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Sample records for inflammation atherosclerosis calcification

  1. Pathology of Human Coronary and Carotid Artery Atherosclerosis and Vascular Calcification in Diabetes Mellitus.

    Science.gov (United States)

    Yahagi, Kazuyuki; Kolodgie, Frank D; Lutter, Christoph; Mori, Hiroyoshi; Romero, Maria E; Finn, Aloke V; Virmani, Renu

    2017-02-01

    The continuing increase in the prevalence of diabetes mellitus in the general population is predicted to result in a higher incidence of cardiovascular disease. Although the mechanisms of diabetes mellitus-associated progression of atherosclerosis are not fully understood, at clinical and pathological levels, there is an appreciation of increased disease burden and higher levels of arterial calcification in these subjects. Plaques within the coronary arteries of patients with diabetes mellitus generally exhibit larger necrotic cores and significantly greater inflammation consisting mainly of macrophages and T lymphocytes relative to patients without diabetes mellitus. Moreover, there is a higher incidence of healed plaque ruptures and positive remodeling in hearts from subjects with type 1 diabetes mellitus and type 2 diabetes mellitus, suggesting a more active atherogenic process. Lesion calcification in the coronary, carotid, and other arterial beds is also more extensive. Although the role of coronary artery calcification in identifying cardiovascular disease and predicting its outcome is undeniable, our understanding of how key hormonal and physiological alterations associated with diabetes mellitus such as insulin resistance and hyperglycemia influence the process of vascular calcification continues to grow. Important drivers of atherosclerotic calcification in diabetes mellitus include oxidative stress, endothelial dysfunction, alterations in mineral metabolism, increased inflammatory cytokine production, and release of osteoprogenitor cells from the marrow into the circulation. Our review will focus on the pathophysiology of type 1 diabetes mellitus- and type 2 diabetes mellitus-associated vascular disease with particular focus on coronary and carotid atherosclerotic calcification. © 2016 American Heart Association, Inc.

  2. BMD PREDICTION OF DEATH IS ENCAPSULATED BY THE MORPHOLOGICAL ATHEROSCLEROSIS CALCIFICATION DISTRIBUTION (MACD) INDEX

    DEFF Research Database (Denmark)

    Ganz, Melanie; Nielsen, Mads; Karsdal, Morten

    2009-01-01

    .3±0.3 years and of which CVD, cancer, and all cause deaths were recorded. The spine BMD and aortic calcification markers, AC24 and the recently proposed Morphological Atherosclerosis Calcification Distribution (MACD) index, were quantified from DXA scans and lateral X-rays respectively. The MACD...

  3. Raman spectroscopy imaging reveals interplay between atherosclerosis and medial calcification in the human aorta

    Science.gov (United States)

    You, Amanda Y. F.; Bergholt, Mads S.; St-Pierre, Jean-Philippe; Kit-Anan, Worrapong; Pence, Isaac J.; Chester, Adrian H.; Yacoub, Magdi H.; Bertazzo, Sergio; Stevens, Molly M.

    2017-01-01

    Medial calcification in the human aorta accumulates during aging and is known to be aggravated in several diseases. Atherosclerosis, another major cause of cardiovascular calcification, shares some common aggravators. However, the mechanisms of cardiovascular calcification remain poorly understood. To elucidate the relationship between medial aortic calcification and atherosclerosis, we characterized the cross-sectional distributions of the predominant minerals in aortic tissue, apatite and whitlockite, and the associated extracellular matrix. We also compared the cellular changes between atherosclerotic and nonatherosclerotic human aortic tissues. This was achieved through the development of Raman spectroscopy imaging methods that adapted algorithms to distinguish between the major biomolecules present within these tissues. We present a relationship between apatite, cholesterol, and triglyceride in atherosclerosis, with the relative amount of all molecules concurrently increased in the atherosclerotic plaque. Further, the increase in apatite was disproportionately large in relation to whitlockite in the aortic media directly underlying a plaque, indicating that apatite is more pathologically significant in atherosclerosis-aggravated medial calcification. We also discovered a reduction of β-carotene in the whole aortic intima, including a plaque in atherosclerotic aortic tissues compared to nonatherosclerotic tissues. This unprecedented biomolecular characterization of the aortic tissue furthers our understanding of pathological and physiological cardiovascular calcification events in humans. PMID:29226241

  4. Molecular Imaging of Inflammation in Atherosclerosis

    Science.gov (United States)

    Wildgruber, Moritz; Swirski, Filip K.; Zernecke, Alma

    2013-01-01

    Acute rupture of vulnerable plaques frequently leads to myocardial infarction and stroke. Within the last decades, several cellular and molecular players have been identified that promote atherosclerotic lesion formation, maturation and plaque rupture. It is now widely recognized that inflammation of the vessel wall and distinct leukocyte subsets are involved throughout all phases of atherosclerotic lesion development. The mechanisms that render a stable plaque unstable and prone to rupture, however, remain unknown and the identification of the vulnerable plaque remains a major challenge in cardiovascular medicine. Imaging technologies used in the clinic offer minimal information about the underlying biology and potential risk for rupture. New imaging technologies are therefore being developed, and in the preclinical setting have enabled new and dynamic insights into the vessel wall for a better understanding of this complex disease. Molecular imaging has the potential to track biological processes, such as the activity of cellular and molecular biomarkers in vivo and over time. Similarly, novel imaging technologies specifically detect effects of therapies that aim to stabilize vulnerable plaques and silence vascular inflammation. Here we will review the potential of established and new molecular imaging technologies in the setting of atherosclerosis, and discuss the cumbersome steps required for translating molecular imaging approaches into the clinic. PMID:24312156

  5. Osteocalcin, Vascular Calcification, and Atherosclerosis: A Systematic Review and Meta-analysis

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    Sophie A. Millar

    2017-07-01

    Full Text Available BackgroundOsteocalcin (OC is an intriguing hormone, concomitantly being the most abundant non-collagenous peptide found in the mineralized matrix of bone, and expanding the endocrine function of the skeleton with far-reaching extra-osseous effects. A new line of enquiry between OC and vascular calcification has emerged in response to observations that the mechanism of vascular calcification resembles that of bone mineralisation. To date, studies have reported mixed results. This systematic review and meta-analysis aimed to identify any association between OC and vascular calcification and atherosclerosis.Methods and resultsDatabases were searched for original, peer reviewed human studies. A total of 1,453 articles were retrieved, of which 46 met the eligibility criteria. Overall 26 positive, 17 negative, and 29 neutral relationships were reported for assessments between OC (either concentration in blood, presence of OC-positive cells, or histological staining for OC and extent of calcification or atherosclerosis. Studies that measured OC-positive cells or histological staining for OC reported positive relationships (11 studies. A higher percentage of Asian studies found a negative relationship (36% in contrast to European studies (6%. Studies examining carboxylated and undercarboxylated forms of OC in the blood failed to report consistent results. The meta-analysis found no significant difference between OC concentration in the blood between patients with “atherosclerosis” and control (p = 0.13, n = 1,197.ConclusionNo definitive association was determined between OC and vascular calcification or atherosclerosis; however, the presence of OC-positive cells and histological staining had a consistent positive correlation with calcification or atherosclerosis. The review highlighted several themes, which may influence OC within differing populations leading to inconclusive results. Large, longitudinal studies are required to further

  6. Toll-Like Receptors, Inflammation, and Calcific Aortic Valve Disease

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    Carmen García-Rodríguez

    2018-03-01

    Full Text Available Inflammation, the primary response of innate immunity, is essential to initiate the calcification process underlying calcific aortic valve disease (CAVD, the most prevalent valvulopathy in Western countries. The pathogenesis of CAVD is multifactorial and includes inflammation, hemodynamic factors, fibrosis, and active calcification. In the development of CAVD, both innate and adaptive immune responses are activated, and accumulating evidences show the central role of inflammation in the initiation and propagation phases of the disease, being the function of Toll-like receptors (TLR particularly relevant. These receptors act as sentinels of the innate immune system by recognizing pattern molecules from both pathogens and host-derived molecules released after tissue damage. TLR mediate inflammation via NF-κB routes within and beyond the immune system, and play a crucial role in the control of infection and the maintenance of tissue homeostasis. This review outlines the current notions about the association between TLR signaling and the ensuing development of inflammation and fibrocalcific remodeling in the pathogenesis of CAVD. Recent data provide new insights into the inflammatory and osteogenic responses underlying the disease and further support the hypothesis that inflammation plays a mechanistic role in the initiation and progression of CAVD. These findings make TLR signaling a potential target for therapeutic intervention in CAVD.

  7. Heme oxygenase-1, oxidation, inflammation and atherosclerosis

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    Jesus A Araujo

    2012-07-01

    Full Text Available Atherosclerosis is an inflammatory process of the vascular wall characterized by the infiltration of lipids and inflammatory cells. Oxidative modifications of infiltrating low density lipoproteins and induction of oxidative stress play a major role in lipid retention in the vascular wall, uptake by macrophages and generation of foam cells, a hallmark of this disorder. The vasculature has a plethora of protective resources against oxidation and inflammation, many of them regulated by the Nrf2 transcription factor. Heme oxygenase-1 (HO-1 is a Nrf2-regulated gene that plays a critical role in the prevention of vascular inflammation. It is the inducible isoform of heme oxygenase, responsible for the oxidative cleavage of heme groups leading to the generation of biliverdin, carbon monoxide and release of ferrous iron. HO-1 has important antioxidant, antiinflammatory, antiapoptotic, antiproliferative and immunomodulatory effects in vascular cells, most of which play a significant role in the protection against atherogenesis. HO-1 may also be an important feature in macrophage differentiation and polarization to certain subtypes. The biological effects of HO-1 are largely attributable to its enzymatic activity, which can be conceived as a system with three arms of action, corresponding to its three enzymatic byproducts. HO-1 mediated vascular protection may be due to a combination of systemic and vascular local effects. It is usually expressed at low levels but can be highly upregulated in the presence of several proatherogenic stimuli. The HO-1 system is amenable for use in the development of new therapies, some of them currently under experimental and clinical trials. Interestingly, in contrast to the HO-1 antiatherogenic actions, the expression of its transcriptional regulator Nrf2 leads to proatherogenic effects instead. This article reviews the evidence that supports the antiatherogenic role of HO-1, potential pathways and mechanisms mediating

  8. Dual roles of heparanase in vascular calcification associated with human carotid atherosclerosis

    DEFF Research Database (Denmark)

    Aldi, S.; Eriksson, L.; Kronqvist, M.

    2017-01-01

    Vascular intimal calcification is a hallmark of advanced atherosclerosis and an active process akin to bone remodeling. Heparanase (HPSE) is an endo-β-glucuronidase, which cleaves glycosaminoglycan chains of heparan sulfate proteoglycans. The role of heparanase in osteogenesis and bone remodeling...

  9. Inflammation and immune system interactions in atherosclerosis

    NARCIS (Netherlands)

    Legein, Bart; Temmerman, Lieve; Biessen, Erik A. L.; Lutgens, Esther

    2013-01-01

    Cardiovascular disease (CVD) is the leading cause of mortality worldwide, accounting for 16.7 million deaths each year. The underlying cause of the majority of CVD is atherosclerosis. In the past, atherosclerosis was considered to be the result of passive lipid accumulation in the vessel wall.

  10. RIP3-dependent necrosis induced inflammation exacerbates atherosclerosis

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    Meng, Lingjun, E-mail: menglingjun@nibs.ac.cn [College of Biological Sciences, China Agricultural University, Beijing 100094 (China); National Institute of Biological Sciences, Beijing 102206 (China); Jin, Wei [Institute for Immunology, Tsinghua University, Beijing 100084 (China); Wang, Yuhui [Institute of Cardiovascular Sciences, Health Science Center, Peking University, Beijing 100191 (China); Huang, Huanwei; Li, Jia; Zhang, Cai [National Institute of Biological Sciences, Beijing 102206 (China)

    2016-04-29

    Atherothrombotic vascular disease is already the leading cause of mortality worldwide. Atherosclerosis shares features with diseases caused by chronic inflammation. More attention should concentrates on the innate immunity effect atherosclerosis progress. RIP3 (receptor-interacting protein kinase 3) act through the transcription factor named Nr4a3 (Nuclear orphan receptors) to regulate cytokine production. Deletion RIP3 decreases IL-1α production. Injection of anti-IL-1α antibody protects against the progress of atherosclerosis in ApoE −/− mice. RIP3 as a molecular switch in necrosis, controls macrophage necrotic death caused inflammation. Inhibiting necrosis will certainly reduce atherosclerosis through limit inflammation. Necrotic cell death caused systemic inflammation exacerbated cardiovascular disease. Inhibition of necrosis may yield novel therapeutic targets for treatment in years to come. - Highlights: • RIP3 regulate the Nr4a3 to control cytokine production. • Deletion RIP3 decreases IL-1a production. • Injection anti-IL-1a antibody protects against the progress of atherosclerosis. • RIP3 controls macrophage necrotic dead caused inflammation.

  11. RIP3-dependent necrosis induced inflammation exacerbates atherosclerosis

    International Nuclear Information System (INIS)

    Meng, Lingjun; Jin, Wei; Wang, Yuhui; Huang, Huanwei; Li, Jia; Zhang, Cai

    2016-01-01

    Atherothrombotic vascular disease is already the leading cause of mortality worldwide. Atherosclerosis shares features with diseases caused by chronic inflammation. More attention should concentrates on the innate immunity effect atherosclerosis progress. RIP3 (receptor-interacting protein kinase 3) act through the transcription factor named Nr4a3 (Nuclear orphan receptors) to regulate cytokine production. Deletion RIP3 decreases IL-1α production. Injection of anti-IL-1α antibody protects against the progress of atherosclerosis in ApoE −/− mice. RIP3 as a molecular switch in necrosis, controls macrophage necrotic death caused inflammation. Inhibiting necrosis will certainly reduce atherosclerosis through limit inflammation. Necrotic cell death caused systemic inflammation exacerbated cardiovascular disease. Inhibition of necrosis may yield novel therapeutic targets for treatment in years to come. - Highlights: • RIP3 regulate the Nr4a3 to control cytokine production. • Deletion RIP3 decreases IL-1a production. • Injection anti-IL-1a antibody protects against the progress of atherosclerosis. • RIP3 controls macrophage necrotic dead caused inflammation.

  12. [Chronic mild inflammation links obesity, metabolic syndrome, atherosclerosis and diabetes].

    Science.gov (United States)

    Andel, M; Polák, J; Kraml, P; Dlouhý, P; Stich, V

    2009-01-01

    Chronic low grade inflammation is relatively new concept in metabolic medicine. This concept describes the relations between the inflammation and adipose tissue, insulin resistence, atherosclerosis and type 2 diabetes mellitus. Macrophages and lymphocytes deposed in adipose tissue produce proinflammatory cytokines which directly or through the CRP liver secretion are targeting endothelial cells, hepatocytes and beta cells of Langerhans islets of pancreas. The dysfunction of these cells follows often further disturbances and in case of beta cells - the cell death. The connection between the adipose tissue insulin resistence, atherosclerosis and type 2 diabetes was earlier described with endocrine and metabolic descriptors. The concept of chronic low grade inflammation creates also another description of multilateral connections in metabolic syndome. The salicylates and the drugs related to them seem to have some glucose lowering properties. The recent development in the field ofchronic low grade inflammation represents also certain therapeutic hope for antiinflammatory intervention in type 2 diabetes.

  13. Relation between intracranial artery calcifications and aortic atherosclerosis in ischemic stroke patients.

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    Bugnicourt, Jean-Marc; Chillon, Jean-Marc; Tribouilloy, Christophe; Canaple, Sandrine; Lamy, Chantal; Massy, Ziad A; Godefroy, Olivier

    2010-08-01

    We previously demonstrated a strong relation between carotid atherosclerosis (defined as carotid artery stenosis > or =50%) and intracranial artery calcification (IAC) in ischemic stroke patients. The purpose of this study was to evaluate the relation between aortic atherosclerosis and IAC. Four hundred fifty-four patients with ischemic stroke were included. Complex aortic plaques (CAP) were assessed by transesophageal echocardiography (TEE) and defined as plaques > or =4 mm thick or with mobile components in the proximal aorta. IAC were assessed in the seven major cerebral arteries and a semiquantitative score system was applied, ranging from 0 (no calcification) to 7. Forty-two patients (9.3%) had CAP. Patients with CAP were older compared with patients without CAP (73.6 vs. 63.6 years, p vs. 1.8; p stroke or TIA (OR 3.3; 95%CI 1.5-7.0; p = 0.002), carotid artery stenosis > or =50% (OR 3.7; 95%CI 1.7-8.0; p = 0.001), chronic kidney disease (OR 3.8; 95%CI 1.9-7.8; p stroke patients, the absence of IAC strongly points to the lack of CAP. However, these results warrant confirmation in prospective studies before concluding the non-utility of the use of TEE to exclude CAP as a potential source of cerebral embolism in patients without IAC.

  14. Effect of uremia on HDL composition, vascular inflammation, and atherosclerosis in wild-type mice

    DEFF Research Database (Denmark)

    Bang, Christian A; Bro, Susanne; Bartels, Emil D

    2007-01-01

    Wild-type mice normally do not develop atherosclerosis, unless fed cholic acid. Uremia is proinflammatory and increases atherosclerosis 6- to 10-fold in apolipoprotein E-deficient mice. This study examined the effect of uremia on lipoproteins, vascular inflammation, and atherosclerosis in wild...... in cholic acid-fed sham mice. The results suggest that moderate uremia neither induces aortic inflammation nor atherosclerosis in C57BL/6J mice despite increased LDL/HDL cholesterol ratio and altered HDL composition....

  15. Bisphosphonates, atherosclerosis and vascular calcification: update and systematic review of clinical studies

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    Caffarelli C

    2017-10-01

    Full Text Available Carla Caffarelli,1 Andrea Montagnani,2 Ranuccio Nuti,1 Stefano Gonnelli1 1Department of Medicine, Surgery and Neuroscience, University of Siena, Italy; 2Division of Internal Medicine, General Hospital Misericordia, Grosseto, Italy Background: Epidemiologic and clinical data have suggested the existence of a biologic linkage between the bone system and the vascular system. Bisphosphonates (BPs are effective inhibitors of bone resorption and are currently considered the drugs of choice for the prevention and treatment of osteoporosis and related fractures. Data from several publications have suggested that BPs may also be effective in reducing the atherosclerotic process and vascular calcification, but the results of these studies are contrasting. This review aimed to allow a better understanding of the relationships between BPs and atherosclerosis in humans.Materials and methods: Electronic databases of Pubmed-Medline, Cochrane Library and SCOPUS from inception to June 30, 2016 were searched. The full texts of the articles potentially eligible were carefully assessed and reviewed. Finally, 20 studies were found to be eligible and were included in the systematic review. All included studies were published between 2000 and 2014.Results: In several studies, etidronate limited the progression of aortic and coronary calcification in hemodialysis patients, whereas the nitrogen-containing-BPs given orally did not significantly reduce vascular calcifications in patients with chronic kidney disease, kidney trasplant or in those with osteoporosis. Nitrogen-containing-BPs present favorable effects both on vessel wall thickness and on arterial elasticity due to both a reduction in serum lipids and the interaction of BPs with the bone tissue, with the consequent release of bone turnover markers and cytokines into the bloodstream.Conclusion: To sum up, the BPs seem to have the potential of influencing atherosclerosis and calcium homeostasis at the level of

  16. Inflammation of vertebral bone associated with acute calcific tendinitis of the longus colli muscle

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    Mihmanli, I.; Kanberoglu, K. [Dept. of Radiology, Istanbul Univ. (Turkey); Karaarslan, E. [Intermed Medical Center, Nisantasi, Istanbul (Turkey)

    2001-12-01

    We present a case of acute retropharyngeal calcific tendinitis with characteristic findings on radiographic, computed tomography, and magnetic resonance imaging (MRI). To our knowledge, this is the first acute retropharyngeal calcific tendinitis report having inflammation of both the vertebra itself and the longus colli muscle diagnosed on MRI. In patients with neck pain, acute retropharyngeal calcific tendinitis should be kept in mind in the differential diagnosis, even if these patients had vertebral pathological signals on MRI. (orig.)

  17. Inflammation of vertebral bone associated with acute calcific tendinitis of the longus colli muscle

    International Nuclear Information System (INIS)

    Mihmanli, I.; Kanberoglu, K.; Karaarslan, E.

    2001-01-01

    We present a case of acute retropharyngeal calcific tendinitis with characteristic findings on radiographic, computed tomography, and magnetic resonance imaging (MRI). To our knowledge, this is the first acute retropharyngeal calcific tendinitis report having inflammation of both the vertebra itself and the longus colli muscle diagnosed on MRI. In patients with neck pain, acute retropharyngeal calcific tendinitis should be kept in mind in the differential diagnosis, even if these patients had vertebral pathological signals on MRI. (orig.)

  18. Chronic skin inflammation accelerates macrophage cholesterol crystal formation and atherosclerosis

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    Ng, Qimin; Sanda, Gregory E.; Dey, Amit K.; Teague, Heather L.; Sorokin, Alexander V.; Dagur, Pradeep K.; Silverman, Joanna I.; Harrington, Charlotte L.; Rodante, Justin A.; Rose, Shawn M.; Varghese, Nevin J.; Belur, Agastya D.; Goyal, Aditya; Gelfand, Joel M.; Springer, Danielle A.; Bleck, Christopher K.E.; Thomas, Crystal L.; Yu, Zu-Xi; Winge, Mårten C.G.; Kruth, Howard S.; Marinkovich, M. Peter; Joshi, Aditya A.; Playford, Martin P.; Mehta, Nehal N.

    2018-01-01

    Inflammation is critical to atherogenesis. Psoriasis is a chronic inflammatory skin disease that accelerates atherosclerosis in humans and provides a compelling model to understand potential pathways linking these diseases. A murine model capturing the vascular and metabolic diseases in psoriasis would accelerate our understanding and provide a platform to test emerging therapies. We aimed to characterize a new murine model of skin inflammation (Rac1V12) from a cardiovascular standpoint to identify novel atherosclerotic signaling pathways modulated in chronic skin inflammation. The RacV12 psoriasis mouse resembled the human disease state, including presence of systemic inflammation, dyslipidemia, and cardiometabolic dysfunction. Psoriasis macrophages had a proatherosclerotic phenotype with increased lipid uptake and foam cell formation, and also showed a 6-fold increase in cholesterol crystal formation. We generated a triple-genetic K14-RacV12–/+/Srb1–/–/ApoER61H/H mouse and confirmed psoriasis accelerates atherogenesis (~7-fold increase). Finally, we noted a 60% reduction in superoxide dismutase 2 (SOD2) expression in human psoriasis macrophages. When SOD2 activity was restored in macrophages, their proatherogenic phenotype reversed. We demonstrate that the K14-RacV12 murine model captures the cardiometabolic dysfunction and accelerates vascular disease observed in chronic inflammation and that skin inflammation induces a proatherosclerotic macrophage phenotype with impaired SOD2 function, which associated with accelerated atherogenesis. PMID:29321372

  19. The effects of 3-month atorvastatin therapy on arterial inflammation, calcification, abdominal adipose tissue and circulating biomarkers

    Energy Technology Data Exchange (ETDEWEB)

    Wu, Yen-Wen [National Taiwan University Hospital, Department of Internal Medicine, Taipei (China); National Taiwan University Hospital, Department of Nuclear Medicine, Taipei (China); Kao, Hsian-Li; Chen, Ming-Fong; Lin, Lian-Yu; Wang, Yi-Chih; Lin, Yen-Hung; Lin, Hung-Ju; Huang, Por-Jau [National Taiwan University Hospital, Department of Internal Medicine, Taipei (China); Huang, Chi-Lun [Tao-Yuan General Hospital, Department of Internal Medicine, Tao-Yuan (China); Tzen, Kai-Yuan; Yen, Ruoh-Fang [National Taiwan University Hospital, Department of Nuclear Medicine, Taipei (China); Chi, Yu-Chiao [National Taiwan University, Graduate Institute of Clinical Medicine, College of Medicine, Taipei (China); Yang, Wei-Shiung [National Taiwan University Hospital, Department of Internal Medicine, Taipei (China); National Taiwan University, Graduate Institute of Clinical Medicine, College of Medicine, Taipei (China)

    2012-03-15

    {sup 18}F-Fluorodeoxyglucose (FDG) positron emission tomography (PET)/CT has the potential to track vascular inflammation and monitor therapeutic response. The purpose of this study was to determine the association between arterial inflammation, calcification and serological biomarkers in subjects with atherosclerosis, and to assess their therapeutic response to 12-week atorvastatin treatment. Forty-three statin-naive subjects with atherosclerosis received atorvastatin (40 mg/day) for 12 weeks and underwent {sup 18}F-FDG PET/CT, coronary calcification and abdominal adipose tissue volume measurements. A panel of serological biomarkers was analysed. Arterial inflammation was measured at seven arterial segments and normalized to venous FDG activity to produce target to background ratios (TBR). Thirty-four subjects without cardiovascular disease who repeated PET 1-4 years apart for routine health check-ups were retrospectively evaluated for comparison. The baseline mean TBR values in atherosclerotic patients were positively correlated with age (R = 0.36), body mass index (R = 0.54), abdominal visceral adipose tissue volume (R = 0.65), coronary calcification score (R = 0.40), levels of low-density lipoprotein cholesterol (R = 0.54), matrix metalloproteinase (MMP)-9 (R = 0.46) and fatty acid binding protein 4 (FABP4) (R = 0.67, all p < 0.05). The TBR as well as high-sensitivity C-reactive protein (hsCRP), E-selectin, MMP-9, monocyte chemotactic protein 1, FABP4 and follistatin values were reduced significantly after the 12-week atorvastatin treatment. The TBR reduction marginally correlated with changes in MMP-9 levels (R = 0.56, p = 0.05). The control group, whose median age was younger, by comparison had lower hsCRP and arterial TBR than the subjects with atherosclerosis (all p < 0.05), and moreover had a slight but insignificant increase in mean TBR at their 2.5{+-}0.8 year follow-up. The medium dose of atorvastatin over a 12-week period resulted in a significant

  20. The effects of 3-month atorvastatin therapy on arterial inflammation, calcification, abdominal adipose tissue and circulating biomarkers

    International Nuclear Information System (INIS)

    Wu, Yen-Wen; Kao, Hsian-Li; Chen, Ming-Fong; Lin, Lian-Yu.; Wang, Yi-Chih; Lin, Yen-Hung; Lin, Hung-Ju; Huang, Por-Jau; Huang, Chi-Lun; Tzen, Kai-Yuan; Yen, Ruoh-Fang; Chi, Yu-Chiao; Yang, Wei-Shiung

    2012-01-01

    18 F-Fluorodeoxyglucose (FDG) positron emission tomography (PET)/CT has the potential to track vascular inflammation and monitor therapeutic response. The purpose of this study was to determine the association between arterial inflammation, calcification and serological biomarkers in subjects with atherosclerosis, and to assess their therapeutic response to 12-week atorvastatin treatment. Forty-three statin-naive subjects with atherosclerosis received atorvastatin (40 mg/day) for 12 weeks and underwent 18 F-FDG PET/CT, coronary calcification and abdominal adipose tissue volume measurements. A panel of serological biomarkers was analysed. Arterial inflammation was measured at seven arterial segments and normalized to venous FDG activity to produce target to background ratios (TBR). Thirty-four subjects without cardiovascular disease who repeated PET 1-4 years apart for routine health check-ups were retrospectively evaluated for comparison. The baseline mean TBR values in atherosclerotic patients were positively correlated with age (R = 0.36), body mass index (R = 0.54), abdominal visceral adipose tissue volume (R = 0.65), coronary calcification score (R = 0.40), levels of low-density lipoprotein cholesterol (R = 0.54), matrix metalloproteinase (MMP)-9 (R = 0.46) and fatty acid binding protein 4 (FABP4) (R = 0.67, all p < 0.05). The TBR as well as high-sensitivity C-reactive protein (hsCRP), E-selectin, MMP-9, monocyte chemotactic protein 1, FABP4 and follistatin values were reduced significantly after the 12-week atorvastatin treatment. The TBR reduction marginally correlated with changes in MMP-9 levels (R = 0.56, p = 0.05). The control group, whose median age was younger, by comparison had lower hsCRP and arterial TBR than the subjects with atherosclerosis (all p < 0.05), and moreover had a slight but insignificant increase in mean TBR at their 2.5±0.8 year follow-up. The medium dose of atorvastatin over a 12-week period resulted in a significant reduction of

  1. Modulation of genes involved in inflammation and cell death in atherosclerosis-susceptible mice

    NARCIS (Netherlands)

    Zadelaar, Anna Susanne Maria

    2006-01-01

    In this thesis we focus on atherosclerosis as the main cause of cardiovascular disease. Since inflammation and cell death are important processes in the onset and progression of atherosclerosis, we investigate the role of several genes involved in inflammation and cell death in the vessel wall and

  2. Effects of dietary calcium on atherosclerosis, aortic calcification, and icterus in rabbits fed a supplemental cholesterol diet

    Directory of Open Access Journals (Sweden)

    Culley Nathan C

    2006-06-01

    Full Text Available Abstract Background Vascular calcification is implicated in myocardial infarction, instability and rigidity of the aortic wall, and bioprosthetic failures. Although an increase in the calcium (Ca content in atherogenic diets has been shown to decrease atherosclerosis in rabbits, whether Ca supplementation and deficiency can affect atherosclerosis-related aortic calcification remains unknown. Results New Zealand White male rabbit littermates were fed an atherogenic diet containing 0.5% cholesterol and 2% peanut oil. The Ca content of the diet, which normally contains 1%, was adjusted to 0.5 or 3%. Segments of thoracic aortas were dissected from rabbits for histological evaluations and Ca and Pi determinations. Rabbits with calcium supplementation were maintained for 4 months, whereas those with calcium deficiency were maintained for 2 1/2 months due to severe icterus beyond this stage. The ratios of intimal to medial areas and calcified to intimal areas were used to semi-quantify lesion accumulation and calcification, respectively. Icterus was estimated from the extent of yellowing of the skin, sclera, and mucous membranes along with gross evidence of hepatic lipidosis and/or biliary obstructions. Statistical analysis of 16 matched littermates shows that Ca supplementation significantly decreased the lesions by 41% (p Conclusion Ca supplementation to an atherogenic diet inhibits atherosclerosis, aortic calcification, and icterus, whereas a Ca deficient-diet promotes them.

  3. Alloxan-induced diabetes exacerbates coronary atherosclerosis and calcification in Ossabaw miniature swine with metabolic syndrome.

    Science.gov (United States)

    Badin, Jill K; Kole, Ayeeshik; Stivers, Benjamin; Progar, Victor; Pareddy, Anisha; Alloosh, Mouhamad; Sturek, Michael

    2018-03-09

    There is a preponderance of evidence implicating diabetes with increased coronary artery disease (CAD) and calcification (CAC) in human patients with metabolic syndrome (MetS), but the effect of diabetes on CAD severity in animal models remains controversial. We investigated whether diabetes exacerbates CAD/CAC and intracellular free calcium ([Ca 2+ ] i ) dysregulation in the clinically relevant Ossabaw miniature swine model of MetS. Sixteen swine, eight with alloxan-induced diabetes, were fed a hypercaloric, atherogenic diet for 6 months. Alloxan-induced pancreatic beta cell damage was examined by immunohistochemical staining of insulin. The metabolic profile was confirmed by body weight, complete blood panel, intravenous glucose tolerance test (IVGTT), and meal tolerance test. CAD severity was assessed with intravascular ultrasound and histology. [Ca 2+ ] i handling in coronary smooth muscle (CSM) cells was assessed with fura-2 ratiometric imaging. Fasting and post-prandial blood glucose, total cholesterol, and serum triglycerides were elevated in MetS-diabetic swine. This group also exhibited hypoinsulinemia during IVGTT and less pancreatic beta cell mass when compared to lean and MetS-nondiabetic swine. IVUS analysis revealed that MetS-diabetic swine had greater percent wall coverage, percent plaque burden, and calcium index when compared to lean and MetS-nondiabetic swine. Fura-2 imaging of CSM [Ca 2+ ] i revealed that MetS-nondiabetic swine exhibited increased sarcoplasmic reticulum Ca 2+ store release and Ca 2+ influx through voltage-gated Ca 2+ channels compared to lean swine. MetS-diabetic swine exhibited impaired Ca 2+ efflux. Diabetes exacerbates coronary atherosclerosis and calcification in Ossabaw miniature swine with MetS, accompanied by progression of [Ca 2+ ] i dysregulation in advanced CAD/CAC. These results recapitulate increased CAD in humans with diabetes and establish Ossabaw miniature swine as an animal model for future Met

  4. A novel ultrasound-based vascular calcification score (CALCS) to detect subclinical atherosclerosis.

    Science.gov (United States)

    Flore, R; Zocco, M A; Ainora, M E; Fonnesu, C; Nesci, A; Gasbarrini, A; Ponziani, F R

    2018-02-01

    To quantify non-coronary vascular calcifications (VC) in asymptomatic patients at low-intermediate cardiovascular risk by a new color Doppler ultrasound (DUS)-based score (the carotid, aortic, lower limbs calcium score, CALCs), and to correlate this score with classical parameters associated with cardiovascular risk [carotid intima media thickness (IMT), and arterial stiffness (AS)]. All consecutive asymptomatic patients who underwent a screening DUS of non-coronary circulation were evaluated and patients at low-intermediate cardiovascular risk were selected according to Framingham risk score (FRS). Among them, we enrolled 70 patients with US evidence of VC and 71 age, sex and FRS matched controls. The presence of VC was correlated with classical markers of cardiovascular risk, such as AS and intima-media thickness (IMT). AS, expressed as pulse wave velocity (PWV) and arterial distensibility, carotid IMT and CALCs were measured for both groups. AS and c-IMT were assessed by a new Radio-Frequency (RF) DUS-based method. CALCs was generated by our previously described B-mode DUS-based method according to number/size of VC in 11 non-coronary segments (range 0-33). Patients with VC presented higher AS and IMT values than controls (PWV 8.34±0.98 m/s vs. 6.74±0.68 m/s, p<0.0001; arterial distensibility 267±12 mm vs. 315±65 mm, p=0.001; IMT 687±132 mm vs. 572±91 mm, p<0.0001). Mean CALCs of patients with VC was 8.41±7.78. CALCs were significantly correlated with c-IMT (p<0.0001; r=0.3), PWV (p<0.0001; r=0.4) and arterial distensibility (p=0.002; r=-0.1). DUS-based CALCs is highly correlated with other validated markers of subclinical atherosclerosis, such as c-IMT and AS. Our results demonstrated the ability of CALCs to identify individual predictive factors beyond the traditional risk factors by quantifying an interesting and novel step of the atherogenic process. Future studies on larger series and with adequate follow up are necessary to confirm these results and

  5. Relationship of Aortic Wall Distensibility to Mitral and Aortic Valve Calcification: The Multi-Ethnic Study of Atherosclerosis.

    Science.gov (United States)

    Cohoon, Kevin P; Criqui, Michael H; Budoff, Matthew J; Lima, Joao A; Blaha, Michael J; Decker, Paul A; Durazo, Ramon; Liu, Kiang; Kramer, Holly

    2018-05-01

    Data are limited on whether valvular calcification is associated with aortic wall stiffness. We tested whether aortic valve calcification (AVC) and/or mitral valve calcification (MVC) is inversely associated with aortic distensibility (AD). Cross-sectional study conducted in a subset of the Multi-Ethnic Study of Atherosclerosis (MESA) included 3676 MESA participants aged 44 to 84 years with AD measured with magnetic resonance imaging and with AVC and MVC measured with noncontrast cardiac computed tomography scans. Both AVC and MVC were divided into 3 categories: zero, AVC and MVC, while 6% (n = 211) and 4% (n = 156) had low, and 6% (n = 209) and 4% (n = 155) had high values of AVC and MVC, respectively. The AVC was independently associated with AD after adjusting for age, gender, and ethnicity ( P = .035). No association was noted between AVC groups and AD after adjustment for all covariates or MVC groups and AD in any model.

  6. Atherosclerosis and liver inflammation induced by increased dietary cholesterol intake: A combined transcriptomics and metabolomics analysis

    NARCIS (Netherlands)

    Kleemann, R.; Verschuren, L.; Erk, M.J. van; Nikolsky, Y.; Cnubben, N.H.P.; Verheij, E.R.; Smilde, A.K.; Hendriks, H.F.J.; Zadelaar, A.S.M.; Smith, G.J.; Kaznacheev, V.; Nikolskaya, T.; Melnikov, A.; Hurt-Camejo, E.; Greef, J. van der; Ommen, B. van; Kooistra, T.

    2007-01-01

    Background: Increased dietary cholesterol intake is associated with atherosclerosis. Atherosclerosis development requires a lipid and an inflammatory component. It is unclear where and how the inflammatory component develops. To assess the role of the liver in the evolution of inflammation, we

  7. Induction of calcification by serum depletion in cell culture: a model for focal calcification in aortas related to atherosclerosis

    Directory of Open Access Journals (Sweden)

    Villar Maria T

    2008-01-01

    Full Text Available Abstract Background Since aortic calcification has been shown to initiate in the lower zone of well-thickened plaques (LZP adjacent to the aortic media of rabbits fed supplemental cholesterol diets, a restricted supply of serum to vascular cells could play a role in vascular calcification. This study was designed to use a cell culture model to support this hypothesis. Results Rabbit aortic smooth muscle cells were grown to confluence in a culture media containing 10 % fetal bovine serum (FBS. The confluent cells were then exposed to the media for 2 hrs with or without serum at a Ca × P ion product range of 4.5–9.4 mM2. In contrast to the cells cultured in the presence of FBS, confluent cells in its absence displayed marked mineral-positive alizarin red staining and infrared absorption of mineral phosphate. A kinetic parameter C1/2 was used to designate the concentration of serum or its protein constituents needed to reduce the deposition of Ca and P by half. The C1/2 for FBS and rabbit serum was 0.04–0.07 % The C1/2 value for rabbit serum proteins was 13.5 μg/ml corresponding to the protein concentration in 0.06 % of serum. This C1/2 was markedly smaller than 86.2 μg/ml for bovine serum albumin present in 0.37 % serum (p Conclusion The aortic smooth muscle cell culture model suggests that serum depletion may play a role in the initiation of aortic calcification. The serum exhibits remarkable ability to inhibit cell-mediated calcification.

  8. Proatherogenic pathways leading to vascular calcification

    International Nuclear Information System (INIS)

    Mazzini, Michael J.; Schulze, P. Christian

    2006-01-01

    Cardiovascular disease is the leading cause of morbidity and mortality in the western world and atherosclerosis is the major common underlying disease. The pathogenesis of atherosclerosis involves local vascular injury, inflammation and oxidative stress as well as vascular calcification. Vascular calcification has long been regarded as a degenerative process leading to mineral deposition in the vascular wall characteristic for late stages of atherosclerosis. However, recent studies identified vascular calcification in early stages of atherosclerosis and its occurrence has been linked to clinical events in patients with cardiovascular disease. Its degree correlates with local vascular inflammation and with the overall impact and the progression of atherosclerosis. Over the last decade, diverse and highly regulated molecular signaling cascades controlling vascular calcification have been described. Local and circulating molecules such as osteopontin, osteoprogerin, leptin and matrix Gla protein were identified as critical regulators of vascular calcification. We here review the current knowledge on molecular pathways of vascular calcification and their relevance for the progression of cardiovascular disease

  9. The effect of aging on atherosclerotic plaque inflammation and molecular calcification: A PET CT imaging study

    DEFF Research Database (Denmark)

    Blomberg, Björn; Thomassen, Anders; Simonsen, Jane Angel

    Aim: Aging is an important independent risk factor for the inception and maturation of atherosclerotic plaques. This study aimed to investigate the effect of aging on atherosclerotic plaque inflammation and molecular calcification. Methods: Thirteen healthy volunteers without traditional......SUV) [Mean SUVAORTA - Mean SUVBLOOD POOL]. Furthermore, the average maximum 18F-NaF cSUV was determined in the coronary arteries. Calculating regression and correlation coefficients summarized the data. Results: A quadratic relationship was observed between aging and aortic 18F-FDG avidity. A second order...... polynomial regression established that aging is a strong predictor of the degree of aortic plaque inflammation (R2 = 0.71, F statistic = 11.98, P = 0.002). A linear relationship was observed between aging and molecular calcification. Linear regression established that aging is a predictor of both the degree...

  10. Liraglutide Reduces Both Atherosclerosis and Kidney Inflammation in Moderately Uremic LDLr-/- Mice.

    Directory of Open Access Journals (Sweden)

    Line S Bisgaard

    Full Text Available Chronic kidney disease (CKD leads to uremia. CKD is characterized by a gradual increase in kidney fibrosis and loss of kidney function, which is associated with a progressive increase in risk of atherosclerosis and cardiovascular death. To prevent progression of both kidney fibrosis and atherosclerosis in uremic settings, insight into new treatment options with effects on both parameters is warranted. The GLP-1 analogue liraglutide improves glucose homeostasis, and is approved for treatment of type 2 diabetes. Animal studies suggest that GLP-1 also dampens inflammation and atherosclerosis. Our aim was to examine effects of liraglutide on kidney fibrosis and atherosclerosis in a mouse model of moderate uremia (5/6 nephrectomy (NX. Uremic (n = 29 and sham-operated (n = 14 atherosclerosis-prone low density lipoprotein receptor knockout mice were treated with liraglutide (1000 μg/kg, s.c. once daily or vehicle for 13 weeks. As expected, uremia increased aortic atherosclerosis. In the remnant kidneys from NX mice, flow cytometry revealed an increase in the number of monocyte-like cells (CD68+F4/80-, CD4+, and CD8+ T-cells, suggesting that moderate uremia induced kidney inflammation. Furthermore, markers of fibrosis (i.e. Col1a1 and Col3a1 were upregulated, and histological examinations showed increased glomerular diameter in NX mice. Importantly, liraglutide treatment attenuated atherosclerosis (~40%, p < 0.05 and reduced kidney inflammation in NX mice. There was no effect of liraglutide on expression of fibrosis markers and/or kidney histology. This study suggests that liraglutide has beneficial effects in a mouse model of moderate uremia by reducing atherosclerosis and attenuating kidney inflammation.

  11. Serum phosphate is associated with aortic valve calcification in the Multi-ethnic Study of Atherosclerosis (MESA).

    Science.gov (United States)

    Linefsky, Jason P; O'Brien, Kevin D; Sachs, Michael; Katz, Ronit; Eng, John; Michos, Erin D; Budoff, Matthew J; de Boer, Ian; Kestenbaum, Bryan

    2014-04-01

    This study sought to investigate associations of phosphate metabolism biomarkers with aortic valve calcification (AVC). Calcific aortic valve disease (CAVD) is a common progressive condition that involves inflammatory and calcification mediators. Currently there are no effective medical treatments, but mineral metabolism pathways may be important in the development and progression of disease. We examined associations of phosphate metabolism biomarkers, including serum phosphate, urine phosphate, parathyroid hormone (PTH) and serum fibroblast growth factor (FGF)-23, with CT-assessed AVC at study baseline and in short-term follow-up in 6814 participants of the Multi-Ethnic Study of Atherosclerosis (MESA). At baseline, AVC prevalence was 13.2%. Higher serum phosphate levels were associated with significantly greater AVC prevalence (relative risk 1.3 per 1 mg/dL increment, 95% confidence incidence: 1.1 to 1.5, pAVC. Average follow-up CT evaluation was 2.4 years (range 0.9-4.9 years) with an AVC incidence of 4.1%. Overall, phosphate metabolism biomarkers were not associated with incident AVC except in the top FGF-23 quartile. Serum phosphate levels are significantly associated with AVC prevalence. Further study of phosphate metabolism as a modifiable risk factor for AVC is warranted. Published by Elsevier Ireland Ltd.

  12. Breast arterial calcification and risk of carotid atherosclerosis: Focusing on the preferentially affected layer of the vessel wall

    Energy Technology Data Exchange (ETDEWEB)

    Sedighi, Nahid, E-mail: nsedighi@sina.tums.ac.ir [Department of Radiology, Shariati Hospital, Tehran University of Medical Sciences. North Kargar Ave., Tehran 14114 (Iran, Islamic Republic of); Radmard, Amir Reza, E-mail: radmard@ams.ac.ir [Department of Radiology, Shariati Hospital, Tehran University of Medical Sciences. North Kargar Ave., Tehran 14114 (Iran, Islamic Republic of); Radmehr, Ali, E-mail: radmehr@sina.tums.ac.ir [Department of Radiology, Shariati Hospital, Tehran University of Medical Sciences. North Kargar Ave., Tehran 14114 (Iran, Islamic Republic of); Hashemi, Pari, E-mail: phtums@yahoo.com [Department of Radiology, Shariati Hospital, Tehran University of Medical Sciences. North Kargar Ave., Tehran 14114 (Iran, Islamic Republic of); Hajizadeh, Abdolmahmoud, E-mail: mroomezi@yahoo.com [Department of Radiology, Shariati Hospital, Tehran University of Medical Sciences. North Kargar Ave., Tehran 14114 (Iran, Islamic Republic of); Taheri, Amir Pejman Hashemi, E-mail: hashemip@sina.tums.ac.ir [Department of Radiology, Shariati Hospital, Tehran University of Medical Sciences. North Kargar Ave., Tehran 14114 (Iran, Islamic Republic of)

    2011-08-15

    Objective: To assess the relationship between breast arterial calcification (BAC) detected on screening mammography and atherosclerosis of carotid arteries considering the most likely involved layer of the arterial wall. Materials and methods: A total of 537 consecutive women who underwent screening mammography were enrolled in this study. Seventy-nine subjects having BAC, aged 46-75 years, and 125 age-matched controls from those without BAC were selected for ultrasound examination of carotid arteries assessing intima-media thickness (IMT) and plaque presence. Participants were divided into three groups of risk including, low-risk: IMT < 0.6 mm without plaque, medium-risk: 0.6 mm {<=} IMT {<=} 0.8 mm without plaque and high-risk: IMT > 0.8 mm and/or plaque. Risk factors for atherosclerosis were obtained from medical records for independent effects. Results: BAC was present in 14.7% of mammograms. According to multivariable logistic regression analyses, significant association was identified between the carotid atherosclerosis risk and presence of BAC. Compared to women with IMT < 0.6 mm, those with 0.6 mm {<=} IMT{<=} 0.8 mm and IMT > 0.8 mm had OR (95% CI) of 4.88 (1.47-16.16) and 23.36 (4.54-120.14), respectively. The OR (95% CI) for carotid plaque was 3.13 (1.3-7.57). There was no interaction between IMT category and plaque. Significant associations were also detected with postmenopausal duration (P = 0.02) and hypertension (P = 0.004). Conclusion: The risk of carotid atherosclerosis increases with the presence of BAC. Women with BAC are more likely to have thicker IMT than plaque, which could be attributed to the preferentially similar affected layer of media causing thick IMT rather than plaque.

  13. Breast arterial calcification and risk of carotid atherosclerosis: Focusing on the preferentially affected layer of the vessel wall

    International Nuclear Information System (INIS)

    Sedighi, Nahid; Radmard, Amir Reza; Radmehr, Ali; Hashemi, Pari; Hajizadeh, Abdolmahmoud; Taheri, Amir Pejman Hashemi

    2011-01-01

    Objective: To assess the relationship between breast arterial calcification (BAC) detected on screening mammography and atherosclerosis of carotid arteries considering the most likely involved layer of the arterial wall. Materials and methods: A total of 537 consecutive women who underwent screening mammography were enrolled in this study. Seventy-nine subjects having BAC, aged 46-75 years, and 125 age-matched controls from those without BAC were selected for ultrasound examination of carotid arteries assessing intima-media thickness (IMT) and plaque presence. Participants were divided into three groups of risk including, low-risk: IMT 0.8 mm and/or plaque. Risk factors for atherosclerosis were obtained from medical records for independent effects. Results: BAC was present in 14.7% of mammograms. According to multivariable logistic regression analyses, significant association was identified between the carotid atherosclerosis risk and presence of BAC. Compared to women with IMT 0.8 mm had OR (95% CI) of 4.88 (1.47-16.16) and 23.36 (4.54-120.14), respectively. The OR (95% CI) for carotid plaque was 3.13 (1.3-7.57). There was no interaction between IMT category and plaque. Significant associations were also detected with postmenopausal duration (P = 0.02) and hypertension (P = 0.004). Conclusion: The risk of carotid atherosclerosis increases with the presence of BAC. Women with BAC are more likely to have thicker IMT than plaque, which could be attributed to the preferentially similar affected layer of media causing thick IMT rather than plaque.

  14. Short-term changes in arterial inflammation predict long-term changes in atherosclerosis progression

    Energy Technology Data Exchange (ETDEWEB)

    Joseph, Philip [Massachusetts General Hospital and Harvard Medical School, Cardiology Division and Cardiac MR PET CT Program, Boston, MA (United States); McMaster University, Population Health Research Institute, Department of Medicine, and Department of Radiology, Hamilton, ON (Canada); Ishai, Amorina; Tawakol, Ahmed [Massachusetts General Hospital and Harvard Medical School, Cardiology Division and Cardiac MR PET CT Program, Boston, MA (United States); Mani, Venkatesh [Icahn School of Medicine at Mount Sinai School of Medicine, Translational and Molecular Imaging Institute and Department of Radiology, New York, NY (United States); Kallend, David [The Medicines Company, Parsippany, NJ (United States); Rudd, James H.F. [University of Cambridge, Division of Cardiovascular Medicine, Cambridge (United Kingdom); Fayad, Zahi A. [Icahn School of Medicine at Mount Sinai School of Medicine, Translational and Molecular Imaging Institute and Department of Radiology, New York, NY (United States); Icahn School of Medicine at Mount Sinai School of Medicine, Hess CSM Building Floor TMII, Rm S1-104, Translational and Molecular Imaging Institute and Department of Radiology, New York, NY (United States)

    2017-01-15

    It remains unclear whether changes in arterial wall inflammation are associated with subsequent changes in the rate of structural progression of atherosclerosis. In this sub-study of the dal-PLAQUE clinical trial, multi-modal imaging was performed using 18-fludeoxyglucose (FDG) positron emission tomography (PET, at 0 and 6 months) and magnetic resonance imaging (MRI, at 0 and 24 months). The primary objective was to determine whether increasing FDG uptake at 6 months predicted atherosclerosis progression on MRI at 2 years. Arterial inflammation was measured by the carotid FDG target-to-background ratio (TBR), and atherosclerotic plaque progression was defined as the percentage change in carotid mean wall area (MWA) and mean wall thickness (MWT) on MRI between baseline and 24 months. A total of 42 participants were included in this sub-study. The mean age of the population was 62.5 years, and 12 (28.6 %) were women. In participants with (vs. without) any increase in arterial inflammation over 6 months, the long-term changes in both MWT (% change MWT: 17.49 % vs. 1.74 %, p = 0.038) and MWA (% change MWA: 25.50 % vs. 3.59 %, p = 0.027) were significantly greater. Results remained significant after adjusting for clinical and biochemical covariates. Individuals with no increase in arterial inflammation over 6 months had no significant structural progression of atherosclerosis over 24 months as measured by MWT (p = 0.616) or MWA (p = 0.373). Short-term changes in arterial inflammation are associated with long-term structural atherosclerosis progression. These data support the concept that therapies that reduce arterial inflammation may attenuate or halt progression of atherosclerosis. (orig.)

  15. Short-term changes in arterial inflammation predict long-term changes in atherosclerosis progression

    International Nuclear Information System (INIS)

    Joseph, Philip; Ishai, Amorina; Tawakol, Ahmed; Mani, Venkatesh; Kallend, David; Rudd, James H.F.; Fayad, Zahi A.

    2017-01-01

    It remains unclear whether changes in arterial wall inflammation are associated with subsequent changes in the rate of structural progression of atherosclerosis. In this sub-study of the dal-PLAQUE clinical trial, multi-modal imaging was performed using 18-fludeoxyglucose (FDG) positron emission tomography (PET, at 0 and 6 months) and magnetic resonance imaging (MRI, at 0 and 24 months). The primary objective was to determine whether increasing FDG uptake at 6 months predicted atherosclerosis progression on MRI at 2 years. Arterial inflammation was measured by the carotid FDG target-to-background ratio (TBR), and atherosclerotic plaque progression was defined as the percentage change in carotid mean wall area (MWA) and mean wall thickness (MWT) on MRI between baseline and 24 months. A total of 42 participants were included in this sub-study. The mean age of the population was 62.5 years, and 12 (28.6 %) were women. In participants with (vs. without) any increase in arterial inflammation over 6 months, the long-term changes in both MWT (% change MWT: 17.49 % vs. 1.74 %, p = 0.038) and MWA (% change MWA: 25.50 % vs. 3.59 %, p = 0.027) were significantly greater. Results remained significant after adjusting for clinical and biochemical covariates. Individuals with no increase in arterial inflammation over 6 months had no significant structural progression of atherosclerosis over 24 months as measured by MWT (p = 0.616) or MWA (p = 0.373). Short-term changes in arterial inflammation are associated with long-term structural atherosclerosis progression. These data support the concept that therapies that reduce arterial inflammation may attenuate or halt progression of atherosclerosis. (orig.)

  16. An alternative method for quantifying coronary artery calcification: the multi-ethnic study of atherosclerosis (MESA).

    Science.gov (United States)

    Liang, C Jason; Budoff, Matthew J; Kaufman, Joel D; Kronmal, Richard A; Brown, Elizabeth R

    2012-07-02

    Extent of atherosclerosis measured by amount of coronary artery calcium (CAC) in computed tomography (CT) has been traditionally assessed using thresholded scoring methods, such as the Agatston score (AS). These thresholded scores have value in clinical prediction, but important information might exist below the threshold, which would have important advantages for understanding genetic, environmental, and other risk factors in atherosclerosis. We developed a semi-automated threshold-free scoring method, the spatially weighted calcium score (SWCS) for CAC in the Multi-Ethnic Study of Atherosclerosis (MESA). Chest CT scans were obtained from 6814 participants in the Multi-Ethnic Study of Atherosclerosis (MESA). The SWCS and the AS were calculated for each of the scans. Cox proportional hazards models and linear regression models were used to evaluate the associations of the scores with CHD events and CHD risk factors. CHD risk factors were summarized using a linear predictor. Among all participants and participants with AS > 0, the SWCS and AS both showed similar strongly significant associations with CHD events (hazard ratios, 1.23 and 1.19 per doubling of SWCS and AS; 95% CI, 1.16 to 1.30 and 1.14 to 1.26) and CHD risk factors (slopes, 0.178 and 0.164; 95% CI, 0.162 to 0.195 and 0.149 to 0.179). Even among participants with AS = 0, an increase in the SWCS was still significantly associated with established CHD risk factors (slope, 0.181; 95% CI, 0.138 to 0.224). The SWCS appeared to be predictive of CHD events even in participants with AS = 0, though those events were rare as expected. The SWCS provides a valid, continuous measure of CAC suitable for quantifying the extent of atherosclerosis without a threshold, which will be useful for examining novel genetic and environmental risk factors for atherosclerosis.

  17. An alternative method for quantifying coronary artery calcification: the multi-ethnic study of atherosclerosis (MESA

    Directory of Open Access Journals (Sweden)

    Liang C

    2012-07-01

    Full Text Available Abstract Background Extent of atherosclerosis measured by amount of coronary artery calcium (CAC in computed tomography (CT has been traditionally assessed using thresholded scoring methods, such as the Agatston score (AS. These thresholded scores have value in clinical prediction, but important information might exist below the threshold, which would have important advantages for understanding genetic, environmental, and other risk factors in atherosclerosis. We developed a semi-automated threshold-free scoring method, the spatially weighted calcium score (SWCS for CAC in the Multi-Ethnic Study of Atherosclerosis (MESA. Methods Chest CT scans were obtained from 6814 participants in the Multi-Ethnic Study of Atherosclerosis (MESA. The SWCS and the AS were calculated for each of the scans. Cox proportional hazards models and linear regression models were used to evaluate the associations of the scores with CHD events and CHD risk factors. CHD risk factors were summarized using a linear predictor. Results Among all participants and participants with AS > 0, the SWCS and AS both showed similar strongly significant associations with CHD events (hazard ratios, 1.23 and 1.19 per doubling of SWCS and AS; 95% CI, 1.16 to 1.30 and 1.14 to 1.26 and CHD risk factors (slopes, 0.178 and 0.164; 95% CI, 0.162 to 0.195 and 0.149 to 0.179. Even among participants with AS = 0, an increase in the SWCS was still significantly associated with established CHD risk factors (slope, 0.181; 95% CI, 0.138 to 0.224. The SWCS appeared to be predictive of CHD events even in participants with AS = 0, though those events were rare as expected. Conclusions The SWCS provides a valid, continuous measure of CAC suitable for quantifying the extent of atherosclerosis without a threshold, which will be useful for examining novel genetic and environmental risk factors for atherosclerosis.

  18. Relationship of aortic valve calcification with coronary artery calcium severity: the Multi-Ethnic Study of Atherosclerosis (MESA).

    Science.gov (United States)

    Nasir, Khurram; Katz, Ronit; Al-Mallah, Mouaz; Takasu, Junichiro; Shavelle, David M; Carr, Jeffery J; Kronmal, Richard; Blumenthal, Roger S; O'Brien, Kevin; Budoff, Matthew J

    2010-01-01

    Aortic valve calcification (AVC) and atherosclerosis share causative and pathologic features. We evaluated the relationship between AVC and coronary artery calcium (CAC) severity in the Multi-Ethnic Study of Atherosclerosis (MESA). Men and women aged 45-84 years (n=6809; mean age, 62 years) were studied. The presence and burden of AVC and CAC were determined by noncontrast cardiac computed tomography. Relative risk regression was used to model the probability of AVC as a function of CAC > 0 as well as CAC categories (0, 1-99, 100-399, and > or = 400) with the reference group being CAC=0. The prevalence of AVC and CAC was 13% and 50%, respectively. Among those without CAC, the prevalence of AVC was 5% and increased across levels of CAC severity such that 14%, 25%, and 38% had AVC with increasing CAC scores of 1-99, 100-399, and > or = 400, respectively (P for trendAVC among those with mild CAC (1-99) was 1.83 (95% CI, 1.45-2.31) and increased to 3.36 (95% CI, 2.56-4.42) for CAC > or = 400. Similar statistically significant increased risk of AVC was found when CAC was assessed as a continuous variable. Our study shows that AVC is independently associated with increasing severity of CAC. 2010 Society of Cardiovascular Computed Tomography. Published by Elsevier Inc. All rights reserved.

  19. Intracranial atherosclerosis and inflammation: Lessons from the East and the West

    Directory of Open Access Journals (Sweden)

    Juan F Arenillas

    2015-01-01

    Full Text Available Intracranial atherosclerosis (ICAS is a major cause of ischemic stroke worldwide. Patients affected by this disease have a high risk of suffering further ischemic strokes and other major vascular events despite the best medical therapy available. However, identification of factors that characterize a high-risk ICAS patient is a clinical problem that is yet to be solved. Inflammation is known to play a crucial role in all the stages of atherosclerosis affecting extracranial arterial beds but its role in ICAS is not firmly established. Circulating inflammatory biomarkers may represent a valuable tool to assess the importance of systemic and local (intraplaque inflammation in ICAS pathogenesis. In this article, we have reviewed studies with inflammatory biomarkers performed in symptomatic and asymptomatic ICAS patients published in the recent literature. Their findings strongly support the hypothesis that inflammation determines the risk of progression and complication of symptomatic ICAS.

  20. Lower Extremity Arterial Calcification as a Predictor of Coronary Atherosclerosis in Patients with Peripheral Arterial Disease

    International Nuclear Information System (INIS)

    Shin, Hwa Seon; Jung Park, Mi; Nyeo Jeon, Kyung; Min Cho, Jae; Soo Bae, Kyung; Seob Choi, Dae; Boem Na, Jae; Cheol Choi, Ho; Young Choi, Hye; Eun Kim, Ji; Bueum Cho, Soo; Eun Park, Sung

    2016-01-01

    Until now, there has been no study on the relationship between the calcification of the lower extremity arteries and significant coronary arterial disease (CAD). To evaluate whether lower extremity calcium scores (LECS) are associated with CAD and whether this can predict multivessel-CAD in patients with peripheral arterial disease (PAD). We retrospectively enrolled 103 PAD patients without cardiac symptoms or known CAD. All patients underwent cardiac computed tomography (CT) and lower extremity CT within 1 month and were categorized as nonsignificant CAD, single-CAD, or multivessel-CAD. The coronary calcium scores (CCS) were quantitatively measured according to the Agatston method and LECS were semi-quantitatively measured according to the presence of lower extremity calcification in the segment. The extent of CAD was evaluated according to the presence of ≥ 50% luminal diameter stenosis in the segment of CAD. LECS in multivessel-CAD were significantly higher than those in nonsignificant CAD (10.0 ± 5.8 versus 4.0 ± 3.1, P < 0.001). LECS significantly correlated with CCS (r = 0.831, P < 0.001) and the extent of CAD (r = 0.631, P < 0.001). Multivariate regression analysis demonstrated LECS and log-transformed CCS were independent predictors for multivessel-CAD. In receiver operating characteristic curve analysis, the diagnostic performance of LECS was 0.807 (95% confidence interval = 0.724-0.891, P < 0.001) for predicting multivessel-CAD. Peripheral arterial calcification is significantly correlated with CAD extent in patients with PAD. Peripheral arterial calcification can be a useful marker for predicting multivessel-CAD

  1. Liraglutide Reduces Both Atherosclerosis and Kidney Inflammation in Moderately Uremic LDLr-/- Mice

    DEFF Research Database (Denmark)

    Bisgaard, Line S; Bosteen, Markus H; Fink, Lisbeth N

    2016-01-01

    Chronic kidney disease (CKD) leads to uremia. CKD is characterized by a gradual increase in kidney fibrosis and loss of kidney function, which is associated with a progressive increase in risk of atherosclerosis and cardiovascular death. To prevent progression of both kidney fibrosis and atherosc......Chronic kidney disease (CKD) leads to uremia. CKD is characterized by a gradual increase in kidney fibrosis and loss of kidney function, which is associated with a progressive increase in risk of atherosclerosis and cardiovascular death. To prevent progression of both kidney fibrosis...... aim was to examine effects of liraglutide on kidney fibrosis and atherosclerosis in a mouse model of moderate uremia (5/6 nephrectomy (NX)). Uremic (n = 29) and sham-operated (n = 14) atherosclerosis-prone low density lipoprotein receptor knockout mice were treated with liraglutide (1000 μg/kg, s.......c. once daily) or vehicle for 13 weeks. As expected, uremia increased aortic atherosclerosis. In the remnant kidneys from NX mice, flow cytometry revealed an increase in the number of monocyte-like cells (CD68+F4/80-), CD4+, and CD8+ T-cells, suggesting that moderate uremia induced kidney inflammation...

  2. Hypercholesterolemia Tunes Hematopoietic Stem/Progenitor Cells for Inflammation and Atherosclerosis.

    Science.gov (United States)

    Ma, Xiaojuan; Feng, Yingmei

    2016-07-19

    As the pathological basis of cardiovascular disease (CVD), atherosclerosis is featured as a chronic inflammation. Hypercholesterolemia is an independent risk factor for CVD. Accumulated studies have shown that hypercholesterolemia is associated with myeloid cell expansion, which stimulates innate and adaptive immune responses, strengthens inflammation, and accelerates atherosclerosis progression. Hematopoietic stem/progenitor cells (HSPC) in bone marrow (BM) expresses a panel of lipoprotein receptors to control cholesterol homeostasis. Deficiency of these receptors abrogates cellular cholesterol efflux, resulting in HSPC proliferation and differentiation in hypercholesterolemic mice. Reduction of the cholesterol level in the lipid rafts by infusion of reconstituted high-density lipoprotein (HDL) or its major apolipoprotein, apoA-I, reverses hypercholesterolemia-induced HSPC expansion. Apart from impaired cholesterol metabolism, inhibition of reactive oxygen species production suppresses HSPC activation and leukocytosis. These data indicate that the mechanisms underlying the effects of hypercholesterolemia on HSPC proliferation and differentiation could be multifaceted. Furthermore, dyslipidemia also regulates HSPC-neighboring cells, resulting in HSPC mobilization. In the article, we review how hypercholesterolemia evokes HSPC activation and mobilization directly or via its modification of BM microenvironment. We hope this review will bring light to finding key molecules to control HSPC expansion, inflammation, and atherosclerosis for the treatment of CVD.

  3. Development of a Patient-Specific Multi-Scale Model to Understand Atherosclerosis and Calcification Locations: Comparison with In vivo Data in an Aortic Dissection

    Science.gov (United States)

    Alimohammadi, Mona; Pichardo-Almarza, Cesar; Agu, Obiekezie; Díaz-Zuccarini, Vanessa

    2016-01-01

    Vascular calcification results in stiffening of the aorta and is associated with hypertension and atherosclerosis. Atherogenesis is a complex, multifactorial, and systemic process; the result of a number of factors, each operating simultaneously at several spatial and temporal scales. The ability to predict sites of atherogenesis would be of great use to clinicians in order to improve diagnostic and treatment planning. In this paper, we present a mathematical model as a tool to understand why atherosclerotic plaque and calcifications occur in specific locations. This model is then used to analyze vascular calcification and atherosclerotic areas in an aortic dissection patient using a mechanistic, multi-scale modeling approach, coupling patient-specific, fluid-structure interaction simulations with a model of endothelial mechanotransduction. A number of hemodynamic factors based on state-of-the-art literature are used as inputs to the endothelial permeability model, in order to investigate plaque and calcification distributions, which are compared with clinical imaging data. A significantly improved correlation between elevated hydraulic conductivity or volume flux and the presence of calcification and plaques was achieved by using a shear index comprising both mean and oscillatory shear components (HOLMES) and a non-Newtonian viscosity model as inputs, as compared to widely used hemodynamic indicators. The proposed approach shows promise as a predictive tool. The improvements obtained using the combined biomechanical/biochemical modeling approach highlight the benefits of mechanistic modeling as a powerful tool to understand complex phenomena and provides insight into the relative importance of key hemodynamic parameters. PMID:27445834

  4. Nanoparticles containing a liver X receptor agonist inhibit inflammation and atherosclerosis.

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    Zhang, Xue-Qing; Even-Or, Orli; Xu, Xiaoyang; van Rosmalen, Mariska; Lim, Lucas; Gadde, Suresh; Farokhzad, Omid C; Fisher, Edward A

    2015-01-28

    Liver X receptor (LXR) signaling pathways regulate lipid metabolism and inflammation, which has generated widespread interest in developing synthetic LXR agonists as potential therapeutics for the management of atherosclerosis. In this study, it is demonstrated that nanoparticles (NPs) containing the synthetic LXR agonist GW3965 (NP-LXR) exert anti-inflammatory effects and inhibit the development of atherosclerosis without causing hepatic steatosis. These NPs are engineered through self-assembly of a biodegradable diblock poly(lactide-co-glycolide)-b-poly(ethylene glycol) (PLGA-b-PEG) copolymer. NP-LXR is significantly more effective than free GW3965 at inducing LXR-target gene expression and suppressing inflammatory factors in macrophages in vitro and in vivo. Additionally, the NPs elicit negligible lipogenic gene stimulation in the liver. Using the Ldlr (-/-) mouse model of atherosclerosis, abundant colocalization of fluorescently labeled NPs within plaque macrophages following systemic administration is seen. Notably, six intravenous injections of NP-LXR over 2 weeks markedly reduce the CD68-positive cell (macrophage) content of plaques (by 50%) without increasing total cholesterol or triglycerides in the liver and plasma. Together, these findings identify GW3965-encapsulated PLGA-b-PEG NPs as a promising nanotherapeutic approach to combat atherosclerosis, providing the benefits of LXR agonists without their adverse effects on hepatic and plasma lipid metabolism. © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  5. A crucial role for CDC42 in senescence-associated inflammation and atherosclerosis.

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    Takashi K Ito

    Full Text Available Risk factors for atherosclerosis accelerate the senescence of vascular endothelial cells and promote atherogenesis by inducing vascular inflammation. A hallmark of endothelial senescence is the persistent up-regulation of pro-inflammatory genes. We identified CDC42 signaling as a mediator of chronic inflammation associated with endothelial senescence. Inhibition of CDC42 or NF-κB signaling attenuated the sustained up-regulation of pro-inflammatory genes in senescent human endothelial cells. Endothelium-specific activation of the p53/p21 pathway, a key mediator of senescence, also resulted in up-regulation of pro-inflammatory molecules in mice, which was reversed by Cdc42 deletion in endothelial cells. Likewise, endothelial-specific deletion of Cdc42 significantly attenuated chronic inflammation and plaque formation in atherosclerotic mice. While inhibition of NF-κB suppressed the pro-inflammatory responses in acute inflammation, the influence of Cdc42 deletion was less marked. Knockdown of cdc-42 significantly down-regulated pro-inflammatory gene expression and restored the shortened lifespan to normal in mutant worms with enhanced inflammation. These findings indicate that the CDC42 pathway is critically involved in senescence-associated inflammation and could be a therapeutic target for chronic inflammation in patients with age-related diseases without compromising host defenses.

  6. MITRAL ANNULAR CALCIFICATION IN ELDERLY PATIENTS: RELATIONSHIP WITH CLINICAL MANIFESTATIONS AND RISK FACTORS OF CARDIOVASCULAR DISEASES CAUSED BY ATHEROSCLEROSIS

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    G. M. Urvacheva

    2011-01-01

    Full Text Available The aim – to study the association of the mitral annular calcification (MAC with traditional risk factors and clinical manifestations of atherosclerosisin patients aged over 65 years without diabetes.Materials and methods. The prospective study included 100 patients over 65 years with MAC consistently identified among 910 ambulatory patients after transthoracic Doppler echocardiography in relation to the symptoms of cardiovascular disease. The comparison group consisted of 65 consecutively examined patients aged over 65 with no MAC.Results. When comparing risk factors in patients with and without MAC, MAC statistically significant differences was found with age (72,4 ± 5,4 and 70,2 ± 4,3 years, respectively; p = 0,006, the incidence of hypertension of moderate and severe degree (99 % and 90.8 % of patients, p = 0.012, levels of total cholesterol – TC (6,91 ± 0,92 and 6,2 ± 0,90 mmol / l, p = 0.0008 and lipoproteinlow density (3,57 ± 0,95 and 2,96 ± 0,96 mmol / l, p = 0.004 in subgroups of patients aged 65 to 70 years. In multivariate analysis remained statistically significant association of MAC only with age (p = 0,025, β = 0,173 and total cholesterol levels (p = 0,040; β = 0,160. Averages of the coefficient of atherogenicity of blood lipids, systolic and diastolic blood pressure, C-reactive protein, body mass index, waist circumference, the frequency of smoking, and risk assessment on a scale of SCORE in groups of patients with and without MAC did not differ significantly. In patients with MAC was higher incidence of myocardial infarction (p = 0.024 and more often than in patients without MAC, diagnosed coronary heart disease (p = 0.029. In the multivariate analysis adjusted for age and total cholesterol level is set significantly associated with the presence and extent of MAC with symptomatic atherosclerotic peripheral arterial disease (p < 0,00001; β = 0,410.Conclusion. In patients with MAC older than 65 years without diabetes

  7. Modulation of ambient temperature promotes inflammation and initiates atherosclerosis in wild type C57BL/6 mice

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    Daniel A. Giles

    2016-11-01

    Full Text Available Objectives: Obesity and obesity-associated inflammation is central to a variety of end-organ sequelae including atherosclerosis, a leading cause of death worldwide. Although mouse models have provided important insights into the immunopathogenesis of various diseases, modeling atherosclerosis in mice has proven difficult. Specifically, wild-type (WT mice are resistant to developing atherosclerosis, while commonly used genetically modified mouse models of atherosclerosis are poor mimics of human disease. The lack of a physiologically relevant experimental model of atherosclerosis has hindered the understanding of mechanisms regulating disease development and progression as well as the development of translational therapies. Recent evidence suggests that housing mice within their thermoneutral zone profoundly alters murine physiology, including both metabolic and immune processes. We hypothesized that thermoneutral housing would allow for augmentation of atherosclerosis induction and progression in mice. Methods: ApoE−/− and WT mice were housed at either standard (TS or thermoneutral (TN temperatures and fed either a chow or obesogenic “Western” diet. Analysis included quantification of (i obesity and obesity-associated downstream sequelae, (ii the development and progression of atherosclerosis, and (iii inflammatory gene expression pathways related to atherosclerosis. Results: Housing mice at TN, in combination with an obesogenic “Western” diet, profoundly augmented obesity development, exacerbated atherosclerosis in ApoE−/− mice, and initiated atherosclerosis development in WT mice. This increased disease burden was associated with altered lipid profiles, including cholesterol levels and fractions, and increased aortic plaque size. In addition to the mild induction of atherosclerosis, we similarly observed increased levels of aortic and white adipose tissue inflammation and increased circulating immune cell expression of pathways

  8. Periodontal Pathogens and Atherosclerosis: Implications of Inflammation and Oxidative Modification of LDL

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    Tomoko Kurita-Ochiai

    2014-01-01

    Full Text Available Inflammation is well accepted to play a crucial role in the development of atherosclerotic lesions, and recent studies have demonstrated an association between periodontal disease and cardiovascular disease. Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, causative agents of destructive chronic inflammation in the periodontium, can accelerate atheroma deposition in animal models. Emerging evidence suggests that vaccination against virulence factors of these pathogens and anti-inflammatory therapy may confer disease resistance. In this review, we focus on the role of inflammatory mechanisms and oxidative modification in the formation and activation of atherosclerotic plaques accelerated by P. gingivalis or A. actinomycetemcomitans in an ApoE-deficient mouse model and high-fat-diet-fed mice. Furthermore, we examine whether mucosal vaccination with a periodontal pathogen or the anti-inflammatory activity of catechins can reduce periodontal pathogen-accelerated atherosclerosis.

  9. Macrophage mitochondrial oxidative stress promotes atherosclerosis and nuclear factor-κB-mediated inflammation in macrophages.

    Science.gov (United States)

    Wang, Ying; Wang, Gary Z; Rabinovitch, Peter S; Tabas, Ira

    2014-01-31

    Mitochondrial oxidative stress (mitoOS) has been shown to correlate with the progression of human atherosclerosis. However, definitive cell type-specific causation studies in vivo are lacking, and the molecular mechanisms of potential proatherogenic effects remain to be determined. Our aims were to assess the importance of macrophage mitoOS in atherogenesis and to explore the underlying molecular mechanisms. We first validated Western diet-fed Ldlr(-/-) mice as a model of human mitoOS-atherosclerosis association by showing that non-nuclear oxidative DNA damage, a marker of mitoOS in lesional macrophages, correlates with aortic root lesion development. To investigate the importance of macrophage mitoOS, we used a genetic engineering strategy in which the OS suppressor catalase was ectopically expressed in mitochondria (mCAT) in macrophages. MitoOS in lesional macrophages was successfully suppressed in these mice, and this led to a significant reduction in aortic root lesional area. The mCAT lesions had less monocyte-derived cells, less Ly6c(hi) monocyte infiltration into lesions, and lower levels of monocyte chemotactic protein-1. The decrease in lesional monocyte chemotactic protein-1 was associated with the suppression of other markers of inflammation and with decreased phosphorylation of RelA (NF-κB p65), indicating decreased activation of the proinflammatory NF-κB pathway. Using models of mitoOS in cultured macrophages, we showed that mCAT suppressed monocyte chemotactic protein-1 expression by decreasing the activation of the IκB-kinase β-RelA NF-κB pathway. MitoOS in lesional macrophages amplifies atherosclerotic lesion development by promoting NF-κB-mediated entry of monocytes and other inflammatory processes. In view of the mitoOS-atherosclerosis link in human atheromata, these findings reveal a potentially new therapeutic target to prevent the progression of atherosclerosis.

  10. Gla-rich protein is involved in the cross-talk between calcification and inflammation in osteoarthritis.

    Science.gov (United States)

    Cavaco, Sofia; Viegas, Carla S B; Rafael, Marta S; Ramos, Acácio; Magalhães, Joana; Blanco, Francisco J; Vermeer, Cees; Simes, Dina C

    2016-03-01

    Osteoarthritis (OA) is a whole-joint disease characterized by articular cartilage loss, tissue inflammation, abnormal bone formation and extracellular matrix (ECM) mineralization. Disease-modifying treatments are not yet available and a better understanding of osteoarthritis pathophysiology should lead to the discovery of more effective treatments. Gla-rich protein (GRP) has been proposed to act as a mineralization inhibitor and was recently shown to be associated with OA in vivo. Here, we further investigated the association of GRP with OA mineralization-inflammation processes. Using a synoviocyte and chondrocyte OA cell system, we showed that GRP expression was up-regulated following cell differentiation throughout ECM calcification, and that inflammatory stimulation with IL-1β results in an increased expression of COX2 and MMP13 and up-regulation of GRP. Importantly, while treatment of articular cells with γ-carboxylated GRP inhibited ECM calcification, treatment with either GRP or GRP-coated basic calcium phosphate (BCP) crystals resulted in the down-regulation of inflammatory cytokines and mediators of inflammation, independently of its γ-carboxylation status. Our results strengthen the calcification inhibitory function of GRP and strongly suggest GRP as a novel anti-inflammatory agent, with potential beneficial effects on the main processes responsible for osteoarthritis progression. In conclusion, GRP is a strong candidate target to develop new therapeutic approaches.

  11. Effect of vitamin K2 on progression of atherosclerosis and vascular calcification in nondialyzed patients with chronic kidney disease stages 3-5.

    Science.gov (United States)

    Kurnatowska, Ilona; Grzelak, Piotr; Masajtis-Zagajewska, Anna; Kaczmarska, Magdalena; Stefańczyk, Ludomir; Vermeer, Cees; Maresz, Katarzyna; Nowicki, Michał

    2015-01-01

    Observational studies have shown that high dietary intake of vitamin K2 is associated with reduced risk of coronary vascular disease and vascular calcification. We assessed the effect of vitamin K2 substitution on the progression of atherosclerosis and calcification in nondialyzed patients with CKD stages 3-5. The study included 42 nondialyzed patients with CKD. The following measurements were taken at baseline and after 270 ±12 days of supplementation with vitamin K2 at a dose of 90 μg (menaquinone, MK-7) together with 10 μg of cholecalciferol (K+D group) or 10 μg of cholecalciferol (group D): common carotid intima-media thickness (CCA-IMT), coronary artery calcification score (CACS), basic biochemical parameters, lipids, and calcification modulators: matrix Gla protein (MGP), desphosphorylated-uncarboxylated MGP (dp-ucMGP), osteoprotegerin (OPG), fetuin A, osteocalcin (OC), and fibroblast growth factor 23. The increase of CCA-IMT was significantly lower in the K+D group compared with the D group: from 0.95 ±0.2 mm to 1.01 ±0.3, P = 0.003 vs from 1.02 ±0.2 mm to 1.16 ±0.3, P = 0.003 (ΔCCA-IMT, 0.06 ±0.08 vs 0.136 ±0.05 mm, P = 0.005, respectively). The increase in CACS was slightly lower in the K+D group than in the D group (ΔCACS, 58.1 ±106.5 AU vs 74.4 ±127.1 AU, P = 0.7). In the K+D group, a significant decrease in the level of dp-ucMGP and total OC was observed. A 270-day course of vitamin K2 administration in patients with CKD stages 3-5 may reduce the progression of atherosclerosis, but does not significantly affect the progression of calcification. Vitamin K2 significantly changes the levels of calcification promoters and inhibitors: dp-ucMGP, OC, and OPG.

