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Sample records for experimental myocardial necrosis

  1. Comparative evaluation of HMG CoA reductase inhibitors in experimentally-induced myocardial necrosis: Biochemical, morphological and histological studies.

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    Variya, Bhavesh C; Patel, Snehal S; Trivedi, Jinal I; Gandhi, Hardik P; Rathod, S P

    2015-10-05

    The present study was carried out to evaluate the protective effect of different statins on isoproterenol (ISO) induced myocardial necrosis. Atorvastatin, rosuvastatin, fluvastatin, simvastatin and pravastatin (10 mg/kg/day) were administered for 12 weeks. After pretreatment of 12 weeks myocardial necrosis was induced by subsequent injection of ISO (85 mg/kg/day, s.c.) to wistar rats. Serum biochemical parameters like glucose, lipid profile, cardiac markers and transaminases were evaluated. Animals were killed and heart was excised for histopathology and antioxidant study. Statins pretreated rats showed significant protection against ISO induced elevation in serum biochemical parameters and serum level of cardiac marker enzymes and transaminase level as compared to ISO control group. Mild to moderate protection was observed in different statins treated heart in histopathology and TTC stained sections. Result from our study also revealed that statins could efficiently protect against ISO intoxicated myocardial necrosis by impairing membrane bound enzyme integrity and endogenous antioxidant enzyme levels. Amongst all statins used, rosuvastatin and pravastatin were found to have maximum cardio-protective activity against ISO induced myocardial necrosis as compared to other statins. Copyright © 2015 Elsevier B.V. All rights reserved.

  2. Ischemic preconditioning: Protection against myocardial necrosis and apoptosis

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    Efstathios K Iliodromitis

    2007-11-01

    Full Text Available Efstathios K Iliodromitis1, Antigone Lazou2, Dimitrios Th Kremastinos112nd University Department of Cardiology, Medical School, University of Athens, Greece; 2Lab of Animal Physiology, School of Biology, Aristotle University of Thessaloniki, GreeceAbstract: The phenomenon of ischemic preconditioning has been recognized as one of the most potent mechanisms to protect against myocardial ischemic injury. In experimental animals and humans, a brief period of ischemia has been shown to protect the heart from more prolonged episodes of ischemia, reducing infarct size, attenuating the incidence, and severity of reperfusion-induced arrhythmias, and preventing endothelial cell dysfunction. Although the exact mechanism of ischemic preconditioning remains obscure, several reports indicate that this phenomenon may be a form of receptor-mediated cardiac protection and that the underlying intracellular signal transduction pathways involve activation of a number of protein kinases, including protein kinase C, and mitochondrial KATP channels. Apoptosis, a genetically programmed form of cell death, has been associated with cardiomyocyte cell loss in a variety of cardiac pathologies, including cardiac failure and those related to ischemia/reperfusion injury. While ischemic preconditioning significantly reduces DNA fragmentation and apoptotic myocyte death associated with ischemia-reperfusion, the potential mechanisms underlying this effect have not been fully clarified. A comprehensive understanding of these mechanisms and application to clinical scenarios will provide new directions in research and translate this information into new treatment approaches for reducing the extent of ischemia/reperfusion injury.Keywords: preconditioning, ischemia, reperfusion, necrosis, apoptosis

  3. INFLAMMATORY REACTIONS IN EXPERIMENTAL MYOCARDIAL DAMAGE

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    L. D. Khidirova

    2015-12-01

    Full Text Available Aim. To study the role of hormonal and metabolic changes specific to myocardial infarction in the development of inflammatory reactions in the experimental non-coronarogenic myocardial damage. Material and methods. Wistar male rats weighing 180–220 g (n=80 were used in the study. Metabolic myocardial infarction in intact rats and rats with alloxan diabetes was induced by epinephrine injected subcutaneously as single dose or daily (7 days. Myocardial infarction was verified by ECG analysis, and by histological control. Nitroblue tetrazolium test (NBT-test both spontaneous and zymosan induced NBT-test was used to determine the oxygen-dependent functional activity of neutrophils and their biocidal reserve. Determination of cationic proteins in neutrophils of peripheral blood was performed using lysosomal-cationic test. Results. Increase in oxygen-dependent neutrophil biocidal activity was found as well as reduction in biocidal reserves. Indicators of zymosan induced NBT-test raised according to aggravation of hormonal changes much slower: alloxan increased them by 10% only , epinephrine single dose — by 35%, long-term epinephrine administration simultaneously with alloxan — by 54%. At the same time oxygen-independent neutrophil activity determined by intra-neutrophil cationic proteins level was significantly reduced. Blood levels of pro-inflammatory cytokines raised according to progression of the changes in myocardium: tumor necrosis factor-α (from 5.5±0.03 to 12.6±1.23 pg/ml and interleukin-1β (from 6.0±0.18 to 11.1±0.78 pg/ml. Conclusion. Experimental model of hormonal changes specific to myocardial infarction detected a relationship between inflammatory reactions accompanying myocardial damage and increased catecholamine production.

  4. INFLAMMATORY REACTIONS IN EXPERIMENTAL MYOCARDIAL DAMAGE

    Directory of Open Access Journals (Sweden)

    L. D. Khidirova

    2012-01-01

    Full Text Available Aim. To study the role of hormonal and metabolic changes specific to myocardial infarction in the development of inflammatory reactions in the experimental non-coronarogenic myocardial damage. Material and methods. Wistar male rats weighing 180–220 g (n=80 were used in the study. Metabolic myocardial infarction in intact rats and rats with alloxan diabetes was induced by epinephrine injected subcutaneously as single dose or daily (7 days. Myocardial infarction was verified by ECG analysis, and by histological control. Nitroblue tetrazolium test (NBT-test both spontaneous and zymosan induced NBT-test was used to determine the oxygen-dependent functional activity of neutrophils and their biocidal reserve. Determination of cationic proteins in neutrophils of peripheral blood was performed using lysosomal-cationic test. Results. Increase in oxygen-dependent neutrophil biocidal activity was found as well as reduction in biocidal reserves. Indicators of zymosan induced NBT-test raised according to aggravation of hormonal changes much slower: alloxan increased them by 10% only , epinephrine single dose — by 35%, long-term epinephrine administration simultaneously with alloxan — by 54%. At the same time oxygen-independent neutrophil activity determined by intra-neutrophil cationic proteins level was significantly reduced. Blood levels of pro-inflammatory cytokines raised according to progression of the changes in myocardium: tumor necrosis factor-α (from 5.5±0.03 to 12.6±1.23 pg/ml and interleukin-1β (from 6.0±0.18 to 11.1±0.78 pg/ml. Conclusion. Experimental model of hormonal changes specific to myocardial infarction detected a relationship between inflammatory reactions accompanying myocardial damage and increased catecholamine production.

  5. [Histoautoradiographic study of the heart in experimental myocardial ischemia].

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    Makhova, A N; Shliapnikov, V N

    1979-01-01

    Autoradiographic examinations of the heart muscle in experimental myocardial necroses using 3H-thymidine, revealed a high DNA synthesis in the connective tissue cells in the zone of necrosis in the acute period of infarction and its subsequent decrease. Deviations from this regularity were observed when relapses of necrosis developed. The activation of DNA synthesis occurred to a lesser extent in stromal cells of the periinfarction and remote zones of the heart. Muscle cells incorporated 3H-thymidine extremely rarely. When myocardial infarction was combined with aterosclerosis, relapses of necrosis occurred frequently, and morphological changes in many arteries and veins were accompanied by 3H-thymidine incorporation into the nuclei of the endothelium, smooth cells and adventitial cells. Inhibition of DNA synthesis in connective tissue cells of various heart zones was observed in cases of combined myocardial infarction and aterosclerosis and hypertension.

  6. Temporal Trends in the Prevalence, Severity, and Localization of Myocardial Ischemia and Necrosis at Myocardial Perfusion Imaging After Myocardial Infarction.

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    Nudi, Francesco; Schillaci, Orazio; Di Belardino, Natale; Versaci, Francesco; Tomai, Fabrizio; Pinto, Annamaria; Neri, Giandomenico; Procaccini, Enrica; Nudi, Alessandro; Frati, Giacomo; Biondi-Zoccai, Giuseppe

    2017-10-15

    The definition, presentation, and management of myocardial infarction (MI) have changed substantially in the last decade. Whether these changes have impacted on the presence, severity, and localization of necrosis at myocardial perfusion imaging (MPI) has not been appraised to date. Subjects undergoing MPI and reporting a history of clinical MI were shortlisted. We focused on the presence, severity, and localization of necrosis at MPI with a retrospective single-center analysis. A total of 10,476 patients were included, distinguishing 5 groups according to the period in which myocardial perfusion scintigraphy had been performed (2004 to 2005, 2006 to 2007, 2008 to 2009, 2010 to 2011, 2012 to 2013). Trend analysis showed over time a significant worsening in baseline features (e.g., age, diabetes mellitus, and Q waves at electrocardiogram), whereas medical therapy and revascularization were offered with increasing frequency. Over the years, there was also a lower prevalence of normal MPI (from 16.8% to 13.6%) and ischemic MPI (from 35.6% to 32.8%), and a higher prevalence of ischemic and necrotic MPI (from 12.0% to 12.7%) or solely necrotic MPI (from 35.7% to 40.9%, p necrosis (from 19.8% to 8.2%) and moderate necrosis (from 8.5% to 7.8%, p = 0.028). These trends were largely confirmed at regional level and after propensity score matching. In conclusion, the outlook of stable patients with previous MI has substantially improved in the last decade, with a decrease in the severity of residual myocardial ischemia and necrosis, despite an apparent worsening in baseline features. Copyright © 2017 Elsevier Inc. All rights reserved.

  7. [Integrated assessment of serum homeostasis shifts in experimental myocardial infarction].

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    Lebedeva, M A; Medvedeva, U S; Mirzoyan, R S; Maslennikov, D V; Zolotov, N N; Karganov, M Yu

    2013-01-01

    Dynamic changes in serum homeostasis of rats with experimental myocardial infarction evolution using the method of laser correlation spectroscopy were studied. The presence of necrotic myocardial damage was confirmed by electrocardiographic, histological and biochemical methods. Increased contribution of small particles in the acute period of myocardial infarction was detected, which indicates products of catabolism accumulation in serum and changing the level of some proteins. Comparison of subfractional content of sera from rats with varying degrees of extension of myocardial necrosis through the ventricular wall revealed the predominance of particles of low molecular size (up to 10 nm) in animals with transmural infarction and middle-size fraction (50-120 nm) in animals with non-transmural infarction. These results are consistent with the clinical data obtained by this method in patients with Q-wave and non-Q-wave myocardial infarction.

  8. Provoking conditions, management and outcomes of type 2 myocardial infarction and myocardial necrosis.

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    Smilowitz, Nathaniel R; Weiss, Matthew C; Mauricio, Rina; Mahajan, Asha M; Dugan, Kaitlyn E; Devanabanda, Arvind; Pulgarin, Claudia; Gianos, Eugenia; Shah, Binita; Sedlis, Steven P; Radford, Martha; Reynolds, Harmony R

    2016-09-01

    Type 2 myocardial infarction (MI) is defined as myocardial necrosis (myonecrosis) due to an imbalance in supply and demand with clinical evidence of ischemia. Some clinical scenarios of supply-demand mismatch predispose to myonecrosis but limit the identification of symptoms and ECG changes referable to ischemia; therefore, the MI definition may not be met. Factors that predispose to type 2 MI and myonecrosis without definite MI, approaches to treatment, and outcomes remain poorly characterized. Patients admitted to an academic medical center with an ICD-9 diagnosis of secondary myocardial ischemia or non-primary diagnosis of non-ST-elevation MI were retrospectively reviewed. Cases were classified as either MI (n=255) or myonecrosis without definite MI (n=220) based on reported symptoms, ischemic ECG changes, and new wall motion abnormalities. Conditions associated with type 2 MI or myonecrosis included non-cardiac surgery (38%), anemia or bleeding requiring transfusion (32%), sepsis (31%), tachyarrhythmia (23%), hypotension (22%), respiratory failure (23%), and severe hypertension (8%). Inpatient mortality was 5%, with no difference between patients with MI and those with myonecrosis (6% vs. 5%, p=0.41). At discharge, only 43% of patients received aspirin and statin therapy. Type 2 MI and myonecrosis occur frequently in the setting of supply-demand mismatch due to non-cardiac surgery, sepsis, or anemia. Myonecrosis without definite MI is associated with similar in-hospital mortality as type 2 MI; both groups warrant further workup for cardiovascular disease. Antiplatelet and statin prescriptions were infrequent at discharge, reflecting physician uncertainty about the role of secondary prevention in these patients. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

  9. Tumor necrosis factor-alpha increases myocardial microvascular transport in vivo

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    Hansen, P R; Svendsen, J H; Høyer, Christian S

    1994-01-01

    ng/kg for 60 min) on myocardial microvascular transport of a small hydrophilic indicator was examined by the single-injection, residue-detection method. Intracoronary infusion of rTNF-alpha increased myocardial microvascular transport after 120 min. This increase was preceded by a sustained decline...... in cardiac output and was associated with the appearance of areas with myocardial necrosis in the regional left ventricular wall. The myocardial plasma flow rate and maximum plasma flow rate in response to a 30-s coronary occlusion were not influenced by rTNF-alpha, although a decrease in the myocardial...... hydrophilic molecules across the myocardial microvascular barrier in vivo and induce a prolonged decrease in cardiac performance. These effects may be important elements in myocardial pathophysiology....

  10. Magnetic resonance versus technetium-99m pyrophosphate scintigraphy in the detection of perioperative myocardial necrosis

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    Monte, Guilherme Urpia; Drager, Luciano Ferreira; Souza, Fabio Solano de Freitas; Avila, Luiz Francisco Rodrigues de; Parga Filho, Jose Rodrigues; Cesar, Luiz Antonio Machado; Izaki, Marisa; Meneghetti, Jose Claudio; Rochitte, Carlos Eduardo; Kalil Filho, Roberto [Universidade de Sao Paulo (USP), SP (Brazil). Hospital das Clinicas. Instituto do Coracao (InCor)]. E-mail: gumonte@cardiol.br

    2008-07-01

    Background: Perioperative myocardial infarction (POMI) is a complication of coronary artery bypass grafting (CABG) with a potential prognostic impact. Technetium-99m pyrophosphate myocardial scintigraphy (MS) is used in the diagnosis of POMI; however it shows a limited sensitivity for subendocardial lesions. Cardiovascular magnetic resonance imaging (CMRI), in turn, has a high accuracy in the detection of myocardial necrosis. Objective: To compare CMRI and MS for the detection of POMI after CABG. Methods: A total of 24 patients with chronic coronary artery disease were studied using the delayed contrast enhanced CMRI and MS before and after CABG by analyzing the development of areas of perioperative myocardial necrosis (POMI). Biochemical markers of myocardial injury (CKMB and troponin I) were also determined before and after surgery. Results: Nineteen patients completed the study. Of these, 6 (32%) presented POMI on CMRI and 4 (21%) on MS (p = NS). Of the 323 left ventricular segments assessed, 17 (5.3%) showed perioperative necrosis on CMRI and 7 (2.2%) on MS (p = 0.013). moderate agreement was observed between the methods (kappa 0.46). There was disagreement regarding the diagnosis of POMI in 4 (21%) cases, most of them with small areas of perioperative necrosis on CMRI which were not visualized on MS. In all cases with POMI on CMRI, significant CKMB and troponin I elevations were observed. Conclusion: Moderate diagnostic agreement was observed between the methods for the detection of POMI, but CMRI enabled visualization of small areas of perioperative myocardial necrosis which were not identified on MS and were associated with elevation of biochemical markers of myocardial injury. (author)

  11. Tumor necrosis factor-alpha increases myocardial microvascular transport in vivo

    DEFF Research Database (Denmark)

    Hansen, P R; Svendsen, Jesper Hastrup; Høyer, S

    1994-01-01

    Tumor necrosis factor-alpha (TNF-alpha) is a primary mediator in the pathogenesis of tissue injury, and high circulating levels of TNF-alpha are found in a variety of pathological conditions. In open-chest anesthetized dogs, the effects of intracoronary recombinant human TNF-alpha (rTNF-alpha; 10...... hydrophilic molecules across the myocardial microvascular barrier in vivo and induce a prolonged decrease in cardiac performance. These effects may be important elements in myocardial pathophysiology....