  12. Deficiency of ABCA1 and ABCG1 in Macrophages Increases Inflammation and Accelerates Atherosclerosis in Mice

    Science.gov (United States)

    Westerterp, Marit; Murphy, Andrew J.; Wang, Mi; Pagler, Tamara A.; Vengrenyuk, Yuliya; Kappus, Mojdeh S.; Gorman, Darren J.; Nagareddy, Prabhakara R.; Zhu, Xuewei; Abramowicz, Sandra; Parks, John S.; Welch, Carrie; Fisher, Edward A.; Wang, Nan; Yvan-Charvet, Laurent; Tall, Alan R.

    2013-01-01

    Rationale Plasma HDL levels are inversely correlated with atherosclerosis. Although it is widely assumed that this is due to the ability of HDL to promote cholesterol efflux from macrophage foam cells, direct experimental support for this hypothesis is lacking. Objective To assess the role of macrophage cholesterol efflux pathways in atherogenesis. Methods and Results We developed MAC-ABCDKO mice with efficient deletion of the ATP Binding Cassette Transporters A1 and G1 (ABCA1 and ABCG1) in macrophages but not in hematopoietic stem or progenitor populations. MAC-ABCDKO bone marrow (BM) was transplanted into Ldlr-/- recipients. On the chow diet, these mice had similar plasma cholesterol and blood monocyte levels but increased atherosclerosis compared to controls. On the Western type diet (WTD), MAC-ABCDKO BM transplanted Ldlr-/- mice had disproportionate atherosclerosis, considering they also had lower VLDL/LDL cholesterol levels than controls. ABCA1/G1 deficient macrophages in lesions showed increased inflammatory gene expression. Unexpectedly, WTD-fed MAC-ABCDKO BM transplanted Ldlr-/- mice displayed monocytosis and neutrophilia in the absence of HSPC proliferation. Mechanistic studies revealed increased expression of M-CSF and G-CSF in splenic macrophage foam cells, driving BM monocyte and neutrophil production. Conclusion These studies 1) show that macrophage deficiency of ABCA1/G1 is pro-atherogenic likely by promoting plaque inflammation and 2) uncover a novel positive feedback loop in which cholesterol-laden splenic macrophages signal BM progenitors to produce monocytes, with suppression by macrophage cholesterol efflux pathways. PMID:23572498

  13. Acute and chronic effects of treatment with mesenchymal stromal cells on LPS-induced pulmonary inflammation, emphysema and atherosclerosis development.

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    P Padmini S J Khedoe

    Full Text Available COPD is a pulmonary disorder often accompanied by cardiovascular disease (CVD, and current treatment of this comorbidity is suboptimal. Systemic inflammation in COPD triggered by smoke and microbial exposure is suggested to link COPD and CVD. Mesenchymal stromal cells (MSC possess anti-inflammatory capacities and MSC treatment is considered an attractive treatment option for various chronic inflammatory diseases. Therefore, we investigated the immunomodulatory properties of MSC in an acute and chronic model of lipopolysaccharide (LPS-induced inflammation, emphysema and atherosclerosis development in APOE*3-Leiden (E3L mice.Hyperlipidemic E3L mice were intranasally instilled with 10 μg LPS or vehicle twice in an acute 4-day study, or twice weekly during 20 weeks Western-type diet feeding in a chronic study. Mice received 0.5x106 MSC or vehicle intravenously twice after the first LPS instillation (acute study or in week 14, 16, 18 and 20 (chronic study. Inflammatory parameters were measured in bronchoalveolar lavage (BAL and lung tissue. Emphysema, pulmonary inflammation and atherosclerosis were assessed in the chronic study.In the acute study, intranasal LPS administration induced a marked systemic IL-6 response on day 3, which was inhibited after MSC treatment. Furthermore, MSC treatment reduced LPS-induced total cell count in BAL due to reduced neutrophil numbers. In the chronic study, LPS increased emphysema but did not aggravate atherosclerosis. Emphysema and atherosclerosis development were unaffected after MSC treatment.These data show that MSC inhibit LPS-induced pulmonary and systemic inflammation in the acute study, whereas MSC treatment had no effect on inflammation, emphysema and atherosclerosis development in the chronic study.

  14. Thoracic aorta calcification but not inflammation is associated with increased cardiovascular disease risk: results of the CAMONA study

    Energy Technology Data Exchange (ETDEWEB)

    Blomberg, Bjoern A. [Odense University Hospital, Department of Nuclear Medicine, Odense C (Denmark); University Medical Center Utrecht, Department of Radiology and Nuclear Medicine, Utrecht (Netherlands); Jong, Pim A. de; Lam, Marnix G.E.; Mali, Willem P.T.M. [University Medical Center Utrecht, Department of Radiology and Nuclear Medicine, Utrecht (Netherlands); Thomassen, Anders [Odense University Hospital, Department of Nuclear Medicine, Odense C (Denmark); Vach, Werner [University Medical Center Freiburg, Clinical Epidemiology, Institute of Medical Biometry and Medical Informatics, Freiburg (Germany); Olsen, Michael H. [Odense University Hospital, The Cardiovascular and Metabolic Preventive Clinic, Department of Endocrinology, Center for Individualized Medicine in Arterial Diseases, Odense (Denmark); Narula, Jagat [Mount Sinai Hospital, Icahn School of Medicine, New York, NY (United States); Alavi, Abass [Hospital of the University of Pennsylvania, Department of Radiology, Philadelphia, PA (United States); Hoeilund-Carlsen, Poul F. [Odense University Hospital, Department of Nuclear Medicine, Odense C (Denmark); University of Southern Denmark, Institute of Clinical Research, Odense (Denmark)

    2017-02-15

    Arterial inflammation and vascular calcification are regarded as early prognostic markers of cardiovascular disease (CVD). In this study we investigated the relationship between CVD risk and arterial inflammation ({sup 18}F-FDG PET/CT imaging), vascular calcification metabolism (Na{sup 18}F PET/CT imaging), and vascular calcium burden (CT imaging) of the thoracic aorta in a population at low CVD risk. Study participants underwent blood pressure measurements, blood analyses, and {sup 18}F-FDG and Na{sup 18}F PET/CT imaging. In addition, the 10-year risk for development of CVD, based on the Framingham risk score (FRS), was estimated. CVD risk was compared across quartiles of thoracic aorta {sup 18}F-FDG uptake, Na{sup 18}F uptake, and calcium burden on CT. A total of 139 subjects (52 % men, mean age 49 years, age range 21 - 75 years, median FRS 6 %) were evaluated. CVD risk was, on average, 3.7 times higher among subjects with thoracic aorta Na{sup 18}F uptake in the highest quartile compared with those in the lowest quartile of the distribution (15.5 % vs. 4.2 %; P < 0.001). CVD risk was on average, 3.7 times higher among subjects with a thoracic aorta calcium burden on CT in the highest quartile compared with those in the lowest two quartiles of the distribution (18.0 % vs. 4.9 %; P < 0.001). CVD risk was similar in subjects in all quartiles of thoracic aorta {sup 18}F-FDG uptake. Our findings indicate that an unfavourable CVD risk profile is associated with marked increases in vascular calcification metabolism and vascular calcium burden of the thoracic aorta, but not with arterial inflammation. (orig.)

  15. Ten-year trends in coronary calcification in individuals without clinical cardiovascular disease in the multi-ethnic study of atherosclerosis.

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    Diane E Bild

    Full Text Available Coronary heart disease (CHD incidence has declined significantly in the US, as have levels of major coronary risk factors, including LDL-cholesterol, hypertension and smoking, but whether trends in subclinical atherosclerosis mirror these trends is not known.To describe recent secular trends in subclinical atherosclerosis as measured by serial evaluations of coronary artery calcification (CAC prevalence in a population over 10 years, we measured CAC using computed tomography (CT and CHD risk factors in five serial cross-sectional samples of men and women from four race/ethnic groups, aged 55-84 and without clinical cardiovascular disease, who were members of Multi-Ethnic Study of Atherosclerosis (MESA cohort from 2000 to 2012. Sample sizes ranged from 1062 to 4837. After adjusting for age, gender, and CT scanner, the prevalence of CAC increased across exams among African Americans, whose prevalence of CAC was 52.4% in 2000-02, 50.4% in 2003-04, 60.0% is 2005-06, 57.4% in 2007-08, and 61.3% in 2010-12 (p for trend <0.001. The trend was strongest among African Americans aged 55-64 [prevalence ratio for 2010-12 vs. 2000-02, 1.59 (95% confidence interval 1.06, 2.39; p = 0.005 for trend across exams]. There were no consistent trends in any other ethnic group. Risk factors generally improved in the cohort, and adjustment for risk factors did not change trends in CAC prevalence.There was a significant secular trend towards increased prevalence of CAC over 10 years among African Americans and no change in three other ethnic groups. Trends did not reflect concurrent general improvement in risk factors. The trend towards a higher prevalence of CAC in African Americans suggests that CHD risk in this population is not improving relative to other groups.

  16. PREVALENCE OF METABOLIC SYNDROME IN PATIENTS WITH PSORIATIC ARTHRITIS: ITS ASSOCIATION WITH INFLAMMATION AND SUBCLINICAL ATHEROSCLEROSIS

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    E. I. Markelova

    2016-01-01

    Full Text Available Metabolic syndrome (MS is a cluster of metabolic disorders giving rise to atherosclerotic  cardiovascular diseases (CVD. The combination  of inflammatory activity and a high spread of traditional  risk factors (RF for CVD in patients with psoriatic arthritis (PsA permits them to be referred to as a higher cardiovascular risk group as compared to the general population.Objective: to estimate the spread of MS and its association with inflammation and subclinical atherosclerosis in patients with PsA.Subjects and methods. This investigation enrolled 128 patients with PsA (61.7% women and 38.3% men; their median age was 43 [34; 49.5] years; the duration of PsA and psoriasis – 7 [3; 13] and 15 [6; 26] years, respectively. There was a preponderance of patients with moderate (3.7 ≥ DAS > 2.4 and high (DAS > 3.7 disease activity: 33 (25.8% and 74 (57.8%, respectively. MS was diagnosed on the basis of the 2011 National  Guidelines of the Russian Cardiology Society for Cardiovascular Prevention.  All the patients underwent carotid Doppler ultrasound (CDU for the diagnosis of subclinical atherosclerosis. Results and discussion. MS was diagnosed in 49 (38.3% patients with PsA. The most common  MS criteria were abdominal  obesity in 72 (56.3% and dyslipidemia [an elevation of low-density lipoproteins (LDL  level in 101 (78.9%, and a decrease in high-density lipoproteins (HDL  level in 65 (50.8]. Hypertension was diagnosed in 32 (25%. 65 (50.8% patients were found to have subclinical atherosclerosis,  as evidenced by CDU.The patients with MS were older than those without this condition  (46 [43; 52] and 39 [31; 46] years, respectively; p < 0.0001. These groups did not differ in PsA duration (15 [7; 29] and 15 [5.5; 25] years respectively; p = 0.47. The patients with MS had higher DAS values (4.4 [3.2; 5.6] and 3.6 [2.5; 4.7], respectively; p = 0.02; mean intima media thickness (IMT  (0.78 [0.72; 0.86] and 0.73 [0.66; 0.77] mm; p < 0.0001 and

  17. Insights From Pre-Clinical and Clinical Studies on the Role of Innate Inflammation in Atherosclerosis Regression

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    Karishma Rahman

    2018-05-01

    Full Text Available Atherosclerosis, the underlying cause of coronary artery (CAD and other cardiovascular diseases, is initiated by macrophage-mediated immune responses to lipoprotein and cholesterol accumulation in artery walls, which result in the formation of plaques. Unlike at other sites of inflammation, the immune response becomes maladaptive and inflammation fails to resolve. The most common treatment for reducing the risk from atherosclerosis is low density lipoprotein cholesterol (LDL-C lowering. Studies have shown, however, that while significant lowering of LDL-C reduces the risk of heart attacks to some degree, there is still residual risk for the majority of the population. We and others have observed “residual inflammatory risk” of atherosclerosis after plasma cholesterol lowering in pre-clinical studies, and that this phenomenon is clinically relevant has been dramatically reinforced by the recent Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS trial. This review will summarize the role of the innate immune system, specifically macrophages, in atherosclerosis progression and regression, as well as the pre-clinical and clinical models that have provided significant insights into molecular pathways involved in the resolution of plaque inflammation and plaque regression. Partnered with clinical studies that can be envisioned in the post-CANTOS period, including progress in developing targeted plaque therapies, we expect that pre-clinical studies advancing on the path summarized in this review, already revealing key mechanisms, will continue to be essential contributors to achieve the goals of dampening plaque inflammation and inducing its resolution in order to maximize the therapeutic benefits of conventional risk factor modifications, such as LDL-C lowering.

  18. The effect of aging on aortic atherosclerotic plaque inflammation and molecular calcification: A FDG and NaF PET CT imaging study

    DEFF Research Database (Denmark)

    Blomberg, Björn; Thomassen, Anders; Hildebrandt, Malene

    2013-01-01

    Objectives: Aging is an important independent determinant of plaque biology. This study aimed to investigate the effect of aging on atherosclerotic plaque inflammation and calcification metabolism. Methods: Thirteen healthy volunteers without traditional cardiovascular risk factors were...... and correlation coefficients summarized the data. Results: A quadratic relationship was observed between aging and aortic 18-FDG and aortic Na-18F avidity. A second order polynomial regression established that aging is a predictor of the degree of aortic plaque inflammation (R = 0.524; F statistic = 4.93; P = 0...... data, a quadratic relationship appears to exist between aging and plaque inflammation. Furthermore, a quadratic relationship was observed between aging and plaque calcification metabolism. In line with these observations, a linear relationship was observed between atherosclerotic plaque inflammation...

  19. The effect of aging on aortic atherosclerotic plaque inflammation and molecular calcification: A FDG and NaF PET CT imaging study

    DEFF Research Database (Denmark)

    Blomberg, Björn; Thomassen, Anders; Hildebrandt, Malene

    2013-01-01

    prospectively assessed by 18-FDG (inflammation) and Sodium 18-Fluoride (Na-18F) (calcification metabolism) PET CT imaging. Global aortic uptake of 18-FDG and Na-18F was quantified by subtracting the blood pool SUVmean from the aortic SUVmax (cSUV) [maximum SUVaorta - mean SUVblood pool]. Calculating regression...

  20. Factors associated with early atherosclerosis and arterial calcifications in young subjects with a benign phenotype of obesity.

    Science.gov (United States)

    Gilardini, Luisa; Pasqualinotto, Lucia; Di Matteo, Silvia; Caffetto, Katherine; Croci, Marina; Girola, Andrea; Invitti, Cecilia

    2011-08-01

    We assessed (i) the association between early arterial disease and factors linked to adiposity, dietary habits, and family in a young cohort of 151 obese children and adolescents with less than or equal to one cardiovascular (CV) risk factor, (ii) whether in subjects with carotid calcifications there was an imbalance of calcium-phosphorus homeostasis. Measurement included: carotid ultrasound, oral glucose tolerance test, anthropometry, body composition, dietary history, white blood cells count, lipids, uric acid, adiponectin, insulin, C-reactive protein, plasminogen activator inhibitor 1 (PAI-1), 25-hydroxyvitamin D, parathyroid hormone (PTH), calcium and phosphorus. Obese children with carotid artery intima media thickness (cIMT) values >75° percentile (0.55 mm), compared to those with lower cIMT, were more obese, more often pubertal and had higher prevalence of family history of CV disease (CVD) (P < 0.05), higher plasma PAI-1 and uric acid (P < 0.001) and lower adiponectin (P < 0.05) and high-density lipoprotein (HDL) cholesterol levels (P < 0.05). After adjustment for sex, age, puberty, obesity, and insulin levels, only PAI-I remained significantly different between the two groups (10.9 (7.2-29.8) vs. 6.2 (4.3-10.6) ng/ml, P < 0.001). Dietary intake did not affect cIMT values. Eight percent of subjects showed nonatherosclerotic carotid calcifications with patchy pattern. These children had a worse lipid profile (P < 0.05) and higher plasma PTH levels (48.6 ± 21.5 vs 38.5 ± 16.9 pg/ml, P < 0.05) that were inversely associated with 25-hydroxyvitamin D levels (r = 0.245, P < 0.01). Present results suggest that (i) several adiposity-related factors may play a role in promoting the development of early arterial diseases in young subjects with a benign phenotype of obesity, (ii) a PTH rise resulting from a subclinical imbalance in calcium-phosphorus homeostasis may affect the biological process of vascular calcifications.

  1. Effect of tocopherol on atherosclerosis, vascular function, and inflammation in apolipoprotein E knockout mice with subtotal nephrectomy.

    Science.gov (United States)

    Shing, Cecilia M; Fassett, Robert G; Peake, Jonathan M; Coombes, Jeff S

    2014-12-01

    Inflammation and endothelial dysfunction contribute to cardiovascular disease, prevalent in chronic kidney disease (CKD). Antioxidant supplements such as tocopherols may reduce inflammation and atherosclerosis. This study aimed to investigate the effect of tocopherol supplementation on vascular function, aortic plaque formation, and inflammation in apolipoprotein E(-/-) mice with 5/6 nephrectomy as a model of combined cardiovascular and kidney disease. Nephrectomized mice were assigned to a normal chow diet group (normal chow), a group receiving 1000 mg/kg diet of α-tocopherol supplementation or a group receiving 1000 mg/kg diet mixed-tocopherol (60% γ-tocopherol). Following 12 weeks, in vitro aortic endothelial-independent relaxation was enhanced with both α-tocopherol and mixed-tocopherol (P tocopherol enhanced aortic contraction at noradrenaline concentrations of 3 × 10(-7) M to 3 × 10(-5) M (P tocopherol reduced systemic concentrations of IL-6 (P tocopherol also reduced MCP-1 (P tocopherol supplementation when compared to normal chow (P Tocopherol supplementation favorably influenced vascular function and cytokine profile, while it was also effective in reducing atherosclerosis in the apolipoprotein E(-/-) mouse with CKD. © 2014 John Wiley & Sons Ltd.

  2. Chitotriosidase enzyme activity: is this a possible chronic inflammation marker in children with common variable immunodeficiency and early atherosclerosis?

    Science.gov (United States)

    Azarsız, Elif; Karaca, Neslihan; Levent, Erturk; Kutukculer, Necil; Sozmen, Eser

    2017-11-01

    Background Common variable immunodeficiency is a rare clinically symptomatic primary immunodeficiency disorder which manifests a wide variability of symptoms, complications. Atherosclerosis in common variable immunodeficiency patients has not been investigated yet contrary to other severe clinical complications. We aimed to investigate the chitotriosidase enzyme's role as an inflammation and atherosclerosis marker in paediatric common variable immunodeficiency patients. Methods Common variable immunodeficiency patients (n = 24) and healthy controls (n = 23) evaluated for chitotriosidase activity with other inflammation markers (hsCRP, myeloperoxidase, serum amyloid A, ferritin), lipid profile and echocardiographic findings (carotid artery intima media thickness - cIMT, brachial artery flow-mediated vazodilatation - FMD%). Results In patients, the mean chitotriosidase activity (8.98 ± 6.28) was significantly higher than the controls (5.17 ± 3.42) ( P = 0.014). Chitotriosidase showed positive relation with hs-CRP ( P = 0.011) and SAA ( P = 0.011) but had no relation with ferritin ( P = 0.155), HDL ( P = 0.152) or LDL-cholesterol ( P = 0.380). Mean cIMT increased in patients compared with the controls ( P variable immunodeficiency patients demonstrated in vivo the presence of activated macrophages indicating ongoing inflammation. Echocardiographic diastolic functional deficiency, increased cIMT and decreased FMD% may be accepted as early atherosclerotic findings, but none of them showed relationship with chitotriosidase activities.

  3. Associations of Cigarette Smoking With Subclinical Inflammation and Atherosclerosis: ELSA-Brasil (The Brazilian Longitudinal Study of Adult Health).

    Science.gov (United States)

    Kianoush, Sina; Yakoob, Mohammad Yawar; Al-Rifai, Mahmoud; DeFilippis, Andrew P; Bittencourt, Marcio S; Duncan, Bruce B; Bensenor, Isabela M; Bhatnagar, Aruni; Lotufo, Paulo A; Blaha, Michael J

    2017-06-24

    There is a need to identify sensitive biomarkers of early tobacco-related cardiovascular disease. We examined the association of smoking status, burden, time since quitting, and intensity, with markers of inflammation and subclinical atherosclerosis. We studied 14 103 participants without clinical cardiovascular disease in ELSA-Brasil (Brazilian Longitudinal Study of Adult Health). We evaluated baseline cross-sectional associations between smoking parameters and inflammation (high-sensitivity C-reactive protein [hsCRP]) and measures of subclinical atherosclerosis (carotid intima-media thickness, ankle-brachial index, and coronary artery calcium [CAC]). The cohort included 1844 current smokers, 4121 former smokers, and 8138 never smokers. Mean age was 51.7±8.9 years; 44.8% were male. After multivariable adjustment, compared with never smokers, current smokers had significantly higher levels of hsCRP (β=0.24, 0.19-0.29 mg/L; P media thickness (β=0.03, 0.02-0.04 mm; P 0 (odds ratio: 1.83; 95% confidence interval, 1.46-2.30; P media thickness levels and odds of ankle-brachial index ≤1.0 and CAC >0 were lower with increasing time since quitting ( P 0 ( P =0.03) after adjusting for duration of smoking. Strong associations were observed between smoking status, burden, and intensity with inflammation (hsCRP) and subclinical atherosclerosis (carotid intima-media thickness, ankle-brachial index, CAC). These markers of early cardiovascular disease injury may be used for the further study and regulation of traditional and novel tobacco products. © 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

  4. A CD1d-dependent lipid antagonist to NKT cells ameliorates atherosclerosis in ApoE-/- mice by reducing lesion necrosis and inflammation.

    Science.gov (United States)

    Li, Yi; Kanellakis, Peter; Hosseini, Hamid; Cao, Anh; Deswaerte, Virginie; Tipping, Peter; Toh, Ban-Hock; Bobik, Alex; Kyaw, Tin

    2016-02-01

    Atherosclerosis-related deaths from heart attacks and strokes remain leading causes of global mortality, despite the use of lipid-lowering statins. Thus, there is an urgent need to develop additional therapies. Reports that NKT cells promote atherosclerosis and an NKT cell CD1d-dependent lipid antagonist (DPPE-PEG350, 1,2-dipalmitoyl-sn-glycero-3-phosphoethanolamine-N[methoxy(polyethyleneglycol)-350]) reduces allergen-induced inflammation led us to investigate its therapeutic potential in preventing the development and progression of experimental atherosclerosis. DPPE-PEG350 was administered to hyperlipidaemic ApoE(-/-) mice with/without established atherosclerosis. Atherosclerosis and immune cells were assessed in the aortic sinus lesions. Lesion expression of monocyte chemoattractant protein-1 (MCP-1) and vascular cell adhesion protein-1 (VCAM-1) responsible for inflammatory immune cell recruitment as well as mRNA expression of IFNγ and its plasma levels were investigated. Necrotic cores and lesion smooth muscle and collagen contents important in plaque stability were determined as were plasma lipid levels. DPPE-PEG350 reduced atherosclerosis development and delayed progression of established atherosclerosis without affecting plasma lipids. CD4 and CD8 T cells and B cells in atherosclerotic lesions were decreased in DPPE-PEG350-treated mice. Lesion MCP-1 and VCAM-1 protein expression and necrotic core size were reduced without affecting lesion smooth muscle and collagen content. IFNγ and lymphocytes were unaffected by the treatment. The attenuation of progression of established atherosclerosis together with reduced development of atherosclerosis in hyperlipidaemic mice by the NKT antagonist, without affecting NKT cell or other lymphocyte numbers, suggests that targeting lesion inflammation via CD1d-dependent activation of NKT cells using DPPE-PEG350 has a therapeutic potential in treating atherosclerosis. Published on behalf of the European Society of

  5. HMGB1 in vascular diseases : Its role in vascular inflammation and atherosclerosis

    NARCIS (Netherlands)

    de Souza, A. W. S.; Westra, J.; Limburg, P. C.; Bijl, M.; Kallenberg, C. G. M.

    2012-01-01

    The nuclear protein high mobility group box 1 (HMGB1) has been suggested to be involved in the pathogenesis of several vascular diseases such as systemic vasculitis and atherosclerosis. In systemic vasculitides including ANCA-associated vasculitis and Kawasaki disease, serum HMGB1 levels are higher

  6. Endothelial GPR124 Exaggerates the Pathogenesis of Atherosclerosis by Activating Inflammation

    Directory of Open Access Journals (Sweden)

    Dong-Mei Gong

    2018-01-01

    Full Text Available Background/Aims: Endothelial cell dysfunction is the principal pathological process underlying atherosclerotic cardiovascular disease. G protein-coupled receptor 124 (GPR124, an orphan receptor in the adhesion GPCR subfamily, promotes angiogenesis in the brain. In the present study, we explored the role of endothelial GPR124 in the development and progression of atherosclerosis in adult mice. Methods: Using tetracycline-inducible transgenic systems, we generated mice expressing GPR124 specifically under control of the Tie-2 promoter. The animal model of atherosclerosis was constructed by intravenously injecting AAV-PCSK9DY into tetracycline-regulated mice and feeding the mice a high-fat diet for 16 consecutive weeks. Biochemical analysis and immunohistochemistry methods were used to address the role and mechanism of GPR124 in the pathological process of atherosclerosis. Results: Higher TC (total cholesterol and LDL-C (low density lipoprotein cholesterol levels in serum and greater lipid deposition in the aortic sinus were found in atherosclerotic mice with GPR124 overexpression, coincident with the elevated proliferation of smooth muscle cells. We observed an elevation of ONOO- in the aortic sinus in this model by using immunofluorescence, and the experiments showed that the specific overexpression of GPR124 in the endothelium induced the up-regulation of CD68, NLRP3 and caspase-1 levels in the aortic sinus. Conclusion: The above results indicate that manipulating GPR124 in the endothelium may contribute to delayed pathological progression of atherosclerosis.

  7. Addition of Aspirin to a Fish Oil Rich Diet Decreases Inflammation and Atherosclerosis in ApoE-Null Mice

    Science.gov (United States)

    Sorokin, Alexander V.; Yang, Zhi-Hong; Vaisman, Boris L.; Thacker, Seth; Yu, Zu-Xi; Sampson, Maureen; Serhan, Charles N.; Remaley, Alan T.

    2016-01-01

    Aspirin (ASA) is known to alter the production of potent inflammatory lipid mediators, but whether it interacts with omega-3 fatty acids (FA) from fish oil to affect atherosclerosis has not been determined. The goal was to investigate the impact of a fish oil enriched diet alone and in combination with ASA on the production of lipid mediators and atherosclerosis. ApoE−/− female mice were fed for 13 weeks one of the four following diets: Omega-3 FA deficient (OD), Omega-3 FA Rich (OR) (1.8 g Omega-3 FAs/kg • diet per day), Omega-3 FA Rich plus ASA (ORA) (0.1 g ASA/kg • diet per day), or an Omega-3 FA deficient plus ASA (ODA) with supplement levels equivalent to human doses. Plasma lipids, atherosclerosis, markers of inflammation, hepatic gene expression and aortic lipid mediators were determined. Hepatic omega-3 FAs were markedly higher in OR (9.9-fold) and ORA (7-fold) groups. Mice in both OR and ORA groups had 40% less plasma cholesterol in VLDL and LDL fractions, but aortic plaque area formation was only significantly lower in the ORA group (5.5%) compared to the OD group (2.5%). Plasma PCSK9 protein levels were approximately 70% lower in the OR and ORA groups. Pro-inflammatory aortic lipid mediators were 50–70% lower in the ODA group than in the OD group and more than 50% lower in the ORA group. In summary, less aortic plaque lesions and aortic pro-inflammatory lipid mediators were observed in mice on the fish oil diet plus ASA versus just the fish oil diet. PMID:27394692

  8. Associations Between Cardiovascular Risk Factors, Inflammation, and Progression of Carotid Atherosclerosis Among Smokers.

    Science.gov (United States)

    Zingg, Sarah; Collet, Tinh-Hai; Locatelli, Isabella; Nanchen, David; Depairon, Michèle; Bovet, Pascal; Cornuz, Jacques; Rodondi, Nicolas

    2016-06-01

    The high risk of cardiovascular events in smokers requires adequate control of other cardiovascular risk factors (CVRFs) to curtail atherosclerosis progression. However, it is unclear which CVRFs have the most influence on atherosclerosis progression in smokers. In 260 smokers aged 40-70 included in a smoking cessation trial, we analyzed the association between traditional CVRFs, high-sensitivity C-reactive protein (hs-CRP), smoking cessation and 3-year progression of carotid intima-media thickness (CIMT, assessed by repeated ultrasound measurements) in a longitudinal multivariate model. Participants (mean age 52 years, 47% women) had a mean smoking duration of 32 years with a median daily consumption of 20 cigarettes. Baseline CIMT was 1185 μm (95% confidence interval [CI]: 1082-1287) and increased by 93 μm (95% CI: 25-161) and 108 μm (95% CI: 33-183) after 1 and 3 years, respectively. Age, male sex, daily cigarette consumption, systolic blood pressure (SBP), but neither low-density lipoprotein cholesterol nor hs-CRP, were independently associated with baseline CIMT (all P ≤ .05). Baseline SBP, but neither low-density lipoprotein cholesterol nor hs-CRP, was associated with 3-year atherosclerosis progression (P = .01 at 3 years). The higher the SBP at baseline, the steeper was the CIMT increase over 3-year follow-up. We found an increase of 26 μm per each 10-mmHg raise in SBP at 1 year and an increase of 39 μm per each 10 mmHg raise in SBP at 3 years. Due to insufficient statistical power, we could not exclude an effect of smoking abstinence on CIMT progression. Control of blood pressure may be an important factor to limit atherosclerosis progression in smokers, besides support for smoking cessation. Among 260 smokers aged 40-70 years with a mean smoking duration of 32 years, baseline SBP was associated with atherosclerosis progression over 3 years, as measured by CIMT (P = .01 at 3 years), independently of smoking variables and other CVRFs. The higher the

  9. Early atherosclerosis and vascular inflammation in mice with diet-induced type 2 diabetes

    DEFF Research Database (Denmark)

    Bartels, E D; Bang, C A; Nielsen, L B

    2009-01-01

    and the median lesion area was 8.0 times higher than in fat-fed wild-type mice (P = 0.001). Intracellular adhesion molecule-1 staining of the aortic endothelium was most pronounced in the fat-fed apoB transgenic mice. CONCLUSIONS: Our findings suggest that diet-induced type 2 diabetes causes early......BACKGROUND: Obesity and type 2 diabetes increase the risk of atherosclerosis. It is unknown to what extent this reflects direct effects on the arterial wall or secondary effects of hyperlipidaemia. MATERIALS AND METHODS: The effect of obesity and type 2 diabetes on the development...

  10. Neighborhood characteristics influence DNA methylation of genes involved in stress response and inflammation: The Multi-Ethnic Study of Atherosclerosis.

    Science.gov (United States)

    Smith, Jennifer A; Zhao, Wei; Wang, Xu; Ratliff, Scott M; Mukherjee, Bhramar; Kardia, Sharon L R; Liu, Yongmei; Roux, Ava V Diez; Needham, Belinda L

    2017-08-01

    Living in a disadvantaged neighborhood is associated with poor health outcomes even after accounting for individual-level socioeconomic factors. The chronic stress of unfavorable neighborhood conditions may lead to dysregulation of the stress reactivity and inflammatory pathways, potentially mediated through epigenetic mechanisms such as DNA methylation. We used multi-level models to examine the relationship between 2 neighborhood conditions and methylation levels of 18 genes related to stress reactivity and inflammation in purified monocytes from 1,226 participants of the Multi-Ethnic Study of Atherosclerosis (MESA), a population-based sample of US adults. Neighborhood socioeconomic disadvantage, a summary of 16 census-based metrics, was associated with DNA methylation [False discovery rate (FDR) q-value ≤ 0.1] in 2 out of 7 stress-related genes evaluated (CRF, SLC6A4) and 2 out of 11 inflammation-related genes (F8, TLR1). Neighborhood social environment, a summary measure of aesthetic quality, safety, and social cohesion, was associated with methylation in 4 of the 7 stress-related genes (AVP, BDNF, FKBP5, SLC6A4) and 7 of the 11 inflammation-related genes (CCL1, CD1D, F8, KLRG1, NLRP12, SLAMF7, TLR1). High socioeconomic disadvantage and worse social environment were primarily associated with increased methylation. In 5 genes with significant associations between neighborhood and methylation (FKBP5, CD1D, F8, KLRG1, NLRP12), methylation was associated with gene expression of at least one transcript. These results demonstrate that multiple dimensions of neighborhood context may influence methylation levels and subsequent gene expression of stress- and inflammation-related genes, even after accounting for individual socioeconomic factors. Further elucidating the molecular mechanisms underlying these relationships will be important for understanding the etiology of health disparities.

  11. microRNAs in the regulation of dendritic cell functions in inflammation and atherosclerosis.

    Science.gov (United States)

    Busch, Martin; Zernecke, Alma

    2012-08-01

    Atherosclerosis has been established as a chronic inflammatory disease of the vessel wall. Among the mononuclear cell types recruited to the lesions, specialized dendritic cells (DCs) have gained increasing attention, and their secretory products and interactions shape the progression of atherosclerotic plaques. The regulation of DC functions by microRNAs (miRNAs) may thus be of primary importance in disease. We here systematically summarize the biogenesis and functions of miRNAs and provide an overview of miRNAs in DCs, their targets, and potential implications for atherosclerosis, with a particular focus on the best characterized miRNAs in DCs, namely, miR-155 and miR-146. MiRNA functions in DCs range from regulation of lipid uptake to cytokine production and T cell responses with a complex picture emerging, in which miRNAs cooperate or antagonize DC behavior, thereby promoting or counterbalancing inflammatory responses. As miRNAs regulate key functions of DCs known to control atherosclerotic vascular disease, their potential as a therapeutic target holds promise and should be attended to in future research.

  12. Effect of 12-O-tetradecanoylphorbol-13-acetate-induced psoriasis-like skin lesions on systemic inflammation and atherosclerosis in hypercholesterolaemic apolipoprotein E deficient mice

    DEFF Research Database (Denmark)

    Madsen, Marie; Hansen, Peter Riis; Nielsen, Lars Bo

    2016-01-01

    BACKGROUND: Risk of cardiovascular disease is increased in patients with psoriasis, but molecular mechanisms linking the two conditions have not been clearly established. Lack of appropriate animal models has hampered generation of new knowledge in this area of research and we therefore sought...... to develop an animal model with combined atherosclerosis and psoriasis-like skin inflammation. METHODS: Topical 12-O-tetradecanoylphorbol-13-acetate (TPA) was applied to the ears twice per week for 8 weeks in atherosclerosis-prone apolipoprotein E deficient (ApoE(-/-)) mice. RESULTS: TPA led to localized...

  13. The relationship between aortic calcification on chest radiography and ionizing radiation in RERF's Adult Health Study

    International Nuclear Information System (INIS)

    Yamada, M.; Suzuki, G.; Masunari, N.; Kasagi, F.

    2003-01-01

    Aortic calcification has been reported to be an indicator of atherosclerosis and a predictor of coronary heart disease. However, the relationship between aortic calcification and conventional coronary risk factors or recently reported coronary risk factors including ionizing radiation, which is one kind of oxidative stress, has not been established. Objective: To investigate the relationship between aortic calcification and ionizing radiation in a longitudinal study design. The study cohort comprises the Radiation Effects Research Foundation's Adult Health Study participants which include atomic-bomb survivors and sex- and age-matched controls. A total of 522 men and 938 women identified as not having aortic calcification based on plain chest X-ray examinations at baseline examination between 1991 and 1993 were assessed regarding the presence of aortic calcification (mild/ severe calcification) about 10 years later. The relationship between cumulative incidence of aortic calcification and atomic-bomb radiation was analyzed using logistic regression analysis after adjusting for sex, age, and other coronary risk factors such as blood pressure, total cholesterol, and inflammation markers. Age-adjusted cumulative incidence of aortic calcification showed a possible increase with atomic-bomb radiation dose for both total aortic calcification and severe aortic calcification. But after adjusting for other coronary risk factors such as smoking, SBP, total cholesterol, HDL-cholesterol, hemoglobin A1c, and leukocyte neutropils, radiation dose was not a significant predictor of cumulative incidence of severe aortic calcification. Age-adjusted increase of cumulative incidence of aortic calcification with atomic-bomb radiation dose suggests ionizing radiation is one predictor of atheroscelerosis. Nevertheless, its predictive impact may not be as significant as conventional coronary risk factors

  14. Metabolomic and Genomic Markers of Atherosclerosis as Related to Oxidative Stress, Inflammation, and Vascular Function in Twin Astronauts

    Science.gov (United States)

    Lee, Stuart M. C.; Rana, Brinda K.; Stenger, Michael B.; Sears, Dorothy D.; Smith, Scott M.; Zwart, Sara R.; Macias, Brandon R.; Hargans, Alan R.; Sharma, Kumar; De Vivo, Immaculata

    2017-01-01

    BACKGROUND: Future human space travel will consist primarily of long-duration missions onboard the International Space Station (ISS) or exploration-class missions to Mars, its moons, or nearby asteroids. Astronauts participating in long-duration missions may be at an increased risk of oxidative stress and inflammatory damage due to radiation, psychological stress, altered physical activity, nutritional insufficiency, and hyperoxia during extravehicular activity. By studying one identical twin during his 1-year ISS mission and his ground-based twin, this work extends a current NASA-funded investigation to determine whether these spaceflight factors contribute to an accelerated progression of atherosclerosis. This study of twins affords a unique opportunity to examine spaceflight-related atherosclerosis risk that is independent of the confounding factors associated with different genotypes. PURPOSE: The purpose of this investigation was to determine whether biomarkers of oxidative and inflammatory stress are elevated during and after long-duration spaceflight and determine if a relation exists between levels of these biomarkers and structural and functional indices of atherosclerotic risk measured in the carotid and brachial arteries. These physiological and biochemical data will be extended by using an exploratory approach to investigate the relationship between intermediate phenotypes and risk factors for atherosclerosis and the metabolomic signature from plasma and urine samples. Since metabolites are often the indirect products of gene expression, we simultaneously assessed gene expression and DNA methylation in leukocytes. HYPOTHESIS: We predict that, compared to the ground-based twin, the space-flown twin will experience elevated biomarkers of oxidative stress and inflammatory damage, altered arterial structure and function, accelerated telomere shortening, dysregulation of genes associated with oxidative stress and inflammation, and a metabolic profile shift

  15. Individual serum saturated fatty acids and markers of chronic subclinical inflammation: the Insulin Resistance Atherosclerosis Study.

    Science.gov (United States)

    Santaren, Ingrid D; Watkins, Steven M; Liese, Angela D; Wagenknecht, Lynne E; Rewers, Marian J; Haffner, Steven M; Lorenzo, Carlos; Festa, Andreas; Bazinet, Richard P; Hanley, Anthony J

    2017-11-01

    Recent evidence has documented distinct effects of individual saturated FAs (SFAs) on cardiometabolic outcomes, with potential protective effects from odd- and very long-chain SFAs (VLSFAs). Cross-sectional and prospective associations of individual serum SFAs (12:0, 14:0, 15:0, 16:0, 18:0, 20:0, 22:0, and total SFA) with proinflammatory biomarkers and adiponectin were investigated in 555 adults from the IRAS. Principal component analysis (PCA) of proinflammatory markers yielded three clusters: principal component (PC) 1: fibrinogen, white cell count, C-reactive protein; PC 2: plasminogen activator inhibitor-1 (PAI-1), TNF-α, IL-18; PC 3: IL-6 and IL-8. Cross-sectional analyses on proinflammatory PCs and adiponectin, and prospective analyses on 5 year PAI-1 and fibrinogen concentrations were conducted with multiple regression. Total SFA and 16:0 were positively associated with PC 1 and PC 2, and negatively associated with adiponectin. The 14:0 was positively associated with PC 1 and negatively associated with adiponectin. In contrast, 15:0, 20:0, and 22:0 were negatively associated with PC 2, and 20:0 and 22:0 were positively associated with adiponectin. The 18:0 was negatively associated with PC 3. Prospectively, 15:0, 18:0, 20:0, and 22:0 were negatively associated with 5 year PAI-1 concentrations. The results demonstrate that individual SFAs have distinct roles in subclinical inflammation, highlighting the unique metabolic impacts of individual SFAs. Copyright © 2017 by the American Society for Biochemistry and Molecular Biology, Inc.

  16. Atorvastatin Protects Vascular Smooth Muscle Cells From TGF-β1-Stimulated Calcification by Inducing Autophagy via Suppression of the β-Catenin Pathway

    Directory of Open Access Journals (Sweden)

    Demin Liu

    2014-01-01

    Full Text Available Background: Arterial calcification is a major event in the progression of atherosclerosis. It is reported that statins exhibit various protective effects against vascular smooth muscle cell (VSMC inflammation and proliferation in cardiovascular remodeling. Although statins counteract atherosclerosis, the molecular mechanisms of statins on the calcium release from VSMCs have not been clearly elucidated. Methods: Calcium content of VSMCs was measured using enzyme-linked immunosorbent assay (ELISA. The expression of proteins involved in cellular transdifferentiation was analyzed by western blot. Cell autophagy was measured by fluorescence microscopic analysis for acridine orange staining and transmission electron microscopy analysis. The autophagic inhibitors (3-MA, chloroquine, NH4Cl and bafilomycin A1 and β-catenin inhibitor JW74 were used to assess the effects of atorvastatin on autophagy and the involvement of β-catenin on cell calcification respectively. Furthermore, cell transfection was performed to overexpress β-catenin. Results: In VSMCs, atorvastatin significantly suppressed transforming growth factor-β1 (TGF-β1-stimulated calcification, accompanied by the induction of autophagy. Downregulation of autophagy with autophagic inhibitors significantly suppressed the inhibitory effect of atorvastatin on cell calcification. Moreover, the beneficial effect of atorvastatin on calcification and autophagy was reversed by β-catenin overexpression. Conversely, JW74 supplement enhanced this effect. Conclusion: These data demonstrated that atorvastatin protect VSMC from TGF-β1-stimulated calcification by inducing autophagy through suppression of the β-catenin pathway, identifying autophagy induction might be a therapeutic strategy for use in vascular calcification.

  17. Inflammasomes and Atherosclerosis

    Directory of Open Access Journals (Sweden)

    S. Vallurupalli, MD

    2016-09-01

    Full Text Available Inflammation plays an important role in atherosclerosis. Inflammasomes play a crucial role in innate immunity, which mediates the body’s response to various pathogens. Of the different types of inflammasomes, NLRP3 has been implicated in atherosclerosis through the production of proinflammatory cytokines, IL-1β and IL-18. This review describes the role of the NLRP3 inflammasome in atherosclerosis and discusses potential therapeutic targets in the inflammasome pathway.

  18. Microvascular inflammation in atherosclerosis

    Directory of Open Access Journals (Sweden)

    Laura Vitiello

    2014-06-01

    Full Text Available Atherogenesis is the pathogenetic process leading to formation of the atheroma lesion. It is associated to a chronic inflammatory state initially stimulated by an aberrant accumulation of lipid molecules beyond the endothelial barrier. This event triggers a cascade of deleterious events mainly through immune cell stimulation with the consequent liberation of potent pro-inflammatory and tissue damaging mediators. The atherogenetic process implies marked modifications of endothelial cell functions and a radical change in the endothelial–leukocyte interaction pattern. Moreover, accumulating evidence shows an important link between microvascular and inflammatory responses and major cardiovascular risk factors. This review illustrates the current knowledge on the effects of obesity, hypercholesterolemia and diabetes on microcirculation; their pathophysiological implications will be discussed.

  19. Inflammation, thrombosis, and atherosclerosis

    DEFF Research Database (Denmark)

    de Maat, M.P.M.; Bladbjerg, E.M.; Drivsholm, T.

    2003-01-01

    artery and the assessment of plaque occurrence. Plasma samples were analyzed for the concentration of C-reactive protein (CRP), fibrinogen, d-dimer, plasminogen activator inhibitor type-1 (PAI-1) antigen and activity, tissue-type plasminogen activator (t-PA) antigen and activity, factor VII (FVII......) antigen, FVII coagulant activity (FVII:C) and activated FVII (FVIIa). DNA variations were determined for fibrinogen, PAI-1, t-PA, FVII, factor XIII and methylene tetrahydrofolate reductase (MTHFR). Subjects with high IMT (upper 10% of distribution, n = 63) had higher CRP levels [2.2 mg L-1 (SE 0.3)] than...... subjects with IMT in the lowest tertile (n = 217) [1.7 mg L-1 (SE 0.1), P = 0.04], whereas there was no association between the hemostatic variables and IMT. There was an association between fibrinogen and d-dimer concentrations and number of plaques (P

  20. Nonalcoholic fatty liver disease (NAFLD – a new factor that interplays between inflammation, malnutrition, and atherosclerosis in elderly hemodialysis patients

    Directory of Open Access Journals (Sweden)

    Mikolasevic I

    2014-08-01

    remarkable positive correlation between NAFLD and high-sensitivity C-reactive protein (hs-CRP (r=0.659; P<0.0001 and consequent negative correlation with the nutritional parameter, serum albumin (r=-0.321; P=0.004. Interestingly, we showed that in contrast to the general population, where NAFLD is associated with obesity, in the present study, there was no statistically significant association between NAFLD and overnutrition in elderly HD patients. Furthermore, the presence of NAFLD, low serum albumin levels, and high hs-CRP were strong predictors of poor outcome in our elderly HD patients. Conclusion: Our results indicated that NAFLD probably interplays between inflammation, malnutrition, and atherosclerosis in elderly HD patients. NAFLD could be a new factor that contributes to type 2 malnutrition in elderly HD patients, who may be amenable to adequate nutritional and HD support. Keywords: cardiovascular risk, serum albumin, high-sensitivity C-reactive protein (hs-CRP

  1. Increased levels of the calcification marker matrix Gla Protein and the inflammatory markers YKL-40 and CRP in patients with type 2 diabetes and ischemic heart disease

    DEFF Research Database (Denmark)

    Thomsen, Stine B; Rathcke, Camilla N; Zerahn, Bo

    2010-01-01

    . In the present study levels of markers of calcification (MGP) and inflammation (YKL-40, hsCRP) were evaluated in patients with T2 D and/or ischemic heart disease (IHD). MATERIALS AND METHODS: The study population consisted of 1) patients with T2D (n = 45); 2) patients with IHD (n = 37); patients with both T2D......OBJECTIVE AND DESIGN: Low grade inflammation is of pathogenic importance in atherosclerosis and in the development of cardiovascular disease (CVD) and type 2 diabetes (T2D). Matrix GLA protein (MGP), an inhibitor of medial calcification of arteries, is increased in patients with atherosclerosis...... and IHD (n = 20) and 4) healthy controls (n = 20). Biochemical parameters were measured in venous blood samples. RESULTS: Levels of MGP, YKL-40 and hsCRP were increased in patients with IHD and/or T2D (p T2D and IHD had higher MGP levels (p

  2. Exposure to ambient air pollution and calcification of the mitral annulus and aortic valve: the multi-ethnic study of atherosclerosis (MESA).

    Science.gov (United States)

    Tibuakuu, Martin; Jones, Miranda R; Navas-Acien, Ana; Zhao, Di; Guallar, Eliseo; Gassett, Amanda J; Sheppard, Lianne; Budoff, Matthew J; Kaufman, Joel D; Michos, Erin D

    2017-12-21

    Long-term exposure to high ambient air pollution has been associated with coronary artery calcium (CAC), a marker of cardiovascular disease (CVD). Calcifications of left-sided heart valves are also markers of CVD risk. We investigated whether air pollution was associated with valvular calcification and its progression. We studied 6253 MESA participants aged 45-84 years who underwent two cardiac CT scans 2.5 years apart to quantify aortic valve calcium (AVC) and mitral annular calcium (MAC). CAC was included for the same timeframe for comparison with AVC/MAC. Ambient particulate matter AVC and MAC at baseline were 13% and 9% respectively, compared to 50% prevalence of CAC. The adjusted prevalence ratios of AVC and MAC for each 5 μg/m 3 higher PM 2.5 was 1.19 (95% CI 0.87, 1.62) and 1.20 (0.81, 1.77) respectively, and for CAC was 1.14 (1.01, 1.27). Over 2.5 years, the mean change in Agatston units/year for each 5 μg/m 3 higher PM 2.5 concentration was 0.29 (-5.05, 5.63) for AVC and 4.38 (-9.13, 17.88) for MAC, compared to 8.66 (0.61, 16.71) for CAC. We found no significant associations of NOx with AVC and MAC. Our findings suggest a trend towards increased 2.5-year progression of MAC with exposure to outdoor PM 2.5 , although this association could not be confirmed. Additional well-powered studies with longer periods of follow-up are needed to further study associations of air pollution with valvular calcium. Although MESA is not a clinical trial, this cohort is registered at ClinicalTrials.gov Identifier: NCT00005487; Date of registration May 25, 2000.

  3. Molecular imaging of inflammation in the ApoE -/- mouse model of atherosclerosis with IodoDPA

    Energy Technology Data Exchange (ETDEWEB)

    Foss, Catherine A., E-mail: cfoss1@jhmi.edu [Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD 21287 (United States); Bedja, Djahida [Department of Medicine, Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD 21287 (United States); Faculty of Medicine and Health Sciences, Macquarie University, Sydney (Australia); Mease, Ronnie C.; Wang, Haofan [Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD 21287 (United States); Kass, David A. [Department of Medicine, Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD 21287 (United States); Chatterjee, Subroto [Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21287 (United States); Pomper, Martin G. [Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD 21287 (United States)

    2015-05-22

    Background: Atherosclerosis is a common and serious vascular disease predisposing individuals to myocardial infarction and stroke. Intravascular plaques, the pathologic lesions of atherosclerosis, are largely composed of cholesterol-laden luminal macrophage-rich infiltrates within a fibrous cap. The ability to detect those macrophages non-invasively within the aorta, carotid artery and other vessels would allow physicians to determine plaque burden, aiding management of patients with atherosclerosis. Methods and results: We previously developed a low-molecular-weight imaging agent, [{sup 125}I]iodo-DPA-713 (iodoDPA), which selectively targets macrophages. Here we use it to detect both intravascular macrophages and macrophage infiltrates within the myocardium in the ApoE -/- mouse model of atherosclerosis using single photon emission computed tomography (SPECT). SPECT data were confirmed by echocardiography, near-infrared fluorescence imaging and histology. SPECT images showed focal uptake of radiotracer at the aortic root in all ApoE -/- mice, while the age-matched controls were nearly devoid of radiotracer uptake. Focal radiotracer uptake along the descending aorta and within the myocardium was also observed in affected animals. Conclusions: IodoDPA is a promising new imaging agent for atherosclerosis, with specificity for the macrophage component of the lesions involved. - Highlights: • [{sup 125}I]iodoDPA SPECT detects atherosclerotic plaques in ApoE -/- mice with high contrast. • Plaques are detected in ApoE -/- mice regardless of diet with iodoDPA. • iodoDPA has very low uptake in healthy tissue including healthy TSPO + tissues at 24 h.

  4. Molecular imaging of inflammation in the ApoE -/- mouse model of atherosclerosis with IodoDPA

    International Nuclear Information System (INIS)

    Foss, Catherine A.; Bedja, Djahida; Mease, Ronnie C.; Wang, Haofan; Kass, David A.; Chatterjee, Subroto; Pomper, Martin G.

    2015-01-01

    Background: Atherosclerosis is a common and serious vascular disease predisposing individuals to myocardial infarction and stroke. Intravascular plaques, the pathologic lesions of atherosclerosis, are largely composed of cholesterol-laden luminal macrophage-rich infiltrates within a fibrous cap. The ability to detect those macrophages non-invasively within the aorta, carotid artery and other vessels would allow physicians to determine plaque burden, aiding management of patients with atherosclerosis. Methods and results: We previously developed a low-molecular-weight imaging agent, [ 125 I]iodo-DPA-713 (iodoDPA), which selectively targets macrophages. Here we use it to detect both intravascular macrophages and macrophage infiltrates within the myocardium in the ApoE -/- mouse model of atherosclerosis using single photon emission computed tomography (SPECT). SPECT data were confirmed by echocardiography, near-infrared fluorescence imaging and histology. SPECT images showed focal uptake of radiotracer at the aortic root in all ApoE -/- mice, while the age-matched controls were nearly devoid of radiotracer uptake. Focal radiotracer uptake along the descending aorta and within the myocardium was also observed in affected animals. Conclusions: IodoDPA is a promising new imaging agent for atherosclerosis, with specificity for the macrophage component of the lesions involved. - Highlights: • [ 125 I]iodoDPA SPECT detects atherosclerotic plaques in ApoE -/- mice with high contrast. • Plaques are detected in ApoE -/- mice regardless of diet with iodoDPA. • iodoDPA has very low uptake in healthy tissue including healthy TSPO + tissues at 24 h

  5. Cardiovascular calcification. An inflammatory disease

    International Nuclear Information System (INIS)

    New, S.E.P.; Aikawa, E.

    2011-01-01

    Cardiovascular calcification is an independent risk factor for cardiovascular morbidity and mortality. This disease of dysregulated metabolism is no longer viewed as a passive degenerative disease, but instead as an active process triggered by pro-inflammatory cues. Furthermore, a positive feedback loop of calcification and inflammation is hypothesized to drive disease progression in arterial calcification. Both calcific aortic valve disease and atherosclerotic arterial calcification may possess similar underlying mechanisms. Early histopathological studies first highlighted the contribution of inflammation to cardiovascular calcification by demonstrating the accumulation of macrophages and T lymphocytes in 'early' lesions within the aortic valves and arteries. A series of in vitro work followed, which gave a mechanistic insight into the stimulation of smooth muscle cells to undergo osteogenic differentiation and mineralization. The emergence of novel technology, in the form of animal models and more recently molecular imaging, has enabled accelerated progression of this field, by providing strong evidence regarding the concept of this disorder as an inflammatory disease. Although there are still gaps in our knowledge of the mechanisms behind this disorder, this review discusses the various studies that have helped form the concept of the inflammation-dependent cardiovascular calcification paradigm. (author)

  6. Pericardial and thoracic peri-aortic adipose tissues contribute to systemic inflammation and calcified coronary atherosclerosis independent of body fat composition, anthropometric measures and traditional cardiovascular risks

    International Nuclear Information System (INIS)

    Yun, Chun-Ho; Lin, Tin-Yu; Wu, Yih-Jer; Liu, Chuan-Chuan; Kuo, Jen-Yuan; Yeh, Hung-I.; Yang, Fei-Shih; Chen, Su-Chiu; Hou, Charles Jia-Yin; Bezerra, Hiram G.; Hung, Chung-Lieh; Cury, Ricardo C.

    2012-01-01

    Background: Coronary atherosclerosis has traditionally been proposed to be associated with several cardiovascular risk factors and anthropometric measures. However, clinical data regarding the independent value of visceral adipose tissue in addition to such traditional predictors remains obscure. Materials and methods: We subsequently studied 719 subjects (age: 48.1 ± 8.3 years, 25% females) who underwent multidetector computed tomography (MDCT) for coronary calcium score (CCS) quantification. Baseline demographic data and anthropometric measures were taken with simultaneous body fat composition estimated. Visceral adipose tissue of pericardial and thoracic peri-aortic fat was quantified by MDCT using TeraRecon Aquarius workstation (San Mateo, CA). Traditional cardiovascular risk stratification was calculated by metabolic (NCEP ATP III) and Framingham (FRS) scores and high-sensitivity CRP (Hs-CRP) was taken to represent systemic inflammation. The independent value of visceral adipose tissue to systemic inflammation and CCS was assessed by utilizing multivariable regression analysis. Results: Of all subjects enrolled in this study, the mean values for pericardial and peri-aortic adipose tissue were 74.23 ± 27.51 and 7.23 ± 3.69 ml, respectively. Higher visceral fat quartile groups were associated with graded increase of risks for cardiovascular diseases. Both adipose burdens strongly correlated with anthropometric measures including waist circumference, body weight and body mass index (all p < 0.001). In addition, both visceral amount correlates well with ATP and FRS scores, all lipid profiles and systemic inflammation marker in terms of Hs-CRP (all p < 0.001). After adjustment for baseline variables, both visceral fat were independently related to Hs-CRP levels (all p < 0.05), but only pericardial fat exerted independent role in coronary calcium deposit. Conclusion: Both visceral adipose tissues strongly correlated with systemic inflammation beyond traditional

  7. Germinated Brown Rice Attenuates Atherosclerosis and Vascular Inflammation in Low-Density Lipoprotein Receptor-Knockout Mice.

    Science.gov (United States)

    Zhao, Ruozhi; Ghazzawi, Nora; Wu, Jiansu; Le, Khuong; Li, Chunyang; Moghadasian, Mohammed H; Siow, Yaw L; Apea-Bah, Franklin B; Beta, Trust; Yin, Zhengfeng; Shen, Garry X

    2018-05-02

    The present study investigates the impact of germinated brown rice (GBR) on atherosclerosis and the underlying mechanism in low-density lipoprotein receptor-knockout (LDLr-KO) mice. The intensity of atherosclerosis in aortas of LDLr-KO mice receiving diet supplemented with 60% GBR (weight/weight) was significantly less than that in mice fed with 60% white rice (WR) or control diet ( p mice fed with WR diet was significantly more than that from mice receiving the control diet ( p mice in comparison to the WR diet ( p mice compared to WR. The anti-atherosclerotic effect of GBR in LDLr-KO mice at least in part results from its anti-inflammatory activity.

  8. Deficiency of ATP-binding cassette transporters A1 and G1 in macrophages increases inflammation and accelerates atherosclerosis in mice.

    Science.gov (United States)

    Westerterp, Marit; Murphy, Andrew J; Wang, Mi; Pagler, Tamara A; Vengrenyuk, Yuliya; Kappus, Mojdeh S; Gorman, Darren J; Nagareddy, Prabhakara R; Zhu, Xuewei; Abramowicz, Sandra; Parks, John S; Welch, Carrie; Fisher, Edward A; Wang, Nan; Yvan-Charvet, Laurent; Tall, Alan R

    2013-05-24

    Plasma high-density lipoprotein levels are inversely correlated with atherosclerosis. Although it is widely assumed that this is attributable to the ability of high-density lipoprotein to promote cholesterol efflux from macrophage foam cells, direct experimental support for this hypothesis is lacking. To assess the role of macrophage cholesterol efflux pathways in atherogenesis. We developed mice with efficient deletion of the ATP-binding cassette transporters A1 and G1 (ABCA1 and ABCG1) in macrophages (MAC-ABC(DKO) mice) but not in hematopoietic stem or progenitor populations. MAC-ABC(DKO) bone marrow (BM) was transplanted into Ldlr(-/-) recipients. On the chow diet, these mice had similar plasma cholesterol and blood monocyte levels but increased atherosclerosis compared with controls. On the Western-type diet, MAC-ABC(DKO) BM-transplanted Ldlr(-/-) mice had disproportionate atherosclerosis, considering they also had lower very low-density lipoprotein/low-density lipoprotein cholesterol levels than controls. ABCA1/G1-deficient macrophages in lesions showed increased inflammatory gene expression. Unexpectedly, Western-type diet-fed MAC-ABC(DKO) BM-transplanted Ldlr(-/-) mice displayed monocytosis and neutrophilia in the absence of hematopoietic stem and multipotential progenitor cells proliferation. Mechanistic studies revealed increased expressions of machrophage colony stimulating factor and granulocyte colony stimulating factor in splenic macrophage foam cells, driving BM monocyte and neutrophil production. These studies show that macrophage deficiency of ABCA1/G1 is proatherogenic likely by promoting plaque inflammation and uncover a novel positive feedback loop in which cholesterol-laden splenic macrophages signal BM progenitors to produce monocytes, with suppression by macrophage cholesterol efflux pathways.

  9. Non-invasive assessment of coronary calcification

    International Nuclear Information System (INIS)

    Vliegenthart, Rozemarijn; Oei, Hok-Hay S.; Hofman, Albert; Oudkerk, Matthijs; Witteman, Jackqueline C. M.

    2004-01-01

    Electron-beam tomography (EBT) and multi-detector computed tomography (MDCT) enable the noninvasive assessment of coronary calcification. The amount of coronary calcification, as detected by EBT, has a close relation with the amount of coronary atherosclerosis, which is the substrate for the occurrence of myocardial infarction and sudden cardiac death. Calcification of the coronary arteries can be seen as a cumulative measure of life-time exposure to cardiovascular risk factors. Several studies have shown that the amount of coronary calcification is associated with the risk of coronary heart disease. Therefore, coronary calcification is a promising method for non-invasive detection of asymptomatic subjects at high risk of developing coronary heart disease. Whether measurement of coronary calcification also increases the predictive power of coronary events based on cardiovascular risk factors is topic of current research

  10. Hepatocellular calcification

    DEFF Research Database (Denmark)

    Ladefoged, Claus; Frifelt, J J

    1987-01-01

    Autopsy of a twenty year old girl dying from complications of renal and cardiac failure demonstrated severe hepatocellular calcification, a rare finding. The pathogenesis is thought to be a combination of dystrophic calcification caused by severe centrilobular necrosis and metastatic calcificatio...

  11. Development of an inflammation imaging tracer, 111In-DOTA-DAPTA, targeting chemokine receptor CCR5 and preliminary evaluation in an ApoE-/- atherosclerosis mouse model.

    Science.gov (United States)

    Wei, Lihui; Petryk, Julia; Gaudet, Chantal; Kamkar, Maryam; Gan, Wei; Duan, Yin; Ruddy, Terrence D

    2018-02-07

    Chemokine receptor 5 (CCR5) plays an important role in atherosclerosis. Our objective was to develop a SPECT tracer targeting CCR5 for imaging plaque inflammation by radiolabeling D-Ala-peptide T-amide (DAPTA), a CCR5 antagonist, with 111 In. 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA) conjugated DAPTA (DOTA-DAPTA) was labeled with 111 In. Cell uptake studies were conducted in U87-CD4-CCR5 and U87-MG cells. Biodistribution was determined in C57BL/6 mice. Autoradiography, en face and Oil Red O (ORO) imaging studies were performed in ApoE -/- mice. DOTA-DAPTA was radiolabeled with 111 In with high radiochemical purity (> 98%) and specific activity (70 MBq·nmol). 111 In-DOTA-DAPTA exhibited fast blood and renal clearance and high spleen uptake. The U87-CD4-CCR5 cells had significantly higher uptake in comparison to the U87-MG cells. The cell uptake was reduced by three times with DAPTA, indicating the receptor specificity of the uptake. Autoradiographic images showed significantly higher lesion uptake of 111 In-DOTA-DAPTA in ApoE -/- mice than that in C57BL/6 mice. The tracer uptake in 4 month old ApoE -/- high fat diet (HFD) mice with blocking agent was twofold lower than the same mice without the blocking agent, demonstrating the specificity of the tracer for the CCR5 receptor. 111 In-DOTA-DAPTA, specifically targeting chemokine receptor CCR5, is a potential SPECT agent for imaging inflammation in atherosclerosis.

  12. An essential role for diet in exercise-mediated protection against dyslipidemia, inflammation and atherosclerosis in ApoE⁻/⁻ mice.

    Directory of Open Access Journals (Sweden)

    Liliana Cesar

    2011-02-01

    Full Text Available Diet and exercise promote cardiovascular health but their relative contributions to atherosclerosis are not fully known. The transition from a sedentary to active lifestyle requires increased caloric intake to achieve energy balance. Using atherosclerosis-prone ApoE-null mice we sought to determine whether the benefits of exercise for arterial disease are dependent on the food source of the additional calories.Mice were fed a high-fat diet (HF for 4.5 months to initiate atherosclerosis after which time half were continued on HF while the other half were switched to a high protein/fish oil diet (HP. Half of each group underwent voluntary running. Food intake, running distance, body weight, lipids, inflammation markers, and atherosclerotic plaque were quantified. Two-way ANOVA tests were used to assess differences and interactions between groups. Exercised mice ran approximately 6-km per day with no difference between groups. Both groups increased food intake during exercise and there was a significant main effect of exercise F((1,44 = 9.86, p<0.01 without interaction. Diet or exercise produced significant independent effects on body weight (diet: F(1,52 = 6.85, p = 0.012; exercise: F(1,52 = 9.52, p<0.01 with no significant interaction. The combination of HP diet and exercise produced a greater decrease in total cholesterol (F(1, 46 = 7.9, p<0.01 and LDL (F(1, 46 = 7.33, p<0.01 with a large effect on the size of the interaction. HP diet and exercise independently reduced TGL and VLDL (p<0.05 and 0.001 respectively. Interleukin 6 and C-reactive protein were highest in the HF-sedentary group and were significantly reduced by exercise only in this group. Plaque accumulation in the aortic arch, a marker of cardiovascular events was reduced by the HP diet and the effect was significantly potentiated by exercise only in this group resulting in significant plaque regression (F1, 49 = 4.77, p<0.05.In this model exercise is

  13. AGE and their receptor RAGE in systemic autoimmune diseases : An inflammation propagating factor contributing to accelerated atherosclerosis

    NARCIS (Netherlands)

    Nienhuis, Hans L. A.; Westra, Johanna; Smit, Andries J.; Limburg, Pieter C.; Kallenberg, Cees G. M.; Bijl, Marc

    2009-01-01

    Systemic autoimmune diseases are associated with inflammation, and oxidative stress favouring the formation of advanced glycation endproducts (AGE), able to modulate cellular functions by activation of receptor for advanced glycation endproducts (RAGE). As RAGE expression is increased in an

  14. Self-reported experiences of discrimination and inflammation among men and women: The multi-ethnic study of atherosclerosis.

    Science.gov (United States)

    Kershaw, Kiarri N; Lewis, Tené T; Diez Roux, Ana V; Jenny, Nancy S; Liu, Kiang; Penedo, Frank J; Carnethon, Mercedes R

    2016-04-01

    To examine associations of lifetime and everyday discrimination with inflammation independent of sociodemographic characteristics. Cross-sectional associations of self-reported experiences of everyday discrimination and lifetime discrimination with interleukin-6 (IL-6) and C-reactive protein (CRP) were examined by gender in a multiethnic sample of 3,099 men and 3,468 women aged 45-84 years. Everyday discrimination, lifetime discrimination due to any attribution, and lifetime discrimination attributed to race/ethnicity were based on self-report, and IL-6 and CRP were assayed from blood samples. Among women, higher levels of all 3 discrimination measures were significantly associated with higher IL-6 in models adjusted for sociodemographic characteristics, recent infection, anti-inflammatory medication use, and hormone replacement therapy use. All associations were attenuated with adjustment for body mass index (BMI). For men, everyday discrimination was inversely associated with IL-6 in all adjusted models. Lifetime discrimination was not related to IL-6 among men. Discrimination was unassociated with CRP in all models for both men and women. The association between discrimination and inflammation varied by gender and marker of inflammation. These findings highlight the complex relationship between discrimination and cardiovascular disease (CVD) risk and point to areas in need of further research. (PsycINFO Database Record (c) 2016 APA, all rights reserved).

  15. Association between air pollution and coronary artery calcification within six metropolitan areas in the USA (the Multi-Ethnic Study of Atherosclerosis and Air Pollution): a longitudinal cohort study.

    Science.gov (United States)

    Kaufman, Joel D; Adar, Sara D; Barr, R Graham; Budoff, Matthew; Burke, Gregory L; Curl, Cynthia L; Daviglus, Martha L; Diez Roux, Ana V; Gassett, Amanda J; Jacobs, David R; Kronmal, Richard; Larson, Timothy V; Navas-Acien, Ana; Olives, Casey; Sampson, Paul D; Sheppard, Lianne; Siscovick, David S; Stein, James H; Szpiro, Adam A; Watson, Karol E

    2016-08-13

    g PM2.5/m(3) and 7.2-139.2 parts per billion (ppb) NOX. For each 5 μg PM2.5/m(3) increase, coronary calcium progressed by 4.1 Agatston units per year (95% CI 1.4-6.8) and for each 40 ppb NOX coronary calcium progressed by 4.8 Agatston units per year (0.9-8.7). Pollutant exposures were not associated with intima-media thickness change. The estimate for the effect of a 5 μg/m(3) higher long-term exposure to PM2.5 in intima-media thickness was -0.9 μm per year (95% CI -3.0 to 1.3). For 40 ppb higher NOX, the estimate was 0.2 μm per year (-1.9 to 2.4). Increased concentrations of PM2.5 and traffic-related air pollution within metropolitan areas, in ranges commonly encountered worldwide, are associated with progression in coronary calcification, consistent with acceleration of atherosclerosis. This study supports the case for global efforts of pollution reduction in prevention of cardiovascular diseases. US Environmental Protection Agency and US National Institutes of Health. Copyright © 2016 Elsevier Ltd. All rights reserved.

  16. TNF-α production in NKT cell hybridoma is regulated by sphingosine-1-phosphate: implications for inflammation in atherosclerosis.

    Science.gov (United States)

    Ito, Shiori; Iwaki, Soichiro; Kondo, Rie; Satoh, Masashi; Iwabuchi, Kazuya; Ohkawa, Ryunosuke; Mishima, Yuko; Yatomi, Yutaka; Furumoto, Tomoo; Tsutsui, Hiroyuki; Fujii, Satoshi

    2014-06-01

    Natural killer T (NKT) cells are unique T lymphocytes that recognize glycolipid antigen and produce various cytokines. NKT cells accelerate atherosclerosis in mice. Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid and regulates T-lymphocyte trafficking. We aimed to determine the effects of S1P on the production of proinflammatory cytokine, tumor necrosis factor (TNF)-α, in NKT cell hybridomas and mouse NKT cells. NKT cell hybridomas and sorted mouse NKT cells were stimulated with S1P and α-galactosylceramide (α-GalCer), the major ligand to produce cytokines in NKT cells. TNF-α mRNA expression and protein production were determined by real-time PCR and ELISA, respectively. Cell migration was assayed using chemotaxicell. Plasma S1P was measured using HPLC. Hybridomas expressed S1P receptors, S1P1, S1P2, and S1P4. S1P and α-GalCer increased TNF-α mRNA expression and protein production. S1P enhanced TNF-α induction by α-GalCer. S1P receptor antagonists decreased the TNF-α mRNA expression induced by S1P. FTY720, an immunosuppressive S1P receptor modulator, also decreased the TNF-α mRNA expression. The migration of NKT cell hybridomas was increased by S1P. FTY720 reduced the migration induced by S1P. S1P also increased the TNF-α mRNA expression in mouse NKT cells. Plasma TNF-α levels in patients with high plasma S1P (≥500 nmol/l) were higher than those in patients with low S1P (NKT cells and enhances TNF-α production. TNF-α overproduction may induce atherogenic inflammatory responses. S1P may serve as a novel therapeutic target for amelioration of vascular inflammatory diseases.

  17. Curcuma oil attenuates accelerated atherosclerosis and macrophage foam-cell formation by modulating genes involved in plaque stability, lipid homeostasis and inflammation.

    Science.gov (United States)

    Singh, Vishal; Rana, Minakshi; Jain, Manish; Singh, Niharika; Naqvi, Arshi; Malasoni, Richa; Dwivedi, Anil Kumar; Dikshit, Madhu; Barthwal, Manoj Kumar

    2015-01-14

    In the present study, the anti-atherosclerotic effect and the underlying mechanism of curcuma oil (C. oil), a lipophilic fraction from turmeric (Curcuma longa L.), was evaluated in a hamster model of accelerated atherosclerosis and in THP-1 macrophages. Male golden Syrian hamsters were subjected to partial carotid ligation (PCL) or FeCl3-induced arterial oxidative injury (Ox-injury) after 1 week of treatment with a high-cholesterol (HC) diet or HC diet plus C. oil (100 and 300 mg/kg, orally). Hamsters fed with the HC diet were analysed at 1, 3 and 5 weeks following carotid injury. The HC diet plus C. oil-fed group was analysed at 5 weeks. In hyperlipidaemic hamsters with PCL or Ox-injury, C. oil (300 mg/kg) reduced elevated plasma and aortic lipid levels, arterial macrophage accumulation, and stenosis when compared with those subjected to arterial injury alone. Similarly, elevated mRNA transcripts of matrix metalloproteinase-2 (MMP-2), MMP-9, cluster of differentiation 45 (CD45), TNF-α, interferon-γ (IFN-γ), IL-1β and IL-6 were reduced in atherosclerotic arteries, while those of transforming growth factor-β (TGF-β) and IL-10 were increased after the C. oil treatment (300 mg/kg). The treatment with C. oil prevented HC diet- and oxidised LDL (OxLDL)-induced lipid accumulation, decreased the mRNA expression of CD68 and CD36, and increased the mRNA expression of PPARα, LXRα, ABCA1 and ABCG1 in both hyperlipidaemic hamster-derived peritoneal and THP-1 macrophages. The administration of C. oil suppressed the mRNA expression of TNF-α, IL-1β, IL-6 and IFN-γ and increased the expression of TGF-β in peritoneal macrophages. In THP-1 macrophages, C. oil supplementation prevented OxLDL-induced production of TNF-α and IL-1β and increased the levels of TGF-β. The present study shows that C. oil attenuates arterial injury-induced accelerated atherosclerosis, inflammation and macrophage foam-cell formation.

  18. Immune-Mediated Inflammation Promotes Subclinical Atherosclerosis in Recent-Onset Psoriatic Arthritis Patients without Conventional Cardiovascular Risk Factors

    Directory of Open Access Journals (Sweden)

    Rodolfo A. Kolliker Frers

    2018-02-01

    Full Text Available Studies on the inflammatory burden in recent-onset psoriatic arthritis (PsA patients without conventional cardiovascular risk factors (CVRFs are not available. This preliminary study focuses on cardiovascular risk in cutaneous psoriasis (CPs and recent-onset PsA patients. Blood biochemistry (glucose, cholesterol, uric acid, lipid profile and apolipoprotein B was analyzed using standard kits. Proatherogenic inflammation markers, C-reactive protein (CRP and interleukin-6 (IL-6, and endothelial activators monocyte chemoattractant protein-1 (MCP-1 and soluble intercellular adhesion molecule-1 (sICAM-1, were determined by enzyme-linked immunosorbent assay. Ultrasound images allowed measuring carotid intima–media thickness (cIMT. Our study first shows an increase in cIMT, and in serum levels of sICAM-1 and CRP in recent-onset PsA patients not presenting conventional CVRFs over the non-medicated time-period, from disease diagnosis to the beginning of pharmacological treatment, compared with healthy subjects. The outcome highlights the importance of monitoring serum level of sICAM1, CRP, and cIMT, and the value of primary prevention in psoriatic patients even with no history of cardiovascular events.

  19. Acute calcific retropharyngeal tendinitis

    International Nuclear Information System (INIS)

    Gonzalez, I.; Mendoza, M.; Aperribay, M.; Recondo, J.A.

    1998-01-01

    Acute calcific tendinitis results from the deposition of calcium hydroxyapatite crystals in peri articular muscular attachments. It usually develops in extremities, most often in shoulders and hips. Although the incidence is much lower, it has been reported to occur in the neck region, where it involves the tendons insertion of the longs colli muscle. We present a case of acute neck pain caused by a calcareous deposition in the tendon of the longs colli muscle, producing inflammation. We describe the clinical and radiologic features (plain radiography, CT,MRI) associated with this entire. (Author) 7 refs

  20. Coronary atherosclerosis in sudden cardiac death: An autopsy study

    Directory of Open Access Journals (Sweden)

    Sudha M

    2009-10-01

    Full Text Available Background: The incidence of ischemic heart disease (IHD has markedly increased in India over the past few years. Considering the variations in racial, dietary and lifestyle patterns in our population, it is essential to study the biology of coronary atherosclerosis in our patients. Vulnerable plaques have a large number of foam cells, extracellular lipid, thin fibrous caps and clusters of inflammatory cells and are more prone to rupture. These plaques are nourished by the microvessels arising from the vasa vasorum of the blood vessels and by lumen-derived microvessels through the fibrous cap. This autopsy study was designed to analyse the coronary arterial tree in cases of sudden cardiac death, classify coronary atherosclerotic plaques and to assess the factors contributing to vulnerability of the plaques including inflammation, calcification and microvascular density. Materials and Methods: Seven cases of sudden cardiac death were included in the study. The hearts were perfusion-fixed and the coronary arteries along with their main branches were dissected and studied. The location of the plaques, type of plaques, presence of inflammation and calcification were assessed. The cap thickness and microvessel density per 1000um 2 were assessed. The statistical significance was estimated. Results and Conclusions: Extensive high-grade coronary atherosclerotic disease was seen in all sudden cardiac death cases. Majority of the plaques were vulnerable. High-grade inflammation was seen in most of the vulnerable and ruptured plaques. All the ruptured plaques were uncalcified indicating that calcification probably stabilizes the plaques and protects against rupture. Increased microvessel density was noted in ruptured plaques compared to vulnerable plaques. However, it was not statistically significant.

  1. Computed Tomographic Distinction of Intimal and Medial Calcification in the Intracranial Internal Carotid Artery

    OpenAIRE

    Kockelkoren, Remko; Vos, Annelotte; Van Hecke, Wim; Vink, Aryan; Bleys, Ronald L. A. W.; Verdoorn, Daphne; Mali, Willem P. Th. M.; Hendrikse, Jeroen; Koek, Huiberdina L.; de Jong, Pim A.; De Vis, Jill B.

    2017-01-01

    BACKGROUND: Intracranial internal carotid artery (iICA) calcification is associated with stroke and is often seen as a proxy of atherosclerosis of the intima. However, it was recently shown that these calcifications are predominantly located in the tunica media and internal elastic lamina (medial calcification). Intimal and medial calcifications are thought to have a different pathogenesis and clinical consequences and can only be distinguished through ex vivo histological analysis. Therefore...