  12. Myocardial uptake of indium-111-labeled antimyosin in acute subendocardial infarction: Clinical, histochemical, and autoradiographic correlation of myocardial necrosis

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    Hendel, R.C.; McSherry, B.A.; Leppo, J.A. (Univ. of Massachusetts Medical Center, Worcester (USA))

    1990-11-01

    Indium-111-labeled antimyosin has been utilized in the diagnosis and localization of acute transmural myocardial infarction. The present report describes a patient who presented with a massive subendocardial infarction. Two days after the injection of antimyosin, the patient's clinical status markedly deteriorated and he expired. Postmortem examination demonstrated severe three-vessel coronary artery disease with extensive myocyte death in the endocardium. Autoradiography and histochemical staining of the prosected heart demonstrated high correlation for myocardial necrosis and corresponded to clinical evidence for diffuse subendocardial infarction.

  13. Detecting Acute Myocardial Infarction by Diffusion-Weighted versus T2-Weighted Imaging and Myocardial Necrosis Markers.

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    Jin, Jiyang; Chen, Min; Li, Yongjun; Wang, YaLing; Zhang, Shijun; Wang, Zhen; Wang, Lin; Ju, Shenghong

    2016-10-01

    We used a porcine model of acute myocardial infarction to study the signal evolution of ischemic myocardium on diffusion-weighted magnetic resonance images (DWI). Eight Chinese miniature pigs underwent percutaneous left anterior descending or left circumflex coronary artery occlusion for 90 minutes followed by reperfusion, which induced acute myocardial infarction. We used DWI preprocedurally and hourly for 4 hours postprocedurally. We acquired turbo inversion recovery magnitude T2-weighted images (TIRM T2WI) and late gadolinium enhancement images from the DWI slices. We measured the serum myocardial necrosis markers myoglobin, creatine kinase-MB isoenzyme, and cardiac troponin I at the same time points as the magnetic resonance scanning. We used histochemical staining to confirm injury. All images were analyzed qualitatively. Contrast-to-noise ratio (the contrast between infarcted and healthy myocardium) and relative signal index were used in quantitative image analysis. We found that DWI identified myocardial signal abnormity early (acute myocardial infarction and identified the infarct-related high signal more often than did TIRM T2WI: 7 of 8 pigs (87.5%) versus 3 of 8 (37.5%) ( P =0.046). Quantitative image analysis yielded a significant difference in contrast-to-noise ratio and relative signal index between infarcted and normal myocardium on DWI. However, within 4 hours after infarction, the serologic myocardial injury markers were not significantly positive. We conclude that DWI can be used to detect myocardial signal abnormalities early after acute myocardial infarction-identifying the infarction earlier than TIRM T2WI and widely used clinical serologic biomarkers.

  14. miR-874 regulates myocardial necrosis by targeting caspase-8

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    Wang, K; Liu, F; Zhou, L-Y; Ding, S-L; Long, B; Liu, C-Y; Sun, T; Fan, Y-Y; Sun, L; Li, P-F

    2013-01-01

    Cardiomyocyte death is an important reason for the cardiac syndromes, such as heart failure (HF) and myocardial infarction (MI). In the heart diseases, necrosis is one of the main forms of cell death. MicroRNAs (miRNAs) are a class of small non-coding RNAs that mediate post-transcriptional gene silencing. Hitherto, it is not yet clear whether miRNA can regulate necrosis in cardiomyocyte. In this work, we performed a microarray to detect miRNAs in response to H2O2 treatment, and the results showed that miR-874 was substantially increased. We further studied the function of miR-874, and observed that knockdown of miR-874 attenuated necrosis in the cellular model and also MI in the animal model. We searched for the downstream mediator of miR-874 and identified that caspase-8 was a target of miR-874. Caspase-8 was able to antagonize necrosis. When suppressed by miR-874, caspase-8 lost the ability to repress necrotic program. In exploring the molecular mechanism by which miR-874 expression is regulated, we identified that Foxo3a could transcriptionally repress miR-874 expression. Foxo3a transgenic or knockout mice exhibited a low or high expression level of miR-874, and a reduced or enhanced necrosis and MI. Our present study reveals a novel myocardial necrotic regulating model, which is composed of Foxo3a, miR-874 and caspase-8. Modulation of their levels may provide a new approach for tackling myocardial necrosis. PMID:23828572

  15. Myocyte necrosis underlies progressive myocardial dystrophy in mouse dsg2-related arrhythmogenic right ventricular cardiomyopathy.

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    Pilichou, Kalliopi; Remme, Carol Ann; Basso, Cristina; Campian, Maria E; Rizzo, Stefania; Barnett, Phil; Scicluna, Brendon P; Bauce, Barbara; van den Hoff, Maurice J B; de Bakker, Jacques M T; Tan, Hanno L; Valente, Marialuisa; Nava, Andrea; Wilde, Arthur A M; Moorman, Antoon F M; Thiene, Gaetano; Bezzina, Connie R

    2009-08-03

    Mutations in the cardiac desmosomal protein desmoglein-2 (DSG2) are associated with arrhythmogenic right ventricular cardiomyopathy (ARVC). We studied the explanted heart of a proband carrying the DSG2-N266S mutation as well as transgenic mice (Tg-NS) with cardiac overexpression of the mouse equivalent of this mutation, N271S-dsg2, with the aim of investigating the pathophysiological mechanisms involved. Transgenic mice recapitulated the clinical features of ARVC, including sudden death at young age, spontaneous ventricular arrhythmias, cardiac dysfunction, and biventricular dilatation and aneurysms. Investigation of transgenic lines with different levels of transgene expression attested to a dose-dependent dominant-negative effect of the mutation. We demonstrate for the first time that myocyte necrosis is the key initiator of myocardial injury, triggering progressive myocardial damage, including an inflammatory response and massive calcification within the myocardium, followed by injury repair with fibrous tissue replacement, and myocardial atrophy. These observations were supported by findings in the explanted heart from the patient. Insight into mechanisms initiating myocardial damage in ARVC is a prerequisite to the future development of new therapies aimed at delaying onset or progression of the disease.

  16. MicroRNA-103/107 Regulate Programmed Necrosis and Myocardial Ischemia/Reperfusion Injury Through Targeting FADD.

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    Wang, Jian-Xun; Zhang, Xiao-Jie; Li, Qian; Wang, Kun; Wang, Yin; Jiao, Jian-Qin; Feng, Chang; Teng, Sun; Zhou, Lu-Yu; Gong, Ying; Zhou, Zhi-Xia; Liu, Jia; Wang, Jian-Ling; Li, Pei-feng

    2015-07-31

    Necrosis is one of the main forms of cardiomyocyte death in heart disease. Recent studies have demonstrated that certain types of necrosis are regulated and programmed dependent on the activation of receptor-interacting serine/threonine-protein kinase (RIPK) 1 and 3 which may be negatively regulated by Fas-associated protein with death domain (FADD). In addition, microRNAs and long noncoding RNAs have been shown to play important roles in various biological processes recently. The purpose of this study was to test the hypothesis that microRNA-103/107 and H19 can participate in the regulation of RIPK1- and RIPK3-dependent necrosis in fetal cardiomyocyte-derived H9c2 cells and myocardial infarction through targeting FADD. Our results show that FADD participates in H2O2-induced necrosis by influencing the formation of RIPK1 and RIPK3 complexes in H9c2 cells. We further demonstrate that miR-103/107 target FADD directly. Knockdown of miR-103/107 antagonizes necrosis in the cellular model and also myocardial infarction in a mouse ischemia/reperfusion model. The miR-103/107-FADD pathway does not participate in tumor necrosis factor-α-induced necrosis. In exploring the molecular mechanism by which miR-103/107 are regulated, we show that long noncoding RNA H19 directly binds to miR-103/107 and regulates FADD expression and necrosis. Our results reveal a novel myocardial necrosis regulation model, which is composed of H19, miR-103/107, and FADD. Modulation of their levels may provide a new approach for preventing myocardial necrosis. © 2015 American Heart Association, Inc.

  17. [Extension of necrosis in the acute phase of myocardial infarct. Clinical picture and prognosis].

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    Maresta, A; Melandri, G; Leghissa, R; Magnani, B

    1983-12-01

    In a consecutive series of 297 patients prospectively evaluated at the time of admission for an acute myocardial infarction, the extension of necrosis was found to occur in 16,4% of the cases. The electrocardiographic site of extension was the same as during the initial episode in over 75% of cases suggesting the possibility of a similar pathogenetic mechanism and the involvement of the same coronary district. Patients in Killip class I were respectively 61% and 45% before and after the extension, in class II 33% and 14%, in class III 6% and 14%, in class IV 0 and 27% (p less than 0,001). In-hospital mortality was 16,1% without and 38,8% with extension (p less than 0,001). The peak level of CPK-MB was an average of 110 +/- 45 U/1 before and 96 +/- 34 after the extension (p = N.S.). It was not possible to recognize the patients at risk of extension according to the traditional clinical parameters (age, sex, site of necrosis, transmural involvement, residual angina, Norris index and Killip class before the extension). It is concluded that the protection of the myocardium at risk is of primary importance in the setting of acute myocardial infarction, regardless of the possibility of saving areas already compromised at the time of admission or the hypothetical "border zone".

  18. [The effect of a new phenylalkyl taurine derivative on the size of the necrotic area in experimental myocardial infarct in rats].

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    Sapronov, N S; Torkunov, P A; Eliseev, V V; Krylova, I B; Evdokimova, N R

    1999-01-01

    The study of an anti-ischemic action of a new phenilalkyl taurin derivative TAU-60 has discovered that this drug attenuates ECG signs of myocardial infarction and reduces the size of necrosis zone on the anterior wall of the left ventricular myocardium in rats with experimental myocardial infarction.

  19. Experimental Approaches to Acute Myocardial Infarction

    NARCIS (Netherlands)

    D.B. Uitterdijk (André)

    2015-01-01

    markdownabstractAbstract This thesis is dedicated to i) novel methods and optimization studies to improve the diagnosis of myocardial ischemia and myocardial infarction as well as fundamental studies that precede novel therapies for myocardial infarction. In part ii) 2 novel, adjunctive therapies

  20. Autonomic nervous system instability, tetanic necrosis of the heart and myocardial TNFalpha expression in a tetanus fatal case.

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    Pomara, Cristoforo; Neri, Margherita; Riezzo, Irene; Turillazzi, Emanuela; Fineschi, Vittorio

    2009-08-21

    The cardiovascular manifestations of tetanus consist of disturbances of heart rate and rhythm, blood pressure instability, arrhythmias, myocardial dysfunction and sympathetic overactivity. It was suggested that either a sudden loss of catecholamine stimulation or myocardial damage caused by the direct action of the tetanus toxin, could be involved in cardiac dysfunction described in tetanus. However, histologic evidence of myocardial necrosis in tetanus was demonstrated in few cases. We report a fatal case of tetanus in which we investigated the cardiac morphology and the expression of TNFalpha to elucidate the heart involvement in this case. Since it is well known that myocardial damage caused by catecholamines can induce synthesis of cytokines by myocytes, cytokines, specifically those with known cardiodepressant properties such as TNF-alpha, could be an alternative mechanism involved in cardiac dysfunction in the setting of tetanus.

  1. Cardioprotective effect of Sida rhomboidea. Roxb extract against isoproterenol induced myocardial necrosis in rats.

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    Thounaojam, Menaka C; Jadeja, Ravirajsinh N; Ansarullah; Karn, Sanjay S; Shah, Jigar D; Patel, Dipak K; Salunke, Sunita P; Padate, Geeta S; Devkar, Ranjitsinh V; Ramachandran, A V

    2011-05-01

    The present study investigates cardioprotective effect of Sida rhomboidea. Roxb (SR) extract on heart weight, plasma lipid profile, plasma marker enzymes, lipid peroxidation, endogenous enzymatic and non-enzymatic antioxidants and membrane bound ATPases against isoproterenol (IP) induced myocardial necrosis (MN) in rats. Rats treated with IP (85 mg/kg, s.c.) recorded significant (p<0.05) increment in heart weight, plasma lipid profile, plasma marker enzymes of cardiac damage, cardiac lipid peroxidation (LPO) and activity levels of Ca(+2) ATPase whereas there was significant (p<0.05) decrease in plasma HDL, cardiac endogenous enzymatic and non-enzymatic antioxidants, Na(+)-K(+) ATPase and Mg(+2) ATPase. Pre-treatment with SR extract (400 mg/kg per day, p.o.) for 30 consecutive days followed by IP injections on days 29th and 30th, showed significant (p<0.05) decrease in heart weight, plasma lipid profile, plasma marker enzymes of cardiac damage, cardiac lipid peroxidation, Ca(+2) ATPase and significant increase in plasma HDL, cardiac endogenous enzymatic and non-enzymatic antioxidants, Na(+)-K(+) ATPase and Mg(+2) ATPase compared to IP treated group. Hence, this study is the first scientific report on cardioprotective effect of SR against IP induced MN in rats. Copyright © 2010 Elsevier GmbH. All rights reserved.

  2. Quantifying the Release of Biomarkers of Myocardial Necrosis from Cardiac Myocytes and Intact Myocardium.

    Science.gov (United States)

    Marjot, Jack; Kaier, Thomas E; Martin, Eva D; Reji, Shiney S; Copeland, O'Neal; Iqbal, Mohammed; Goodson, Bob; Hamren, Sarah; Harding, Sian E; Marber, Michael S

    2017-05-01

    Myocardial infarction is diagnosed when biomarkers of cardiac necrosis exceed the 99th centile, although guidelines advocate even lower concentrations for early rule-out. We examined how many myocytes and how much myocardium these concentrations represent. We also examined if dietary troponin can confound the rule-out algorithm. Individual rat cardiac myocytes, rat myocardium, ovine myocardium, or human myocardium were spiked into 400-μL aliquots of human serum. Blood was drawn from a volunteer after ingestion of ovine myocardium. High-sensitivity assays were used to measure cardiac troponin T (cTnT; Roche, Elecsys), cTnI (Abbott, Architect), and cardiac myosin-binding protein C (cMyC; EMD Millipore, Erenna®). The cMyC assay could only detect the human protein. For each rat cardiac myocyte added to 400 μL of human serum, cTnT and cTnI increased by 19.0 ng/L (95% CI, 16.8-21.2) and 18.9 ng/L (95% CI, 14.7-23.1), respectively. Under identical conditions cTnT, cTnI, and cMyC increased by 3.9 ng/L (95% CI, 3.6-4.3), 4.3 ng/L (95% CI, 3.8-4.7), and 41.0 ng/L (95% CI, 38.0-44.0) per μg of human myocardium. There was no detectable change in cTnI or cTnT concentration after ingestion of sufficient ovine myocardium to increase cTnT and cTnI to approximately 1 × 108 times their lower limits of quantification. Based on pragmatic assumptions regarding cTn and cMyC release efficiency, circulating species, and volume of distribution, 99th centile concentrations may be exceeded by necrosis of 40 mg of myocardium. This volume is much too small to detect by noninvasive imaging. © 2017 American Association for Clinical Chemistry.

  3. Peak longitudinal strain most accurately reflects myocardial segmental viability following acute myocardial infarction - an experimental study in open-chest pigs.

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    Aarsaether, Erling; Rösner, Assami; Straumbotn, Espen; Busund, Rolf

    2012-05-29

    The extension and the transmurality of the myocardial infarction are of high predictive value for clinical outcome. The aim of the study was to characterize the ability of longitudinal, circumferential and radial strain measured by 2-dimensional speckle tracking echocardiography (2D-STE) to predict the extent of necrosis in myocardial segments following acute myocardial infarction and to separate transmural necrotic segments from non-transmural necrotic segments in a full 18-segment porcine model. 2D-STE strain was assessed in long- and short-axis following myocardial infarction in ten open-chest anesthetized pigs. Strain was defined according to systolic peak values. In segments displaying both negative and positive peaks, only the peak with the highest absolute value was utilized. Necrosis was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining and expressed as percent of each myocardial segment. Significant correlations were found between the extension of necrosis and all measured parameters of myocardial deformation (p transmural necrotic segments (>50% necrosis) from predominantly viable segments (0-50% necrosis) was significantly larger for longitudinal strain (AUC = 0.98, CI = 0.97-1.00) when compared with circumferential strain (AUC = 0.91, CI = 0.84-0.97, p transmural necrosis. Peak strain values derived from 2D-STE correlate well with the extent of necrosis in myocardial segments following acute myocardial infarction. Longitudinal strain most accurately reflects myocardial segmental viability in this setting.

  4. Diagnosis of Coronary Heart Diseases Using Gene Expression Profiling; Stable Coronary Artery Disease, Cardiac Ischemia with and without Myocardial Necrosis.

    Directory of Open Access Journals (Sweden)

    Nabila Kazmi

    Full Text Available Cardiovascular disease (including coronary artery disease and myocardial infarction is one of the leading causes of death in Europe, and is influenced by both environmental and genetic factors. With the recent advances in genomic tools and technologies there is potential to predict and diagnose heart disease using molecular data from analysis of blood cells. We analyzed gene expression data from blood samples taken from normal people (n = 21, non-significant coronary artery disease (n = 93, patients with unstable angina (n = 16, stable coronary artery disease (n = 14 and myocardial infarction (MI; n = 207. We used a feature selection approach to identify a set of gene expression variables which successfully differentiate different cardiovascular diseases. The initial features were discovered by fitting a linear model for each probe set across all arrays of normal individuals and patients with myocardial infarction. Three different feature optimisation algorithms were devised which identified two discriminating sets of genes, one using MI and normal controls (total genes = 6 and another one using MI and unstable angina patients (total genes = 7. In all our classification approaches we used a non-parametric k-nearest neighbour (KNN classification method (k = 3. The results proved the diagnostic robustness of the final feature sets in discriminating patients with myocardial infarction from healthy controls. Interestingly it also showed efficacy in discriminating myocardial infarction patients from patients with clinical symptoms of cardiac ischemia but no myocardial necrosis or stable coronary artery disease, despite the influence of batch effects and different microarray gene chips and platforms.

  5. Requirement for Tumor Necrosis Factor Receptor 2 Expression on Vascular Cells To Induce Experimental Cerebral Malaria

    OpenAIRE

    Stoelcker, Benjamin; Hehlgans, Thomas; Weigl, Karin; Bluethmann, Horst; Grau, Georges E.; Männel, Daniela N.

    2002-01-01

    Using tumor necrosis factor receptor type 2 (TNFR2)-deficient mice and generating bone marrow chimeras which express TNFR2 on either hematopoietic or nonhematopoietic cells, we demonstrated the requirement for TNFR2 expression on tissue cells to induce lethal cerebral malaria. Thus, TNFR2 on the brain vasculature mediates tumor necrosis factor-induced neurovascular lesions in experimental cerebral malaria.

  6. Spontaneous and bilateral necrosis of the femoral head in a young experimental beagle dog.

    Science.gov (United States)

    Kobayashi, Ryosuke; Kurotaki, Tetsuro; Yamada, Naoaki; Kumabe, Shino; Doi, Takuya; Wako, Yumi; Tsuchitani, Minoru

    2015-04-01

    This report describes the pathological characterizations of a rare case of necrosis of the femoral head that was spontaneous, bilateral, avascular and nontraumatic. A 14-month-old beagle dog was presented with pain in the hind limbs. At necropsy, the articular surface in the bilateral femoral head was markedly irregular. There were no gross abnormalities other than in the hip joints. Microscopically, a wide range of trabecular bone necrosis localized in the subchondral area was observed in both femoral heads. In the right femoral head, fibrosis and proliferative vessels were noted in the subchondral area. The articular cartilage was thickened irregularly, but there was no evidence of cartilage necrosis. The bone marrow adjacent to the affected area showed severe depression. In the metaphysis, atrophic bone marrow, but not bone necrosis, was observed. This was a rare case of spontaneous necrosis of the femoral head in an experimental beagle dog.

  7. Tumor necrosis factor-alpha increases myocardial microvascular transport in vivo

    DEFF Research Database (Denmark)

    Hansen, P R; Svendsen, J H; Høyer, Christian S

    1994-01-01

    Tumor necrosis factor-alpha (TNF-alpha) is a primary mediator in the pathogenesis of tissue injury, and high circulating levels of TNF-alpha are found in a variety of pathological conditions. In open-chest anesthetized dogs, the effects of intracoronary recombinant human TNF-alpha (rTNF-alpha; 100...

  8. Efficacy of tumor necrosis factor-alpha and antibiotics in therapy of experimental murine staphylococcal mastitis.

    Science.gov (United States)

    Sanchez, M S; Ford, C W; Yancey, R J

    1994-05-01

    The mouse model was used to determine the efficacy of the cytokine, tumor necrosis factor-alpha, and antibiotic in treatment of experimentally induced staphylococcal mastitis. Recombinant human tumor necrosis factor-alpha alone administered to the mammary glands of lactating mice recruited significantly more polymorphonuclear neutrophils into the gland by 4 h posttreatment than did the untreated control. One hundred times less recombinant mouse tumor necrosis factor-alpha than human tumor necrosis factor-alpha was required to enhance the killing of Staphylococcus aureus within the gland. Human tumor necrosis factor-alpha effectively enhanced the killing of the bacteria when it was administered 4 to 0 h prior to infection, but not 4 h after infection. When mice were first pretreated with tumor necrosis factor-alpha, infected, and then treated with antibiotics (ciprofloxacin and pirlimycin, but not cloxacillin), the combination of antibiotic and cytokine significantly reduced the number of bacteria within the gland compared with that for mice treated with antibiotic alone, cytokine alone, or placebo. Recombinant tumor necrosis factor-alpha may be an effective adjunct to antimicrobial therapy in treatment of staphylococcal mastitis in the bovine.

  9. Cardioprotective effect of Nerium oleander flower against isoproterenol-induced myocardial oxidative stress in experimental rats.

    Science.gov (United States)

    Gayathri, Veeraraghavan; Ananthi, Subhash; Chandronitha, Chandranayagam; Ramakrishnan, Ganapathy; Lakshmisundaram, Raman; Sundaram, Raman Lakshmi; Vasanthi, Hannah R

    2011-03-01

    Nerium oleander Linn (NOL) an evergreen shrub belonging to the Apocynaceae family has been reported to have a wide spectrum of bioactivities. In in vitro study, the free radical scavenging potential of the hydroethanolic extract of N oleander Linn (ENO) flower and its fractions (glycosidic and nonglycosidic) were studied using 2, 2(')-azino-di [3-ethylbenzthiazoline sulphonate] (ABTS(*+) ) and 1, 1-diphenyl-2-picrylhydrazyl (DPPH*) scavenging assay. ENO exhibited better radical scavenging activities than its fractions. Furthermore, the cardioprotective role of ENO (10, 30, 100 mg/kg, per oral [po]) was tested against isoproterenol-induced myocardial toxicity (ISO, 120 mg/kg per day, subcutaneously [sc], for 2 days at 48 hours interval) in experimental rats when compared to propranolol (5 mg/kg, po) which was the standard. Pretreatment with ENO (10, 30, and 100 mg/kg) and propranolol for 2 weeks followed by ISO challenge in rats prevented the elevation of marker enzymes such as lactate dehydrogenase (LDH), γ-glutamyl transferase (GGT), creatine kinase (CK-MB and creatine phosphokinase [CPK]), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) in plasma. In addition, pretreatment with ENO and propranolol significantly attenuated the lipid peroxidation by maintaining the levels of enzymatic (superoxide dismutase and glutathione peroxidase) and nonenzymatic antioxidants (reduced glutathione and nitrite), which was also confirmed histologically. Taken together, the current study indicates that the hydroalcoholic extract of N oleander Linn flowers aid in cardioprotection probably by improving the antioxidant defense system during experimental myocardial necrosis.

  10. Peak longitudinal strain most accurately reflects myocardial segmental viability following acute myocardial infarction - an experimental study in open-chest pigs

    OpenAIRE

    Aarsæther, Erling Johan; Røsner, Assami; Straumbotn, Espen; Busund, Rolf

    2012-01-01

    The extension and the transmurality of the myocardial infarction are of high predictive value for clinical outcome. The aim of the study was to characterize the ability of longitudinal, circumferential and radial strain measured by 2-dimensional speckle tracking echocardiography (2D-STE) to predict the extent of necrosis in myocardial segments following acute myocardial infarction and to separate transmural necrotic segments from non-transmural necrotic segments in a full 18-segment porcine m...

  11. Cardioprotective effect of amlodipine in oxidative stress induced by experimental myocardial infarction in rats

    Directory of Open Access Journals (Sweden)

    Sudhira Begum

    2007-12-01

    Full Text Available The present study investigated whether the administration of amlodipine ameliorates oxidative stress induced by experimental myocardial infarction in rats. Adrenaline was administered and myocardial damage was evaluated biochemically [significantly increased serum aspertate aminotransferase (AST, lactate dehydrogenase (LDH and malondialdehyde (MDA levels of myocardial tissue] and histologically (morphological changes of myocardium. Amlodipine was administered as pretreatment for 14 days in adrenaline treated rats. Statistically significant amelioration in all the biochemical parameters supported by significantly improved myocardial morphology was observed in amlodipine pretreatment. It was concluded that amlodipine afforded cardioprotection by reducing oxidative stress induced in experimental myocardial infarction of catecholamine assault.

  12. Myocardial repolarization dispersion and autonomic nerve activity in a canine experimental acute myocardial infarction model.

    Science.gov (United States)

    Piccirillo, Gianfranco; Moscucci, Federica; D'Alessandro, Gaetana; Pascucci, Matteo; Rossi, Pietro; Han, Seongwook; Chen, Lan S; Lin, Shien-Fong; Chen, Peng-Sheng; Magrì, Damiano

    2014-01-01

    Evidence from a canine experimental acute myocardial infarction (MI) model shows that until the seventh week after MI, the relationship between stellate ganglion nerve activity (SGNA) and vagal nerve activity (VNA) progressively increases. The purpose of this study was to evaluate how autonomic nervous system activity influences temporal myocardial repolarization dispersion at this period. We analyzed autonomic nerve activity as well as QT and RR variability from recordings previously obtained in nine dogs. From a total of 48 short-term ECG segments, 24 recorded before and 24 recorded 7 weeks after experimentally-induced MI, we obtained three indices of temporal myocardial repolarization dispersion: QTe (from Q-wave to T-wave end), QTp (from Q-wave to T-wave peak), and Te (from T-wave peak to T-wave end) variability index (QTeVI, QTpVI, TeVI). We also performed heart rate variability power spectral analysis on the same segments. After MI, all the QT variables increased QTeVI (median [interquartile range]) (from -1.76[0.82] to -1.32[0.68]), QTeVI (from -1.90[1.01] to -1.45[0.78]), and TeVI (from -0.72[0.67] to -0.22[1.00]), whereas all RR spectral indices decreased (P <.001 for all). Distinct circadian rhythms in QTeVI (P <.05,) QTpVI (P <.001) and TeVI (P <.05) appeared after MI with circadian variations resembling that of SGNA/VNA. The morning QTpVI and TeVI acrophases approached the SGNA/VNA acrophase. Conversely, the evening QTeVI acrophase coincided with another SGNA/VNA peak. After MI, regression analysis detected a positive relationship between SGNA/VNA and TeVI (R(2): 0.077; β: 0.278; p< 0.001). Temporal myocardial repolarization dispersion shows a circadian variation after MI reaching its peak at a time when sympathetic is highest and vagal activity lowest. © 2013 Heart Rhythm Society Published by Heart Rhythm Society All rights reserved.

  13. Desferal-Induced Inhibition of Lipid Peroxidation Processes in Experimental Pancreatic Necrosis

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    Yu. P. Orlov

    2007-01-01

    Full Text Available Objective: To experimentally reduce the activity of hyperoxidative processes in experimental pancreatic necrosis, by pread-ministering desferal as a Fe2+ chelator, and to determine the implication of ionized iron in the intensification of endotoxi-cosis, one of the leading risk factors of multiple organ dysfunctions.Subjects and methods. An experiment was carried out in 60 albino male rats in which pancreatic necrosis was simulated, by administering 0.25 ml of autobile per kg into the pancreas and by ligating the common bile duct just at the mouth of the duodenum. The parameters of endogenous intoxication (the levels of oligopeptides and the rate of free radical oxidation processes were estimated in the experiment. The impact of prophylactic desferal administration on the parameters was also evaluated.Results. It has been ascertained that pread-ministration (3 hours before the simulation of pancreatic necrosis of desferal in a dose of 80 mg/kg can prevent the potentiation of LPO processes, which substantially reduces endotoxicosis that develops in pancreatic necrosis.Conclusion. The findings give grounds to use desferal in clinical practice as a pathogenetically warranted agent to perform an abolishing therapy for one of the pathogenetic factors (oxidative stress in acute progressive pancreatitis. 

  14. Effect of Glucocorticoids on Ultrastructure of Myocardial Muscle in the Course of Experimentally Induced Acute Myocardial Ischemia

    Directory of Open Access Journals (Sweden)

    Piotr Kuropka

    2017-01-01

    Full Text Available The search for effective methods of myocardial cytoprotection against ischemia is the most significant issue in modern cardiology and cardiac surgery. Glucocorticoids are deemed very strong modulators of inflammatory response and thus can potentially protect heart muscle from postreperfusion injury and myocardial ischemia during cardiac surgery. Ultrastructural examination of the left ventricle heart samples revealed that the intravenous application of dexamethasone and hydrocortisone proved to exert cytoprotective effect on cardiomyocytes during experimentally induced acute ischemia in rats.

  15. Renal sympathetic denervation improves myocardial apoptosis in rats with isoproterenol-induced heart failure by downregulation of tumor necrosis factor-α and nuclear factor-κB.

    Science.gov (United States)

    Yao, Wei; Wang, Neng; Qian, Jin; Bai, Lu; Zheng, Xiaoxin; Hou, Guo; Qiu, Xuan; Yang, Bo

    2017-11-01

    Chronic congestive heart failure (CHF) is the end outcome of organic heart diseases and one of the major diseases harmful to human health. Renal sympathetic denervation (RSD) is the anatomical basis of transcatheter renal sympathetic nerve ablation within the renal artery. To date, the roles of norepinephrine and angiotensin II (Ang II) in myocardial apoptosis and their underlying mechanisms have not been well explored. The aim of the present study was to verify the hypothesis that RSD is likely to inhibit myocardial apoptosis by inhibiting the release of norepinephrine and Ang II. An isoproterenol-induced CHF rat model was established, and the effects of RSD on myocardial apoptosis were examined using flow cytometry and TUNEL staining. The expression of factors associated with myocardial apoptosis, including p53, tumor necrosis factor-α (TNF-α), nuclear factor-κB (NF-κB), caspase-2 and -3, were measured using quantitative polymerase chain reaction and western blot analysis. The results indicated that the mRNA levels of p53, TNF-α, NF-κB, caspase-2 and -3 were significantly reduced in the myocardial tissues of rats in the CHF+RSD group when compared with the levels in the CHF+sham group (PRSD group in comparison with the CHF+sham group (PRSD group compared with that in the CHF+sham group (PRSD in the treatment of CHF.

  16. Grade 3 ischemia on the admission electrocardiogram predicts rapid progression of necrosis over time and less myocardial salvage by primary angioplasty.