  2. Göttingen minipig model of diet-induced atherosclerosis: influence of mild streptozotocin-induced diabetes on lesion severity and markers of inflammation evaluated in obese, obese and diabetic, and lean control animals

    DEFF Research Database (Denmark)

    Ludvigsen, Trine Pagh; Kirk, Rikke Kaae; Christoffersen, Berit Østergaard

    2015-01-01

    in human patients, inclusion of this disease aspect in the characterization of a such model, is highly relevant. The objective of this study was to evaluate the effect of mild streptozotocin-induced diabetes on ex- and in vivo end-points in a diet-induced atherosclerotic minipig model. Castrated male...... Göttingen minipigs were fed standard chow (CD), atherogenic diet alone (HFD) or with superimposed mild streptozotocin-induced diabetes (HFD-D). Circulating markers of inflammation (C-reactive protein (CRP), oxidized low-density lipoprotein (oxLDL), plasminogen activator inhibitor-1, lipid and glucose......From a pharmacological perspective, readily-available, well-characterized animal models of cardiovascular disease, including relevant in vivo markers of atherosclerosis are important for evaluation of novel drug candidates. Furthermore, considering the impact of diabetes mellitus on atherosclerosis...

  3. Arterial calcification: friend or foe?

    Science.gov (United States)

    Nicoll, Rachel; Henein, Michael Y

    2013-07-31

    There is a significant relationship between the presence, extent and progression of coronary artery calcification (CAC) and cardiovascular (CV) events and mortality in both CV and renal patients and CAC scoring can provide improved predictive ability over risk factor scoring alone. There is also a close relationship between CAC presence and atherosclerotic plaque burden, with angiography studies showing very high sensitivity but poor specificity of CAC score for predicting obstructive disease. Nevertheless, there are objections to CAC screening because of uncertainties and lack of studies showing improved outcome. Furthermore, histopathology studies indicate that heavily calcified plaque is unlikely to result in a CV event, while the vulnerable plaque tends to be uncalcified or 'mixed', suggesting that calcification may be protective. This scenario highlights a number of paradoxes, which may indicate that the association between CAC and CV events is spurious, following from the adoption of CAC as a surrogate for high plaque burden, which itself is a surrogate for the presence of vulnerable plaque. Since studies indicate that arterial calcification is a complex, organised and regulated process similar to bone formation, there is no particular reason why it should be a reliable indicator of either the plaque burden or the risk of a future CV event. We suggest that it is time to divorce arterial calcification from atherosclerosis and to view it as a distinct pathology in its own right, albeit one which frequently coexists with atherosclerosis and is related to it for reasons which are not yet fully understood. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

  4. Implication of progranulin and C1q/TNF-related protein-3 (CTRP3) on inflammation and atherosclerosis in subjects with or without metabolic syndrome.

    Science.gov (United States)

    Yoo, Hye Jin; Hwang, Soon Young; Hong, Ho Cheol; Choi, Hae Yoon; Yang, Sae Jeong; Choi, Dong Seop; Baik, Sei Hyun; Blüher, Matthias; Youn, Byung-Soo; Choi, Kyung Mook

    2013-01-01

    Progranulin and C1q/TNF-related protein-3 (CTRP3) were recently discovered as novel adipokines which may link obesity with altered regulation of glucose metabolism, chronic inflammation and insulin resistance. We examined circulating progranulin and CTRP3 concentrations in 127 subjects with (n = 44) or without metabolic syndrome (n = 83). Furthermore, we evaluated the relationship of progranulin and CTRP3 levels with inflammatory markers and cardiometabolic risk factors, including high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), estimated glomerular filtration rate (eGFR), and adiponectin serum concentrations, as well as carotid intima-media thickness (CIMT). Circulating progranulin levels are significantly related with inflammatory markers, hsCRP (r = 0.30, P = 0.001) and IL-6 (r = 0.30, P = 0.001), whereas CTRP3 concentrations exhibit a significant association with cardiometabolic risk factors, including waist circumference (r = -0.21), diastolic blood pressure (r = -0.21), fasting glucose (r = -0.20), triglyceride (r = -0.34), total cholesterol (r = -0.25), eGFR (r = 0.39) and adiponectin (r = 0.26) levels. Serum progranulin concentrations were higher in patients with metabolic syndrome than those of the control group (199.55 [179.33, 215.53] vs. 185.10 [160.30, 204.90], P = 0.051) and the number of metabolic syndrome components had a significant positive correlation with progranulin levels (r = 0.227, P = 0.010). In multiple regression analysis, IL-6 and triglyceride levels were significant predictors of serum progranulin levels (R(2) = 0.251). Furthermore, serum progranulin level was an independent predictor for increased CIMT in subjects without metabolic syndrome after adjusting for other cardiovascular risk factors (R(2) = 0.365). Serum progranulin levels are significantly associated with systemic inflammatory markers and were an independent predictor for

  5. Implication of progranulin and C1q/TNF-related protein-3 (CTRP3 on inflammation and atherosclerosis in subjects with or without metabolic syndrome.

    Directory of Open Access Journals (Sweden)

    Hye Jin Yoo

    Full Text Available Progranulin and C1q/TNF-related protein-3 (CTRP3 were recently discovered as novel adipokines which may link obesity with altered regulation of glucose metabolism, chronic inflammation and insulin resistance.We examined circulating progranulin and CTRP3 concentrations in 127 subjects with (n = 44 or without metabolic syndrome (n = 83. Furthermore, we evaluated the relationship of progranulin and CTRP3 levels with inflammatory markers and cardiometabolic risk factors, including high-sensitivity C-reactive protein (hsCRP, interleukin-6 (IL-6, estimated glomerular filtration rate (eGFR, and adiponectin serum concentrations, as well as carotid intima-media thickness (CIMT.Circulating progranulin levels are significantly related with inflammatory markers, hsCRP (r = 0.30, P = 0.001 and IL-6 (r = 0.30, P = 0.001, whereas CTRP3 concentrations exhibit a significant association with cardiometabolic risk factors, including waist circumference (r = -0.21, diastolic blood pressure (r = -0.21, fasting glucose (r = -0.20, triglyceride (r = -0.34, total cholesterol (r = -0.25, eGFR (r = 0.39 and adiponectin (r = 0.26 levels. Serum progranulin concentrations were higher in patients with metabolic syndrome than those of the control group (199.55 [179.33, 215.53] vs. 185.10 [160.30, 204.90], P = 0.051 and the number of metabolic syndrome components had a significant positive correlation with progranulin levels (r = 0.227, P = 0.010. In multiple regression analysis, IL-6 and triglyceride levels were significant predictors of serum progranulin levels (R(2 = 0.251. Furthermore, serum progranulin level was an independent predictor for increased CIMT in subjects without metabolic syndrome after adjusting for other cardiovascular risk factors (R(2 = 0.365.Serum progranulin levels are significantly associated with systemic inflammatory markers and were an independent predictor for atherosclerosis in

  6. Increased arterial inflammation in individuals with stage 3 chronic kidney disease

    International Nuclear Information System (INIS)

    Takx, Richard A.P.; MacNabb, Megan H.; Emami, Hamed; Abdelbaky, Amr; Lavender, Zachary R.; Singh, Parmanand; Di Carli, Marcelo; Taqueti, Viviany; Foster, Courtney; Mann, Jessica; Comley, Robert A.; Weber, Chek Ing Kiu; Tawakol, Ahmed

    2016-01-01

    While it is well known that patients with chronic kidney disease (CKD) are at increased risk for the development and progression of atherosclerosis, it is not known whether arterial inflammation is increased in mild CKD. The aim of this study was to compare arterial inflammation using 18 F-FDG PET/CT in patients with CKD and in matched controls. This retrospective study included 128 patients undergoing FDG PET/CT imaging for clinical indications, comprising 64 patients with stage 3 CKD and 64 control patients matched by age, gender, and cancer history. CKD was defined according to guidelines using a calculated glomerular filtration rate (eGFR). Arterial inflammation was measured in the ascending aorta as FDG uptake on PET. Background FDG uptake (venous, subcutaneous fat and muscle) were recorded. Coronary artery calcification (CAC) was assessed using the CT images. The impact of CKD on arterial inflammation and CAC was then assessed. Arterial inflammation was higher in patients with CKD than in matched controls (standardized uptake value, SUV: 2.41 ± 0.49 vs. 2.16 ± 0.43; p = 0.002). Arterial SUV correlated inversely with eGFR (r = -0.299, p = 0.001). Venous SUV was also significantly elevated in patients with CKD, while subcutaneous fat and muscle tissue SUVs did not differ between groups. Moreover, arterial SUV remained significantly elevated in patients with CKD compared to controls after correcting for muscle and fat background, and also remained significant after adjusting for clinical risk factors. Further, CKD was associated with arterial inflammation (SUV) independent of the presence of subclinical atherosclerosis (CAC). Moderate CKD is associated with increased arterial inflammation beyond that of controls. Further, the increased arterial inflammation is independent of presence of subclinical atherosclerosis. Current risk stratification tools may underestimate the presence of atherosclerosis in patients with CKD and thereby the risk of cardiovascular

  7. Increased arterial inflammation in individuals with stage 3 chronic kidney disease

    Energy Technology Data Exchange (ETDEWEB)

    Takx, Richard A.P. [Massachusetts General Hospital and Harvard Medical School, Cardiac MR PET CT Program, Boston, MA (United States); University Medical Center Utrecht, Department of Radiology, Utrecht (Netherlands); MacNabb, Megan H.; Emami, Hamed; Abdelbaky, Amr; Lavender, Zachary R. [Massachusetts General Hospital and Harvard Medical School, Cardiac MR PET CT Program, Boston, MA (United States); Singh, Parmanand [Massachusetts General Hospital and Harvard Medical School, Cardiac MR PET CT Program, Boston, MA (United States); New York Presbyterian Hospital, Weill Cornell Medical College, Division of Cardiology, New York, NY (United States); Di Carli, Marcelo; Taqueti, Viviany; Foster, Courtney [Brigham and Women' s Hospital and Harvard Medical School, Division of Radiology, Department of Medicine, Boston, MA (United States); Mann, Jessica; Comley, Robert A.; Weber, Chek Ing Kiu [F. Hoffmann-La Roche Ltd., Basel (Switzerland); Tawakol, Ahmed [Massachusetts General Hospital and Harvard Medical School, Cardiac MR PET CT Program, Boston, MA (United States); Massachusetts General Hospital and Harvard Medical School, Cardiology Division, Boston, MA (United States); Massachusetts General Hospital, Boston, MA (United States)

    2016-02-15

    While it is well known that patients with chronic kidney disease (CKD) are at increased risk for the development and progression of atherosclerosis, it is not known whether arterial inflammation is increased in mild CKD. The aim of this study was to compare arterial inflammation using {sup 18}F-FDG PET/CT in patients with CKD and in matched controls. This retrospective study included 128 patients undergoing FDG PET/CT imaging for clinical indications, comprising 64 patients with stage 3 CKD and 64 control patients matched by age, gender, and cancer history. CKD was defined according to guidelines using a calculated glomerular filtration rate (eGFR). Arterial inflammation was measured in the ascending aorta as FDG uptake on PET. Background FDG uptake (venous, subcutaneous fat and muscle) were recorded. Coronary artery calcification (CAC) was assessed using the CT images. The impact of CKD on arterial inflammation and CAC was then assessed. Arterial inflammation was higher in patients with CKD than in matched controls (standardized uptake value, SUV: 2.41 ± 0.49 vs. 2.16 ± 0.43; p = 0.002). Arterial SUV correlated inversely with eGFR (r = -0.299, p = 0.001). Venous SUV was also significantly elevated in patients with CKD, while subcutaneous fat and muscle tissue SUVs did not differ between groups. Moreover, arterial SUV remained significantly elevated in patients with CKD compared to controls after correcting for muscle and fat background, and also remained significant after adjusting for clinical risk factors. Further, CKD was associated with arterial inflammation (SUV) independent of the presence of subclinical atherosclerosis (CAC). Moderate CKD is associated with increased arterial inflammation beyond that of controls. Further, the increased arterial inflammation is independent of presence of subclinical atherosclerosis. Current risk stratification tools may underestimate the presence of atherosclerosis in patients with CKD and thereby the risk of

  8. Dietary fatty acids on aortic root calcification in mice with metabolic syndrome.

    Science.gov (United States)

    Naranjo, Maria C; Bermudez, Beatriz; Garcia, Indara; Lopez, Sergio; Abia, Rocio; Muriana, Francisco J G; Montserrat-de la Paz, Sergio

    2017-04-19

    Metabolic syndrome (MetS) is associated with obesity, dyslipidemia, type 2 diabetes, and chronic low-grade inflammation. The aim of this study was to determine the role of high-fat low-cholesterol diets (HFLCDs) rich in SFAs (HFLCD-SFAs), MUFAs (HFLCD-MUFAs) or MUFAs plus omega-3 long-chain PUFAs (HFLCD-PUFAs) on vascular calcification by the modulation of the RANKL/RANK/OPG system in the aortic roots of Lep ob/ob LDLR -/- mice. Animals fed with HFLCD-SFAs had increased weight and a greater atheroma plaque size, calcification, and RANKL/CATHK expression in the aortic root than mice on MUFA-enriched diets, with an increasing OPG expression in the aortic roots of the latter. Our study demonstrates that compared to dietary SFAs, MUFAs from olive oil protect against atherosclerosis by interfering with vascular calcification via the RANKL/RANK/OPG system in the setting of MetS. These findings open opportunities for developing novel nutritional strategies with olive oil as the most important dietary source of MUFAs (notably oleic acid) to prevent cardiovascular complications in MetS.

  9. Phosphate and Cardiovascular Disease beyond Chronic Kidney Disease and Vascular Calcification

    Directory of Open Access Journals (Sweden)

    Sinee Disthabanchong

    2018-01-01

    Full Text Available Phosphate is essential for life but its accumulation can be detrimental. In end-stage renal disease, widespread vascular calcification occurs as a result of chronic phosphate load. The accumulation of phosphate is likely to occur long before the rise in serum phosphate above the normal range since several observational studies in both general population and early-stage CKD patients have identified the relationship between high-normal serum phosphate and adverse cardiovascular outcomes. Consumption of food high in phosphate increases both fasting and postprandial serum phosphate and habitual intake of high phosphate diet is associated with aging, cardiac hypertrophy, endothelial dysfunction, and subclinical atherosclerosis. The decline in renal function and dietary phosphate load can increase circulating fibroblast growth factor-23 (FGF-23 which may have a direct impact on cardiomyocytes. Increased FGF-23 levels in both CKD and general populations are associated with left ventricular hypertrophy, congestive heart failure, atrial fibrillation, and mortality. Increased extracellular phosphate directly affects endothelial cells causing cell apoptosis and vascular smooth muscle cells (VSMCs causing transformation to osteogenic phenotype. Excess of calcium and phosphate in the circulation can promote the formation of protein-mineral complex called calciprotein particles (CPPs. In CKD, these CPPs contain less calcification inhibitors, induce inflammation, and promote VSMC calcification.

  10. Computed Tomographic Distinction of Intimal and Medial Calcification in the Intracranial Internal Carotid Artery

    NARCIS (Netherlands)

    Kockelkoren, Remko; Vos, Annelotte; Van Hecke, Wim; Vink, Aryan; Bleys, Ronald L A W; Verdoorn, Daphne; Mali, Willem P Th M; Hendrikse, Jeroen; Koek, Huiberdina L; de Jong, Pim A; De Vis, Jill B

    2017-01-01

    BACKGROUND: Intracranial internal carotid artery (iICA) calcification is associated with stroke and is often seen as a proxy of atherosclerosis of the intima. However, it was recently shown that these calcifications are predominantly located in the tunica media and internal elastic lamina (medial

  11. Deficiency of ATP-Binding Cassette Transporters A1 and G1 in Macrophages Increases Inflammation and Accelerates Atherosclerosis in Mice

    NARCIS (Netherlands)

    Westerterp, Marit; Murphy, Andrew J.; Wang, Mi; Pagler, Tamara A.; Vengrenyuk, Yuliya; Kappus, Mojdeh S.; Gorman, Darren J.; Nagareddy, Prabhakara R.; Zhu, Xuewei; Abramowicz, Sandra; Parks, John S.; Welch, Carrie; Fisher, Edward A.; Wang, Nan; Yvan-Charvet, Laurent; Tall, Alan R.

    2013-01-01

    Rationale: Plasma high-density lipoprotein levels are inversely correlated with atherosclerosis. Although it is widely assumed that this is attributable to the ability of high-density lipoprotein to promote cholesterol efflux from macrophage foam cells, direct experimental support for this

  12. Alcohol and atherosclerosis

    Directory of Open Access Journals (Sweden)

    DA LUZ PROTASIO L.

    2001-01-01

    Full Text Available Atherosclerosis is manifested as coronary artery disease (CAD, ischemic stroke and peripheral vascular disease. Moderate alcohol consumption has been associated with reduction of CAD complications. Apparently, red wine offers more benefits than any other kind of drinks, probably due to flavonoids. Alcohol alters lipoproteins and the coagulation system. The flavonoids induce vascular relaxation by mechanisms that are both dependent and independent of nitric oxide, inhibits many of the cellular reactions associated with atherosclerosis and inflammation, such as endothelial expression of vascular adhesion molecules and release of cytokines from polymorphonuclear leukocytes. Hypertension is also influenced by the alcohol intake. Thus, heavy alcohol intake is almost always associated with systemic hypertension, and hence shall be avoided. In individuals that ingest excess alcohol, there is higher risk of coronary occlusion, arrhythmias, hepatic cirrhosis, upper gastrointestinal cancers, fetal alcohol syndrome, murders, sex crimes, traffic and industrial accidents, robberies, and psychosis. Alcohol is no treatment for atherosclerosis; but it doesn't need to be prohibited for everyone. Thus moderate amounts of alcohol (1-2 drinks/day, especially red wine, may be allowed for those at risk for atherosclerosis complications.

  13. Periodontal Disease Is an Independent Predictor of Intracardiac Calcification

    Directory of Open Access Journals (Sweden)

    Gregg S. Pressman

    2013-01-01

    Full Text Available Background. Periodontitis is the most common chronic inflammatory condition worldwide and is associated with incident coronary disease. Hypothesis. We hypothesized that periodontal disease would also be associated with cardiac calcification, a condition which shares many risk factors with atherosclerosis and is considered a marker of subclinical atherosclerosis. Methods. Cross-sectional study at two sites (USA and Japan involving subjects with both clinical echocardiograms and detailed dental examinations. Semiquantitative scoring systems were used to assess severity of periodontal disease and echocardiographic calcification. Results. Fifty-six of 73 subjects (77% had cardiac calcifications, and 51% had moderate to severe periodontal disease (score > 2. In unadjusted analysis, a significant relationship between periodontal score and cardiac calcification (Spearman rho = 0.4, P=0.001 was noted, with increases in mean calcification score seen across increasing levels of periodontal disease. On multivariate logistic regression, adjusted for age, gender, race, glomerular filtration rate, and traditional risk factors, this association remained significant (P=0.024. There was no significant interaction by study site, race, or gender. Conclusions. In a multiracial population, we found a significant association between the degree of periodontal disease, a chronic inflammatory condition, and cardiac calcification. Further, higher periodontal scores were associated with greater degrees of calcification.

  14. Periodontal disease is an independent predictor of intracardiac calcification.

    Science.gov (United States)

    Pressman, Gregg S; Qasim, Atif; Verma, Nitin; Miyamae, Masami; Arishiro, Kumiko; Notohara, Yasuhiro; Crudu, Vitalie; Figueredo, Vincent M

    2013-01-01

    Periodontitis is the most common chronic inflammatory condition worldwide and is associated with incident coronary disease. We hypothesized that periodontal disease would also be associated with cardiac calcification, a condition which shares many risk factors with atherosclerosis and is considered a marker of subclinical atherosclerosis. Cross-sectional study at two sites (USA and Japan) involving subjects with both clinical echocardiograms and detailed dental examinations. Semiquantitative scoring systems were used to assess severity of periodontal disease and echocardiographic calcification. Fifty-six of 73 subjects (77%) had cardiac calcifications, and 51% had moderate to severe periodontal disease (score > 2). In unadjusted analysis, a significant relationship between periodontal score and cardiac calcification (Spearman rho = 0.4, P = 0.001) was noted, with increases in mean calcification score seen across increasing levels of periodontal disease. On multivariate logistic regression, adjusted for age, gender, race, glomerular filtration rate, and traditional risk factors, this association remained significant (P = 0.024). There was no significant interaction by study site, race, or gender. In a multiracial population, we found a significant association between the degree of periodontal disease, a chronic inflammatory condition, and cardiac calcification. Further, higher periodontal scores were associated with greater degrees of calcification.

  15. Decreased naive and increased memory CD4(+ T cells are associated with subclinical atherosclerosis: the multi-ethnic study of atherosclerosis.

    Directory of Open Access Journals (Sweden)

    Nels C Olson

    Full Text Available Adaptive immunity has been implicated in atherosclerosis in animal models and small clinical studies. Whether chronic immune activation is associated with atherosclerosis in otherwise healthy individuals remains underexplored. We hypothesized that activation of adaptive immune responses, as reflected by higher proportions of circulating CD4(+ memory cells and lower proportions of naive cells, would be associated with subclinical atherosclerosis.We examined cross-sectional relationships of circulating CD4(+ naive and memory T cells with biomarkers of inflammation, serologies, and subclinical atherosclerosis in 912 participants of the Multi-Ethnic Study of Atherosclerosis (MESA. Circulating CD4(+ naive cells were higher in women than men and decreased with age (all p-values <0.0001. European-Americans had higher levels of naive cells and lower levels of memory cells compared with African-Americans and Hispanic-Americans (all p-values ≤0.0005. Lower naive/higher memory cells were associated with interleukin-6 levels. In multivariate models, cytomegalovirus (CMV and H. Pylori titers were strongly associated with higher memory and lower naive cells (all p-values <0.05. Higher memory cells were associated with coronary artery calcification (CAC level in the overall population [β-Coefficient (95% confidence interval (CI  = 0.20 (0.03, 0.37]. Memory and naive (inversely cells were associated with common carotid artery intimal media thickness (CC IMT in European-Americans [memory: β =  0.02 (0.006, 0.04; naive: β = -0.02 (-0.004, -0.03].These results demonstrate that the degree of chronic adaptive immune activation is associated with both CAC and CC IMT in otherwise healthy individuals, consistent with the known role of CD4(+ T cells, and with innate immunity (inflammation, in atherosclerosis. These data are also consistent with the hypothesis that immunosenescence accelerates chronic diseases by putting a greater burden on the innate

  16. [Transdisciplinary Approach for Sarcopenia. Sarcopenia and atherosclerosis].

    Science.gov (United States)

    Kohara, Katsuhiko

    2014-10-01

    Risk factors for sarcopenia, including aging, inflammation, oxidative stress, and sedentary life style, are also known as risks for atherosclerosis. Sarcopenia and atherosclerosis relate each other. We found that sarcopenia, especially sarcopenic visceral obesity in male subjects, was associated with higher arterial stiffness and central blood pressure. We also observed that leptin resistance may underlie the link between sarcopenia, sarcopenic obesity and atherosclerosis. In epidemiological studies, it has been demonstrated sarcopenic indices were associated with cardiovascular death. These findings indicate that sarcopenia could be regarded as risk factor for atherosclerosis and cardiovascular events.

  17. Proliferating macrophages prevail in atherosclerosis.

    Science.gov (United States)

    Randolph, Gwendalyn J

    2013-09-01

    Macrophages accumulate in atherosclerotic lesions during the inflammation that is part of atherosclerosis development and progression. A new study in mice indicates that the accumulation of macrophages in atherosclerotic plaques depends on local macrophage proliferation rather than the recruitment of circulating monocytes.

  18. Calcific aortic valve damage as a risk factor for cardiovascular events

    International Nuclear Information System (INIS)

    Wasilewski, Jarosław; Mirota, Kryspin; Wilczek, Krzysztof; Głowacki, Jan; Poloński, Lech

    2012-01-01

    Aortic valve calcification (AVC) is a common disease of the elderly. It is a progressive disease ranging from mild valve thickening to severe calcification with aortic valve stenosis. Risk factors for AVC are similar to those for atherosclerosis: age, gender, hypercholesterolemia, diabetes, hypertension, smoking and renal failure. AVC shares many similarities to atherosclerosis, including inflammatory cells and calcium deposits, and correlates with coronary plaque burden. Presence of AVC is associated with increased risk of adverse cardiovascular events. The objective for this review is to discuss the clinical features, natural history and prognostic significance of aortic valve calcifications, including mechanical and hemodynamic factors of flow distribution

  19. Cell Phenotype Transitions in Cardiovascular Calcification

    Directory of Open Access Journals (Sweden)

    Luis Hortells

    2018-03-01

    Full Text Available Cardiovascular calcification was originally considered a passive, degenerative process, however with the advance of cellular and molecular biology techniques it is now appreciated that ectopic calcification is an active biological process. Vascular calcification is the most common form of ectopic calcification, and aging as well as specific disease states such as atherosclerosis, diabetes, and genetic mutations, exhibit this pathology. In the vessels and valves, endothelial cells, smooth muscle cells, and fibroblast-like cells contribute to the formation of extracellular calcified nodules. Research suggests that these vascular cells undergo a phenotypic switch whereby they acquire osteoblast-like characteristics, however the mechanisms driving the early aspects of these cell transitions are not fully understood. Osteoblasts are true bone-forming cells and differentiate from their pluripotent precursor, the mesenchymal stem cell (MSC; vascular cells that acquire the ability to calcify share aspects of the transcriptional programs exhibited by MSCs differentiating into osteoblasts. What is unknown is whether a fully-differentiated vascular cell directly acquires the ability to calcify by the upregulation of osteogenic genes or, whether these vascular cells first de-differentiate into an MSC-like state before obtaining a “second hit” that induces them to re-differentiate down an osteogenic lineage. Addressing these questions will enable progress in preventative and regenerative medicine strategies to combat vascular calcification pathologies. In this review, we will summarize what is known about the phenotypic switching of vascular endothelial, smooth muscle, and valvular cells.

  20. The effect of PPE-induced emphysema and chronic LPS-induced pulmonary inflammation on atherosclerosis development in APOE*3-LEIDEN mice

    NARCIS (Netherlands)

    Khedoe, P.P.S.J.; Wong, M.C.; Wagenaar, G.T.M.; Plomp, J.J.; Eck, M. van; Havekes, L.M.; Rensen, P.C.N.; Hiemstra, P.S.; Berbée, J.F.P.

    2013-01-01

    Background: Chronic obstructive pulmonary disease (COPD) is characterized by pulmonary inflammation, airways obstruction and emphysema, and is a risk factor for cardiovascular disease (CVD). However, the contribution of these individual COPD components to this increased risk is unknown. Therefore,

  1. Association of mitral annulus calcification, aortic valve calcification with carotid intima media thickness

    Directory of Open Access Journals (Sweden)

    Scuteri Angelo

    2004-10-01

    Full Text Available Abstract Background Mitral annular calcification (MAC and aortic annular calcification (AVC may represent a manifestation of generalized atherosclerosis in the elederly. Alterations in vascular structure, as indexed by the intima media thickness (IMT, are also recognized as independent predictors of adverse cardiovascular outcomes. Aim To examine the relationship between the degree of calcification at mitral and/or aortic valve annulus and large artery structure (thickness. Methods We evaluated 102 consecutive patients who underwent transthoracic echocardiography and carotid artery echoDoppler for various indications; variables measured were: systemic blood pressure (BP, pulse pressure (PP=SBP-DBP, body mass index (BMI, fasting glucose, total, HDL, LDL chlolesterol, triglycerides, cIMT. The patients were divided according to a grading of valvular/annular lesions independent scores based on acoustic densitometry: 1 = annular/valvular sclerosis/calcification absence; 2 = annular/valvular sclerosis; 3 = annular calcification; 4 = annular-valvular calcification; 5 = valvular calcification with no recognition of the leaflets. Results Patient score was the highest observed for either valvular/annulus. Mean cIMT increased linearly with increasing valvular calcification score, ranging from 3.9 ± 0.48 mm in controls to 12.9 ± 1.8 mm in those subjects scored 5 (p 0.0001. Conclusion MAC and AVC score can identify subgroups of patients with different cIMT values which indicate different incidence and prevalence of systemic artery diseases. This data may confirm MAC-AVC as a useful important diagnostic parameter of systemic atherosclerotic disease.

  2. Role of Platelet-derived Microvesicles as Crosstalk Mediators in Atherothrombosis and Future Pharmacology Targets: a Link between Inflammation, Atherosclerosis and Thrombosis

    Directory of Open Access Journals (Sweden)

    Lina Badimon

    2016-08-01

    Full Text Available Reports in the last decade have suggested that the role of platelets in atherosclerosis and its thrombotic complications may be mediated, in part, by local secretion of platelet-derived microvesicles (pMVs, small cell blebs released during the platelet activation process. MVs are the most abundant cell-derived microvesicle subtype in the circulation. High concentrations of circulating MVs have been reported in patients with atherosclerosis, acute vascular syndromes, and/or diabetes mellitus, suggesting a potential correlation between the quantity of microvesicles and the clinical severity of the atherosclerotic disease. pMVs are considered to be biomarkers of disease but new information indicates that pMVs are also involved in signaling functions. pMVs evoke or promote haemostatic and inflammatory responses, neovascularization, cell survival and apoptosis, processes involved in the pathophysiology of cardiovascular disease. This review is focused on the complex cross-talk between platelet-derived microvesicles, inflammatory cells and vascular elements and their relevance in the development of the atherosclerotic disease and its clinical outcomes, providing an updated state-of-the art of pMV involvement in atherothrombosis and pMV potential use as therapeutic agent influencing cardiovascular biomedicine in the future.

  3. Early life socioeconomic adversity is associated in adult life with chronic inflammation, carotid atherosclerosis, poorer lung function and decreased cognitive performance: a cross-sectional, population-based study

    Directory of Open Access Journals (Sweden)

    Sattar Naveed

    2011-01-01

    Full Text Available Abstract Background Socioeconomic gradients in health persist despite public health campaigns and improvements in healthcare. The Psychosocial and Biological Determinants of Ill-health (pSoBid study was designed to uncover novel biomarkers of chronic disease that may help explain pathways between socioeconomic adversity and poorer physical and mental health. Methods We examined links between indicators of early life adversity, possible intermediary phenotypes, and markers of ill health in adult subjects (n = 666 recruited from affluent and deprived areas. Classical and novel risk factors for chronic disease (lung function and atherosclerosis and for cognitive performance were assessed, and associations sought with early life variables including conditions in the parental home, family size and leg length. Results Associations were observed between father's occupation, childhood home status (owner-occupier; overcrowding and biomarkers of chronic inflammation and endothelial activation in adults (C reactive protein, interleukin 6, intercellular adhesion molecule; P P Conclusions Adverse levels of biomarkers of ill health in adults appear to be influenced by father's occupation and childhood home conditions. Chronic inflammation and endothelial activation may in part act as intermediary phenotypes in this complex relationship. Reducing the 'health divide' requires that these life course determinants are taken into account.

  4. Prevalence, Vascular Distribution, and Multiterritorial Extent of Subclinical Atherosclerosis in a Middle-Aged Cohort

    DEFF Research Database (Denmark)

    Fernández-Friera, Leticia; Peñalvo, José L; Fernández-Ortiz, Antonio

    2015-01-01

    age, 45.8 years; 63% male) to evaluate the systemic extent of atherosclerosis in the carotid, abdominal aortic, and iliofemoral territories by 2-/3-dimensional ultrasound and coronary artery calcification by computed tomography. The extent of subclinical atherosclerosis, defined as presence of plaque...

  5. Atherosclerosis VII

    International Nuclear Information System (INIS)

    Fidge, N.H.; Nestel, P.J.; Flinders Univ., Adelaide

    1986-01-01

    In these proceedings the major themes of the conference have been preserved and comprise epidemiology, lipoproteins, pathogenesis, and clinical, therapeutic and nutritional aspects. The diet-lipidcoronary artery disease hypothesis has been strengthened significantly. Several long-awaited trials, reviewed here, have provided very strong support for the rationale for treating hyperlipidemia. A strategy for the prevention of atherosclerosis was defined at the conference. The genesis of atherosclerosis was shown to be more firmly grounded in the influx of lipoprotein into the arterial wall. The regulation of these processes and the rapid advances made possible by new technology were detailed in several sessions. Important new developments in the clinical area and in pharmacology give promise of greatly improved management of established disease. However, the possibility of mounting large-scale preventive measures in the near future, was given credence in the epidemiology and nutrition workshops. (Auth.)

  6. Function and Therapeutic Potential of Mesenchymal Stem Cells in Atherosclerosis

    Directory of Open Access Journals (Sweden)

    Feifei Li

    2017-05-01

    Full Text Available Atherosclerosis is a complicated disorder and largely attributable to dyslipidaemia and chronic inflammation. Despite therapeutic advances over past decades, atherosclerosis remains the leading cause of mortality worldwide. Due to their capability of immunomodulation and tissue regeneration, mesenchymal stem cells (MSCs have evolved as an attractive therapeutic agent in various diseases including atherosclerosis. Accumulating evidences support the protective role of MSCs in all stages of atherosclerosis. In this review, we highlight the current understanding of MSCs including their characteristics such as molecular markers, tissue distribution, migratory property, immune-modulatory competence, etc. We also summarize MSC functions in animal models of atherosclerosis. MSC transplantation is able to modulate cytokine and chemokine secretion, reduce endothelial dysfunction, promote regulatory T cell function, decrease dyslipidemia, and stabilize vulnerable plaques during atherosclerosis development. In addition, MSCs may migrate to lesions where they develop into functional cells during atherosclerosis formation. Finally, the perspectives of MSCs in clinical atherosclerosis therapy are discussed.

  7. Aluminum Chloride Pretreatment of Elastin Inhibits Elastolysis by Matrix Metalloproteinases and Leads to Inhibition of Elastin-Oriented Calcification

    OpenAIRE

    Bailey, Michael; Xiao, Hui; Ogle, Matthew; Vyavahare, Naren

    2001-01-01

    Calcification of elastin occurs in many pathological cardiovascular diseases including atherosclerosis. We have previously shown that purified elastin when subdermally implanted in rats undergoes severe calcification and aluminum chloride (AlCl3) pretreatment of elastin inhibits calcification. In the present study we investigated whether matrix metalloproteinase (MMP) binding to elastin and elastin degradation is prevented by AlCl3 pretreatment. Subdermal implantation of AlCl3-pretreated elas...

  8. Computed Tomographic Distinction of Intimal and Medial Calcification in the Intracranial Internal Carotid Artery.

    Science.gov (United States)

    Kockelkoren, Remko; Vos, Annelotte; Van Hecke, Wim; Vink, Aryan; Bleys, Ronald L A W; Verdoorn, Daphne; Mali, Willem P Th M; Hendrikse, Jeroen; Koek, Huiberdina L; de Jong, Pim A; De Vis, Jill B

    2017-01-01

    Intracranial internal carotid artery (iICA) calcification is associated with stroke and is often seen as a proxy of atherosclerosis of the intima. However, it was recently shown that these calcifications are predominantly located in the tunica media and internal elastic lamina (medial calcification). Intimal and medial calcifications are thought to have a different pathogenesis and clinical consequences and can only be distinguished through ex vivo histological analysis. Therefore, our aim was to develop CT scoring method to distinguish intimal and medial iICA calcification in vivo. First, in both iICAs of 16 cerebral autopsy patients the intimal and/or medial calcification area was histologically assessed (142 slides). Brain CT images of these patients were matched to the corresponding histological slides to develop a CT score that determines intimal or medial calcification dominance. Second, performance of the CT score was assessed in these 16 patients. Third, reproducibility was tested in a separate cohort. First, CT features of the score were circularity (absent, dot(s), medial and a lower sum intimal calcifications. Second, in the 16 patients the concordance between the CT score and the dominant calcification type was reasonable. Third, the score showed good reproducibility (kappa: 0.72 proportion of agreement: 0.82) between the categories intimal, medial or absent/indistinguishable. The developed CT score shows good reproducibility and can differentiate reasonably well between intimal and medial calcification dominance in the iICA, allowing for further (epidemiological) studies on iICA calcification.

  9. Prevalence, Impact, and Predictive Value of Detecting Subclinical Coronary and Carotid Atherosclerosis in Asymptomatic Adults

    DEFF Research Database (Denmark)

    Baber, Usman; Mehran, Roxana; Sartori, Samantha

    2015-01-01

    BACKGROUND: Although recent studies suggest that measuring coronary artery calcification (CAC) may be superior to indirect atherosclerotic markers in predicting cardiac risk, there are limited data evaluating imaging-based biomarkers that directly quantify atherosclerosis in different vascular beds...

  10. Effects of a vildagliptin/metformin combination on markers of atherosclerosis, thrombosis, and inflammation in diabetic patients with coronary artery disease

    Directory of Open Access Journals (Sweden)

    Klempfner Robert

    2012-06-01

    Full Text Available Abstract Background Diabetic patients present with an accelerated atherosclerotic process and an increased risk for future cardiovascular events. In addition to the risk imposed by the disease itself, pharmacological treatment adds also a sizable risk, especially if certain classes of antidiabetic drugs are employed. Animal evidence indicates that dipeptidyl peptidase-4 inhibitors have anti-atherosclerotic effects, yet clinical data are scarcely available. Design We plan to prospectively investigate the effects of dipeptidyl peptidase-4 inhibition with vildagliptin on a number of atherothrombotic markers and adipokines in patients with proven atherosclerosis and type 2 diabetes. The selected markers are: interleukin-6, high sensitivity C reactive protein, interleukin 1-beta, total adiponectin levels, matrix metallo-proteinase 9 and platelet reactivity testing. Sixty eligible patients will be randomized in a 2:1 ratio to vildagliptin/metformin or metformin only treatment, for a 3-month duration treatment. Blood sampling for the proposed investigations will be taken at enrollment and immediately after completion of the study period. Discussion Demonstrating antiatherothrombotic properties of dipeptidyl peptidase-4 inhibitors on proven markers is of substantial clinical significance. Coupled with their proven good safety profile these findings could translate into a significant clinical benefit.

  11. Early life socioeconomic adversity is associated in adult life with chronic inflammation, carotid atherosclerosis, poorer lung function and decreased cognitive performance: a cross-sectional, population-based study

    LENUS (Irish Health Repository)

    Packard, Chris J

    2011-01-17

    Abstract Background Socioeconomic gradients in health persist despite public health campaigns and improvements in healthcare. The Psychosocial and Biological Determinants of Ill-health (pSoBid) study was designed to uncover novel biomarkers of chronic disease that may help explain pathways between socioeconomic adversity and poorer physical and mental health. Methods We examined links between indicators of early life adversity, possible intermediary phenotypes, and markers of ill health in adult subjects (n = 666) recruited from affluent and deprived areas. Classical and novel risk factors for chronic disease (lung function and atherosclerosis) and for cognitive performance were assessed, and associations sought with early life variables including conditions in the parental home, family size and leg length. Results Associations were observed between father\\'s occupation, childhood home status (owner-occupier; overcrowding) and biomarkers of chronic inflammation and endothelial activation in adults (C reactive protein, interleukin 6, intercellular adhesion molecule; P < 0.0001) but not number of siblings and leg length. Lung function (forced expiratory volume in 1 second) and cognition (Choice Reaction Time, the Stroop test, Auditory Verbal Learning Test) were likewise related to early life conditions (P < 0.001). In multivariate models inclusion of inflammatory variables reduced the impact and independence of early life conditions on lung function and measures of cognitive ability. Including variables of adult socioeconomic status attenuated the early life associations with disease biomarkers. Conclusions Adverse levels of biomarkers of ill health in adults appear to be influenced by father\\'s occupation and childhood home conditions. Chronic inflammation and endothelial activation may in part act as intermediary phenotypes in this complex relationship. Reducing the \\'health divide\\' requires that these life course determinants are taken into account.

  12. Calcific periarthritis of the elbow presenting as acute tennis elbow.

    Science.gov (United States)

    Jawad, F; Jawad, A S M

    2014-01-01

    A 28-year-old woman presented with sudden acute lateral epicondylitis. There was no history of preceding trauma or repetitive use of the arm. Because of the acute onset and signs of acute inflammation, an X-ray was arranged. The X-ray showed a hyperdense calcified elongated globule distal to the lateral epicondyle. A diagnosis of calcific periarthritis (calcium apatite) of the elbow was made. Calcific periarthritis has rarely been reported as a cause of acute elbow pain.

  13. Growth Pattern of Atherosclerotic Calcifications

    DEFF Research Database (Denmark)

    Larsen, Lene Lillemark; Ganz, Melanie; Dam, Erik

    2008-01-01

    of the calcifications are matched longitudinally using thin plate spline registration and area overlap calculations. The growth of the calcifications is measured by the distribution of the geometry statistics of the calcifications. The method was evaluated on 135 subjects with a total number of 611 calcifications. Our...

  14. Calcific Uremic Arteriolopathy: Pathophysiology, Reactive Oxygen Species and Therapeutic Approaches

    Directory of Open Access Journals (Sweden)

    Kurt M. Sowers

    2010-01-01

    Full Text Available Calcific uremic arteriolopathy (CUA/calciphylaxis is an important cause of morbidity and mortality in patients with chronic kidney disease requiring renal replacement. Once thought to be rare, it is being increasingly recognized and reported on a global scale. The uremic milieu predisposes to multiple metabolic toxicities including increased levels of reactive oxygen species and inflammation. Increased oxidative stress and inflammation promote this arteriolopathy by adversely affecting endothelial function resulting in a prothrombotic milieu and significant remodeling effects on vascular smooth muscle cells. These arteriolar pathological effects include intimal hyperplasia, inflammation, endovascular fibrosis and vascular smooth muscle cell apoptosis and differentiation into bone forming osteoblast-like cells resulting in medial calcification. Systemic factors promoting this vascular condition include elevated calcium, parathyroid hormone and hyperphosphatemia with consequent increases in the calcium × phosphate product. The uremic milieu contributes to a marked increased in upstream reactive oxygen species—oxidative stress and subsequent downstream increased inflammation, in part, via activation of the nuclear transcription factor NFκB and associated downstream cytokine pathways. Consitutive anti-calcification proteins such as Fetuin-A and matrix GLA proteins and their signaling pathways may be decreased, which further contributes to medial vascular calcification. The resulting clinical entity is painful, debilitating and contributes to the excess morbidity and mortality associated with chronic kidney disease and end stage renal disease. These same histopathologic conditions also occur in patients without uremia and therefore, the term calcific obliterative arteriolopathy could be utilized in these conditions.

  15. Associations of Triiodothyronine Levels with Carotid Atherosclerosis and Arterial Stiffness in Hemodialysis Patients

    Science.gov (United States)

    Kircelli, Fatih; Asci, Gulay; Carrero, Juan Jesus; Gungor, Ozkan; Demirci, Meltem Sezis; Ozbek, Suha Sureyya; Ceylan, Naim; Ozkahya, Mehmet; Toz, Huseyin; Ok, Ercan

    2011-01-01

    Summary Background and objectives End-stage renal disease is linked to alterations in thyroid hormone levels and/or metabolism, resulting in a high prevalence of subclinical hypothyroidism and low triiodothyronine (T3) levels. These alterations are involved in endothelial damage, cardiac abnormalities, and inflammation, but the exact mechanisms are unclear. In this study, we investigated the relationship between serum free-T3 (fT3) and carotid artery atherosclerosis, arterial stiffness, and vascular calcification in prevalent patients on conventional hemodialysis. Design, setting, participants, & measurements 137 patients were included. Thyroid-hormone levels were determined by chemiluminescent immunoassay, carotid artery–intima media thickness (CA-IMT) by Doppler ultrasonography, carotid-femoral pulse wave velocity (c-f PWV), and augmentation index by Sphygmocor device, and coronary artery calcification (CAC) scores by multi-slice computerized tomography. Results Mean fT3 level was 3.70 ± 1.23 pmol/L. Across decreasing fT3 tertiles, c-f PWV and CA-IMT values were incrementally higher, whereas CACs were not different. In adjusted ordinal logistic regression analysis, fT3 level (odds ratio, 0.81; 95% confidence interval, 0.68 to 0.97), age, and interdialytic weight gain were significantly associated with CA-IMT. fT3 level was associated with c-f PWV in nondiabetics but not in diabetics. In nondiabetics (n = 113), c-f PWV was positively associated with age and systolic BP but negatively with fT3 levels (odds ratio = 0.57, 95% confidence interval 0.39 to 0.83). Conclusions fT3 levels are inversely associated with carotid atherosclerosis but not with CAC in hemodialysis patients. Also, fT3 levels are inversely associated with surrogates of arterial stiffness in nondiabetics. PMID:21836150

  16. NMR imaging of human atherosclerosis

    International Nuclear Information System (INIS)

    Toussaint, J.F.

    1995-01-01

    Diagnosis and prognosis of atherosclerosis can no longer be evaluated with morphological parameters only. A description of atherosclerotic plaque composition is necessary to study the mechanisms of plaque rupture, which depends on collagenous cap and lipid core thicknesses. NMR, as a biochemical imaging technique, allows visualization of these components using T1 contrast (mobile lipids), T2 contrast (cap vs. core), spin density (calcifications), diffusion imaging, 1H and 13C spectroscopy. Today, these imaging sequences allow to study in vitro the effects of interventional techniques such as angioplasty or atherectomy. Clinical investigations begin, which will attempt to develop in vivo microscopy and test the ability of NMR to predict plaque rupture. (author). 13 refs., 7 figs

  17. A Review of the Effect of Diet on Cardiovascular Calcification

    Directory of Open Access Journals (Sweden)

    Rachel Nicoll

    2015-04-01

    Full Text Available Cardiovascular (CV calcification is known as sub-clinical atherosclerosis and is recognised as a predictor of CV events and mortality. As yet there is no treatment for CV calcification and conventional CV risk factors are not consistently correlated, leaving clinicians uncertain as to optimum management for these patients. For this reason, a review of studies investigating diet and serum levels of macro- and micronutrients was carried out. Although there were few human studies of macronutrients, nevertheless transfats and simple sugars should be avoided, while long chain ω-3 fats from oily fish may be protective. Among the micronutrients, an intake of 800 μg/day calcium was beneficial in those without renal disease or hyperparathyroidism, while inorganic phosphorus from food preservatives and colas may induce calcification. A high intake of magnesium (≥380 mg/day and phylloquinone (500 μg/day proved protective, as did a serum 25(OHD concentration of ≥75 nmol/L. Although oxidative damage appears to be a cause of CV calcification, the antioxidant vitamins proved to be largely ineffective, while supplementation of α-tocopherol may induce calcification. Nevertheless other antioxidant compounds (epigallocatechin gallate from green tea and resveratrol from red wine were protective. Finally, a homocysteine concentration >12 µmol/L was predictive of CV calcification, although a plasma folate concentration of >39.4 nmol/L could both lower homocysteine and protect against calcification. In terms of a dietary programme, these recommendations indicate avoiding sugar and the transfats and preservatives found in processed foods and drinks and adopting a diet high in oily fish and vegetables. The micronutrients magnesium and vitamin K may be worthy of further investigation as a treatment option for CV calcification.

  18. Metabonomics-based omics study and atherosclerosis

    OpenAIRE

    Wu, Duo-jiao; Zhu, Bi-jun; Wang, Xiang-dong

    2011-01-01

    Atherosclerosis results from dyslipidemia and systemic inflammation, associated with the strong metabolism and interaction between diet and disease. Strategies based on the global profiling of metabolism would be important to define the mechanisms involved in pathological alterations. Metabonomics is the quantitative measurement of the dynamic multiparametric metabolic response of living systems to pathophysiological stimuli or genetic modification. Metabonomics has been used in combination w...

  19. Neutrophils in atherosclerosis. A brief overview

    NARCIS (Netherlands)

    Hartwig, H.; Silvestre Roig, C.; Daemen, M.; Lutgens, E.; Soehnlein, O.

    2015-01-01

    Atherosclerosis is a chronic inflammation of the arterial wall and the continuous infiltration of leukocytes into the plaque enhances the progression of the lesion. Because of the scarce detection of neutrophils in atherosclerotic plaques compared to other immune cells, their contribution was

  20. Genetics in arterial calcification: pieces of a puzzle and cogs in a wheel.

    Science.gov (United States)

    Rutsch, Frank; Nitschke, Yvonne; Terkeltaub, Robert

    2011-08-19

    Artery calcification reflects an admixture of factors such as ectopic osteochondral differentiation with primary host pathological conditions. We review how genetic factors, as identified by human genome-wide association studies, and incomplete correlations with various mouse studies, including knockout and strain analyses, fit into "pieces of the puzzle" in intimal calcification in human atherosclerosis, and artery tunica media calcification in aging, diabetes mellitus, and chronic kidney disease. We also describe in sharp contrast how ENPP1, CD73, and ABCC6 serve as "cogs in a wheel" of arterial calcification. Specifically, each is a minor component in the function of a much larger network of factors that exert balanced effects to promote and suppress arterial calcification. For the network to normally suppress spontaneous arterial calcification, the "cogs" ENPP1, CD73, and ABCC6 must be present and in working order. Monogenic ENPP1, CD73, and ABCC6 deficiencies each drive a molecular pathophysiology of closely related but phenotypically different diseases (generalized arterial calcification of infancy (GACI), pseudoxanthoma elasticum (PXE) and arterial calcification caused by CD73 deficiency (ACDC)), in which premature onset arterial calcification is a prominent but not the sole feature.

  1. [Disk calcifications in children].

    Science.gov (United States)

    Schmit, P; Fauré, C; Denarnaud, L

    1985-05-01

    It is not unusual for intervertebral disk calcifications to be detected in pediatric practice, the 150 or so cases reported in the literature probably representing only a small proportion of lesions actually diagnosed. Case reports of 33 children with intervertebral disk calcifications were analyzed. In the majority of these patients (31 of 33) a diagnosis of "idiopathic" calcifications had been made, the cervical localization of the lesions being related to repeated ORL infections and/or trauma. A pre-existing pathologic factor was found in two cases (one child with juvenile rheumatoid arthritis treated by corticoids and one child with Williams and Van Beuren's syndrome). An uncomplicated course was noted in 31 cases, the symptomatology (pain, spinal stiffness and febricula) improving after several days. Complications developed in two cases: one child had very disabling dysphagia due to an anteriorly protruding cervical herniated disc and surgery was necessary; the other child developed cervicobrachial neuralgia due to herniated disc protrusion into the cervical spinal canal, but symptoms regressed within several days although calcifications persisted unaltered. These findings and the course of the rare complications documented in the literature suggest the need for the most conservative treatment possible in cases of disc calcifications in children.

  2. Calcific shoulder joint periarthritis. Disappearance of calcifications after laser therapy

    Energy Technology Data Exchange (ETDEWEB)

    Gussetti, P; Moroso, P; Palazzo, C

    1986-01-01

    The authors report their results in the laser therapy of 30 calcific joint periarthritis. In two out of the ten radiographed cases, at the end of therapy, the complete disappearance of calcifications has been shown and in one case a decrease in calcification volume has been demonstrated. In the follow up after 6 months, 80% of clinically checked patients had no painful relapse.

  3. Proinflammatory Status, Genetics and Atherosclerosis

    Czech Academy of Sciences Publication Activity Database

    Poledne, R.; Lorenzová, A.; Stávek, P.; Valenta, Zdeněk; Hubáček, J.; Suchánek, R.; Piťha, J.

    2009-01-01

    Roč. 58, Suppl. 2 (2009), S111-S118 ISSN 0862-8408 R&D Projects: GA MŠk(CZ) 1M06014 Grant - others:GA MŠk(CZ) 1M0510 Program:1M Institutional research plan: CEZ:AV0Z10300504 Keywords : atherosclerosis * inflammation * C-reactive protein * genetics Subject RIV: EB - Genetics ; Molecular Biology Impact factor: 1.430, year: 2009 http://www.biomed.cas.cz/physiolres/pdf/58%20Suppl%202/58_S111.pdf

  4. [Vascular Calcification - Pathological Mechanism and Clinical Application - . Role of vascular smooth muscle cells in vascular calcification].

    Science.gov (United States)

    Kurabayashi, Masahiko

    2015-05-01

    Vascular calcification is commonly seen with aging, chronic kidney disese (CKD), diabetes, and atherosclerosis, and is closely associated with cardiovascular morbidity and mortality. Vascular calcification has long been regarded as the final stage of degeneration and necrosis of arterial wall and a passive, unregulated process. However, it is now known to be an active and tightly regulated process involved with phenotypic transition of vascular smooth muscle cells (VSMC) that resembles bone mineralization. Briefly, calcium deposits of atherosclerotic plaque consist of hydroxyapatite and may appear identical to fully formed lamellar bone. By using a genetic fate mapping strategy, VSMC of the vascular media give rise to the majority of the osteochondrogenic precursor- and chondrocyte-like cells observed in the calcified arterial media of MGP (- / -) mice. Osteogenic differentiation of VSMC is characterized by the expression of bone-related molecules including bone morphogenetic protein (BMP) -2, Msx2 and osteopontin, which are produced by osteoblasts and chondrocytes. Our recent findings are that (i) Runx2 and Notch1 induce osteogenic differentiation, and (ii) advanced glycation end-product (AGE) /receptor for AGE (RAGE) and palmitic acid promote osteogenic differentiation of VSMC. To understand of the molecular mechanisms of vascular calcification is now under intensive research area.

  5. Immune Response to Lipoproteins in Atherosclerosis

    Directory of Open Access Journals (Sweden)

    Sonia Samson

    2012-01-01

    Full Text Available Atherosclerosis, the underlying cause of cardiovascular disease, is characterized by chronic inflammation and altered immune response. Cholesterol is a well-known risk factor associated with the development of cardiovascular diseases. Elevated serum cholesterol is unique because it can lead to development of atherosclerosis in animals and humans even in the absence of other risk factors. Modifications of low-density lipoproteins mediated by oxidation, enzymatic degradation, and aggregation result in changes in their function and activate both innate and adaptive immune system. Oxidized low-density lipoprotein (LDL has been identified as one of the most important autoantigens in atherosclerosis. This escape from self-tolerance is dependent on the formation of oxidized phospholipids. The emerging understanding of the importance of immune responses against oxidized LDL in atherosclerosis has focused attention on the possibility of development of novel therapy for atherosclerosis. This review provides an overview of immune response to lipoproteins and the fascinating possibility of developing an immunomodulatory therapy for atherosclerosis.

  6. Vinpocetine attenuates lipid accumulation and atherosclerosis formation

    International Nuclear Information System (INIS)

    Cai, Yujun; Li, Jian-Dong; Yan, Chen

    2013-01-01

    Highlights: •Vinpocetine attenuates hyperlipidemia-induced atherosclerosis in a mouse model. •Vinpocetine antagonizes ox-LDL uptake and accumulation in macrophages. •Vinpocetine blocks the induction of ox-LDL receptor LOX-1 in vitro and in vivo. -- Abstract: Atherosclerosis, the major cause of myocardial infarction and stroke, is a chronic arterial disease characterized by lipid deposition and inflammation in the vessel wall. Cholesterol, in low-density lipoprotein (LDL), plays a critical role in the pathogenesis of atherosclerosis. Vinpocetine, a derivative of the alkaloid vincamine, has long been used as a cerebral blood flow enhancer for treating cognitive impairment. Recent study indicated that vinpocetine is a potent anti-inflammatory agent. However, its role in the pathogenesis of atherosclerosis remains unexplored. In the present study, we show that vinpocetine significantly reduced atherosclerotic lesion formation in ApoE knockout mice fed with a high-fat diet. In cultured murine macrophage RAW264.7 cells, vinpocetine markedly attenuated oxidized LDL (ox-LDL) uptake and foam cell formation. Moreover, vinpocetine greatly blocked the induction of ox-LDL receptor 1 (LOX-1) in cultured macrophages as well as in the LOX-1 level in atherosclerotic lesions. Taken together, our data reveal a novel role of vinpocetine in reduction of pathogenesis of atherosclerosis, at least partially through suppressing LOX-1 signaling pathway. Given the excellent safety profile of vinpocetine, this study suggests vinpocetine may be a therapeutic candidate for treating atherosclerosis

  7. Oral microbiota in patients with atherosclerosis.

    Science.gov (United States)

    Fåk, Frida; Tremaroli, Valentina; Bergström, Göran; Bäckhed, Fredrik

    2015-12-01

    Recent evidence suggests that the microbiota may be considered as an environmental factor that contributes to the development of atherosclerosis. Periodontal disease has been associated with cardio- and cerebrovascular events, and inflammation in the periodontium is suggested to increase the systemic inflammatory level of the host, which may in turn influence plaque composition and rupture. We previously showed that bacteria from the oral cavity and the gut could be found in atherosclerotic plaques. To elucidate whether the oral microbiota composition differed between patients with asymptomatic and symptomatic atherosclerosis we performed pyrosequencing of the oral microbiota of 92 individuals including patients with asymptomatic and symptomatic atherosclerosis and control individuals without carotid plaques or previous stroke or myocardial infarction. The overall microbial structure was similar in controls and atherosclerosis patients, but patients with symptomatic atherosclerosis had higher relative abundance of Anaeroglobus (mean 0.040% (SD 0.049)) than the control group (0.010% (SD 0.028)) (P = 0.03). Using linear regression analysis, we found that Parvimonas associated positively with uCRP and Capnocytophaga, Catonella and Lactobacillus associated with blood lipid markers. In conclusion, abundance of Anaeroglobus in the oral cavity could be associated with symptomatic atherosclerosis. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

  8. Vinpocetine attenuates lipid accumulation and atherosclerosis formation

    Energy Technology Data Exchange (ETDEWEB)

    Cai, Yujun [Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester, 601 Elmwood Ave, Rochester, NY 14642 (United States); Li, Jian-Dong [Center for Inflammation, Immunity and Infection, and Department of Biology, Georgia State University, Atlanta, GA 30303 (United States); Yan, Chen, E-mail: Chen_Yan@urmc.rochester.edu [Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester, 601 Elmwood Ave, Rochester, NY 14642 (United States)

    2013-05-10

    Highlights: •Vinpocetine attenuates hyperlipidemia-induced atherosclerosis in a mouse model. •Vinpocetine antagonizes ox-LDL uptake and accumulation in macrophages. •Vinpocetine blocks the induction of ox-LDL receptor LOX-1 in vitro and in vivo. -- Abstract: Atherosclerosis, the major cause of myocardial infarction and stroke, is a chronic arterial disease characterized by lipid deposition and inflammation in the vessel wall. Cholesterol, in low-density lipoprotein (LDL), plays a critical role in the pathogenesis of atherosclerosis. Vinpocetine, a derivative of the alkaloid vincamine, has long been used as a cerebral blood flow enhancer for treating cognitive impairment. Recent study indicated that vinpocetine is a potent anti-inflammatory agent. However, its role in the pathogenesis of atherosclerosis remains unexplored. In the present study, we show that vinpocetine significantly reduced atherosclerotic lesion formation in ApoE knockout mice fed with a high-fat diet. In cultured murine macrophage RAW264.7 cells, vinpocetine markedly attenuated oxidized LDL (ox-LDL) uptake and foam cell formation. Moreover, vinpocetine greatly blocked the induction of ox-LDL receptor 1 (LOX-1) in cultured macrophages as well as in the LOX-1 level in atherosclerotic lesions. Taken together, our data reveal a novel role of vinpocetine in reduction of pathogenesis of atherosclerosis, at least partially through suppressing LOX-1 signaling pathway. Given the excellent safety profile of vinpocetine, this study suggests vinpocetine may be a therapeutic candidate for treating atherosclerosis.

  9. Incidental internal carotid artery calcifications on temporal bone CT in children

    Energy Technology Data Exchange (ETDEWEB)

    Koch, Bernadette; Jones, Blaise [Cincinnati Children' s Hospital Medical Center, Department of Radiology, Cincinnati, OH (United States); Blackham, Aaron [University of Cincinnati College of Medicine, Cincinnati, OH (United States)

    2007-02-15

    Incidental internal carotid artery (ICA) calcifications are occasionally noted on CT images of the brain and temporal bone. In adults, incidental calcifications have been correlated with increased incidence of hypercholesterolemia, cardiac disease, diabetes and carotid stenosis. To determine the incidence of incidental calcifications of the carotid siphon on temporal bone CT in children. We retrospectively reviewed 24 months of consecutive temporal bone CT examinations in children aged 18 years and younger. CT examinations on 663 patients were reviewed and the presence or absence of ICA calcifications was ranked as absent, questionable or definitive. In patients in whom definitive calcifications were identified, hospital charts were reviewed for evidence of diabetes mellitus, hypercholesterolemia, hypertriglyceridemia, hyperlipidemia and chronic renal disease as potential causes of early atherosclerosis. Of the 663 patients, 25% had definitive calcifications within the wall of the ICA: 6% of children younger than 2 years and 28% of children 12-19 years of age. Incidentally noted ICA calcifications are a common finding on temporal bone CT in children, most likely a physiologic response to turbulent flow at natural bends in the artery rather than secondary to underlying disease predisposing to early atherosclerotic calcification. (orig.)

  10. Incidental internal carotid artery calcifications on temporal bone CT in children

    International Nuclear Information System (INIS)

    Koch, Bernadette; Jones, Blaise; Blackham, Aaron

    2007-01-01

    Incidental internal carotid artery (ICA) calcifications are occasionally noted on CT images of the brain and temporal bone. In adults, incidental calcifications have been correlated with increased incidence of hypercholesterolemia, cardiac disease, diabetes and carotid stenosis. To determine the incidence of incidental calcifications of the carotid siphon on temporal bone CT in children. We retrospectively reviewed 24 months of consecutive temporal bone CT examinations in children aged 18 years and younger. CT examinations on 663 patients were reviewed and the presence or absence of ICA calcifications was ranked as absent, questionable or definitive. In patients in whom definitive calcifications were identified, hospital charts were reviewed for evidence of diabetes mellitus, hypercholesterolemia, hypertriglyceridemia, hyperlipidemia and chronic renal disease as potential causes of early atherosclerosis. Of the 663 patients, 25% had definitive calcifications within the wall of the ICA: 6% of children younger than 2 years and 28% of children 12-19 years of age. Incidentally noted ICA calcifications are a common finding on temporal bone CT in children, most likely a physiologic response to turbulent flow at natural bends in the artery rather than secondary to underlying disease predisposing to early atherosclerotic calcification. (orig.)

  11. Regressing Atherosclerosis by Resolving Plaque Inflammation

    Science.gov (United States)

    2017-07-01

    regression requires the alteration of macrophages in the plaques to a tissue repair “alternatively” activated state. This switch in activation state... tissue repair “alternatively” activated state. This switch in activation state requires the action of TH2 cytokines interleukin (IL)-4 or IL-13. To...regulation of tissue macrophage and dendritic cell population dynamics by CSF-1. J Exp Med. 2011;208(9):1901–1916. 35. Xu H, Exner BG, Chilton PM

  12. Regressing Atherosclerosis by Resolving Plaque Inflammation

    Science.gov (United States)

    2017-07-01

    of Cardiology, Mount Sinai School of Medicine, New York, New York, USA. 3Department of Biomedical Sciences and School of Electrical Engineering and...Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 240 Longwood Ave., Boston, MA 02115, USA Dr. S. Jon KAIST Institute for the...Choi Center for Convergence Bioceramic Materials, Convergence R&D Division, Korea Institute of Ceramic Engineering and Technology, 202

  13. Radiological patterns of thyroid calcifications

    International Nuclear Information System (INIS)

    Lim, Jun; Sim, Do Chul; Park, Seog Hee; Kim, Choon Yul; Bahk, Yong Whee

    1986-01-01

    The purpose of this study was to analyse the various patterns of calcification demonstrated in the anterior and lateral neck roentgenograms of 213 unselected patients with thyroid enlargement. The patterns of thyroid calcifications were correlated with clinical, surgical and histological findings. The results were as follows: 1. Of 213 cases of thyroid enlargement, 180 cases were benign and 168 cases were female. 2. The calcification rate was high in the chronic thyroid enlargement. 3. The incidence of calcification was 30.2% in the malignancy and 17.2% in the benign disease. There was no calcification in the Hashimoto's disease. 4. The nodular calcification was demonstrated in the both benign and malignant disease but curvilinear calcification was predominantly seen in benign disease.

  14. Computed Tomographic Distinction of Intimal and Medial Calcification in the Intracranial Internal Carotid Artery.

    Directory of Open Access Journals (Sweden)

    Remko Kockelkoren

    Full Text Available Intracranial internal carotid artery (iICA calcification is associated with stroke and is often seen as a proxy of atherosclerosis of the intima. However, it was recently shown that these calcifications are predominantly located in the tunica media and internal elastic lamina (medial calcification. Intimal and medial calcifications are thought to have a different pathogenesis and clinical consequences and can only be distinguished through ex vivo histological analysis. Therefore, our aim was to develop CT scoring method to distinguish intimal and medial iICA calcification in vivo.First, in both iICAs of 16 cerebral autopsy patients the intimal and/or medial calcification area was histologically assessed (142 slides. Brain CT images of these patients were matched to the corresponding histological slides to develop a CT score that determines intimal or medial calcification dominance. Second, performance of the CT score was assessed in these 16 patients. Third, reproducibility was tested in a separate cohort.First, CT features of the score were circularity (absent, dot(s, <90°, 90-270° or 270-360°, thickness (absent, ≥1.5mm, or <1.5mm, and morphology (indistinguishable, irregular/patchy or continuous. A high sum of features represented medial and a lower sum intimal calcifications. Second, in the 16 patients the concordance between the CT score and the dominant calcification type was reasonable. Third, the score showed good reproducibility (kappa: 0.72 proportion of agreement: 0.82 between the categories intimal, medial or absent/indistinguishable.The developed CT score shows good reproducibility and can differentiate reasonably well between intimal and medial calcification dominance in the iICA, allowing for further (epidemiological studies on iICA calcification.

  15. Oxyradical Stress, Endocannabinoids, and Atherosclerosis

    Directory of Open Access Journals (Sweden)

    Anberitha T. Matthews

    2015-12-01

    Full Text Available Atherosclerosis is responsible for most cardiovascular disease (CVD and is caused by several factors including hypertension, hypercholesterolemia, and chronic inflammation. Oxidants and electrophiles have roles in the pathophysiology of atherosclerosis and the concentrations of these reactive molecules are an important factor in disease initiation and progression. Overactive NADPH oxidase (Nox produces excess superoxide resulting in oxidized macromolecules, which is an important factor in atherogenesis. Although superoxide and reactive oxygen species (ROS have obvious toxic properties, they also have fundamental roles in signaling pathways that enable cells to adapt to stress. In addition to inflammation and ROS, the endocannabinoid system (eCB is also important in atherogenesis. Linkages have been postulated between the eCB system, Nox, oxidative stress, and atherosclerosis. For instance, CB2 receptor-evoked signaling has been shown to upregulate anti-inflammatory and anti-oxidative pathways, whereas CB1 signaling appears to induce opposite effects. The second messenger lipid molecule diacylglycerol is implicated in the regulation of Nox activity and diacylglycerol lipase β (DAGLβ is a key biosynthetic enzyme in the biosynthesis eCB ligand 2-arachidonylglycerol (2-AG. Furthermore, Nrf2 is a vital transcription factor that protects against the cytotoxic effects of both oxidant and electrophile stress. This review will highlight the role of reactive oxygen species (ROS in intracellular signaling and the impact of deregulated ROS-mediated signaling in atherogenesis. In addition, there is also emerging knowledge that the eCB system has an important role in atherogenesis. We will attempt to integrate oxidative stress and the eCB system into a conceptual framework that provides insights into this pathology.

  16. Subclinical coronary atherosclerosis and neighbourhood deprivation in an urban region

    International Nuclear Information System (INIS)

    Dragano, Nico; Hoffmann, Barbara; Stang, Andreas; Moebus, Susanne; Verde, Pablo E.; Weyers, Simone; Moehlenkamp, Stefan; Schmermund, Axel; Mann, Klaus; Joeckel, Karl-Heinz; Erbel, Raimund; Siegrist, Johannes

    2009-01-01

    Inhabitants of deprived neighbourhoods are at higher risk of coronary heart disease. In this study we investigate the hypothesis that social inequalities at neighbourhood level become already manifest in subclinical coronary atherosclerosis, as defined by electron-beam computed tomography derived measures. Coronary artery calcification was assessed as a marker of atherosclerosis in a population based sample of 4301 men and women (45-75 years) without a history of coronary heart disease. Participants lived in three adjacent cities in Germany and were examined between 2000 and 2003 as part of the Heinz Nixdorf Recall Study. Individual level data was combined with neighbourhood level information about unemployment, welfare and living space per inhabitant. This dataset was analysed with descriptive and multilevel regression methods. An association between neighbourhood deprivation and subclinical coronary calcification was observed. After adjustment for age and individual socioeconomic status male inhabitants of high unemployment neighbourhoods had an odds ratio of 1.45 (1.11, 1.96) of exhibiting a high calcification score (>75th percentile) compared to men living in low unemployment areas. The respective odds for women was 1.29 (0.97, 1.70). Additional explorative analyses suggest that clustering of unhealthy lifestyles in deprived neighbourhoods contributes to the observed association. In conclusion, findings suggest that certain neighbourhood characteristics promote the emergence of coronary atherosclerosis. This might point to a pathway from neighbourhood deprivation to manifest coronary heart disease

  17. Oral microbiota in patients with atherosclerosis

    DEFF Research Database (Denmark)

    Fåk, Frida; Tremaroli, Valentina; Bergström, Göran

    2015-01-01

    BACKGROUND AND AIMS: Recent evidence suggests that the microbiota may be considered as an environmental factor that contributes to the development of atherosclerosis. Periodontal disease has been associated with cardio- and cerebrovascular events, and inflammation in the periodontium is suggested...... to increase the systemic inflammatory level of the host, which may in turn influence plaque composition and rupture. We previously showed that bacteria from the oral cavity and the gut could be found in atherosclerotic plaques. METHODS: To elucidate whether the oral microbiota composition differed between...... patients with asymptomatic and symptomatic atherosclerosis we performed pyrosequencing of the oral microbiota of 92 individuals including patients with asymptomatic and symptomatic atherosclerosis and control individuals without carotid plaques or previous stroke or myocardial infarction. RESULTS...

  18. Calcific retropharyngeal tendinitis

    International Nuclear Information System (INIS)

    Karasick, D.; Karasick, S.

    1981-01-01

    Calcific retropharyngeal tendinitis is an imflammation of the longus colli muscle tendon which is located on the anterior surface of the verterbral column extending from the atlas to the third thoracic vertebra. The acute inflammatory condition is selflimiting with symptoms consisting of a gradually increasing neck pain often associated with throat pain and difficulty swallowing. The pain is aggravated by head and neck movement. Clinically the condition can be confused with retropharyngeal absecess, meningitis, infectious spondylitis, and post-traumatic muscle spasm. The radiographic features of this condition consist of pre-vertebral soft tissue swelling from C1 to C4 and amorphous calcific density in the longus colli tendon anterior to the body of C2 and inferior to the anterior arch of C1. (orig.)

  19. Applying nanomedicine in maladaptive inflammation and angiogenesis

    NARCIS (Netherlands)

    Alaarg, Amr; Pérez-Medina, Carlos; Metselaar, Josbert M.; Nahrendorf, Matthias; Fayad, Zahi A.; Storm, Gert; Mulder, Willem J. M.

    2017-01-01

    Inflammation and angiogenesis drive the development and progression of multiple devastating diseases such as atherosclerosis, cancer, rheumatoid arthritis, and inflammatory bowel disease. Though these diseases have very different phenotypic consequences, they possess several common

  20. The biology of atherosclerosis: general paradigms and distinct pathogenic mechanisms among HIV-infected patients.

    Science.gov (United States)

    Lo, Janet; Plutzky, Jorge

    2012-06-01

    Complications of atherosclerosis, including myocardial infarction and stroke, are the leading cause of death and disability worldwide. Recent data strongly implicate cardiovascular death as a contributor to mortality among patients with human immunodeficiency virus (HIV) infection, with evidence suggesting increased incidence of atherosclerosis among these patients. Therefore, greater understanding of atherosclerotic mechanisms and how these responses may be similar or distinct in HIV-infected patients is needed. Key concepts in atherosclerosis are reviewed, including the evidence that inflammation and abnormal metabolism are major drivers of atherosclerosis, and connected to the current literature regarding atherosclerosis in the context of HIV.

  1. Serum Fetuin-A Levels in Patients with Bilateral Basal Ganglia Calcification.

    Science.gov (United States)

    Demiryurek, Bekir Enes; Gundogdu, Asli Aksoy

    2018-02-14

    The idiopathic basal ganglia calcification (Fahr syndrome) may occur due to senility. Fetuin-A is a negative acute phase reactant which inhibits calcium-phosphorus precipitation and vascular calcification. In this study, we aimed to evaluate whether serum fetuin-A levels correlate with bilateral basal ganglia calcification. Forty-five patients who had bilateral basal ganglia calcification on brain CT were selected according to the inclusion and exclusion criteria, and 45 age and gender-matched subjects without basal ganglia calcification were included for the control group. Serum fetuin-A levels were measured from venous blood samples. All participants were divided into two groups; with and without basal ganglia calcification. These groups were divided into subgroups regarding age (18-32 and 33-45 years of age) and gender (male, female). We detected lower levels of serum fetuin-A in patients with basal ganglia calcification compared with the subjects without basal ganglia calcification. In all subgroups (female, male, 18-32 years and 33-45 years), mean fetuin-A levels were significantly lower in patients with basal ganglia calcification (p = 0.017, p = 0.014, p = 0.024, p = 0.026, p = 0.01 respectively). And statistically significantly lower levels of fetuin-A was found to be correlated with the increasing densities of calcification in the calcified basal ganglia group (p-value: <0.001). Considering the role of fetuin-A in tissue calcification and inflammation, higher serum fetuin-A levels should be measured in patients with basal ganglia calcification. We believe that the measurement of serum fetuin-A may play a role in the prediction of basal ganglia calcification as a biomarker. Copyright © 2017 Elsevier B.V. All rights reserved.

  2. Life stress and atherosclerosis: a pathway through unhealthy lifestyle.

    Science.gov (United States)

    Mainous, Arch G; Everett, Charles J; Diaz, Vanessa A; Player, Marty S; Gebregziabher, Mulugeta; Smith, Daniel W

    2010-01-01

    To examine the relationship between a general measure of chronic life stress and atherosclerosis among middle aged adults without clinical cardiovascular disease via pathways through unhealthy lifestyle characteristics. We conducted an analysis of The Multi-Ethnic Study of Atherosclerosis (MESA). The MESA collected in 2000 includes 5,773 participants, aged 45-84. We computed standard regression techniques to examine the relationship between life stress and atherosclerosis as well as path analysis with hypothesized paths from stress to atherosclerosis through unhealthy lifestyle. Our outcome was sub-clinical atherosclerosis measured as presence of coronary artery calcification (CAC). A logistic regression adjusted for potential confounding variables along with the unhealthy lifestyle characteristics of smoking, excessive alcohol use, high caloric intake, sedentary lifestyle, and obesity yielded no significant relationship between chronic life stress (OR 0.93, 95% CI 0.80-1.08) and CAC. However, significant indirect pathways between chronic life stress and CAC through smoking (p = .007), and sedentary lifestyle (p = .03) and caloric intake (.002) through obesity were found. These results suggest that life stress is related to atherosclerosis once paths of unhealthy coping behaviors are considered.

  3. Endogenous hydrogen sulfide is involved in the pathogenesis of atherosclerosis

    International Nuclear Information System (INIS)

    Qiao, Wang; Chaoshu, Tang; Hongfang, Jin; Junbao, Du

    2010-01-01

    Atherosclerosis is a chronic, complex, and progressive pathological process in large and medium sized arteries. The exact mechanism of this process remains unclear. Hydrogen sulfide (H 2 S), a novel gasotransmitter, was confirmed as playing a major role in the pathogenesis of many cardiovascular diseases. It plays a role in vascular smooth muscle cell (VSMC) proliferation and apoptosis, participates in the progress of hyperhomocysteinemia (HHCY), inhibits atherogenic modification of LDL, interferes with vascular calcification, intervenes with platelet function, and there are interactions between H 2 S and inflammatory processes. The role of H 2 S in atherosclerotic pathogenesis highlights the mysteries of atherosclerosis and inspires the search for innovative therapeutic strategies. Here, we review the studies to date that have considered the role of H 2 S in atherosclerosis.

  4. Influence of Erythrocyte Membrane Stability in Atherosclerosis.

    Science.gov (United States)

    da Silva Garrote-Filho, Mario; Bernardino-Neto, Morun; Penha-Silva, Nilson

    2017-04-01

    The purpose of this study is to show how an excess of cholesterol in the erythrocyte membrane contributes stochastically to the progression of atherosclerosis, leading to damage in blood rheology and O 2 transport, deposition of cholesterol (from trapped erythrocytes) in an area of intraplaque hemorrhage, and local exacerbation of oxidative stress. Cholesterol contained in the membrane of erythrocytes trapped in an intraplaque hemorrhage contributes to the growth of the necrotic nucleus. There is even a relationship between the amount of cholesterol in the erythrocyte membrane and the severity of atherosclerosis. In addition, the volume variability among erythrocytes, measured by RDW, is predictive of a worsening of this disease. Erythrocytes contribute to the development of atherosclerosis in several ways, especially when trapped in intraplate hemorrhage. These erythrocytes are oxidized and phagocytosed by macrophages. The cholesterol present in the membrane of these erythrocytes subsequently contributes to the growth of the atheroma plaque. In addition, when they rupture, erythrocytes release hemoglobin, which leads to the generation of free radicals. Finally, increased RDW may predict the worsening of atherosclerosis, due to the effects of inflammation and oxidative stress on erythropoiesis and erythrocyte volume. A better understanding of erythrocyte participation in atherosclerosis may contribute to the improvement of the prevention and treatment strategies of this disease.

  5. Medial arterial calcification, calcific aortic stenosis and mitral annular calcification in a diabetic patient with severe autonomic neuropathy.

    LENUS (Irish Health Repository)

    Cronin, C C

    2012-02-03

    Medial arterial calcification (Monckeberg\\'s arteriosclerosis) is well described in diabetic patients with autonomic neuropathy. There is also a high prevalence of diabetes mellitus among subjects with calcific aortic stenosis and mitral annular calcification. We describe a diabetic patient with autonomic neuropathy and extensive medial arterial calcification who also had calcification of the aortic valve and of the mitral valve annulus. We propose that autonomic neuropathy may play a role in calcification of these structures at the base of the heart.