    Science.gov (United States)

    Billgren, Therese; Maynard, Charles; Christian, Timothy F; Rahman, Mohmmad A; Saeed, Mahammad; Hammill, Stephen C; Wagner, Galen S; Birnbaum, Yochai

    2005-07-01

    Among patients with ST-elevation acute myocardial infarction, those with terminal QRS distortion (grade 3 ischemia) have higher mortality and larger infarct size (IS) than patients without QRS distortion (grade 2 ischemia). We assessed the relation of baseline electrocardiographic ischemia grades to area at risk (AR) and myocardial salvage [100 (AR-IS)/AR] in 79 patients who underwent primary angioplasty for first ST-elevation acute myocardial infarction and had technetium Tc 99m sestamibi single-photon emission computed tomography before angioplasty (AR) and at predischarge (IS). Patients were classified as having grade 2 ischemia (ST elevation without terminal QRS distortion in any of the leads, n = 48), grade 2.5 ischemia (ST elevation with terminal QRS distortion in 1 lead, n = 16), or grade 3 ischemia (ST elevation with terminal QRS distortion in >2 adjacent leads, n = 15). Time to treatment was comparable among groups. AR was comparable among groups (38% +/- 20%, 33% +/- 23%, and 34% +/- 23%, respectively; P = .70). There were no differences among groups in residual myocardial perfusion (severity index 0.28 +/- 0.12, 0.29 +/- 0.16, and 0.30 +/- 0.15 in grades 2, 2.5, and 3 ischemia, respectively; P = .97). In contrast, there was a trend toward lower myocardial salvage (45% +/- 32%) in the grade 3 group than in the grade 2 (65% +/- 33%) and grade 2.5 (65% +/- 40%) groups ( P = .16). Salvage was dependent on time only in the grade 3 group. Spearman rank correlation coefficients between time to treatment and percentage salvage were 0.003 ( P = .99), -0.24 ( P = .38), and -0.63 ( P = .022) for grades 2, 2.5, and 3, respectively. Patients with grade 3 ischemia have rapid progression of necrosis over time and less myocardial salvage. This admission pattern is a predictor of myocardial salvage by primary angioplasty.

  17. Diabetes subdiagnosticado e necrose miocárdica: preditores de hiperglicemia no infarto do miocárdio Unrecognized diabetes and myocardial necrosis: predictors of hyperglycemia in myocardial infarction

    Directory of Open Access Journals (Sweden)

    Renata Teixeira Ladeira

    2013-05-01

    Full Text Available FUNDAMENTO: Hiperglicemia na fase aguda do infarto do miocárdio é importante fator prognóstico. Entretanto, sua fisiopatologia não está completamente elucidada. OBJETIVO: Analisar simultaneamente correlação entre hiperglicemia e marcadores bioquímicos relacionados ao estresse,metabolismo glicídico e lipídico, coagulação, inflamação e necrose miocárdica. MÉTODOS: Oitenta pacientes com infarto agudo do miocárdio foram incluídos prospectivamente. Os parâmetros analisados foram: glicose, hormônios do estresse (cortisol e norepinefrina, fatores do metabolismo glicídico [hemoglobina glicada (HbA1c, insulina], lipoproteínas (colesterol total, LDL, HDL, LDL eletronegativa minimamente modificada e adiponectina, glicerídeos (triglicérides, VLDL e ácido graxo, fatores da coagulação (fator VII, fibrinogênio,inibidor do ativador do plasminogênio-1, inflamação (proteína C reativa ultrassensível e necrose miocárdica (CK-MB e troponina. Variáveis contínuas foram convertidas em graus de pertinência por intermédio de lógica fuzzy. RESULTADOS: Houve correlação significativa entre hiperglicemia e metabolismo glicídico (p BACKGROUND: Hyperglycemia in the acute phase of myocardial infarction is an important prognostic factor. However, its pathophysiology is not fully understood. OBJECTIVE: To analyze simultaneously the correlation between hyperglycemia and biochemical markers related to stress, glucose and lipid metabolism, coagulation, inflammation, and myocardial necrosis. METHODS Eighty patients with acute myocardial infarction were prospectively included. The following parameters were analyzed: blood glucose; stress hormones (cortisol and norepinephrine; glucose metabolism factors [glycated hemoglobin (HbA1c; insulin]; lipoproteins (total cholesterol, LDL, HDL, minimally modified electronegative LDL, and adiponectin; glycerides (triglycerides, VLDL and fatty acids; coagulation factors (factor VII, fibrinogen, plasminogen

  18. Experimental Myocardial Infarction Upregulates Circulating Fibroblast Growth Factor‐23

    Science.gov (United States)

    Andrukhova, Olena; Slavic, Svetlana; Odörfer, Kathrin I; Erben, Reinhold G

    2015-01-01

    ABSTRACT Myocardial infarction (MI) is a major cause of death worldwide. Epidemiological studies have linked vitamin D deficiency to MI incidence. Because fibroblast growth factor‐23 (FGF23) is a master regulator of vitamin D hormone production and has been shown to be associated with cardiac hypertrophy per se, we explored the hypothesis that FGF23 may be a previously unrecognized pathophysiological factor causally linked to progression of cardiac dysfunction post‐MI. Here, we show that circulating intact Fgf23 was profoundly elevated, whereas serum vitamin D hormone levels were suppressed, after induction of experimental MI in rat and mouse models, independent of changes in serum soluble Klotho or serum parathyroid hormone. Both skeletal and cardiac expression of Fgf23 was increased after MI. Although the molecular link between the cardiac lesion and circulating Fgf23 concentrations remains to be identified, our study has uncovered a novel heart–bone–kidney axis that may have important clinical implications and may inaugurate the new field of cardio‐osteology. © 2015 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research (ASBMR). PMID:25858796

  19. A CMR study of the effects of tissue edema and necrosis on left ventricular dyssynchrony in acute myocardial infarction: implications for cardiac resynchronization therapy

    Directory of Open Access Journals (Sweden)

    Manka Robert

    2012-07-01

    Full Text Available Abstract Background In acute myocardial infarction (AMI, both tissue necrosis and edema are present and both might be implicated in the development of intraventricular dyssynchrony. However, their relative contribution to transient dyssynchrony is not known. Cardiovascular magnetic resonance (CMR can detect necrosis and edema with high spatial resolution and it can quantify dyssynchrony by tagging techniques. Methods Patients with a first AMI underwent percutaneous coronary interventions (PCI of the infarct-related artery within 24 h of onset of chest pain. Within 5–7 days after the event and at 4 months, CMR was performed. The CMR protocol included the evaluation of intraventricular dyssynchrony by applying a novel 3D-tagging sequence to the left ventricle (LV yielding the CURE index (circumferential uniformity ratio estimate; 1 = complete synchrony. On T2-weighted images, edema was measured as high-signal (>2 SD above remote tissue along the LV mid-myocardial circumference on 3 short-axis images (% of circumference corresponding to the area-at-risk. In analogy, on late-gadolinium enhancement (LGE images, necrosis was quantified manually as percentage of LV mid-myocardial circumference on 3 short-axis images. Necrosis was also quantified on LGE images covering the entire LV (expressed as %LV mass. Finally, salvaged myocardium was calculated as the area-at-risk minus necrosis (expressed as % of LV circumference. Results After successful PCI (n = 22, 2 female, mean age: 57 ± 12y, peak troponin T was 20 ± 36ug/l and the LV ejection fraction on CMR was 41 ± 8%. Necrosis mass was 30 ± 10% and CURE was 0.91 ± 0.05. Edema was measured as 58 ± 14% of the LV circumference. In the acute phase, the extent of edema correlated with dyssynchrony (r2 = −0.63, p 2 = −0.19, p = 0.05. PCI resulted in salvaged myocardium of 27 ± 14%. LV dyssynchrony (=CURE decreased at 4 months from 0.91

  20. Nutraceutical inherent of Spinacia oleracea Linn. methanolic leaf extract ameliorates isoproterenol induced myocardial necrosis in male albino Wistar rats via mitigating inflammation.

    Science.gov (United States)

    Vutharadhi, Shivaranjani; Jolapuram, Umamaheswari; Kodidhela, Lakshmi Devi

    2017-01-01

    Cardiovascular diseases (CVDs) remain the principal cause of death in both developed and developing countries. The present study was intended to appraise the nutraceutical inherent of HPLC standardized Spinacia oleracea methanolic leaf extract (SoLE) in isoproterenol (ISO) induced male albino Wistar rats via activation of pro-inflammatory signaling pathway that drives myocardial necrosis. Biochemical analysis of ISO injected rats showed significant alterations in the activities of homocysteine, paraoxonase, lecithin cholesterol acyltransferase, C-reactive protein, myeloperoxidase and caspase-3 which were further confirmed by the histopathological examination. In addition, it also flaunted a significant increase in pro-inflammatory cytokines, such as TNF-α, IL-1β, IL-6 in ISO administered rats when compared with normal control rats. Pretreatment with SoLE (100, 200, and 300mg/kg bw) along with positive control gallic acid, significantly prevented all the adverse effects in ISO administered rats in a dose dependent manner. These results also reiterated the expected amelioration of myocardial necrosis in ISO induced MI rats conveying anti-atherogenic, anti-apoptotic and anti-inflammatory activities of SoLE. Copyright © 2016 Elsevier Masson SAS. All rights reserved.

  1. Dual antiplatelet response during PCI: VerifyNow P2Y12 predicts myocardial necrosis and thromboxane B2 generation confirms wide variation in aspirin response.

    Science.gov (United States)

    Good, Richard I S; McGarrity, Anne; James, Tina E; Miller, Helen; McConnachie, Alex; Goodall, Alison H; Oldroyd, Keith G

    2015-06-01

    There remains concern that the antiplatelet effects of aspirin and clopidogrel vary between patients and poor responders may be at increased risk of adverse events. However, the optimal method of measuring aspirin and/or clopidogrel response remains unresolved. We compared three methods of measuring clopidogrel response recommended by a recent consensus statement for the European Society of Cardiology, and investigated a novel approach to measuring aspirin response in patients established on both aspirin and clopidogrel. In addition, we investigated whether any of these assays predict peri-procedural myocardial necrosis following percutaneous coronary intervention (PCI). A cross-section of 323 patients attending for PCI was tested for clopidogrel response using VerifyNow P2Y12, VASP Platelet Reactivity Index (VASP-PRI) and whole blood impedance aggregometry (WBPA). Aspirin response was assessed by measuring the residual ability of platelets to generate thromboxane, calculated as the difference between thromboxane B2 levels in serum and plasma, [TxB2]S-P. Peri-procedural myocardial necrosis was determined by a change in troponin I >0.2 μmol/l. Patients demonstrated wide variation in response to both aspirin and clopidogrel. Correlation between VerifyNow P2Y12 and VASP-PRI was good (r=0.702, paspirin response in patients taking dual antiplatelet therapy. Copyright © 2015 Elsevier Ltd. All rights reserved.

  2. Scintigraphic myocardial imaging with sup(99m)Tc-labelled pyrophosphate of experimentally produced cardiomyopathy in dogs

    Energy Technology Data Exchange (ETDEWEB)

    Duska, F.; Novak, J.; Vizda, J.; Kubicek, J.; Kafka, P.; Mazurova, Y.; Bradna, P.

    1981-12-01

    Scintigraphic examination of the myocardium using sup(99m)Tc-labelled pyrophosphate was carried out in 10 dogs with experimentally produced cardiomyopathy. This was brought by introvenous administration of high doses of adrenalin and theophylline. The scan was positive in 8 out of 10 dogs. Hot foci were very extensive. The degree of accumulation was however low (2+). Histological examination of the myocardium using the light microscope showed only scarcely distinguishable damage to the tissue without the presence of necrosis. ECG examinations were normal in all cases. By means of sup(99m)Tc-labelled pyrophosphate even very small myocardial disorders can thus be detected. This fact may be of clinical importance for an early diagnosis of heart lesions.

  3. Influence of isoproterenol on myocardial energetics. Experimental and clinical investigations.

    Science.gov (United States)

    Hasenfuss, G; Holubarsch, C; Blanchard, E M; Mulieri, L A; Alpert, N R; Just, H

    1989-01-01

    The influence of isoproterenol on myocardial performance and energetics was investigated in normal guinea pig myocardium and in patients with normal left ventricular function. The in vitro experiments were performed by simultaneous isometric force and heat measurements using sensitive antimony-bismuth thermopiles. Following the application of isoproterenol (10(-8) M) isometric peak twitch tension and tension-time integral increased significantly by 185% and 142%, respectively. Tension-independent heat which reflects high energy phosphate hydrolysis of excitation-contraction coupling increased by 183%. Tension-dependent heat reflecting the high energy phosphate hydrolysis of the crossbridges increased by 417%. The ratio of tension-dependent heat to tension-time integral increased by 131%. The recovery/initial heat ratio, reflecting the efficiency of the recovery metabolism, and the resting metabolism did not significantly change. In the patients the effect of isoproterenol on myocardial energetics was evaluated in terms of myocardial efficiency. Following isoproterenol administration, left ventricular systolic stress-time integral decreased by 49% due to reductions in end-diastolic pressure, end-diastolic volume and duration of systole. Pressure-volume work remained unchanged. Myocardial oxygen consumption per minute increased in proportion to heart rate. The ratio of myocardial oxygen consumption per beat to left ventricular systolic stress-time integral increased significantly by 95%. External myocardial efficiency was unaltered. Thus, isoproterenol increases the energy turnover of excitation-contraction coupling and increases the energy consumption of the crossbridges disproportionately to developed tension-time integral in the guinea pig heart.

  4. Experimental myocardial stem cell therapy for ST-elevation myocardial infarction

    DEFF Research Database (Denmark)

    Kastrup, Jens; Mygind, Naja D; Qayyum, Abbas A

    2016-01-01

    Ischemic heart disease (IHD) is one of the leading causes of death worldwide and is characterized by the formation of atherosclerotic plaques in the coronary arteries reducing the blood supply to the heart muscle causing ischemia. IHD can result in ST-elevation myocardial infarction (STEMI...

  5. Localization of anti-mitochondrial antibody in experimental canine myocardial infarcts.

    OpenAIRE

    Willerson, J T; Kulkarni, P; Stone, M; Lewis, S E; Eigenbrodt, E; Bonte, F J; Parkey, R W; Buja, L M

    1980-01-01

    Alterations in cell and subcellular membrane integrity occur during evolving ischemic myocardial injury. We tested the hypothesis that an antibody against human liver mitochondria [anti-mitochondrial antibody developing in a patient with primary biliary cirrhosis] could identify altered cell membrane integrity in experimental canine myocardial infarcts. The proximal left anterior descending coronary arteries of 12 dogs were ligated and 1 hr later 131I-labeled F(ab')2 fragments from either a c...

  6. Experimental myocardial stem cell therapy for ST-elevation myocardial infarction

    DEFF Research Database (Denmark)

    Kastrup, Jens; Mygind, Naja D; Qayyum, Abbas A

    2016-01-01

    Ischemic heart disease (IHD) is one of the leading causes of death worldwide and is characterized by the formation of atherosclerotic plaques in the coronary arteries reducing the blood supply to the heart muscle causing ischemia. IHD can result in ST-elevation myocardial infarction (STEMI...... interest in the last 10-15 years especially after STEMI. Many preclinical and clinical studies have shown encouraging results but also very diverse clinical outcomes after stem cell treatment. This diversity in results may be explained by different factors, such as cell isolation technique, infarct...

  7. Changes in Coronary Blood Flow After Acute Myocardial Infarction: Insights From a Patient Study and an Experimental Porcine Model.

    Science.gov (United States)

    de Waard, Guus A; Hollander, Maurits R; Teunissen, Paul F A; Jansen, Matthijs F; Eerenberg, Elise S; Beek, Aernout M; Marques, Koen M; van de Ven, Peter M; Garrelds, Ingrid M; Danser, A H Jan; Duncker, Dirk J; van Royen, Niels

    2016-03-28

    The aim of this study was to determine the effects of an acute myocardial infarction (AMI) on baseline and hyperemic flow in both culprit and nonculprit arteries. An impaired coronary flow reserve (CFR) after AMI is related to worse outcomes. The individual contribution of resting and hyperemic flow to the reduction of CFR is unknown. Furthermore, it is unclear whether currently used experimental models of AMI resemble the clinical situation with respect to coronary flow parameters. Intracoronary Doppler flow velocity measurements were obtained in culprit and nonculprit arteries immediately after successfully revascularized ST-segment elevation myocardial infarction (n = 40). Stable patients without obstructive coronary artery disease served as control subjects and were selected by propensity-score matching (n = 40). Similar measurements in an AMI porcine model were taken both before and immediately after 75-min balloon occlusion of the left circumflex artery (n = 11). In the culprit artery, CFR was 36% lower than in matched control subjects (Δ = -0.9; 1.8 ± 0.9 vs. 2.8 ± 0.7; p infarct size as a percentage of the left ventricle in both patients (r = -0.48; p = 0.001) and swine (r = -0.61; p = 0.047). CFR in both culprit and nonculprit coronary arteries decreases after AMI with contributions from both an increased baseline flow and a decreased hyperemic flow. The decreased CFR after AMI in culprit and nonculprit vessels is not a result of pre-existing microvascular dysfunction, but represents a combination of post-occlusive hyperemia, myocardial necrosis, hemorrhagic microvascular injury, compensatory hyperkinesis, and neurohumoral vasoconstriction. Copyright © 2016 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

  8. Experimental myocardial stem cell therapy for ST-elevation myocardial infarction

    DEFF Research Database (Denmark)

    Kastrup, Jens; Mygind, Naja D; Qayyum, Abbas A

    2016-01-01

    Ischemic heart disease (IHD) is one of the leading causes of death worldwide and is characterized by the formation of atherosclerotic plaques in the coronary arteries reducing the blood supply to the heart muscle causing ischemia. IHD can result in ST-elevation myocardial infarction (STEMI...... interest in the last 10-15 years especially after STEMI. Many preclinical and clinical studies have shown encouraging results but also very diverse clinical outcomes after stem cell treatment. This diversity in results may be explained by different factors, such as cell isolation technique, infarct......), chronic IHD and heart failure. The patients suffer from chest pain (angina), dyspnea and a reduced quality of life. Common for all these conditions is loss of functional cardiomyocytes and endothelial cells. Stem cell therapy to regenerate injured myocardium is a new treatment option which has gained much...

  9. Experimental myocardial stem cell therapy for ST-elevation myocardial infarction

    DEFF Research Database (Denmark)

    Kastrup, Jens; Mygind, Naja D.; Qayyum, Abbas A.

    2016-01-01

    Ischemic heart disease (IHD) is one of the leading causes of death worldwide and is characterized by the formation of atherosclerotic plaques in the coronary arteries reducing the blood supply to the heart muscle causing ischemia. IHD can result in ST-elevation myocardial infarction (STEMI......), chronic IHD and heart failure. The patients suffer from chest pain (angina), dyspnea and a reduced quality of life. Common for all these conditions is loss of functional cardiomyocytes and endothelial cells. Stem cell therapy to regenerate injured myocardium is a new treatment option which has gained much...... interest in the last 10-15 years especially after STEMI. Many preclinical and clinical studies have shown encouraging results but also very diverse clinical outcomes after stem cell treatment. This diversity in results may be explained by different factors, such as cell isolation technique, infarct...

  10. Susceptibility of Koi and Yellow Perch to infectious hematopoietic necrosis virus by experimental exposure

    Science.gov (United States)

    Palmer, Alexander D.; Emmenegger, Eveline J.

    2014-01-01

    Infectious hematopoietic necrosis virus (IHNV) is a novirhabdoviral pathogen that originated in western North America among anadromous Pacific salmonids. Severe disease epidemics in the late 1970s resulting from IHNV's invasion into farmed Rainbow Trout Oncorhynchus mykiss in North America, Asia, and Europe emphasized IHNV's ability to adapt to new hosts under varying rearing conditions. Yellow Perch Perca flavescens and Koi Carp Cyprinus carpio (hereafter, “Koi”) are aquaculture-reared fish that are highly valued in sport fisheries and the ornamental fish trade, respectively, but it is unknown whether these fish species are vulnerable to IHNV infection. In this study, we exposed Yellow Perch, Koi, and steelhead (anadromous Rainbow Trout) to IHNV by intraperitoneal injection (106 PFU/fish) and by immersion (5.7×105 PFU/mL) for 7 h, and monitored fish for 28 d. The extended immersion exposure and high virus concentrations used in the challenges were to determine if the tested fish had any level of susceptibility. After experimental exposure, Yellow Perch and Koi experienced low mortality (35%). Virus was found in dead fish of all species tested and in surviving Yellow Perch by plaque assay and quantitative reverse transcription polymerase chain reaction (qPCR), with a higher prevalence in Yellow Perch than Koi. Infectious virus was also detected in Yellow Perch out to 5 d after bath challenge. These findings indicate that Yellow Perch and Koi are highly resistant to IHNV disease under the conditions tested, but Yellow Perch are susceptible to infection and may serve as possible virus carriers.

  11. Effect of Curcuma longa and Ocimum sanctum on myocardial apoptosis in experimentally induced myocardial ischemic-reperfusion injury

    Science.gov (United States)

    Mohanty, Ipseeta; Arya, Dharamvir Singh; Gupta, Suresh Kumar

    2006-01-01

    Background In the present investigation, the effect of Curcuma longa (Cl) and Ocimum sanctum (Os) on myocardial apoptosis and cardiac function was studied in an ischemia and reperfusion (I-R) model of myocardial injury. Methods Wistar albino rats were divided into four groups and orally fed saline once daily (sham, control IR) or Cl (100 mg/kg; Cl-IR) or Os (75 mg/kg; Os-IR) respectively for 1 month. On the 31st day, in the rats of the control IR, Cl-IR and Os-IR groups LAD occlusion was undertaken for 45 min, and reperfusion was allowed for 1 h. The hemodynamic parameters{mean arterial pressure (MAP), heart rate (HR), left ventricular end-diastolic pressure (LVEDP), left ventricular peak positive (+) LVdP/dt (rate of pressure development) and negative (-) LVdP/dt (rate of pressure decline)} were monitored at pre-set points throughout the experimental duration and subsequently, the animals were sacrificed for immunohistopathological (Bax, Bcl-2 protein expression & TUNEL positivity) and histopathological studies. Results Chronic treatment with Cl significantly reduced TUNEL positivity (p < 0.05), Bax protein (p < 0.001) and upregulated Bcl-2 (p < 0.001) expression in comparison to control IR group. In addition, Cl demonstrated mitigating effects on several myocardial injury induced hemodynamic {(+)LVdP/dt, (-) LVdP/dt & LVEDP} and histopathological perturbations. Chronic Os treatment resulted in modest modulation of the hemodynamic alterations (MAP, LVEDP) but failed to demonstrate any significant antiapoptotic effects and prevent the histopathological alterations as compared to control IR group. Conclusion In the present study, significant cardioprotection and functional recovery demonstrated by Cl may be attributed to its anti-apoptotic property. In contrast to Os, Cl may attenuate cell death due to apoptosis and prevent the impairment of cardiac performance. PMID:16504000

  12. Reduction of the ischaemia of the myocard by labetalol after experimental myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Glogar, D.H.; Kloner, R.A.; Zilcher, H.; Weber, H.; Kaindl, F. (Vienna Univ. (Austria). Kardiologische Klinik; Peter Bent Brigham Hospital, Boston, MA (USA))

    1981-01-01

    After experimental myocardial infarction in 28 dogs coronary blood supply was measured by Tc-99-labelled microspheres. The effect of different doses of labetalol on infarct size was observed. Infarct size was measured by autoradiography. In a dose of 0.5 mg/kg labetalol is blocking predominant beta receptors and does not influence infarct extension. Labetalol in a dose of more than 5 mg/kg (alpha- and betareceptors are blocked) reduces significantly infarct extension. Alpha- and beta-blocking with labetalol is a potential favourable intervention during fresh myocardial infarction.

  13. Selective cyclooxygenase-2 inhibition protects against myocardial damage in experimental acute ischemia

    Directory of Open Access Journals (Sweden)

    Alberto Carnieto Jr.

    2009-03-01

    Full Text Available BACKGROUND: Acute myocardial infarction is associated with tissue inflammation. Early coronary reperfusion clearly improves the outcome but may help propagate the inflammatory response and enhance tissue damage. Cyclooxygenase-2 is an enzyme that catalyzes the initial step in the formation of inflammatory prostaglandins from arachidonic acid. Cyclooxygenase-2 levels are increased when ischemic cardiac events occur. The overall function of COX-2 in the inflammatory process generated by myocardial ischemic damage has not yet been elucidated. GOAL: The objective of this study was to determine whether a selective cyclooxygenase-2 inhibitor (rofecoxib could alter the evolution of acute myocardial infarction after reperfusion. METHODS AND RESULTS: This study was performed with 48 mongrel dogs divided into two groups: controls and those treated with the drug. All animals were prepared for left anterior descending coronary artery occlusion. The dogs then underwent 180 minutes of coronary occlusion, followed by 30 minutes of reperfusion. Blood samples were collected from the venous sinus immediately before coronary occlusion and after 30 minutes of reperfusion for measurements of CPK-MB, CPK-MBm and troponin I. During the experiment we observed the mean blood pressure, heart rate and coronary flow. The coronary flow and heart rate did not change, but in the control group, there was blood pressure instability, in addition to maximal levels of CPK-MB post-infarction. The same results were observed for CPK-MBm and troponin I. CONCLUSION: In a canine model of myocardial ischemia-reperfusion, selective inhibition of Cyclooxygenase-2 with rofecoxib was not associated with early detrimental effects on the hemodynamic profile or the gross extent of infarction; in fact, it may be beneficial by limiting cell necrosis.

  14. Genetic inhibition of protein kinase Cε attenuates necrosis in experimental pancreatitis

    Science.gov (United States)

    Liu, Yannan; Tan, Tanya; Jia, Wenzhuo; Lugea, Aurelia; Mareninova, Olga; Waldron, Richard T.; Pandol, Stephen J.

    2014-01-01

    Understanding the regulation of death pathways, necrosis and apoptosis, in pancreatitis is important for developing therapies directed to the molecular pathogenesis of the disease. Protein kinase Cε (PKCε) has been previously shown to regulate inflammatory responses and zymogen activation in pancreatitis. Furthermore, we demonstrated that ethanol specifically activated PKCε in pancreatic acinar cells and that PKCε mediated the sensitizing effects of ethanol on inflammatory response in pancreatitis. Here we investigated the role of PKCε in the regulation of death pathways in pancreatitis. We found that genetic deletion of PKCε resulted in decreased necrosis and severity in the in vivo cerulein-induced pancreatitis and that inhibition of PKCε protected the acinar cells from CCK-8 hyperstimulation-induced necrosis and ATP reduction. These findings were associated with upregulation of mitochondrial Bak and Bcl-2/Bcl-xL, proapoptotic and prosurvival members in the Bcl-2 family, respectively, as well as increased mitochondrial cytochrome c release, caspase activation, and apoptosis in pancreatitis in PKCε knockout mice. We further confirmed that cerulein pancreatitis induced a dramatic mitochondrial translocation of PKCε, suggesting that PKCε regulated necrosis in pancreatitis via mechanisms involving mitochondria. Finally, we showed that PKCε deletion downregulated inhibitors of apoptosis proteins, c-IAP2, survivin, and c-FLIPs while promoting cleavage/inactivation of receptor-interacting protein kinase (RIP). Taken together, our findings provide evidence that PKCε activation during pancreatitis promotes necrosis through mechanisms involving mitochondrial proapoptotic and prosurvival Bcl-2 family proteins and upregulation of nonmitochondrial pathways that inhibit caspase activation and RIP cleavage/inactivation. Thus PKCε is a potential target for prevention and/or treatment of acute pancreatitis. PMID:25035113

  15. Mechanisms of tumor necrosis in photodynamic therapy with a chlorine photosensitizer: experimental studies

    Science.gov (United States)

    Privalov, Valeriy A.; Lappa, Alexander V.; Bigbov, Elmir N.

    2011-02-01

    A photodynamic therapy experiment on 118 inbred white mice with transplanted Ehrlich's tumor (mouse mammary gland adenocarcinoma) is performed to reveal mechanisms of necrosis formation. In 7-10 days the tumor of 1-1.5 cm diameter is formed under skin at the injection point, and PDT procedure is applied. There were used a chlorine type photosensitizer RadachlorineTM and 662 nm wavelength diode laser. The drug is injected by intravenously at the dose of 40 mg/kg; the irradiation is executed in 2-2.5 hours at the surface dose of about 200 J/cm2. Each of the mice had a photochemical reaction in form of destructive changes at the irradiation region with subsequent development of dry coagulation necrosis. After rejection of the necrosis there occurred epithelization of defect tissues in a tumor place. Histological investigations were conducted in different follow-up periods, in 5 and 30 min, 1, 3, 6, and 12 hours, 1, 3, 7 and 28 days after irradiation. They included optical microscopy, immune marker analysis, morphometry with measurements of volume density of epithelium, tumor stroma and necroses, vascular bed. The investigations showed that an important role in damaging mechanisms of photodynamic action belongs to hypoxic injuries of tumor mediated by micro vascular disorders and blood circulatory disturbances. The injuries are formed in a few stages: microcirculation angiospasm causing vessel paresis, irreversible stases in capillaries, diapedetic hemorrhages, thromboses, and thrombovasculitis. It is marked mucoid swelling and fibrinoid necrosis of vascular tissue. Progressive vasculitises result in total vessel obliteration and tumor necrosis.

  16. Lowering Interleukin-12 Activity Improves Myocardial and Vascular Function Compared With Tumor Necrosis Factor-a Antagonism or Cyclosporine in Psoriasis.

    Science.gov (United States)

    Ikonomidis, Ignatios; Papadavid, Evangelia; Makavos, George; Andreadou, Ioanna; Varoudi, Maria; Gravanis, Kostas; Theodoropoulos, Kostas; Pavlidis, George; Triantafyllidi, Helen; Moutsatsou, Paraskevi; Panagiotou, Christina; Parissis, John; Iliodromitis, Efstathios; Lekakis, John; Rigopoulos, Dimitrios

    2017-09-01

    Interleukin (IL)-12 activity is involved in the pathogenesis of psoriasis and acute coronary syndromes. We investigated the effects of IL-12 inhibition on vascular and left ventricular (LV) function in psoriasis. One hundred fifty psoriasis patients were randomized to receive an anti-IL-12/23 (ustekinumab, n=50), anti-tumor necrosis factor-a (TNF-α; etanercept, n=50), or cyclosporine treatment (n=50). At baseline and 4 months post-treatment, we measured (1) LV global longitudinal strain, twisting, and percent difference between peak twisting and untwisting at mitral valve opening (%untwMVO) using speckle-tracking echocardiography, (2) coronary flow reserve, (3) pulse wave velocity and augmentation index, (4) circulating NT-proBNP (N-terminal pro-B-type natriuretic peptide), TNF-α, IL-6, IL-12, IL-17, malondialdehyde, and fetuin-a. Compared with baseline, all patients had improved global longitudinal strain (median values: -17.7% versus -19.5%), LV twisting (12.4° versus 14°), %untwMVO (27.8% versus 35%), and coronary flow reserve (2.8 versus 3.1) and reduced circulating NT-proBNP, IL-17, TNF-α, and IL-6 post-treatment (Ppsoriasis, IL-12/23 inhibition results in a greater improvement of coronary, arterial, and myocardial function than TNF-α inhibition or cyclosporine treatment. URL: http://www.clinicaltrials.gov. Unique identifier: NCT02144857. © 2017 American Heart Association, Inc.

  17. Closed-chest experimental porcine model of acute myocardial infarction-reperfusion.

    Science.gov (United States)

    Pérez de Prado, Armando; Cuellas-Ramón, Carlos; Regueiro-Purriños, Marta; Gonzalo-Orden, J Manuel; Pérez-Martínez, Claudia; Altónaga, José R; García-Iglesias, M José; Orden-Recio, M Asunción; García-Marín, Juan F; Fernández-Vázquez, Felipe

    2009-01-01

    Progress in cardiovascular regenerative medicine research requires the availability of appropriate experimental animal models that are as close to humans as feasible. Our objective was to assess the validity of a porcine endovascular model of myocardial infarction and reperfusion. Fifteen domestic pigs (Large White race) were anesthetized and pre-medicated with amiodarone. Endovascular fluoroscopy-guided coronary procedures were performed to occlude the mid-left anterior descending artery using a coronary angioplasty balloon. Occlusion was confirmed by angiography and electrocardiography. After 75 min the balloon catheter system was withdrawn and the presence of reperfusion flow was verified. The animals were sacrificed after 1 and 2 weeks of follow-up, the hearts were explanted, and the extent of myocardial infarction with respect to the left ventricle was quantified. Overall survival rate was 67%. Five animals died prematurely: 3 showing signs of heart failure, 1 had reperfusion failure (final TIMI flow grade 1) and 1 succumbed to acute stress. The most common adverse event was ventricular fibrillation (87% of the animals) and defibrillation was effective in all affected animals. The extent of myocardial infarct in the animals followed-up for 1 and 2 weeks was similar (20.4+/-4.3% vs. 20.9+/-2.8%, respectively; p=0.8) but was significantly greater in the animals that died prematurely (29.5+/-3.6%, p=0.02). The endovascular porcine model we have explored constitutes a feasible and reproducible alternative for the evaluation of human myocardial infarction and reperfusion.