  6. A CT study of the prevalence of carotid artery calcification in dental patients

    International Nuclear Information System (INIS)

    Yoon, Suk Ja; Lee, Jae Seo; Yoon, Woong

    2006-01-01

    Stroke is one of the leading causes of death in Korea. Atherosclerotic disease in the carotid artery bifurcation is the most common cause of stroke. The carotid artery calcification is easily appreciated by CT(Computed tomography). CT is often taken in a dental hospital for the diagnosis of inflammation. injury, cyst or tumor on maxillofacial region. However, there was no report of carotid artery calcification on CT in dental patients. The presence of carotid artery calcification was evaluated by an experienced radiologist on CT scans of 287 patients (166 males, 121 females, average age 42, range 6 to 86 years) and the medical history of the patient and the interpretation of CT were reviewed. Carotid artery calcification was detected on CT scans of 57 patients (19.8%; 35 males, 22 females). All the male patients with carotid artery calcification were older than 50, and all the female patients with carotid artery calcification were older than 60. Among the 57 patients, 10 had Diabetes mellitus, 20 had cardiovascular disease, 3 had history of stroke and 3 underwent radiation therapy for head and neck cancer. Carotid artery calcification was not included in the interpretation of CT of dental patients except one patient. The prevalence of carotid artery calcification on CT of dental patients was about 20% in this study. Carotid artery calcification should be included in the interpretation of CT of dental patients

  7. Vaccination against atherosclerosis

    NARCIS (Netherlands)

    Es, Thomas van

    2009-01-01

    Atherosclerosis, the predominantly underlying pathology of cardiovascular events, is the consequence of lipid deposition in the arterial wall, mostly as consequence of high levels of serum cholesterol. Treatment of atherosclerosis is mainly focused at the reduction of cholesterol levels by lipid

  8. Phytosterols and atherosclerosis

    DEFF Research Database (Denmark)

    Schrøder, Malene

    Cardiovascular disease (CVD) is the major cause of premature deaths worldwide. Coronary heart disease is the most common CVD, caused by atherosclerosis in the coronary arteries. Atherosclerosis is a multifactorial disease influenced by both genetic and environmental factors. WHO has in 2007 listed...... in its “Guidelines for assessment and management of cardiovascular risk” the following risk factors to influence progressive atherosclerosis: hypertension, abnormal blood lipids, diabetes, unhealthy diet, physical inactivity and smoking. Phytosterols (plant sterols and plant stanols) are known...... their blood cholesterol levels. The aim of this Ph.D. project was to investigate the effects of phytosterols on the development of atherosclerosis in the aorta of heterozygous Watanabe Heritable Hyperlipidemic (WHHL) rabbits. The main advantage of animal studies to human studies in atherosclerosis research...

  9. Myocardial blood flow reserve is impaired in patients with aortic valve calcification and unobstructed epicardial coronary arteries.

    Science.gov (United States)

    Nel, Karen; Nam, Michael C Y; Anstey, Chris; Boos, Christopher J; Carlton, Edward; Senior, Roxy; Kaski, Juan Carlos; Khattab, Ahmed; Shamley, Delva; Byrne, Christopher D; Stanton, Tony; Greaves, Kim

    2017-12-01

    Although calcific aortic valve disease (CAVD) is associated with coronary atherosclerosis, it is not known whether early CAVD is associated with coronary microcirculatory dysfunction (CMD). We sought to investigate the relationship between myocardial blood flow reserve (MBFR) - a measure of CMD, and early CAVD in the absence of obstructive epicardial coronary artery disease. We also determined whether this relationship was independent of coronary artery disease (CAD) and hs-CRP, a marker of systemic inflammation. 183 patients with chest pain and unobstructed coronary arteries were studied. Aortic valve calcification score (AVCS), coronary total plaque length (TPL), and coronary calcium score were quantified from multislice CT. MBFR was assessed using vasodilator myocardial contrast echocardiography. Hs-CRP was measured from venous blood using a particle-enhanced immunoassay. Mean (±SD) participant age was 59.8 (9.6) years. Mean AVCS was 68 (258) AU, TPL was 15.6 (22.2) mm, and median coronary calcification score was 43.5AU. Mean MBFR was 2.20 (0.52). Mean hs-CRP was 2.52 (3.86) mg/l. Multivariable linear regression modelling incorporating demographics, coronary plaque characteristics, MBFR, and inflammatory markers, demonstrated that age (β=0.05, 95% CI: 0.02, 0.08, P=0.007), hs-CRP (β=0.09, CI: 0.02, 0.16, P=0.010) and diabetes (β=1.03, CI: 0.08, 1.98, P=0.033), were positively associated with AVCS. MBFR (β=-0.87, CI: -1.44, -0.30, P=0.003), BMI (β=-0.11, CI: -0.21, -0.01, P=0.033), and LDL (β=-0.32, CI: -0.61, -0.03, P=0.029) were negatively associated with AVCS. TPL and coronary calcium score were not independently associated with AVCS when included in the regression model. Coronary microvascular function as determined by measurement of myocardial blood flow reserve is independently associated with early CAVD. This effect is independent of the presence of coronary artery disease and also systemic inflammation. Copyright © 2017 Elsevier B.V. All rights

  10. Recent advances in pathogenesis, assessment, and treatment of atherosclerosis [version 1; referees: 3 approved

    Directory of Open Access Journals (Sweden)

    J. David Spence

    2016-07-01

    Full Text Available In recent years, there have been a number of advances in the pathogenesis and treatment of atherosclerosis and in assessing prognosis in carotid atherosclerosis. Risk stratification to improve vascular prevention by identifying patients most likely to benefit from intensive therapy is much improved by measuring carotid plaque burden. In patients with asymptomatic carotid stenosis, a number of modalities can be used to identify the 10-15% who could benefit from endarterectomy or stenting. Transcranial Doppler embolus detection, echolucency and ulceration on 3D ultrasound, intraplaque hemorrhage on magnetic resonance imaging (MRI, and reduced cerebrovascular reserve are useful already; new approaches including plaque texture on ultrasound and imaging of plaque inflammation and early calcification on positron emission tomography/computed tomography (PET/CT are in development. The discovery that the intestinal microbiome produces vasculotoxic metabolites from dietary constituents such as carnitine in meat (particularly red meat and phosphatidylcholine from egg yolk and other sources has revolutionized nutritional aspects of vascular prevention. Because many of these vasculotoxic metabolites are removed by the kidney, it is particularly important in patients with renal failure to limit their intake of red meat and egg yolk. A new approach to lowering low-density lipoprotein (LDL cholesterol by blocking the action of an enzyme that destroys LDL receptors promises to revolutionize vascular prevention once less costly treatments are developed, and a new approach to vascular prevention—“treating arteries instead of risk factors”—shows promise but requires randomized trials. These advances all promise to help in the quest to prevent strokes in high-risk patients.

  11. Intraosseous migration of tendinous calcifications: two case reports

    Energy Technology Data Exchange (ETDEWEB)

    Marinetti, A.; Sessa, M.; Falzone, A.; Della Sala, S.W. [Santa Maria del Carmine Hospital, Department of Radiology, Rovereto, TN (Italy)

    2018-01-15

    Calcific tendinopathy of the rotator cuff is a common cause of shoulder pain. Inflammation of the rotator cuff tendons may be complicated by adjacent bone erosion and subsequent migration of calcific deposits within the bone resulting in marrow inflammation. Bone marrow involvement is not readily visible using X-ray and ultrasound (US) and further testing is necessary. Magnetic resonance imaging (MRI) is a highly sensitive technique that can detect a focal bone T1 and T2-weighted hypointensity with bone marrow edema-like signal and cortical erosion. These findings can mislead the radiologist by suggesting an infectious or neoplastic lesion, often requiring further evaluation with computed tomography (CT) and biopsy. We report two cases of patients with shoulder pain in which different radiological approaches were used with pathological confirmation in one of them. In the first case, MRI revealed significant bone involvement in the head of the humerus and cortical erosion of the greater tuberosity. A CT examination and a biopsy was necessary for a final diagnosis of inflammatory bone reaction from intraosseous migration of tendinous calcifications. In the second case, similar MRI findings prompted re-evaluation of imaging to make a diagnosis of intraosseous migration of tendinous calcifications, obviating the need to perform CT and biopsy. We illustrate MRI signs of this complication that we think would allow to narrow the differential diagnosis potentially avoiding biopsy and additional CT examinations. (orig.)

  12. Intraosseous migration of tendinous calcifications: two case reports

    International Nuclear Information System (INIS)

    Marinetti, A.; Sessa, M.; Falzone, A.; Della Sala, S.W.

    2018-01-01

    Calcific tendinopathy of the rotator cuff is a common cause of shoulder pain. Inflammation of the rotator cuff tendons may be complicated by adjacent bone erosion and subsequent migration of calcific deposits within the bone resulting in marrow inflammation. Bone marrow involvement is not readily visible using X-ray and ultrasound (US) and further testing is necessary. Magnetic resonance imaging (MRI) is a highly sensitive technique that can detect a focal bone T1 and T2-weighted hypointensity with bone marrow edema-like signal and cortical erosion. These findings can mislead the radiologist by suggesting an infectious or neoplastic lesion, often requiring further evaluation with computed tomography (CT) and biopsy. We report two cases of patients with shoulder pain in which different radiological approaches were used with pathological confirmation in one of them. In the first case, MRI revealed significant bone involvement in the head of the humerus and cortical erosion of the greater tuberosity. A CT examination and a biopsy was necessary for a final diagnosis of inflammatory bone reaction from intraosseous migration of tendinous calcifications. In the second case, similar MRI findings prompted re-evaluation of imaging to make a diagnosis of intraosseous migration of tendinous calcifications, obviating the need to perform CT and biopsy. We illustrate MRI signs of this complication that we think would allow to narrow the differential diagnosis potentially avoiding biopsy and additional CT examinations. (orig.)

  13. Connective tissue diseases and noninvasive evaluation of atherosclerosis

    Directory of Open Access Journals (Sweden)

    Ardita G

    2014-06-01

    Full Text Available Giorgio Ardita, Giacomo Failla, Paolo Maria Finocchiaro, Francesco Mugno, Luigi Attanasio, Salvatore Timineri, Michelangelo Maria Di SalvoCardiovascular Department, Angiology Unit, Ferrarotto Hospital, Catania, ItalyAbstract: Connective tissue diseases (CTDs are associated with increased risk of cardiovascular disease due to accelerated atherosclerosis. In patients with autoimmune disorders, in addition to traditional risk factors, an immune-mediated inflammatory process of the vasculature seems to contribute to atherogenesis. Several pathogenetic mechanisms have been proposed, including chronic inflammation and immunologic abnormalities, both able to produce vascular damage. Macrovascular atherosclerosis can be noninvasively evaluated by ultrasound measurement of carotid or femoral plaque. Subclinical atherosclerosis can be evaluated by well-established noninvasive techniques which rely on ultrasound detection of carotid intima-media thickness. Flow-mediated vasodilatation and arterial stiffness are considered markers of endothelial dysfunction and subclinical atherosclerosis, respectively, and have been recently found to be impaired early in a wide spectrum of autoimmune diseases. Carotid intima-media thickness turns out to be a leading marker of subclinical atherosclerosis, and many studies recognize its role as a predictor of future vascular events, both in non-CTD individuals and in CTD patients. In rheumatic diseases, flow-mediated dilatation and arterial stiffness prove to be strongly correlated with inflammation, disease damage index, and with subclinical atherosclerosis, although their prognostic role has not yet been conclusively shown. Systemic lupus erythematosus, rheumatoid arthritis, and likely antiphospholipid syndrome are better associated with premature and accelerated atherosclerosis. Inconclusive results were reported in systemic sclerosis.Keywords: rheumatic disease, subclinical atherosclerosis, arterial stiffness

  14. Role of parnaparin in atherosclerosis.

    Science.gov (United States)

    Bonomini, Francesca; Taurone, Samanta; Parnigotto, Pierpaolo; Zamai, Loris; Rodella, Luigi F; Artico, Marco; Rezzani, Rita

    2016-12-01

    Atherosclerosis is characterized by a proliferation of vascular smooth muscle cells (VSMCs) and their migration to the intima, which induces thickening of the intima itself, but the mechanism remains poorly understood. Low molecular weight heparin (LMWH) inhibits the proliferation of VSMCs. Previous studies have shown that a LMWH, parnaparin (PNP), acts on the processes of atherogenesis and atheroprogression in experimental animal models. The aim of this study was to investigate the involvement of oxidative stress, inflammation and VSMCs in the regulation of vascular wall homeostasis. We also considered the possibility of restoring vascular pathological changes using PNP treatment. In order to evaluate vascular remodelling in this study we have analysed the morphological changes in aortas of an animal model of atherosclerosis, apolipoprotein E-deficient mice (ApoE-/-) fed with a normal or a western diet without treatment or treated with PNP. We also analysed, by immunohistochemistry, the expression of proteins linked to atherogenesis and atheroprogression - an enzyme involved in oxidative stress, iNOS, examples of inflammatory mediators, such as tumour necrosis factor alpha (TNF-α), interleukins 1 and 6 (IL-1 and IL-6), and markers of VSMC changes, in particular plasminogen activator inhibitor-1 and thrombospondin-1 (PAI-1 and TSP-1). Our results could suggest that PNP downregulates VSMC proliferation and migration, mediated by PAI-1 and TSP-1, and reduces inflammation and oxidative stress in vessels. These data suggested that LMWH, in particular PNP, could be a theoretically practical tool in the prevention of atherosclerotic vascular modification. © 2017 The Authors. International Journal of Experimental Pathology © 2017 International Journal of Experimental Pathology.

  15. Vitamin K status and vascular calcification: evidence from observational and clinical studies.

    Science.gov (United States)

    Shea, M Kyla; Holden, Rachel M

    2012-03-01

    Vascular calcification occurs when calcium accumulates in the intima (associated with atherosclerosis) and/or media layers of the vessel wall. Coronary artery calcification (CAC) reflects the calcium burden within the intima and media of the coronary arteries. In population-based studies, CAC independently predicts cardiovascular disease (CVD) and mortality. A preventive role for vitamin K in vascular calcification has been proposed based on its role in activating matrix Gla protein (MGP), a calcification inhibitor that is expressed in vascular tissue. Although animal and in vitro data support this role of vitamin K, overall data from human studies are inconsistent. The majority of population-based studies have relied on vitamin K intake to measure status. Phylloquinone is the primary dietary form of vitamin K and available supplementation trials, albeit limited, suggest phylloquinone supplementation is relevant to CAC. Yet observational studies have found higher dietary menaquinone, but not phylloquinone, to be associated with less calcification. Vascular calcification is highly prevalent in certain patient populations, especially in those with chronic kidney disease (CKD), and it is plausible vitamin K may contribute to reducing vascular calcification in patients at higher risk. Subclinical vitamin K deficiency has been reported in CKD patients, but studies linking vitamin K status to calcification outcomes in CKD are needed to clarify whether or not improving vitamin K status is associated with improved vascular health in CKD. This review summarizes the available evidence of vitamin K and vascular calcification in population-based studies and clinic-based studies, with a specific focus on CKD patients.

  16. Combined presence of aortic valve calcification and mitral annular calcification as a marker of the extent and vulnerable characteristics of coronary artery plaque assessed by 64-multidetector computed tomography.

    Science.gov (United States)

    Utsunomiya, Hiroto; Yamamoto, Hideya; Kunita, Eiji; Kitagawa, Toshiro; Ohashi, Norihiko; Oka, Toshiharu; Yamazato, Ryo; Horiguchi, Jun; Kihara, Yasuki

    2010-11-01

    We examined the association of aortic valve calcification (AVC) and mitral annular calcification (MAC) to coronary atherosclerosis using 64-multidetector computed tomography (MDCT). Valvular calcification is considered a manifestation of atherosclerosis. The impact of multiple heart valve calcium deposits on the distribution and characteristics of coronary plaque is unknown. We evaluated 322 patients referred for 64-MDCT, and assessed valvular calcification and the extent of calcified (CAP), mixed (MCAP), and noncalcified coronary atherosclerotic plaque (NCAP) in accordance with the 17-coronary segments model. We assessed the vulnerable characteristics of coronary plaque with positive remodeling, low-density plaque (CT density ≤38 Hounsfield units), and the presence of adjacent spotty calcification. In 49 patients with both AVC and MAC, the segment numbers of CAP and MCAP were larger than in those with a lack of valvular calcification and an isolated AVC (pNCAP. Moreover, it was also related to the presence of coronary plaque with all three vulnerable characteristics (OR 4.87, 95%CI 1.85-12.83, p=0.001). The combined presence of AVC and MAC is highly associated with the presence, extent, and vulnerable characteristics of coronary plaque identified by 64-MDCT. Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

  17. Premature subclinical atherosclerosis in children and young adults with juvenile idiopathic arthritis

    DEFF Research Database (Denmark)

    Bohr, Anna-Helene; Fuhlbrigge, Robert C; Karup Pedersen, Freddy

    2016-01-01

    Many studies show that Juvenile Idiopathic Arthritis (JIA) is associated with early subclinical signs of atherosclerosis. Chronic inflammation per se may be an important driver but other known risk factors, such as dyslipidemia, hypertension, insulin insensitivity, a physically inactive lifestyle...

  18. Atherosclerosis: Hypotheses and theories

    Directory of Open Access Journals (Sweden)

    E. A. Yuryeva

    2014-01-01

    Full Text Available The article gives basic theories of the pathogenesis of atherosclerosis, including inflammatory, cholesterol, lipid, lipoprotein, iron ones, as a result of metabolic syndrome, oxidative stress. In spite of carefully and deeply developed and ongoing elaborated pathogenesis theories, the etiological factors of atherosclerosis remain unknown so far. The age-related aspect of the disease is discussed; atherosclerosis is considered to be a childhood-onset disease that manifests itself at a later age. The authors propose an experimental and clinical evidence-based concept of the common etiology of syndromes of atherosclerosis, namely: the body's endogenous intoxication that is permanent or periodically progressive may be a primary cause of altered conformation of different protein molecules with their higher ability to adsorb the trace elements consolidating the structural changes. This change of proteins diminishes their functions and determines their antigenic properties, which is attended by the development of different pathogenic components in relation to the body's individual features.

  19. The Biochemistry of atherosclerosis

    National Research Council Canada - National Science Library

    Scanu, Angelo M; Getz, Godfrey S; Wissler, Robert W

    1979-01-01

    In this first full-length review of the biochemical parameters and their part in the pathogenesis of atherosclerosis, the reader will discover a range of coverage concerning basic etiological factors...

  20. Hepatic JAK2 protects against atherosclerosis through circulating IGF-1.

    Science.gov (United States)

    Sivasubramaniyam, Tharini; Schroer, Stephanie A; Li, Angela; Luk, Cynthia T; Shi, Sally Yu; Besla, Rickvinder; Dodington, David W; Metherel, Adam H; Kitson, Alex P; Brunt, Jara J; Lopes, Joshua; Wagner, Kay-Uwe; Bazinet, Richard P; Bendeck, Michelle P; Robbins, Clinton S; Woo, Minna

    2017-07-20

    Atherosclerosis is considered both a metabolic and inflammatory disease; however, the specific tissue and signaling molecules that instigate and propagate this disease remain unclear. The liver is a central site of inflammation and lipid metabolism that is critical for atherosclerosis, and JAK2 is a key mediator of inflammation and, more recently, of hepatic lipid metabolism. However, precise effects of hepatic Jak2 on atherosclerosis remain unknown. We show here that hepatic Jak2 deficiency in atherosclerosis-prone mouse models exhibited accelerated atherosclerosis with increased plaque macrophages and decreased plaque smooth muscle cell content. JAK2's essential role in growth hormone signalling in liver that resulted in reduced IGF-1 with hepatic Jak2 deficiency played a causal role in exacerbating atherosclerosis. As such, restoring IGF-1 either pharmacologically or genetically attenuated atherosclerotic burden. Together, our data show hepatic Jak2 to play a protective role in atherogenesis through actions mediated by circulating IGF-1 and, to our knowledge, provide a novel liver-centric mechanism in atheroprotection.

  1. Osteocalcin expression by circulating endothelial progenitor cells in patients with coronary atherosclerosis.

    Science.gov (United States)

    Gössl, Mario; Mödder, Ulrike I; Atkinson, Elizabeth J; Lerman, Amir; Khosla, Sundeep

    2008-10-14

    This study was designed to test whether patients with coronary atherosclerosis have increases in circulating endothelial progenitor cells (EPCs) expressing an osteogenic phenotype. Increasing evidence indicates a link between bone and the vasculature, and bone marrow and circulating osteogenic cells have been identified by staining for the osteoblastic marker, osteocalcin (OCN). Endothelial progenitor cells contribute to vascular repair, but repair of vascular injury may result in calcification. Using cell surface markers (CD34, CD133, kinase insert domain receptor [KDR]) to identify EPCs, we examined whether patients with coronary atherosclerosis had increases in the percentage of EPCs expressing OCN. We studied 72 patients undergoing invasive coronary assessment: control patients (normal coronary arteries and no endothelial dysfunction, n = 21) versus 2 groups with coronary atherosclerosis-early coronary atherosclerosis (normal coronary arteries but with endothelial dysfunction, n = 22) and late coronary atherosclerosis (severe, multivessel coronary artery disease, n = 29). Peripheral blood mononuclear cells were analyzed using flow cytometry. Compared with control patients, patients with early or late coronary atherosclerosis had significant increases (approximately 2-fold) in the percentage of CD34+/KDR+ and CD34+/CD133+/KDR+ cells costaining for OCN. Even larger increases were noted in the early and late coronary atherosclerosis patients in the percentage of CD34+/CD133-/KDR+ cells costaining for OCN (5- and 2-fold, p < 0.001 and 0.05, respectively). A higher percentage of EPCs express OCN in patients with coronary atherosclerosis compared with subjects with normal endothelial function and no structural coronary artery disease. These findings have potential implications for the mechanisms of vascular calcification and for the development of novel markers for coronary atherosclerosis.

  2. The Prebiotic Inulin Aggravates Accelerated Atherosclerosis in Hypercholesterolemic APOE*3-Leiden Mice

    OpenAIRE

    Lisa R. Hoving; Margreet R. de Vries; Rob C. M. de Jong; Saeed Katiraei; Amanda Pronk; Paul H. A. Quax; Vanessa van Harmelen; Ko Willems van Dijk

    2018-01-01

    The prebiotic inulin has proven effective at lowering inflammation and plasma lipid levels. As atherosclerosis is provoked by both inflammation and hyperlipidemia, we aimed to determine the effect of inulin supplementation on atherosclerosis development in hypercholesterolemic APOE*3-Leiden (E3L) mice. Male E3L mice were fed a high-cholesterol (1%) diet, supplemented with or without 10% inulin for 5 weeks. At week 3, a non-constrictive cuff was placed around the right femoral artery to induce...

  3. Animal Models of Calcific Aortic Valve Disease

    Directory of Open Access Journals (Sweden)

    Krista L. Sider

    2011-01-01

    Full Text Available Calcific aortic valve disease (CAVD, once thought to be a degenerative disease, is now recognized to be an active pathobiological process, with chronic inflammation emerging as a predominant, and possibly driving, factor. However, many details of the pathobiological mechanisms of CAVD remain to be described, and new approaches to treat CAVD need to be identified. Animal models are emerging as vital tools to this end, facilitated by the advent of new models and improved understanding of the utility of existing models. In this paper, we summarize and critically appraise current small and large animal models of CAVD, discuss the utility of animal models for priority CAVD research areas, and provide recommendations for future animal model studies of CAVD.

  4. Calcification in a pleural mesothelioma

    International Nuclear Information System (INIS)

    Nichols, D.M.; Johnson, M.A.

    1983-01-01

    Extensive calcification in a rapidly growing malignant mixed mesothelioma of the pleura was observed on plain radiography and computed tomography of the chest in a patient with a long history of asbestos exposure and chronic renal failure

  5. Calcifications simulating peroneus longus tendinitis

    International Nuclear Information System (INIS)

    Carvalho, A. de; Illum, F.; Joergensen, J.

    1984-01-01

    In two patients with sprains of the ankle joint calcification adjacent to the posterior tibial margin was evident in the lateral projection of a standard radiographic examination. Calcifying peroneus longus tendinitis was suggested. Further tangential views and computed tomography (CT) scan disclosed, however, that the calcifications in both patients were located in the tibial insertion of the posterior and inferior tibio-fibular ligament. In such cases, a correct diagnosis will avoid unnecessary treatment for a non-existent tendinitis. (orig.)

  6. Inflammatory markers and extent and progression of early atherosclerosis

    DEFF Research Database (Denmark)

    Willeit, Peter; Thompson, Simon G; Agewall, Stefan

    2016-01-01

    BACKGROUND: Large-scale epidemiological evidence on the role of inflammation in early atherosclerosis, assessed by carotid ultrasound, is lacking. We aimed to quantify cross-sectional and longitudinal associations of inflammatory markers with common-carotid-artery intima-media thickness (CCA-IMT)...

  7. Seasonal variation in thoracic vessel calcifications: Evidence from a chest computed tomography study

    Energy Technology Data Exchange (ETDEWEB)

    Vehmas, Tapio; Leino-Arjas, Paeivi (Health and Work Ability, Finnish Inst. of Occupational Health, Helsinki (Finland)), e-mail: tapio.vehmas@ttl.fi; Hiltunen, Asta (Dept. of Radiology, Central Hospital of Laensi-Pohja, Kemi (Finland))

    2010-01-15

    Background: Cardiovascular disease incidence and mortality exhibit a winter peak and a summer trough, a fact that could have radiological manifestations. Purpose: To identify possible seasonal trends in the occurrence of thoracic vessel calcifications. Material and Methods: 505 male construction workers (aged 39-80 years) were each imaged once with chest spiral computed tomography (CT) during a 2-year period. Based on visual assessment of calcified plaques (0=no, 1=slight, 2=moderate, 3=extensive calcification), sum scores of atherosclerosis in coronary arteries, in the thoracic aorta, in the pre-cervical artery bases, and overall were constructed. The scores were regressed on the annual rank number of the CT day. Results: By using the cubic regression model, seasonal variation in calcified plaques in coronary arteries (P=0.003), in pre-cervical artery origins (P=0.015), and in the overall sum score (P=0.004) was observed. The peak occurred in January-February and the nadir in August. Depending on the model, about 2-3% of the variation in atherosclerotic calcifications could be explained by the season of imaging. Conclusion: The observed seasonal trend in calcifications parallels with mortality reports. Seasonal variations should be considered in atherosclerosis treatment studies. Confirmatory studies using modern imaging technology are needed in different countries and geographical locations, preferably with repeat imaging of the same individuals

  8. Tortuosity and calcification of the splenic artery. More than an additional finding

    International Nuclear Information System (INIS)

    Golder, W.A.

    2008-01-01

    Tortuosity of the splenic artery and calcification of the vessel wall are typical additional findings on plain abdominal x-ray. The combination of both anomalies is common in elderly persons presenting without symptoms of splenic ischemia. Its pathogenesis is thought to be multifactorial. In infancy and childhood, the splenic artery is stretched in its entire course. A growing difference between the length of the vessel and the distance between its origin and the splenic hilum gives rise to tortuosity. The artery's proximal segment is involved more frequently and more severely than the distal one. The tortuous route of the vessel is accentuated by the direction of its major branches, which is roughly perpendicular to the main trajectory. Neither tortuosity nor calcification should be taken to be risk factors for the comparatively common splenic artery aneurysm. Calcific deposits are not confined to the media but are also detected in the intima of the vascular wall. Critical narrowings of the lumen arising on the calcium deposits are not observed. Calcifying atherosclerosis of the splenic artery is comparable to medial sclerosis of the peripheral arteries frequently noticed in diabetics and dialysis patients. Only the less important calcification of the intima may be attributed to mechanisms of the hydrohemodynamic theory of atherosclerosis. The spleen's blood storage capacity may contribute to the characteristic age-dependent alterations of the shape and course of the splenic artery. (orig.) [de

  9. Nuclear medicine and atherosclerosis

    International Nuclear Information System (INIS)

    Sinzinger, H.; Virgolini, I.

    1990-01-01

    Although the pathomechanisms of atherosclerosis are well known, their radioisotopic monitoring is still in its early childhood. The current radioisotope techniques are of only limited value for contributing to the clinical diagnosis of atherosclerosis. The limited reaction time of cellular blood constituents (platelets, monocytes) with the vascular surface at the injury site makes it very difficult to catch the point of injury. Lipoproteins excellently allow receptor imaging, while vascular monitoring is only of scientific interest at present. Labelling and subsequent imaging of components of the coagulation cascade have not succeeded so far, nor have attempts using unspecific labels such as porphyrin, polyclonal IgG and Fc fragments, for example. Preliminary evidence indicates that radioisotopic techniques may be of great benefit in the future in elucidating functional aspects of the disease, while they do not contribute to examining the stage and extent of atherosclerosis. (orig.)

  10. Sphingosine 1-Phosphate and Atherosclerosis

    Science.gov (United States)

    Yatomi, Yutaka

    2018-01-01

    Sphingosine 1-phosphate (S1P) is a potent lipid mediator that works on five kinds of S1P receptors located on the cell membrane. In the circulation, S1P is distributed to HDL, followed by albumin. Since S1P and HDL share several bioactivities, S1P is believed to be responsible for the pleiotropic effects of HDL. Plasma S1P levels are reportedly lower in subjects with coronary artery disease, suggesting that S1P might be deeply involved in the pathogenesis of atherosclerosis. In basic experiments, however, S1P appears to possess both pro-atherosclerotic and anti-atherosclerotic properties; for example, S1P possesses anti-apoptosis, anti-inflammation, and vaso-relaxation properties and maintains the barrier function of endothelial cells, while S1P also promotes the egress and activation of lymphocytes and exhibits pro-thrombotic properties. Recently, the mechanism for the biased distribution of S1P on HDL has been elucidated; apolipoprotein M (apoM) carries S1P on HDL. ApoM is also a modulator of S1P, and the metabolism of apoM-containing lipoproteins largely affects the plasma S1P level. Moreover, apoM modulates the biological properties of S1P. S1P bound to albumin exerts both beneficial and harmful effects in the pathogenesis of atherosclerosis, while S1P bound to apoM strengthens anti-atherosclerotic properties and might weaken the pro-atherosclerotic properties of S1P. Although the detailed mechanisms remain to be elucidated, apoM and S1P might be novel targets for the alleviation of atherosclerotic diseases in the future. PMID:28724841

  11. Chronic Intermittent Hypoxia Induces Atherosclerosis

    OpenAIRE

    Savransky, Vladimir; Nanayakkara, Ashika; Li, Jianguo; Bevans, Shannon; Smith, Philip L.; Rodriguez, Annabelle; Polotsky, Vsevolod Y.

    2007-01-01

    Rationale: Obstructive sleep apnea, a condition leading to chronic intermittent hypoxia (CIH), is associated with hyperlipidemia, atherosclerosis, and a high cardiovascular risk. A causal link between obstructive sleep apnea and atherosclerosis has not been established.

  12. Diagnosis of calcification on abdominal radiographs

    International Nuclear Information System (INIS)

    Lamb, C.R.; Kleine, L.J.; McMillan, M.C.

    1991-01-01

    A wide variety of normal and pathologic factors may induce intraabdominal calcification. In general, the most reliable indication of the cause of a calcification is its location; therefore, if the affected organ can be identified the radiographic diagnosis is often straightforward or, at least, limited to relatively few possibilities. With this principle in mind, a series of patients with abdominal calcification are described for the purpose of illustrating the appearance of calcification of various abdominal organs. In addition, etiology for the calcification in each patient is discussed. Certain extraabdominal calcifications which may be seen on abdominal radiographs are also mentioned

  13. Association between asymptomatic inflammatory prostatitis NIH category IV and prostatic calcification in patients with obstructive benign prostatic hyperplasia.

    Science.gov (United States)

    Engelhardt, Paul F; Seklehner, Stephan; Brustmann, Herman; Riedl, Claus R; Lusuardi, Lukas

    2016-06-01

    The aim of this study was to evaluate the incidence of prostatic calcification and prostatitis NIH category IV in patients with obstructive BPH. Ninety-six patients with obstructive BPH who had undergone transurethral electroresection of the prostate gland were evaluated. In accordance with a preoperative transrectal ultrasound examination, patients were divided into one group with prostatic calcification (N.=31) and one without (N.=65). Prostatitis NIH category IV was classified according to the grading system by Irani. Correlations between the incidence of prostatic calcification, histological prostatitis, PSA, uric acid, cholesterol, triglycerides, CRP, IPSS, IIEF-25, and NIC-CPSI were analyzed. A stone analysis of prostatic calcification was performed using X-ray powder diffraction. Sixty-nine (71.9%) patients had NIH category IV prostatitis, accounting for 83.9% of those with prostatic calcification versus 66.1% of those without (Pprostatic calcification and the severity of inflammation (Pprostatic calcifications were elevated levels of uric acid. Such patients were 1.4times more likely of having calcifications in the prostate gland (OR=1.4, Pprostatic calcification. These were significantly more common in patients with NIH category IV prostatitis.

  14. Incidence of Deflux® calcification masquerading as distal ureteric calculi on ultrasound.

    Science.gov (United States)

    Yankovic, Francisca; Swartz, Robert; Cuckow, Peter; Hiorns, Melanie; Marks, Stephen D; Cherian, Abraham; Mushtaq, Imran; Duffy, Patrick; Smeulders, Naima

    2013-12-01

    Dextranomer-hyaluronic acid (Deflux(®)), the most widely used compound in the endoscopic treatment of vesico-ureteric reflux (VUR) today, is believed to provoke only minimal inflammation. Reports of calcification of Deflux(®) are increasing. We ascertain the incidence of Deflux(®) calcification appearing as distal ureteric calculi on ultrasound. Three cases (2 external patients) of ureteroscopy for calcified submucosal Deflux(®) prompted a retrospective review of the notes and imaging of all children treated with Deflux(®) for VUR between December 2000 and January 2011 at Great Ormond Street Hospital. 232 children (M:F = 5:3) received Deflux(®) for VUR at median age 2 years (range 2 months-12 years). Follow-up annual ultrasound, performed in all, identified calcification in 2. The interval between Deflux(®) injection and presentation of its calcification was 4 years. 104 of the 232 children had been followed up for 4-10 years. Considering the observed lag-period, after 4 years the incidence of calcification of Deflux(®) on ultrasound was 2% (2/104). Patients should be warned that calcification of Deflux(®) can occur. Misinterpretation as ureteric stones is common and may lead to unnecessary ureteroscopy. In this series, the incidence of calcification of Deflux(®) on ultrasound after 4 years was 2%. Copyright © 2012 Journal of Pediatric Urology Company. Published by Elsevier Ltd. All rights reserved.

  15. Vasoreactivity, Inflammation and vascular effects of Thiazolidinediones in Insulin resistance

    NARCIS (Netherlands)

    Martens, Fabrice Marcel Anne Clément

    2006-01-01

    In the pathophysiology of atherosclerosis, based on the respons to injury mechanism, the pathophysiological phenomenons endothelial dysfunction and inflammation are playing a pivitol role. Endothelial dysfunction is characterized by a shift towards reduced vasodilation, a pro-inflammatory state,

  16. What Is Atherosclerosis?

    Science.gov (United States)

    ... builds up in the renal arteries. These arteries supply oxygen-rich blood to your kidneys. Over time, chronic kidney disease causes a slow loss of kidney function. The main function of the kidneys is to remove waste and extra water from the body. Overview The cause of atherosclerosis ...

  17. A Novel Method for Determining Calcification Composition

    National Research Council Canada - National Science Library

    Maidment, Andrew D

    2005-01-01

    Breast calcifications can be divided into two broad categories. Type I are composed of calcium oxylate while type II calcifications all have some phosphorus content most typically calcium hydroxyapatite...

  18. Differential expression of TRAIL and its receptors relative to calcification in AAA

    International Nuclear Information System (INIS)

    Liu, Xun; Winrow, Vivienne R.; Horrocks, Michael; Stevens, Cliff R.

    2007-01-01

    Abdominal aortic aneurysm (AAA) is commonly associated with atherosclerosis. Human AAA tissue displays cells undergoing all stages of apoptosis. Tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induces apoptosis in tumour cells but not in normal cells. It has death receptors and decoy receptors. An inhibitor of TRAIL, osteoprotegerin (OPG), is involved in osteogenesis and vascular calcification. We investigated TRAIL and its receptors in AAA compared within normal aorta (NA). Both qualitative and quantitative analyses of calcification in AAA walls were determined using Von Kossa staining and pre-operation computer tomography (CT) scans. There was a significant difference in calcification level at different locations in the AAA wall (p < 0.05). Apoptosis was confirmed in AAA by TUNEL assay. A significant difference in TRAIL and its receptor expression was observed between normal aortae and AAA (p < 0.05). Significant differences were also observed between tissues displaying different extents of calcification for TRAIL mRNA (p < 0.05) by RT-PCR examination and OPG protein (p < 0.01) by protein blotting examination. We propose that this pattern of expression of TRAIL and its receptors may contribute to AAA formation and calcification in the AAA wall

  19. [¹⁸F]-fluorodeoxyglucose PET imaging of atherosclerosis

    DEFF Research Database (Denmark)

    Blomberg, Björn Alexander; Høilund-Carlsen, Poul Flemming

    2015-01-01

    [(18)F]-fluorodeoxyglucose PET ((18)FDG PET) imaging has emerged as a promising tool for assessment of atherosclerosis. By targeting atherosclerotic plaque glycolysis, a marker for plaque inflammation and hypoxia, (18)FDG PET can assess plaque vulnerability and potentially predict risk...... of atherosclerosis-related disease, such as stroke and myocardial infarction. With excellent reproducibility, (18)FDG PET can be a surrogate end point in clinical drug trials, improving trial efficiency. This article summarizes key findings in the literature, discusses limitations of (18)FDG PET imaging...

  20. Box-Cox transformation of left-censored data with application to the analysis of coronary artery calcification and pharmacokinetic data.

    Science.gov (United States)

    Han, Cong; Kronmal, Richard

    2004-12-15

    Box-Cox transformation is investigated for regression models for left-censored data. Examples are provided using coronary calcification data from the Multi-Ethnic Study of Atherosclerosis and pharmacokinetic data of a nicotine nasal spray. Copyright 2004 John Wiley & Sons, Ltd.

  1. Coffee consumption and coronary calcification - The Rotterdam Coronary Calcification Study

    NARCIS (Netherlands)

    van Woudenbergh, Geertruida J.; Vliegenthart, Rozemarijn; van Rooij, Frank J. A.; Hofman, Albert; Oudkerk, Matthijs; Witteman, Jacqueline C. M.; Geleijnse, Johanna M.

    Background-The role of coffee in the cardiovascular system is not yet clear. We examined the relation of coffee intake with coronary calcification in a population-based cohort. Methods and Results-The study involved 1570 older men and women without coronary heart disease who participated in the

  2. Coffee consumption and coronary calcification: The Rotterdam coronary calcification study

    NARCIS (Netherlands)

    G.J. van Woudenbergh (Geertruida); R. Vliegenthart (Rozemarijn); F.J.A. van Rooij (Frank); A. Hofman (Albert); M. Oudkerk (Matthijs); J.C.M. Witteman (Jacqueline); J.M. Geleijnse (Marianne)

    2008-01-01

    textabstractBACKGROUND - The role of coffee in the cardiovascular system is not yet clear. We examined the relation of coffee intake with coronary calcification in a population-based cohort. METHODS AND RESULTS - The study involved 1570 older men and women without coronary heart disease who

  3. Coffee Consumption and Coronary Calcification: The Rotterdam Coronary Calcification Study

    NARCIS (Netherlands)

    Woudenbergh, van G.J.; Vliegenthart, R.; Rooij, van F.J.A.; Hofman, A.; Oudkerk, M.; Witteman, J.C.M.; Geleijnse, J.M.

    2008-01-01

    Background¿ The role of coffee in the cardiovascular system is not yet clear. We examined the relation of coffee intake with coronary calcification in a population-based cohort. Methods and Results¿ The study involved 1570 older men and women without coronary heart disease who participated in the

  4. Intracranial calcification in central diabetes insipidus

    International Nuclear Information System (INIS)

    Al-Kandari, Salwa R.; Pandey, Tarun; Badawi, Mona H.

    2008-01-01

    Intracranial calcification is a known but extremely rare complication of diabetes insipidus. To date, only 16 patients have been reported and all had the peripheral (nephrogenic) type of diabetes insipidus. We report a child with intracranial calcification complicating central diabetes insipidus. We also report a child with nephrogenic diabetes insipidus, and compare the patterns of intracranial calcification. (orig.)

  5. Intracranial calcification in central diabetes insipidus

    Energy Technology Data Exchange (ETDEWEB)

    Al-Kandari, Salwa R. [Al Razi Hospital, Department of Clinical Radiology, Kuwait (Kuwait); Pandey, Tarun [Al Razi Hospital, Department of Clinical Radiology, Kuwait (Kuwait); University of Arkansas for Medical Sciences, Radiology Department, Little Rock, AR (United States); Badawi, Mona H. [Al-Adan Hospital, Department of Paediatrics, Kuwait (Kuwait)

    2008-01-15

    Intracranial calcification is a known but extremely rare complication of diabetes insipidus. To date, only 16 patients have been reported and all had the peripheral (nephrogenic) type of diabetes insipidus. We report a child with intracranial calcification complicating central diabetes insipidus. We also report a child with nephrogenic diabetes insipidus, and compare the patterns of intracranial calcification. (orig.)

  6. Calcification of peritoneal carcinomatosis from gastric carcinoma

    International Nuclear Information System (INIS)

    Matsuoka, Y.; Itai, Y.; Ohtomo, K.; Nishikawa, J.; Sasaki, Y.

    1991-01-01

    Peritoneal calcification is noted in peritoneal dissemination from serious cystoadenocarcinoma of the ovary, pseudomyxoma peritonei and meconium peritonitis. This article discusses a case of peritoneal disseminated calcification from gastric carcinoma. To the author's knowledge, this is the first report in English literature of gastric cancer showing peritoneal calcification. (author). 10 refs.; 1 fig

  7. Vitamin K-antagonists accelerate atherosclerotic calcification and induce a vulnerable plaque phenotype.

    Directory of Open Access Journals (Sweden)

    Leon J Schurgers

    Full Text Available Vitamin K-antagonists (VKA are treatment of choice and standard care for patients with venous thrombosis and thromboembolic risk. In experimental animal models as well as humans, VKA have been shown to promote medial elastocalcinosis. As vascular calcification is considered an independent risk factor for plaque instability, we here investigated the effect of VKA on coronary calcification in patients and on calcification of atherosclerotic plaques in the ApoE(-/- model of atherosclerosis.A total of 266 patients (133 VKA users and 133 gender and Framingham Risk Score matched non-VKA users underwent 64-slice MDCT to assess the degree of coronary artery disease (CAD. VKA-users developed significantly more calcified coronary plaques as compared to non-VKA users. ApoE(-/- mice (10 weeks received a Western type diet (WTD for 12 weeks, after which mice were fed a WTD supplemented with vitamin K(1 (VK(1, 1.5 mg/g or vitamin K(1 and warfarin (VK(1&W; 1.5 mg/g & 3.0 mg/g for 1 or 4 weeks, after which mice were sacrificed. Warfarin significantly increased frequency and extent of vascular calcification. Also, plaque calcification comprised microcalcification of the intimal layer. Furthermore, warfarin treatment decreased plaque expression of calcification regulatory protein carboxylated matrix Gla-protein, increased apoptosis and, surprisingly outward plaque remodeling, without affecting overall plaque burden.VKA use is associated with coronary artery plaque calcification in patients with suspected CAD and causes changes in plaque morphology with features of plaque vulnerability in ApoE(-/- mice. Our findings underscore the need for alternative anticoagulants that do not interfere with the vitamin K cycle.

  8. Inflammation: a trigger for acute coronary syndrome

    International Nuclear Information System (INIS)

    SAGER, Hendrik B.; NAHRENDORF, Matthias

    2016-01-01

    Atherosclerosis is a chronic inflammatory disease of the vessel wall and a major cause of death worldwide. One of atherosclerosis’ most dreadful complications are acute coronary syndromes that comprise ST-segment elevation myocardial infarction, non-ST-segment elevation myocardial infarction, and unstable angina. We now understand that inflammation substantially contributes to the initiation, progression, and destabilization of atherosclerosis. In this review, we will focus on the role of inflammatory leukocytes, which are the cellular protagonists of vascular inflammation, in triggering disease progression and, ultimately, the destabilization that causes acute coronary syndromes.

  9. Probiotics and atherosclerosis – a new challenge?

    Directory of Open Access Journals (Sweden)

    Chan Yee Kwan

    2012-06-01

    Full Text Available Background Atherosclerosis is the major cause of cardiovascular disease and stroke, which are among the top 10 leading causes of death worldwide. Pathogen-associated molecular patterns (PAMPs can activate toll-like receptors (TLRs and activate nuclear factor kappa B (NFκB signaling, a central pathway in inflammation, which regulates genes that encode proinflammatory molecules essential in atherogenesis. Lipopolysaccharides (LPS, which is unique to gram negative bacteria, as well as peptidoglycan (PGN, which is found in gram positive bacteria are PAMPS and ligands of TLR4 and TLR2, respectively, both of which are essential in plaque progression in atherosclerosis. Gastrointestinal tract is suggested to be the major site for absorption and translocation of TLR2 and TLR4 stimulants. Inflammation can result in a ‘leaky gut’ that leads to higher bacterial translocation, eventually the accumulation of LPS and PGN would activate TLRs and trigger inflammation through NFκB and promote further systemic complication like atherosclerosis. Probiotics, can protect the intestinal barrier to reduce bacterial translocation and have potential systemic anti-inflammatory properties.To evaluate whether probiotics can help reduce atherosclerotic development using in vivo study.Apolipoprotein E knockout (ApoE−/ −  mice were fed on high fat diet alone, with telmisartan (Tel (1 or 5 mg/kg/day, positive controls or with probiotics (VSL#3/LGG with or without Tel (1 mg/kg/day for 12 weeks.Probiotics, Tel, or a combination of both reduced lesion size at the aortic root significantly; VSL#3 reduced serum inflammatory adhesion molecules soluble E- (sE-selectin, soluble intercellular adhesion molecule 1 (sICAM-1, soluble vascular cell adhesion molecule 1 (sVCAM-1, and plaque disrupting factor matrix metalloproteinase (MMP-9 significantly; probiotics and Tel at 5 mg/kg/day could induce changes in gut microbiota population; the efficiency of lesion reduction seemed

  10. Cardiac and pericardial calcifications on chest radiographs

    Energy Technology Data Exchange (ETDEWEB)

    Ferguson, E.C., E-mail: ecferguson@hotmail.co [University of Texas Medical School at Houston, Department of Diagnostic and Interventional Imaging, Section of Thoracic Imaging, Houston, TX 77030 (United States); Berkowitz, E.A. [University of Texas Medical School at Houston, Department of Diagnostic and Interventional Imaging, Section of Thoracic Imaging, Houston, TX 77030 (United States)

    2010-09-15

    Many types of cardiac and pericardial calcifications identified on chest radiographs can be recognized and distinguished based on characteristic locations and appearances. The purpose of this review is to emphasize the importance of detecting cardiac and pericardial calcifications on chest radiographs, and to illustrate and describe the various types of calcifications that may be encountered and how they may be differentiated from one another. Each type of cardiac and pericardial calcification is discussed, its location and appearance described, and its significance explained. Recognizing and understanding these calcifications is important as they are often encountered in daily practice and play an important role in patient care.

  11. Intracranial atherosclerosis: current concepts.

    Science.gov (United States)

    Arenillas, Juan F

    2011-01-01

    The most relevant ideas discussed in this article are described here. Intracranial atherosclerotic disease (ICAD) represents the most common cause of ischemic stroke worldwide. Its importance in whites may have been underestimated. New technical developments, such as high-resolution MRI, allow direct assessment of the intracranial atherosclerotic plaque, which may have a profound impact on ICAD diagnosis and therapy in the near future. Early detection of ICAD may allow therapeutic intervention while the disease is still asymptomatic. The Barcelonès Nord and Maresme Asymptomatic Intracranial Atherosclerosis Study is presented here. The main prognostic factors that characterize the patients who are at a higher risk for ICAD recurrence are classified and discussed. The best treatment for ICAD remains to be established. The Stenting Versus Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis Study is currently ongoing to address this crucial issue. These and other topics will be discussed at the Fifth International Intracranial Atherosclerosis Conference (Valladolid, Spain, autumn 2011).

  12. Where Does Inflammation Fit?

    Science.gov (United States)

    Biasucci, Luigi M; La Rosa, Giulio; Pedicino, Daniela; D'Aiello, Alessia; Galli, Mattia; Liuzzo, Giovanna

    2017-09-01

    This review focuses on the complex relationship between inflammation and the onset of acute coronary syndrome and heart failure. In the last few years, two important lines of research brought new and essential information to light in the pathogenesis of acute coronary syndrome: a) the understanding of the immune mediate mechanisms of inflammation in Ischemic Heart Disease (IHD) and b) evidence that the inflammatory mechanisms associated with atherosclerosis and its complications can be modulated by anti-inflammatory molecules. A large amount of data also suggests that inflammation is a major component in the development and exacerbation of heart failure (HF), in a symbiotic relationship. In particular, recent evidence underlies peculiar aspects of the phenomenon: oxidative stress and autophagy; DAMPS and TLR-4 signaling activation; different macrophages lineage and the contribution of NLRP-3 inflammasome; adaptive immune system. A possible explanation that could unify the pathogenic mechanism of these different conditions is the rising evidence that increased bowel permeability may allow translation of gut microbioma product into the circulation. These findings clearly establish the role of inflammation as the great trigger for two of the major cardiovascular causes of death and morbidity. Further studies are needed, to better clarify the issue and to define more targeted approaches to reduce pathological inflammation while preserving the physiological one.

  13. Suppression of atherosclerosis by synthetic REV-ERB agonist

    Energy Technology Data Exchange (ETDEWEB)

    Sitaula, Sadichha [Department of Molecular Therapeutics, The Scripps Research Institute, Jupiter, FL 33458 (United States); Billon, Cyrielle [Department of Pharmacological & Physiological Science, Saint Louis University School of Medicine, St. Louis, MO 63104 (United States); Kamenecka, Theodore M.; Solt, Laura A. [Department of Molecular Therapeutics, The Scripps Research Institute, Jupiter, FL 33458 (United States); Burris, Thomas P., E-mail: burristp@slu.edu [Department of Pharmacological & Physiological Science, Saint Louis University School of Medicine, St. Louis, MO 63104 (United States)

    2015-05-08

    The nuclear receptors for heme, REV-ERBα and REV-ERBβ, play important roles in the regulation of metabolism and inflammation. Recently it was demonstrated that reduced REV-ERBα expression in hematopoetic cells in LDL receptor null mice led to increased atherosclerosis. We sought to determine if synthetic REV-ERB agonists that we have developed might have the ability to suppress atherosclerosis in this model. A previously characterized synthetic REV-ERB agonist, SR9009, was used to determine if activation of REV-ERB activity would affect atherosclerosis in LDL receptor deficient mice. Atherosclerotic plaque size was significantly reduced (p < 0.05) in mice administered SR9009 (100 mg/kg) for seven weeks compared to control mice (n = 10 per group). SR9009 treatment of bone marrow-derived mouse macrophages (BMDM) reduced the polarization of BMDMs to proinflammatory M1 macrophage while increasing the polarization of BMDMs to anti-inflammatory M2 macrophages. Our results suggest that pharmacological targeting of REV-ERBs may be a viable therapeutic option for treatment of atherosclerosis. - Highlights: • Synthetic REV-ERB agonist treatment reduced atherosclerosis in a mouse model. • Pharmacological activation of REV-ERB decreased M1 macrophage polarization. • Pharmacological activation of REV-ERB increased M2 macrophage polarization.

  14. Thymoma calcification: Is it clinically meaningful?

    Directory of Open Access Journals (Sweden)

    Alkaied Homam

    2011-08-01

    Full Text Available Abstract Among anterior mediastinal lesions, thymoma is the most common. Thymomas are tumors of thymic epithelial cell origin that are distinguished by inconsistent histological and biologic behavior. Chest imaging studies typically show a round or lobulated tumor in the anterior mediastinum. Calcifications in thymomas are classically punctuate or amorphous, positioned within the lesion. Chest computed tomography (CT features suggesting higher risk thymoma consist of tumor heterogeneity, vascular involvement, lobulation, pulmonary nodules, lymphadenopathy, and pleural manifestations. Imaging findings have an imperfect ability to predict stage and prognosis for thymoma patients. Our objective is to highlight the clinical implications of thymoma calcifications on the diagnosis, clinical manifestation and prognosis. A pubmed and google search was performed using the following words: thymoma calcification, calcified thymus, mediastinal calcification, anterior mediastinal calcification, and calcified thymoma. After reviewing 370 articles, 32 eligible articles describing thymoma calcifications were found and included in this review. Although the presence of thymus calcifications was more common in patients with invasive thymomas, they were present in significant portion of non-invasive thymomas. The presence of calcifications was not a significant factor in differentiating between benign and malignant thymoma. As a result, the type, location, size or other characteristics of thymus gland calcifications were not relevant features in clinical and radiologic diagnosis of thymoma. The histopathological diagnosis is still the only possible way to confirm the neoplastic nature of thymoma. All types of thymomas should be evaluated and managed independently of the presence of calcifications.

  15. Coral calcification and ocean acidification

    Science.gov (United States)

    Jokiel, Paul L.; Jury, Christopher P.; Kuffner, Ilsa B.

    2016-01-01

    Over 60 years ago, the discovery that light increased calcification in the coral plant-animal symbiosis triggered interest in explaining the phenomenon and understanding the mechanisms involved. Major findings along the way include the observation that carbon fixed by photosynthesis in the zooxanthellae is translocated to animal cells throughout the colony and that corals can therefore live as autotrophs in many situations. Recent research has focused on explaining the observed reduction in calcification rate with increasing ocean acidification (OA). Experiments have shown a direct correlation between declining ocean pH, declining aragonite saturation state (Ωarag), declining [CO32_] and coral calcification. Nearly all previous reports on OA identify Ωarag or its surrogate [CO32] as the factor driving coral calcification. However, the alternate “Proton Flux Hypothesis” stated that coral calcification is controlled by diffusion limitation of net H+ transport through the boundary layer in relation to availability of dissolved inorganic carbon (DIC). The “Two Compartment Proton Flux Model” expanded this explanation and synthesized diverse observations into a universal model that explains many paradoxes of coral metabolism, morphology and plasticity of growth form in addition to observed coral skeletal growth response to OA. It is now clear that irradiance is the main driver of net photosynthesis (Pnet), which in turn drives net calcification (Gnet), and alters pH in the bulk water surrounding the coral. Pnet controls [CO32] and thus Ωarag of the bulk water over the diel cycle. Changes in Ωarag and pH lag behind Gnet throughout the daily cycle by two or more hours. The flux rate Pnet, rather than concentration-based parameters (e.g., Ωarag, [CO3 2], pH and [DIC]:[H+] ratio) is the primary driver of Gnet. Daytime coral metabolism rapidly removes DIC from the bulk seawater. Photosynthesis increases the bulk seawater pH while providing the energy that drives

  16. Calcific retropharyngeal tendinitis. [Radiological findings

    Energy Technology Data Exchange (ETDEWEB)

    Karasick, D.; Karasick, S.

    1981-12-01

    Calcific retropharyngeal tendinitis is an imflammation of the longus colli muscle tendon which is located on the anterior surface of the verterbral column extending from the atlas to the third thoracic vertebra. The acute inflammatory condition is selflimiting with symptoms consisting of a gradually increasing neck pain often associated with throat pain and difficulty swallowing. The pain is aggravated by head and neck movement. Clinically the condition can be confused with retropharyngeal absecess, meningitis, infectious spondylitis, and post-traumatic muscle spasm. The radiographic features of this condition consist of pre-vertebral soft tissue swelling from C1 to C4 and amorphous calcific density in the longus colli tendon anterior to the body of C2 and inferior to the anterior arch of C1.

  17. Humic acid in drinking well water induces inflammation through reactive oxygen species generation and activation of nuclear factor-κB/activator protein-1 signaling pathways: A possible role in atherosclerosis

    Energy Technology Data Exchange (ETDEWEB)

    Hseu, You-Cheng [Department of Cosmeceutics, China Medical University, Taichung 40402, Taiwan (China); Department of Molecular and Cellular Oncology, University of Texas, MD Anderson Cancer Center, TX 77030 (United States); Senthil Kumar, K.J. [Department of Cosmeceutics, China Medical University, Taichung 40402, Taiwan (China); Chen, Chih-Sheng; Cho, Hsin-Ju; Lin, Shu-Wei; Shen, Pei-Chun [Institute of Nutrition, China Medical University, Taichung 40402, Taiwan (China); Lin, Cheng-Wen [Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung 40402, Taiwan (China); Lu, Fung-Jou [Institute of Medicine, Chun Shan Medical University, Taichung 40201, Taiwan (China); Yang, Hsin-Ling, E-mail: hlyang@mail.cmu.edu.tw [Institute of Nutrition, China Medical University, Taichung 40402, Taiwan (China); Department of Molecular and Cellular Oncology, University of Texas, MD Anderson Cancer Center, TX 77030 (United States)

    2014-01-15

    Humic acid (HA) has been implicated as one of the etiological factors in the peripheral vasculopathy of blackfoot disease (BFD) in Taiwan. However, the underlying pathophysiological mechanisms of BFD are not well defined. In this study, we used an in vitro and in vivo model, in which HA (25–200 μg/mL) activated macrophages to produce pro-inflammatory molecules by activating their transcriptional factors. HA exposure induced NO and PGE{sub 2} production followed by induction of iNOS and COX-2 through NF-κB/AP-1 transactivation in macrophages. In addition, the production of TNF-α and IL-1β was significantly increased by HA. Moreover, HA-induced iNOS and COX-2 expression were down-regulated by the NF-κB and AP-1 inhibitors pyrrolidine dithiocarbamate (PDTC) and Tanshinone, respectively. Furthermore, generations of ROS and nitrotyrosine, as well as activation of the AKT and MAPKs signaling cascades were observed after HA exposure. Specifically, HA-induced NF-κB activation was mediated by ROS and AKT, and that HA-induced AP-1 activation was mediated by JNK and ERK. Notably, HA-mediated AKT, JNK, and ERK activation was ROS-independent. The inflammatory potential of HA was correlated with increased expression of HO-1 and Nrf2. Furthermore, an in vivo study confirms that mice exposed to HA, the serum levels of TNF-α and IL-1β was significantly increased in a dose-dependent manner. This report marks the first confirmation that environmental exposure of HA induces inflammation in macrophages, which may be one of the main causes of early atherogenesis in blackfoot disease. - Highlights: • Humic acid (HA) induce pro-inflammatory cytokines and mediators in macrophages. • HA-induced inflammation is mediated by ROS and NF-κB/AP-1 signaling pathways. • The inflammatory potential of HA correlated with activation of Nrf2/HO-1 genes. • HA exposure to mice increased pro-inflammatory cytokines production in vivo. • HA may be one of the main causes of early

  18. Humic acid in drinking well water induces inflammation through reactive oxygen species generation and activation of nuclear factor-κB/activator protein-1 signaling pathways: A possible role in atherosclerosis

    International Nuclear Information System (INIS)

    Hseu, You-Cheng; Senthil Kumar, K.J.; Chen, Chih-Sheng; Cho, Hsin-Ju; Lin, Shu-Wei; Shen, Pei-Chun; Lin, Cheng-Wen; Lu, Fung-Jou; Yang, Hsin-Ling

    2014-01-01

    Humic acid (HA) has been implicated as one of the etiological factors in the peripheral vasculopathy of blackfoot disease (BFD) in Taiwan. However, the underlying pathophysiological mechanisms of BFD are not well defined. In this study, we used an in vitro and in vivo model, in which HA (25–200 μg/mL) activated macrophages to produce pro-inflammatory molecules by activating their transcriptional factors. HA exposure induced NO and PGE 2 production followed by induction of iNOS and COX-2 through NF-κB/AP-1 transactivation in macrophages. In addition, the production of TNF-α and IL-1β was significantly increased by HA. Moreover, HA-induced iNOS and COX-2 expression were down-regulated by the NF-κB and AP-1 inhibitors pyrrolidine dithiocarbamate (PDTC) and Tanshinone, respectively. Furthermore, generations of ROS and nitrotyrosine, as well as activation of the AKT and MAPKs signaling cascades were observed after HA exposure. Specifically, HA-induced NF-κB activation was mediated by ROS and AKT, and that HA-induced AP-1 activation was mediated by JNK and ERK. Notably, HA-mediated AKT, JNK, and ERK activation was ROS-independent. The inflammatory potential of HA was correlated with increased expression of HO-1 and Nrf2. Furthermore, an in vivo study confirms that mice exposed to HA, the serum levels of TNF-α and IL-1β was significantly increased in a dose-dependent manner. This report marks the first confirmation that environmental exposure of HA induces inflammation in macrophages, which may be one of the main causes of early atherogenesis in blackfoot disease. - Highlights: • Humic acid (HA) induce pro-inflammatory cytokines and mediators in macrophages. • HA-induced inflammation is mediated by ROS and NF-κB/AP-1 signaling pathways. • The inflammatory potential of HA correlated with activation of Nrf2/HO-1 genes. • HA exposure to mice increased pro-inflammatory cytokines production in vivo. • HA may be one of the main causes of early atherogenesis

  19. Toll-Like Receptor-2 Mediates Diet and/or Pathogen Associated Atherosclerosis: Proteomic Findings

    OpenAIRE

    Madan, Monika; Amar, Salomon

    2008-01-01

    Accumulating evidence implicates a fundamental link between the immune system and atherosclerosis. Toll-like receptors are principal sensors of the innate immune system. Here we report an assessment of the role of the TLR2 pathway in atherosclerosis associated with a high-fat diet and/or bacteria in ApoE(+/-) mice.To explore the role of TLR2 in inflammation- and infection-associated atherosclerosis, 10 week-old ApoE(+/-)-TLR2(+/+), ApoE(+/-)-TLR2(+/-) and ApoE(+/-)-TLR2(-/-) mice were fed eit...

  20. A review of plant-based compounds and medicinal plants effective on atherosclerosis

    Directory of Open Access Journals (Sweden)

    Mehrnoosh Sedighi

    2017-01-01

    Full Text Available Atherosclerosis is one of the most important cardiovascular diseases that involve vessels through the development of fatty streaks and plaques. Plant-based compounds can help treat or prevent atherosclerosis through affecting the involved factors. The main purpose of this review article is to investigate and introduce medicinal plants and their potential activities regarding antioxidant properties, effective on lipids level and development of plaque, atherosclerosis, and progression of atherosclerosis as well as the development of cardiovascular disease and ischemia. To search for the relevant articles indexed in Information Sciences Institute, PubMed, Scientific Information Database, IranMedex, and Scopus between 1980 and 2013, with further emphasis on those indexed from 2004 to 2015, we used these search terms: atherosclerosis, antioxidant, cholesterol, inflammation, and the medicinal plants below. Then, the articles with inclusion criteria were used in the final analysis of the findings. Plant-based active compounds, including phenols, flavonoids, and antioxidants, can be effective on atherosclerosis predisposing factors and hence in preventing this disease and associated harmful complications, especially through reducing cholesterol, preventing increase in free radicals, and ultimately decreasing vascular plaque and vascular resistance. Hence, medicinal plants can contribute to treating atherosclerosis and preventing its progression through reducing cholesterolemia, free radicals, inflammation, vascular resistance, and certain enzymes. They, alone or in combination with hypocholesterolemic drugs, can therefore be useful for patients with hyperlipidemia and its complications.

  1. Foraminiferal calcification and CO2

    Science.gov (United States)

    Nooijer, L. D.; Toyofuku, T.; Reichart, G. J.

    2017-12-01

    Ongoing burning of fossil fuels increases atmospheric CO2, elevates marine dissolved CO2 and decreases pH and the saturation state with respect to calcium carbonate. Intuitively this should decrease the ability of CaCO3-producing organisms to build their skeletons and shells. Whereas on geological time scales weathering and carbonate deposition removes carbon from the geo-biosphere, on time scales up to thousands of years, carbonate precipitation increases pCO2 because of the associated shift in seawater carbon speciation. Hence reduced calcification provides a potentially important negative feedback on increased pCO2 levels. Here we show that foraminifera form their calcium carbonate by active proton pumping. This elevates the internal pH and acidifies the direct foraminiferal surrounding. This also creates a strong pCO2 gradient and facilitates the uptake of DIC in the form of carbon dioxide. This finding uncouples saturation state from calcification and predicts that the added carbon due to ocean acidification will promote calcification by these organisms. This unknown effect could add substantially to atmospheric pCO2 levels, and might need to be accounted for in future mitigation strategies.

  2. The Relationship of Body Composition and Coronary Artery Calcification in Apparently Healthy Korean Adults

    Directory of Open Access Journals (Sweden)

    Jung-Hee Yu

    2013-03-01

    Full Text Available BackgroundWe investigated the association of coronary artery calcium score (CACS with body composition and insulin resistance in apparently healthy Korean adults.MethodsNine hundred forty-five participants (mean age, 48.9 years; 628 men in a medical check-up program were selected for analysis. Body composition was assessed by bioelectrical impedance analysis (BIA. Insulin resistance was evaluated using the homeostasis model assessment of insulin resistance (HOMA-IR. The CACS was assessed by multidetector computed tomography.ResultsOne hundred forty-six subjects (15.4% showed coronary artery calcification and 148 subjects (15.7% had metabolic syndrome. CACS showed a significant positive correlation with age, fasting glucose level, waist circumference (WC, blood pressure, hemoglobin A1c, HOMA-IR, and waist-hip ratio (WHR assessed by BIA. CACS had a negative correlation with high density lipoprotein cholesterol (HDL-C. Subjects with high CACS showed significantly higher mean WHRs and lower mean values for lean body mass compared with subjects without coronary artery calcification. In logistic regression analyses with coronary artery calcification as the dependent variable, the highest quartile of WHR showed a 3.125-fold increased odds ratio for coronary artery calcification compared with the lowest quartile after adjustment for confounding variables. When receiver operating characteristics analyses were performed with coronary artery calcification as the result variable, WHR showed the largest area under the curve (AUC value among other variables except for age and WC in women (AUC=0.696 for WHR, 0.790 for age, and 0.719 for WC in women.ConclusionIn our study population of apparently healthy Korean adults, WHR was the most significant predictor for coronary artery calcification among other confounding factors, suggesting that it may have implication as a marker for early atherosclerosis.

  3. Association between circulating vitamin K1 and coronary calcium progression in community-dwelling adults: the Multi-Ethnic Study of Atherosclerosis

    Science.gov (United States)

    While animal studies found vitamin K treatment reduced vascular calcification, human data are limited. Using a case-cohort design, we determined the association between vitamin K status and coronary artery calcium (CAC) progression in the Multi-ethnic Study of Atherosclerosis. Serum phylloquinone (v...

  4. Validation of a Radiography-Based Quantification Designed to Longitudinally Monitor Soft Tissue Calcification in Skeletal Muscle.

    Science.gov (United States)

    Moore, Stephanie N; Hawley, Gregory D; Smith, Emily N; Mignemi, Nicholas A; Ihejirika, Rivka C; Yuasa, Masato; Cates, Justin M M; Liu, Xulei; Schoenecker, Jonathan G

    2016-01-01

    Soft tissue calcification, including both dystrophic calcification and heterotopic ossification, may occur following injury. These lesions have variable fates as they are either resorbed or persist. Persistent soft tissue calcification may result in chronic inflammation and/or loss of function of that soft tissue. The molecular mechanisms that result in the development and maturation of calcifications are uncertain. As a result, directed therapies that prevent or resorb soft tissue calcifications remain largely unsuccessful. Animal models of post-traumatic soft tissue calcification that allow for cost-effective, serial analysis of an individual animal over time are necessary to derive and test novel therapies. We have determined that a cardiotoxin-induced injury of the muscles in the posterior compartment of the lower extremity represents a useful model in which soft tissue calcification develops remote from adjacent bones, thereby allowing for serial analysis by plain radiography. The purpose of the study was to design and validate a method for quantifying soft tissue calcifications in mice longitudinally using plain radiographic techniques and an ordinal scoring system. Muscle injury was induced by injecting cardiotoxin into the posterior compartment of the lower extremity in mice susceptible to developing soft tissue calcification. Seven days following injury, radiographs were obtained under anesthesia. Multiple researchers applied methods designed to standardize post-image processing of digital radiographs (N = 4) and quantify soft tissue calcification (N = 6) in these images using an ordinal scoring system. Inter- and intra-observer agreement for both post-image processing and the scoring system used was assessed using weighted kappa statistics. Soft tissue calcification quantifications by the ordinal scale were compared to mineral volume measurements (threshold 450.7mgHA/cm3) determined by μCT. Finally, sample-size calculations necessary to discriminate

  5. Calcium intake is not associated with increased coronary artery calcification: the Framingham Study.

    Science.gov (United States)

    Samelson, Elizabeth J; Booth, Sarah L; Fox, Caroline S; Tucker, Katherine L; Wang, Thomas J; Hoffmann, Udo; Cupples, L Adrienne; O'Donnell, Christopher J; Kiel, Douglas P

    2012-12-01

    Adequate calcium intake is known to protect the skeleton. However, studies that have reported adverse effects of calcium supplementation on vascular events have raised widespread concern. We assessed the association between calcium intake (from diet and supplements) and coronary artery calcification, which is a measure of atherosclerosis that predicts risk of ischemic heart disease independent of other risk factors. This was an observational, prospective cohort study. Participants included 690 women and 588 men in the Framingham Offspring Study (mean age: 60 y; range: 36-83 y) who attended clinic visits and completed food-frequency questionnaires in 1998-2001 and underwent computed tomography scans 4 y later in 2002-2005. The mean age-adjusted coronary artery-calcification Agatston score decreased with increasing total calcium intake, and the trend was not significant after adjustment for age, BMI, smoking, alcohol consumption, vitamin D-supplement use, energy intake, and, for women, menopause status and estrogen use. Multivariable-adjusted mean Agatston scores were 2.36, 2.52, 2.16, and 2.39 (P-trend = 0.74) with an increasing quartile of total calcium intake in women and 4.32, 4.39, 4.19, and 4.37 (P-trend = 0.94) in men, respectively. Results were similar for dietary calcium and calcium supplement use. Our study does not support the hypothesis that high calcium intake increases coronary artery calcification, which is an important measure of atherosclerosis burden. The evidence is not sufficient to modify current recommendations for calcium intake to protect skeletal health with respect to vascular calcification risk.

  6. Atherosclerosis across 4000 years of human history: the Horus study of four ancient populations.

    Science.gov (United States)

    Thompson, Randall C; Allam, Adel H; Lombardi, Guido P; Wann, L Samuel; Sutherland, M Linda; Sutherland, James D; Soliman, Muhammad Al-Tohamy; Frohlich, Bruno; Mininberg, David T; Monge, Janet M; Vallodolid, Clide M; Cox, Samantha L; Abd el-Maksoud, Gomaa; Badr, Ibrahim; Miyamoto, Michael I; el-Halim Nur el-Din, Abd; Narula, Jagat; Finch, Caleb E; Thomas, Gregory S

    2013-04-06

    Atherosclerosis is thought to be a disease of modern human beings and related to contemporary lifestyles. However, its prevalence before the modern era is unknown. We aimed to evaluate preindustrial populations for atherosclerosis. We obtained whole body CT scans of 137 mummies from four different geographical regions or populations spanning more than 4000 years. Individuals from ancient Egypt, ancient Peru, the Ancestral Puebloans of southwest America, and the Unangan of the Aleutian Islands were imaged. Atherosclerosis was regarded as definite if a calcified plaque was seen in the wall of an artery and probable if calcifications were seen along the expected course of an artery. Probable or definite atherosclerosis was noted in 47 (34%) of 137 mummies and in all four geographical populations: 29 (38%) of 76 ancient Egyptians, 13 (25%) of 51 ancient Peruvians, two (40%) of five Ancestral Puebloans, and three (60%) of five Unangan hunter gatherers (p=NS). Atherosclerosis was present in the aorta in 28 (20%) mummies, iliac or femoral arteries in 25 (18%), popliteal or tibial arteries in 25 (18%), carotid arteries in 17 (12%), and coronary arteries in six (4%). Of the five vascular beds examined, atherosclerosis was present in one to two beds in 34 (25%) mummies, in three to four beds in 11 (8%), and in all five vascular beds in two (1%). Age at time of death was positively correlated with atherosclerosis (mean age at death was 43 [SD 10] years for mummies with atherosclerosis vs 32 [15] years for those without; phuman beings raises the possibility of a more basic predisposition to the disease. National Endowment for the Humanities, Paleocardiology Foundation, The National Bank of Egypt, Siemens, and St Luke's Hospital Foundation of Kansas City. Copyright © 2013 Elsevier Ltd. All rights reserved.

  7. Acute Retropharyngeal Calcific Tendinitis in an Unusual Location: a Case Report in a Patient with Rheumatoid Arthritis and Atlantoaxial Subluxation

    Energy Technology Data Exchange (ETDEWEB)

    Lee, Seung Hun; Joo, Kyung Bin; Lee, Kyu Hoon; Uhm, Wan Sik [Hanyang University Hospital, Seoul (Korea, Republic of)

    2011-08-15

    Retropharyngeal calcific tendinitis is defined as inflammation of the longus colli muscle and is caused by the deposition of calcium hydroxyapatite crystals, which usually involves the superior oblique fibers of the longus colli muscle from C1-3. Diagnosis is usually made by detecting amorphous calcification and prevertebral soft tissue swelling on radiograph, CT or MRI. In this report, we introduce a case of this disease which was misdiagnosed as a retropharyngeal tuberculous abscess, or a muscle strain of the ongus colli muscle. No calcifications were visible along the vertical fibers of the longus colli muscle. The lesion was located anterior to the C4-5 disc, in a rheumatoid arthritis patient with atlantoaxial subluxation. Calcific tendinitis of the longus colli muscle at this location in a rheumatoid arthritis patient has not been reported in the English literature.

  8. Alcohol and atherosclerosis

    Directory of Open Access Journals (Sweden)

    Murilo Foppa

    2001-02-01

    Full Text Available Observational studies have attributed a protective effect to alcohol consumption on the development of atherosclerosis and cardiovascular morbidity and mortality. Alcohol intake in the amount of one to two drinks per day results in an estimated 20-40% reduction in cardiovascular events. An additional protective effect, according to major cohort studies, has been attributed to wine, probably due to antioxidant effects and platelet antiaggregation agents. On the other hand, the influence of different patterns of alcohol consumption and environmental factors may explain a great part of the additional effect of wine. Protection may be mediated by modulation of other risk factors, because alcohol increases HDL-C, produces a biphasic response on blood pressure, and modulates the endothelial function, while it neither increases body weight nor impairs glucose-insulin homeostasis. Alcohol may also have a direct effect on atherogenesis. Despite these favorable effects, the current evidence is not enough to justify prescribing alcohol to prevent cardiovascular disease.

  9. Phytosterols and atherosclerosis

    DEFF Research Database (Denmark)

    Schrøder, Malene

    for decades for their natural ability to reduce cholesterol levels in the blood. In the last decade numerous food products added phytosterol esters have been placed on the market, e.g. yellow fat spread, yoghurt, dressing. The products are being marketed as a natural means for people who want to lower...... or advanced lesion) and quantitatively by stereological methods applied to evaluate the area of the intima and the ratio of intima:media on cross sections from three defined places on the aorta. The biochemical endpoint was the cholesterol content in the inner layer of the entire aorta, which is considered...... than 3% brassicasterol are not accepted on the European market. The aim of the study was to investigate the effect of dietary supplementation of RSO derived sterol, with high content of brassicasterols, and stanol esters on the development of atherosclerosis in cholesterol-fed heterozygous WHHL rabbits...

  10. THE MAMMOGRAPHIC CALCIFICATIONS IN BREAST CANCER

    Institute of Scientific and Technical Information of China (English)

    Tang Ruiying; Liu Jingxian; Gaowen

    1998-01-01

    Objective: This study was performed to exam the relativeship between mammographic calcifications and breast cancer. Methods: All of the 184 patients with breast diseases underwent mammography before either an open biopsy or a mastectomy. The presence,morphology, and distribution of calcifications visualized on mammograms for breast cancer were compared with the controls who remained cancer free. Statistical comparisons were made by using the x2 test. Results:Of the 184 patients with breast diaeases, 93 malignant and 91 benign lesions were histologically confirmed.Calcifications were visualized on mammograms in 60(64%) of 93 breast cancers and 26 (28%) of 91 non breast cancers. The estimated odds ratio (OR) of breast cancer was 4.5 in women with calcifications seen on mammograms, compared with those having none (P<0.01). Of the 60 breast carcinomas having mammographic calcifications, 28 (47%) were infiltrating ductal carcinomas.There were only 8 (24%) cases with infiltrating ductal cancers in the group of without calcifications seen on the mammograms (P<0.05). Conclusion: Our finding suggests that mammographic calcification appears to be a risk factor for breast cancer. The granular and linear cast type calcification provide clues to the presence of breast cancer, especially when the carcinomas without associated masses were seen on mammograms.

  11. Vascular Adventitia Calcification and Its Underlying Mechanism.

    Directory of Open Access Journals (Sweden)

    Na Li

    Full Text Available Previous research on vascular calcification has mainly focused on the vascular intima and media. However, we show here that vascular calcification may also occur in the adventitia. The purpose of this work is to help elucidate the pathogenic mechanisms underlying vascular calcification. The calcified lesions were examined by Von Kossa staining in ApoE-/- mice which were fed high fat diets (HFD for 48 weeks and human subjects aged 60 years and older that had died of coronary heart disease, heart failure or acute renal failure. Explant cultured fibroblasts and smooth muscle cells (SMCswere obtained from rat adventitia and media, respectively. After calcification induction, cells were collected for Alizarin Red S staining. Calcified lesions were observed in the aorta adventitia and coronary artery adventitia of ApoE-/-mice, as well as in the aorta adventitia of human subjects examined. Explant culture of fibroblasts, the primary cell type comprising the adventitia, was successfully induced for calcification after incubation with TGF-β1 (20 ng/ml + mineralization media for 4 days, and the phenotype conversion vascular adventitia fibroblasts into myofibroblasts was identified. Culture of SMCs, which comprise only a small percentage of all cells in the adventitia, in calcifying medium for 14 days resulted in significant calcification.Vascular calcification can occur in the adventitia. Adventitia calcification may arise from the fibroblasts which were transformed into myofibroblasts or smooth muscle cells.