  18. Dietary fenugreek (Trigonella foenum-graecum seeds and garlic (Allium sativum alleviates oxidative stress in experimental myocardial infarction

    Directory of Open Access Journals (Sweden)

    P. Mukthamba

    2017-06-01

    Full Text Available Soluble fiber-rich fenugreek seeds (Trigonella foenum-graecum and garlic (Allium sativum are understood to exert cholesterol-lowering and antioxidant effects. The cardioprotective influence of a combination of fenugreek seeds and garlic by their antioxidant influence was evaluated in hypercholesterolemic rats administered isoproterenol. Wistar rats were maintained on high-cholesterol diet for 8 weeks along with dietary interventions of fenugreek (10%, garlic (2% and their combination. Myocardial infarction was induced with isoproterenol injection. Increased circulatory troponin, disturbed activities of cardiac ATPases, increased serum iron and decreased ceruloplasmin confirmed myocardial infarction. Elevated lipid peroxides accompanied with reduced antioxidant molecules caused by isoproterenol and altered activities of antioxidant enzymes in serum and heart in induced myocardial necrosis were countered by dietary fenugreek, garlic, and fenugreek + garlic. Dietary fenugreek seeds and garlic ameliorated isoproterenol-induced compromised antioxidant status, the cardioprotective effect being higher by the combination of fenugreek seeds and garlic.

  19. Fate of redspotted grouper nervous necrosis virus (RGNNV) in experimentally challenged Manila clam Ruditapes philippinarum.

    Science.gov (United States)

    Volpe, E; Pagnini, N; Serratore, P; Ciulli, S

    2017-06-19

    Redspotted grouper nervous necrosis virus (RGNNV), genus Betanodavirus, family Nodaviridae, is the causative agent of viral encephalopathy and retinopathy (otherwise known as viral nervous necrosis) and can infect several fish species worldwide. Betanodaviruses, including RGNNV, are very resilient in the aquatic environment, and their presence has already been reported in several wild marine species including invertebrates. In order to investigate the interaction between a bivalve mollusc (Manila clam Ruditapes philippinarum) and RGNNV, we optimised a culture-based method. The bioaccumulation of the pathogenic RGNNV by R. philippinarum and the potential shedding of viable RGNNV from RGNNV-exposed clams were evaluated through a culture-based method. R. philippinarum clearly accumulated viable RGNNV in their hepatopancreatic tissue and were able to release viable RGNNV via faecal matter and filtered water into the surrounding environment. The role of clams as bioaccumulators and shedders of viable RGGNV could put susceptible cohabiting cultured fish at risk. RGNNV-contaminated molluscs could behave as reservoirs for this virus and may modify the virus epidemiology.

  20. [Experimental study on avascular necrosis of femoral head in chickens induced by different glucocorticoides].

    Science.gov (United States)

    Xiao, Chun-Sheng; Lin, Na; Lin, Shi-Fu; Wan, Rong; Chen, Wei-Heng

    2010-03-01

    To study the effects of Methylprednisolone and Dexamethasone on the avascular necrosis of femoral head in chickens. Thirty-six chickens were randomly divided into 6 groups (n = 6): control group (group A), Methylprednisolone low dose group (group B), Methylprednisolone large dose group (group C), small dose Dexamethasone and horse serum group (group D), middle dose Dexamethasone and horse serum group (group E), and Dexamethasone large dose group (group F). On the 6th and 12th weeks, blood samples were obtained to determine the level of total cholesterol triglyeride (TG), high density lipoprotein (HDL) and low density lipoprotein (LDL). On the 12th week, femoral heads were taken off. Paraffin tissue sections were prepared to detect histopathologic change with hematoxylin and eosin staining. On the 6th week, compared with group A, the level of CHO increased significantly in group C and group F (P < 0.05), and TG increased in group B, C and group E, while HDL decreased in group B, C and group E. On the 12th week, the level of TG and CHO increased in group B, C, E and group F, and HDL decreased in group C, D and group E (P < 0.05). LDL was not detected in most chickens. The ratio of empty lacuna was higher in group C and group E compared with those of the control group (P < 0.05). Methylprednisolone is easier to induce osteonecrosis of femoral head than Dexamethasone. The condition of metabolic disorder in blood may be the basic pathomechanism of steroid-induced necrosis of femoral head.

  1. Assessment of myocardial ischemia and viability using tissue Doppler and deformation imaging: the lessons from the experimental studies.

    Science.gov (United States)

    Thibault, H; Derumeaux, G

    2008-01-01

    Tissue Doppler imaging and strain rate imaging are quantitative methods for assessing myocardial function and have been shown to overcome the limitations of current ultrasound methods in assessing the complex changes in regional myocardial function that occur in differing ischemic substrates. Tissue Doppler imaging (TDI) measures in real time the myocardial velocity gradient which is an index of myocardial deformation. Strain and strain rate (SR) imaging has been shown to be a sensitive technique for quantifying regional myocardial deformation. Strain rate is less load-dependent that strain and provides therefore a better measure of contractility. In the setting of ischemia, experimental studies have shown that strain imaging was an accurate method for quantitative evaluation of regional myocardial function and may yield important physiological data. In myocardial infarction, transmural extension of scar distribution in the infarct zone is proportionally related to the reduction in systolic function measured by the radial transmural velocity gradient or by strain rate imaging. Measurement of both systolic and post-systolic deformation both at rest and during a graded dobutamine infusion may help to distinguish between transmural and non transmural infarcts. In conclusion, strain imaging has the ability to evaluate of regional myocardial function. Strain rate has not replaced conventional grey-scale imaging in the assessment of regional left ventricular function and the implement of these new indices in the routine clinical practice will need additional clinical and large-scale studies.

  2. Early detection of doxorubicin myocardial injury by ultrasonic tissue characterization in an experimental animal model

    Directory of Open Access Journals (Sweden)

    Romano Minna Moreira

    2012-10-01

    Full Text Available Abstract In the clinical setting, the early detection of myocardial injury induced by doxorubicin (DXR is still considered a challenge. To assess whether ultrasonic tissue characterization (UTC can identify early DXR-related myocardial lesions and their correlation with collagen myocardial percentages, we studied 60 rats at basal status and prospectively after 2mg/Kg/week DXR endovenous infusion. Echocardiographic examinations were conducted at baseline and at 8,10,12,14 and 16 mg/Kg DXR cumulative dose. The left ventricle ejection fraction (LVEF, shortening fraction (SF, and the UTC indices: corrected coefficient of integrated backscatter (IBS (tissue IBS intensity/ phantom IBS intensity (CC-IBS and the cyclic variation magnitude of this intensity curve (MCV were measured. The variation of each parameter of study through DXR dose was expressed by the average and standard error at specific DXR dosages and those at baseline. The collagen percent (% was calculated in six control group animals and 24 DXR group animals. CC-IBS increased (1.29±0.27 x 1.1±0.26-basal; p=0.005 and MCV decreased (9.1± 2.8 x 11.02±2.6-basal; p=0.006 from 8 mg/Kg to 16mg/Kg DXR. LVEF presented only a slight but significant decrease (80.4±6.9% x 85.3±6.9%-basal, p=0.005 from 8 mg/Kg to 16 mg/Kg DXR. CC-IBS was 72.2% sensitive and 83.3% specific to detect collagen deposition of 4.24%(AUC=0.76. LVEF was not accurate to detect initial collagen deposition (AUC=0.54. In conclusion: UTC was able to early identify the DXR myocardial lesion when compared to LVEF, showing good accuracy to detect the initial collagen deposition in this experimental animal model.

  3. Early detection of doxorubicin myocardial injury by ultrasonic tissue characterization in an experimental animal model.

    Science.gov (United States)

    Romano, Minna Moreira Dias; Pazin-Filho, Antônio; O'Connel, João Lucas; Simões, Marcus Vinícius; Schmidt, André; Campos, Érica C; Rossi, Marcos; Maciel, Benedito Carlos

    2012-10-10

    In the clinical setting, the early detection of myocardial injury induced by doxorubicin (DXR) is still considered a challenge. To assess whether ultrasonic tissue characterization (UTC) can identify early DXR-related myocardial lesions and their correlation with collagen myocardial percentages, we studied 60 rats at basal status and prospectively after 2 mg/Kg/week DXR endovenous infusion. Echocardiographic examinations were conducted at baseline and at 8, 10, 12, 14 and 16 mg/Kg DXR cumulative dose. The left ventricle ejection fraction (LVEF), shortening fraction (SF), and the UTC indices: corrected coefficient of integrated backscatter (IBS) (tissue IBS intensity/ phantom IBS intensity) (CC-IBS) and the cyclic variation magnitude of this intensity curve (MCV) were measured. The variation of each parameter of study through DXR dose was expressed by the average and standard error at specific DXR dosages and those at baseline. The collagen percent (%) was calculated in six control group animals and 24 DXR group animals. CC-IBS increased (1.29±0.27 x 1.1±0.26-basal; p=0.005) and MCV decreased (9.1± 2.8 x 11.02±2.6-basal; p=0.006) from 8 mg/Kg to 16 mg/Kg DXR. LVEF presented only a slight but significant decrease (80.4±6.9% x 85.3±6.9%-basal, p=0.005) from 8 mg/Kg to 16 mg/Kg DXR. CC-IBS was 72.2% sensitive and 83.3% specific to detect collagen deposition of 4.24% (AUC=0.76). LVEF was not accurate to detect initial collagen deposition (AUC=0.54). UTC was able to early identify the DXR myocardial lesion when compared to LVEF, showing good accuracy to detect the initial collagen deposition in this experimental animal model.

  4. Theoretic model of myocardial revascularization by far infrared laser and experimental validation

    Science.gov (United States)

    Luo, Le; Chen, Xing; Zhang, Ting; Zong, Ren-He; Deng, Shan-Xi

    2009-03-01

    A theoretic model of myocardial revascularization by a far infrared laser has been established and a quantificational relationship between the aperture of laser channel and parameters of laser has been concluded according to thermodynamics and the law of interaction of far infrared laser and myocardium. The experiment of a carbon dioxide laser revascularization in porcine myocardium has been done for different laser powers and irradiation time. The relative errors between experimental result and theoretic computation are from 13% to 22%. The reasons that cause the errors have been studied in detail.

  5. A secondary wave of neutrophil infiltration causes necrosis and ulceration in lesions of experimental American cutaneous leishmaniasis.

    Science.gov (United States)

    Peniche, Alex G; Bonilla, Diana L; Palma, Gloria I; Melby, Peter C; Travi, Bruno L; Osorio, E Yaneth

    2017-01-01

    We evaluated the importance of neutrophils in the development of chronic lesions caused by L. Viannia spp. using the hamster as experimental model of American Cutaneous Leishmaniasis (ACL). Neutrophils infiltrated the lesion within the first six hours post-infection. Inhibition of this early infiltration using a polyclonal antibody or cyclophosphamide was associated with transient parasite control but the protective effect vanished when lesions became clinically apparent. At lesion onset (approximately 10 days p.i.), there was an increased proportion of both uninfected and infected macrophages, and subsequently a second wave of neutrophils infiltrated the lesion (after 19 days p.i.) This second neutrophil infiltration was associated with lesion necrosis and ulceration (R2 = 0.75) and maximum parasite burden. Intradermal delivery of N-formylmethionyl-leucyl-phenylalanine (fMLP), aimed to increase neutrophil infiltration, resulted in larger lesions with marked necrosis and higher parasite burden than in mock treated groups (pnecrosis in ACL. The overall results indicate that neutrophils were unable to clear the infection in this model, and that the second wave of neutrophils played an important role in the severity of ACL.

  6. Detection of acute myocardial infarction in spontaneously hypertensive rats by /sup 99m/Tc-Pyrrolidino methyl tetracycline

    Energy Technology Data Exchange (ETDEWEB)

    Zmbova, B.; Tadzer, I.; Stakic, D.; Bogdanova, V.; Stojanova, D.

    1983-01-01

    The myocardial infarct induced by isoproterenol in spontaneously hypertensive rats accumulates higher activities of /sup 99/sup(m)Tc-PM tetracycline compared with the cardiac infarct in normotensive rats caused by the same method. The isoproterenol model of the myocardial necrosis was induced in intact rats without opening the thorax and is a convenient method for experimental radioisotope studies.

  7. Neurogenic cardiomyopathy in rabbits with experimentally induced rabies.

    Science.gov (United States)

    Kesdangsakonwut, S; Sunden, Y; Yamada, K; Nishizono, A; Sawa, H; Umemura, T

    2015-05-01

    Cardiomyopathies have been rarely described in rabbits. Here we report myocardial necrosis of the ventricular wall in rabbits with experimentally induced rabies. Myocardial lesions were found only in rabbits with brain lesions, and the severity of the cardiac lesions was proportional to that of the brain lesions. Neither the frequency nor the cumulative dose of anesthesia was related to the incidence or the severity of the myocardial lesions. The myocardial lesions were characterized by degeneration and/or necrosis of myocardial cells and were accompanied by contraction band necrosis, interstitial fibrosis, and infiltration of inflammatory cells. The brain lesions due to rabies virus infection were most prominent in the cerebral cortex, thalamus, hypothalamus, brainstem, and medulla. Rabies virus antigen was not found in the hearts of any rabbits. Based on these findings, the myocardial lesions were classified as neurogenic cardiomyopathy. © The Author(s) 2014.

  8. {sup 99m}Tc-annexin V and {sup 111}In-antimyosin antibody uptake in experimental myocardial infarction in rats

    Energy Technology Data Exchange (ETDEWEB)

    Sarda-Mantel, Laure; Rouzet, Francois; Martet, Genevieve; Raguin, Olivier; Vrigneaud, Jean-Marc; Guludec, Dominique Le [Bichat Hospital AP-HP, EA 3512, Nuclear Medicine Department, Paris (France); Michel, Jean-Baptiste; Louedec, Liliane [INSERM U460, UFR Bichat, Paris (France); Vanderheyden, Jean-Luc [Theseus Imaging Corporation, Boston, MA (United States); Hervatin, Florence [Bichat Hospital AP-HP, EA 3512, Nuclear Medicine Department, Paris (France); CGA/SHFS, Orsay (France); Khaw, Ban An [Bouve College of Pharmacy and Health Sciences, Center for Drug Targeting and Analysis, Boston, MA (United States)

    2006-03-15

    {sup 99m}Tc-annexin V (ANX) allows scintigraphic detection of apoptotic cells via specific binding to exposed phosphatidylserine. In myocardial infarction, apoptosis of myocytes is variable and depends especially on the presence or absence of coronary reperfusion. In this study, ANX uptake in non-reperfused experimental myocardial infarcts was compared with uptake of a marker of myocyte necrosis ({sup 111}In-antimyosin antibodies, AM) and an immunohistochemical marker of apoptosis (Apostain). The left anterior coronary artery was ligated in 47 Wistar rats, which were then injected with ANX (n=20), AM (n=21) or both (n=6). Myocardial uptake of ANX and AM was determined at 2 h (n=14), 4 h (n=14) and 24 h (n=19) after coronary ligation (CL), by quantitative autoradiography with (n=23) or without (n=24) gamma imaging. Heart-to-lung ratios (HLRs) and infarct-to-remote myocardium activity ratios (INRs) were calculated on the scintigrams and autoradiograms respectively. Cardiac sections were stained with haematoxylin-eosin and Apostain. The above studies were repeated in 12 normal rats. All rats with CL showed increased ANX and AM uptake in cardiac areas on scintigrams 24 h after CL, with HLRs higher than in controls: 3.1{+-}0.6 versus 1.5{+-}0.3 (p=0.001) for ANX and 1.99{+-}0.44 versus 1.01{+-}0.05 (p<0.0005) for AM. Autoradiography showed intense ANX and AM uptake in infarcts, with comparable topography and INRs at 2 h, 4 h and 24 h after CL (4.6{+-}0.9 versus 5.0{+-}1.8 at 24 h), while Apostain staining was very low (0.06{+-}0.06% of cells). In this model of persistent CL, we observed increased ANX uptake in injured myocardium, comparable in intensity, topography and kinetics to that of AM. There was only minimal Apostain staining in the same areas. (orig.)