  12. Calcifications of the bladder in schistosomiasis

    International Nuclear Information System (INIS)

    Wechmar, M. von; Vogel, H.

    1989-01-01

    In schistosomiasis calcification of the urinary bladder are characteristic signs that allow a corresponding diagnosis in endemic regions. Problems concerning differential diagnosis occur only in very rare cases. The calcifications of the bladder can be easily detected by native diagnostics. A late complication in an affected bladder is often a bladder carcinoma. (orig.) [de

  13. A quantitative approach of abdominal aortic atherosclerosis with x-ray computed tomography

    International Nuclear Information System (INIS)

    Watanabe, Hiromi; Kubota, Kazuo; Ito, Kengo; Ono, Shuichi; Matsuzawa, Taiju

    1983-01-01

    Currently epidemiologic studies of aortic atherosclerosis are most commonly done by the conventional roentgenological or pathological methods before and after death respectively. Pathological method is difficult and only possible after death. Roentgenological method is simple and useful before death, but its inability to evaluate atherosclerosis in a constant manner is serious drawback. A simple and quantitative method for epidemiological and clinical study of atherosclerosis has been needed. It this study, we examined the usefulness of Calcification Index (C.I.) caliculated from CT films for the evaluation of abdominal aortic atherosclerosis. We analysed 42 patients (32 males, 10 females). They recieved abdominal CT examination and died within a year. First, we got C.I. from their CT films. Then we got Surface Involved (S.I.) of atherosclerotic lesion from their autopsied abdominal aorta with pathological observation. The correlation coefficient between C.I. and S.I. was 0.83 (p<0.001). So we may use C.I. for the evaluation of abdominal aortic atherosclerosis. (author)

  14. Intracranial calcification on paediatric computed tomography

    International Nuclear Information System (INIS)

    Kendall, B.; Cavanagh, N.

    1986-01-01

    An analysis of the computed tomograms of 18000 children examined consecutively form the basis of an assessment of the diagnostic significance of intracranial calcification. The low incidence of physiological calcification in the pineal and choroid of about 2% up to the age of 8 years, but increasing 5-fold by the age of 15 years, is confirmed. Pathological calcification occurred in 1.6%, the commonest causes being neoplasms (43%), neuroectodermal syndromes (20%) and infections (12%). Diffuse basal ganglia calcification (15%) bore little relation to the diverse clinical symptomatology, and routine bio-chemical studies showed a disorder of metabolism to be present in only 6 cases. Calcification has not been previously noted in acute haemorrhagic leukoencephalitis, Pertussis or Cocksackie encephalitis, infantile neuraxonal dystrophy, Marinesco-Sjoegren syndrome or in the basal ganglia in neurofibromatosis. (orig.)

  15. The Prebiotic Inulin Aggravates Accelerated Atherosclerosis in Hypercholesterolemic APOE*3-Leiden Mice.

    Science.gov (United States)

    Hoving, Lisa R; de Vries, Margreet R; de Jong, Rob C M; Katiraei, Saeed; Pronk, Amanda; Quax, Paul H A; van Harmelen, Vanessa; Willems van Dijk, Ko

    2018-02-03

    The prebiotic inulin has proven effective at lowering inflammation and plasma lipid levels. As atherosclerosis is provoked by both inflammation and hyperlipidemia, we aimed to determine the effect of inulin supplementation on atherosclerosis development in hypercholesterolemic APOE*3-Leiden ( E3L ) mice. Male E3L mice were fed a high-cholesterol (1%) diet, supplemented with or without 10% inulin for 5 weeks. At week 3, a non-constrictive cuff was placed around the right femoral artery to induce accelerated atherosclerosis. At week 5, vascular pathology was determined by lesion thickness, vascular remodeling, and lesion composition. Throughout the study, plasma lipids were measured and in week 5, blood monocyte subtypes were determined using flow cytometry analysis. In contrast to our hypothesis, inulin exacerbated atherosclerosis development, characterized by increased lesion formation and outward vascular remodeling. The lesions showed increased number of macrophages, smooth muscle cells, and collagen content. No effects on blood monocyte composition were found. Inulin significantly increased plasma total cholesterol levels and total cholesterol exposure. In conclusion, inulin aggravated accelerated atherosclerosis development in hypercholesterolemic E3L mice, accompanied by adverse lesion composition and outward remodeling. This process was not accompanied by differences in blood monocyte composition, suggesting that the aggravated atherosclerosis development was driven by increased plasma cholesterol.

  16. The Prebiotic Inulin Aggravates Accelerated Atherosclerosis in Hypercholesterolemic APOE*3-Leiden Mice

    Directory of Open Access Journals (Sweden)

    Lisa R. Hoving

    2018-02-01

    Full Text Available The prebiotic inulin has proven effective at lowering inflammation and plasma lipid levels. As atherosclerosis is provoked by both inflammation and hyperlipidemia, we aimed to determine the effect of inulin supplementation on atherosclerosis development in hypercholesterolemic APOE*3-Leiden (E3L mice. Male E3L mice were fed a high-cholesterol (1% diet, supplemented with or without 10% inulin for 5 weeks. At week 3, a non-constrictive cuff was placed around the right femoral artery to induce accelerated atherosclerosis. At week 5, vascular pathology was determined by lesion thickness, vascular remodeling, and lesion composition. Throughout the study, plasma lipids were measured and in week 5, blood monocyte subtypes were determined using flow cytometry analysis. In contrast to our hypothesis, inulin exacerbated atherosclerosis development, characterized by increased lesion formation and outward vascular remodeling. The lesions showed increased number of macrophages, smooth muscle cells, and collagen content. No effects on blood monocyte composition were found. Inulin significantly increased plasma total cholesterol levels and total cholesterol exposure. In conclusion, inulin aggravated accelerated atherosclerosis development in hypercholesterolemic E3L mice, accompanied by adverse lesion composition and outward remodeling. This process was not accompanied by differences in blood monocyte composition, suggesting that the aggravated atherosclerosis development was driven by increased plasma cholesterol.

  17. Atherosclerosis of the carotid artery: evaluation by magnetic resonance angiography.

    Science.gov (United States)

    Wildy, K S; Yuan, C; Tsuruda, J S; Ferguson, M S; Wen, N; Subramaniam, D S; Strandness, D E

    1996-01-01

    Carotid artery atherosclerotic plaques (APs) can lead to brain ischemia, an event shown to correlate with both the degree of stenosis and the composition of the AP. Currently, accurate estimates of stenosis can be obtained by either x-ray angiography or three-dimensional time-of-flight (TOF) magnetic resonance angiography (MRA). Our purpose was to determine whether three-dimensional TOF MRA images could also provide information on plaque location, morphology, and composition. Seven pre-endarterectomy patients underwent three-dimensional TOF MRA. After endarterectomy, plaque histology was evaluated. Three-dimensional TOF MRA images contained sufficient soft tissue contrast to differentiate the plaques from the surrounding tissues in all cases. Estimation of plaque morphology had 80% correlation with histology. Finally, intraplaque hemorrhage and calcification were deplicted as regions of moderately high and very low intensity, respectively. These preliminary results suggest that three-dimensional TOF MRA may be useful in studying the development and progression of carotid atherosclerosis.

  18. [The receptor theory of atherosclerosis].

    Science.gov (United States)

    Likhoded, V G; Bondarenko, V M; Gintsburg, A L

    2010-01-01

    Lipopolysaccharides of Gram-negative bacteria can interact with Toll-like receptor 4 (TLR4) and induce atheroma formation. The risk of atherosclerosis is decreased in case of TLR4 mutation. Other bacterial ligands and endogenous ligands of TLRs can also be involved in induction of atherogenesis. The general concept of atherosclerosis pathogentsis is presented. According to this concept atherogenesis can be initiated by some reactions resulting from interaction of exogenous and endogenous microbial ligands with Toll-like receptors.

  19. Ageing induced vascular smooth muscle cell senescence in atherosclerosis.

    Science.gov (United States)

    Uryga, Anna K; Bennett, Martin R

    2016-04-15

    Atherosclerosis is a disease of ageing in that its incidence and prevalence increase with age. However, atherosclerosis is also associated with biological ageing, manifest by a number of typical hallmarks of ageing in the atherosclerotic plaque. Thus, accelerated biological ageing may be superimposed on the effects of chronological ageing in atherosclerosis. Tissue ageing is seen in all cells that comprise the plaque, but particularly in vascular smooth muscle cells (VSMCs). Hallmarks of ageing include evidence of cell senescence, DNA damage (including telomere attrition), mitochondrial dysfunction, a pro-inflammatory secretory phenotype, defects in proteostasis, epigenetic changes, deregulated nutrient sensing, and exhaustion of progenitor cells. In this model, initial damage to DNA (genomic, telomeric, mitochondrial and epigenetic changes) results in a number of cellular responses (cellular senescence, deregulated nutrient sensing and defects in proteostasis). Ultimately, ongoing damage and attempts at repair by continued proliferation overwhelm reparative capacity, causing loss of specialised cell functions, cell death and inflammation. This review summarises the evidence for accelerated biological ageing in atherosclerosis, the functional consequences of cell ageing on cells comprising the plaque, and the causal role that VSMC senescence plays in atherogenesis. © 2015 The Authors. The Journal of Physiology © 2015 The Physiological Society.

  20. Genomic Analysis of Circulating Cells: A Window into Atherosclerosis

    Science.gov (United States)

    Kang, Ju-Gyeong; Patino, Willmar D.; Matoba, Satoaki; Hwang, Paul M.

    2006-01-01

    Translational studies using genomic techniques in cardiovascular diseases are still in their infancy. Access to disease-associated cardiovascular tissues from patients has been a major impediment to progress in contrast to the diagnostic advances made by oncologists using gene expression on readily available tumor samples. Nonetheless, progress is being made for atherosclerosis by carefully designed experiments using diseased tissue or surrogate specimens. This review details the rationale and findings of a study using freshly isolated blood mononuclear cells from patients undergoing carotid endarterectomy due to atherosclerotic stenosis and from matched normal subjects. Using this cardiovascular tissue surrogate, the mRNA levels of the Finkel-Biskis-Jinkins osteosarcoma (FOS) gene in circulating monocytes were found to correlate with atherosclerosis severity in patients, and with HMG CoA reductase inhibitor (statin) therapy in normal subjects. The major finding of this investigation is discussed in relation to observations from other human atherosclerosis gene expression studies. These distinct studies converge to demonstrate the unequivocal importance of inflammation in atherosclerosis. Although the clinical utility of the specific findings remains open, the identification of similar genes by different investigations serves to validate their reports. They also provide us with insights into pathogenesis that may impact future translational applications. PMID:16781950

  1. Basic mechanisms in intracranial large-artery atherosclerosis: advances and challenges.

    Science.gov (United States)

    Arenillas, Juan F; Alvarez-Sabín, José

    2005-01-01

    Intracranial large-artery atherosclerosis is a major cause of ischemic stroke worldwide. Patients affected by this disease are at a high risk of suffering recurrent ischemic events despite antithrombotic therapy. Progression and a greater extent of intracranial atherosclerosis imply a higher risk for recurrence. Studies performed by our group in patients with symptomatic intracranial large-artery atherosclerosis have shown that: (1) C-reactive protein predicts its progression and recurrence, suggesting that inflammation may play a deleterious role in this condition; (2) a high level of the anti-angiogenic endostatin is also associated with a progressive and recurrent intracranial atherosclerosis, which might support a beneficial role for angiogenesis in this group of patients; and (3) elevated lipoprotein(a) concentration and diabetes mellitus characterize those patients with a higher number of intracranial stenoses. 2005 S. Karger AG, Basel

  2. Association between the surfactant protein D (SFTPD) gene and subclinical carotid artery atherosclerosis

    DEFF Research Database (Denmark)

    Sorensen, Grith L; Bladbjerg, Else Marie; Steffensen, Rudi

    2016-01-01

    OBJECTIVE: Surfactant protein D (SP-D) is a defense collectin with inflammation-modulating properties. SP-D deficiency inhibits atherosclerosis in vivo, and the circulatory SP-D levels have been previously associated with cardiovascular disease mortality. We hypothesized that plasma SP-D (p......SP-D) and SP-D gene (SFTPD) single nucleotide polymorphisms (SNPs) are risk factors for atherosclerosis. METHODS: We evaluated individuals who were all 60 years old and participated in The Glostrup Population Study. Subclinical atherosclerosis was diagnosed based on the ultrasonographic measurement of intima......: The results do not support that pSP-D levels influence the development of subclinical atherosclerosis. However, the SFTPD SNP data support previous observations from animal studies that SP-D plays a role in the etiology of atherosclerotic disease development. The nominal significant effects are likely...

  3. [Potential protective role of nitric oxide and Hsp70 linked to functional foods in the atherosclerosis].

    Science.gov (United States)

    Camargo, Alejandra B; Manucha, Walter

    Atherosclerosis, one of the main pathologic entities considered epidemic and a worldwide public health problem, is currently under constant review as regards its basic determining mechanisms and therapeutic possibilities. In this regard, all patients afflicted with the disease exhibit mitochondrial dysfunction, oxidative stress and inflammation. Interestingly, nitric oxide - a known vasoactive messenger gas - has been closely related to the inflammatory, oxidative and mitochondrial dysfunctional process that characterizes atherosclerosis. In addition, it has recently been demonstrated that alterations in the bioavailability of nitric oxide would induce the expression of heat shock proteins. This agrees with the use of functional foods as a strategy to prevent both vascular aging and the development of atherosclerosis. Finally, a greater knowledge regarding the mechanisms implied in the development of atherosclerosis will enable proposing new and possible hygiene, health and therapeutic interventions. Copyright © 2016 Sociedad Española de Arteriosclerosis. Publicado por Elsevier España, S.L.U. All rights reserved.

  4. Nanomedicine highlights in atherosclerosis

    International Nuclear Information System (INIS)

    Karagkiozaki, Varvara

    2013-01-01

    Atherosclerosis is a multifactorial disease and many different approaches have been attempted for its accurate diagnosis and treatment. The disease is induced by a low-grade inflammatory process in the vascular wall, leading through a cascade of events to the eventual formation of atheromatous plaque and arterial stenosis. Different types of cells participate in the process making more difficult to recognize the potential cellular targets within the plaques for their effective treatment. The rise of nanomedicine over the last decade has provided new types of drug delivery nanosystems that are able to be delivered to a specific diseased site of the vessel for imaging while simultaneously act as therapeutic agents. In this paper, a review of the recent advances in nanomedicine that has provided novel insights to the disease diagnosis and treatment will be given in line with different nanotechnology-based approaches to advance the cardiovascular stents. The main complications of bare metal stents such as restenosis and of drug-eluting stents which is the late stent thrombosis are analyzed to comprehend the demand for emerging therapeutic strategies based on nanotechnology.

  5. Nanomedicine highlights in atherosclerosis

    Energy Technology Data Exchange (ETDEWEB)

    Karagkiozaki, Varvara, E-mail: vakaragk@physics.auth.gr [Aristotle University of Thessaloniki, Nanomedicine Group, Laboratory for Thin Films-Nanosystems and Nanometrology (LTFN), Physics Department (Greece)

    2013-04-15

    Atherosclerosis is a multifactorial disease and many different approaches have been attempted for its accurate diagnosis and treatment. The disease is induced by a low-grade inflammatory process in the vascular wall, leading through a cascade of events to the eventual formation of atheromatous plaque and arterial stenosis. Different types of cells participate in the process making more difficult to recognize the potential cellular targets within the plaques for their effective treatment. The rise of nanomedicine over the last decade has provided new types of drug delivery nanosystems that are able to be delivered to a specific diseased site of the vessel for imaging while simultaneously act as therapeutic agents. In this paper, a review of the recent advances in nanomedicine that has provided novel insights to the disease diagnosis and treatment will be given in line with different nanotechnology-based approaches to advance the cardiovascular stents. The main complications of bare metal stents such as restenosis and of drug-eluting stents which is the late stent thrombosis are analyzed to comprehend the demand for emerging therapeutic strategies based on nanotechnology.

  6. Association between gamma-glutamyltransferase and coronary artery calcification.

    Science.gov (United States)

    Atar, Asli I; Yilmaz, Omer C; Akin, Kayihan; Selcoki, Yusuf; Er, Okan; Eryonucu, Beyhan

    2013-08-20

    The exact mechanisms behind the association between atherosclerosis and gamma-glutamyltransferase (GGT) are unclear. Coronary artery calcification (CAC) detected by computerized tomography is an important marker of atherosclerosis and its severity correlates with coronary plaque burden. The aim of this study was to investigate if serum GGT levels are associated with CAC in patients without known coronary heart disease (CHD) who had low-intermediate risk for CHD. Two hundred and seventy two patients who had low-intermediate risk for coronary artery disease were included in the study. Serum GGT levels were measured spectrophotometrically. CACS (Agatston method) were performed using a 64-slice computerized tomography scanner. The patients were grouped according to their GGT values in four quartiles. Patients in higher GGT quartiles had elevated CAC score (P<0.001). Patients in higher GGT quartiles were predominantly males (P<0.001) and were more likely to be smoking (P=0.004), and have elevated uric acid (P<0.001), fasting blood glucose (P<0.001), CRP levels (P=0.003) and 10-year total cardiovascular risk (P=0.007) and low HDL levels (P<0.001). Positive correlations were found between log GGT and CAC (r=0.233, P<0.001). In the multivariate analysis GGT, age, smoking and serum uric acid levels appeared as independent factors predictive of presence of CAC. We demonstrated a significant correlation between serum GGT levels and CAC and CHD risk factors. Serum GGT level was an independent marker of CAC. Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.

  7. Psychosocial predictors of coronary artery calcification progression in postmenopausal women.

    Science.gov (United States)

    Low, Carissa A; Matthews, Karen A; Kuller, Lewis H; Edmundowicz, Daniel

    2011-01-01

    Coronary artery calcification (CAC) has been associated with psychosocial factors in some but not all cross-sectional analyses. The goal of this study was to determine whether positive and negative psychosocial factors prospectively predict CAC progression in postmenopausal women. Participants from the Healthy Women Study who also participated in the Pittsburgh Mind-Body Center protocol (n = 149) completed self-report psychosocial measures before two electron beam computed tomographic scans of CAC separated by an average of 3.3 years. Results of exploratory factor analysis were used to create aggregate psychosocial indices: psychological risk (depressive symptoms, perceived stress, cynicism, and anger-in) and psychosocial resources (optimism, purpose in life, mastery, self-esteem, and social support). The psychological risk index predicted significantly greater CAC progression over 3 years (β = 0.16, p = .035, ΔR(2) = 0.03), whereas the psychosocial resources index was not predictive of CAC progression (β = -0.08, p = .30, ΔR(2) = 0.01). On individual scales, higher scores on cynicism emerged as a significant predictor of CAC progression, along with a trend linking anger-in to atherosclerosis progression. A post hoc analysis showed a significant interaction between cynicism and anger-in (β = 0.20, p = .01, ΔR(2) = 0.03), such that women reporting high levels of both cynicism and anger suppression exhibited the most CAC progression. These findings highlight psychosocial risk factors that may accelerate the progression of subclinical atherosclerosis in older women, suggest the potential importance of examining combinations of psychosocial risk factors, and identify potential targets for psychological interventions to reduce cardiovascular risk.

  8. Calcifications in the breast in Filaria loa infection

    Energy Technology Data Exchange (ETDEWEB)

    Novak, R. (Karolinska Sjukhuset, Stockholm (Sweden). Dept. of Diagnostic Radiology)

    A 40-year-old patient underwent mammography for evaluation of a mass. Atypical calcifications were observed in the opposite breast. Two types of calcification were observed: One type was spiral-shaped and the other type rod-shaped. These calcifications were caused by Filaria loa. Parasitic calcifications in the breast are uncommon. (orig.).

  9. [Orbital inflammation].

    Science.gov (United States)

    Mouriaux, F; Coffin-Pichonnet, S; Robert, P-Y; Abad, S; Martin-Silva, N

    2014-12-01

    Orbital inflammation is a generic term encompassing inflammatory pathologies affecting all structures within the orbit : anterior (involvement up to the posterior aspect of the globe), diffuse (involvement of intra- and/or extraconal fat), apical (involvement of the posterior orbit), myositis (involvement of only the extraocular muscles), dacryoadenitis (involvement of the lacrimal gland). We distinguish between specific inflammation and non-specific inflammation, commonly referred to as idiopathic inflammation. Specific orbital inflammation corresponds to a secondary localization of a "generalized" disease (systemic or auto-immune). Idiopathic orbital inflammation corresponds to uniquely orbital inflammation without generalized disease, and thus an unknown etiology. At the top of the differential diagnosis for specific or idiopathic orbital inflammation are malignant tumors, represented most commonly in the adult by lympho-proliferative syndromes and metastases. Treatment of specific orbital inflammation begins with treatment of the underlying disease. For idiopathic orbital inflammation, treatment (most often corticosteroids) is indicated above all in cases of visual loss due to optic neuropathy, in the presence of pain or oculomotor palsy. Copyright © 2014 Elsevier Masson SAS. All rights reserved.

  10. Atypical calcific tendinitis with cortical erosions

    International Nuclear Information System (INIS)

    Kraemer, E.J.; El-Khoury, G.Y.

    2000-01-01

    Objective. To present and discuss six cases of calcific tendinitis in atypical locations (one at the insertion of the pectoralis major and five at the insertion of the gluteus maximus).Patients and results. All cases were associated with cortical erosions, and five had soft tissue calcifications. The initial presentation was confusing and the patients were suspected of having infection or neoplastic disease.Conclusion. Calcific tendinitis is a self-limiting condition. It is important to recognize the imaging features of this condition to avoid unnecessary investigation and surgery. (orig.)

  11. Imaging findings in acute calcific prevertebral tendinitis

    International Nuclear Information System (INIS)

    Grassi, Caio Giometti; Diniz, Fabio de Vilhena; Garcia, Marcio Ricardo Taveira; Gomes, Regina Lucia Elia; Daniel, Mauro Miguel; Funari, Marcelo Buarque de Gusmao

    2011-01-01

    Acute calcific prevertebral tendinitis is a benign and rare condition that presents calcification of the superior oblique fibers of longus colli muscle with local inflammatory reaction. Such condition is one of the less common presentations of calcium hydroxyapatite deposition disease. Clinical signs are usually acute neck pain and odynophagia, and it may be misdiagnosed as retropharyngeal abscess, spondylodiscitis or traumatic injury. The imaging findings in calcific prevertebral tendinitis are pathognomonic. The knowledge of such findings is extremely important to avoid unnecessary interventions in a patient presenting a condition with a good response to conservative treatment. (author)

  12. Imaging findings in acute calcific prevertebral tendinitis

    Energy Technology Data Exchange (ETDEWEB)

    Grassi, Caio Giometti; Diniz, Fabio de Vilhena; Garcia, Marcio Ricardo Taveira; Gomes, Regina Lucia Elia; Daniel, Mauro Miguel; Funari, Marcelo Buarque de Gusmao [Hospital Israelita Albert Einstein (HIAE), Sao Paulo, SP (Brazil). Imaging Dept.

    2011-09-15

    Acute calcific prevertebral tendinitis is a benign and rare condition that presents calcification of the superior oblique fibers of longus colli muscle with local inflammatory reaction. Such condition is one of the less common presentations of calcium hydroxyapatite deposition disease. Clinical signs are usually acute neck pain and odynophagia, and it may be misdiagnosed as retropharyngeal abscess, spondylodiscitis or traumatic injury. The imaging findings in calcific prevertebral tendinitis are pathognomonic. The knowledge of such findings is extremely important to avoid unnecessary interventions in a patient presenting a condition with a good response to conservative treatment. (author)

  13. MRI of the basal ganglia calcification

    International Nuclear Information System (INIS)

    Maeda, Masayuki; Murata, Tetsuhito; Kimura, Hirohiko

    1992-01-01

    MR imaging was performed for 11 patients (9 in Down's syndrome and 2 in idiopathic intracerebral calcification) who showed calcifications in bilateral basal ganglia on CT. High signal intensity in the basal ganglia was found only in one patient with idiopathic intracerebral calcification on T1-weighted image. The calcified areas of all patients in Down's syndrome did not show high signal intensity on T1-weighted image. The exact reasons why MRI exhibits the different signal intensities in calcified tissue on T1-weighted image are unknown. Further clinical investigations will be needed. (author)

  14. Tracheobronchial calcification in adult health study subjects

    International Nuclear Information System (INIS)

    Fukuya, Tatsuro; Mihara, Futoshi; Kudo, Sho; Russell, W.J.; Delongchamp, R.R.; Vaeth, M.; Hosoda, Yutaka.

    1988-04-01

    Tracheobronchial calcification is reportedly more frequent in women than in men. Ten cases of extensive tracehobronchial calcification were identified on chest radiographs of 1,152 consecutively examined Adult Health Study subjects, for a prevalence of 0.87 %. An additional 51 subjects having this coded diagnosis were identified among 11,758 members of this fixed population sample. Sixty of the 61 subjects were women. The manifestations and extent of this type of calcification and its correlations with clinical and histopathologic features, which have not been previously reported, are described here. (author)

  15. The multi-functionality of CD40L and its receptor CD40 in atherosclerosis

    NARCIS (Netherlands)

    Lievens, Dirk; Eijgelaar, Wouter J.; Biessen, Erik A. L.; Daemen, Mat J. A. P.; Lutgens, Esther

    2009-01-01

    Disrupting the CD40-CD40L co-stimulatory pathway reduces atherosclerosis and induces a stable atherosclerotic plaque phenotype that is low in inflammation and high in fibrosis. Therefore, inhibition of the CD40-CD40L pathway is an attractive therapeutic target to reduce clinical complications of

  16. ACE inhibition with perindopril and biomarkers of atherosclerosis and thrombosis : Results from the PERTINENT study

    NARCIS (Netherlands)

    Ceconi, C.; Fox, K.M.; Remme, W.J.; Simoons, M.L.; Deckers, J.W.; Bertrand, M.; Parrinello, G.; Kluft, C.; Blann, A.; Cokkinos, D.; Ferrari, R.

    2009-01-01

    The PERTINENT study measured biomarkers of atherosclerosis and thrombosis in a stable coronary artery disease population from EUROPA receiving ACE inhibition with perindopril 8 mg/day or placebo. Biomarkers of inflammation, C-reactive protein (CRP), fibrinogen, and tumor necrosis factor-alpha

  17. Disrupting functional interactions between platelet chemokines inhibits atherosclerosis in hyperlipidemic mice

    DEFF Research Database (Denmark)

    Koenen, Rory R; von Hundelshausen, Philipp; Nesmelova, Irina V

    2009-01-01

    Atherosclerosis is characterized by chronic inflammation of the arterial wall due to chemokine-driven mononuclear cell recruitment. Activated platelets can synergize with chemokines to exacerbate atherogenesis; for example, by deposition of the chemokines platelet factor-4 (PF4, also known as CXC...

  18. Isolated splenic calcifications in two patients with portal hypertension

    International Nuclear Information System (INIS)

    Aleixandre, A.; Cugat, A.; Ruiz, A.; Marti-Bonmati, L.; Tardaguila, F.

    2002-01-01

    Calcification of the walls of the veins of the portal hypertension (PHT) (1-0), is uncommon. Calcification of the intra splenic vessels is exceptional. We report two cases of isolated calcification of intra splenic vessels, without calcification of the splenoportal venous axis, in patients with liver cirrhosis and PHT. The calcification was not clear. Computed tomography identified the calcification as linear tubular, branched structures located in the wall of intra splenic vessels. magnetic resonance imaging disclosed signs of cirrhosis and PHT but did not show the splenic classifications because of technical limitations. The cause of these calcifications was sustained PHT due to chronic liver disease. (Author) 15 refs

  19. ATP-Binding Cassette Transporters, Atherosclerosis, and Inflammation

    NARCIS (Netherlands)

    Westerterp, Marit; Bochem, Andrea E.; Yvan-Charvet, Laurent; Murphy, Andrew J.; Wang, Nan; Tall, Alan R.

    2014-01-01

    Although recent genome-wide association studies have called into question the causal relationship between high-density lipoprotein (HDL) cholesterol levels and cardiovascular disease, ongoing research in animals and cells has produced increasing evidence that cholesterol efflux pathways mediated by

  20. CD40 in clinical inflammation: From multiple sclerosis to atherosclerosis

    NARCIS (Netherlands)

    Laman, J.D.; Boer, M. de; Hart, B.A. 't

    1998-01-01

    The interactions of CD40 and CD40L have been known for some time to critically regulate B-cell responses with respect to proliferation, isotype switching, antibody production, and memory formation. More recent findings demonstrated that CD40 can be expressed on several other antigen-presenting cell

  1. Breast skin calcifications: Mammographic recognition and confirmation

    International Nuclear Information System (INIS)

    Berkowitz, J.E.; Gatewood, O.M.B.; Gayler, B.W.

    1987-01-01

    The authors found microcalcifications in the skin of the breast to occur in 8% of patients undergoing mammography, a prevalence much higher than what has been previously reported. Usually in incidental finding, breast skin calcifications are readily recognized when they are multiple, bilateral, coarse, or polygonal with a central radiolucency; when they are located in a peripheral portion of the breast on at least one view, or when they are serendipitously imaged within the skin. One hundred patients with breast skin calcifications were studied. In 15 patients in whom clustered dermal calcifications simulated parenchymal microcalcifications, template-guided tangential views permitted precise skin localization. Three of those patients had been referred for needle localization before biopsy and four after failed biopsy for clustered microcalcifications. Dermal calcifications can pose a vexing problem in the management of microcalcifications of the breast. A high index of suspicion is warrented in order to forestall unnecessary or unsuccessful biopsies

  2. Paradiaphyseal calcific tendinitis with cortical bone erosion.

    Science.gov (United States)

    Fritz, P; Bardin, T; Laredo, J D; Ziza, J M; D'Anglejan, G; Lansaman, J; Bucki, B; Forest, M; Kuntz, D

    1994-05-01

    To determine the clinical, radiologic, and histologic features of calcific tendinitis with cortical bone erosion. The records of 6 patients with paradiaphyseal calcific tendinitis and adjacent bone cortex erosion were reviewed. Calcific tendinitis involved the linea aspera in 4 patients, the bicipital groove in 1 patient, and the deltoid insertion in another. Calcium deposits were associated with cortical bone erosions, revealed on plain radiographs in 4 patients and computed tomography scans in 2. Bone scans were performed in 2 patients and showed local hyperfixation of the isotope. In 4 patients, suspicion of a neoplasm led to a biopsy. Calcium deposits appeared to be surrounded by a foreign body reaction with numerous giant cells. Apatite crystals were identified by transmission electron microscopy and elemental analysis in 1 surgical sample. Paradiaphyseal calcific tendinitis with cortical bone erosion is an uncommon presentation of apatite deposition disease.

  3. Evaluation of pineal calcification in children

    International Nuclear Information System (INIS)

    Ando, Kazuo; Odagiri, Kunio; Fujiwara, Takuya; Tanohata, Kazunori; Matsui, Kengo; Okano, Shigeki.

    1987-01-01

    The study cases were 804 patients who had received either CT or plain radiographs for some reasons. Their ages ranged from newborn to 15 years old. Twenty four patients had the pineal calcification, in which one patient had the pineal region tumor and 4 patients had precocious puberty. The incidence of the pineal calcification was observed on CT as 0.2, 5.8, and 14 % in their age of 0 to 5, 6 to 10, and 11 to 15 years old, respectively. On the other hand, this finding was detected only in 0, 1.1, and 1.2 % on plain radiographs. In conclusion, pineal calcification on CT may suggest the pathological state in children. Although it is observed in a minority of normal children, such a calcification could be looked upon as not only pineal region tumor but precocious puberty and other intracranial disorders with suspicion. (author)

  4. Topical thrombin-related corneal calcification.

    Science.gov (United States)

    Kiratli, Hayyam; Irkeç, Murat; Alaçal, Sibel; Söylemezoğlu, Figen

    2006-09-01

    To report a highly unusual case of corneal calcification after brief intraoperative use of topical thrombin. A 44-year-old man underwent sclerouvectomy for ciliochoroidal leiomyoma, during which 35 UNIH/mL lyophilized bovine thrombin mixed with 9 mL of diluent containing 1500 mmol/mL calcium chloride was used. From the first postoperative day, corneal and anterior lenticular capsule calcifications developed, and corneal involvement slightly enlarged thereafter. A year later, 2 corneal punch biopsies confirmed calcification mainly in the Bowman layer. Topical treatment with 1.5% ethylenediaminetetraacetic acid significantly restored corneal clarity. Six months later, a standard extracapsular cataract extraction with intraocular lens placement improved visual acuity to 20/60. This case suggests that topical thrombin drops with elevated calcium concentrations may cause acute corneal calcification in Bowman layer and on the anterior lens capsule.

  5. A Study of Carotid Intimomedial Thickness as a Primary Marker of Atherosclerosis in Patients with Rheumatoid Arthritis.

    Directory of Open Access Journals (Sweden)

    Shivani Patel

    2016-01-01

    RA is a chronic disease associatedd with chronic subclinical inflammation. In view of the consequentr high risk of atherosclerosis seen in these patients CIMT may serve as an early surrogate marker of atherosclerosis. We can identify these high risk subgroups of patients with a simple, reliable, inexpensive, and non-invasive bedside carotid Doppler sonogram even in resource poor countries such as India. In our view physicians should be vigilant to identify and screen regularly for atherosclerosis with CIMT in RA patients, so that prompt early management can prevent the cardiovascular complications.

  6. Calcific myonecrosis: keys to early recognition

    International Nuclear Information System (INIS)

    Holobinko, Newt J.; Scerpella, Patrick R.; Hojnowski, Leonard; Damron, Timothy A.

    2003-01-01

    Calcific myonecrosis is a rare, late sequela of trauma occurring almost exclusively in the lower extremity which may be confused with an aggressive primary neoplasm. The platelike mineralization pattern seen on radiographs is characteristic but not widely recognized by clinicians. Three cases of calcific myonecrosis are reported, unique in that two presented for care following infection and that one had extended to involve the muscle compartments of the foot, a previously unreported site. (orig.)

  7. Tumor-like calcifications with scleroderma

    International Nuclear Information System (INIS)

    Meyer, E.; Kulenkampff, H.A.; Kortenhaus, H.

    1987-01-01

    In patients with progressive scleroderma, interstitial calcifications are present to a varying extent. They are mostly located in the soft tissues of the fingers, resembling points, commas or dashes. They may also appear as 'calcinosis universalis' and reach a considerable size. Thus they mimic proliferative tumors. Scintigraphy, proving the existence of further calcifications can be helpful. We report the case of a female patient who presented with such a 'pseudotumor' of unusual size, site and extent in the lumbar region. (orig.) [de

  8. Novel navigation technique for the endodontic treatment of a molar with pulp canal calcification and apical pathology.

    Science.gov (United States)

    Shi, Xilin; Zhao, Shiyong; Wang, Weidong; Jiang, Qianzhou; Yang, Xuechao

    2018-04-01

    Apical periodontitis, the inflammation of periapical tissue, commonly requires root canal treatment to achieve apical healing. However, if it is accompanied by pulp canal calcification, the treatment becomes complicated, and locating the root canal can be challenging. This case report describes a novel approach for treating a molar with pulp canal calcification and apical pathology. Due to the risk of perforation during treatment, a digitally printed template was used to assist in accurately locating the root canal. After six months, the patient was asymptomatic and the periradicular radiolucency was gradually reducing in size. © 2017 Australian Society of Endodontology Inc.

  9. Are air pollution and traffic noise independently associated with atherosclerosis: the Heinz Nixdorf Recall Study.

    Science.gov (United States)

    Kälsch, Hagen; Hennig, Frauke; Moebus, Susanne; Möhlenkamp, Stefan; Dragano, Nico; Jakobs, Hermann; Memmesheimer, Michael; Erbel, Raimund; Jöckel, Karl-Heinz; Hoffmann, Barbara

    2014-04-01

    Living close to high traffic has been linked to subclinical atherosclerosis, however it is not clear, whether fine particulate matter (PM) air pollution or noise, two important traffic-related exposures, are responsible for the association. We investigate the independent associations of long-term exposure to fine PM and road traffic noise with thoracic aortic calcification (TAC), a reliable measure of subclinical atherosclerosis. We used baseline data (2000-2003) from the German Heinz Nixdorf Recall Study, a population-based cohort of 4814 randomly selected participants. We assessed residential long-term exposure to PM with a chemistry transport model, and to road traffic noise using façade levels from noise models as weighted 24 h mean noise (Lden) and night-time noise (Lnight). Thoracic aortic calcification was quantified from non-contrast enhanced electron beam computed tomography. We used multiple linear regression to estimate associations of environmental exposures with ln(TAC+1), adjusting for each other, individual, and neighbourhood characteristics. In 4238 participants (mean age 60 years, 49.9% male), PM2.5 (aerodynamic diameter ≤2.5 µm) and Lnight are both associated with an increasing TAC-burden of 18.1% (95% CI: 6.6; 30.9%) per 2.4 µg/m(3) PM2.5 and 3.9% (95% CI 0.0; 8.0%) per 5dB(A) Lnight, respectively, in the full model and after mutual adjustment. We did not observe effect measure modification of the PM2.5 association by Lnight or vice versa. Long-term exposure to fine PM and night-time traffic noise are both independently associated with subclinical atherosclerosis and may both contribute to the association of traffic proximity with atherosclerosis.

  10. Periodontal Disease-Induced Atherosclerosis and Oxidative Stress

    Directory of Open Access Journals (Sweden)

    Tomoko Kurita-Ochiai

    2015-09-01

    Full Text Available Periodontal disease is a highly prevalent disorder affecting up to 80% of the global population. Recent epidemiological studies have shown an association between periodontal disease and cardiovascular disease, as oxidative stress plays an important role in chronic inflammatory diseases such as periodontal disease and cardiovascular disease. In this review, we focus on the mechanisms by which periodontopathic bacteria cause chronic inflammation through the enhancement of oxidative stress and accelerate cardiovascular disease. Furthermore, we comment on the antioxidative activity of catechin in atherosclerosis accelerated by periodontitis.

  11. Potential Mechanisms Linking Atherosclerosis and Increased Cardiovascular Risk in COPD: Focus On Sirtuins

    Science.gov (United States)

    Corbi, Graziamaria; Bianco, Andrea; Turchiarelli, Viviana; Cellurale, Michele; Fatica, Federica; Daniele, Aurora; Mazzarella, Gennaro; Ferrara, Nicola

    2013-01-01

    The development of atherosclerosis is a multi-step process, at least in part controlled by the vascular endothelium function. Observations in humans and experimental models of atherosclerosis have identified monocyte recruitment as an early event in atherogenesis. Chronic inflammation is associated with ageing and its related diseases (e.g., atherosclerosis and chronic obstructive pulmonary disease). Recently it has been discovered that Sirtuins (NAD+-dependent deacetylases) represent a pivotal regulator of longevity and health. They appear to have a prominent role in vascular biology and regulate aspects of age-dependent atherosclerosis. Many studies demonstrate that SIRT1 exhibits anti-inflammatory properties in vitro (e.g., fatty acid-induced inflammation), in vivo (e.g., atherosclerosis, sustainment of normal immune function in knock-out mice) and in clinical studies (e.g., patients with chronic obstructive pulmonary disease). Because of a significant reduction of SIRT1 in rodent lungs exposed to cigarette smoke and in lungs of patients with chronic obstructive pulmonary disease (COPD), activation of SIRT1 may be a potential target for chronic obstructive pulmonary disease therapy. We review the inflammatory mechanisms involved in COPD-CVD coexistence and the potential role of SIRT1 in the regulation of these systems. PMID:23774840

  12. Procyanidins-crosslinked aortic elastin scaffolds with distinctive anti-calcification and biological properties.

    Science.gov (United States)

    Wang, Xiaoya; Zhai, Wanyin; Wu, Chengtie; Ma, Bing; Zhang, Jiamin; Zhang, Hongfeng; Zhu, Ziyan; Chang, Jiang

    2015-04-01

    Elastin, a main component of decellularized extracellular matrices and elastin-containing materials, has been used for tissue engineering applications due to their excellent biocompatibility. However, elastin is easily calcified, leading to the decrease of life span for elastin-based substitutes. How to inhibit the calcification of elastin-based scaffolds, but maintain their good biocompatibility, still remains significantly challenging. Procyanidins (PC) are a type of natural polyphenols with crosslinking ability. To investigate whether pure elastin could be crosslinked by PC with anti-calcification effect, PC was first used to crosslink aortic elastin. Results show that PC can crosslink elastin and effectively inhibit elastin-initiated calcification. Further experiments reveal the possible mechanisms for the anti-calcification of PC crosslinking including (1) inhibiting inflammation cell attachment, and secretion of inflammatory factors such as MMPs and TNF-α, (2) preventing elastin degradation by elastase, and (3) direct inhibition of mineral nucleation in elastin. Moreover, the PC-crosslinked aortic elastin maintains natural structure with high pore volume (1111 μL/g), large pore size (10-300 μm) and high porosity (75.1%) which facilitates recellularization of scaffolds in vivo, and displays excellent hemocompatibility, anti-thrombus and anti-inflammatory potential. The advantages of PC-crosslinked porous aortic elastin suggested that it can serve as a promising scaffold for tissue engineering. Copyright © 2015 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.

  13. Clinical and imaging features associated with intracranial internal carotid artery calcifications in patients with ischemic stroke

    Energy Technology Data Exchange (ETDEWEB)

    Yilmaz, Arda [Mersin University, Department of Neurology, Faculty of Medicine, Mersin (Turkey); Akpinar, Erhan [Hacettepe University, Department of Radiology, Faculty of Medicine, Ankara (Turkey); Topcuoglu, Mehmet Akif; Arsava, Ethem Murat [Hacettepe University, Department of Neurology, Faculty of Medicine, Ankara (Turkey)

    2015-05-01

    Intracranial internal carotid artery calcifications (ICAC), a frequent finding on imaging studies, are predictive of future stroke risk in population-based studies. The clinical significance of this observation among ischemic stroke patients is however less clear. In this study, we analyzed ICAC burden in relation to vascular risk factor profile, stroke etiology, and extent of craniocervical vascular calcifications in a consecutive series of ischemic stroke patients. The burden of ICAC was determined both on non-contrast CT and CT-angiography source images by semiquantitative scoring algorithms. The distribution of vascular risk factors, etiologic stroke subtype, and calcification burden in other craniocervical arteries was assessed among patients with no ICAC, mild-moderate ICAC, and severe ICAC. Of 319 patients included into the study, 28 % had no ICAC, 35 % had mild-moderate ICAC, and 37 % had severe ICAC on CT angiography. Independent factors associated with ICAC burden in multivariate analysis included age (p < 0.001), diabetes mellitus (p = 0.006), and coronary artery disease (p < 0.001). Furthermore, a stroke etiology of large artery atherosclerosis or cardioaortic embolism was significantly related to higher ICAC burden (p = 0.006). Patients with severe ICAC were more likely to harbor calcifications in other vascular beds (p < 0.001). All of these findings persisted when analyses were repeated with CT-based ICAC burden assessments. ICAC burden reflects a continuum of atherosclerotic disease involving carotid arteries together with other craniocervical vascular beds. ICAC is significantly associated with stroke of large vessel or cardioembolic origin. This information might help the clinician in prioritizing etiologic work-up in the acute period. (orig.)

  14. Evaluation of carotid intima-media thickness in children with migraine: a marker of subclinical atherosclerosis.

    Science.gov (United States)

    Poyrazoglu, Hatice Gamze; Vurdem, Umit Erkan; Arslan, Alev; Uytun, Salih

    2016-10-01

    Migraine is a commonly seen neurovascular disorder during childhood. Inflammation induced by the activation of cytokines and neuropeptides is implied in its pathophysiology. There is an association between inflammation and atherosclerosis in patients with migraine. In addition, there is a strong correlation between early atherosclerotic wall lesions and carotid intima-media thickness (CIMT). The study population consisted of 57 migraine patients aged 5-17 years, as well as 47 healthy children who served as the control group. Those migraine patients who were not receiving any medications at the interictal period were compared to healthy controls in terms of their measured lipid levels, thyroid function, vitamin B12 levels, serum iron levels, iron binding capacity, complete blood count, C-reactive protein (CRP) levels, and carotid intima-media thickness (CIMT) scores, which may comprise risk factors for atherosclerosis. When children in the migraine and control groups were compared in terms of those risk factors that are known to be related to vascular changes, no significant differences were found. However, a significant difference was detected in CIMT values (P < 0.05). Atherosclerosis commences in childhood, and there is a long period of time before the onset of ischemic symptoms occurs. In children with migraine, an evaluation of CIMT can be used as a non-invasive imaging modality to detect atherosclerosis, which develops in the context of chronic inflammation. In this way, measures to reduce morbidity and mortality, which may result from cardiovascular diseases, can be implemented.

  15. The relation between coronary artery calcification in asymptomatic subjects and both traditional risk factors and living in the city centre

    DEFF Research Database (Denmark)

    Lambrechtsen, J; Gerke, Oke; Egstrup, Kenneth

    2012-01-01

    atherosclerosis. The relationship between CAC and several demographic and clinical parameters were evaluated using multivariate logistic regression. Results:  A total of 1225 individuals participated in the study, of whom 250 (20%) were living in the centres of major Danish cities. Gender and age showed......Objective:  To evaluate the association between the risk factor of living in the city centre as a surrogate for air pollution and the presence of coronary artery calcification (CAC) in a population of asymptomatic Danish subjects. Design and subjects:  A random sample of 1825 men and women...

  16. [Macrophage activation in atherosclerosis. Message 1: Activation of macrophages normally and in atherosclerotic lesions].

    Science.gov (United States)

    Nikiforov, N G; Kornienko, V Y; Karagodin, V P; Orekhov, A N

    2015-01-01

    Macrophages play important role in initiation and progression of inflammation in atherosclerosis. Plaque macrophages were shown to exhibit a phenotypic range that is intermediate between two extremes, M1 (proinflammatory) and M2 (anti-inflammatory). Indeed, in atherosclerosis, macrophages demonstrate phenotypic plasticity to rapidly adjust to changing microenvironmental conditions. In plaque macrophages demonstrate different phenotypes, and besides macrophage phenotypes could be changed. Phenotypes M1, M2, M4, Mhem, HA-mac, M(Hb) u Mox are described in the article. Ability of macrophages change their phenotype also considered.

  17. Vascular ossification – calcification in metabolic syndrome, type 2 diabetes mellitus, chronic kidney disease, and calciphylaxis – calcific uremic arteriolopathy: the emerging role of sodium thiosulfate

    Directory of Open Access Journals (Sweden)

    Sowers James R

    2005-03-01

    Full Text Available Abstract Background Vascular calcification is associated with metabolic syndrome, diabetes, hypertension, atherosclerosis, chronic kidney disease, and end stage renal disease. Each of the above contributes to an accelerated and premature demise primarily due to cardiovascular disease. The above conditions are associated with multiple metabolic toxicities resulting in an increase in reactive oxygen species to the arterial vessel wall, which results in a response to injury wound healing (remodeling. The endothelium seems to be at the very center of these disease processes, acting as the first line of defense against these multiple metabolic toxicities and the first to encounter their damaging effects to the arterial vessel wall. Results The pathobiomolecular mechanisms of vascular calcification are presented in order to provide the clinician – researcher a database of knowledge to assist in the clinical management of these high-risk patients and examine newer therapies. Calciphylaxis is associated with medial arteriolar vascular calcification and results in ischemic subcutaneous necrosis with vulnerable skin ulcerations and high mortality. Recently, this clinical syndrome (once thought to be rare is presenting with increasing frequency. Consequently, newer therapeutic modalities need to be explored. Intravenous sodium thiosulfate is currently used as an antidote for the treatment of cyanide poisioning and prevention of toxicities of cisplatin cancer therapies. It is used as a food and medicinal preservative and topically used as an antifungal medication. Conclusion A discussion of sodium thiosulfate's dual role as a potent antioxidant and chelator of calcium is presented in order to better understand its role as an emerging novel therapy for the clinical syndrome of calciphylaxis and its complications.

  18. High prevalence of COPD in atherosclerosis patients

    Directory of Open Access Journals (Sweden)

    Tuleta I

    2017-10-01

    Full Text Available Izabela Tuleta, Tarik Farrag, Laura Busse, Carmen Pizarro, Christian Schaefer, Simon Pingel, Georg Nickenig, Dirk Skowasch, Nadjib Schahab Department of Internal Medicine II – Cardiology, Pulmonology and Angiology, University of Bonn, Bonn, Germany Abstract: Atherosclerosis and COPD are both systemic inflammatory diseases that may influence each other. The aim of the present study was to determine the prevalence of COPD in patients with cerebral and/or peripheral artery disease and to assess factors associated with the presence of COPD. Following the diagnosis of cerebral and/or peripheral artery disease by means of duplex sonography, 166 consecutive patients underwent body plethysmography with capillary blood gas analysis. Thereafter, blood tests with determination of different parameters such as lipid profile, inflammatory and coagulation markers were conducted in remaining 136 patients who fulfilled inclusion criteria of the study. Thirty-six out of 136 patients suffered from COPD, mostly in early stages of the disease. Residual volume indicating emphysema was increased (162.9%±55.9% vs 124.5%±37.0%, p<0.05 and diffusion capacity was decreased (55.1%±19.5% vs 75.3%±18.6%, p<0.05 in COPD patients vs non-COPD group. In capillary blood gas analysis, COPD patients had lower partial pressure of oxygen (70.9±11.5 vs 75.2±11.0 mmHg, p<0.05 and higher partial pressure of carbon dioxide (36.8±7.5 vs 34.4±4.4 mmHg, p<0.05 compared with non-COPD individuals. Presence of COPD was associated with predominance of diabetes mellitus, interleukin-8-related systemic neutrophilic inflammation and anemia. In conclusion, COPD is highly prevalent in patients with atherosclerotic artery disease. Keywords: cerebral artery disease, peripheral artery disease, lung function, capillary blood gas, diabetes mellitus, inflammation, interleukin-8, anemia

  19. Heart failure due to severe myocardial calcification

    International Nuclear Information System (INIS)

    Takahashi, Shouichi; Maida, Kiyoshi; Yokoyama, Hitoshi; Tanaka, Shigeo

    1993-01-01

    A 28-year-old female who had had irradiation on the chest wall at the age of 5 as a remedy for keloid granulation after burn, recently developed congestive heart failure. Severe tricuspid regurgitation was demonstrated by echocardiography with a certain calcification in the cardiac shadow on chest radiogram. Calcified right ventricle and ventricular septum were noticed operatively, which disturbed ventricular motion and also caused tricuspid valve deformity. These calcified myocardium apparently corresponded with the irradiation field. After tricuspid valve replacement, she regained physical activity satisfactorily without congestive heart failure. Because she had no other known causes of cardiac calcification such as hypercalcemia, myocarditis, myocardial infarction or renal diseases, irradiation on the chest wall could be responsible for the severe myocardial calcification. (author)

  20. CT brain demonstration of basal ganglion calcification in adult HIV ...

    African Journals Online (AJOL)

    brain barrier has been postulated. Calcification of the basal ganglia in encephalopathic HIV/AIDS children has been relatively well documented. Only two adult HIV cases with basal ganglion calcification (BGC) have been reported in the literature.

  1. Idiopathic Pulmonary Calcification and Ossification in an Elderly ...

    African Journals Online (AJOL)

    Histology of tissue from autopsy showed intraparenchymal pulmonary calcification and ossification with marrow elements. Idiopathic pulmonary calcification and ossification is rare. At autopsy, she was also found to have had bilateral subarachnoid haemorrhage (SAH), a diagnosis missed during clinical evaluation.

  2. Double Trouble Foraminiferal Calcification in a Changing Ocean

    NARCIS (Netherlands)

    Van Dijk, I.E.Y.

    2017-01-01

    Within the project ‘Double Trouble: Foraminiferal Calcification in a Changing Ocean’, I tried to illuminate mechanisms determining element incorporation in foraminifera with different calcification strategies. In particular, I aimed to assess the interplay between ocean acidification and

  3. Double Trouble : Foraminiferal calcification in a changing ocean

    NARCIS (Netherlands)

    van Dijk, I.E.Y.

    2017-01-01

    Within the project ‘Double Trouble: Foraminiferal Calcification in a Changing Ocean’, I tried to illuminate mechanisms determining element incorporation in foraminifera with different calcification strategies. In particular, I aimed to assess the interplay between ocean acidification and

  4. Genetic associations with valvular calcification and aortic stenosis

    DEFF Research Database (Denmark)

    Thanassoulis, George; Campbell, Catherine Y; Owens, David S

    2013-01-01

    Limited information is available regarding genetic contributions to valvular calcification, which is an important precursor of clinical valve disease.......Limited information is available regarding genetic contributions to valvular calcification, which is an important precursor of clinical valve disease....

  5. Platelets and their chemokines in atherosclerosis – clinical applications

    Directory of Open Access Journals (Sweden)

    Philipp evon Hundelshausen

    2014-08-01

    Full Text Available The concept of platelets as important players in the process of atherogenesis has become increasingly accepted due to accumulating experimental and clinical evidence. Despite the progress in understanding the molecular details of atherosclerosis, particularly by using animal models, the inflammatory and thrombotic roles of activated platelet s especially in the human system remain difficult to dissect, as often only the complications of atherosclerosis i.e. stroke and myocardial infarction are definable but not the plaque burden.Platelet indices including platelet count and mean platelet volume and soluble mediators released by activated platelets are associated with atherosclerosis. The chemokine CXCL4 has multiple atherogenic activities e.g. altering the differentiation of T cells and macrophages by inhibiting neutrophil and monocyte apoptosis and by increasing the uptake of oxLDL and synergizing with CCL5. CCL5 is released and deposited on endothelium by activated platelets thereby triggering atherogenic monocyte recruitment, which can be attenuated by blocking the corresponding chemokine receptor CCR5. Atheroprotective and plaque stabilizing properties are attributed to CXCL12, which plays an important role in regenerative processes by attracting progenitor cells. Its release from luminal attached platelets accelerates endothelial healing after injury. Platelet surface molecules GPIIb/IIIa, GP1bα, P-selectin, JAM-A and the CD40/CD40L dyade are crucially involved in the interaction with endothelial cells, leukocytes and matrix molecules affecting atherogenesis. Beyond the effects on the arterial inflammatory infiltrate, platelets affect cholesterol metabolism by binding, modifying and endocytosing LDL particles via their scavenger receptors and contribute to the formation of lipid laden macrophages. Current medical therapies for the prevention of atherosclerotic therapies enable the elucidation of mechanisms linking platelets to inflammation

  6. Bilateral basal ganglia calcifications visualised on CT scan.

    OpenAIRE

    Brannan, T S; Burger, A A; Chaudhary, M Y

    1980-01-01

    Thirty-eight cases of basal ganglia calcification imaged on computed axial tomography were reviewed. Most cases were felt to represent senescent calcification. The possibility of a vascular aetiology in this group is discussed. A less common group of patients was identified with calcification secondary to abnormalities in calcium metabolism or radiation therapy. Three cases of basal ganglia calcifications were detected in juvenile epileptic patients receiving chronic anticonvulsants. These ca...

  7. Innate lymphoid cells in atherosclerosis.

    Science.gov (United States)

    Engelbertsen, Daniel; Lichtman, Andrew H

    2017-12-05

    The family of innate lymphoid cells (ILCs) consisting of NK cells, lymphoid tissue inducer cells and the 'helper'-like ILC subsets ILC1, ILC2 and ILC3 have been shown to have important roles in protection against microbes, regulation of inflammatory diseases and involved in allergic reactions. ILC1s produce IFN-γ upon stimulation with IL-12 and IL-18, ILC2s produce IL-5 and IL-13 responding to IL-33 and IL-25 while ILC3s produce IL-17 and IL-22 after stimulation with IL-23 or IL-1. Although few studies have directly investigated the role for ILCs in atherosclerosis, several studies have investigated transcription factors and cytokines shared by ILCs and T helper cells. In this review we summarize our current understanding of the role of ILC in atherosclerosis and discuss future directions. Copyright © 2017. Published by Elsevier B.V.

  8. Non-invasive diagnostic methods for atherosclerosis and use in assessing progression and regression in hypercholesterolemia

    International Nuclear Information System (INIS)

    Tsushima, Motoo; Fujii, Shigeki; Yutani, Chikao; Yamamoto, Akira; Naitoh, Hiroaki.

    1990-01-01

    We evaluated the wall thickening and stenosis rate (ASI), the calcification rate (ACI), and the wall thickening and calcification stenosis rate (SCI) of the lower abdominal aorta calculated by the 12 sector method from simple or enhanced computed tomography. The intra-observer variation of the calculation of ASI was 5.7% and that of ACI was 2.4%. In 9 patients who underwent an autopsy examination, ACI was significantly correlated with the rate of the calcification dimension to the whole objective area of the abdominal aorta (r=0.856, p<0.01). However, there were no correlations between ASI and the surface involvement or the atherosclerotic index obtained by the point-counting method of the autopsy materials. In the analysis of 40 patients with atherosclerotic vascular diseases, ASI and ACI were also highly correlated with the percentage volume of the arterial wall in relation to the whole volume of the observed artery (r=0.852, p<0.0001) and also the percentage calcification volume (r=0.913, p<0.0001) calculated by the computed method, respectively. The percentage of atherosclerotic vascular diseases increased in the group of both high ASI (over 10%) and high ACI (over 20%). We used SCI as a reliable index when the progression and regression of atherosclerosis was considered. Among patients of hypercholesterolemia consisting of 15 with familial hypercholesterolemia (FH) and 6 non-FH patients, the change of SCI (d-SCI) was significantly correlated with the change of total cholesterol concentration (d-TC) after the treatment (r=0.466, p<0.05) and the change of the right Achilles' tendon thickening (d-ATT) was also correlated with d-TC (r=0.634, p<0.005). However, no correlation between d-SCI and d-ATT was observed. In conclusion, CT indices of atherosclerosis were useful as a noninvasive quantitative diagnostic method and we were able to use them to assess the progression and regression of atherosclerosis. (author)

  9. Vascular and valvular calcifications in chronic hemodialysis patients

    Directory of Open Access Journals (Sweden)

    María Elena Bruzzone

    2014-12-01

    Full Text Available Introduction: Vascular and valvular calcifications are a frequent complication in dialyzed patients and are connected to an increased morbi-mortality. Many radiological methods (TAC multiple slices and with electrons emission have been used to investigate the presence of vascular calcifications in this population, but only few works have been focused on simple radiology. Objectives: The objectives of this work are to evaluate vascular calcifications by means of Kauppila index in hemodialysis prevalent patients, identify linked risk factors and determine their association with heart valves calcification. Methods: 95 stable patients under hemodialysis were surveyed during a period of 6 months longer. Abdominal Rx simple profile were performed on all patients to evaluate calcification of abdominal aorta by Kauppila index and twodimensional echocardiogram to detect valvular calcifications. Data were collected about sex, age, diabetes, Hypertension, tabaquism, dislipemia and bone-mineral metabolism. Results: 64.5% of the patients showed vascular calcifications. Average Kauppila index was 6.25. Age and time on dialysis correlated with vascular calcifications. In 31.6 % of individuals valvular calcifications were found, which presented significant association with diabetes and Kauppila Index. Conclusions: Vascular and valvular calcifications were frequent in the surveyed population. Kauppila index correlated with age, time on dialysis and valvular calcifications. Heart valves calcification was associated with diabetes.

  10. Atherosclerosis in Juvenile Idiopathic Arthritis

    Directory of Open Access Journals (Sweden)

    Ewa Jednacz

    2012-01-01

    Full Text Available Atherosclerosis is a chronic inflammatory disease of the arteries. Clinical consequences of the atherosclerotic process occur in the adult population, however atherosclerotic process begins in childhood. The classic risk factors for atherosclerosis include obesity, dyslipidaemia, age, gender or family history. In recent years, attention has been drawn to the similarity between atherosclerotic inflammatory processes and inflammatory changes in the course of systemic connective tissue disease, in particular systemic lupus etythematosus (SLE or rheumatoid arthritis (RA. There is also observed the similarity of the pathogenetic background of development of atherosclerosis and juvenile idiopathic arthritis (JIA. Elevated levels of pro-inflammatory cytokines are observed in the course of juvenile idiopathic arthritis. Also homocysteine concentrations, which may play a significant role in the development of atherosclerotic lesions, are observed higher in patients with JIA. Some studies revealed higher carotid intima-media thickness (IMT index values in children with JIA. In view of the fact that atherosclerotic process begins as early as in childhood, the introduction of appropriate preventive measures in children is a matter of utmost importance.

  11. Beyond Framingham risk factors and coronary calcification: does aortic valve calcification improve risk prediction? The Heinz Nixdorf Recall Study.

    Science.gov (United States)

    Kälsch, Hagen; Lehmann, Nils; Mahabadi, Amir A; Bauer, Marcus; Kara, Kaffer; Hüppe, Patricia; Moebus, Susanne; Möhlenkamp, Stefan; Dragano, Nico; Schmermund, Axel; Stang, Andreas; Jöckel, Karl-Heinz; Erbel, Raimund

    2014-06-01

    Aortic valve calcification (AVC) is considered a manifestation of atherosclerosis. In this study, we investigated whether AVC adds to cardiovascular risk prediction beyond Framingham risk factors and coronary artery calcification (CAC). A total of 3944 subjects from the population based Heinz Nixdorf Recall Study (59.3±7.7 years; 53% females) were evaluated for coronary events, stroke, and cardiovascular disease (CVD) events (including all plus CV death) over 9.1±1.9 years. CT scans were performed to quantify AVC. Cox proportional hazards regressions and Harrell's C were used to examine AVC as event predictor in addition to risk factors and CAC. During follow-up, 138 (3.5%) subjects experienced coronary events, 101 (2.6%) had a stroke, and 257 (6.5%) experienced CVD events. In subjects with AVC>0 versus AVC=0 the incidence of coronary events was 8.0% versus 3.0% (pAVC scores (pAVC scores (3rd tertile) remained independently associated with coronary events (HR 2.21, 95% CI 1.28 to 3.81) and CVD events (HR 1.67, 95% CI 1.08 to 2.58). After further adjustment for CAC score, HRs were attenuated (coronary events 1.55, 95% CI 0.89 to 2.69; CVD events 1.29, 95% CI 0.83 to 2.00). When adding AVC to the model containing traditional risk factors and CAC, Harrell's C indices did not increase for coronary events (from 0.744 to 0.744) or CVD events (from 0.759 to 0.759). AVC is associated with incident coronary and CVD events independent of Framingham risk factors. However, AVC fails to improve cardiovascular event prediction over Framingham risk factors and CAC. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

  12. Magnetic Nanoparticles Conjugated with Peptides Derived from Monocyte Chemoattractant Protein-1 as a Tool for Targeting Atherosclerosis

    Directory of Open Access Journals (Sweden)

    Chung-Wei Kao

    2018-05-01

    Full Text Available Atherosclerosis is a multifactorial inflammatory disease that may progress silently for long period, and it is also widely accepted as the main cause of cardiovascular diseases. To prevent atherosclerotic plaques from generating, imaging early molecular markers and quantifying the extent of disease progression are desired. During inflammation, circulating monocytes leave the bloodstream and migrate into incipient lipid accumulation in the artery wall, following conditioning by local growth factors and proinflammatory cytokines; therefore, monocyte accumulation in the arterial wall can be observed in fatty streaks, rupture-prone plaques, and experimental atherosclerosis. In this work, we synthesized monocyte-targeting iron oxide magnetic nanoparticles (MNPs, which were incorporated with the peptides derived from the chemokine receptor C-C chemokine receptor type 2 (CCR2-binding motif of monocytes chemoattractant protein-1 (MCP-1 as a diagnostic tool for potential atherosclerosis. MCP-1-motif MNPs co-localized with monocytes in in vitro fluorescence imaging. In addition, with MNPs injection in ApoE knockout mice (ApoE KO mice, the well-characterized animal model of atherosclerosis, MNPs were found in specific organs or regions which had monocytes accumulation, especially the aorta of atherosclerosis model mice, through in vivo imaging system (IVIS imaging and magnetic resonance imaging (MRI. We also performed Oil Red O staining and Prussian Blue staining to confirm the co-localization of MCP-1-motif MNPs and atherosclerosis. The results showed the promising potential of MCP-1-motif MNPs as a diagnostic agent of atherosclerosis.

  13. Reproducibility of coronary calcification detection with electron-beam computed tomography

    International Nuclear Information System (INIS)

    Hernigou, A.; Challande, P.; Boudeville, J.C.; Sene, V.; Grataloup, C.; Plainfosse, M.

    1996-01-01

    If coronary calcification scores obtained with electron-beam computed tomography (EBT) were proved to be correlated to coronary atherosclerosis, the reproducibility of the technique had to be assessed before being useed for patient follow-up. A total of 150 patients, selected as a result of a cholesterol screening programme, were studied by EBT. Twelve contiguous 3-mm-thick transverse slices beginning on the proximal coronary arteries were obtained through the base of the heart. The amount of calcium was evaluated as the calcified area weighted by a coefficient depending on the density peak level. The value was expressed as a logarithmic scale. Intra-observer, inter-observer and inter-examination reproducibilities were calculated. They were 1.9, 1.3 and 7.2%, respectively. These results were good enough to allow the use of EBT for longitudinal studies. The influence of acquisition and calculation conditions on score computation were also analysed. (orig.)

  14. Lack of Correlation Between Depression and Coronary Artery Calcification in a Non-Selected Danish Population

    DEFF Research Database (Denmark)

    Devantier, Torben Albert; Nørgaard, Bjarne Linde; Sand, Niels Peter

    2013-01-01

    BACKGROUND: Depression is associated with coronary artery disease, and atherosclerosis seems to play a central role in this relation. In several studies, multislice computed tomography (CT) has been applied for detection and quantification of coronary artery calcification (CAC) in relation...... to depression. To our knowledge, only one previous study has investigated the relation between CAC and depression in an unselected population. METHODS: A total of 617 persons were randomly selected from the background population. The participants underwent CT of the heart and were screened for depression by use...... of the Major Depression Inventory questionnaire. Quantification of CAC was performed using the Agatston method. The Mann-Whitney U test, Spearman's correlational analysis, and logistic regression were used to assess the association between depression and CAC. RESULTS: The median Agatston score...

  15. Effects of intra-abdominal sepsis on atherosclerosis in mice.

    Science.gov (United States)

    Kaynar, Ata Murat; Yende, Sachin; Zhu, Lin; Frederick, Daniel R; Chambers, Robin; Burton, Christine L; Carter, Melinda; Stolz, Donna Beer; Agostini, Brittani; Gregory, Alyssa D; Nagarajan, Shanmugam; Shapiro, Steven D; Angus, Derek C

    2014-09-03

    Sepsis and other infections are associated with late cardiovascular events. Although persistent inflammation is implicated, a causal relationship has not been established. We tested whether sepsis causes vascular inflammation and accelerates atherosclerosis. We performed prospective, randomized animal studies at a university research laboratory involving adult male ApoE-deficient (ApoE-/-) and young C57B/L6 wild-type (WT) mice. In the primary study conducted to determine whether sepsis accelerates atherosclerosis, we fed ApoE-/- mice (N = 46) an atherogenic diet for 4 months and then performed cecal ligation and puncture (CLP), followed by antibiotic therapy and fluid resuscitation or a sham operation. We followed mice for up to an additional 5 months and assessed atheroma in the descending aorta and root of the aorta. We also exposed 32 young WT mice to CLP or sham operation and followed them for 5 days to determine the effects of sepsis on vascular inflammation. ApoE-/- mice that underwent CLP had reduced activity during the first 14 days (38% reduction compared to sham; P < 0.001) and sustained weight loss compared to the sham-operated mice (-6% versus +9% change in weight after CLP or sham surgery to 5 months; P < 0.001). Despite their weight loss, CLP mice had increased atheroma (46% by 3 months and 41% increase in aortic surface area by 5 months; P = 0.03 and P = 0.004, respectively) with increased macrophage infiltration into atheroma as assessed by immunofluorescence microscopy (0.52 relative fluorescence units (rfu) versus 0.97 rfu; P = 0.04). At 5 months, peritoneal cultures were negative; however, CLP mice had elevated serum levels of interleukin 6 (IL-6) and IL-10 (each at P < 0.05). WT mice that underwent CLP had increased expression of intercellular adhesion molecule 1 in the aortic lumen versus sham at 24 hours (P = 0.01) that persisted at 120 hours (P = 0.006). Inflammatory and adhesion genes (tumor necrosis factor α, chemokine (C-C motif) ligand 2

  16. Usefulness of detecting atherosclerosis by computed tomography. A relation to coronary artery stenosis

    International Nuclear Information System (INIS)

    Takasu, Junichiro; Yamamoto, Rie; Yokoyama, Kenichi

    1999-01-01

    Reports evaluating coronary artery calcification detection by nonenhanced computed tomography (CT) have verified the usefulness for diagnosis of coronary artery disease. In the condition of a mobile CT scanning at a public health examination, however, determination of coronary calcification remains unclear. We investigated, under this scanning condition, a relation between the characteristic of coronary artery calcification determined by conventional CT and coronary disease on arteriogram. The quantification of aortic wall thickening by enhanced CT was examined on the usefulness of detecting coronary artery disease. The CT density score and the characteristics of aortic atherosclerosis for 159 male patients 30 year-old or more (average age 60.7 years) were examined the relation to coronary artery stenoses. The CT density score was the strongest independent variable for determining the existence of coronary disease. The CT density cutoff score for detection of coronary disease was 50 equal to 50 HU the maximal CT density in the coronary arteries. The maximal aortic wall thickness was the strongest significant variable independent of the noted coronary risk factors for the severity of coronary stenosis on arteriogram. (author)

  17. Clinicoradiologic evaluation of styloid process calcification

    International Nuclear Information System (INIS)

    Bagga, Mun Bhawni; Kumar, C. Anand; Yeluri, Garima

    2012-01-01

    This study was performed to investigate the prevalence, morphology, and calcification pattern of the elongated styloid process in the Mathura population and its relation to gender, age, and mandibular movements. The study analyzed digital panoramic radiographs of 2,706 adults. The elongated styloid process was classified with the radiographic appearance based on the morphology and calcification pattern. The limits of mandibular protrusion were evaluated for each subject. The data were analyzed by using a Student's t-test and chi-squared test with significance set at p=0.05. Bilateral elongation having an 'elongated' type styloid process with a 'partially mineralized' pattern was the most frequent type of styloid process. No correlation was found between styloid process type and calcification pattern on the one hand and gender on the other, although elongated styloid was more prevalent in older and male populations (p 0.05). Dentists should recognize the existence of morphological variation in elongated styloid process or Eagle syndrome apparent on panoramic radiographs. We found higher prevalence of elongated styloid process in the population of the Mathura region when compared with other Indian populations. The calcification of the styloid process was more common in the older age group with no correlation to gender, mandibular movement and site. 'Type I' with a 'partially calcified' styloid process was observed more frequently in the population studied.

  18. Penile gangrene due to calcific uremic arteriopathy

    African Journals Online (AJOL)

    2011-06-15

    Jun 15, 2011 ... 2Department of Medicine, Nephrology Unit, 3Department of Medicine, Infectious Disease Unit, King Fahad. Medical City, Riyadh, Kingdom of Saudi Arabia. Correspondence to: Dr. .... Russell R, Brookshire MA, Zekonis M, Moe SM. Distal calcific uremic arteriolopathy in a hemodialysis patient responds to ...

  19. Differential diagnosis of disseminated periventricular calcifications

    International Nuclear Information System (INIS)

    Rieger, P.; Piepgras, U.

    1986-01-01

    Juvenile disseminated periventricular calcifications may occur in tuberous sclerosis, toxoplasmosis, cytomegaly, and in tuberculous meningitis. Cysticercosis, by contrast, does not result in corresponding intracerebral foci until an older age. Differential diagnosis is no problem if clinical findings are typical (tuberous sclerosis) or if serological verification is positive. However, any unclear clinical diagnosis can often be secured by CT. (orig.) [de

  20. Coronary artery calcification in Kawasaki disease

    International Nuclear Information System (INIS)

    Ino, T.; Shimazaki, S.; Akimoto, K.; Park, I.; Nishimoto, K.; Yabuta, K.; Tanaka, A.

    1990-01-01

    To evaluate the angiographic features of coronary lesions in Kawasaki disease with coronary artery calcification, cinefluoroscopy and cineangiography were retrospectively reviewed in 116 patients who had undergone coronary angiography between 1982 and 1989. Angiographic abnormalities of coronary arteries were demonstrated in 55 of 116 patients. In 5 (9.1%) of the 55 patients, 9 with calcification were identified by cinefluoroscopy and chest X-ray. Eight of the 9 calcified lesions showed a circular or ring-shape configuration. Coronary angiography revealed a total occlusion of the right coronary artery with collateral circulation from the distal left coronary artery in 2 patients and a severe stenosis of the right coronary artery in 2 patients, in whom anticoagulant therapy had not been continued during the follow-up periods. The remaining patient in whom anticoagulant therapy had been continued had bilateral aneurysms but no significant stenosis. These results indicate that a ring-shape calcification on chest X-ray in 2 patients with a history of Kawasaki disease may suggest an involvement by coronary artery stenosis even when anticoagulant drugs had been given. Therefore, coronary angiography should be performed to evaluate the stenotic lesions if this type of calcification is found by routine radiographic examination. (orig.)

  1. Sclerosing peritonitis with gross calcification: case report

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Cheung Sook; Kim, Young Jae; Min, Seon Jeong; Cho, Seong Whi; Lee, Gyung Kyu; Lee, Eil Seong; Kang, Ik Won [Hallym University College of Medicine, Seoul (Korea, Republic of)

    2003-09-01

    Sclerosing peritonitis is an uncommon complication of continuous ambulatory peritoneal dialysis (CAPD) and can lead to small bowel dysfunction involving abdominal pain, progressive loss of ultrafiltration, and small intestinal obstruction. Peritoneal thickening, in which calcification can develop, often starts as al small plaque which gradually becomes larger. We report a case of CAPD-related calcifying peritonitis.

  2. Diabetes mellitus, pulmonary tuberculosis and chronic calcific ...

    African Journals Online (AJOL)

    The prevalence of chronic calcific pancreatitis (CCP) was determined in 25 successive patients with both diabetes mellitus and newly diagnosed pulmonary tuberculosis. Twenty patients (80%) were alcoholics and all were black. Of these, 9 (45%) had CCP. In only 3 of these 9 patients was the history compatible with the ...

  3. Diabetes mellitus, pulmonary tuberculosis and chronic calcific ...

    African Journals Online (AJOL)

    The prevalence of chronic calcific pancreatitis (CCP) was determined in 25 successive patients with both diabetes mellitus and newly diagnosed pulmonary tuberculosis. Twenty patients (80%) were alcoholics and all were black. Of these, 9. (45%) had CCP. In only 3 of these 9 patients was the history compatible with the ...

  4. Differential diagnosis of disseminated periventricular calcifications

    Energy Technology Data Exchange (ETDEWEB)

    Rieger, P.; Piepgras, U.

    1986-08-01

    Juvenile disseminated periventricular calcifications may occur in tuberous sclerosis, toxoplasmosis, cytomegaly, and in tuberculous meningitis. Cysticercosis, by contrast, does not result in corresponding intracerebral foci until an older age. Differential diagnosis is no problem if clinical findings are typical (tuberous sclerosis) or if serological verification is positive. However, any unclear clinical diagnosis can often be secured by CT.

  5. Atherosclerosis-Driven Treg Plasticity Results in Formation of a Dysfunctional Subset of Plastic IFNγ+ Th1/Tregs.

    Science.gov (United States)

    Butcher, Matthew J; Filipowicz, Adam R; Waseem, Tayab C; McGary, Christopher M; Crow, Kevin J; Magilnick, Nathaniel; Boldin, Mark; Lundberg, Patric S; Galkina, Elena V

    2016-11-11

    Forkhead box P3 + T regulatory cells (Tregs) are key players in maintaining immune homeostasis. Evidence suggests that Tregs respond to environmental cues to permit or suppress inflammation. In atherosclerosis, Th1-driven inflammation affects Treg homeostasis, but the mechanisms governing this phenomenon are unclear. Here, we address whether atherosclerosis impacts Treg plasticity and functionality in Apoe - /- mice, and what effect Treg plasticity might have on the pathology of atherosclerosis. We demonstrate that atherosclerosis promotes Treg plasticity, resulting in the reduction of CXCR3 + Tregs and the accumulation of an intermediate Th1-like interferon (IFN)-γ + CCR5 + Treg subset (Th1/Tregs) within the aorta. Importantly, Th1/Tregs arise in atherosclerosis from bona fide Tregs, rather than from T-effector cells. We show that Th1/Tregs recovered from atherosclerotic mice are dysfunctional in suppression assays. Using an adoptive transfer system and plasticity-prone Mir146a -/- Tregs, we demonstrate that elevated IFNγ + Mir146a -/- Th1/Tregs are unable to adequately reduce atherosclerosis, arterial Th1, or macrophage content within Apoe -/- mice, in comparison to Mir146a +/+ Tregs. Finally, via single-cell RNA-sequencing and real-time -polymerase chain reaction, we show that Th1/Tregs possess a unique transcriptional phenotype characterized by coexpression of Treg and Th1 lineage genes and a downregulation of Treg-related genes, including Ikzf2, Ikzf4, Tigit, Lilrb4, and Il10. In addition, an ingenuity pathway analysis further implicates IFNγ, IFNα, interleukin-2, interleukin-7, CTLA-4 (cytotoxic T-lymphocyte-associated protein 4), T-cell receptor, and Csnk2b-related pathways in regulating Treg plasticity. Atherosclerosis drives Treg plasticity, resulting in the accumulation of dysfunctional IFNγ + Th1/Tregs that may permit further arterial inflammation and atherogenesis. © 2016 American Heart Association, Inc.

  6. Study of the position of calcification in calcific tendinitis of the shoulder

    International Nuclear Information System (INIS)

    Asakura, Toru; Matsuura, Koumei; Shin, Kunichika; Ooe, Kenjiro

    2011-01-01

    The commonly occurring position of calcification in the calcific tendinitis of the shoulder is said to be the supraspinatus tendon. In the anatomical field, it has been newly discovered that the infraspinatus tendon crosses over the supraspinatus tendon to the superior facet of the greater tuberosity. In this study, we thus attempted to determine the occurring position of calcification on MRI quantitatively. We measured the angle between the bicipital groove and center of calcification, and found it to be 49.5±16.5 degrees. On the other hand, it has been reported that the boundary line between the superior and middle facets is 45.4 degrees externally rotated from the bicipital groove. The protrusion formed at the greater tuberosity at this position imposes mechanical stress on the rotator cuff tendon. As we confirmed that these two angles are very close in this study, it suggests that calcification occurs at the boundary line of the superior and middle facets. Our findings also indicate that calcification often occurs at the infraspinatus tendon. (author)

  7. Plasma apolipoprotein C-III levels, triglycerides, and coronary artery calcification in type 2 diabetics.

    Science.gov (United States)

    Qamar, Arman; Khetarpal, Sumeet A; Khera, Amit V; Qasim, Atif; Rader, Daniel J; Reilly, Muredach P

    2015-08-01

    Triglyceride-rich lipoproteins have emerged as causal risk factors for developing coronary heart disease independent of low-density lipoprotein cholesterol levels. Apolipoprotein C-III (ApoC-III) modulates triglyceride-rich lipoprotein metabolism through inhibition of lipoprotein lipase and hepatic uptake of triglyceride-rich lipoproteins. Mutations causing loss-of-function of ApoC-III lower triglycerides and reduce coronary heart disease risk, suggestive of a causal role for ApoC-III. Little data exist about the relationship of ApoC-III, triglycerides, and atherosclerosis in patients with type 2 diabetes mellitus (T2DM). Here, we examined the relationships between plasma ApoC-III, triglycerides, and coronary artery calcification in patients with T2DM. Plasma ApoC-III levels were measured in a cross-sectional study of 1422 subjects with T2DM but without clinically manifest coronary heart disease. ApoC-III levels were positively associated with total cholesterol (Spearman r=0.36), triglycerides (r=0.59), low-density lipoprotein cholesterol (r=0.16), fasting glucose (r=0.16), and glycosylated hemoglobin (r=0.12; Ptriglycerides (Tobit regression ratio, 1.43; 95% confidence interval, 0.94-2.18; P=0.086) and separately for very low-density lipoprotein cholesterol (Tobit regression ratio, 1.14; 95% confidence interval, 0.75-1.71; P=0.53). In persons with T2DM, increased plasma ApoC-III is associated with higher triglycerides, less favorable cardiometabolic phenotypes, and higher coronary artery calcification, a measure of subclinical atherosclerosis. Therapeutic inhibition of ApoC-III may thus be a novel strategy for reducing plasma triglyceride-rich lipoproteins and cardiovascular risk in T2DM. © 2015 American Heart Association, Inc.

  8. Significance of coronary artery calcification detected incidentally with chest CT

    International Nuclear Information System (INIS)

    Moore, E.H.; Greenberg, R.; Miller, S.W.; Shepard, J.O.; Bourgouin, P.M.; McLoud, T.C.

    1987-01-01

    Coronary artery calcifications are well seen on CT scans because of high contrast resolution. Individual vessels were scored 0-3+ based on degree of calcification in over 40 patients who also underwent cardiac catheterization. Though relatively insensitive, the presence of dense calcifications had a specificity of roughly 60% to 70% for the presence of severe stenosis. In addition, 30 patients with calcification on CT scans and 30 age-matched controls, all of whom underwent thoracotomy, were compared with respect to prior cardiac history, estimated anesthetic risk, and postoperative cardiac complications. Patients with calcifications were more likely to have evidence of coronary disease and/or encounter postoperative cardiac complications

  9. Eosinophil count is positively correlated with coronary artery calcification

    International Nuclear Information System (INIS)

    Tanaka, Muhei; Fukui, Michiaki; Yamasaki, Masahiro; Hasegawa, Goji; Oda, Yohei; Nakamura, Naoto; Tomiyasu, Ki-ichiro; Akabame, Satoshi; Nakano, Koji

    2012-01-01

    Recent studies suggested that allergic disorders and increased eosinophil count were associated with atherosclerosis. The purpose of this study was to assess the relationship between eosinophil count and coronary artery calcification (CAC). We performed a cross-sectional study in 1363 consecutive participants with clinical suspicion of coronary heart disease (CHD). We evaluated the relationships between CAC score determined by multislice CT and peripheral eosinophil count as well as major cardiovascular risk factors, including age, body mass index, smoking status, hypertension, dyslipidemia, diabetes mellitus (DM), high-sensitivity C-reactive protein and estimated glomerular filtration rate (eGFR). Sex (P=0.0004), hypertension (P=0.0002), dyslipidemia (P=0.0004) and DM (P=0.0061) were associated with log (CAC+1), respectively. Positive correlations were found between log (CAC+1), and age (r=0.325, P<0.0001) and eosinophil count (r=0.165, P<0.0001). Negative correlations were found between log (CAC+1) and eGFR (r=-0.166, P<0.0001). Multivariate linear regression analysis demonstrated that age (β=0.314, P<0.0001), sex (β=0.124, P<0.0001), hypertension (β=0.084, P=0.0008), DM (β=0.108, P<0.0001), eGFR (β=-0.079, P=0.0021) and eosinophil count (β=0.147, P<0.0001) were independent determinants of log (CAC+1). In conclusion, eosinophil count correlated positively with CAC in participants with clinical suspicion of CHD. (author)

  10. Fatty Acid binding protein 4 is associated with carotid atherosclerosis and outcome in patients with acute ischemic stroke

    DEFF Research Database (Denmark)

    Holm, Sverre; Ueland, Thor; Dahl, Tuva B

    2011-01-01

    Fatty acid binding protein 4 (FABP4) has been shown to play an important role in macrophage cholesterol trafficking and associated inflammation. To further elucidate the role of FABP4 in atherogenesis in humans, we examined the regulation of FABP4 in carotid atherosclerosis and ischemic stroke....

  11. Pentosan polysulfate inhibits atherosclerosis in Watanabe heritable hyperlipidemic rabbits: differential modulation of metalloproteinase-2 and -9.

    Science.gov (United States)

    Lupia, Enrico; Zheng, Feng; Grosjean, Fabrizio; Tack, Ivan; Doublier, Sophie; Elliot, Sharon J; Vlassara, Helen; Striker, Gary E

    2012-02-01

    Pentosan polysulfate (PPS), a heparinoid compound essentially devoid of anticoagulant activity, modulates cell growth and decreases inflammation. We investigated the effect of PPS on the progression of established atherosclerosis in Watanabe heritable hyperlipidemic (WHHL) rabbits. After severe atherosclerosis developed on an atherogenic diet, WHHL rabbits were treated with oral PPS or tap water for 1 month. The aortic intima-to-media ratio and macrophage infiltration were reduced, plaque collagen content was increased, and plaque fibrous caps were preserved by PPS treatment. Plasma lipid levels and post-heparin hepatic lipase activity remained unchanged. However, net collagenolytic activity in aortic extracts was decreased, and the levels of matrix metalloproteinase (MMP)-2 and tissue inhibitor of metalloproteinase (TIMP) activity were increased by PPS. Moreover, PPS treatment decreased tumor necrosis factor α (TNFα)-stimulated proinflammatory responses, in particular activation of nuclear factor-κB and p38, and activation of MMPs in macrophages. In conclusion, oral PPS treatment prevents progression of established atherosclerosis in WHHL rabbits. This effect may be partially mediated by increased MMP-2 and TIMP activities in the aortic wall and reduced TNFα-stimulated inflammation and MMP activation in macrophages. Thus, PPS may be a useful agent in inhibiting the progression of atherosclerosis.

  12. Calcification in large cell neuroendocrine carcinoma of the lung

    International Nuclear Information System (INIS)

    Takamochi, Kazuya; Yokose, Tomoyuki; Ochiai, Atsushi; Yoshida, Junji; Nishimura, Mitsuyo; Ohmatsu, Hironobu; Nagai, Kanji; Nishiwaki, Yutaka

    2003-01-01

    The aim was to investigate the prevalence of intratumoral calcification in large cell neuroendocrine carcinoma (LCNEC) and to review computed tomography (CT) and histological findings. From August 1992 through March 2000, 35 out of 1183 surgically resected lung cancer patients were histologically diagnosed as having LCNEC at our institute. We reviewed the pain radiographs and CT scans of these 35 LCNEC patients. In LCNEC cases with intratumoral calcification, we examined the size, number, distribution and pattern of intratumoral calcifications visible on the CT scans and the histological features. Three cases (9%) exhibited calcification. The calcifications were recognized by CT scans alone. The CT scans showed punctate or eccentric intratumoral calcifications, which are considered to be a malignant feature, in all three cases. In two cases, the calcifications were histologically confirmed to be located within the necrotic areas of a tumor nest. We found three LCNEC cases with intratumoral calcification. The prevalence of LCNEC calcification was similar to that in previous reports on lung cancer. The mechanism of the intratumoral calcification in our LCNEC cases is speculated to be dystrophic calcification. (author)

  13. Medial arterial calcification in diabetes and its relationship to neuropathy

    DEFF Research Database (Denmark)

    Jeffcoate, W J; Rasmussen, Lars Melholt; Hofbauer, L C

    2009-01-01

    Calcification of the media of arterial walls is common in diabetes and is particularly associated with distal symmetrical neuropathy. Arterial calcification also complicates chronic kidney disease and is an independent risk factor for cardiovascular and all-cause mortality. The term calcification......, such as calcitonin gene-related peptide, which are inherently protective. The association between distal symmetrical neuropathy and calcification of the arterial wall highlights the fact that neuropathy may be an independent risk factor for cardiovascular mortality.......Calcification of the media of arterial walls is common in diabetes and is particularly associated with distal symmetrical neuropathy. Arterial calcification also complicates chronic kidney disease and is an independent risk factor for cardiovascular and all-cause mortality. The term calcification...

  14. Impact of Hydroxychloroquine on Atherosclerosis and Vascular Stiffness in the Presence of Chronic Kidney Disease.

    Directory of Open Access Journals (Sweden)

    Ashutosh M Shukla

    Full Text Available Cardiovascular disease is the largest cause of morbidity and mortality among patients with chronic kidney disease (CKD and end-stage kidney disease, with nearly half of all deaths attributed to cardiovascular disease. Hydroxychloroquine (HCQ, an anti-inflammatory drug, has been shown to have multiple pleiotropic actions relevant to atherosclerosis. We conducted a proof-of-efficacy study to evaluate the effects of hydroxychloroquine in an animal model of atherosclerosis in ApoE knockout mice with and without chronic kidney disease. Forty male, 6-week-old mice were divided into four groups in a 2 x 2 design: sham placebo group; sham treatment group; CKD placebo group; and CKD treatment group. CKD was induced by a two-step surgical procedure. All mice received a high-fat diet through the study duration and were sacrificed after 16 weeks of therapy. Mice were monitored with ante-mortem ultrasonic echography (AUE for atherosclerosis and vascular stiffness and with post-mortem histology studies for atherosclerosis. Therapy with HCQ significantly reduced the severity of atherosclerosis in CKD mice and sham treated mice. HCQ reduced the area of aortic atherosclerosis on en face examination by approximately 60% in HCQ treated groups compared to the non-treated groups. Additionally, therapy with HCQ resulted in significant reduction in vascular endothelial dysfunction with improvement in vascular elasticity and flow patterns and better-preserved vascular wall thickness across multiple vascular beds. More importantly, we found that presence of CKD had no mitigating effect on HCQ's anti-atherosclerotic and vasculoprotective effects. These beneficial effects were not due to any significant effect of HCQ on inflammation, renal function, or lipid profile at the end of 16 weeks of therapy. This study, which demonstrates structural and functional protection against atherosclerosis by HCQ, provides a rationale to evaluate its use in CKD patients. Further studies

  15. C-reactive protein in relation to early atherosclerosis and periodontitis.

    Science.gov (United States)

    Yakob, Maha; Meurman, Jukka H; Jogestrand, Tomas; Nowak, Jacek; Söder, Per-Östen; Söder, Birgitta

    2012-02-01

    Periodontitis may affect atherosclerosis via the chronic inflammation. We investigated high-sensitivity C-reactive protein (hsCRP) in relation to early vascular atherosclerotic changes in non-symptomatic subjects with and without long-term periodontitis. Carotid ultrasonography with calculation of common carotid artery intima-media area (cIMA) was performed, and hsCRP and atherosclerosis risk factors were analysed in randomly chosen 93 patients with periodontitis and 41 controls. The relationship between hsCRP, cIMA and atherosclerosis risk factors was evaluated with multiple logistic regression analysis. Women displayed lower hsCRP (p periodontitis, cIMA values were higher than in controls. Periodontitis appeared to be a major predictor for increased cIMA (odds ratio, 3.82; 95% confidence interval, 1.19-12.26). Neither of these factors was significantly associated with hsCRP which thus appeared not sensitive enough to be a marker for periodontitis or atherosclerosis. Hence, irrespective of low hsCRP levels, periodontitis appeared to increase the risk for atherosclerosis.

  16. Transcriptional profiling uncovers a network of cholesterol-responsive atherosclerosis target genes.

    Directory of Open Access Journals (Sweden)

    Josefin Skogsberg

    2008-03-01

    Full Text Available Despite the well-documented effects of plasma lipid lowering regimes halting atherosclerosis lesion development and reducing morbidity and mortality of coronary artery disease and stroke, the transcriptional response in the atherosclerotic lesion mediating these beneficial effects has not yet been carefully investigated. We performed transcriptional profiling at 10-week intervals in atherosclerosis-prone mice with human-like hypercholesterolemia and a genetic switch to lower plasma lipoproteins (Ldlr(-/-Apo(100/100Mttp(flox/flox Mx1-Cre. Atherosclerotic lesions progressed slowly at first, then expanded rapidly, and plateaued after advanced lesions formed. Analysis of lesion expression profiles indicated that accumulation of lipid-poor macrophages reached a point that led to the rapid expansion phase with accelerated foam-cell formation and inflammation, an interpretation supported by lesion histology. Genetic lowering of plasma cholesterol (e.g., lipoproteins at this point all together prevented the formation of advanced plaques and parallel transcriptional profiling of the atherosclerotic arterial wall identified 37 cholesterol-responsive genes mediating this effect. Validation by siRNA-inhibition in macrophages incubated with acetylated-LDL revealed a network of eight cholesterol-responsive atherosclerosis genes regulating cholesterol-ester accumulation. Taken together, we have identified a network of atherosclerosis genes that in response to plasma cholesterol-lowering prevents the formation of advanced plaques. This network should be of interest for the development of novel atherosclerosis therapies.

  17. Regulation of the renin–angiotensin system in coronary atherosclerosis: A review of the literature

    Directory of Open Access Journals (Sweden)

    Ramadan A Hammoud

    2008-01-01

    Full Text Available Ramadan A Hammoud, Christopher S Vaccari, Sameer H Nagamia, Bobby V KhanEmory University School of Medicine, Division of Cardiology, Grady Memorial Hospital Vascular Research Laboratory, Atlanta, Georgia, USAAbstract: Activation of the renin–angiotensin system (RAS is significant in the pathogenesis of cardiovascular disease and specifically coronary atherosclerosis. There is strong evidence that the RAS has effects on the mechanisms of action of atherosclerosis, including fibrinolytic balance, endothelial function, and plaque stability. Pharmacological inhibition of the renin angiotensin system includes angiotensin converting enzyme (ACE inhibitors, angiotensin receptor blockers (ARBs, and renin inhibitors. These agents have clinical benefits in reducing morbidity and mortality in the management of hypertension. In addition, ACE inhibitors and ARBs have shown to be effective in the management of congestive heart failure and acute myocardial infarction. This review article discusses the biochemical and molecular mechanisms involving the RAS in coronary atherosclerosis as well as the effects of RAS inhibition in clinical studies involving coronary atherosclerosis.Keywords: angiotensin II, atherosclerosis, endothelium, inflammation, vasculature

  18. Telomerase Activation in Atherosclerosis and Induction of Telomerase Reverse Transcriptase Expression by Inflammatory Stimuli in Macrophages

    Science.gov (United States)

    Gizard, Florence; Heywood, Elizabeth B.; Findeisen, Hannes M.; Zhao, Yue; Jones, Karrie L.; Cudejko, Cèline; Post, Ginell R.; Staels, Bart; Bruemmer, Dennis

    2010-01-01

    Objective Telomerase serves as a critical regulator of tissue renewal. Although telomerase activity is inducible in response to various environmental cues, it remains unknown whether telomerase is activated during the inflammatory remodeling underlying atherosclerosis formation. To address this question, we investigated in the present study the regulation of telomerase in macrophages and during atherosclerosis development in LDL-receptor-deficient mice. Methods and Results We demonstrate that inflammatory stimuli activate telomerase in macrophages by inducing the expression of the catalytic subunit telomerase reverse transcriptase (TERT). Reporter and chromatin immunoprecipitation assays identified a previously unrecognized NF-κB response element in the TERT promoter, to which NF-κB is recruited during inflammation. Inhibition of NF-κB signaling completely abolished the induction of TERT expression, characterizing TERT as a bona fide NF-κB target gene. Furthermore, functional experiments revealed that TERT-deficiency results in a senescent cell phenotype. Finally, we demonstrate high levels of TERT expression in macrophages of human atherosclerotic lesions and establish that telomerase is activated during atherosclerosis development in LDL-receptor-deficient mice. Conclusion These results characterize TERT as a previously unrecognized NF-κB target gene in macrophages and demonstrate that telomerase is activated during atherosclerosis. This induction of TERT expression prevents macrophage senescence and may have important implications for the development of atherosclerosis. PMID:21106948

  19. Adipocyte induced arterial calcification is prevented with sodium thiosulfate

    Energy Technology Data Exchange (ETDEWEB)

    Chen, Neal X., E-mail: xuechen@iupui.edu [Divison of Nephrology, Indiana University School of Medicine, Indianapolis, IN (United States); O’Neill, Kalisha; Akl, Nader Kassis [Divison of Nephrology, Indiana University School of Medicine, Indianapolis, IN (United States); Moe, Sharon M. [Divison of Nephrology, Indiana University School of Medicine, Indianapolis, IN (United States); Roudebush VA Medical Center, Indianapolis, IN (United States)

    2014-06-20

    Highlights: • High phosphorus can induce calcification of adipocytes, even when fully differentiated. • Adipocytes can induce vascular calcification in an autocrine manner. • Sodium thiosulfate inhibits adipocyte calcification. - Abstract: Background: Calcification can occur in fat in multiple clinical conditions including in the dermis, breasts and in the abdomen in calciphylaxis. All of these are more common in patients with advanced kidney disease. Clinically, hyperphosphatemia and obesity are risk factors. Thus we tested the hypothesis that adipocytes can calcify in the presence of elevated phosphorus and/or that adipocytes exposed to phosphorus can induce vascular smooth muscle cell (VSMC) calcification. Methods: 3T3-L1 preadipocytes were induced into mature adipocytes and then treated with media containing high phosphorus. Calcification was assessed biochemically and PCR performed to determine the expression of genes for osteoblast and adipocyte differentiation. Adipocytes were also co-cultured with bovine VSMC to determine paracrine effects, and the efficacy of sodium thiosulfate was determined. Results: The results demonstrated that high phosphorus induced the calcification of differentiated adipocytes with increased expression of osteopontin, the osteoblast transcription factor Runx2 and decreased expression of adipocyte transcription factors peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT-enhancer-binding protein α (CEBPα), indicating that high phosphorus led to a phenotypic switch of adipocytes to an osteoblast like phenotype. Sodium thiosulfate, dose dependently decreased adipocyte calcification and inhibited adipocyte induced increase of VSMC calcification. Co-culture studies demonstrated that adipocytes facilitated VSMC calcification partially mediated by changes of secretion of leptin and vascular endothelial growth factor (VEGF) from adipocytes. Conclusion: High phosphorus induced calcification of mature adipocytes, and

  20. Radiological observation of determination of sex by costal cartilage calcification

    International Nuclear Information System (INIS)

    Kang, Shin Hwa; Won, Jong Jin; Rhee, Song Joo; Moon, Moo Chang; Oh, Jong Hyun; Choi, Ki Chul

    1979-01-01

    The difference of patterns of costal cartilage calcification in male and female had been first described by Fischer in 1955. Thereafter several reports were published, but specific clinical significance was not found. During the period from January, 1978 to December, 1978, we, in the Department of Radiology, Jeonbug National University, studied 2164 cases that showed the entire 12 pairs of ribs. Among these we detected 1494 cases of costal cartilage calcification and frequent sites of calcification. Patterns of costal cartilage calcification were classified into six groups- type l: central, type II: marginal, type III: junctional type, type IV: railroad, type V: diffuse, type VI: mixed. Results are as follows; 1. In a total of 2164 cases, calcification of costal cartilage was present in 1494 cases(69.0%). Of 1181 males 780 cases(66.0%) showed calcification, and of 983 females 714 cases (72.6%) showed calcification. 2. In 439 cases of males, except for 341 cases that showed calcification within the first costal cartilage, patterns of costal cartilage calcification were as follows: marginal type in 265 cases (60.4%), junctional type in 134 cases (30.5%), mixed type in 21 cases (0.5%), central type in 17 cases(3.8%), and railroad type in 2 cases (0.5%). Diffuse type was not present. 3. In 492 cases of females, except of 222 cases that showed calcification within the first costal cartilage, patterns of costal cartilage calcification were as follows; central type in 336 cases (68.3%), junctional type in 94 cases(19.1%), mixed type in 24 cases (4.9%), railroad type in 19 cases (3.9%), and diffuse type in 14 cases (2.8%). 4. When central calcification was observed, predictive value to female was 94.7%. When marginal calcification was observed, predictive value to male was 987.4%. 5. Males frequently showed calcification in upper costal cartilages, and females in lower costal cartilages.

  1. Matrix Gla Protein Polymorphisms are Associated with Coronary Artery Calcification in Men

    Science.gov (United States)

    Crosier, Michael D.; Booth, Sarah L.; Peter, Inga; Dawson-Hughes, Bess; Price, Paul A.; O’Donnell, Christopher J.; Hoffmann, Udo; Williamson, Matthew K.; Ordovas, Jose M.

    2009-01-01

    Summary Matrix Gla protein (MGP) is a key regulator of vascular calcification. Genetic variation at the MGP locus could modulate the development of coronary artery calcification (CAC). Our aim was to examine the cross-sectional association between MGP single nucleotide polymorphisms (SNPs) [rs1800802 (T-138C), rs1800801 (G-7A), and rs4236 (Ala102Thr)] and CAC. CAC was measured by multidetector computed tomography (MDCT), in older men and women of European descent, (n = 386; 60 to 80 y of age). Serum MGP was measured by radioimmunoassay. Linear, Tobit and Ordinal regression analyses all revealed that in men, homozygous carriers of the minor allele of rs1800802 , rs1800801 , or rs4236 (minor allele frequency: 21, 38, and 40%, respectively) were associated with a decreased quantity of CAC, relative to major allele carriers. This association was not found in women. Although genetic variation in MGP was associated with serum MGP concentrations, there were no associations between serum MGP and CAC. The results of this study suggest a role for MGP genetic variants in coronary atherosclerosis among men that is not reflected in serum MGP concentrations. PMID:19352064

  2. The Establishment and Characteristics of Rat Model of Atherosclerosis Induced by Hyperuricemia

    Directory of Open Access Journals (Sweden)

    Zhen Liu

    2016-01-01

    Full Text Available Epidemiological studies have identified hyperuricemia as an independent risk factor for cardiovascular disease. However, the mechanism whereby hyperuricemia causes atherosclerosis remains unclear. The objective of the study was to establish a new rat model of hyperuricemia-induced atherosclerosis. Wistar-Kyoto rats were randomly allocated to either a normal diet (ND, high-fat diet (HFD, or high-adenine diet (HAD, followed by sacrifice 4, 8, or 12 weeks later. Serum uric acid and lipid levels were analyzed, pathologic changes in the aorta were observed by hematoxylin and eosin staining, and mRNA expression was evaluated by quantitative real-time polymerase chain reaction. Serum uric acid and TC were significantly increased in the HAD group at 4 weeks compared with the ND group, but there was no significant difference in serum uric acid between the ND and HFD groups. Aorta calcification occurred earlier and was more severe in the HAD group, compared with the HFD group. Proliferating cell nuclear antigen, monocyte chemotactic factor-1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 mRNA levels were increased in the HFD and HAD groups compared with the ND group. This new animal model will be a useful tool for investigating the mechanisms responsible for hyperuricemia-induced atherosclerosis.

  3. Risk of carotid atherosclerosis associated with genetic polymorphisms of apolipoprotein E and inflammatory genes among arsenic exposed residents in Taiwan

    International Nuclear Information System (INIS)

    Hsieh, Y.-C.; Hsieh, F.-I; Lien, L.-M.; Chou, Y.-L.; Chiou, H.-Y.; Chen, C.-J.

    2008-01-01

    Arsenic had been reported to be associated with carotid atherosclerosis. However, there were few studies to evaluate the association between the susceptible gene of lipid metabolism and inflammation and carotid atherosclerosis among arsenic exposure residents. The aim of the study was to investigate the associations between the genetic polymorphisms of APOE and MCP-1 and the risk of carotid atherosclerosis among residents of Lanyang Basin in Taiwan which was a newly confirmed arsenic-endemic area. In total, 479 residents who had been genotyped of these two genes and examined the severity of carotid atherosclerosis were included in this study. The study subjects with carotid intima media thickness (IMT) ≥ 1.0 mm or with the observable plaque in the extracranial carotid artery were diagnosed as carotid atherosclerosis. A significantly age- and gender-adjusted odds ratio of 2.0 for the development of carotid atherosclerosis was observed in study subjects with ε4 allele of APOE than those without ε4 allele. Compared with study subjects who carried wild genotypes of APOE and MCP-1, those with both risk genotypes of APOE and MCP-1 had 2.5-fold risk of carotid atherosclerosis after adjustment for age and gender, revealing a significant dose-response relationship between number of risk genotypes of these genes and risk of carotid atherosclerosis. Additionally, study subjects with two risk genotypes of APOE and MCP-1 and either had ingested well water contained arsenic level > 10 μg/L or had arsenic exposure > 0.22 mg/L-year would have strikingly highest risk of 10.3-fold and 15.7-fold, respectively, for the development carotid atherosclerosis, showing significant joint effect of arsenic exposure and risk genotypes of APOE and MCP-1

  4. Cell cycle and apoptosis genes in atherosclerosis

    NARCIS (Netherlands)

    Boesten, Lianne Simone Mirjam

    2006-01-01

    The work described in this thesis was aimed at identifying the role of cell cycle and apoptosis genes in atherosclerosis. Atherosclerosis is the primary cause of cardiovascular disease, a disorder occurring in the large and medium-sized arteries of the body. Although in the beginning 90s promising

  5. Regulation of T cell responses in atherosclerosis

    NARCIS (Netherlands)

    Puijvelde, Gijsbrecht Henricus Maria van

    2007-01-01

    One of the most important characteristics of atherosclerosis is the chronic inflammatory response in which T cells and NKT cells are very important. In this thesis several methods to modulate the activity of these T and NKT cells in atherosclerosis are described. The induction of regulatory T cells

  6. In-Vivo Assessment of Coronary Atherosclerosis

    NARCIS (Netherlands)

    G.A. Rodriguez-Granillo

    2006-01-01

    textabstractIntravascular ultrasound (IVUS) has emerged as a highly accurate tool for the serial assessment of the natural history of coronary atherosclerosis and to evaluate the effect of different conventional and emerging drug therapies on the progression of atherosclerosis. The

  7. Cytokines in atherosclerosis: an intricate balance

    NARCIS (Netherlands)

    Boshuizen, M.C.S.

    2016-01-01

    Atherosclerosis is the underlying pathology in the majority of clinical manifestations of cardiovascular diseases, which are nowadays the main global cause of mortality. Atherosclerosis is a lipid-driven chronic inflammatory disease of the arterial wall. This inflammatory response, with cytokines as

  8. Inflammation in renal atherosclerotic disease.

    Science.gov (United States)

    Udani, Suneel M; Dieter, Robert S

    2008-07-01

    The study of renal atherosclerotic disease has conventionally focused on the diagnosis and management of renal artery stenosis. With the increased understanding of atherosclerosis as a systemic inflammatory process, there has been increased interest in vascular biology at the microvasculature level. While different organ beds share some features, the inflammation and injury in the microvasculature of the kidney has unique elements as well. Understanding of the pathogenesis yields a better understanding of the clinical manifestations of renal atherosclerotic disease, which can be very subtle. Furthermore, identifying the molecular mechanisms responsible for the progression of kidney damage can also direct clinicians and scientists toward targeted therapies. Existing therapies used to treat atherosclerotic disease in other vascular beds may also play a role in the treatment of renal atherosclerotic disease.

  9. Calcification of intervertebral discs in children

    International Nuclear Information System (INIS)

    Hoermann, D.

    1984-01-01

    Thirteen children with intervertebral disc calcifications of the cervical, thoracal and lumbar spine have been diagnosed since 1970. Most of them were observed over a period of several years. Ten children fell ill with acute pains, but only 2 of them sufferred from a trauma. In 3 cases the features were discovered accidentally combined with malformations of vertebral bodies and congenital diseases. Our results suggest a primary structural inferiority of the calcified discs. The calcifications arise partially from a birth trauma, partially from an unknown etiology. They can last for a long time without symptoms. An acute event effects the pains due to shifting or herniation of calcified disc-fragments. Secondary findings such as decrease of the height of cervical vertebral bodies or destructions of the endplates of thoracal and lumbar vertebral bodies disappear retarded and often incompletely and demand a control for a long time. (orig.)

  10. Associations of serum LDL particle concentration with carotid intima-media thickness and coronary artery calcification.

    Science.gov (United States)

    Zaid, Maryam; Miura, Katsuyuki; Fujiyoshi, Akira; Abbott, Robert D; Hisamatsu, Takashi; Kadota, Aya; Arima, Hisatomi; Kadowaki, Sayaka; Torii, Sayuki; Miyagawa, Naoko; Suzuki, Sentaro; Takashima, Naoyuki; Ohkubo, Takayoshi; Sekikawa, Akira; Maegawa, Hiroshi; Horie, Minoru; Nakamura, Yasuyuki; Okamura, Tomonori; Ueshima, Hirotsugu

    2016-01-01

    Low-density lipoprotein particle (LDL-P) has recently been found to be a stronger predictor of cardiovascular disease (CVD) than LDL-cholesterol (LDL-C). Whether LDL-P is associated with subclinical atherosclerosis, independent of LDL-C, as well as other lipid measures has not been fully examined. We aimed to analyze LDL-P associations with measures of subclinical atherosclerosis. We examined 870 Japanese men randomly selected from Kusatsu City, Shiga, Japan, aged 40-79 years from 2006-2008, free of clinical CVD and not using lipid-lowering medication. Cross-sectional associations of lipid measures with carotid intima-media thickness (cIMT) and coronary artery calcification (CAC; >0 Agatston score) were examined. LDL-P was significantly positively associated with cIMT and maintained this association after adjustments for LDL-C and other lipid measures. Although these lipid measures were positively associated with cIMT, model adjustment for LDL-P removed any significant relationships. Higher LDL-P was associated with a significantly higher odds ratio of CAC and further adjustment for LDL-C did not affect this relationship. In contrast, the LDL-C association with CAC was no longer significant after adjustment for LDL-P. Other lipid measures attenuated associations of LDL-P with CAC. Likewise, associations of these measures with CAC were attenuated when model adjustments for LDL-P were made. In a community-based sample of Japanese men, free of clinical CVD, LDL-P was a robust marker for subclinical atherosclerosis, independent of LDL-C and other lipid measures. Associations of LDL-C and other lipid measures with either cIMT or CAC were generally not independent of LDL-P. Copyright © 2016 National Lipid Association. Published by Elsevier Inc. All rights reserved.

  11. Clinicoradiologic evaluation of styloid process calcification

    Energy Technology Data Exchange (ETDEWEB)

    Bagga, Mun Bhawni [Dept. of Oral Medicine Diagnosis and Radiology, M.N. D.A.V. Dental College and Hospital, Solan (Korea, Republic of); Kumar, C. Anand; Yeluri, Garima [Dept. of Oral Medicine Diagnosis and Radiology, KD Dental College and Hospital, Mathura (Korea, Republic of)

    2012-09-15

    This study was performed to investigate the prevalence, morphology, and calcification pattern of the elongated styloid process in the Mathura population and its relation to gender, age, and mandibular movements. The study analyzed digital panoramic radiographs of 2,706 adults. The elongated styloid process was classified with the radiographic appearance based on the morphology and calcification pattern. The limits of mandibular protrusion were evaluated for each subject. The data were analyzed by using a Student's t-test and chi-squared test with significance set at p=0.05. Bilateral elongation having an 'elongated' type styloid process with a 'partially mineralized' pattern was the most frequent type of styloid process. No correlation was found between styloid process type and calcification pattern on the one hand and gender on the other, although elongated styloid was more prevalent in older and male populations (p<0.05). Further styloid process elongation showed no effect on mandibular protrusive movement (p>0.05). Dentists should recognize the existence of morphological variation in elongated styloid process or Eagle syndrome apparent on panoramic radiographs. We found higher prevalence of elongated styloid process in the population of the Mathura region when compared with other Indian populations. The calcification of the styloid process was more common in the older age group with no correlation to gender, mandibular movement and site. 'Type I' with a 'partially calcified' styloid process was observed more frequently in the population studied.

  12. Aortic stenosis and vascular calcifications in alkaptonuria.

    Science.gov (United States)

    Hannoush, Hwaida; Introne, Wendy J; Chen, Marcus Y; Lee, Sook-Jin; O'Brien, Kevin; Suwannarat, Pim; Kayser, Michael A; Gahl, William A; Sachdev, Vandana

    2012-02-01

    Alkaptonuria is a rare metabolic disorder of tyrosine catabolism in which homogentisic acid (HGA) accumulates and is deposited throughout the spine, large joints, cardiovascular system, and various tissues throughout the body. In the cardiovascular system, pigment deposition has been described in the heart valves, endocardium, pericardium, aortic intima and coronary arteries. The prevalence of cardiovascular disease in patients with alkaptonuria varies in previous reports. We present a series of 76 consecutive adult patients with alkaptonuria who underwent transthoracic echocardiography between 2000 and 2009. A subgroup of 40 patients enrolled in a treatment study underwent non-contrast CT scans and these were assessed for vascular calcifications. Six of the 76 patients had aortic valve replacement. In the remaining 70 patients, 12 patients had aortic sclerosis and 7 patients had aortic stenosis. Unlike degenerative aortic valve disease, we found no correlation with standard cardiac risk factors. There was a modest association between the severity of aortic valve disease and joint involvement, however, we saw no correlation with urine HGA levels. Vascular calcifications were seen in the coronaries, cardiac valves, aortic root, descending aorta and iliac arteries. These findings suggest an important role for echocardiographic screening of alkaptonuria patients to detect valvular heart disease and cardiac CT to detect coronary artery calcifications. Published by Elsevier Inc.

  13. A Case of Chronic Calcific Nonalcoholic Pancreatitis

    Directory of Open Access Journals (Sweden)

    Aaron Kangas-Dick

    2016-01-01

    Full Text Available Tropical Calcific Pancreatitis (TCP is a type of chronic calcific nonalcoholic pancreatitis. Similar to nonalcoholic chronic pancreatitis, it presents in the second and third decades of life; however this type is reported mostly in the developing tropical and subtropical countries. It is associated with the formation of pancreatic calculi and a high probability of developing insulin-dependent diabetes mellitus. Epidemiologic studies have shown that these patients have an increased risk of developing pancreatic carcinoma. The etiology of TCP remains uncertain, with the current consensus suggesting genetics as well as possible toxicity from consuming large amounts of cassava, a tuber. Definite diagnosis of TCP requires younger age of onset, history of malnutrition, and presence of diabetes mellitus along with extensive pancreatic calcification and ductal calculi. When patients meet most but not all of these conditions the term Idiopathic Chronic Pancreatitis (ICP is used. This is a case of a 44-year-old man who presented with most features seen in TCP, and however, was diagnosed with ICP.

  14. Atherosclerosis

    Science.gov (United States)

    ... usually doesn't cause symptoms until it severely narrows or totally blocks an artery. Many people don't know they have it until they have a medical emergency. A physical exam, imaging, and other diagnostic tests can tell ...

  15. Visualization of atherosclerosis as detected by coronary artery calcium and carotid intima-media thickness reveals significant atherosclerosis in a cross-sectional study of psoriasis patients in a tertiary care center.

    Science.gov (United States)

    Santilli, S; Kast, D R; Grozdev, I; Cao, L; Feig, R L; Golden, J B; Debanne, S M; Gilkeson, R C; Orringer, C E; McCormick, T S; Ward, N L; Cooper, K D; Korman, N J

    2016-07-22

    Psoriasis is a chronic inflammatory disease of the skin and joints that may also have systemic inflammatory effects, including the development of cardiovascular disease (CVD). Multiple epidemiologic studies have demonstrated increased rates of CVD in psoriasis patients, although a causal link has not been established. A growing body of evidence suggests that sub-clinical systemic inflammation may develop in psoriasis patients, even from a young age. We aimed to evaluate the prevalence of atherosclerosis and identify specific clinical risk factors associated with early vascular inflammation. We conducted a cross-sectional study of a tertiary care cohort of psoriasis patients using coronary artery calcium (CAC) score and carotid intima-media thickness (CIMT) to detect atherosclerosis, along with high sensitivity C-reactive protein (hsCRP) to measure inflammation. Psoriasis patients and controls were recruited from our tertiary care dermatology clinic. Presence of atherosclerosis was defined using validated numeric values within CAC and CIMT imaging. Descriptive data comparing groups was analyzed using Welch's t test and Pearson Chi square tests. Logistic regression was used to analyze clinical factors associated with atherosclerosis, and linear regression to evaluate the relationship between psoriasis and hsCRP. 296 patients were enrolled, with 283 (207 psoriatic and 76 controls) having all data for the hsCRP and atherosclerosis analysis. Atherosclerosis was found in 67.6 % of psoriasis subjects versus 52.6 % of controls; Psoriasis patients were found to have a 2.67-fold higher odds of having atherosclerosis compared to controls [95 % CI (1.2, 5.92); p = 0.016], after adjusting for age, gender, race, BMI, smoking, HDL and hsCRP. In addition, a non-significant trend was found between HsCRP and psoriasis severity, as measured by PASI, PGA, or BSA, again after adjusting for confounders. A tertiary care cohort of psoriasis patients have a high prevalence of early

  16. Acute Calcific Tendinitis of the Index Finger in a Child.

    Science.gov (United States)

    Walocko, Frances M; Sando, Ian C; Haase, Steven C; Kozlow, Jeffrey H

    2017-09-01

    Calcific tendinitis is characterized by calcium hydroxyapatite crystal deposition within tendons and is a common cause of musculoskeletal pain in adults. Its clinical manifestations may be acute, chronic, or asymptomatic. Acute calcific tendinitis is self-resolving condition that is rarely reported in the pediatric population and may be overlooked for more common processes, leading to unnecessary treatment. A chart reivew was performed of a single case of acute calcific tendonitis of the index finger in a child. We describe a case of calcific tendinitis of the index finger in a 9-year-old boy who was referred to us for a second opinion after surgical exploration of an acutely inflamed digit was recommended based on his initial presentation. The calcifications and symptoms resolved over time without operative management. Although rare in children, acute calcific tendinitis can present similar to an infection. However, appropriate managment is non-operative as the symptoms and radiographic findings resolve over time.

  17. PPARα activation differently affects microparticle content in atherosclerotic lesions and liver of a mouse model of atherosclerosis and NASH.

    Science.gov (United States)

    Baron, Morgane; Leroyer, Aurélie S; Majd, Zouher; Lalloyer, Fanny; Vallez, Emmanuelle; Bantubungi, Kadiombo; Chinetti-Gbaguidi, Giulia; Delerive, Philippe; Boulanger, Chantal M; Staels, Bart; Tailleux, Anne

    2011-09-01

    Atherosclerosis and non-alcoholic fatty liver disease (NAFLD) are complex pathologies characterized by lipid accumulation, chronic inflammation and extensive tissue remodelling. Microparticles (MPs), small membrane vesicles produced by activated and apoptotic cells, might not only be biomarkers, but also functional actors in these pathologies. The apoE2-KI mouse is a model of atherosclerosis and NAFLD. Activation of the nuclear receptor PPARα decreases atherosclerosis and components of non-alcoholic steatohepatitis (NASH) in the apoE2-KI mouse. (1) To determine whether MPs are present in atherosclerotic lesions, liver and plasma during atherosclerosis and NASH progression in apoE2-KI mice, and (2) to study whether PPARα activation modulates MP concentrations. ApoE2-KI mice were fed a Western diet to induce atherosclerosis and NASH. MPs were isolated from atherosclerotic lesions, liver and blood and quantified by flow cytometry. An increase of MPs was observed in the atherosclerotic lesions and in the liver of apoE2-KI mice upon Western diet feeding. PPARα activation with fenofibrate decreased MP levels in the atherosclerotic lesions in a PPARα-dependent manner, but did not influence MP concentrations in the liver. Here we report that MPs are present in atherosclerotic lesions and in the liver of apoE2-KI mice. Their concentration increased during atherosclerosis and NASH development. PPARα activation differentially modulates MP levels in a tissue-specific manner. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

  18. Circulating Endothelial Microparticles: A Key Hallmark of Atherosclerosis Progression

    Directory of Open Access Journals (Sweden)

    Keshav Raj Paudel

    2016-01-01

    Full Text Available The levels of circulating microparticles (MPs are raised in various cardiovascular diseases. Their increased level in plasma is regarded as a biomarker of alteration in vascular function. The prominent MPs present in blood are endothelial microparticles (EMPs described as complex submicron (0.1 to 1.0 μm vesicles like structure, released in response to endothelium cell activation or apoptosis. EMPs possess both physiological and pathological effects and may promote oxidative stress and vascular inflammation. EMPs release is triggered by inducer like angiotensin II, lipopolysaccharide, and hydrogen peroxide leading to the progression of atherosclerosis. However, there are multiple physiological pathways for EMPs generation like NADPH oxidase derived endothelial ROS formation, Rho kinase pathway, and mitogen-activated protein kinases. Endothelial dysfunction is a key initiating event in atherosclerotic plaque formation. Atheroemboli, resulting from ruptured carotid plaques, is a major cause of stroke. Increasing evidence suggests that EMPs play an important role in the pathogenesis of cardiovascular disease, acting as a marker of damage, either exacerbating disease progression or triggering a repair response. In this regard, it has been suggested that EMPs have the potential to act as biomarkers of disease status. This review aims to provide updated information of EMPs in relation to atherosclerosis pathogenesis.

  19. Smoking and atherosclerosis: mechanisms of disease and new therapeutic approaches.

    Science.gov (United States)

    Siasos, Gerasimos; Tsigkou, Vasiliki; Kokkou, Eleni; Oikonomou, Evangelos; Vavuranakis, Manolis; Vlachopoulos, Charalambos; Verveniotis, Alexis; Limperi, Maria; Genimata, Vasiliki; Papavassiliou, Athanasios G; Stefanadis, Christodoulos; Tousoulis, Dimitris

    2014-01-01

    It has been clear that at least 1 billion adults worldwide are smokers and at least 700 million children are passive smokers at home. Smoking exerts a detrimental effect to many organ systems and is responsible for illnesses such as lung cancer, pneumonia, chronic obstructive pulmonary disease, cancer of head and neck, cancer of the urinary and gastrointestinal tract, periodontal disease, cataract and arthritis. Additionally, smoking is an important modifiable risk factor for the development of cardiovascular disease such as coronary artery disease, stable angina, acute coronary syndromes, sudden death, stroke, peripheral vascular disease, congestive heart failure, erectile dysfunction and aortic aneurysms via initiation and progression of atherosclerosis. A variety of studies has proved that cigarette smoking induces oxidative stress, vascular inflammation, platelet coagulation, vascular dysfunction and impairs serum lipid pro-file in both current and chronic smokers, active and passive smokers and results in detrimental effects on the cardiovascular system. The aim of this review is to depict the physical and biochemical properties of cigarette smoke and, furthermore, elucidate the main pathophysiological mechanisms of cigarette-induced atherosclerosis and overview the new therapeutic approaches for smoking cessation and augmentation of cardiovascular health.

  20. Association of Television Viewing Time with Body Composition and Calcified Subclinical Atherosclerosis in Singapore Chinese.

    Directory of Open Access Journals (Sweden)

    Ei Ei Khaing Nang

    Full Text Available Sedentary behavior such as television viewing may be an independent risk factor for coronary heart disease. However, few studies have assessed the impact of television viewing time on coronary artery calcification and it remains unclear how body fat contributes to this relationship. The aim of this study is to evaluate the association between television viewing time and subclinical atherosclerosis and whether effects on visceral or subcutaneous fat may mediate any associations observed.This was a cross-sectional study of 398 Chinese participants (192 men and 206 women from Singapore prospective study. Participants were free from known cardiovascular diseases and underwent interview, health screening, computed tomography scans of coronary arteries and abdomen. Spearman's correlation was used to test the correlation between television viewing time, physical activity, body composition and abdominal fat distribution. The association between television viewing time and subclinical atherosclerosis was assessed by multiple logistic regression analysis.In men, television viewing time was significantly correlated with higher body fat mass index, percent body fat, subcutaneous and visceral fat. These associations were in the same direction, but weaker and not statistically significant in women. Television viewing time (hours/day was associated with subclinical atherosclerosis in men (odds ratio: 1.41, 95% CI: 1.03-1.93 but no significant association was observed in women (odds ratio: 0.88, 95% CI: 0.59-1.31 after adjusting for potential socio-demographic and lifestyle confounders. Further adjustments for biological factors did not affect these associations.Television viewing time was associated with greater adiposity and higher subcutaneous and visceral fat in men. TV viewing time was also associated with subclinical atherosclerosis in men and the potential mechanisms underlying this association require further investigation.

  1. Association of Television Viewing Time with Body Composition and Calcified Subclinical Atherosclerosis in Singapore Chinese.

    Science.gov (United States)

    Nang, Ei Ei Khaing; van Dam, Rob M; Tan, Chuen Seng; Mueller-Riemenschneider, Falk; Lim, Yi Ting; Ong, Kai Zhi; Ee, Siqing; Lee, Jeannette; Tai, E Shyong

    2015-01-01

    Sedentary behavior such as television viewing may be an independent risk factor for coronary heart disease. However, few studies have assessed the impact of television viewing time on coronary artery calcification and it remains unclear how body fat contributes to this relationship. The aim of this study is to evaluate the association between television viewing time and subclinical atherosclerosis and whether effects on visceral or subcutaneous fat may mediate any associations observed. This was a cross-sectional study of 398 Chinese participants (192 men and 206 women) from Singapore prospective study. Participants were free from known cardiovascular diseases and underwent interview, health screening, computed tomography scans of coronary arteries and abdomen. Spearman's correlation was used to test the correlation between television viewing time, physical activity, body composition and abdominal fat distribution. The association between television viewing time and subclinical atherosclerosis was assessed by multiple logistic regression analysis. In men, television viewing time was significantly correlated with higher body fat mass index, percent body fat, subcutaneous and visceral fat. These associations were in the same direction, but weaker and not statistically significant in women. Television viewing time (hours/day) was associated with subclinical atherosclerosis in men (odds ratio: 1.41, 95% CI: 1.03-1.93) but no significant association was observed in women (odds ratio: 0.88, 95% CI: 0.59-1.31) after adjusting for potential socio-demographic and lifestyle confounders. Further adjustments for biological factors did not affect these associations. Television viewing time was associated with greater adiposity and higher subcutaneous and visceral fat in men. TV viewing time was also associated with subclinical atherosclerosis in men and the potential mechanisms underlying this association require further investigation.

  2. Idiopathic Basal Ganglia Calcification Presented with Impulse Control Disorder

    OpenAIRE

    Sahin, Cem; Levent, Mustafa; Akbaba, Gulhan; Kara, Bilge; Yeniceri, Emine Nese; Inanc, Betul Battaloglu

    2015-01-01

    Primary familial brain calcification (PFBC), also referred to as Idiopathic Basal Ganglia Calcification (IBGC) or “Fahr’s disease,” is a clinical condition characterized by symmetric and bilateral calcification of globus pallidus and also basal ganglions, cerebellar nuclei, and other deep cortical structures. It could be accompanied by parathyroid disorder and other metabolic disturbances. The clinical features are dysfunction of the calcified anatomic localization. IBGC most commonly present...

  3. MR imaging of intracranial calcification; experimental and clinical studies

    Energy Technology Data Exchange (ETDEWEB)

    Yoon, Jong Hoon; Kim, Byung Jin; Kim, Yun Hyeon; Seo, Jeong Jin; Kang, Heoung Keun; Yang, Sung Yeul [Chonnam University Medical School, Kwangju (Korea, Republic of)

    1995-05-15

    This study was performed to evaluate MR signal intensity (SI) of calcification and to assess the capability of MRI in detection of various intracranial calcifications. The MR findings and ROI value of experimental model of calcium carbonate suspension according to each concentration (20, 35, 50%) and diameter (1-10 mm) and hydroxyapatite suspension according to each concentration (10, 20, 30, 40, 50%) were analyzed. A specimen of calcification in craniopharyngioma was analyzed for its composition by XRD (X-ray diffractometer) and ICP (inductively coupled plasma) methods. MRI of 34 patients with intracranial calcifications were retrospectively analyzed for signal intensity of the calcification and its capability to detect calcifications according to size, location, and contrast with adjacent lesion. The calcium carbonate phantom with larger diameter and low concentration showed lower signal intensity on T2 than T1WI. Hydroxyapatite phantom showed high signal intensity in 10-30% concentration and low signal intensity in 40-50% concentration on T1 weighted image. The 5 cases of 34 intracranial calcifications showed high signal intensity on T1 weighted image. The capability of MRI in the detection of intracranial calcifications decreased in the circumstances such as small size (< 2.5 mm) and intraventricular location. Although the size of calcification was small, the detection was easy in the good contrast with adjacent lesion. However, the detection of the small sized calcification was easy if the contrast with adjacent lesion was good. Intracranial calcification shows generally low signal intensity on T1 and T2 weighted image with the exception of occasional high SI on T1WI. Detection of intracranial calcification in MRI is affected by its composition, size, location, and contrast with adjacent lesion.

  4. An unusual case of neonatal peritoneal calcifications associated with hydrometrocolpos

    Energy Technology Data Exchange (ETDEWEB)

    Hu, M.X.; Methratta, S. [College of Medicine and Dentistry of New Jersey - New Jersey Medical School, Newark (United States). Dept. of Radiology

    2001-10-01

    Neonatal peritoneal calcifications usually suggest a diagnosis of meconium peritonitis, but in this case, a premature baby girl, peritoneal calcifications were caused by hydrometrocolpos secondary to imperforate hymen, a rare association. The patient presented with respiratory distress and ascites and demonstrated abdominal calcifications on plain film. Other radiographic work-up revealed hydrometrocolpos without evidence of gastrointestinal tract obstruction. The patient was diagnosed and treated for imperforate hymen; she was recovered fully. (orig.)

  5. Prognostic Utility of Neutrophil-to-Lymphocyte Ratio on Adverse Clinical Outcomes in Patients with Severe Calcific Aortic Stenosis.

    Directory of Open Access Journals (Sweden)

    Kyoung Im Cho

    Full Text Available Inflammation is an important factor in the pathogenesis of calcific aortic stenosis (AS. We aimed to evaluate the association between an inflammatory marker, neutrophil-to-lymphocyte ratio (NLR and major adverse cardiovascular events (MACE in patients with severe calcific AS.A total of 336 patients with isolated severe calcific AS newly diagnosed between 2010 and 2015 were enrolled in this study. Using Cox proportional hazards (PH regression models, we investigated the prognostic value of NLR adjusted for baseline covariates including logistic European System for Cardiac Operative Risk Evaluation score (EuroSCORE-I and undergoing aortic valve replacement (AVR. We also evaluated the clinical relevance of NLR risk groups (divided into low, intermediate, high risk as categorized by NLR cutoff values. MACE was defined as a composite of all-cause mortality, cardiac death and non-fatal myocardial infarction during the follow-up period.The inflammatory marker NLR was an independent prognostic factor most significantly associated with MACE [hazard ratio (HR, 1.06; 95% confidence interval (CI, 1.04-1.09; p-value 9, respectively.The findings of the present study demonstrate the potential utility of NLR in risk stratification of patients with severe calcific AS.

  6. Genome-Wide Association Studies Candidate Gene to Dual Modifier of Nonalcoholic Steatohepatitis and Atherosclerosis

    Directory of Open Access Journals (Sweden)

    Clint L. Miller, PhD

    2016-12-01

    Full Text Available Nonalcoholic steatohepatitis is a common disease involving chronic accumulation of fat and inflammation in the liver, often leading to advanced fibrosis, cirrhosis, and cancer. It is known that nonalcoholic steatohepatitis shares many features with atherosclerosis; however, there are still no effective therapeutics. In a recent study published in Nature, investigators demonstrated that mice lacking a high-density lipoprotein–associated gene were surprisingly protected from both steatohepatitis and atherosclerosis through the stabilization of the liver X receptor. This work reveals a timely candidate target for 2 highly prevalent cardiovascular diseases.

  7. The Progression and Early detection of Subclinical Atherosclerosis (PESA) study

    DEFF Research Database (Denmark)

    Fernández-Ortiz, Antonio; Jiménez-Borreguero, L Jesús; Peñalvo, José L

    2013-01-01

    The presence of subclinical atherosclerosis is a likely predictor of cardiovascular events; however, factors associated with the early stages and progression of atherosclerosis are poorly defined.......The presence of subclinical atherosclerosis is a likely predictor of cardiovascular events; however, factors associated with the early stages and progression of atherosclerosis are poorly defined....

  8. Aging, Atherosclerosis, and IGF-1

    Science.gov (United States)

    Higashi, Yusuke; Sukhanov, Sergiy; Anwar, Asif; Shai, Shaw-Yung

    2012-01-01

    Insulin-like growth factor 1 (IGF-1) is an endocrine and autocrine/paracrine growth factor that circulates at high levels in the plasma and is expressed in most cell types. IGF-1 has major effects on development, cell growth and differentiation, and tissue repair. Recent evidence indicates that IGF-1 reduces atherosclerosis burden and improves features of atherosclerotic plaque stability in animal models. Potential mechanisms for this atheroprotective effect include IGF-1–induced reduction in oxidative stress, cell apoptosis, proinflammatory signaling, and endothelial dysfunction. Aging is associated with increased vascular oxidative stress and vascular disease, suggesting that IGF-1 may exert salutary effects on vascular aging processes. In this review, we will provide a comprehensive update on IGF-1's ability to modulate vascular oxidative stress and to limit atherogenesis and the vascular complications of aging. PMID:22491965

  9. Association of gastrocnemius tendon calcification with chondrocalcinosis of the knee

    Energy Technology Data Exchange (ETDEWEB)

    Foldes, K. [Department of Radiology, Veterans Administration Medical Center (VAMC), San Diego, CA (United States)]|[University of California San Diego Medical Center (UCSD), San Diego, CA (United States)]|[National Institute of Rheumatology and Physiotherapy, Budapest (Hungary); Lenchik, L. [Department of Radiology, Veterans Administration Medical Center (VAMC), San Diego, CA (United States)]|[University of California San Diego Medical Center (UCSD), San Diego, CA (United States); Jaovisidha, S. [Department of Radiology, Veterans Administration Medical Center (VAMC), San Diego, CA (United States)]|[University of California San Diego Medical Center (UCSD), San Diego, CA (United States); Clopton, P. [Department of Radiology, Veterans Administration Medical Center (VAMC), San Diego, CA (United States); Sartoris, D.J. [Department of Radiology, Veterans Administration Medical Center (VAMC), San Diego, CA (United States)]|[University of California San Diego Medical Center (UCSD), San Diego, CA (United States); Resnick, D. [Department of Radiology, Veterans Administration Medical Center (VAMC), San Diego, CA (United States)]|[University of California San Diego Medical Center (UCSD), San Diego, CA (United States)

    1996-10-01

    Objective. Chondrocalcinosis of the knee is a common radiological finding in the elderly. However, visualization of chondrocalcinosis may be difficult in patients with advanced cartilage loss.The purpose of this study was to determine sensitivity, specificity, and accuracy of gastrocnemius tendon calcification that might serve as a radiographic marker of chondrocalcinosis in patients with painful knees. Design and patients. We prospectively evaluated 37 knee radiographs in 30 consecutive patients (29 men, 8 women; mean age 67 years, age range 37-90 years) with painful knees who had radiographic evidence of chondrocalcinosis. The frequency of fibrocartilage, hyaline cartilage, and gastrocnemius tendon calcification was determined. For a control group, we evaluated knee radiographs in 65 consecutive patients with knee pain (54 men, 11 women; mean age 59 years, age range 40-93 years) who had no radiological signs of chondrocalcinosis. The frequency of gastrocnemius tendon calcification in the control group was determined. Results. Gastrocnemius tendon calcification was 41% sensitive, 100% specific, and 78% accurate in predicting chondrocalcinosis. The gastrocnemius tendon was calcified on 15 of 37 (41%) radiographs in the experimental group and on 0 of 67 radiographs in the control group. In the chondrocalcinosis group, 23 (62%) had posterior hyaline cartilage calcification, 14 (38%) had anterior hyaline cartilage calcification, 31 (84%) had medial meniscus calcification, and 36 (97%) had lateral meniscus calcification. Conclusions. Our results show that gastrocnemius tendon calcification is an accurate radiographic marker of chondrocalcinosis in patients with knee pain. (orig.). With 2 figs., 2 tabs.

  10. Association of gastrocnemius tendon calcification with chondrocalcinosis of the knee

    International Nuclear Information System (INIS)

    Foldes, K.; Lenchik, L.; Jaovisidha, S.; Clopton, P.; Sartoris, D.J.; Resnick, D.

    1996-01-01

    Objective. Chondrocalcinosis of the knee is a common radiological finding in the elderly. However, visualization of chondrocalcinosis may be difficult in patients with advanced cartilage loss.The purpose of this study was to determine sensitivity, specificity, and accuracy of gastrocnemius tendon calcification that might serve as a radiographic marker of chondrocalcinosis in patients with painful knees. Design and patients. We prospectively evaluated 37 knee radiographs in 30 consecutive patients (29 men, 8 women; mean age 67 years, age range 37-90 years) with painful knees who had radiographic evidence of chondrocalcinosis. The frequency of fibrocartilage, hyaline cartilage, and gastrocnemius tendon calcification was determined. For a control group, we evaluated knee radiographs in 65 consecutive patients with knee pain (54 men, 11 women; mean age 59 years, age range 40-93 years) who had no radiological signs of chondrocalcinosis. The frequency of gastrocnemius tendon calcification in the control group was determined. Results. Gastrocnemius tendon calcification was 41% sensitive, 100% specific, and 78% accurate in predicting chondrocalcinosis. The gastrocnemius tendon was calcified on 15 of 37 (41%) radiographs in the experimental group and on 0 of 67 radiographs in the control group. In the chondrocalcinosis group, 23 (62%) had posterior hyaline cartilage calcification, 14 (38%) had anterior hyaline cartilage calcification, 31 (84%) had medial meniscus calcification, and 36 (97%) had lateral meniscus calcification. Conclusions. Our results show that gastrocnemius tendon calcification is an accurate radiographic marker of chondrocalcinosis in patients with knee pain. (orig.). With 2 figs., 2 tabs

  11. Chronic parotitis with multiple calcifications: Clinical and sialendoscopic findings.

    Science.gov (United States)

    Jáuregui, Emmanuel; Kiringoda, Ruwan; Ryan, William R; Eisele, David W; Chang, Jolie L

    2017-07-01

    To characterize clinical, imaging, and sialendoscopy findings in patients with chronic parotitis and multiple parotid calcifications. Retrospective review. Clinical history, radiographic images and reports, lab tests, and operative reports were reviewed for adult patients with chronic parotitis and multiple parotid calcifications who underwent parotid sialendoscopy. Thirteen of 133 (10%) patients undergoing parotid sialendoscopy for chronic sialadenitis had more than one calcification in the region of the parotid gland. Seven patients (54%) were diagnosed with immune-mediated disease from autoimmune parotitis (positive Sjögren's antibodies or antinuclear antibodies) or human immunodeficiency virus (HIV) disease. The six patients (46%) who did not have an immune-mediated disorder had most calcifications located anterior or along the masseter muscle. Eight of 13 patients (61%) had at least one calculus found in the parotid duct on sialendoscopy. Four patients (38%) had multiple punctate calcifications within the parotid gland, all of whom had either autoimmune parotitis or HIV. None of the proximal or punctate parotid calcifications posterior to the masseter were visualized on sialendoscopy. Chronic parotitis in conjunction with multiple parotid calcifications is uncommon and was identified in 10% of our cohort. We contrast two classifications of parotid calcifications: 1) intraductal stones that cause recurrent duct obstruction and are often located within the main parotid duct along or anterior to the masseter and 2) punctate intraparenchymal parotid gland calcifications that are not visualized on sialendoscopy and may represent underlying inflammatory disease. 4 Laryngoscope, 127:1565-1570, 2017. © 2016 The American Laryngological, Rhinological and Otological Society, Inc.

  12. Inhibitory role of Notch1 in calcific aortic valve disease.

    Directory of Open Access Journals (Sweden)

    Asha Acharya

    Full Text Available Aortic valve calcification is the most common form of valvular heart disease, but the mechanisms of calcific aortic valve disease (CAVD are unknown. NOTCH1 mutations are associated with aortic valve malformations and adult-onset calcification in families with inherited disease. The Notch signaling pathway is critical for multiple cell differentiation processes, but its role in the development of CAVD is not well understood. The aim of this study was to investigate the molecular changes that occur with inhibition of Notch signaling in the aortic valve. Notch signaling pathway members are expressed in adult aortic valve cusps, and examination of diseased human aortic valves revealed decreased expression of NOTCH1 in areas of calcium deposition. To identify downstream mediators of Notch1, we examined gene expression changes that occur with chemical inhibition of Notch signaling in rat aortic valve interstitial cells (AVICs. We found significant downregulation of Sox9 along with several cartilage-specific genes that were direct targets of the transcription factor, Sox9. Loss of Sox9 expression has been published to be associated with aortic valve calcification. Utilizing an in vitro porcine aortic valve calcification model system, inhibition of Notch activity resulted in accelerated calcification while stimulation of Notch signaling attenuated the calcific process. Finally, the addition of Sox9 was able to prevent the calcification of porcine AVICs that occurs with Notch inhibition. In conclusion, loss of Notch signaling contributes to aortic valve calcification via a Sox9-dependent mechanism.

  13. The roentgenographic study of placental calcifications in Korean pregnant

    International Nuclear Information System (INIS)

    Cho, Chung Che

    1980-01-01

    Calcifications in the placenta have been considered as a sign of the maturity because it is found frequently in variable degrees in full-term placentas. The placentas studied were those from deliveries at Chung-Ang University Hospital during the period of January 1978 to June 1980 and were excluded if their deliveries were by Caesarean section. Roentgenographic studies of placenta were performed postnatally in 135 cases delivered from normal pregnant. The results were as follows: 1. The incidence of calcification in the placenta was 53.3%. 2. The tendency of placenta calcification was increased as progress of maturity but not indicated as postmaturity. 3. Calcifications were less correlated with increasing gravidity or maternal age. 4. Calcifications occurred more frequently with increasing birth weight. 5. Calcifications in placentas were more frequently in the neonates with 10 scores of Apgar and normal level of maternal hemoglobin. 6. No significant correlation between incidence of calcification and maternal toxemia was observed. In the pregnant with an episode of previous abortion or S. P. R. M., incidence of calcification was apparently increased but statistically not significant. On the whole, placental calcifications are not harmful and identified as normal or proper aging process

  14. Stent-assisted angioplasty for intracranial atherosclerosis

    International Nuclear Information System (INIS)

    Nakahara, Toshinori; Sakamoto, Shigeyuki; Hamasaki, Osamu; Sakoda, Katsuaki

    2002-01-01

    We report on two patients with intracranial atherosclerosis of the carotid artery or vertebral artery treated with stent-assisted angioplasty. Both patients have severe intracranial atherosclerosis (>70%) with refractory symptoms despite optimal medical treatment. In both patients, a coronary balloon-expandable stent was successfully placed using a protective balloon technique without procedural complications. The patients were asymptomatic and neurologically intact at a mean clinical follow-up of 13 months. Follow-up angiograms did not show restenosis 3 or 4 months after procedure, respectively. Stent-assisted angioplasty for intracranial atherosclerosis in the elective patient has proven effective, with an acceptable low rate of morbidity and mortality. (orig.)

  15. Magnesium intake is inversely associated with coronary artery calcification: the Framingham Heart Study

    Science.gov (United States)

    OBJECTIVES: The aim of this study was to examine whether magnesium intake is associated with coronary artery calcification (CAC) and abdominal aortic calcification (AAC). BACKGROUND: Animal and cell studies suggest that magnesium may prevent calcification within atherosclerotic plaques underlying c...

  16. The time of onset of abnormal calcification in spondylometaepiphyseal dysplasia, short limb-abnormal calcification type

    Energy Technology Data Exchange (ETDEWEB)

    Tueysuez, Beyhan [Istanbul University, Department of Pediatric Genetics, Cerrahpasa Medical School, Istanbul (Turkey); Gazioglu, Nurperi [Istanbul University, Department of Neurosurgery, Cerrahpasa Medical School, Istanbul (Turkey); Uenguer, Savas [Istanbul University, Department of Pediatric Radiology, Cerrahpasa Medical School, Istanbul (Turkey); Aji, Dolly Yafet [Istanbul University, Department of Pediatrics, Cerrahpasa Medical School, Istanbul (Turkey); Tuerkmen, Seval [Istanbul University, Department of Pediatric Genetics, Cerrahpasa Medical School, Istanbul (Turkey); Universitatsklinikum Berlin, Charite Virchow-Klinik, Berlin (Germany)

    2009-01-15

    A 1-month-old boy with shortness of extremities on prenatal US was referred to our department with a provisional diagnosis of achondroplasia. His height was normal but he had short extremities and platyspondyly, premature carpal epiphyses on both hands, and short tubular bones with irregular metaphyses on radiographs. Re-evaluation of the patient at the age of 1 year revealed very short height and premature calcification of the costal cartilages and epiphyses. Spondylometaepiphyseal dysplasia (SMED), short limb-abnormal calcification type was diagnosed. This condition is a very rare autosomal recessively inherited disorder, and most of the patients die in early childhood due to neurological involvement. At the age of 2 years and 5 months, a CT scan showed narrowing of the cervical spinal canal. One month later he died suddenly because of spinal cord injury. In conclusion early diagnosis is very important because the recurrence risk is high and patients may die due to early neurological complications. The time of onset of abnormal calcifications, a diagnostic finding of the disease, is at the age of around 1 year in most patients. When abnormal calcifications are not yet present, but radiological changes associated with SMED are present, this rare disease must be considered. (orig.)

  17. The time of onset of abnormal calcification in spondylometaepiphyseal dysplasia, short limb-abnormal calcification type

    International Nuclear Information System (INIS)

    Tueysuez, Beyhan; Gazioglu, Nurperi; Uenguer, Savas; Aji, Dolly Yafet; Tuerkmen, Seval

    2009-01-01

    A 1-month-old boy with shortness of extremities on prenatal US was referred to our department with a provisional diagnosis of achondroplasia. His height was normal but he had short extremities and platyspondyly, premature carpal epiphyses on both hands, and short tubular bones with irregular metaphyses on radiographs. Re-evaluation of the patient at the age of 1 year revealed very short height and premature calcification of the costal cartilages and epiphyses. Spondylometaepiphyseal dysplasia (SMED), short limb-abnormal calcification type was diagnosed. This condition is a very rare autosomal recessively inherited disorder, and most of the patients die in early childhood due to neurological involvement. At the age of 2 years and 5 months, a CT scan showed narrowing of the cervical spinal canal. One month later he died suddenly because of spinal cord injury. In conclusion early diagnosis is very important because the recurrence risk is high and patients may die due to early neurological complications. The time of onset of abnormal calcifications, a diagnostic finding of the disease, is at the age of around 1 year in most patients. When abnormal calcifications are not yet present, but radiological changes associated with SMED are present, this rare disease must be considered. (orig.)

  18. Premature Calcifications of Costal Cartilages: A New Perspective Premature Calcifications of Costal Cartilages: A New Perspective

    International Nuclear Information System (INIS)

    Rhomberg, W.; Schuster, A.

    2014-01-01

    Calcifications of the costal cartilages occur, as a rule, not until the age of 30 years. The knowledge of the clinical significance of early and extensive calcifications is still incomplete. Materials and Methods. A search was made to find patients below the age of 30 years who showed distinct calcifications of their lower costal cartilages by viewing 360 random samples of intravenous pyelograms and abdominal plain films. The histories, and clinical and laboratory findings of these patients were analyzed. Results. Nineteen patients fulfilled the criteria of premature calcifications of costal cartilages (CCCs). The patients had in common that they were frequently referred to a hospital and were treated by several medical disciplines. Nevertheless many complaints of the patients remained unsolved. Premature CCCs were often associated with rare endocrine disorders, inborn errors of metabolism, and abnormal hematologic findings. Among the metabolic disorders there were 2 proven porphyrias and 7 patients with a suspected porphyria but with inconclusive laboratory findings. Conclusion. Premature CCCs are unlikely to be a normal variant in skeletal radiology. The findings in this small group of patients call for more intensive studies, especially in regard to the putative role of a porphyria

  19. The Relation between Calcium Supplement Consumption and Calcific Shoulder Tendonitis

    Directory of Open Access Journals (Sweden)

    Alireza Rouhani

    2015-10-01

    Full Text Available Background: Calcific tendonitis is a common cause of non-traumatic shoulder pain. Previous studies have suggested a relation between minerals and endocrine and calcium deposition. Thus, hypercalcemia is probably related to calcific tendonitis. This study aims at evaluating the relation found between calcium supplement consumption and calcific shoulder tendonitis. Methods: This analytical-descriptive study was conducted on 250 patients with shoulder pain referring to clinics and emergency department of Shohada Orthopedics Hospital during one year for considering calcific shoulder tendonitis and calcium supplement consumption. Patients with calcific tendonitis were treated and their functional ability was evaluated using DASH questionnaire, pain severity and range of motion (ROM before and after treatment and their correlation with calcium supplement consumption. Results: Calcific tendonitis and calcium consumption were generally seen in 30 (12% and 73 (29.2% cases, respectively. Calcium consumption frequency in patients with calcific tendonitis was significantly higher than the patients who did not consume calcium supplements (76.7% vs. 22.7%. Patients with calcific tendonitis who did not consume calcium supplements suffered from significantly longer periods of shoulder pain. All patients having consumed calcium supplement were female. The group who consumed calcium supplement had significantly severe pain and higher DASH score before and after treatment, while there was no significant difference in number of impaired ROM before and after treatment. Also, there was a negative correlation between calcium supplement consumption, pain severity and DASH score before and after treatment. Conclusion: Calcium supplement consumption is related to calcific tendonitis and is also accompanied with more pain and lower functional ability in patients with calcific tendonitis.    Keywords: Calcific tendonitis; Shoulder; Calcium supplement; Pain

  20. Mouse models for atherosclerosis and pharmaceutical modifiers

    NARCIS (Netherlands)

    Zadelaar, A.S.M.; Kleemann, R.; Verschuren, L.; Vries-van der Weij, J. de; Hoorn, J. van der; Princen, H.M.; Kooistra, T.

    2007-01-01

    Atherosclerosis is a multifactorial highly-complex disease with numerous etiologies that work synergistically to promote lesion development. The ability to develop preventive and ameliorative treatments will depend on animal models that mimic the human subject metabolically and pathophysiologically

  1. A review of Chlamydia pneumoniae and atherosclerosis

    DEFF Research Database (Denmark)

    Lindholt, Jes Sanddal; Fasting, H; Henneberg, E W

    1999-01-01

    Chlamydia pneumoniae is a Gram-negative obligate intracellular bacterium that causes acute upper and lower respiratory infections. Its distribution is worldwide. Seroepidemiological studies have shown an association between C. pneumoniae and atherosclerosis, and the risk of acute myocardial...

  2. Gender-Related Differences in Atherosclerosis

    Czech Academy of Sciences Publication Activity Database

    Mathur, P.; Ošťádal, Bohuslav; Romeo, F.; Mehta, J. L.

    2015-01-01

    Roč. 29, č. 4 (2015), s. 319-327 ISSN 0920-3206 Institutional support: RVO:67985823 Keywords : atherosclerosis * gender Subject RIV: FA - Cardiovascular Diseases incl. Cardiotharic Surgery Impact factor: 3.189, year: 2015

  3. Vitamin K: from coagulation to calcification.

    Science.gov (United States)

    Paakkari, Ilari

    Vitamin K is not only essential for the synthesis of coagulation factors in the liver, but it also strengthens the bones and prevents calcification of the arteries. These effects are mediated through the same mechanism, i.e. carboxylation of Gla target proteins. The discovery of novel Gla proteins that are not associated with blood coagulation or calcium metabolism indicates that vitamin K has additional effects in the pancreas and the central nervous system, for example. As dietary supplements, vitamin K1 of plant origin and vitamins K2 of bacterial origin may exert different effects.

  4. Pulmonary metastatic calcification: a case report

    Energy Technology Data Exchange (ETDEWEB)

    Bozi, Lilian Christine Franchiotti [Radiology, Hospital Universitario Antonio Pedro (HUAP), Niteroi, RJ (Brazil); Melo, Alessandro Severo Alves de; Marchiori, Edson, E-mail: edmarchiori@gmail.com [Department of Radiology, School of Medicine, Universidade Federal Fluminense (UFF), Niteroi, RJ (Brazil)

    2012-09-15

    The present report describes the case of a 48-year-old female patient suffering from chronic renal failure on dialysis for 13 years. She presented with hemoptysis, fever, productive cough and dyspnoea. Chest radiography showed predominance of ill-defined opacities in the middle and lower lung fields, bilaterally. Chest computed tomography showed ground glass opacities associated with poorly defined centrilobular nodules with ground-glass attenuation. The patient was submitted to bronchoalveolar lavage that was negative for mycobacteria and fungi. On the basis of such findings, open lung biopsy was performed, which revealed metastatic pulmonary calcification. (author)

  5. Physical water treatment against calcification and rust

    International Nuclear Information System (INIS)

    Burger, A.

    1995-01-01

    In contrast to Germany, where the installation of small-sized, decentralised plants is still prefered, water supply companies in countries such as Denmark have already for some time successfully been using physical water treatment systems. Although the health and environmental benefits of this non-chemical method of water treatment are undisputed and its proper application is also economically beneficial, there is still a widerspread lack of information as to where such plants can be used. Consequently, older methods are often resorted to combatting calcification and rust. (orig.) [de

  6. Obstructive sleep apnea and inflammation.

    LENUS (Irish Health Repository)

    McNicholas, Walter T

    2012-02-01

    The pathogenesis of cardiovascular complications in obstructive sleep apnea syndrome (OSAS) is not fully understood but is likely multifactorial in origin. Inflammatory processes play an important role in the pathogenesis of atherosclerosis, and circulating levels of several markers of inflammation have been associated with future cardiovascular risk. These include cell adhesion molecules such as intercellular adhesion molecule-1 and selectins, cytokines such as tumour necrosis factor alpha and interleukin 6, chemokines such as interleukin 8, and C-reactive protein. There is also increasing evidence that inflammatory processes play an important role in the cardiovascular pathophysiology of OSAS and many of the inflammatory markers associated with cardiovascular risk have been reported as elevated in patients with OSAS. Furthermore, animal and cell culture studies have demonstrated preferential activation of inflammatory pathways by intermittent hypoxia, which is an integral feature of OSAS. The precise role of inflammation in the development of cardiovascular disease in OSAS requires further study, particularly the relationship with oxidative stress, metabolic dysfunction, and obesity.

  7. Pulp Stone, Haemodialysis, End-stage Renal Disease, Carotid Atherosclerosis

    OpenAIRE

    Patil, Santosh; Sinha, Nidhi

    2013-01-01

    Objectives: The aim of this study was to determine the relationship between the presence of pulp calcification and carotid artery calcification on the dental panoramic radiographs in End Stage Renal Disease (ESRD) patients who were on haemodialysis.

  8. Self-reported Sleep Duration and Subclinical Atherosclerosis in a General Population of Japanese Men

    Science.gov (United States)

    Suzuki, Sentaro; Arima, Hisatomi; Miyazaki, Soichiro; Fujiyoshi, Akira; Kadota, Aya; Takashima, Naoyuki; Hisamatsu, Takashi; Kadowaki, Sayaka; Zaid, Maryam; Torii, Sayuki; Horie, Minoru; Murata, Kiyoshi; Miura, Katsuyuki; Ueshima, Hirotsugu

    2018-01-01

    Aim: There are few data regarding associations between sleep duration and subclinical atherosclerosis in Japan. The aim of this study was to evaluate associations of self-reported sleep duration with calcification in the coronary arteries (CAC) and carotid intima media thickness (IMT) in Japanese men. Methods: This was a cross-sectional survey of 1093 randomly selected men from Kusatsu City, Japan. Average sleep duration on weekdays was estimated through questionnaire; CAC by computed tomography; and carotid IMT by ultrasonography. Results: The prevalence of CAC was 50.0% for participants with sleep duration 0.1). Conclusion: Self-reported sleep duration was not associated with increased CAC or carotid IMT in a general population of Japanese men. PMID:28747590

  9. NMR imaging of human atherosclerosis; Role de l`IRM dans le diagnostic d`atherosclerose

    Energy Technology Data Exchange (ETDEWEB)

    Toussaint, J.F. [Massachusetts General Hospital, Boston, MA (United States)]|[Hopital Cochin, 75 - Paris (France)

    1995-12-31

    Diagnosis and prognosis of atherosclerosis can no longer be evaluated with morphological parameters only. A description of atherosclerotic plaque composition is necessary to study the mechanisms of plaque rupture, which depends on collagenous cap and lipid core thicknesses. NMR, as a biochemical imaging technique, allows visualization of these components using T1 contrast (mobile lipids), T2 contrast (cap vs. core), spin density (calcifications), diffusion imaging, 1H and 13C spectroscopy. Today, these imaging sequences allow to study in vitro the effects of interventional techniques such as angioplasty or atherectomy. Clinical investigations begin, which will attempt to develop in vivo microscopy and test the ability of NMR to predict plaque rupture. (author). 13 refs., 7 figs.