  9. Activation of complement factor B contributes to murine and human myocardial ischemia/reperfusion injury.

    Directory of Open Access Journals (Sweden)

    Nicholas Chun

    Full Text Available The pathophysiology of myocardial injury that results from cardiac ischemia and reperfusion (I/R is incompletely understood. Experimental evidence from murine models indicates that innate immune mechanisms including complement activation via the classical and lectin pathways are crucial. Whether factor B (fB, a component of the alternative complement pathway required for amplification of complement cascade activation, participates in the pathophysiology of myocardial I/R injury has not been addressed. We induced regional myocardial I/R injury by transient coronary ligation in WT C57BL/6 mice, a manipulation that resulted in marked myocardial necrosis associated with activation of fB protein and myocardial deposition of C3 activation products. In contrast, in fB-/- mice, the same procedure resulted in significantly reduced myocardial necrosis (% ventricular tissue necrotic; fB-/- mice, 20 ± 4%; WT mice, 45 ± 3%; P < 0.05 and diminished deposition of C3 activation products in the myocardial tissue (fB-/- mice, 0 ± 0%; WT mice, 31 ± 6%; P<0.05. Reconstitution of fB-/- mice with WT serum followed by cardiac I/R restored the myocardial necrosis and activated C3 deposition in the myocardium. In translational human studies we measured levels of activated fB (Bb in intracoronary blood samples obtained during cardio-pulmonary bypass surgery before and after aortic cross clamping (AXCL, during which global heart ischemia was induced. Intracoronary Bb increased immediately after AXCL, and the levels were directly correlated with peripheral blood levels of cardiac troponin I, an established biomarker of myocardial necrosis (Spearman coefficient = 0.465, P < 0.01. Taken together, our results support the conclusion that circulating fB is a crucial pathophysiological amplifier of I/R-induced, complement-dependent myocardial necrosis and identify fB as a potential therapeutic target for prevention of human myocardial I/R injury.

  10. Elevated interferon gamma expression in the central nervous system of tumour necrosis factor receptor 1-deficient mice with experimental autoimmune encephalomyelitis

    DEFF Research Database (Denmark)

    Wheeler, Rachel D; Zehntner, Simone P; Kelly, Lisa M

    2006-01-01

    Inflammation in the central nervous system (CNS) can be studied in experimental autoimmune encephalomyelitis (EAE). The proinflammatory cytokines interferon-gamma (IFN-gamma) and tumour necrosis factor (TNF) are implicated in EAE pathogenesis. Signals through the type 1 TNF receptor (TNFR1) are r...

  11. [Impacts of early metoprolol intervention on connexin 43 and phosphorylated connexin 43 expression in rabbits with experimental myocardial infarction].

    Science.gov (United States)

    Zhou, M; Lu, Q; Jiang, J Q; Chen, Z N; Gong, Z G; Li, Z G; Fu, W W; Ding, S F

    2017-04-24

    infarction group was less than in sham group, which was significantly upregulated in in early treatment group and routine treatment group when compared with myocardial infarction group, and expression of p-Cx43 was significantly higher in early treatment group than in routine treatment group. (4)The p-Cx43/Cx43 ratio of protein was significantly lower in myocardial infarction group than in sham group (0.165±0.011 vs. 0.363±0.046, P treatment group (0.720±0.063) and routine treatment group (0.364±0.030) than in myocardial infarction group (both P treatment group than in routine treatment group ( P treatment, especially the early metoprolol treatment (within 24 hours after LAD ligation), could significantly improve VFT by ameliorating the distribution and dephosphorylation of myocardial Cx43 in rabbits with experimental myocardial infarction.

  12. Potential advantages of cell administration on the inflammatory response compared to standard ACE inhibitor treatment in experimental myocardial infarction

    Directory of Open Access Journals (Sweden)

    De Camilli Elisa

    2008-06-01

    Full Text Available Abstract Background Bone Marrow (BM progenitor cells can target the site of myocardial injury, contributing to tissue repair by neovascolarization and/or by a possible direct paracrine effect on the inflammatory cascade. Angiotensin Converting Enzyme inhibitors (ACE-I are effective in reducing mortality and preventing left ventricular (LV function deterioration after myocardial infarction. Methods We investigated the short term effects of BM mononuclear cells (BMMNCs therapy on the pro-inflammatory cytokines (pro-CKs and on LV remodelling and compared these effects over a standard ACE-I therapy in a rat model of myocardial cryodamage. Forty two adult inbread Fisher-F344 rats were randomized into three groups: untreated (UT; n = 12, pharmacological therapy (ACE-I; n = 14, receiving quinapril, and cellular therapy (BMMNCs; n = 16, receiving BMMNCs infusion. Rats underwent to a standard echocardiogram in the acute setting and 14 days after the damage, before the sacrifice. Pro-CKs analysis (interleukin (IL1β, IL-6, tumor necrosis factor (TNFα was performed (multiplex proteome arrays on blood samples obtained by direct aorta puncture before the sacrifice; a control group of 6 rats was considered as reference. Results Concerning the extension of the infarcted area as well as the LV dimensions, no differences were observed among the animal groups; treated rats had lower left atrial diameters and higher indexes of LV function. Pro-Cks were increased in infarcted-UT rats if compared with controls, and significantly reduced by BMMNCs and ACE-I ; TNFα inversely correlated with LV fractional shortening. Conclusion After myocardial infarction, both BMMNCs and ACE-I reduce the pattern of pro-Ck response, probably contributing to prevent the deterioration of LV function observed in UT rats.

  13. Myocardial imaging. Coxsackie myocarditis

    Energy Technology Data Exchange (ETDEWEB)

    Wells, R.G.; Ruskin, J.A.; Sty, J.R.

    1986-09-01

    A 3-week-old male neonate with heart failure associated with Coxsackie virus infection was imaged with Tc-99m PYP and TI-201. The abnormal imaging pattern suggested myocardial infarction. Autopsy findings indicated that the cause was myocardial necrosis secondary to an acute inflammatory process. Causes of abnormal myocardial uptake of Tc-99m PYP in pediatrics include infarction, myocarditis, cardiomyopathy, bacterial endocarditis, and trauma. Myocardial imaging cannot provide a specific cause diagnosis. Causes of myocardial infarction in pediatrics are listed in Table 1.

  14. Early detection of doxorubicin myocardial injury by ultrasonic tissue characterization in an experimental animal model

    OpenAIRE

    Romano Minna Moreira; Pazin-Filho Antônio; O’Connel João; Simões Marcus; Schmidt André; Campos Érica C; Rossi Marcos; Maciel Benedito

    2012-01-01

    Abstract In the clinical setting, the early detection of myocardial injury induced by doxorubicin (DXR) is still considered a challenge. To assess whether ultrasonic tissue characterization (UTC) can identify early DXR-related myocardial lesions and their correlation with collagen myocardial percentages, we studied 60 rats at basal status and prospectively after 2mg/Kg/week DXR endovenous infusion. Echocardiographic examinations were conducted at baseline and at 8,10,12,14 and 16 mg/Kg DXR cu...

  15. Experimental validation of contrast-enhanced SSFP cine CMR for quantification of myocardium at risk in acute myocardial infarction.

    Science.gov (United States)

    Nordlund, David; Kanski, Mikael; Jablonowski, Robert; Koul, Sasha; Erlinge, David; Carlsson, Marcus; Engblom, Henrik; Aletras, Anthony H; Arheden, Håkan

    2017-01-30

    Accurate assessment of myocardium at risk (MaR) after acute myocardial infarction (AMI) is necessary when assessing myocardial salvage. Contrast-enhanced steady-state free precession (CE-SSFP) is a recently developed cardiovascular magnetic resonance (CMR) method for assessment of MaR up to 1 week after AMI. Our aim was to validate CE-SSFP for determination of MaR in an experimental porcine model using myocardial perfusion single-photon emission computed tomography (MPS) as a reference standard and to test the stability of MaR-quantification over time after injecting gadolinium-based contrast. Eleven pigs were subjected to either 35 or 40 min occlusion of the left anterior descending artery followed by six hours of reperfusion. A technetium-based perfusion tracer was administered intravenously ten minutes before reperfusion. In-vivo and ex-vivo CE-SSFP CMR was performed followed by ex-vivo MPS imaging. MaR was expressed as % of left ventricular mass (LVM). There was good agreement between MaR by ex-vivo CMR and MaR by MPS (bias: 1 ± 3% LVM, r 2  = 0.92, p myocardial salvage in experimental studies.

  16. Propofol Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor-Alpha Expression and Myocardial Depression through Decreasing the Generation of Superoxide Anion in Cardiomyocytes

    Science.gov (United States)

    Tang, Jing; Hu, Ji-Jie; Lu, Chun-Hua; Liang, Jia-Ni; Xiao, Jin-Fang; Liu, You-Tan; Lin, Chun-Shui; Qin, Zai-Sheng

    2014-01-01

    TNF-α has been shown to be a major factor responsible for myocardial depression in sepsis. The aim of this study was to investigate the effect of an anesthetic, propofol, on TNF-α expression in cardiomyocytes treated with LPS both in vivo and in vitro. In cultured cardiomyocytes, compared with control group, propofol significantly reduced protein expression of gp91phox and phosphorylation of extracellular regulated protein kinases 1/2 (ERK1/2) and p38 MAPK, which associates with reduced TNF-α production. In in vivo mice studies, propofol significantly improved myocardial depression and increased survival rate of mice after LPS treatment or during endotoxemia, which associates with reduced myocardial TNF-α production, gp91phox, ERK1/2, and p38 MAPK. It is concluded that propofol abrogates LPS-induced TNF-α production and alleviates cardiac depression through gp91phox/ERK1/2 or p38 MAPK signal pathway. These findings have great clinical importance in the application of propofol for patients enduring sepsis. PMID:25180066

  17. Kaempferol Attenuates Myocardial Ischemic Injury via Inhibition of MAPK Signaling Pathway in Experimental Model of Myocardial Ischemia-Reperfusion Injury

    Directory of Open Access Journals (Sweden)

    Kapil Suchal

    2016-01-01

    Full Text Available Kaempferol (KMP, a dietary flavonoid, has antioxidant, anti-inflammatory, and antiapoptotic effects. Hence, we investigated the effect of KMP in ischemia-reperfusion (IR model of myocardial injury in rats. We studied male albino Wistar rats that were divided into sham, IR-control, KMP-20 + IR, and KMP 20 per se groups. KMP (20 mg/kg; i.p. was administered daily to rats for the period of 15 days, and, on the 15th day, ischemia was produced by one-stage ligation of left anterior descending coronary artery for 45 min followed by reperfusion for 60 min. After completion of surgery, rats were sacrificed; heart was removed and processed for biochemical, morphological, and molecular studies. KMP pretreatment significantly ameliorated IR injury by maintaining cardiac function, normalizing oxidative stress, and preserving morphological alterations. Furthermore, there was a decrease in the level of inflammatory markers (TNF-α, IL-6, and NFκB, inhibition of active JNK and p38 proteins, and activation of ERK1/ERK2, a prosurvival kinase. Additionally, it also attenuated apoptosis by reducing the expression of proapoptotic proteins (Bax and Caspase-3, TUNEL positive cells, and increased level of antiapoptotic proteins (Bcl-2. In conclusion, KMP protected against IR injury by attenuating inflammation and apoptosis through the modulation of MAPK pathway.

  18. An overview on development and application of an experimental platform for quantitative cardiac imaging research in rabbit models of myocardial infarction.

    Science.gov (United States)

    Feng, Yuanbo; Bogaert, Jan; Oyen, Raymond; Ni, Yicheng

    2014-10-01

    To exploit the advantages of using rabbits for cardiac imaging research and to tackle the technical obstacles, efforts have been made under the framework of a doctoral research program. In this overview article, by cross-referencing the current literature, we summarize how we have developed a preclinical cardiac research platform based on modified models of reperfused myocardial infarction (MI) in rabbits; how the in vivo manifestations of cardiac imaging could be closely matched with those ex vivo macro- and microscopic findings; how these imaging outcomes could be quantitatively analyzed, validated and demonstrated; and how we could apply this cardiac imaging platform to provide possible solutions to certain lingering diagnostic and therapeutic problems in experimental cardiology. In particular, tissue components in acute cardiac ischemia have been stratified and characterized, post-infarct lipomatous metaplasia (LM) as a common but hardly illuminated clinical pathology has been identified in rabbit models, and a necrosis avid tracer as well as an anti-ischemic drug have been successfully assessed for their potential utilities in clinical cardiology. These outcomes may interest the researchers in the related fields and help strengthen translational research in cardiovascular diseases.

  19. The effect of xenon on isoflurane protection against experimental myocardial infarction.

    NARCIS (Netherlands)

    Baumert, J.H.; Hein, M.; Gerets, C.; Baltus, T.; Hecker, K.E.; Rossaint, R.

    2009-01-01

    OBJECTIVES: To investigate if the protective effects of xenon and isoflurane against myocardial ischemia-reperfusion damage would be additive. DESIGN: A prospective, randomized laboratory investigation. SETTING: An animal laboratory of a university hospital. PARTICIPANTS: Thirty-six pigs (female

  20. Progressive left ventricular hypertrophy after withdrawal of long-term ACE inhibition following experimental myocardial infarction

    NARCIS (Netherlands)

    Westendorp, B; Schoemaker, RG; Buikema, H; Boomsma, F; van Veldhuisen, DJ; van Gilsta, WH

    Background: Although discontinuation of chronic ACE inhibitor (ACEi) therapy after myocardial infarction (MI) is common in clinical practice, some clinical studies reported an increased incidence of ischemia-related events after withdrawal. To further address this issue, we assessed hemodynamic,

  1. The endothelial nitric oxide synthase cofactor tetrahydrobiopterin shields the remote myocardium from apoptosis after experimental myocardial infarction in vivo.

    Science.gov (United States)

    Heidrich, Felix M; Jercke, Marcel C; Ritzkat, Anna; Ebner, Annette; Poitz, David M; Pfluecke, Christian; Quick, Silvio; Speiser, Uwe; Simonis, Gregor; Wäßnig, Nadine K; Strasser, Ruth H; Wiedemann, Stephan

    2017-08-23

    Following myocardial infarction (MI), apoptosis occurs early in the remote myocardium and contributes to the processes of myocardial remodeling. Increased nitrosative stress is a well-known and potent inductor of myocardial apoptosis. Excess activation of endothelial nitric oxide synthase (eNOS) increases its uncoupling potential and results in nitrosative stress via formation of peroxynitrite. However, the pathophysiologic role of eNOS signaling in the remote myocardium after MI is as yet undefined. The impact of eNOS activation on pro- and anti-apoptotic signaling in the remote myocardium and the influence of pretreatment with the eNOS cofactor tetrahydrobiopterin (BH4) on eNOS activation, nitrosative stress level and apoptosis induction and execution were studied in a rat myocardial infarction model in vivo. 24 hours after anterior MI, eNOS activity in animals treated with left anterior descending coronary artery ligation (LIG) significantly increased in the posterior left ventricular myocardium as did protein nitrosylation when compared to sham treatment. This was paralleled by induction of apoptosis via both, the extrinsic and intrinsic pathways. Moreover, anti-apoptotic signaling via protein kinase B/Akt and glycogen synthase-kinase 3 beta was suppressed. Notably, pretreatment with the eNOS cofactor BH4 reduced eNOS activation, prevented excess protein nitrosylation, blunted apoptosis induction, facilitated anti-apoptotic signaling and eventually prevented apoptosis execution. Here we showed that 24 hours after experimental MI in rats in vivo, apoptosis was induced in the posterior non-infarcted LV wall. Evidence is presented that pretreatment with the eNOS cofactor BH4 resulted in less nitrosative stress and weakened apoptotic processes, although stabilizers contained did participate in this phenomenon. Because apoptosis is a crucial component of myocardial remodeling, influencing eNOS signaling might be an interesting pharmacological target for the

  2. Cysteinyl leukotriene signaling aggravates myocardial hypoxia in experimental atherosclerotic heart disease

    DEFF Research Database (Denmark)

    Nobili, Elena; Salvado, M Dolores; Folkersen, Lasse Westergaard

    2012-01-01

    Cysteinyl-leukotrienes (cys-LT) are powerful spasmogenic and immune modulating lipid mediators involved in inflammatory diseases, in particular asthma. Here, we investigated whether cys-LT signaling, in the context of atherosclerotic heart disease, compromises the myocardial microcirculation and ...