  10. Coronary artery calcification correlates with the presence and severity of valve calcification.

    Science.gov (United States)

    Koulaouzidis, G; Nicoll, R; MacArthur, T; Jenkins, P J; Henein, M Y

    2013-10-15

    To investigate the prevalence of coronary artery calcification (CAC) in symptomatic individuals with CT evidence for left heart valve calcification, aortic valve (AVC), mitral valve (MAC) or both. This is a retrospective study of 282 consecutive patients with calcification in either the aortic valve or mitral annulus. Calcium scoring of the coronary artery, aortic and mitral valve was measured using the Agatston score. AVC was more prevalent than MAC (64% vs. 2.5%, p AVC + CAC were observed in 53.5%, MAC and CAC in 2.1%, and combined AVC, MAC and CAC in 31.6%. The median CAC score was higher in individuals with combined AVC+MAC, followed by those with AVC and lowest was in the MAC group. The majority (40%) of individuals with AVC had CAC score >400, and only in 16% had CAC = 0. The same pattern was more evident in individuals with AVC + MAC, where 70% had CAC score >400 and only 6% had CAC score of 0. These results were irrespective of gender. There was no correlation between AVC and MAC but there was modest correlation between CAC score and AVC score (r = 0.28, p = 0.0001), MAC (r = 0.36, p = 0.0001) and with combined AVC + MAC (r = 0.5, p = 0.0001). AVC score of 262 had a sensitivity of 78% and specificity of 92% for the prediction of presence of CAC. The presence and extent of calcification in the aortic valve or/and mitral valves are associated with severe coronary artery calcification. © 2013.

  11. The cathelicidin protein CRAMP is a potential atherosclerosis self-antigen in ApoE(-/- mice.

    Directory of Open Access Journals (Sweden)

    Peter M Mihailovic

    Full Text Available Auto-immunity is believed to contribute to inflammation in atherosclerosis. The antimicrobial peptide LL-37, a fragment of the cathelicidin protein precursor hCAP18, was previously identified as an autoantigen in psoriasis. Given the reported link between psoriasis and coronary artery disease, the biological relevance of the autoantigen to atherosclerosis was tested in vitro using a truncated (t form of the mouse homolog of hCAP18, CRAMP, on splenocytes from athero-prone ApoE(-/- mice. Stimulation with tCRAMP resulted in increased CD8+ T cells with Central Memory and Effector Memory phenotypes in ApoE(-/- mice, differentially activated by feeding with normal chow or high fat diet. Immunization of ApoE(-/- with different doses of the shortened peptide (Cramp resulted in differential outcomes with a lower dose reducing atherosclerosis whereas a higher dose exacerbating the disease with increased neutrophil infiltration of the atherosclerotic plaques. Low dose Cramp immunization also resulted in increased splenic CD8+ T cell degranulation and reduced CD11b+CD11c+ conventional dendritic cells (cDCs, whereas high dose increased CD11b+CD11c+ cDCs. Our results identified CRAMP, the mouse homolog of hCAP-18, as a potential self-antigen involved in the immune response to atherosclerosis in the ApoE(-/- mouse model.

  12. Functional blockage of EMMPRIN ameliorates atherosclerosis in apolipoprotein E-deficient mice.

    Science.gov (United States)

    Liu, Hong; Yang, Li-xia; Guo, Rui-wei; Zhu, Guo-Fu; Shi, Yan-Kun; Wang, Xian-mei; Qi, Feng; Guo, Chuan-ming; Ye, Jin-shan; Yang, Zhi-hua; Liang, Xing

    2013-10-09

    Extracellular matrix metalloproteinase inducer (EMMPRIN), a 58-kDa cell surface glycoprotein, has been identified as a key receptor for transmitting cellular signals mediating metalloproteinase activities, as well as inflammation and oxidative stress. Clinical evidence has revealed that EMMPRIN is expressed in human atherosclerotic plaque; however, the relationship between EMMPRIN and atherosclerosis is unclear. To evaluate the functional role of EMMPRIN in atherosclerosis, we treated apolipoprotein E-deficient (ApoE(-/-)) mice with an EMMPRIN function-blocking antibody. EMMPRIN was found to be up-regulated in ApoE(-/-) mice fed a 12-week high-fat diet in contrast to 12 weeks of normal diet. Administration of a function-blocking EMMPRIN antibody (100 μg, twice per week for 4 weeks) to ApoE(-/-) mice, starting after 12 weeks of high-fat diet feeding caused attenuated and more stable atherosclerotic lesions, less reactive oxygen stress generation on plaque, as well as down-regulation of circulating interleukin-6 and monocyte chemotactic protein-1 in ApoE(-/-) mice. The benefit of EMMPRIN functional blockage was associated with reduced metalloproteinases proteolytic activity, which delayed the circulating monocyte transmigrating into atherosclerotic lesions. EMMPRIN antibody intervention ameliorated atherosclerosis in ApoE(-/-) mice by the down-regulation of metalloproteinase activity, suggesting that EMMPRIN may be a viable therapeutic target in atherosclerosis. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

  13. Polyphenols and Oxidative Stress in Atherosclerosis-Related Ischemic Heart Disease and Stroke

    Directory of Open Access Journals (Sweden)

    Yu-Chen Cheng

    2017-01-01

    Full Text Available Good nutrition could maintain health and life. Polyphenols are common nutrient mainly derived from fruits, vegetables, tea, coffee, cocoa, mushrooms, beverages, and traditional medicinal herbs. They are potential substances against oxidative-related diseases, for example, cardiovascular disease, specifically, atherosclerosis-related ischemic heart disease and stroke, which are health and economic problems recognized worldwide. In this study, we reviewed the risk factors for atherosclerosis, including hypertension, diabetes mellitus, hyperlipidemia, obesity, and cigarette smoking as well as the antioxidative activity of polyphenols, which could prevent the pathology of atherosclerosis, including endothelial dysfunction, low-density lipoprotein oxidation, vascular smooth muscle cell proliferation, inflammatory process by monocytes, macrophages or T lymphocytes, and platelet aggregation. The strong radical-scavenging properties of polyphenols would exhibit antioxidative and anti-inflammation effects. Polyphenols reduce ROS production by inhibiting oxidases, reducing the production of superoxide, inhibiting OxLDL formation, suppressing VSMC proliferation and migration, reducing platelet aggregation, and improving mitochondrial oxidative stress. Polyphenol consumption also inhibits the development of hypertension, diabetes mellitus, hyperlipidemia, and obesity. Despite the numerous in vivo and in vitro studies, more advanced clinical trials are necessary to confirm the efficacy of polyphenols in the treatment of atherosclerosis-related vascular diseases.

  14. The role of oxidative stress and NADPH oxidase in the pathogenesis of atherosclerosis

    Directory of Open Access Journals (Sweden)

    Dorota Bryk

    2017-01-01

    Full Text Available Reactive oxygen species (ROS play a key role in the pathogenesis of atherosclerosis. The main mechanisms which are involved are low-density lipoprotein oxidative modification, inactivation of nitric oxide and modulation of redox-sensitive signaling pathways. ROS contribute to several aspects of atherosclerosis including endothelial cell dysfunction, monocyte/macrophage recruitment and activation, stimulation of inflammation, and inducing smooth muscle cell migration and proliferation. NADPH oxidase is the main source of ROS in the vasculature. This enzyme consists of a membrane-bound heterodimer of gp91phox and p22phox, cytosolic regulatory subunits p47phox, p67phox and p40phox, and small GTP-binding proteins rac1 and rac 2. Seven distinct isoforms of this enzyme have been identified, of which four (NOX1, 2, 4 and 5 may have cardiovascular function. In this paper, we review the current state of knowledge concerning the role of oxidative stress and NOX enzymes in pathogenesis of atherosclerosis. Moreover, we analyze the experimental studies that explore the relationship between the NOX family and atherosclerosis.

  15. Periodontitis-activated monocytes/macrophages cause aortic inflammation

    Science.gov (United States)

    Miyajima, Shin-ichi; Naruse, Keiko; Kobayashi, Yasuko; Nakamura, Nobuhisa; Nishikawa, Toru; Adachi, Kei; Suzuki, Yuki; Kikuchi, Takeshi; Mitani, Akio; Mizutani, Makoto; Ohno, Norikazu; Noguchi, Toshihide; Matsubara, Tatsuaki

    2014-01-01

    A relationship between periodontal disease and atherosclerosis has been suggested by epidemiological studies. Ligature-induced experimental periodontitis is an adequate model for clinical periodontitis, which starts from plaque accumulation, followed by inflammation in the periodontal tissue. Here we have demonstrated using a ligature-induced periodontitis model that periodontitis activates monocytes/macrophages, which subsequently circulate in the blood and adhere to vascular endothelial cells without altering the serum TNF-α concentration. Adherent monocytes/macrophages induced NF-κB activation and VCAM-1 expression in the endothelium and increased the expression of the TNF-α signaling cascade in the aorta. Peripheral blood-derived mononuclear cells from rats with experimental periodontitis showed enhanced adhesion and increased NF-κB/VCAM-1 in cultured vascular endothelial cells. Our results suggest that periodontitis triggers the initial pathogenesis of atherosclerosis, inflammation of the vasculature, through activating monocytes/macrophages. PMID:24893991

  16. Liposarcoma of the thigh with mixed calcification and ossification

    Directory of Open Access Journals (Sweden)

    Jeremy R. Child, MD

    2016-09-01

    Full Text Available Liposarcoma is one of the most common soft-tissue sarcomas. Calcification and ossification can occur in liposarcoma; however, the presence of both ossification and calcification is a very rare entity. We present a case of a partially calcified and ossified dedifferentiated liposarcoma of the thigh in a 76-year-old woman, which contained heterologous elements of chondrosarcoma and rhabdomyosarcoma.

  17. Dracunculus medinensis (Guinea worm disease): a rare cause of calcification

    Energy Technology Data Exchange (ETDEWEB)

    Gospos, C.

    1980-01-01

    Tangled whorly calcifications were seen in the abdominal subcutaneous tissues of a negro patient from Africa. The differential diagnosis of such calcifications - rarely observed in Europe - includes a variety of parasites. In this patient, Dracunculus medinensis (guinea worm disease) was the cause.

  18. Cardiovascular calcifications in chronic kidney disease: Potential therapeutic implications

    Directory of Open Access Journals (Sweden)

    Jordi Bover

    2016-11-01

    Full Text Available Cardiovascular (CV calcification is a highly prevalent condition at all stages of chronic kidney disease (CKD and is directly associated with increased CV and global morbidity and mortality. In the first part of this review, we have shown that CV calcifications represent an important part of the CKD–MBD complex and are a superior predictor of clinical outcomes in our patients. However, it is also necessary to demonstrate that CV calcification is a modifiable risk factor including the possibility of decreasing (or at least not aggravating its progression with iatrogenic manoeuvres. Although, strictly speaking, only circumstantial evidence is available, it is known that certain drugs may modify the progression of CV calcifications, even though a direct causal link with improved survival has not been demonstrated. For example, non-calcium-based phosphate binders demonstrated the ability to attenuate the progression of CV calcification compared with the liberal use of calcium-based phosphate binders in several randomised clinical trials. Moreover, although only in experimental conditions, selective activators of the vitamin D receptor seem to have a wider therapeutic margin against CV calcification. Finally, calcimimetics seem to attenuate the progression of CV calcification in dialysis patients. While new therapeutic strategies are being developed (i.e. vitamin K, SNF472, etc., we suggest that the evaluation of CV calcifications could be a diagnostic tool used by nephrologists to personalise their therapeutic decisions.

  19. A comparative study of the identification of rotator cuff calcifications ...

    African Journals Online (AJOL)

    A deposit of calcium in the rotator cuff tendons, also known as calcifying tendinopathy, is a common condition. Calcifications are often associated with significant pain and restriction of shoulder movement. The hypothesis of this retrospective, descriptive study is that ultrasound is more sensitive to detect calcifications in the ...

  20. Acute calcific tendinitis of the finger--a case report.

    LENUS (Irish Health Repository)

    Ali, S N

    2004-07-01

    Acute calcific tendinitis of the hand is rare and often misdiagnosed as infection, fracture or periarthritis. It frequently occurs in peri-menopausal women and is caused by deposits of hydroxyapatite crystals. We describe acute calcific tendinitis of the flexor digitorum superficialis insertion in an elderly man taking oral anticoagulants. The differential diagnoses and recommended treatment are discussed.

  1. [Endomyocardial fibrosis with massive calcification of the left ventricle].

    Science.gov (United States)

    Trigo, Joana; Camacho, Ana; Gago, Paula; Candeias, Rui; Santos, Walter; Marques, Nuno; Matos, Pedro; Brandão, Victor; Gomes, Veloso

    2010-03-01

    Endomyocardial fibrosis is a rare disease, endemic in tropical countries. It is characterized by fibrosis of the endocardium that can extend to myocardium. Important calcification of the endocardium is rare with only a few cases reported in the literature. We report a case of endomyocardial fibrosis in a european caucasian patient, associated with massive calcification of left ventricle.

  2. Calcification within the lesion of an old cerebral infarction

    International Nuclear Information System (INIS)

    Hanyu, Haruo; Hagiwara, Akiyoshi; Yamaguchi, Katsuhiko; Imamura, Toshiharu; Iwamoto, Toshihiko; Katsunuma, Hideyo

    1987-01-01

    We described a 68-year-old woman with marked calcification in the lesion of an old cerebral infarction. Calcified deposits in an old infarcted area of the left middle cerebral artery were demonstrated by CT 9 months after she had suffered a stroke, probably because of an embolism. There have been few reports of calcification associated with cerebral infarction. (author)

  3. Lutein and atherosclerosis: Belfast versus Toulouse revisited.

    Science.gov (United States)

    Howard, A N; Thurnham, D I

    2017-01-01

    In 1995 we reported that mean plasma lutein concentrations in salaried men and women from Toulouse in Southern France were double those in subjects recruited from general practitioner lists in Belfast, Northern Ireland. At the time incidence of coronary heart disease (CHD) in Southern France was among the lowest in Europe and was much higher in Northern Ireland. Plasma lutein is a biomarker of vegetable and fruit intake and evidence suggests that high concentrations are generally associated with better cardiometabolic health. At the time we speculated like others that role of the carotenoids may well have been to prevent oxidation of lipid in the lipoproteins and so reduce the uptake of oxidised lipid by macrophages and its deposition within the intimal layers of the major arteries as plaque. It is now widely accepted that CHD is an inflammatory disease and that macrophages within plaque together with tissue damage contribute to this inflammation. Stimulated macrophages release cytokines to activate the immune system both locally and systemically. Precursor complement proteins in the blood are activated to assist immune cells in phagocytosis and cell repair. Individuals with a history of arteriosclerosis display significantly higher concentrations of complement factors C3 and C3a than subjects without such a history. Metabolism of C3 via the alternate complement pathway can give rise to the membrane attack complex (MAC) which creates a hole or pore in pathogens or host cells, killing the cell. Recent studies in patients with early age related macular disease (AMD) who also exhibit similar elevated concentrations of complement proteins in their blood, showed supplementation with lutein progressively decreased the amount of the MAC and other complement factors in the blood. Lutein was used in the supplementation experiments because it is an important constituent of macular pigment. Thus the healthier cardiometabolic features displayed by the people in Toulouse may

  4. Inflammation and Heart Disease

    Science.gov (United States)

    ... Disease Venous Thromboembolism Aortic Aneurysm More Inflammation and Heart Disease Updated:Jun 13,2017 Understand the risks of ... inflammation causes cardiovascular disease, inflammation is common for heart disease and stroke patients and is thought to be ...

  5. Calcific bursitis mimicking a parosteal osteogenic sarcoma

    International Nuclear Information System (INIS)

    Slavin, J.D. Jr.; Vento, J.A.; Haugh, J.D.; Spencer, R.P.; Connecticut Univ., Farmington

    1986-01-01

    A 43-year-old woman with no history of trauma or major medical illness, presented with a ten day history of right hip and thigh pain. The pain was described as constant, dull, and aching. It was nonradiating and was not relieved by analgesics. Physical examination revealed diffuse tenderness over the right hip and right lateral thigh region; no mass was palpable. The CBC, serum electrolytes, calcium, phosphorus, and alkaline phosphatase determinations were all normal. Radiographs of the right hip demonstrated amorphous soft tissue calcification adjacent to the lateral aspect of the right femur as well as periosteal reaction and apparent destruction in the adjacent bone. Because of these suspicious X-rays findings, the initial working diagnosis was parosteal osteogenic sarcoma. A bone scan was performed two hours after the intravenous administration of 15 millicuries of Tc-99m-MDP. It showed focal uptake overlying the upper femur, approximately where the X-ray had shown periosteal reaction and apparent bony destruction. In addition, the bone images also demonstrated a linear band of activity extending through the soft tissues from the greater trochanter to the lower lateral thigh. Because of the unexpected and quite extensive soft tissue uptake seen on the scan, the possibility that a benign process was involved was then considered seriously for the first time. An open biopsy was then performed. It revealed acute calcific trochanteric bursitis; there was no evidence of bone involvement. The patient was treated conservatively and symptoms gradually resolved. (orig.) [de

  6. Basal ganglia calcification on computed tomography in systemic lupus erythematosus

    International Nuclear Information System (INIS)

    Nagaoka, Shohei; Tani, Kenji; Ishigatsubo, Yoshiaki

    1988-01-01

    The development of basal ganglia calcification was studied in 85 patients with systemic lupus erythematosus (SLE) by computed tomography (CT). Bilateral calcification of the basal ganglia was found to occur in 5 patients (5.9 %) with SLE, but was not seen in patients with rheumatoid arthritis and progressive systemic sclerosis. All were female with a mean age of 42 years (range 29 - 49). The patients with calcification of the basal ganglia had neurological symptoms, such as psychiatric problems (3 cases), grand mal seizures (1 case), CSF abnormalities (2 cases), and EEG changes (4 cases). There were significantly higher incidences of alopecia, cutaneous vasculitis, leukopenia, and thrombocytopenia in the group with calcifications than those in the group with normal CT findings. Circulating immune complexes were detected and LE tests were positive in 2 patients. Endocrinological examination showed no abnormality in any. We suggest that basal ganglia calcification in SLE might be related to cerebral vasculitis. (author)

  7. Recurrent acute low back pain secondary to lumbar epidural calcification

    Energy Technology Data Exchange (ETDEWEB)

    Ziade, M.; Zufferey, P.; So, A.K.L. [Centre Hospitalier Vaudois, Service de Rhumatologie, Lausanne (Switzerland)

    2007-06-15

    Epidural calcification is a rare cause of back pain, and spontaneous epidural calcification has not been reported previously. We describe a patient with acute low back pain and signs of lumbar nerve root compression due to epidural calcification, as demonstrated by CT-scan and MRI. Radiological signs of spondylodiscitis led to a search for an infectious cause, which was negative, and her symptoms responded rapidly to NSAID treatment alone. Her symptoms recurred 18 months later, and further imaging studies again revealed epidural calcification, but with a changed distribution. Her symptoms were relieved once more by NSAID treatment alone. We propose that epidural calcification secondary to aseptic spondylodiscitis is the main cause of acute back pain in this patient. A possible mechanism may be the pro-inflammatory effects of calcium pyrophosphate or hydroxyapatite crystal deposition within the epidural space. (orig.)

  8. Computed tomography of calcification of the basal ganglia

    International Nuclear Information System (INIS)

    Park, Churl Min; Suh, Soo Jhi; Kim, Soon Yong

    1981-01-01

    Calcifications of the basal ganglia are rarely found at routine autopsies and in skull radiographs. CT is superior to the plain skull radiographs in detecting intracranial attenuation differences and may be stated to be the method of choice in the diagnosis of intracranial calcifications. Of 5985 brain CT scans performed in Kyung Hee University Hospital during past 3 years, 36 cases were found to have high attenuation lesions suggesting calcifications within basal ganglia. 1. The incidence of basal ganglia calcification on CT scan was about 0.6%. 2. Of these 36 cases, 34 cases were bilateral and the remainder was unilateral. 3. The plain skull films of 23 cases showed visible calcification of basal ganglia in 3 cases (13%). 4. No specific metabolic disease was noted in the cases

  9. Recurrent acute low back pain secondary to lumbar epidural calcification

    International Nuclear Information System (INIS)

    Ziade, M.; Zufferey, P.; So, A.K.L.

    2007-01-01

    Epidural calcification is a rare cause of back pain, and spontaneous epidural calcification has not been reported previously. We describe a patient with acute low back pain and signs of lumbar nerve root compression due to epidural calcification, as demonstrated by CT-scan and MRI. Radiological signs of spondylodiscitis led to a search for an infectious cause, which was negative, and her symptoms responded rapidly to NSAID treatment alone. Her symptoms recurred 18 months later, and further imaging studies again revealed epidural calcification, but with a changed distribution. Her symptoms were relieved once more by NSAID treatment alone. We propose that epidural calcification secondary to aseptic spondylodiscitis is the main cause of acute back pain in this patient. A possible mechanism may be the pro-inflammatory effects of calcium pyrophosphate or hydroxyapatite crystal deposition within the epidural space. (orig.)

  10. Susceptibility weighted imaging: differentiating between calcification and hemosiderin

    Energy Technology Data Exchange (ETDEWEB)

    Barbosa, Jeam Haroldo Oliveira; Salmon, Carlos Ernesto Garrido, E-mail: jeamharoldo@hotmail.com [Universidade de Sao Paulo (FFCLRP/USP), Ribeirao Preto, SP (Brazil). Faculdade de Filosofia, Ciencias e Letras; Santos, Antonio Carlos [Universidade de Sao Paulo (FMRP/USP), Ribeirao Preto, SP (Brazil). Faculdade de Medicina

    2015-03-15

    Objective: to present a detailed explanation on the processing of magnetic susceptibility weighted imaging (SWI), demonstrating the effects of echo time and sensitive mask on the differentiation between calcification and hemosiderin. Materials and methods: computed tomography and magnetic resonance (magnitude and phase) images of six patients (age range 41-54 years; four men) were retrospectively selected. The SWI images processing was performed using the Matlab's own routine. Results: four out of the six patients showed calcifications at computed tomography images and their SWI images demonstrated hyperintense signal at the calcification regions. The other patients did not show any calcifications at computed tomography, and SWI revealed the presence of hemosiderin deposits with hypointense signal. Conclusion: the selection of echo time and of the mask may change all the information on SWI images, and compromise the diagnostic reliability. Amongst the possible masks, the authors highlight that the sigmoid mask allows for contrasting calcifications and hemosiderin on a single SWI image. (author)

  11. Basal ganglia calcification on computed tomography in systemic lupus erythematosus

    Energy Technology Data Exchange (ETDEWEB)

    Nagaoka, Shohei; Tani, Kenji; Ishigatsubo, Yoshiaki and others

    1988-09-01

    The development of basal ganglia calcification was studied in 85 patients with systemic lupus erythematosus (SLE) by computed tomography (CT). Bilateral calcification of the basal ganglia was found to occur in 5 patients (5.9 %) with SLE, but was not seen in patients with rheumatoid arthritis and progressive systemic sclerosis. All were female with a mean age of 42 years (range 29 - 49). The patients with calcification of the basal ganglia had neurological symptoms, such as psychiatric problems (3 cases), grand mal seizures (1 case), CSF abnormalities (2 cases), and EEG changes (4 cases). There were significantly higher incidences of alopecia, cutaneous vasculitis, leukopenia, and thrombocytopenia in the group with calcifications than those in the group with normal CT findings. Circulating immune complexes were detected and LE tests were positive in 2 patients. Endocrinological examination showed no abnormality in any. We suggest that basal ganglia calcification in SLE might be related to cerebral vasculitis.

  12. Relationship Between Lifelong Exercise Volume and Coronary Atherosclerosis in Athletes.

    Science.gov (United States)

    Aengevaeren, Vincent L; Mosterd, Arend; Braber, Thijs L; Prakken, Niek H J; Doevendans, Pieter A; Grobbee, Diederick E; Thompson, Paul D; Eijsvogels, Thijs M H; Velthuis, Birgitta K

    2017-07-11

    Higher levels of physical activity are associated with a lower risk of cardiovascular events. Nevertheless, there is debate on the dose-response relationship of exercise and cardiovascular disease outcomes and whether high volumes of exercise may accelerate coronary atherosclerosis. We aimed to determine the relationship between lifelong exercise volumes and coronary atherosclerosis. Middle-aged men engaged in competitive or recreational leisure sports underwent a noncontrast and contrast-enhanced computed tomography scan to assess coronary artery calcification (CAC) and plaque characteristics. Participants reported lifelong exercise history patterns. Exercise volumes were multiplied by metabolic equivalent of task (MET) scores to calculate MET-minutes per week. Participants' activity was categorized as 2000 MET-min/wk. A total of 284 men (age, 55±7 years) were included. CAC was present in 150 of 284 participants (53%) with a median CAC score of 35.8 (interquartile range, 9.3-145.8). Athletes with a lifelong exercise volume >2000 MET-min/wk (n=75) had a significantly higher CAC score (9.4 [interquartile range, 0-60.9] versus 0 [interquartile range, 0-43.5]; P =0.02) and prevalence of CAC (68%; adjusted odds ratio [OR adjusted ]=3.2; 95% confidence interval [CI], 1.6-6.6) and plaque (77%; OR adjusted =3.3; 95% CI, 1.6-7.1) compared with exercise (≥9 MET) was associated with CAC (OR adjusted =1.47; 95% CI, 1.14-1.91) and plaque (OR adjusted =1.56; 95% CI, 1.17-2.08). Among participants with CAC>0, there was no difference in CAC score ( P =0.20), area ( P =0.21), density ( P =0.25), and regions of interest ( P =0.20) across exercise volume groups. Among participants with plaque, the most active group (>2000 MET-min/wk) had a lower prevalence of mixed plaques (48% versus 69%; OR adjusted =0.35; 95% CI, 0.15-0.85) and more often had only calcified plaques (38% versus 16%; OR adjusted =3.57; 95% CI, 1.28-9.97) compared with the least active group (2000 MET

  13. Carbon monoxide, smoking, and atherosclerosis

    Energy Technology Data Exchange (ETDEWEB)

    Astrup, P

    1973-10-01

    Studies on the effects of carbon monoxide and smoking on atherosclerosis are reviewed. Nonsmokers do not run the risk of getting significantly elevated carboxyhemoglobin levels from automobile exhaust in the streets, however, they do run the risk of getting elevated carboxyhemoglobin levels from exposure to CO in closed areas such as garages and tunnels. Carboxyhemoglobin levels up to 20 percent may also be found in smokers. The central nervous system seems to be influenced by carboxyhemoglobin concentrations up to 20 percent. The myocardium may also be affected. Experimental work with rabbits exposed to carbon monoxide and cholesterol is described which proved that CO has a damaging effect on arterial walls, leading to increased permeability for various plasma components, to the formation of subendothelial edema, and to increased atheromatosis. The results indicate that the much higher risk of smokers of developing arterial disease in comparison to nonsmokers is mainly due to the inhaled CO in the tobacco smoke and not to nicotine. (Air Pollut. Abstr.)

  14. Noninvasive assessment of preclinical atherosclerosis

    Directory of Open Access Journals (Sweden)

    Helen A Lane

    2006-03-01

    Full Text Available Helen A Lane, Jamie C Smith, J Stephen DaviesDepartment of Endocrinology, University of Wales College of Medicine, Heath Park, Cardiff, Wales, UKAbstract: Initially considered as a semipermeable barrier separating lumen from vessel wall, the endothelium is now recognised as a complex endocrine organ responsible for a variety of physiological processes vital for vascular homeostasis. These include the regulation of vascular tone, luminal diameter, and blood flow; hemostasis and thrombolysis; platelet and leucocyte vessel-wall interactions; the regulation of vascular permeability; and tissue growth and remodelling. The endothelium modulates arterial stiffness, which precedes overt atherosclerosis and is an independent predictor of cardiovascular events. Unsurprisingly, dysfunction of the endothelium may be considered as an early and potentially reversible step in the process of atherogenesis and numerous methods have been developed to assess endothelial status and large artery stiffness. Methodology includes flow-mediated dilatation of the brachial artery, assessment of coronary flow reserve, carotid intimamedia thickness, pulse wave analysis, pulse wave velocity, and plethysmography. This review outlines the various modalities, indications, and limitations of available methods to assess arterial dysfunction and vascular risk.Keywords: endothelial function, vascular risk, vascular stiffness

  15. High prevalence of subclinical atherosclerosis in Brazilian postmenopausal women with low and intermediate risk by Framingham score.

    Science.gov (United States)

    Petisco, Ana Claudia Gomes Pereira; Assef, Jorge Eduardo; de Jesus, Carlos Alberto; Saleh, Mohamed Hassan; Barbosa, Jose Eduardo Martins; Costa de Souza Le Bihan, David; Pinto, Ibraim Masciarelli França; Rolim Fernandes Fontes Pedra, Simone; Barretto, Rodrigo Bellio de Mattos; Sousa, Amanda Guerra de Moraes Rego

    2017-03-01

    Cardiovascular diseases are the leading cause of mortality among women in several countries. Early detection of subclinical atherosclerosis (SA) could enable the adoption of preventive measures to avoid cardiovascular events. This study aimed to determine the prevalence of SA in Brazilian asymptomatic postmenopausal women in Framingham Risk Score (FRS) low and intermediate groups. Computed tomography (CT) and ultrasound (US) scans were performed in 138 asymptomatic postmenopausal women (56.1 ± 4.9 years of age) to survey for coronary artery and aortic calcification (CT scan) and assess carotid intima-media thickness (CIMT) and identify carotid plaques (US). The mean FRS was 2.64 ± 2.13 %. The prevalence of increased CIMT, carotid plaques, increased CIMT and/or plaques, coronary artery calcification (CAC) >0 and aortic calcification (AC) were, respectively, 45.7, 37.7, 62.3, 23.9 and 45.7 %. Normal imaging tests were found in 22.4 %. SA, defined as at least one abnormal imaging test, was associated with age, FRS, waist-to-rip ratio, systolic and diastolic blood pressure, HDL-c and ApoA1 levels, and ApoA1/ApoB ratio. In logistic regression, SA was associated with higher age (OR 1.108, 95 % CI 1.010-1.215, p = 0.029) and lower ApoA1 levels (OR 0.979, 95 % CI 0.960-0.998, p = 0.029). SA was prevalent in Brazilian postmenopausal women with low and intermediate risk groups (FRS) and was associated with higher age and lower levels of ApoA1. Carotid atherosclerosis was the most common presentation of SA in this group.

  16. Persistent low-grade inflammation and regular exercise

    DEFF Research Database (Denmark)

    Astrom, Maj-Briit; Feigh, Michael; Pedersen, Bente Klarlund

    2010-01-01

    Persistent low-grade systemic inflammation is a feature of chronic diseases such as cardiovascular disease (CVD), type 2 diabetes and dementia and evidence exists that inflammation is a causal factor in the development of insulin resistance and atherosclerosis. Regular exercise offers protection ...... diabetes and dementia. We suggest that the anti-inflammatory effects of exercise may be mediated via a long-term effect of exercise leading to a reduction in visceral fat mass and/or by induction of anti-inflammatory cytokines with each bout of exercise....

  17. Impact of long-term corticosteroid therapy on the distribution pattern of lower limb atherosclerosis.

    Science.gov (United States)

    Willenberg, T; Diehm, N; Zwahlen, M; Kalka, C; Do, D-D; Gretener, S; Ortmann, J; Baumgartner, I

    2010-04-01

    Ectopic calcification and mediacalcinosis can be promoted by corticosteroid use. Aim of the present investigation is to describe macrovascular disease features in patients with long-term corticosteroid therapy and symptomatic lower limb peripheral arterial occlusive disease (PAD). A consecutive series of 2783 patients undergoing clinical and angiographic work-up of PAD were screened for long-term (>5 years) corticosteroid use (group A). Comparison was performed to a randomly selected age-, sex- and risk factor-matched PAD control cohort from the same series without corticosteroid use (group B). Patients with diabetes mellitus or severe renal failure were excluded. Arterial calcification was evaluated by qualitative assessment on radiographic images. Severity of atherosclerotic lesions was analysed from angiographic images using a semi-quantitative score (Bollinger score). In general, 12 patients (5 males, mean age 78.5 +/- 9.0 years) with 15 ischaemic limbs qualified to be enrolled in group A and were compared to 23 matching control patients (6 2 males, mean age 79.5 +/- 6 years) with 32 ischaemic limbs. Incompressibility of ankle arteries determined by measurement of the ankle-brachial index was seen in 12 limbs (80%) in group A compared to 3 limbs (9%) in group B (p = 0.0009). No significant difference was found comparing group A and B for segmental calcification, whereas comparison of the atherosclerotic burden using the angiographic severity score showed a significantly higher score at the infragenicular arterial level in group A (p = 0.001). Findings suggest that the long-term corticosteroid therapy is associated with a distally accentuated, calcifying peripheral atherosclerosis inducing arterial incompressibility. This occlusion pattern is comparable to patients with renal failure or diabetes. Further research is required to support our observations.

  18. Imaging pathobiology of carotid atherosclerosis with ultrasmall superparamagnetic particles of iron oxide: an update.

    Science.gov (United States)

    Sadat, Umar; Usman, Ammara; Gillard, Jonathan H

    2017-07-01

    To provide brief overview of the developments regarding use of ultrasmall superparamagnetic particles of iron oxide in imaging pathobiology of carotid atherosclerosis. MRI is a promising technique capable of providing morphological and functional information about atheromatous plaques. MRI using iron oxide particles, called ultrasmall superparamagnetic iron oxide (USPIO) particles, allows detection of macrophages in atherosclerotic tissue. Ferumoxytol has emerged as a new USPIO agent, which has an excellent safety profile. Based on the macrophage-selective properties of ferumoxytol, there is increasing number of recent reports suggesting its effectiveness to detect pathological inflammation. USPIO particles allow magnetic resonance detection of macrophages in atherosclerotic tissue. Ferumoxytol has emerged as a new USPIO agent, with an excellent safety profile. This has the potential to be used for MRI of the pathobiology of atherosclerosis.

  19. Effects of Ramadan Fasting on the Regulation of Inflammation

    Directory of Open Access Journals (Sweden)

    Safieh Ebrahimi

    2016-03-01

    Full Text Available The month of Ramadan, as a model of intermittent fasting, is a valuable opportunity to investigate the effects of dietary modifications on human metabolism. Fasting improves insulin sensitivity, reduces atherogenic risk, oxidative stress, and inflammation. Inflammation plays a key role in the pathogenesis of different disorders including atherosclerosis, metabolic syndrome and cardiovascular diseases. Ramadan fasting can positively modulate cardiovascular risks and improves the metabolic syndrome features through suppression of inflammatory responses. In this review we attempt to present recent studies that addressed the regulatory role(s of this nutritional status on inflammation in patients with inflammatory diseases. These studies suggest that the anti-inflammatory effect of fasting is significant and could be considered as a complementary therapeutic approach in treatment of inflammatory disorders in patients.Keywords: Ramadan fasting, Inflammation, Metabolic syndrome, Cardiovascular diseaseAbstract Abstract Abstract Abstract Abstract Abstract Abstract Abstract Abstract Abstract Abstract Abstract Abstract Abstract Abstract Abstract Abstract Abstract Abstract

  20. Emerging role of FDG-PET/CT in assessing atherosclerosis in large arteries

    International Nuclear Information System (INIS)

    Chen, Wengen; Bural, Gonca G.; Torigian, Drew A.; Alavi, Abass; Rader, Daniel J.

    2009-01-01

    Atherosclerosis is a dynamic inflammatory disorder. The biological composition and inflammatory state of an atherosclerotic plaque, rather than the degree of stenosis or its size are the major determinants of acute clinical events. A noninvasive technique to detect vulnerable atherosclerotic plaque is critically needed. FDG-PET/CT, a combined functional and structural whole-body imaging modality, holds great potential for this purpose. FDG uptake in large arteries has been frequently observed and is associated with cardiovascular risk factors. FDG accumulates in plaque macrophages and uptake is correlated with macrophage density. It is known that vascular FDG uptake and calcification do not overlap significantly and changes of FDG uptake are common, suggesting that FDG uptake may represent a dynamic inflammatory process. It has been reported that vascular FDG uptake can be attenuated by simvastatin in patients, and by the antiinflammatory drug probucol in rabbits. Vascular FDG uptake has been linked to cardiovascular events in some preliminary studies. Data from basic sciences, and animal and clinical studies support the emerging role of FDG-PET/CT in assessing atherosclerosis in large arteries in humans. (orig.)

  1. MicroRNAs as Potential Mediators for Cigarette Smoking Induced Atherosclerosis

    Directory of Open Access Journals (Sweden)

    Yuka Yokoyama

    2018-04-01

    Full Text Available Smoking increases the risk of atherosclerosis-related events, such as myocardial infarction and ischemic stroke. Recent studies have examined the expression levels of altered microRNAs (miRNAs in various diseases. The profiles of tissue miRNAs can be potentially used in diagnosis or prognosis. However, there are limited studies on miRNAs following exposure to cigarette smoke (CS. The present study was designed to dissect the effects and cellular/molecular mechanisms of CS-induced atherosclerogenesis. Apolipoprotein E knockout (ApoE KO mice were exposed to CS for five days a week for two months at low (two puffs/min for 40 min/day or high dose (two puffs/min for 120 min/day. We measured the area of atherosclerotic plaques in the aorta, representing the expression of miRNAs after the exposure period. Two-month exposure to the high dose of CS significantly increased the plaque area in aortic arch, and significantly upregulated the expression of atherosclerotic markers (VCAM-1, ICAM-1, MCP1, p22phox, and gp91phox. Exposure to the high dose of CS also significantly upregulated the miRNA-155 level in the aortic tissues of ApoE KO mice. Moreover, the expression level of miR-126 tended to be downregulated and that of miR-21 tended to be upregulated in ApoE KO mice exposed to the high dose of CS, albeit statistically insignificant. The results suggest that CS induces atherosclerosis through increased vascular inflammation and NADPH oxidase expression and also emphasize the importance of miRNAs in the pathogenesis of CS-induced atherosclerosis. Our findings provide evidence for miRNAs as potential mediators of inflammation and atherosclerosis induced by CS.

  2. Noninvasive ultrasound molecular imaging of the effect of statins on endothelial inflammatory phenotype in early atherosclerosis.

    Directory of Open Access Journals (Sweden)

    Elham Khanicheh

    Full Text Available BACKGROUND/OBJECTIVES: Inflammatory changes on the endothelium are responsible for leukocyte recruitment to plaques in atherosclerosis. Noninvasive assessment of treatment-effects on endothelial inflammation may be of use for managing medical therapy and developing novel therapies. We hypothesized that molecular imaging of vascular cell adhesion molecule-1 (VCAM-1 with contrast enhanced ultrasound (CEU could assess treatment effects on endothelial phenotype in early atherosclerosis. METHODS: Mice with atherosclerosis produced by gene deletion of the LDL-receptor and Apobec-1-editing protein were studied. At 12 weeks of age, mice received 8 weeks of regular chow or atorvastatin-enriched chow (10 mg/kg/day. At 20 weeks, CEU molecular imaging for aortic endothelial VCAM-1 expression was performed with VCAM-1-targeted (MB(VCAM and control microbubbles (MB(Ctr. Aortic wall thickness was assessed with high frequency ultrasound. Histology, immunohistology and Western blot were used to assess plaque burden and VCAM-1 expression. RESULTS: Plaque burden was reduced on histology, and VCAM-1 was reduced on Western blot by atorvastatin, which corresponded to less endothelial expression of VCAM-1 on immunohistology. High frequency ultrasound did not detect differences in aortic wall thickness between groups. In contrast, CEU molecular imaging demonstrated selective signal enhancement for MB(VCAM in non-treated animals (MB(VCAM 2±0.3 vs MB(Ctr 0.7±0.2, p<0.01, but not in statin-treated animals (MB(VCAM 0.8±0.2 vs MB(Ctr 1.0±0.2, p = ns; p<0.01 for the effect of statin on MB(VCAM signal. CONCLUSIONS: Non-invasive CEU molecular imaging detects the effects of anti-inflammatory treatment on endothelial inflammation in early atherosclerosis. This easily accessible, low-cost technique may be useful in assessing treatment effects in preclinical research and in patients.

  3. A Rabbit Model for Testing Helper-Dependent Adenovirus-Mediated Gene Therapy for Vein Graft Atherosclerosis

    Directory of Open Access Journals (Sweden)

    Lianxiang Bi

    2017-12-01

    Full Text Available Coronary artery bypass vein grafts are a mainstay of therapy for human atherosclerosis. Unfortunately, the long-term patency of vein grafts is limited by accelerated atherosclerosis. Gene therapy, directed at the vein graft wall, is a promising approach for preventing vein graft atherosclerosis. Because helper-dependent adenovirus (HDAd efficiently transduces grafted veins and confers long-term transgene expression, HDAd is an excellent candidate for delivery of vein graft-targeted gene therapy. We developed a model of vein graft atherosclerosis in fat-fed rabbits and demonstrated long-term (≥20 weeks persistence of HDAd genomes after graft transduction. This model enables quantitation of vein graft hemodynamics, wall structure, lipid accumulation, cellularity, vector persistence, and inflammatory markers on a single graft. Time-course experiments identified 12 weeks after transduction as an optimal time to measure efficacy of gene therapy on the critical variables of lipid and macrophage accumulation. We also used chow-fed rabbits to test whether HDAd infusion in vein grafts promotes intimal growth and inflammation. HDAd did not increase intimal growth, but had moderate—yet significant—pro-inflammatory effects. The vein graft atherosclerosis model will be useful for testing HDAd-mediated gene therapy; however, pro-inflammatory effects of HdAd remain a concern in developing HDAd as a therapy for vein graft disease.

  4. A Rabbit Model for Testing Helper-Dependent Adenovirus-Mediated Gene Therapy for Vein Graft Atherosclerosis.

    Science.gov (United States)

    Bi, Lianxiang; Wacker, Bradley K; Bueren, Emma; Ham, Ervin; Dronadula, Nagadhara; Dichek, David A

    2017-12-15

    Coronary artery bypass vein grafts are a mainstay of therapy for human atherosclerosis. Unfortunately, the long-term patency of vein grafts is limited by accelerated atherosclerosis. Gene therapy, directed at the vein graft wall, is a promising approach for preventing vein graft atherosclerosis. Because helper-dependent adenovirus (HDAd) efficiently transduces grafted veins and confers long-term transgene expression, HDAd is an excellent candidate for delivery of vein graft-targeted gene therapy. We developed a model of vein graft atherosclerosis in fat-fed rabbits and demonstrated long-term (≥20 weeks) persistence of HDAd genomes after graft transduction. This model enables quantitation of vein graft hemodynamics, wall structure, lipid accumulation, cellularity, vector persistence, and inflammatory markers on a single graft. Time-course experiments identified 12 weeks after transduction as an optimal time to measure efficacy of gene therapy on the critical variables of lipid and macrophage accumulation. We also used chow-fed rabbits to test whether HDAd infusion in vein grafts promotes intimal growth and inflammation. HDAd did not increase intimal growth, but had moderate-yet significant-pro-inflammatory effects. The vein graft atherosclerosis model will be useful for testing HDAd-mediated gene therapy; however, pro-inflammatory effects of HdAd remain a concern in developing HDAd as a therapy for vein graft disease.

  5. Potential Biomarkers of Insulin Resistance and Atherosclerosis in Type 2 Diabetes Mellitus Patients with Coronary Artery Disease

    Directory of Open Access Journals (Sweden)

    Sharifah Intan Qhadijah Syed Ikmal

    2013-01-01

    Full Text Available Type 2 diabetes mellitus patients with coronary artery disease have become a major public health concern. The occurrence of insulin resistance accompanied with endothelial dysfunction worsens the state of atherosclerosis in type 2 diabetes mellitus patients. The combination of insulin resistance and endothelial dysfunction leads to coronary artery disease and ischemic heart disease complications. A recognized biological marker, high-sensitivity C-reactive protein, has been used widely to assess the progression of atherosclerosis and inflammation. Along with coronary arterial damage and inflammatory processes, high-sensitivity C-reactive protein is considered as an essential atherosclerosis marker in patients with cardiovascular disease, but not as an insulin resistance marker in type 2 diabetes mellitus patients. A new biological marker that can act as a reliable indicator of both the exact state of insulin resistance and atherosclerosis is required to facilitate optimal health management of diabetic patients. Malfunctioning of insulin mechanism and endothelial dysfunction leads to innate immune activation and released several biological markers into circulation. This review examines potential biological markers, YKL-40, alpha-hydroxybutyrate, soluble CD36, leptin, resistin, interleukin-18, retinol binding protein-4, and chemerin, as they may play significant roles in insulin resistance and atherosclerosis in type 2 diabetes mellitus patients with coronary artery disease.

  6. Serum magnesium is inversely associated with coronary artery calcification in the Genetics of Atherosclerotic Disease (GEA) study.

    Science.gov (United States)

    Posadas-Sánchez, Rosalinda; Posadas-Romero, Carlos; Cardoso-Saldaña, Guillermo; Vargas-Alarcón, Gilberto; Villarreal-Molina, María Teresa; Pérez-Hernández, Nonanzit; Rodríguez-Pérez, José Manuel; Medina-Urrutia, Aida; Jorge-Galarza, Esteban; Juárez-Rojas, Juan Gabriel; Torres-Tamayo, Margarita

    2016-03-01

    Serum magnesium is inversely associated to coronary artery calcification (CAC) in patients with chronic kidney disease. There is little information on this association in a general healthy population. The aim of this study was to examine the cross-sectional association of serum magnesium levels with CAC. We included 1276 Mexican-mestizo subjects (50 % women), aged 30-75 years, free of symptomatic cardiovascular disease. CAC was quantified by multidetector computed tomography using the method described by Agatston. Cross-sectional associations of serum magnesium with cardiometabolic factors and subclinical atherosclerosis defined as a CAC score > 0, were examined in logistic regression models adjusted for age, sex, education, smoking status, body mass index, systolic blood pressure, physical activity, elevated abdominal visceral tissue, fasting insulin and glucose, alcohol consumption, menopausal status (women only), low (LDL-C) and high density lipoprotein cholesterol (HDL-C), triglycerides, diuretic use, type 2 diabetes mellitus (DM2), and family history of DM2. After full adjustment, subjects in the highest quartile of serum magnesium had 48 % lower odds of hypertension (p = 0.028), 69 % lower odds of DM2 (p = 0.003), and 42 % lower odds of CAC score > 0 (p = 0.016) compared to those with the lowest serum magnesium. The analyses also showed that a 0.17 mg/dL (1SD) increment in serum magnesium was independently associated with 16 % lower CAC (OR 0.84, 95 % CI 0.724-0.986). In a sample of Mexican-mestizo subjects, low serum magnesium was independently associated to higher prevalence not only of hypertension and DM2, but also to coronary artery calcification, which is a marker of atherosclerosis and a predictor of cardiovascular morbidity and mortality.

  7. Association of conjunctival and corneal calcification with vascular calcification among hepatitis-C-seropositive hemodialysis patients.

    Science.gov (United States)

    AbouSeif, Khaled; Sany, Dawlat; Elshahawy, Yasser; Seddik, Ayman; Rahman, Khedr; Gaber, Moustapha

    2016-01-01

    Disorders associated with the hepatitis C virus (HCV) have been reported including cardiovascular, metabolic, and central nervous system diseases. Since chronic HCV infections may be curable, their identification as causal contributors to cardiovascular risk could offer new perspectives in the prevention of cardiovascular disease. The aim of this study is to investigate the association between HCV and aortic arch calcification (AAC) and corneal and conjunctival calcification (CCC) in maintenance hemodialysis (MHD) patients; further, we assessed the correlation of CCC with vascular calcification. A total of 100 patients undergoing hemodialysis (HD) in our hospital were included in this study. Patients underwent a complete ocular examination including intraocular pressure, and CCC was looked for by slit lamp and fundoscopy. CCC was graded according to modified Porter and Crombie classification system described by Tokuyama et al. Helical computerized tomographic chest examination was used to evaluate the grading of AAC. Demographic, hematological, biochemical, and dialysis-related data were obtained. There was significant difference between seropositive (n = 51) and seronegative patients (n = 49) regarding grading of AAC and CCC (P <0.001). Significant positive correlation was found between grading of CCC, AAC, age (P <0.001), duration on HD (P <0.001), HCV-antibody positivity (P <0.001), serum calcium level (P <0.001), serum phosphorus level (P <0.001), calcium × phosphorus product (P <0.001), and i-parathormone level (P < 0.001). In addition, CCC grading positively correlated with AAC. Our results suggest that patients undergoing HD infected with the HCV have high degree of CCC, AAC, and mineral metabolism disorder. The strong correlation between CCC and AAC indicates that CCC evaluation is an easy, fast, non-invasive method, and might be used as an indirect indicator to detect vascular calcification in patients undergoing MHD.

  8. Association of conjunctival and corneal calcification with vascular calcification among hepatitis-C-seropositive hemodialysis patients

    Directory of Open Access Journals (Sweden)

    Khaled AbouSeif

    2016-01-01

    Full Text Available Disorders associated with the hepatitis C virus (HCV have been reported including cardiovascular, metabolic, and central nervous system diseases. Since chronic HCV infections may be curable, their identification as causal contributors to cardiovascular risk could offer new perspectives in the prevention of cardiovascular disease. The aim of this study is to investigate the association between HCV and aortic arch calcification (AAC and corneal and conjunctival calcification (CCC in maintenance hemodialysis (MHD patients; further, we assessed the correlation of CCC with vascular calcification. A total of 100 patients undergoing hemodialysis (HD in our hospital were included in this study. Patients underwent a complete ocular examination including intraocular pressure, and CCC was looked for by slit lamp and fundoscopy. CCC was graded according to modified Porter and Crombie classification system described by Tokuyama et al. Helical computerized tomographic chest examination was used to evaluate the grading of AAC. Demographic, hematological, biochemical, and dialysis-related data were obtained. There was significant difference between seropositive (n = 51 and seronegative patients (n = 49 regarding grading of AAC and CCC (P <0.001. Significant positive correlation was found between grading of CCC, AAC, age (P <0.001, duration on HD (P <0.001, HCV-antibody positivity (P <0.001, serum calcium level (P <0.001, serum phosphorus level (P <0.001, calcium × phosphorus product (P <0.001, and i-parathormone level (P < 0.001. In addition, CCC grading positively correlated with AAC. Our results suggest that patients undergoing HD infected with the HCV have high degree of CCC, AAC, and mineral metabolism disorder. The strong correlation between CCC and AAC indicates that CCC evaluation is an easy, fast, non-invasive method, and might be used as an indirect indicator to detect vascular calcification in patients undergoing MHD.

  9. Cyanotic congenital heart disease and atherosclerosis.

    Science.gov (United States)

    Tarp, Julie Bjerre; Jensen, Annette Schophuus; Engstrøm, Thomas; Holstein-Rathlou, Niels-Henrik; Søndergaard, Lars

    2017-06-01

    Improved treatment options in paediatric cardiology and congenital heart surgery have resulted in an ageing population of patients with cyanotic congenital heart disease (CCHD). The risk of acquired heart disease such as atherosclerosis increases with age.Previous studies have speculated whether patients with CCHD are protected against atherosclerosis. Results have shown that the coronary arteries of patients with CCHD are free from plaques and stenosis. Decreased carotid intima-media thickness and low total plasma cholesterol may indicate a reduced risk of later development of atherosclerosis. However, the evidence is still sparse and questionable, and a reasonable explanation for the decreased risk of developing atherosclerosis in patients with CCHD is still missing.This review provides an overview of what is known about the prevalence and potential causes of the reduced risk of atherosclerosis in patients with CCHD. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

  10. History of hot flashes and aortic calcification among postmenopausal women.

    Science.gov (United States)

    Thurston, Rebecca C; Kuller, Lewis H; Edmundowicz, Daniel; Matthews, Karen A

    2010-03-01

    Menopausal hot flashes are considered largely a quality-of-life issue. However, emerging research also links hot flashes to cardiovascular risk. In some investigations, this risk is particularly apparent among women using hormone therapy. The aim of this study was to determine whether a longer history of reported hot flashes over the study period was associated with greater aortic and coronary artery calcification. Interactions with hormone therapy use were examined in an exploratory fashion. Participants included 302 women participating in the Healthy Women Study, a longitudinal study of cardiovascular risk during perimenopause and postmenopause, which was initiated in 1983. Hot flashes (any/none) were assessed when women were 1, 2, 5, and 8 years postmenopausal. Electron beam tomography measures of coronary artery calcification and aortic calcification were completed in 1997-2004. Associations between the number of visits with report of hot flashes, divided by the number of visits attended, and aortic or coronary artery calcification (transformed) were examined in linear regression models. Interactions by hormone therapy use were evaluated. Among women using hormone therapy, a longer history of reported hot flashes was associated with increased aortic calcification, controlling for traditional cardiovascular risk factors (b = 2.87, SE = 1.21, P history of hot flashes and coronary artery calcification. Among postmenopausal women using hormone therapy, a longer history of reported hot flashes measured prospectively was associated with increased aortic calcification, controlling for traditional cardiovascular risk factors. Hot flashes may signal adverse cardiovascular changes among certain postmenopausal women.

  11. Skeletal maturity assessment using mandibular canine calcification stages

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    Vildana Džemidžić

    2016-11-01

    Full Text Available Objective. The aims of this study were: to investigate the relationship between mandibular canine calcification stages and skeletal maturity; and to evaluate whether the mandibular canine calcification stages may be used as a reliable diagnostic tool for skeletal maturity assessment. Materials and methods. This study included 151 subjects: 81 females and 70 males, with ages ranging from 9 to 16 years (mean age: 12.29±1.86 years. The inclusion criteria for subjects were as follows: age between 9 and 16 years; good general health without any hormonal, nutritional, growth or dental development problems. Subjects who were undergoing or had previously received orthodontic treatment were not included in this study. The calcification stages of the left permanent mandibular canine were assessed according to the method of Demirjian, on panoramic radiographs. Assessment of skeletal maturity was carried out using the cervical vertebral maturation index (CVMI, as proposed by the Hassel-Farman method, on lateral cephalograms. The correlation between the calcification stages of mandibular canine and skeletal maturity was estimated separately for male and female subjects. Results. Correlation coefficients between calcification stages of mandibular canine and skeletal maturity were 0.895 for male and 0.701 for female subjects. Conclusions. A significant correlation was found between the calcification stages of the mandibular canine and skeletal maturity. The calcification stages of the mandibular canine show a satisfactory diagnostic performance only for assessment of pre-pubertal growth phase.

  12. Potential role of proteasome on c-jun related signaling in hypercholesterolemia induced atherosclerosis

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    Erdi Sozen

    2014-01-01

    Full Text Available Atherosclerosis and its complications are major causes of death all over the world. One of the major risks of atherosclerosis is hypercholesterolemia. During atherosclerosis, oxidized low density lipoprotein (oxLDL regulates CD36-mediated activation of c-jun amino terminal kinase-1 (JNK1 and modulates matrix metalloproteinase (MMP induction which stimulates inflammation with an invasion of monocytes. Additionally, inhibition of proteasome leads to an accumulation of c-jun and phosphorylated c-jun and activation of activator protein-1 (AP-1 related increase of MMP expression. We have previously reported a significant increase in cluster of differentiation 36 (CD36 mRNA levels in hypercholesterolemic rabbits and shown that vitamin E treatment prevented the cholesterol induced increase in CD36 mRNA expression. In the present study, our aim is to identify the signaling molecules/transcription factors involved in the progression of atherosclerosis following CD36 activation in an in vivo model of hypercholesterolemic (induced by 2% cholesterol containing diet rabbits. In this direction, proteasomal activities by fluorometry and c-jun, phospo c-jun, JNK1, MMP-9 expressions by quantitative RT-PCR and immunoblotting were tested in aortic tissues. The effects of vitamin E on these changes were also investigated in this model. As a result, c-jun was phosphorylated following decreased proteasomal degradation in hypercholesterolemic group. MMP-9 expression was also increased in cholesterol group rabbits contributing to the development of atherosclerosis. In addition, vitamin E showed its effect by decreasing MMP-9 levels and phosphorylation of c-jun.

  13. Adenocarcinoma of the parotid gland with calcification

    Energy Technology Data Exchange (ETDEWEB)

    Song, Haeng Eun; Koh, Kwang Joon [School of Dentistry, Chonbuk National University, Chonju (Korea, Republic of)

    2002-03-15

    A 78-year-old woman was referred to Chonbuk National University Dental Hospital complaining of facial palsy and palpable mass on the right parotid gland area. Clinical examination showed non-specific findings of the intraoral region, but showed asymmetrical facial appearance. Panoramic view showed a large amorphous calcified mass on the posterior to the mandibular ramus and thin cortical plate of the posterior ramus. Sialogram showed constriction of the main duct and no further filling of striated, intercalated ducts and parenchymal areas. CT scans demonstrated an irregular, infiltrating mass with slight enhancement in the right parotid gland. The mass showed necrotic areas and calcifications. Bone scan showed marked accumulation of {sup 99m}Tc-MDP on the right posterior maxilla. Microscopic findings demonstrated the minimal morphologic alterations and rare mitotic figures within tumor cells, and diagnosed as adenocarcinoma (NOS, Grade II). This report could be aid in the diagnosis of calcified lesions of the salivary gland.

  14. Adenocarcinoma of the parotid gland with calcification

    International Nuclear Information System (INIS)

    Song, Haeng Eun; Koh, Kwang Joon

    2002-01-01

    A 78-year-old woman was referred to Chonbuk National University Dental Hospital complaining of facial palsy and palpable mass on the right parotid gland area. Clinical examination showed non-specific findings of the intraoral region, but showed asymmetrical facial appearance. Panoramic view showed a large amorphous calcified mass on the posterior to the mandibular ramus and thin cortical plate of the posterior ramus. Sialogram showed constriction of the main duct and no further filling of striated, intercalated ducts and parenchymal areas. CT scans demonstrated an irregular, infiltrating mass with slight enhancement in the right parotid gland. The mass showed necrotic areas and calcifications. Bone scan showed marked accumulation of 99m Tc-MDP on the right posterior maxilla. Microscopic findings demonstrated the minimal morphologic alterations and rare mitotic figures within tumor cells, and diagnosed as adenocarcinoma (NOS, Grade II). This report could be aid in the diagnosis of calcified lesions of the salivary gland.

  15. Increased activity of vascular adenosine deaminase in atherosclerosis and therapeutic potential of its inhibition.

    Science.gov (United States)

    Kutryb-Zajac, Barbara; Mateuszuk, Lukasz; Zukowska, Paulina; Jasztal, Agnieszka; Zabielska, Magdalena A; Toczek, Marta; Jablonska, Patrycja; Zakrzewska, Agnieszka; Sitek, Barbara; Rogowski, Jan; Lango, Romuald; Slominska, Ewa M; Chlopicki, Stefan; Smolenski, Ryszard T

    2016-11-01

    Extracellular nucleotides and adenosine that are formed or degraded by membrane-bound ecto-enzymes could affect atherosclerosis by regulating the inflammation and thrombosis. This study aimed to evaluate a relation between ecto-enzymes that convert extracellular adenosine triphosphate to adenine dinucleotide phosphate, adenosine monophosphate, adenosine, and inosine on the surface of the vessel wall with the severity or progression of experimental and clinical atherosclerosis. Furthermore, we tested whether the inhibition of adenosine deaminase will block the development of experimental atherosclerosis. Vascular activities of ecto-nucleoside triphosphate diphosphohydrolase 1, ecto-5'-nucleotidase, and ecto-adenosine deaminase (eADA) were measured in aortas of apolipoprotein E-/- low density lipoprotein receptor (ApoE-/-LDLR-/-) and wild-type mice as well as in human aortas. Plaques were analysed in the entire aorta, aortic root, and brachiocephalic artery by Oil-Red O and Orcein Martius Scarlet Blue staining and vascular accumulation of macrophages. The cellular location of ecto-enzymes was analysed by immunofluorescence. The effect of eADA inhibition on atherosclerosis progression was studied by a 2-month deoxycoformycin treatment of ApoE-/-LDLR-/- mice. The vascular eADA activity prominently increased in ApoE-/-LDLR-/- mice when compared with wild type already at the age of 1 month and progressed along atherosclerosis development, reaching a 10-fold difference at 10 months. The activity of eADA correlated with atherosclerotic changes in human aortas. High abundance of eADA in atherosclerotic vessels originated from activated endothelial cells and macrophages. There were no changes in ecto-nucleoside triphosphate diphosphohydrolase 1 activity, whereas ecto-5'-nucleotidase was moderately decreased in ApoE-/-LDLR-/- mice. Deoxycoformycin treatment attenuated plaque development in aortic root and brachiocephalic artery of ApoE-/-LDLR-/- mice, suppressed vascular

  16. Myocardial Ischaemia, Coronary Atherosclerosis and Pulmonary Pressure Elevation in Antiphospholipid Syndrome Patients.

    Science.gov (United States)

    Padjas, Agnieszka; Płazak, Wojciech; Celińska-Lowenhoff, Magdalena; Mazurek, Adam; Perricone, Carlo; Podolec, Piotr; Musiał, Jacek

    2016-01-01

    Thrombotic events in antiphospholipid syndrome (APS) involve venous and arterial circulation with the possible involvement of coronary or pulmonary microcirculation. To evaluate the influence of antiphospholipid antibodies (aPL) and on myocardial ischaemia assessed by single-photon emission computerized tomography (SPECT), coronary atherosclerosis assessed by multidetector computerized tomography (MDCT) and pulmonary pressure assessed by transthoracic echocardiography (TTE) in patients with primary antiphospholipid syndrome (PAPS). TTE, SPECT (Tc 99m sestamibi) and MDCT-based coronary calcium scoring were performed in 26 consecutive PAPS patients (20 females, 6 males, aged 20-61, mean 39.7) without any signs of other autoimmunological disease and without clinical symptoms of heart disease. Out of 26 patients, TEE showed normal left and right ventricle function in 25 (96.2%) and elevated (≥ 30 mm Hg) right ventricle systolic pressure in 7 (26.9%) patients. SPECT revealed myocardial perfusion defects in 15 (57.7%) patients: exercise-induced in 6 (23.1%) and persistent in 11 (42.3%). MDCT revealed coronary calcifications in 4 (15.4%) patients. The number of plaques ranged from 1 to 11 (median 2), volume 3-201.7 mm³ (median 7), calcium scores 1.3-202.6 (median 5.7). In the group with perfusion defects or coronary calcifications (n = 15), all the patients showed elevated aCL IgG. In most of the relatively young APS patients, without any symptoms of ischemic heart disease, SPECT showed myocardial perfusion defects, and coronary calcifications in 1/6 of them. Right ventricle systolic pressure was elevated in 1/4 of APS patients. These pathologies, well known as cardiovascular risk markers, were associated with elevated levels of the IgG class of both anti-cardiolipin and antiB2 GPI antibodies. Thus, in a high percentage of APS patients, clinically silent myocardial ischaemia, pulmonary pressure elevation and coronary atherosclerosis are present and related to the

  17. The relationship of socioeconomic status with coronary artery calcification and pericardial fat.

    Science.gov (United States)

    Nafakhi, Hussein; Almosawi, Abdulameer; Alnafakh, Hasan; Mousa, Widad

    2017-01-01

    Little data currently exist supporting the correlation of socioeconomic status (SES) to markers of subclinical coronary atherosclerosis. The main aim was to investigate the relationship of SES measured by economic status and educational level with coronary artery calcification (CAC) and pericardial fat volume (PFV) assessed by multi-detector computed tomography (MDCT). A total of 220 consecutive patients with suspected coronary artery disease, who underwent 64-slice MDCT angiography for assessment of coronary atherosclerosis, were recruited between January 2014 and March 2015. Of these, 186 patients were enrolled in this cross sectional study. Low economic status patients showed higher PFV values; median (inter-quartile range [IQR] was 94 [50-140] cm3, p = 0.00001 and r = 0.37, compared to patients with high economic status, and this association persisted even after multiple logistic regression to conventional cardiac risk factors (p = 0.004, CI 7.3-30.4), while patients with low economic status reported a higher calcium score (but statistically non significant) (p = 0.12) compared to high economic status patients. Pa-tients with no formal education showed higher PFV (median [IQR] was 93 [48-140] cm3, p = 0.01) compared to patients with bachelor's degree (median [IQR] was 56 [28-92] cm3), but this association was attenuated after further adjustment for conventional cardiac risk factors (p = 0.1, CI -9.52-10.88), while CAC showed no significant correlation with educational level (p = 0.2, r = 0.117). Socioeconomic status, particularly economic status measure, reported a significant inverse relationship with PFV independent of conventional cardiac risk factors.

  18. Intraocular Lens Calcification; a Clinicopathologic Report

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    Mozhgan Rezaei-Kanavi

    2009-04-01

    Full Text Available

    PURPOSE: To describe the clinical and pathological features of a case of hydrogel intraocular lens (IOL calcification. CASE REPORT: A 48-year-old man underwent explantation of a single-piece hydrophilic acrylic intraocular lens in his left eye because of decreased visual acuity and milky white opalescence of the IOL. The opacified lens was exchanged uneventfully with a hydrophobic acrylic IOL. Gross examination of the explanted IOL disclosed opacification of the optic and haptics. Full-thickness sections of the lens optic were stained with hematoxylin and eosin (H&E, von Kossa and Gram Tworts'. Microscopic examination of the sections revealed fine and diffuse basophilic granular deposits of variable size within the lens optic parallel to the lens curvature but separated from the surface by a moderately clear zone. The deposits were of high calcium content as evident by dark brown staining with von Kossa. Gram Tworts' staining disclosed no microorganisms. CONCLUSION: This report further contributes to the existing literature on hydrogel IOL calcification.

  19. Tofacitinib ameliorates atherosclerosis and reduces foam cell formation in apoE deficient mice.

    Science.gov (United States)

    Wang, Zaicun; Wang, Shumei; Wang, Zunzhe; Yun, Tiantian; Wang, Chenchen; Wang, Huating

    2017-08-19

    Atherosclerosis is a chronic inflammatory cardiovascular disease with high mortality worldwide. Tofacitinib (CP-690,550), an oral small-molecule Janus kinase inhibitor, has been shown to be effective in the treatment of rheumatoid arthritis, autoimmune encephalomyelitis and ulcerative colitis. However, its protective effect against atherosclerosis remains poorly understood. The aim of the present study was to evaluate the effects of Tofacitinib on atherogenic diet (ATD)-induced atherosclerosis using apolipoprotein E deficient (apoE-/-) mice. Atherosclerosis-prone apoE-/- mice were fed with ATD and treated with or without Tofacitinib through intragastrical administration (10 mg kg -1 day -1 ) for 8 weeks. Our results showed that Tofacitinib did not change plasma lipids, while significantly reduced the levels of plasma pro-inflammatory cytokines IL-6 and TNF-α. It also significantly attenuated atherosclerotic plaque lesion in the aortic root and macrophages contained in plaque as shown with Mac2 immuno-staining. Peritoneal macrophages (PMC) were separated from apoE-/- mice fed with 8-week ATD, and then subjected to inflammation tests. Flow cytometry analysis of F4/80 and CD206 and mRNA levels of M1 and M2 macrophages markers showed that M1 macrophages decreased while M2 macrophages increased in Tofacitinib treated group. Expressions of other inflammatory genes also indicated an anti-inflammatory status in mice treated with Tofacitinib. Ox-LDL was used to induce foam cell formation from PMC in wild type mice, and the results displayed a reduced formation of foam cells and decreased inflammation in mice with Tofacitinib administration (1 μM). The mRNA and protein levels of ATP binding cassette subfamily A member 1 (ABCA1), a key gene involved in cholesterol efflux, remarkably increased, while it was absence of alterations in scavenger receptors expression. Therefore, we demonstrated that Tofacitinib could attenuate atherosclerosis and foam cells formation by

  20. Calcification in the portal venous system demonstrated by computed tomography

    Energy Technology Data Exchange (ETDEWEB)

    Hadar, H; Sommer, R

    1983-08-01

    The CT appearance of calcification in the portal venous system in a patient with chronic alcoholic cirrhosis is presented. Reported cases of radiologically detectable calcification in the portal system are rare, and most of them have been associated with longstanding portal hypertension. We presume that with CT this diagnosis will be made more frequently. In the presence of calcification in the portal venous system, portal vein thrombosis is highly probable. This information is of obvious importance to the surgeon contemplating a portal decompressive shunt procedure.

  1. Massive intracranial calcifications in a patient with systemic lupus erythematosus

    International Nuclear Information System (INIS)

    Gasparetto, Emerson L.; Carvalho Neto, Arnolfo de; Ono, Sergio E.

    2004-01-01

    Central nervous system involvement is frequently reported in patients with systemic lupus erythematosus. Computed tomography and magnetic resonance imaging studies usually show brain atrophy, cerebral infarction and/or intracranial bleeding. Extensive intracranial calcification in patients with systemic lupus erythematosus is rare. We report a case of a patient with systemic lupus erythematosus who presented with seizures and massive basal ganglia calcification and mild calcifications in the frontal lobes, seen on the brain computed tomography scan. Magnetic resonance imaging showed hyperintensity on FLAIR images and hypointense signals on T2 * gradient echo images in the basal ganglia. (author)

  2. ATHEROSCLEROSIS DISEASE: A MULTI-FACTORIAL PATHOLOGY

    Directory of Open Access Journals (Sweden)

    Marcieli da Luz Giroldo1; Arienne Serrano Alves1; Francielle Baptista1

    2007-06-01

    Full Text Available Atherosclerosis or arterial stiffening is a gradual disease that restricts the normal blood flow in different areas of body and maylead to secondary illnesses as myocardial infarction and cerebral stroke. Innumerable factors are related to the development ofatherosclerosis, among them are the dyslipidemia; genetic factors; arterial hypertension; diabetes mellitus; obesity; smoking;lack of exercise; pulmonary infection by Chlamydia and stress. Due to multi-factorial atherosclerosis characteristics,innumerable drugs, with differentiated mechanisms of action, are being elaborated to be used in prevention and control of thisdisease. However, beyond the pharmacological therapy, a balanced diet, physical activity and elimination of risk habits, assmoking, also are need for controlling atherosclerosis progression, as well as for the increase of expectative and quality of life

  3. Osteoprotegerin as a marker of atherosclerosis

    DEFF Research Database (Denmark)

    Hosbond, Susanne Elisabeth; Poulsen, Tina Svenstrup; Diederichsen, Axel Cosmus Pyndt

    2012-01-01

    Abstract Objective: Osteoprotegerin (OPG) may be involved in development of atherosclerosis. To evaluate plasma concentrations of OPG in individuals with stable coronary artery disease (CAD), acute coronary syndrome (ACS), peripheral artery disease (PAD) and cerebrovascular disease (CBVD) a syste......Abstract Objective: Osteoprotegerin (OPG) may be involved in development of atherosclerosis. To evaluate plasma concentrations of OPG in individuals with stable coronary artery disease (CAD), acute coronary syndrome (ACS), peripheral artery disease (PAD) and cerebrovascular disease (CBVD...... with clearly defined cohorts qualified for this review. Results: In 11 studies OPG concentrations were elevated. Severity of atherosclerosis was significantly associated with higher OPG concentrations compared to healthy controls. No association between PAD and OPG concentrations was observed. Conclusion: OPG...

  4. Role of gut microbiota in atherosclerosis

    DEFF Research Database (Denmark)

    Jonsson, Annika Lindskog; Bäckhed, Gert Fredrik

    2017-01-01

    describe three pathways by which microbiota might affect atherogenesis. First, local or distant infections might cause a harmful inflammatory response that aggravates plaque development or triggers plaque rupture. Second, metabolism of cholesterol and lipids by gut microbiota can affect the development...... of atherosclerotic plaques. Third, diet and specific components that are metabolized by gut microbiota can have various effects on atherosclerosis; for example, dietary fibre is beneficial, whereas the bacterial metabolite trimethylamine-N-oxide is considered harmful. Although specific bacterial taxa have been...... associated with atherosclerosis, which is supported by increasing mechanistic evidence, several questions remain to be answered to understand fully how the microbiota contributes to atherosclerosis and cardiovascular disease. Such knowledge might pave the way for novel diagnostics and therapeutics based...

  5. Carotid Atherosclerosis and Cognitive Impairment in Nonstroke Patients

    Directory of Open Access Journals (Sweden)

    Wei-Hong Chen

    2017-01-01

    Conclusions: Carotid atherosclerosis can be used to predict the risk of cognitive impairment. Furthermore, diagnosing and treating carotid atherosclerosis at early stage might help clinicians prevent and treat vascular cognitive impairment in nonstroke patients.

  6. Additive effects of lupin protein and phytic acid on aortic calcification in ApoE deficient mice.

    Science.gov (United States)

    Schutkowski, Alexandra; Hirche, Frank; Geissler, Stefanie; Radtke, Juliane; Stangl, Gabriele I

    2015-03-01

    Lupin proteins have repeatedly been shown to exhibit lipid lowering properties and reduce aortic calcification in atherosclerosis models. Despite many efforts on its identification, the component which is responsible for the observed effects is still under debate. Phytic acid which is generally associated with lupin protein isolates has currently been described as bioactive plant compound. The objective of the study was to determine the role of associated phytic acid for the described lupin protein effects. A two-factorial study with ApoE knockout mice was conducted in which mice received lupin protein isolate or casein with or without phytase. Phytic acid was added to the casein diets to a final concentration identical to the lupin protein diets. Here we show that the serum concentrations of cholesterol, lathosterol and desmosterol were lower and the faecal bile acid excretion was higher in the groups fed lupin proteins than in the groups fed casein ( p  < 0.05). Mice that received the lupin protein diet containing phytic acid were characterized by a lower aortic calcification than mice of the other three groups ( p  < 0.05). In conclusion, our results show that the cholesterol lowering properties of lupin protein isolate were not caused by phytic acid. However, the hypocalcific action of lupin proteins appears to depend on the combination of lupin proteins and phytic acid.

  7. Vitamin K2 can suppress the expression of Toll-like receptor 2 (TLR2) and TLR4, and inhibit calcification of aortic intima in ApoE-/- mice as well as smooth muscle cells.

    Science.gov (United States)

    Wang, Zhaojun; Wang, Zhongqun; Zhu, Jie; Long, Xinguang; Yan, Jinchuan

    2018-02-01

    Background and objectives Vascular calcification is a common complication in atherosclerosis. Accumulating evidence showed that Toll-like receptors (TLRs) mediate pro-inflammatory and atherosclerosis. Recent studies demonstrated that vascular calcification is one of the detrimental effects of vitamin K (Vit K) antagonists. However, the effects of Vit K on the expression of TLR2 and 4 and intimal calcification in artery remained unidentified. Methods and results Eighteen ApoE -/- mice were randomly divided into model group, Vit K-treated group, and control group. The mice of model and Vit K-treated group were fed with high-fat diet, while control group mice were fed with normal diet. Mice of Vit K-treated group were administered orally with vitamin K2 (40 mg.kg -1 .day -1 ) for 12 weeks. Twelve weeks later the aortic sections of mice were acquired and stained with hematoxylin and eosin and von Kossa, respectively. Calcium content and activity of alkaline phosphatase (ALP) at aortic tissues were measured. The expression levels of TLR2 and TLR4 in aorta sections were detected by immunohistochemisty and RT-PCR, respectively. The effects of Vit K on cellular calcification were further studied in A7r5 SMCs. Results demonstrated that high-fat diet induced typical atherosclerosis with intimal calcification in ApoE -/- mice, while in Vit K-treated group atherosclerosis and calcium deposits were not serious; Vit K2 also inhibited cellular calcification in A7r5 SMCs. Quantitative analysis showed that calcium and ALP activity at aortic tissues in the Vit K-treated mice were significantly lower than that of the model group ( P < 0.01); Compared to the control group, the expression levels of TLR2 and TLR4 in the model group were significantly higher ( P < 0.05), while in Vit K-treated group the levels of TLR2 and 4 were significantly lower than that in the model group. Furthermore, the content of calcium was positively related to the expression levels of TLR2 and TLR4

  8. Toll-like receptor-2 mediates diet and/or pathogen associated atherosclerosis: proteomic findings.

    Science.gov (United States)

    Madan, Monika; Amar, Salomon

    2008-09-12

    Accumulating evidence implicates a fundamental link between the immune system and atherosclerosis. Toll-like receptors are principal sensors of the innate immune system. Here we report an assessment of the role of the TLR2 pathway in atherosclerosis associated with a high-fat diet and/or bacteria in ApoE(+/-) mice. To explore the role of TLR2 in inflammation- and infection-associated atherosclerosis, 10 week-old ApoE(+/-)-TLR2(+/+), ApoE(+/-)-TLR2(+/-) and ApoE(+/-)-TLR2(-/-) mice were fed either a high fat diet or a regular chow diet. All mice were inoculated intravenously, once per week for 24 consecutive weeks, with 50 microl live Porphyromonas gingivalis (P.g) (10(7) CFU) or vehicle (normal saline). Animals were euthanized 24 weeks after the first inoculation. ApoE(+/-)-TLR2(+/+) mice showed a significant increase in atheromatous lesions in proximal aorta and aortic tree compared to ApoE(+/-)-TLR2(+/-) and ApoE(+/-)-TLR2(-/-) mice for all diet conditions. They also displayed profound changes in plaque composition, as evidenced by increased macrophage infiltration and apoptosis, increased lipid content, and decreased smooth muscle cell mass, all reflecting an unstable plaque phenotype. SAA levels from ApoE(+/-)-TLR2(+/+) mice were significantly higher than from ApoE(+/-)-TLR2(+/-) and ApoE(+/-)-TLR2(-/-) mice. Serum cytokine analysis revealed increased levels of pro-inflammatory cytokines in ApoE(+/-)-TLR2(+/+) mice compared to ApoE(+/-)-TLR2(+/-) and TLR2(-/-) mice, irrespective of diet or bacterial challenge. ApoE(+/-)-TLR2(+/+) mice injected weekly for 24 weeks with FSL-1 (a TLR2 agonist) also demonstrated significant increases in atherosclerotic lesions, SAA and serum cytokine levels compared to ApoE(+/-)-TLR2(-/-) mice under same treatment condition. Finally, mass-spectrometry (MALDI-TOF-MS) of aortic samples analyzed by 2-dimensional gel electrophoresis differential display, identified 6 proteins upregulated greater than 2-fold in ApoE(+/-)-TLR2(+/+) mice

  9. Toll-like receptor-2 mediates diet and/or pathogen associated atherosclerosis: proteomic findings.

    Directory of Open Access Journals (Sweden)

    Monika Madan

    2008-09-01

    Full Text Available Accumulating evidence implicates a fundamental link between the immune system and atherosclerosis. Toll-like receptors are principal sensors of the innate immune system. Here we report an assessment of the role of the TLR2 pathway in atherosclerosis associated with a high-fat diet and/or bacteria in ApoE(+/- mice.To explore the role of TLR2 in inflammation- and infection-associated atherosclerosis, 10 week-old ApoE(+/--TLR2(+/+, ApoE(+/--TLR2(+/- and ApoE(+/--TLR2(-/- mice were fed either a high fat diet or a regular chow diet. All mice were inoculated intravenously, once per week for 24 consecutive weeks, with 50 microl live Porphyromonas gingivalis (P.g (10(7 CFU or vehicle (normal saline. Animals were euthanized 24 weeks after the first inoculation. ApoE(+/--TLR2(+/+ mice showed a significant increase in atheromatous lesions in proximal aorta and aortic tree compared to ApoE(+/--TLR2(+/- and ApoE(+/--TLR2(-/- mice for all diet conditions. They also displayed profound changes in plaque composition, as evidenced by increased macrophage infiltration and apoptosis, increased lipid content, and decreased smooth muscle cell mass, all reflecting an unstable plaque phenotype. SAA levels from ApoE(+/--TLR2(+/+ mice were significantly higher than from ApoE(+/--TLR2(+/- and ApoE(+/--TLR2(-/- mice. Serum cytokine analysis revealed increased levels of pro-inflammatory cytokines in ApoE(+/--TLR2(+/+ mice compared to ApoE(+/--TLR2(+/- and TLR2(-/- mice, irrespective of diet or bacterial challenge. ApoE(+/--TLR2(+/+ mice injected weekly for 24 weeks with FSL-1 (a TLR2 agonist also demonstrated significant increases in atherosclerotic lesions, SAA and serum cytokine levels compared to ApoE(+/--TLR2(-/- mice under same treatment condition. Finally, mass-spectrometry (MALDI-TOF-MS of aortic samples analyzed by 2-dimensional gel electrophoresis differential display, identified 6 proteins upregulated greater than 2-fold in ApoE(+/--TLR2(+/+ mice fed the high fat

  10. [Psychosocial factors as predictors of atherosclerosis and cardiovascular events: contribution from animal models].

    Science.gov (United States)

    Alboni, Paolo; Alboni, Marco

    2006-11-01

    Conventional risk factors (abnormal lipids, hypertension, etc.) are independent predictors of atherosclerosis and cardiovascular events; however, these factors are not specific since about half patients with acute myocardial infarction paradoxically result at low cardiovascular risk. Recent prospective studies provide convincing evidence that some psychosocial factors are independent predictors of atherosclerosis and cardiovascular events, as well. Psychosocial factors that promote atherosclerosis can be divided into two general categories: chronic stressors, including social isolation/low social support and work stress (subordination without job control) and emotional factors, including affective disorders such as depression, severe anxiety and hostility/anger. The emotional factors, such as the chronic stressors, activate the biological mechanisms of chronic stress: increased activity of the hypothalamic-pituitary-adrenal axis, sympathetic system and inflammation processes, which have atherogenic effects, and an increase in blood coagulation. In spite of the amount of published data, psychosocial factors receive little attention in the medical setting. About 30 years ago, Kuller defined the criteria for a causal relation between a risk factor and atherosclerosis and cardiac events. The first of these criteria states that experimental research should demonstrate that any new factor would increase the extent of atherosclerosis or its complications in suitable animal models. We carried out a bibliographic research in order to investigate whether the results of the studies dealing with animal examination and experimentation support the psychosocial factors as predictors of atherosclerosis. Contributions related to some of the psychosocial factors such as social isolation, subordination and hostility/anger have been found. In these studies atherosclerotic extension has been evaluated at necroscopy; however, the incidence of cardiovascular events has not been

  11. Infrapopliteal calcification patterns in critical limb ischemia: diagnostic, pathologic and therapeutic implications in the search for the endovascular holy grail.

    Science.gov (United States)

    Mustapha, Jihad A; Diaz-Sandoval, Larry J; Saab, Fadi

    2017-06-01

    Critical limb ischemia (CLI) represents the terminal stage of peripheral arterial disease (PAD) and is characterized by multilevel and multivessel disease. Amongst patients with infrainguinal disease, approximately one third have predominantly isolated infrapopliteal disease and the remaining two thirds, a combination of femoropopliteal and infrapopliteal disease. Isolated infrapopliteal disease is mainly seen in the elderly, diabetic, or dialysis-dependent patients. These patients have higher risk of amputation and shorter amputation-free survival. Infrapopliteal disease presents with either complex high-grade calcified tandem lesions in multiple vessels or with long chronic total occlusion (CTO) segments with plaques characterized by higher calcium and lower fibro-fatty content than the inflow vessels, as arterial calcium deposition increases as we progress distally in the arterial tree. Vascular calcification occurs in both intima and media. Intimal calcification leads to development of calcified atheroma and occlusive lesions. Medial calcification leads to stiffening and decrease in arterial wall elasticity and compliance leading to atherosclerosis, reduced perfusion, and PAD, increasing cardiovascular mortality among patients with end-stage renal disease. This article attempts to review the implications of the diverse pathologic patterns of calcium distribution in infrapopliteal vessels of CLI patients, on the diagnostic modalities, technological developments, and the evolution of therapeutic approaches to improve outcomes among these patients. A critical analysis of the currently available data is provided, pointing to the surprising omission on the role of calcium on outcomes, and future directions are discussed. Is infrapopliteal calcium a roadblock or the avenue towards new paths? Necessity remains the mother of invention.

  12. Quantitative X-ray CT analysis of calcification of the abdominal aorta and its relationship to obesity

    International Nuclear Information System (INIS)

    Shinagawa, Toshio; Hiraiwa, Yoshio; Mizuno, Seio; Kusunoki, Norio; Nitta, Yu; Matsubara, Takao; Iwainaka, Yoichi; Konishi, Hideo

    1992-01-01

    Quantitative analysis of abdominal aorta calcification by X-ray CT is useful method for non-invasive diagnosis of atherosclerosis. We recently examined the relationship between the X-ray CT measurement of abdominal aorta calcification and the degree of obesity. For this purpose, the body mass index (BMI) and the subcutaneous fat thickness (determined by X-ray CT at the umbilical level) were analyzed in relation to the abdominal aorta calcification index (ACI) in 845 patients (453 males and 392 females aged 40-79 years). Patients with BMI under 20 were classified as 'lean', those with BMI between 20-26 as 'normal' and those with BMI over 26 as 'obese'. 1. Among males, the ACI was highest in lean individuals and lowest in obese individuals. The difference in ACI between lean and obese males was significant in the middle aged group (40-65 years). Among females, no relationship was observed between the degree of obesity and ACI. 2. Among males, ACI was higher in individuals with low subcutaneous fat thickness and lower in individuals with greater subcutaneous fat thickness. The difference was significant in the middle aged group. Among females, no relationship was observed between the two parameters. 3. When the visceral fat to subcutaneous fat ratio (V/S) in 85 males and females aged 60-69 years was analyzed in relation to ACI, ACI tended to decrease as the V/S increased, in both males and females. 4. Relationships between BMI and subcutaneous fat thickness, between BMI and lipids and between lipids and ACI were also analyzed. (author)

  13. Nutrigenetics and nutrigenomics of atherosclerosis.

    Science.gov (United States)

    Merched, Aksam J; Chan, Lawrence

    2013-06-01

    The latest genome-wide association studies (GWAS) have re-energized our effort to understand the genetic basis of atherosclerotic cardiovascular disease. Although the knowledge generated by GWAS has confirmed that mediators of inflammation and perturbed lipid metabolism are major players in cardiovascular disease (CVD) development, much of individual disease heritability remains unexplained by the variants identified through GWAS. Moreover, results from interventions that aim at the pharmaceutical modification of lipid parameters fall short of expectation. These elusive treatment goals based on heritability studies highlight a key supportive, and perhaps even primary, role of nutritional therapy to achieve better health outcomes. Nonetheless, effective and specific interventions for CVD prevention using principles of "personalized" nutrition require a better knowledge of gene-diet interactions, an area that remains poorly explored. Dietary fatty acids such as omega-3 polyunsaturated fatty acids (PUFAs) are an excellent example of a widely studied "environment" that interacts with the genetic makeup in relation to CVD. A thorough exploration of the nutrigenomics and nutrigenetics of omega-3 PUFAs is key to understanding the etiology, and developing effective preventive measures. In this review, we will summarize the current state of knowledge of genetic interactions with omega-3 PUFAs in modulating lipid metabolism and inflammation, and defining health outcomes. Nutrigenetics and nutrigenomics are still in their infancy with respect to CVD prediction and therapy. Integration of the progress in the omics, including metabolomics, lipidomics, transcriptomics, and proteomics, coupled with advances in nutrigenomic and nutrigenetic research will move us towards personalized medicine as the ultimate paradigm of responsible clinical practice.

  14. A Waving Horn on the Big Mitral Annulus Calcification: Caseous Calcification of the Mitral Annulus with Abscess Formation

    Directory of Open Access Journals (Sweden)

    Li-Tan Yang

    2014-06-01

    Full Text Available Caseous calcification of the mitral annulus (CCMA is a rare variant of mitral annular calcification. It comprises a combination of calcium, fatty acids, and cholesterol, and is characterized by heterogeneity in echocardiographic images, with peripheral areas of calcification surrounding a central area of echolucency, resembling a periannular mass. Here, we describe a case of CCMA combined with a mitral annulus abscess, manifesting as a waving, horn-like structure. Although the image characteristics of the posterior mitral annulus suggested CCMA, additional findings warranted further work-up and studies.

  15. Association of aortic valve calcification to the presence, extent, and composition of coronary artery plaque burden: from the Rule Out Myocardial Infarction using Computer Assisted Tomography (ROMICAT) trial.

    Science.gov (United States)

    Mahabadi, Amir A; Bamberg, Fabian; Toepker, Michael; Schlett, Christopher L; Rogers, Ian S; Nagurney, John T; Brady, Thomas J; Hoffmann, Udo; Truong, Quynh A

    2009-10-01

    Aortic valve calcification (AVC) is associated with cardiovascular risk factors and coronary artery calcification. We sought to determine whether AVC is associated with the presence and extent of overall plaque burden, as well as to plaque composition (calcified, mixed, and noncalcified). We examined 357 subjects (mean age 53 +/- 12 years, 61% male) who underwent contrast-enhanced electrocardiogram-gated 64-slice multidetector computed tomography from the ROMICAT trial for the assessment of presence and extent of coronary plaque burden according to the 17-coronary segment model and presence of AVC. Patients with AVC (n = 37, 10%) were more likely than those without AVC (n = 320, 90%) to have coexisting presence of any coronary plaque (89% vs 46%, P AVC had >3-fold increase odds of having any plaque (adjusted odds ratio [OR] 3.6, P = .047) and an increase of 2.5 segments of plaque (P AVC. When stratified by plaque composition, AVC was associated most with calcified plaque (OR 5.2, P = .004), then mixed plaque (OR 3.2, P = .02), but not with noncalcified plaque (P = .96). Aortic valve calcification is associated with the presence and greater extent of coronary artery plaque burden and may be part of the later stages of the atherosclerosis process, as its relation is strongest with calcified plaque, less with mixed plaque, and nonsignificant with noncalcified plaque. If AVC is present, consideration for aggressive medical therapy may be warranted.

  16. Association of the C-Reactive Protein Gene (CRP rs1205 C>T Polymorphism with Aortic Valve Calcification in Patients with Aortic Stenosis

    Directory of Open Access Journals (Sweden)

    Ewa Wypasek

    2015-10-01

    Full Text Available Elevation in C-reactive protein (CRP levels have been shown in patients with aortic valve stenosis (AS. Minor allele of the CRP gene (CRP rs1205 C>T polymorphism has been associated with lower plasma CRP concentrations in cohorts of healthy and atherosclerotic patients. Considering the existing similarities between atherosclerosis and AS, we examined the effect of CRP rs1205 C>T polymorphism on the AS severity. Three hundred consecutive Caucasian patients diagnosed with AS were genotyped for the rs1205 C>T polymorphism using the TaqMan assay. Severity of the AS was assessed using transthoracic echocardiography. The degree of calcification was analyzed semi-quantitatively. Carriers of the rs1205 T allele were characterized by elevated serum CRP levels (2.53 (1.51–3.96 vs. 1.68 (0.98–2.90 mg/L, p < 0.001 and a higher proportion of the severe aortic valve calcification (70.4% vs. 55.1%, p = 0.01 compared with major homozygotes. The effect of CRP rs1205 polymorphism on CRP levels is opposite in AS-affected than in unaffected subjects, suggesting existence of a disease-specific molecular regulatory mechanism. Furthermore, rs1205 variant allele predisposes to larger aortic valve calcification, potentially being a novel genetic risk marker of disease progression.

  17. New modalities of ultrasound-based intima-media thickness, arterial stiffness and non-coronary vascular calcifications detection to assess cardiovascular risk.

    Science.gov (United States)

    Flore, R; Ponziani, F R; Tinelli, G; Arena, V; Fonnesu, C; Nesci, A; Santoro, L; Tondi, P; Santoliquido, A

    2015-04-01

    Carotid intima-media thickness (c-IMT), arterial stiffness (AS) and vascular calcification (VC) are now considered important new markers of atherosclerosis and have been associated with increased prevalence of cardiovascular events. An accurate, reproducible and easy detection of these parameters could increase the prognostic value of the traditional cardiovascular risk factors in many subjects at low and intermediate risk. Today, c-IMT and AS can be measured by ultrasound, while cardiac computed tomography is the gold standard to quantify coronary VC, although concern about the reproducibility of the former and the safety of the latter have been raised. Nevertheless, a safe and reliable method to quantify non-coronary (i.e., peripheral) VC has not been detected yet. To review the most innovative and accurate ultrasound-based modalities of c-IMT and AS detection and to describe a novel UltraSound-Based Carotid, Aortic and Lower limbs Calcification Score (USB-CALCs, simply named CALC), allowing to quantify peripheral calcifications. Finally, to propose a system for cardiovascular risk reclassification derived from the global evaluation of "Quality Intima-Media Thickness", "Quality Arterial Stiffness", and "CALC score" in addition to the Framingham score.

  18. Clinical significance of intramammary arterial calcifications in diabetic women

    Directory of Open Access Journals (Sweden)

    Milošević Zorica

    2004-01-01

    Full Text Available Background. It is well known that intramammary arterial calcifications diagnosed by mammography as a part of generalized diabetic macroangiopathy may be an indirect sign of diabetes mellitus. Hence, the aim of this study was to determine the incidence of intramammary arterial calcifications, the patient’s age when the calcifications occur, as well as to observe the influence of diabetic polineuropathy, type, and the duration of diabetes on the onset of calcifications, in comparison with nondiabetic women. Methods. Mammographic findings of 113 diabetic female patients (21 with type 1 diabetes and 92 with type 2, as well as of 208 nondiabetic women (the control group were analyzed in the prospective study. The data about the type of diabetes, its duration, and polineuropathy were obtained using the questionnaire. Statistical differences were determined by Mann-Whitney test. Results. Intramammary arterial calcifications were identified in 33.3% of the women with type 1 diabetes, in 40.2% with type 2, and in 8.2% of the women from the control group, respectively. The differences comparing the women with type 1, as well as type 2 diabetes and the controls were statistically significant (p=0.0001. Women with intramammary arterial calcifications and type 1 diabetes were younger comparing to the control group (median age 52 years, comparing to 67 years of age, p=0.001, while there was no statistically significant difference in age between the women with calcifications and type 2 diabetes (61 years of age in relation to the control group (p=0.176. The incidence of polineuropathy in diabetic women was higher in the group with intramammary arterial calcifications (52.3% in comparison to the group without calcifications (26.1%, (p=0.005. The association between intramammary arterial calcifications and the duration of diabetes was not found. Conclusion. The obtained results supported the theory that intramammary arterial calcifications, detected by

  19. Prevalence of carotid and pulp calcifications: a correlation using digital panoramic radiographs

    International Nuclear Information System (INIS)

    Clark, Stephen J.; Scheetz, James P.; Khan, Zafrulla; Farman, Allan G.; Horsley, Scott H.; Beckstrom, Brice

    2009-01-01

    To compare the prevalence of pulp calcification with that of carotid calcification using digital panoramic dental radiographs. Digital panoramic radiographs of patients at a dental oncology clinic were included if (1) the carotid artery bifurcation region was visible bilaterally and (2) the patient had non-restored or minimally restored molars and/or canines. An endodontist evaluated the images for pulpal calcifications in the selected teeth. An oral and maxillofacial radiologist independently evaluated the same images for calcifications in the carotid bifurcation region. Odds-ratio and Pearson χ 2 were used for data analysis. Presence of pulpal calcification was also evaluated as a screening test for the presence of carotid calcification. A total of 247 panoramic radiographs were evaluated. 32% (n=80) had pulpal calcifications and 25% (n=61) had carotid calcifications with 12% (n=29) having both carotid and pulp calcifications. A significantly higher prevalence of both pulp and carotid calcification was found in subjects older than age 60 years compared to younger age groups. Accuracy of pulpal calcification in screening for carotid calcification was 66.4%. Both pulp and carotid calcifications were more prevalent in older individuals. The presence of pulp calcification was not a strong predictor for the presence of carotid calcification. (orig.)

  20. Prevalence of carotid and pulp calcifications: a correlation using digital panoramic radiographs

    Energy Technology Data Exchange (ETDEWEB)

    Clark, Stephen J. [School of Dentistry, University of Louisville, Department of Periodontics, Endodontics and Dental Hygiene, Louisville, KY (United States); Scheetz, James P.; Khan, Zafrulla [University of Louisville, Department of Diagnostic Sciences, Prosthodontics and Restorative Dentistry, School of Dentistry, Louisville, KY (United States); Farman, Allan G. [School of Dentistry, University of Louisville, Department of Periodontics, Endodontics and Dental Hygiene, Louisville, KY (United States); Horsley, Scott H.; Beckstrom, Brice

    2009-03-15

    To compare the prevalence of pulp calcification with that of carotid calcification using digital panoramic dental radiographs. Digital panoramic radiographs of patients at a dental oncology clinic were included if (1) the carotid artery bifurcation region was visible bilaterally and (2) the patient had non-restored or minimally restored molars and/or canines. An endodontist evaluated the images for pulpal calcifications in the selected teeth. An oral and maxillofacial radiologist independently evaluated the same images for calcifications in the carotid bifurcation region. Odds-ratio and Pearson {chi}{sup 2} were used for data analysis. Presence of pulpal calcification was also evaluated as a screening test for the presence of carotid calcification. A total of 247 panoramic radiographs were evaluated. 32% (n=80) had pulpal calcifications and 25% (n=61) had carotid calcifications with 12% (n=29) having both carotid and pulp calcifications. A significantly higher prevalence of both pulp and carotid calcification was found in subjects older than age 60 years compared to younger age groups. Accuracy of pulpal calcification in screening for carotid calcification was 66.4%. Both pulp and carotid calcifications were more prevalent in older individuals. The presence of pulp calcification was not a strong predictor for the presence of carotid calcification. (orig.)

  1. High-grade histologic features of DCIS are associated with R5 rather than R3 calcifications in breast screening mammography.

    LENUS (Irish Health Repository)

    Hayes, Brian D

    2013-01-01

    Mammographic calcification is an important radiologic feature of early breast carcinoma whose index of suspicion for malignancy may be reported by a five-tier R-category system. This study aims to describe the histologic diagnoses underlying screen-detected mammographic calcifications using both digital and screen-film mammography, and to correlate these findings with radiologic R-categories. Patients attending the Merrion Breast Screening Unit in Dublin between 2000 and 2011 were identified, who underwent needle-core biopsy for assessment of mammographic calcifications without associated mass or architectural distortion. Radiologic R-category was correlated with biopsy and excision histology reports. A total of 776 cases of calcification were identified, involving 769 individual patients. The radiologic R-categories were as follows: R3 513 (66.1%), R4 192 (24.7%), R5 71 (9.1%). The positive predictive values for malignancy were R3 32.6%, R4 69.8%, R5 95.8%. Several histologic features of DCIS were associated with R5 rather than R3 radiology: high nuclear grade, solid or cribriform architecture, necrosis, periductal inflammation or fibrosis, and associated microinvasive or invasive carcinoma. Mammographic lesions and histologic whole and invasive tumors increased in size from R3 to R5. Radiologic size of calcifications correlated with whole (but not invasive) tumor size, although it tended to underestimate it by several millimeters. Digital-detected calcifications were more likely than screen-film detected to be categorized as R3 and less likely R4 or R5, and there was no significant difference in positive predictive value between the two imaging techniques in any R-category. In conclusion, histologic features of DCIS, in particular those associated with high grade, are associated with R5 radiology. There is no significant difference in positive predictive value for malignancy in any R-category between digital and screen-film mammography.

  2. National Coral Reef Monitoring Program: Calcification Rates of Crustose Coralline Algae Derived from Calcification Accretion Units (CAUs) Deployed across Marianas Archipelago in 2011

    Data.gov (United States)

    National Oceanic and Atmospheric Administration, Department of Commerce — Calcification accretion units, or CAUs, are used to assess the current effects of changes in seawater carbonate chemistry on calcification and accretion rates of...

  3. National Coral Reef Monitoring Program: Calcification Rates of Crustose Coralline Algae Derived from Calcification Accretion Units (CAUs) Deployed across the Pacific Remote Island Areas since 2011

    Data.gov (United States)

    National Oceanic and Atmospheric Administration, Department of Commerce — Calcification accretion units, or CAUs, are used to assess the current effects of changes in seawater carbonate chemistry on calcification and accretion rates of...

  4. National Coral Reef Monitoring Program: Calcification Rates of Crustose Coralline Algae Derived from Calcification Accretion Units (CAUs) Deployed across American Samoa in 2012

    Data.gov (United States)

    National Oceanic and Atmospheric Administration, Department of Commerce — Calcification accretion units, or CAUs, are used to assess the current effects of changes in seawater carbonate chemistry on calcification and accretion rates of...

  5. National Coral Reef Monitoring Program: Calcification Rates of Crustose Coralline Algae Derived from Calcification Accretion Units (CAUs) Deployed across the Hawaiian Archipelago in 2010

    Data.gov (United States)

    National Oceanic and Atmospheric Administration, Department of Commerce — Calcification accretion units, or CAUs, are used to assess the current effects of changes in seawater carbonate chemistry on calcification and accretion rates of...

  6. Cardiovascular calcifications in chronic kidney disease: Potential therapeutic implications.

    Science.gov (United States)

    Bover, Jordi; Ureña-Torres, Pablo; Górriz, José Luis; Lloret, María Jesús; da Silva, Iara; Ruiz-García, César; Chang, Pamela; Rodríguez, Mariano; Ballarín, José

    Cardiovascular (CV) calcification is a highly prevalent condition at all stages of chronic kidney disease (CKD) and is directly associated with increased CV and global morbidity and mortality. In the first part of this review, we have shown that CV calcifications represent an important part of the CKD-MBD complex and are a superior predictor of clinical outcomes in our patients. However, it is also necessary to demonstrate that CV calcification is a modifiable risk factor including the possibility of decreasing (or at least not aggravating) its progression with iatrogenic manoeuvres. Although, strictly speaking, only circumstantial evidence is available, it is known that certain drugs may modify the progression of CV calcifications, even though a direct causal link with improved survival has not been demonstrated. For example, non-calcium-based phosphate binders demonstrated the ability to attenuate the progression of CV calcification compared with the liberal use of calcium-based phosphate binders in several randomised clinical trials. Moreover, although only in experimental conditions, selective activators of the vitamin D receptor seem to have a wider therapeutic margin against CV calcification. Finally, calcimimetics seem to attenuate the progression of CV calcification in dialysis patients. While new therapeutic strategies are being developed (i.e. vitamin K, SNF472, etc.), we suggest that the evaluation of CV calcifications could be a diagnostic tool used by nephrologists to personalise their therapeutic decisions. Copyright © 2016 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.

  7. Basal Ganglia Calcification with Tetanic Seizure Suggest Mitochondrial Disorder

    OpenAIRE

    Finsterer, Josef; Enzelsberger, Barbara; Bastowansky, Adam

    2017-01-01

    Patient: Female, 65 Final Diagnosis: Mitochondrial disorder Symptoms: Headache ? tetanic seizure Medication: Diazepam Clinical Procedure: Admission Specialty: Neurology Objective: Challenging differential diagnosis Background: Basal ganglia calcification (BGC) is a rare sporadic or hereditary central nervous system (CNS) abnormality, characterized by symmetric or asymmetric calcification of the basal ganglia. Case Report: We report the case of a 65-year-old Gypsy female who was admitted for a...

  8. Prostate calcifications: A case series supporting the microbial biofilm theory

    Directory of Open Access Journals (Sweden)

    Tommaso Cai

    2018-05-01

    Full Text Available Purpose: Prostate calcifications are a common finding during transrectal prostate ultrasound in both healthy subjects and patients, but their etiopathogenesis and clinical significance are not fully understood. We aimed to establish a new methodology for evaluating the role of microbial biofilms in the genesis of prostate calcifications. Materials and Methods: Ten consecutive patients who had undergone radical prostatectomy were enrolled in this study. All of the patients presented with prostate calcifications during transrectal ultrasound evaluation before surgery and underwent Meares-Stamey tests and clinical evaluation with the National Institutes of Health Chronic Prostatitis Symptom Index and the International Prostate Symptom Score. At the time of radical prostatectomy, the prostate specimen, after removal, was analyzed with ultrasonography under sterile conditions in the operating room. Core biopsy specimens were taken from the site of prostate calcification and subjected to ultrastructural and microbiological analysis. Results: The results of the Meares-Stamey test showed only 1 of 10 patients (10% with positive cultures for Escherichia coli. Two of five patients (40% had positive cultures from prostate biopsy specimens. Enterococcus faecalis, Enterococcus raffinosus, and Citrobacter freundii were isolated. Ultrastructural analysis of the prostate biopsy specimens showed prostate calcifications in 6 of 10 patients (60%, and a structured microbial biofilm in 1 patient who had positive cultures for E. faecalis and E. raffinosus. Conclusions: Although the findings are supported by a low number of patients, this study highlights the validity of the proposed methodology for investigating the role of bacterial biofilms in the genesis of prostate calcification.

  9. Ocean acidification reduces growth and calcification in a marine dinoflagellate.

    Directory of Open Access Journals (Sweden)

    Dedmer B Van de Waal

    Full Text Available Ocean acidification is considered a major threat to marine ecosystems and may particularly affect calcifying organisms such as corals, foraminifera and coccolithophores. Here we investigate the impact of elevated pCO2 and lowered pH on growth and calcification in the common calcareous dinoflagellate Thoracosphaera heimii. We observe a substantial reduction in growth rate, calcification and cyst stability of T. heimii under elevated pCO2. Furthermore, transcriptomic analyses reveal CO2 sensitive regulation of many genes, particularly those being associated to inorganic carbon acquisition and calcification. Stable carbon isotope fractionation for organic carbon production increased with increasing pCO2 whereas it decreased for calcification, which suggests interdependence between both processes. We also found a strong effect of pCO2 on the stable oxygen isotopic composition of calcite, in line with earlier observations concerning another T. heimii strain. The observed changes in stable oxygen and carbon isotope composition of T. heimii cysts may provide an ideal tool for reconstructing past seawater carbonate chemistry, and ultimately past pCO2. Although the function of calcification in T. heimii remains unresolved, this trait likely plays an important role in the ecological and evolutionary success of this species. Acting on calcification as well as growth, ocean acidification may therefore impose a great threat for T. heimii.

  10. Prevalence of breast arterial calcification in hypertensive patients

    International Nuclear Information System (INIS)

    Cetin, M.; Cetin, R.; Tamer, N.

    2004-01-01

    AIM: To determine the age-specific prevalence of breast arterial calcifications in patients with systemic hypertension. METHODS: The mammograms and patient records of 2406 women who underwent screening or diagnostic mammography were reviewed retrospectively. Mammograms were evaluated for the presence of arterial calcification and results were coded. Hypertension was defined as use of anti-hypertensive agents and diabetes was defined as use of oral hypoglycaemic agents or insulin. RESULTS: The prevalence of breast arterial calcification among hypertensives (17.6%) was lower than among diabetics (25.4%). The prevalence in the non-diabetic, non-hypertensive group was lowest (7.3%). The prevalence increased with age in all three groups. The highest prevalence was found in diabetics older than 60 years (81.8%). Breast arterial calcification was not found among women younger than 40 years. CONCLUSION: Breast arterial calcification is associated with hypertension and prevalence increases with age. Breast arterial calcification on mammograms may indicate unsuspected hypertension especially in non-diabetic patients

  11. Evaluation of laryngeal cartilage calcification in computed tomography

    International Nuclear Information System (INIS)

    Laskowska, K.; Serafin, Z.; Lasek, W.; Maciejewski, M.; Wieczor, W.; Wisniewski, S.

    2008-01-01

    Computed tomography (CT) is one of the basic methods used for laryngeal carcinoma diagnostics. Osteosclerotic and osteolytic changes of the cartilages are considered as a common radiologic symptom of laryngeal neoplasms. The aim of this paper was to evaluate the prevalence of both osteosclerotic changes and focal calcification defects, which may be suggestive of osteolysis. Calcification was assessed in the thyroid, the cricoid and the arytenoids cartilages on CT images of the neck. We have retrospectively analyzed neck CT examinations of 50 patients without any laryngeal pathology in anamnesis. The grade and symmetry of calcifications was assessed in the thyroid, the cricoid and the arytenoids cartilages. Calcification of the laryngeal cartilages was present in 83% of the patients. Osteosclerotic lesions of the thyroid cartilage were seen in 70% of the patients (asymmetric in 60% of them), of the cricoid catrilage in 50% (asymmetric in 60%), and of the arytenoid cartilages in 24% (asymmetric in 67%). Focal calcification defects were present in the thyroid cartilage in 56% of the patients (asymmetric in 67% of them), in the cricoid catrilage in 8% (asymmetric in all cases), and in the arytenoid cartilages in 20% (asymmetric in 90%). Osteosclerotic changes and focal calcification defects, which may suggest osteolysis, were found in most of the patients. Therefore, they cannot be used as crucial radiological criteria of neoplastic invasion of laryngeal cartilages. (authors)

  12. Fruit Intake and Abdominal Aortic Calcification in Elderly Women: A Prospective Cohort Study

    Directory of Open Access Journals (Sweden)

    Nicola P. Bondonno

    2016-03-01

    Full Text Available Cardiovascular disease (CVD is the leading cause of death worldwide. There is a consistent inverse relationship between fruit intake with CVD events and mortality in cross-sectional and prospective observational studies, but the relationship of fruit intake with measurements of atherosclerosis in humans is less clear. Nutritional effects on abdominal aortic calcification (AAC, a marker for subclinical intimal and medial atherosclerotic vascular disease, have not been studied previously. The aim of this study was to examine the cross-sectional relationship of total and individual fruit (apple, pear, orange and other citrus, and banana intake with AAC, scored between 0 and 24. The current study assessed baseline data for a cohort of 1052 women over 70 years of age who completed both a food frequency questionnaire assessing fruit intake, and underwent AAC measurement using dual energy X-ray absorptiometry. AAC scores were significantly negatively correlated with total fruit and apple intakes (p < 0.05, but not with pear, orange or banana intakes (p > 0.25. In multivariable-adjusted logistic regression, each standard deviation (SD; 50 g/day increase in apple intake was associated with a 24% lower odds of having severe AAC (AAC score >5 (odd ratio OR: 0.76 (0.62, 0.93, p = 0.009. Total and other individual fruit intake were not associated with increased odds of having severe AAC. Apple but not total or other fruit intake is independently negatively associated with AAC in older women.

  13. Fruit Intake and Abdominal Aortic Calcification in Elderly Women: A Prospective Cohort Study

    Science.gov (United States)

    Bondonno, Nicola P.; Lewis, Joshua R.; Prince, Richard L.; Lim, Wai H.; Wong, Germaine; Schousboe, John T.; Woodman, Richard J.; Kiel, Douglas P.; Bondonno, Catherine P.; Ward, Natalie C.; Croft, Kevin D.; Hodgson, Jonathan M.

    2016-01-01

    Cardiovascular disease (CVD) is the leading cause of death worldwide. There is a consistent inverse relationship between fruit intake with CVD events and mortality in cross-sectional and prospective observational studies, but the relationship of fruit intake with measurements of atherosclerosis in humans is less clear. Nutritional effects on abdominal aortic calcification (AAC), a marker for subclinical intimal and medial atherosclerotic vascular disease, have not been studied previously. The aim of this study was to examine the cross-sectional relationship of total and individual fruit (apple, pear, orange and other citrus, and banana) intake with AAC, scored between 0 and 24. The current study assessed baseline data for a cohort of 1052 women over 70 years of age who completed both a food frequency questionnaire assessing fruit intake, and underwent AAC measurement using dual energy X-ray absorptiometry. AAC scores were significantly negatively correlated with total fruit and apple intakes (p 0.25). In multivariable-adjusted logistic regression, each standard deviation (SD; 50 g/day) increase in apple intake was associated with a 24% lower odds of having severe AAC (AAC score >5) (odd ratio OR): 0.76 (0.62, 0.93), p = 0.009). Total and other individual fruit intake were not associated with increased odds of having severe AAC. Apple but not total or other fruit intake is independently negatively associated with AAC in older women. PMID:26978394

  14. Inherited disorders of HDL metabolism and atherosclerosis

    NARCIS (Netherlands)

    Hovingh, G Kees; de Groot, E.P.; van der Steeg, Wim; Boekholdt, S Matthijs; Hutten, Barbara A; Kuivenhoven, J.A.; Kastelein, John J P

    PURPOSE OF REVIEW: Genetic disorders of HDL metabolism are rare and, as a result, the assessment of atherosclerosis risk in individuals suffering from these disorders has been difficult. Ultrasound imaging of carotid arteries has provided a tool to assess the risk in hereditary hypo and

  15. Inherited disorders of HDL metabolism and atherosclerosis

    NARCIS (Netherlands)

    Hovingh, G. Kees; de Groot, Eric; van der Steeg, Wim; Boekholdt, S. Matthijs; Hutten, Barbara A.; Kuivenhoven, Jan Albert; Kastelein, John J. P.

    2005-01-01

    Purpose of review Genetic disorders of HDL metabolism are rare and, as a result, the assessment of atherosclerosis risk in individuals suffering from these disorders has been difficult. Ultrasound imaging of carotid arteries has provided a tool to assess the risk in hereditary hypo and

  16. Effects of apolipoprotein M in uremic atherosclerosis

    DEFF Research Database (Denmark)

    Bosteen, Markus Høybye; Madsen Svarrer, Eva Martha; Bisgaard, Line Stattau

    2017-01-01

    BACKGROUND AND AIMS: Chronic kidney disease is characterized by uremia and causes premature death, partly due to accelerated atherosclerosis. Apolipoprotein (apo) M is a plasma carrier protein for the lipid sphingosine-1-phosphate (S1P). The Apom-S1P complex associates with HDL, and may contribute...

  17. Cyanotic congenital heart disease and atherosclerosis

    DEFF Research Database (Denmark)

    Tarp, Julie Bjerre; Jensen, Annette Schophuus; Engstrøm, Thomas

    2017-01-01

    Improved treatment options in paediatric cardiology and congenital heart surgery have resulted in an ageing population of patients with cyanotic congenital heart disease (CCHD). The risk of acquired heart disease such as atherosclerosis increases with age.Previous studies have speculated whether...

  18. Overview of Atherosclerosis and Chemical Stressors

    Science.gov (United States)

    Dr. Cascio’s presentation at the workshop titled, “titled “Understanding the Combined Effects of Environmental Chemical and Non-Chemical Stressors: Atherosclerosis as a Model” will highlight atherosclerosis’s rapidly growing role as a cause of increa...

  19. Single-Cell RNA-Seq Reveals the Transcriptional Landscape and Heterogeneity of Aortic Macrophages in Murine Atherosclerosis.

    Science.gov (United States)

    Cochain, Clément; Vafadarnejad, Ehsan; Arampatzi, Panagiota; Jaroslav, Pelisek; Winkels, Holger; Ley, Klaus; Wolf, Dennis; Saliba, Antoine-Emmanuel; Zernecke, Alma

    2018-03-15

    Rationale: It is assumed that atherosclerotic arteries contain several macrophage subsets endowed with specific functions. The precise identity of these subsets is poorly characterized as they ha ve been defined by the expression of a restricted number of markers. Objective: We have applied single-cell RNA-seq as an unbiased profiling strategy to interrogate and classify aortic macrophage heterogeneity at the single-cell level in atherosclerosis. Methods and Results: We performed single-cell RNA sequencing of total aortic CD45 + cells extracted from the non-diseased (chow fed) and atherosclerotic (11 weeks of high fat diet) aorta of Ldlr -/- mice. Unsupervised clustering singled out 13 distinct aortic cell clusters. Among the myeloid cell populations, Resident-like macrophages with a gene expression profile similar to aortic resident macrophages were found in healthy and diseased aortae, whereas monocytes, monocyte-derived dendritic cells (MoDC), and two populations of macrophages were almost exclusively detectable in atherosclerotic aortae, comprising Inflammatory macrophages showing enrichment in I l1b , and previously undescribed TREM2 hi macrophages. Differential gene expression and gene ontology enrichment analyses revealed specific gene expression patterns distinguishing these three macrophage subsets and MoDC, and uncovered putative functions of each cell type. Notably, TREM2 hi macrophages appeared to be endowed with specialized functions in lipid metabolism and catabolism, and presented a gene expression signature reminiscent of osteoclasts, suggesting a role in lesion calcification. TREM2 expression was moreover detected in human lesional macrophages. Importantly, these macrophage populations were present also in advanced atherosclerosis and in Apoe -/- aortae, indicating relevance of our findings in different stages of atherosclerosis and mouse models. Conclusions: These data unprecedentedly uncovered the transcriptional landscape and phenotypic

  20. [Prevalence and risk factors of extra-coronary artery disease in patients with diabetes which confirmed atherosclerosis of coronary arteries].

    Science.gov (United States)

    Gracheva, S A; Biragova, M S; Glazunova, A M; Klefortova, I I; Melkozerov, K V; Shamkhalova, M Sh; Dzhavelidze, M I; Soldatova, T V; Il'in, A V; Deev, A D; Shestakova, M V; Tugeeva, E F; Buziashvili, Iu I

    2014-01-01

    model identified diabetes, reduced renal function, previous myocardial infarction, smoking, ADMA and fibrinogen as factors associated with presence of multifocal atherosclerosis. Coexistence of atherosclerosis in two or more vascular beds was more frequent in P with diabetes and hemodynamically significant CA atherosclerosis than in PWD. It was associated with renal and cardiac dysfunction, excessive activation of mediators of inflammation, hemostasis, and factors of endothelial damage.

  1. Bovine pericardium coated with biopolymeric films as an alternative to prevent calcification: In vitro calcification and cytotoxicity results

    International Nuclear Information System (INIS)

    Nogueira, Grinia M.; Rodas, Andrea C.D.; Weska, Raquel F.; Aimoli, Cassiano G.; Higa, Olga Z.; Maizato, Marina; Leiner, Adolfo A.; Pitombo, Ronaldo N.M.; Polakiewicz, Bronislaw; Beppu, Marisa M.

    2010-01-01

    Bovine pericardium, for cardiac valve fabrication, was coated with either chitosan or silk fibroin film. In vitro calcification tests of coated and non coated bovine pericardium were performed in simulated body fluid solution in order to investigate potential alternatives to minimize calcification on implanted heart valves. Complementary, morphology was assessed by scanning electron microscopy - SEM; X-ray diffraction (XRD) and infrared spectroscopy (FTIR-ATR) were performed for structural characterization of coatings and biocompatibility of chitosan. Silk fibroin films were assayed by in vitro cytotoxicity and endothelial cell growth tests. Bovine pericardium coated with silk fibroin or chitosan did not present calcification during in vitro calcification tests, indicating that these biopolymeric coatings do not induce bovine pericardium calcification. Chitosan and silk fibroin films were characterized as non cytotoxic and silk fibroin films presented high affinity to endothelial cells. The results indicate that bovine pericardium coated with silk fibroin is a potential candidate for cardiac valve fabrication, since the affinity of silk fibroin to endothelial cells can be explored to induce the tissue endothelization and therefore, increase valve durability by increasing their mechanical resistance and protecting them against calcification.

  2. Breast arterial calcifications are correlated with subsequent development of coronary artery calcifications, but their aetiology is predominantly different

    Energy Technology Data Exchange (ETDEWEB)

    Maas, Angela H.E.M. [Department of Cardiology, Isala Klinieken, Groot Wezenland 20, 8011 JW Zwolle (Netherlands)], E-mail: a.maas@diagram-zwolle.nl; Schouw, Yvonne T. van der; Atsma, Femke [Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Heidelberglaan 100, 3584CX Utrecht (Netherlands); Beijerinck, David; Deurenberg, Jan J.M. [Preventicon Breast Cancer Screening Center, Stationsplein 91, 3511ED Utrecht (Netherlands); Mali, Willem P.Th.M. [Department of Radiology, University Medical Center Utrecht, Heidelberglaan 100, 3584CX Utrecht (Netherlands); Graaf, Y. van der [Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Heidelberglaan 100, 3584CX Utrecht (Netherlands)

    2007-09-15

    Objective: To study whether calcifications in breast arteries, as seen on mammograms, predict future development of coronary artery calcifications. Methods: We studied 499 women, aged 49-70 years, participating in a breast cancer screening program and investigated whether arterial calcifications in the breast (BAC) are associated with coronary arterial calcifications (CAC) after 9 years follow-up. Mammograms were reviewed for the presence of BAC. CAC was assessed by multi slice computed tomography (MSCT). With logistic regression analysis the independent effect of various risk factors on BAC and CAC was measured. Results: BAC was present in 58 of 499 women (12%) and CAC score > 0 was present in 262 of 499 women (53%). BAC was strongly associated with CAC (OR 3.2, 95% CI 1.71-6.04) and this remained significant after adjustment for age at baseline and the duration of follow-up (OR 2.1, 95% CI 1.10-4.23). Most CV risk factors were associated with CAC but not with BAC. Only parity was significantly associated with both increased CAC (OR 2.1, 95% CI 1.21-3.60) and increased BAC (OR 5.3, 95% CI 1.23-22.43). Breastfeeding was associated with BAC (OR 3.4, 95% CI 1.40-8.23) but not with CAC (OR 1.3, 95% CI 0.84-1.93). Conclusion: Breast arterial calcifications are predictive of subsequent development of calcifications in the coronary arteries.

  3. The role of T and B cells in human atherosclerosis and atherothrombosis.

    Science.gov (United States)

    Ammirati, E; Moroni, F; Magnoni, M; Camici, P G

    2015-02-01

    Far from being merely a passive cholesterol accumulation within the arterial wall, the development of atherosclerosis is currently known to imply both inflammation and immune effector mechanisms. Adaptive immunity has been implicated in the process of disease initiation and progression interwined with traditional cardiovascular risk factors. Although the body of knowledge regarding the correlation between atherosclerosis and immunity in humans is growing rapidly, a relevant proportion of it derives from studies carried out in animal models of cardiovascular disease (CVD). However, while the mouse is a well-suited model, the results obtained therein are not fully transferrable to the human setting due to intrinsic genomic and environmental differences. In the present review, we will discuss mainly human findings, obtained either by examination of post-mortem and surgical atherosclerotic material or through the analysis of the immunological profile of peripheral blood cells. In particular, we will discuss the findings supporting a pro-atherogenic role of T cell subsets, such as effector memory T cells or the potential protective function of regulatory T cells. Recent studies suggest that traditional T cell-driven B2 cell responses appear to be atherogenic, while innate B1 cells appear to exert a protective action through the secretion of naturally occurring antibodies. The insights into the immune pathogenesis of atherosclerosis can provide new targets in the quest for novel therapeutic targets to abate CVD morbidity and mortality. © 2014 British Society for Immunology.

  4. Persistent low-grade inflammation and regular exercise

    DEFF Research Database (Denmark)

    Åström, Maj-brit; Feigh, Michael; Pedersen, Bente Klarlund

    2010-01-01

    against all of these diseases and recent evidence suggests that the protective effect of exercise may to some extent be ascribed to an anti-inflammatory effect of regular exercise. Visceral adiposity contributes to systemic inflammation and is independently associated with the occurrence of CVD, type 2...... diabetes and dementia. We suggest that the anti-inflammatory effects of exercise may be mediated via a long-term effect of exercise leading to a reduction in visceral fat mass and/or by induction of anti-inflammatory cytokines with each bout of exercise.......Persistent low-grade systemic inflammation is a feature of chronic diseases such as cardiovascular disease (CVD), type 2 diabetes and dementia and evidence exists that inflammation is a causal factor in the development of insulin resistance and atherosclerosis. Regular exercise offers protection...

  5. Endothelial Lipase Concentrations Are Increased in Metabolic Syndrome and Associated with Coronary Atherosclerosis.

    Directory of Open Access Journals (Sweden)

    2005-12-01

    Full Text Available BACKGROUND: Endothelial lipase (EL, a new member of the lipase family, has been shown to modulate high-density lipoprotein (HDL-C metabolism and atherosclerosis in mouse models. We hypothesized that EL concentrations would be associated with decreased HDL-C and increased atherosclerosis in humans. METHODS AND FINDINGS: Healthy individuals with a family history of premature coronary heart disease (n = 858 were recruited as part of the Study of the Inherited Risk of Atherosclerosis. Blood was drawn in the fasting state before and, in a subgroup (n = 510, after administration of a single dose of intravenous heparin. Plasma lipids were measured enzymatically, lipoprotein subclasses were assessed by nuclear magnetic resonance, and coronary artery calcification (CAC was quantified by electron beam computed tomography. Plasma EL mass was measured using a newly developed enzyme-linked immunosorbent assay. Median EL mass in pre-heparin plasma was 442 (interquartile range = 324-617 ng/ml. Median post-heparin mass was approximately 3-fold higher, 1,313 (888-1,927 ng/ml. The correlation between pre-heparin EL mass and post-heparin EL mass was 0.46 (p < 0.001. EL mass concentrations in both pre- and post-heparin plasma significantly correlated with all NCEP ATPIII-defined metabolic syndrome factors: waist circumference (r = 0.28 and 0.22, respectively, p < 0.001 for each, blood pressure (r = 0.18 and 0.24, p < 0.001 for each, triglycerides (r = 0.22, p < 0.001; and 0.13, p = 0.004, HDL cholesterol (r = -0.11, p = 0.002; and -0.18, p < 0.001, and fasting glucose (r = 0.11 and 0.16, p = 0.001 for both. EL mass in both routine (odds ratio [OR] = 1.67, p = 0.01 and post-heparin (OR = 2.42, p = 0.003 plasma was associated with CAC as determined by ordinal regression after adjustment for age, gender, waist circumference, vasoactive medications, hormone replacement therapy (women, and established cardiovascular risk factors. CONCLUSIONS: We report, to our knowledge

  6. Kaempferol and inflammation: From chemistry to medicine.

    Science.gov (United States)

    Devi, Kasi Pandima; Malar, Dicson Sheeja; Nabavi, Seyed Fazel; Sureda, Antoni; Xiao, Jianbo; Nabavi, Seyed Mohammad; Daglia, Maria

    2015-09-01

    Inflammation is an important process of human healing response, wherein the tissues respond to injuries induced by many agents including pathogens. It is characterized by pain, redness and heat in the injured tissues. Chronic inflammation seems to be associated with different types of diseases such as arthritis, allergies, atherosclerosis, and even cancer. In recent years natural product based drugs are considered as the novel therapeutic strategy for prevention and treatment of inflammatory diseases. Among the different types of phyto-constituents present in natural products, flavonoids which occur in many vegetable foods and herbal medicines are considered as the most active constituent, which has the potency to ameliorate inflammation under both in vitro and in vivo conditions. Kaempferol is a natural flavonol present in different plant species, which has been described to possess potent anti-inflammatory properties. Despite the voluminous literature on the anti-inflammatory effects of kaempferol, only very limited review articles has been published on this topic. Hence the present review is aimed to provide a critical overview on the anti-inflammatory effects and the mechanisms of action of kaempferol, based on the current scientific literature. In addition, emphasis is also given on the chemistry, natural sources, bioavailability and toxicity of kaempferol. Copyright © 2015 Elsevier Ltd. All rights reserved.

  7. Osteoprotegerin and biomarkers of vascular inflammation in type 2 diabetes.

    LENUS (Irish Health Repository)

    O'Sullivan, Eoin P

    2010-09-01

    Osteoprotegerin (OPG), receptor activator for nuclear factor kappa beta ligand (RANKL) and tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) are newly discovered members of the tumour necrosis factor-alpha receptor superfamily. While their role in bone metabolism is well described, their function within the vasculature is poorly understood. OPG inhibits vascular calcification in vitro and high serum levels have been demonstrated in type 2 diabetes, but serum RANKL and TRAIL and their potential correlation with well-established biomarkers of subclinical vascular inflammation such as high-sensitivity C-reactive protein (hsCRP) and interleukin-6 (IL-6) have not been described.

  8. The association of breast arterial calcification and metabolic syndrome

    Directory of Open Access Journals (Sweden)

    Seyma Yildiz

    2014-01-01

    Full Text Available OBJECTIVES: We investigated the relationship between metabolic syndrome and breast arterial calcification detected via mammography in a cohort of postmenopausal subjects. METHODS: Among 837 patients referred to our radiology department for mammographic screening, 310 postmenopausal females (105 patients with and 205 patients without breast arterial calcification aged 40 to 73 (mean 55.9±8.4 years were included in this study. The groups were compared with respect to clinical characteristics and metabolic syndrome criteria. Univariate and multivariate analyses identified the factors related to breast arterial calcification. RESULTS: Age, postmenopausal duration and the frequencies of diabetes mellitus, hypertension and metabolic syndrome were significantly higher in the subjects with breast arterial calcification than in those without (p<0.05. Multivariate analysis indicated that age (OR = 1.3, 95% CI = 1.1-1.6, p = 0.001 and metabolic syndrome (OR = 4.0, 95% CI = 1.5−10.4, p = 0.005 were independent predictors of breast arterial calcification detected via mammography. The independent predictors among the features of metabolic syndrome were low levels of high-density lipoproteins (OR = 8.1, 95% CI = 1.0−64.0, p = 0.047 and high blood pressure (OR = 8.7, 95% CI = 1.5−49.7, p = 0.014. CONCLUSIONS: The likelihood of mammographic detection of breast arterial calcification increases with age and in the presence of hypertension or metabolic syndrome. For patients undergoing screening mammography who present with breast arterial calcification, the possibility of metabolic syndrome should be considered. These patients should be informed of their cardiovascular risk factors and counseled on appropriate lifestyle changes.

  9. Effects of long- and short-term darbepoetin-α treatment on oxidative stress, inflammation and endothelial injury in ApoE knockout mice.

    Science.gov (United States)

    Özdemir, Evrim Dursun; Hanikoglu, Aysegul; Cort, Aysegul; Ozben, Beste; Suleymanlar, Gultekin; Ozben, Tomris

    2017-07-01

    Atherosclerosis and atherosclerosis-related complications are the main cause of death in the world. Vascular injury in response to inflammation and enhanced oxidant stress promotes endothelial dysfunction and leads to atherosclerotic lesions. Low-dose treatment with darbepoetin-α may be a potential therapeutic tool for endothelial injury and atherosclerosis. In order to study the effect of darbepoetin-α on endothelial injury and atherosclerosis, we used ApoE-/- mice as the atherosclerotic mice model. We monitored atherosclerosis and plaque formation histochemically in ApoE knockout mice at early and late stages of atherosclerosis. Darbepoetin-α was injected intraperitoneally at a dose of 0.1 μg/kg to ApoE-/- mice. The results of 2 ApoE-/- mice groups injected with darbepoetin-α (early and late stages of atherosclerosis) were compared to the results of the corresponding saline injected ApoE-/- mice groups and the control (C57BL/6) mice. Lipid profile (total cholesterol, triglyceride), inflammation (CRP, IL-6, histamine), endothelial injury (ICAM-1, selectin) and oxidative stress markers (lipid peroxidation, protein oxidation) were significantly increased in 4 atherosclerotic groups compared to the control group. Short-term darbepoetin-α had no marked effects on indicators of inflammation and endothelial injury in the ApoE knockout mice groups compared to the ApoE knockout mice not treated with darbepoetin-α, however, darbepoetin-α significantly decreased 8-isoprostane and protein carbonyl content. Long term darbepoetin-α treatment reduced oxidative stress in ApoE-/- mice. This study contributes to understanding and elucidating the biochemical changes occurring during early and late stages of atherosclerosis development regarding lipid profile, inflammation, endothelial injury and oxidative stress markers.

  10. The Interleukin-6 inflammation pathway from cholesterol to aging – Role of statins, bisphosphonates and plant polyphenols in aging and age-related diseases

    Directory of Open Access Journals (Sweden)

    Omoigui Sota

    2007-03-01

    Full Text Available Abstract We describe the inflammation pathway from Cholesterol to Aging. Interleukin 6 mediated inflammation is implicated in age-related disorders including Atherosclerosis, Peripheral Vascular Disease, Coronary Artery Disease, Osteoporosis, Type 2 Diabetes, Dementia and Alzheimer's disease and some forms of Arthritis and Cancer. Statins and Bisphosphonates inhibit Interleukin 6 mediated inflammation indirectly through regulation of endogenous cholesterol synthesis and isoprenoid depletion. Polyphenolic compounds found in plants, fruits and vegetables inhibit Interleukin 6 mediated inflammation by direct inhibition of the signal transduction pathway. Therapeutic targets for the control of all the above diseases should include inhibition of Interleukin-6 mediated inflammation.

  11. Osteoprotegerin as a Marker of Atherosclerosis in Diabetic Patients

    Directory of Open Access Journals (Sweden)

    Areti Augoulea

    2013-01-01

    Full Text Available Atherosclerosis is the principal cause of cardiovascular disease (CVD and has many risk factors, among which is diabetes. Osteoprotegerin (OPG is a soluble glycoprotein, involved in bone metabolism. OPG is also found in other tissues, and studies have shown that it is expressed in vascular smooth muscle cells. OPG has been implicated in various inflammations and also has been linked to diabetes mellitus. Increased serum OPG levels were found in patients with diabetes and poor glycemic control. Furthermore, prepubertal children with type 1 diabetes have significantly increased OPG levels. Receptor activator of nuclear factor kappa-B ligand (RANKL is not found in the vasculature in normal conditions, but may appear in calcifying areas. OPG and RANKL are important regulators of mineral metabolism in both bone and vascular tissues. Few data are available on the relationship between plasma OPG/RANKL levels and endothelial dysfunction as assessed using noninvasive methods like ultrasound indexes, neither in the general population nor, more specifically, in diabetic patients. The aim of our review study was to investigate, based on the existing data, these interrelationships in order to identify a means of predicting, via noninvasive methods, later development of endothelial dysfunction and vascular complications in diabetic patients.

  12. The Interaction Between IGF-1, Atherosclerosis and Vascular Aging

    Science.gov (United States)

    Higashi, Yusuke; Quevedo, Henry C.; Tiwari, Summit; Sukhanov, Sergiy; Shai, Shaw-Yung; Anwar, Asif; Delafontaine, Patrice

    2014-01-01

    The process of vascular aging encompasses alterations in the function of endothelial (EC) and vascular smooth muscle cells (VSMCs) via oxidation, inflammation, cell senescence and epigenetic modifications, increasing the probability of atherosclerosis. Aged vessels exhibit decreased endothelial antithrombogenic properties, increased reactive oxygen species (ROS) generation and inflammatory signaling, increased migration of VSMCs to the subintimal space, impaired angiogenesis and increased elastin degradation. The key initiating step in atherogenesis is subendothelial accumulation of apolipoprotein-B containing low density lipoproteins resulting in activation of endothelial cells and recruitment of monocytes. Activated endothelial cells secrete “chemokines” that interact with cognate chemokine receptors on monocytes and promote directional migration. Recruitment of immune cells establishes a pro-inflammatory status, further causing elevated oxidative stress, which in turn triggers a series of events including apoptotic or necrotic death of vascular and non-vascular cells. Increased oxidative stress is also considered to be a key factor in mechanisms of aging-associated changes in tissue integrity and function. Experimental evidence indicates that insulin-like growth factor-1 (IGF-1) exerts anti-oxidant, anti-inflammatory and pro-survival effects on the vasculature, reducing atherosclerotic plaque burden and promoting features of atherosclerotic plaque stability. PMID:24943302

  13. [Placental atherosclerosis and markers of endothelial dysfunction in infants born to mothers with gestational diabetes].

    Science.gov (United States)

    López Morales, Cruz Mónica; Brito Zurita, Olga Rosa; González Heredia, Ricardo; Cruz López, Miguel; Méndez Padrón, Araceli; Matute Briseño, Juan Antonio

    2016-08-05

    The pathophysiology of gestational diabetes itself causes hyperstimulation of adipose tissue and of the placenta cells increasing the production of inflammatory cytokines, which cause changes in the tissues exposed such as the placenta and foetus. Therefore, the objective of this study was to compare metabolic markers and endothelial dysfunction in umbilical cord blood, as well as to determine the presence of atherosclerosis in the placentas of newborn infants of patients with gestational diabetes and in patients with normally progressing pregnancies. An analytical cross-sectional study was carried out in 84 patients, obtaining data such as age, smoking and weight gain in pregnancy; the gestational age of the newborns was determined by Capurro, and their weight and destination subsequent to birth, the placentas were also collected in order to look for atherosclerosis through histological studies and glucose, insulin, VLDL-C, HDL-C, triglycerides, cholesterol, fibrinogen, PCR and markers of endothelial dysfunction (adiponectin, VCAM-1, ICAM-1 and IL-6) were determined in blood samples obtained from the umbilical cord. Placental atherosclerosis presented in 28.94% of the group with gestational diabetes compared to 10.52% of the group with normally progressing pregnancies (P=.044); differences were found in glucose, cholesterol, triglycerides, fibrinogen, HOMA-IR, PCR-us, HDL-C, not in VLDL-C. Twenty-one point five percent of the newborns of the gestational diabetes patients required hospitalization, against 5.2% in the control group, Pregnancies that involve diabetes have higher proportion of atherosclerosis, hospitalization of the newborn, insulin resistance, as well as elevation of markers associated with inflammation and endothelial dysfunction in umbilical cord blood. Copyright © 2016 Elsevier España, S.L.U. All rights reserved.

  14. Thymic Stromal Lymphopoietin Attenuates the Development of Atherosclerosis in ApoE−/− Mice

    Science.gov (United States)

    Yu, Kunwu; Zhu, Pengfei; Dong, Qian; Zhong, Yucheng; Zhu, Zhengfeng; Lin, Yingzhong; Huang, Ying; Meng, Kai; Ji, Qingwei; Yi, Guiwen; Zhang, Wei; Wu, Bangwei; Mao, Yi; Cheng, Peng; Zhao, Xiaoqi; Mao, Xiaobo; Zeng, Qiutang

    2013-01-01

    Background Thymic stromal lymphopoietin (TSLP) is a cytokine with multiple effects on the body. For one thing, TSLP induces Th2 immunoreaction and facilitates allergic reaction; for another, it promotes the differentiation of naturally occurring CD4+CD25+Foxp3+ regulatory T cells (nTregs) and maintains immune tolerance. However, the exact role of TSLP in atherosclerosis remains unknown. Methods and Results In vitro, we examined the phenotype of TSLP‐conditioned bone marrow dendritic cells (TSLP‐DCs) of apolipoprotein E–deficient (ApoE−/−) mice and their capacity to induce the differentiation of Tregs. Our results indicated that TSLP‐DCs obtained the characteristics of tolerogenic dendritic cells and increased a generation of CD4+ latency‐associated peptide (LAP)+ Tregs and nTregs when cocultured with naive T cells. In addition, the functional relevance of TSLP and TSLP‐DCs in the development of atherosclerosis was also determined. Interestingly, we found that TSLP was almost absent in cardiovascular tissue of ApoE−/− mice, and TSLP administration increased the levels of antioxidized low‐density lipoprotein IgM and IgG1, but decreased the levels of IgG2a in plasma. Furthermore, mice treated with TSLP and TSLP‐DCs developed significantly fewer (32.6% and 28.2%, respectively) atherosclerotic plaques in the aortic root compared with controls, along with increased numbers of CD4+LAP+ Tregs and nTregs in the spleen and decreased inflammation in the aorta, which could be abrogated by anti‐TGF‐β antibody. Conclusions Our results revealed a protective role for TSLP in atherosclerosis that is possibly mediated by reestablishing a tolerogenic immune response, which may represent a novel possibility for treatment or prevention of atherosclerosis. PMID:23985377

  15. Intranasal delivery of E-selectin reduces atherosclerosis in ApoE-/- mice.

    Directory of Open Access Journals (Sweden)

    Xinhui Li

    Full Text Available Mucosal tolerance to E-selectin prevents stroke and protects against ischemic brain damage in experimental models of stroke studying healthy animals or spontaneously hypertensive stroke-prone rats. A reduction in inflammation and neural damage was associated with immunomodulatory or "tolerogenic" responses to E-selectin. The purpose of the current study on ApoE deficient mice is to assess the capacity of this stroke prevention innovation to influence atherosclerosis, a major underlying cause for ischemic strokes; human E-selectin is being translated as a potential clinical prevention strategy for secondary stroke. Female ApoE-/- mice received intranasal delivery of E-selectin prior to (pre-tolerization or simultaneously with initiation of a high-fat diet. After 7 weeks on the high-fat diet, lipid lesions in the aorta, serum triglycerides, and total cholesterol were assessed as markers of atherosclerosis development. We also assessed E-selectin-specific antibodies and cytokine responses, in addition to inflammatory responses that included macrophage infiltration of the aorta and altered gene expression profiles of aortic mRNA. Intranasal delivery of E-selectin prior to initiation of high-fat chow decreased atherosclerosis, serum total cholesterol, and expression of the leucocyte chemoattractant CCL21 that is typically upregulated in atherosclerotic lesions of ApoE-/- mice. This response was associated with the induction of E-selectin specific cells producing the immunomodulatory cytokine IL-10 and immunosuppressive antibody isotypes. Intranasal administration of E-selectin generates E-selectin specific immune responses that are immunosuppressive in nature and can ameliorate atherosclerosis, a major risk factor for ischemic stroke. These results provide additional preclinical support for the potential of induction of mucosal tolerance to E-selectin to prevent stroke.

  16. Sodium Thiosulfate Therapy for Calcific Uremic Arteriolopathy

    Science.gov (United States)

    Brunelli, Steven M.; Meade, Debra; Wang, Weiling; Hymes, Jeffrey; Lacson, Eduardo

    2013-01-01

    Summary Background and objective Calcific uremic arteriolopathy (CUA) is an often fatal condition with no effective treatment. Multiple case reports and case series have described intravenous sodium thiosulfate (STS) administration in CUA, but no studies have systematically evaluated this treatment. Design, setting, participants, & measurements This study included 172 patients undergoing maintenance hemodialysis who had CUA and were treated with STS between August 2006 and June 2009 at Fresenius Medical Care North America. Of these, 85% completed STS therapy. Clinical, laboratory, and mortality data were abstracted from clinical information systems. Responses to survey questionnaires sent to treating physicians regarding patient-level outcomes were available for 53 patients. Effect on CUA lesions and mortality were summarized as CUA outcomes. Relevant laboratory measures, weight (using pairwise comparisons of values before, during, and after STS), and adverse events were summarized as safety parameters. Results Mean age of the cohort was 55 years, and 74% of patients were women. Median STS dose was 25 g, and median number of doses was 38. Among surveyed patients, CUA completely resolved in 26.4%, markedly improved in 18.9%, improved in 28.3%, and did not improve in 5.7%; in the remaining patients (20.8%), the response was unknown. One-year mortality in patients treated with STS was 35%. Adverse events, laboratory abnormalities, and weight-related changes were mild. Significant reductions in serum phosphorous (P=0.02) and parathyroid hormone (P=0.01) were noted during STS treatment in patients who completed the therapy. Conclusions Although conclusive evidence regarding its efficacy is lacking, a majority of patients who received STS demonstrated clinical improvement in this study. PMID:23520041

  17. Distinct lipid a moieties contribute to pathogen-induced site-specific vascular inflammation.

    Directory of Open Access Journals (Sweden)

    Connie Slocum

    2014-07-01

    Full Text Available Several successful pathogens have evolved mechanisms to evade host defense, resulting in the establishment of persistent and chronic infections. One such pathogen, Porphyromonas gingivalis, induces chronic low-grade inflammation associated with local inflammatory bone loss and systemic inflammation manifested as atherosclerosis. P. gingivalis expresses an atypical lipopolysaccharide (LPS structure containing heterogeneous lipid A species, that exhibit Toll-like receptor-4 (TLR4 agonist or antagonist activity, or are non-activating at TLR4. In this study, we utilized a series of P. gingivalis lipid A mutants to demonstrate that antagonistic lipid A structures enable the pathogen to evade TLR4-mediated bactericidal activity in macrophages resulting in systemic inflammation. Production of antagonistic lipid A was associated with the induction of low levels of TLR4-dependent proinflammatory mediators, failed activation of the inflammasome and increased bacterial survival in macrophages. Oral infection of ApoE(-/- mice with the P. gingivalis strain expressing antagonistic lipid A resulted in vascular inflammation, macrophage accumulation and atherosclerosis progression. In contrast, a P. gingivalis strain producing exclusively agonistic lipid A augmented levels of proinflammatory mediators and activated the inflammasome in a caspase-11-dependent manner, resulting in host cell lysis and decreased bacterial survival. ApoE(-/- mice infected with this strain exhibited diminished vascular inflammation, macrophage accumulation, and atherosclerosis progression. Notably, the ability of P. gingivalis to induce local inflammatory bone loss was independent of lipid A expression, indicative of distinct mechanisms for induction of local versus systemic inflammation by this pathogen. Collectively, our results point to a pivotal role for activation of the non-canonical inflammasome in P. gingivalis infection and demonstrate that P. gingivalis evades immune

  18. Reduced calcification decreases photoprotective capability in the coccolithophorid Emiliania huxleyi.

    Science.gov (United States)

    Xu, Kai; Gao, Kunshan

    2012-07-01

    Intracellular calcification of coccolithophores generates CO₂ and consumes additional energy for acquisition of calcium and bicarbonate ions; therefore, it may correlate with photoprotective processes by influencing the energetics. To address this hypothesis, a calcifying Emiliania huxleyi strain (CS-369) was grown semi-continuously at reduced (0.1 mM, LCa) and ambient Ca²⁺ concentrations (10 mM, HCa) for 150 d (>200 generations). The HCa-grown cells had higher photosynthetic and calcification rates and higher contents of Chl a and carotenoids compared with the naked (bearing no coccoliths) LCa-grown cells. When exposed to stressfull levels of photosynthetically active radiation (PAR), LCa-grown cells displayed lower photochemical yield and less efficient non-photochemical quenching (NPQ). When the LCa- or HCa-grown cells were inversely shifted to their counterpart medium, LCa to HCa transfer increased photosynthetic carbon fixation (P), calcification rate (C), the C/P ratio, NPQ and pigment contents, whereas those shifted from HCa to LCa exhibited the opposite effects. Increased NPQ, carotenoids and quantum yield were clearly linked with increased or sustained calcification in E. huxleyi. The calcification must have played a role in dissipating excessive energy or as an additional drainage of electrons absorbed by the photosynthetic antennae. This phenomenon was further supported by testing two non-calcifying strains, which showed insignificant changes in photosynthetic carbon fixation and NPQ when transferred to LCa conditions.

  19. Left ventricular calcification following postpartum toxic shock syndrome

    Directory of Open Access Journals (Sweden)

    Stella C Pak

    2018-01-01

    Full Text Available Toxic shock syndrome (TSS is a rare but lethal clinical event that can occur during the postpartum period. Early recognition and intervention is critical to improve patient outcomes. This is a case of TSS complicated by cardiac arrest and left ventricular calcification. This is a case report of streptococcal TSS in a 29-year-old female in the postpartum period who presented with fever, abdominal distension, and a purpuric rash. Her hospital course was characterized by multiple organ failure, including respiratory distress syndrome, liver failure, renal failure, and coagulopathy. She was found to have acute compartment syndrome, which resulted in a below-the-knee amputation. She deteriorated further after experiencing cardiac arrest and the development of hypoxic-ischemic encephalopathy with hemorrhagic transformation. A computed tomography scan of the chest revealed evidence of dystrophic myocardial calcification in the left ventricle. She improved clinically but remained ventilator dependent upon discharge to an extended acute care facility. Sepsis-induced cardiomyopathy can result in myocardial calcification. As dystrophic calcification can significantly affect cardiac function, clinicians should rule out cardiac calcification in patients who have had severe septic shock.

  20. Gene expression analysis in calcific tendinopathy of the rotator cuff

    Directory of Open Access Journals (Sweden)

    F Oliva

    2011-06-01

    Full Text Available We evaluated the expression of several genes involved in tissue remodelling and bone development in patients with calcific tendinopathy of the rotator cuff. Biopsies from calcified and non-calcified areas were obtained from 10 patients (8 women and 2 men; average age: 55 years; range: 40-68 with calcific tendinopathy of the rotator cuff. To evaluate the expression of selected genes, RNA extraction, cDNA synthesis and quantitative polymerase chain reaction (PCR were performed. A significantly increased expression of tissue transglutaminase (tTG2 and its substrate, osteopontin, was detected in the calcific areas compared to the levels observed in the normal tissue from the same subject with calcific tendinopathy, whereas a modest increase was observed for catepsin K. There was also a significant decrease in mRNA expression of Bone Morphogenetic Protein (BMP4 and BMP6 in the calcific area. BMP-2, collagen V and vascular endothelial growth factor (VEGF did not show significant differences. Collagen X and matrix metalloproteinase (MMP-9 were not detectable. A variation in expression of these genes could be characteristic of this form tendinopathy, since an increased level of these genes has not been detected in other forms of tendon lesions.

  1. Weight-loss changes PPAR expression, reduces atherosclerosis and improves cardiovascular function in obese insulin-resistant mice

    Energy Technology Data Exchange (ETDEWEB)

    Verreth, Wim; Verhamme, Peter; Pelat, Michael; Ganame, Javier; Bielicki, John K.; Mertens, Ann; Quarck, Rozenn; Benhabiles, Nora; Marguerie, Gerard; Mackness, Bharti; Mackness, Mike; Ninio, Ewa; Herregods, Marie-Christine; Balligand, Jean-Luc; Holvoet, Paul

    2003-09-01

    Weight-loss in obese insulin-resistant, but not in insulin-sensitive, persons reduces CHD risk. It is not known to what extent changes in the adipose gene expression profile are important for reducing CHD risk. We studied the effect of diet restriction-induced weight-loss on gene expression in adipose tissue, atherosclerosis and cardiovascular function in mice with combined leptin and LDL-receptor deficiency. Obesity, hypertriglyceridemia and insulin-resistance are associated with hypertension, impaired left ventricle function and accelerated atherosclerosis in those mice. Diet restriction during 12 weeks caused a 45% weight-loss and changes in the gene expression in adipose tissue of PPARa and PPAR? and of key genes regulating glucose transport and insulin sensitivity, lipid metabolism, oxidative stress and inflammation, most of which are under the transcriptional control of PPARs. These changes were associated with increased insulin-sensitivity, decreased hypertriglyceridemia, reduced mean 24-hour blood pressure and heart rate, restored circadian variations of blood pressure and heart rate, increased ejection fraction, and reduced atherosclerosis. Thus, induction of PPARa and PPAR? in adipose tissue is a key mechanism for reducing atherosclerosis and improving cardiovascular function resulting from weight-loss. Our observations point to the critical role of PPARs in the pathogenesis of cardiovascular features of the metabolic syndrome.

  2. Coronary atherosclerosis: Significance of autophagic armour.

    Science.gov (United States)

    Arora, Mansi; Kaul, Deepak

    2012-09-26

    Autophagy is a lysosomal degradation pathway of cellular components such as organelles and long-lived proteins. Though a protective role for autophagy has been established in various patho-physiologic conditions such as cancer, neurodegeneration, aging and heart failure, a growing body of evidence now reveals a protective role for autophagy in atherosclerosis, mainly by removing oxidatively damaged organelles and proteins and also by promoting cholesterol egress from the lipid-laden cells. Recent studies by Razani et al and Liao et al unravel novel pathways that might be involved in autophagic protection and in this commentary we highlight the importance of autophagy in atherosclerosis in the light of these two recent papers.

  3. Atherosclerosis and Nanotechnology: Diagnostic and Therapeutic Applications.

    Science.gov (United States)

    Kratz, Jeremy D; Chaddha, Ashish; Bhattacharjee, Somnath; Goonewardena, Sascha N

    2016-02-01

    Over the past several decades, tremendous advances have been made in the understanding, diagnosis, and treatment of coronary artery disease (CAD). However, with shifting demographics and evolving risk factors we now face new challenges that must be met in order to further advance are management of patients with CAD. In parallel with advances in our mechanistic appreciation of CAD and atherosclerosis, nanotechnology approaches have greatly expanded, offering the potential for significant improvements in our diagnostic and therapeutic management of CAD. To realize this potential we must go beyond to recognize new frontiers including knowledge gaps between understanding atherosclerosis to the translation of targeted molecular tools. This review highlights nanotechnology applications for imaging and therapeutic advancements in CAD.

  4. mTOR drives cerebral blood flow and memory deficits in LDLR-/- mice modeling atherosclerosis and vascular cognitive impairment.

    Science.gov (United States)

    Jahrling, Jordan B; Lin, Ai-Ling; DeRosa, Nicholas; Hussong, Stacy A; Van Skike, Candice E; Girotti, Milena; Javors, Martin; Zhao, Qingwei; Maslin, Leigh Ann; Asmis, Reto; Galvan, Veronica

    2018-01-01

    We recently showed that mTOR attenuation blocks progression and abrogates established cognitive deficits in Alzheimer's disease (AD) mouse models. These outcomes were associated with the restoration of cerebral blood flow (CBF) and brain vascular density (BVD) resulting from relief of mTOR inhibition of NO release. Recent reports suggested a role of mTOR in atherosclerosis. Because mTOR drives aging and vascular dysfunction is a universal feature of aging, we hypothesized that mTOR may contribute to brain vascular and cognitive dysfunction associated with atherosclerosis. We measured CBF, BVD, cognitive function, markers of inflammation, and parameters of cardiovascular disease in LDLR -/- mice fed maintenance or high-fat diet ± rapamycin. Cardiovascular pathologies were proportional to severity of brain vascular dysfunction. Aortic atheromas were reduced, CBF and BVD were restored, and cognitive dysfunction was attenuated potentially through reduction in systemic and brain inflammation following chronic mTOR attenuation. Our studies suggest that mTOR regulates vascular integrity and function and that mTOR attenuation may restore neurovascular function and cardiovascular health. Together with our previous studies in AD models, our data suggest mTOR-driven vascular damage may be a mechanism shared by age-associated neurological diseases. Therefore, mTOR attenuation may have promise for treatment of cognitive impairment in atherosclerosis.

  5. RENAL INVOLVEMENT IN SUBJECTS WITH PERIPHERAL ATHEROSCLEROSIS

    International Nuclear Information System (INIS)

    FAWZY, A.; IBRAHIM, S.

    2008-01-01

    Ischemic nephropathy is an important cause of renal failure.Sub-clinical renal function abnormalities may exist in patients with extra renal atherosclerosis and may precede the onset of overt ischemic nephropathy. To assess the impact of extrarenal atherosclerosis on the kidney, the study evaluated renal function in 50 subjects with differing degrees of peripheral atherosclerosis without manifest clinical or laboratory signs of ischemic nephropathy and renovascular hypertension.All laboratory testing including total LDL and HDL-cholesterol, triglycerides, ultrasonography with Doppler analysis for the localization of peripheral vascular disease (carotid and lower limb arteries), and non-invasive evaluation of renal function by radionuclide studies of renal plasma flow (MAG3 clearance) and glomerular filtration (DTPA clearance) were determined as well as smoking habit was recorded. By combining sonographic data on arterial tree stenosis (ATS), the subjects were grouped according to the atherosclerotic vascular damage (ATS involvement). The results showed no change in plasma creatinine while DTPA clearance was increased from 91.58±26.53 to 93.47±24.82 ml/min/1.73 m. MAG3 clearance was progressively declined with the severity of vascular damage from 244.86 ± 60.60 to 173.59±58.74 ml/min/1.73 m.Stepwise, multiple regression analysis indicated that MAG3 clearance was best explained by ATS involvement (standardized B coefficient -0.40; P< 0.001), smoking habit (-0.34;P=0.004) and serum LDL-cholesterol (-0.24; P<0.035).It could be concluded that the renal hemodynamic profile in atherosclerotic patients might constitute functional evidence of the silent phase of ischemic renal disease. The findings suggest that renal function should be carefully assessed in patients with extrarenal atherosclerosis, particularly in those with classic cardiovascular risk factors

  6. Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming

    DEFF Research Database (Denmark)

    Zimmer, Sebastian; Grebe, Alena; Bakke, Siril S

    2016-01-01

    -containing lipoproteins in the subendothelial space causes a local overabundance of free cholesterol. Because cholesterol accumulation and deposition of cholesterol crystals (CCs) trigger a complex inflammatory response, we tested the efficacy of the cyclic oligosaccharide 2-hydroxypropyl-β-cyclodextrin (CD), a compound...... of CD as well as for augmented reverse cholesterol transport. Because CD treatment in humans is safe and CD beneficially affects key mechanisms of atherogenesis, it may therefore be used clinically to prevent or treat human atherosclerosis....

  7. Incretin hormones as immunomodulators of atherosclerosis

    Directory of Open Access Journals (Sweden)

    Nuria eAlonso

    2012-09-01

    Full Text Available Atherosclerosis results from endothelial cell dysfunction and inflammatory processes affecting both macro-and microvasculature which are involved in vascular diabetic complications. Glucagon-like peptide 1 (GLP-1 is an incretin hormone responsible for amplification of insulin secretion when nutrients are given orally as opposed to intravenously and it retains its insulinotropic activity in patients with type 2 diabetes mellitus (T2D. GLP-1 based therapies, such as GLP-1 receptor (R agonists and inhibitors of dipeptidyl peptidase 4 (DPP-4, an enzyme that degrades endogenous GLP-1 are routinely used to treat patients with T2D. Recent experimental model studies have established that GLP-1R mRNA is widely expressed in several immune cells. Moreover, its activation contributes to the regulation of both thymocyte and peripheral T cells proliferation and is involved in the maintenance of peripheral regulatory T cells. GLP-1 R is also expressed in endothelial and smooth muscle cells. The effect of incretin hormones on atherosclerogenesis have recently been studied in animal models of apolipoprotein E-deficient mice (apo E-/-. These studies have demonstrated that treatment with incretin hormones or related compounds suppresses the progression of atherosclerosis and macrophage infiltration in the arterial wall as well as a marked anti-oxidative and anti-inflammatory effect on endothelial cells. This effect may have a major impact on the attenuation of atherosclerosis and may help