  3. Cysteinyl leukotriene signaling aggravates myocardial hypoxia in experimental atherosclerotic heart disease.

    Directory of Open Access Journals (Sweden)

    Elena Nobili

    Full Text Available BACKGROUND: Cysteinyl-leukotrienes (cys-LT are powerful spasmogenic and immune modulating lipid mediators involved in inflammatory diseases, in particular asthma. Here, we investigated whether cys-LT signaling, in the context of atherosclerotic heart disease, compromises the myocardial microcirculation and its response to hypoxic stress. To this end, we examined Apoe(-/- mice fed a hypercholesterolemic diet and analysed the expression of key enzymes of the cys-LT pathway and their receptors (CysLT1/CysLT2 in normal and hypoxic myocardium as well as the potential contribution of cys-LT signaling to the acute myocardial response to hypoxia. METHODS AND PRINCIPAL FINDINGS: Myocardial biopsies from Apoe(-/- mice demonstrated signs of chronic inflammation with fibrosis, increased apoptosis and expression of IL-6, as compared to biopsies from C57BL/6J control mice. In addition, we found increased leukotriene C(4 synthase (LTC(4S and CysLT1 expression in the myocardium of Apoe(-/- mice. Acute bouts of hypoxia further induced LTC(4S expression, increased LTC(4S enzyme activity and CysLT1 expression, and were associated with increased extension of hypoxic areas within the myocardium. Inhibition of cys-LT signaling by treatment with montelukast, a selective CysLT1 receptor antagonist, during acute bouts of hypoxic stress reduced myocardial hypoxic areas in Apoe(-/- mice to levels equal to those observed under normoxic conditions. In human heart biopsies from 14 patients with chronic coronary artery disease mRNA expression levels of LTC(4S and CysLT1 were increased in chronic ischemic compared to non-ischemic myocardium, constituting a molecular basis for increased cys-LT signaling. CONCLUSION: Our results suggest that CysLT1 antagonists may have protective effects on the hypoxic heart, and improve the oxygen supply to areas of myocardial ischemia, for instance during episodes of sleep apnea.

  4. Assessing the role of eptifibatide in patients with diffuse coronary disease undergoing drug-eluting stenting: the INtegrilin plus STenting to Avoid myocardial Necrosis Trial.

    Science.gov (United States)

    Biondi-Zoccai, Giuseppe; Valgimigli, Marco; Margheri, Massimo; Marzocchi, Antonio; Lettieri, Corrado; Stabile, Amerigo; Petronio, A Sonia; Binetti, Giorgio; Bolognese, Leonardo; Bellone, Pietro; Sardella, Gennaro; Contarini, Marco; Sheiban, Imad; Marra, Sebastiano; Piscione, Federico; Romeo, Francesco; Colombo, Antonio; Sangiorgi, Giuseppe

    2012-05-01

    The optimal antiplatelet regimen in elective patients undergoing complex percutaneous coronary interventions (PCIs) is uncertain. We aimed to assess the impact of glycoprotein IIb/IIIa (GpIIb/IIIa) inhibition with eptifibatide in clinically stable subjects with diffuse coronary lesions. Patients with stable coronary artery disease undergoing PCI by means of implantation of >33 mm of drug-eluting stent were single-blindedly randomized to heparin plus eptifibatide versus heparin alone. The primary end point was the rate of abnormal post-PCI creatine kinase-MB mass values. Secondary end points were major adverse cardiovascular events (MACEs) (ie, cardiac death, myocardial infarction, or urgent revascularization) and MACE plus bailout GpIIb/IIIa inhibitor use. The study was stopped for slow enrollment and funding issues after including a total of 91 patients: 44 were randomized to heparin plus eptifibatide, and 47, to heparin alone. Analysis for the primary end point showed a trend toward lower rates of abnormal post-PCI creatine kinase-MB mass values in the heparin-plus-eptifibatide group (18 [41%]) versus the heparin-alone group (26 [55%], relative risk 0.74 [95% CI 0.48-1.15], P = .169). Similar nonstatistically significant trends were found for rates of MACE, their components, or MACE plus bailout GpIIb/IIIa inhibitors (all P > .05). Notably, heparin plus eptifibatide proved remarkably safe because major bleedings or minor bleeding was uncommon and nonsignificantly different in both groups (all P > .05). Given its lack of statistical power, the INSTANT study cannot definitively provide evidence against or in favor of routine eptifibatide administration in stable patients undergoing implantation of multiple drug-eluting stent for diffuse coronary disease. However, the favorable trend evident for the primary end point warrants further larger randomized studies. Copyright © 2012 Mosby, Inc. All rights reserved.

  5. The effect of clomethiazole on plasma concentrations of interleukin-6, -8, -1beta, tumor necrosis factor-alpha, and neutrophil adhesion molecule expression during experimental extracorporeal circulation.

    LENUS (Irish Health Repository)

    Harmon, D

    2012-02-03

    Clomethiazole (CMZ), a neuroprotective drug, has antiinflammatory actions. We investigated the effects of CMZ administration on plasma concentrations of interleukin (IL)-6, IL-8, IL-1beta, tumor necrosis factor-alpha, and neutrophil adhesion molecule expression during experimental extracorporeal circulation. Five healthy volunteers each donated 500 mL of blood, which was subsequently divided into equal portions. Identical extracorporeal circuits were simultaneously primed with donated blood (250 mL) and circulated for 2 h at 37 degrees C. CMZ was added to 1 of the circuits of each pair to achieve a total plasma concentration of 40 micro mol\\/L. Blood samples were withdrawn at (i) donation, (ii) immediately after addition of CMZ, and at (iii) 30, 60, 90, and 120 min after commencing circulation. Plasma concentrations of IL-6, IL-8, and tumor necrosis factor-alpha were less in the CMZ group compared with control after 60 min of circulation (2.2 [0.3] versus 3.2 [0.4], 14.9 [4.8] versus 21.9 [18.4], 63.3 [43.5] versus 132.2 [118.9] pg\\/mL, respectively, P < 0.05). After 120 min of circulation, neutrophils from CMZ-treated circuits showed significantly less CD18 expression compared with control (237.5 [97.4] versus 280.5 [111.5], P = 0.03). The addition of CMZ to experimental extracorporeal circuits decreases the inflammatory response. This effect may be of clinical benefit by decreasing inflammatory-mediated neurological injury during cardiopulmonary bypass. IMPLICATIONS: Enhancement of gamma-aminobutyric acid(A)-mediated effects by clomethiazole (CMZ) and associated neuroprotection has been established in animal models of cerebral ischemia. In an ex vivo study, we demonstrated antiinflammatory activity of CMZ in experimental extracorporeal circulation. This represents a potential neuroprotective mechanism of CMZ in patients undergoing coronary artery bypass surgery.

  6. Neutrophil accumulation in experimental myocardial infarcts: relation with extent of injury and effect of reperfusion

    Energy Technology Data Exchange (ETDEWEB)

    Chatelain, P.; Latour, J.G.; Tran, D.; de Lorgeril, M.; Dupras, G.; Bourassa, M.

    1987-05-01

    The effects of reperfusion on the myocardial accumulation of neutrophils and their role in the extent of injury were investigated in a canine preparation with a 3 hr coronary occlusion followed by 21 hr of reperfusion. The left anterior descending coronary artery (LAD) was permanently occluded in group 1 and reperfused after 3 hr in four others (groups 2 to 5). All but group 5 received lidocaine (1 mg/min over 8 hr). A critical stenosis was produced and left in place at reperfusion only in group 2. In groups 1 and 2, /sup 111/In-labeled autologous neutrophils were injected at the time of coronary occlusion. Group 4 animals were rendered leukopenic 2 hr before the coronary ligature and throughout the experiment by injection of an antineutrophil rabbit serum. Quantification of the radioactivity by digitized scintigraphy of the heart slices revealed an 80% increase in neutrophil accumulation in the infarct region after reperfusion (group 2) as compared with permanent occlusion (group 1). Gamma counting of myocardial tissue samples showed that the neutrophil accumulation ratio in the subendocardial central zone of the infarct was increased five times by reperfusion, whereas no difference was evident in the subepicardium. Infarct size and myocardial area at risk were not statistically different among the five groups. However LAD flow in the leukopenic group (group 4) was significantly higher 30 min after reperfusion (40.0 +/- 5 ml/min) when compared with the preocclusion value (21.7 +/- 4 ml/min). In contrast, in a parallel experiment without leukopenia (group 3), LAD flow after reperfusion did not differ from the preocclusion value.

  7. Blockade of KCa3.1 Attenuates Left Ventricular Remodeling after Experimental Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Chen-Hui Ju

    2015-07-01

    Full Text Available Background/Aims: After myocardial infarction (MI, cardiac fibrosis greatly contributes to left ventricular remodeling and heart failure. The intermediate-conductance calcium-activated potassium Channel (KCa3.1 has been recently proposed as an attractive target of fibrosis. The present study aimed to detect the effects of KCa3.1 blockade on ventricular remodeling following MI and its potential mechanisms. Methods: Myocardial expression of KCa3.1 was initially measured in a mouse MI model by Western blot and real time-polymerase chain reaction. Then after treatment with TRAM-34, a highly selective KCa3.1 blocker, heart function and fibrosis were evaluated by echocardiography, histology and immunohistochemistry. Furthermore, the role of KCa3.1 in neonatal mouse cardiac fibroblasts (CFs stimulated by angiotensin II (Ang II was tested. Results: Myocardium expressed high level of KCa3.1 after MI. Pharmacological blockade of KCa3.1 channel improved heart function and reduced ventricular dilation and fibrosis. Besides, a lower prevalence of myofibroblasts was found in TRAM-34 treatment group. In vitro studies KCa3.1 was up regulated in CFs induced by Ang II and suppressed by its blocker.KCa3.1 pharmacological blockade attenuated CFs proliferation, differentiation and profibrogenic genes expression and may regulating through AKT and ERK1/2 pathways. Conclusion: Blockade of KCa3.1 is able to attenuate ventricular remodeling after MI through inhibiting the pro-fibrotic effects of CFs.

  8. Increased severity of experimental autoimmune encephalomyelitis, chronic macrophage/microglial reactivity, and demyelination in transgenic mice producing tumor necrosis factor-alpha in the central nervous system

    DEFF Research Database (Denmark)

    Taupin, V; Renno, T; Bourbonnière, L

    1997-01-01

    Tumor necrosis factor-alpha (TNF-alpha) is an inflammatory cytokine implicated in a number of autoimmune diseases. Apoptotic cell death is induced by TNF-alpha in vitro, and has been suggested as one cause of autoimmune pathology, including autoimmune demyelinating diseases where oligodendrocytes...... and showed no spontaneous pathology, but they developed experimental autoimmune encephalomyelitis (EAE) with greater severity than nontransgenic controls when immunized with MBP in adjuvant. Unlike nontransgenic controls, EAE then progressed to a nonabating demyelinating disease. Macrophage....../microglial reactivity was evident in demyelinating lesions in spinal cord, but T cells were not detected during chronic disease. The participation of TNF-alpha in the demyelinating process is thus more probably due to the perpetuation of macrophage/microglial activation than to direct cytotoxicity of myelin...

  9. Preventive effects of p-coumaric acid on cardiac hypertrophy and alterations in electrocardiogram, lipids, and lipoproteins in experimentally induced myocardial infarcted rats.

    Science.gov (United States)

    Roy, Abhro Jyoti; Stanely Mainzen Prince, P

    2013-10-01

    The present study evaluated the preventive effects of p-coumaric acid on cardiac hypertrophy and alterations in electrocardiogram, lipids, and lipoproteins in experimentally induced myocardial infarcted rats. Rats were pretreated with p-coumaric acid (8 mg/kg body weight) daily for a period of 7 days and then injected with isoproterenol (100mg/kg body weight) on 8th and 9th day to induce myocardial infarction. Myocardial infarction induced by isoproterenol was indicated by increased level of cardiac sensitive marker and elevated ST-segments in the electrocardiogram. Also, the levels/concentrations of serum and heart cholesterol, triglycerides and free fatty acids were increased in myocardial infarcted rats. Isoproterenol also increased the levels of serum low density and very low density lipoprotein cholesterol and decreased the levels of high density lipoprotein cholesterol. It also enhanced the activity of liver 3-hydroxy-3 methyl glutaryl-Coenzyme-A reductase. p-Coumaric acid pretreatment revealed preventive effects on all the biochemical parameters and electrocardiogram studied in myocardial infarcted rats. The in vitro study confirmed the free radical scavenging property of p-coumaric acid. Thus, p-coumaric acid prevented cardiac hypertrophy and alterations in lipids, lipoproteins, and electrocardiogram, by virtue of its antihypertrophic, antilipidemic, and free radical scavenging effects in isoproterenol induced myocardial infarcted rats. Copyright © 2013 Elsevier Ltd. All rights reserved.

  10. Increased pulmonary secretion of tumor necrosis factor-alpha in calves experimentally infected with bovine respiratory syncytial virus

    DEFF Research Database (Denmark)

    Rontved, C. M.; Tjørnehøj, Kirsten; Viuff, B.

    2000-01-01

    Bovine respiratory syncytial virus (BRSV) is an important cause of respiratory disease among calves in the Danish cattle industry. An experimental BRSV infection model was used to study the pathogenesis of the disease in calves. Broncho alveolar lung lavage (BAL) was performed on 28 Jersey calves...

  11. Cardiovascular Magnetic Resonance Relaxometry Predicts Regional Functional Outcome After Experimental Myocardial Infarction.

    Science.gov (United States)

    Haberkorn, Sebastian M; Jacoby, Christoph; Ding, Zhaoping; Keul, Petra; Bönner, Florian; Polzin, Amin; Levkau, Bodo; Schrader, Jürgen; Kelm, Malte; Flögel, Ulrich

    2017-08-01

    Cardiovascular magnetic resonance with gadolinium-based contrast agents has established as gold standard for tissue characterization after myocardial infarction (MI). Beyond accurate diagnosis, the value of cardiovascular magnetic resonance to predict the outcome after MI has yet to be substantiated. Recent cardiovascular magnetic resonance approaches were systematically compared for quantification of tissue injury and functional impairment after MI using murine models with permanent left anterior descending coronary artery ligation (n=14) or 50 minutes ischemia/reperfusion (n=13). Cardiovascular magnetic resonance included native/postcontrast T1 maps, T2 maps, and late gadolinium enhancement at days 1 and 21 post-MI. For regional correlation of parametric and functional measures, the left ventricle was analyzed over 200 sectors. For T1 mapping, we used retrospective triggering with variable flip angle analysis. Sectoral analysis of native T1 maps already revealed in the acute phase after MI substantial discrepancies in myocardial tissue texture between the 2 MI models (native T1 day 1: permanent ligation, 1280.0±162.6 ms; ischemia/reperfusion, 1115.0±140.5 ms; Pfunctional outcome (left ventricular ejection fraction day 21: permanent ligation, 24.5±7.0%; ischemia/reperfusion, 33.7±11.6%; Pfunction in corresponding areas at day 21 demonstrated for early native T1 values the best correlation with the later functional impairment (R2 =0.94). The present T1 mapping approach permits accurate characterization of local tissue injury and holds the potential for sensitive and graduated prognosis of the functional outcome after MI without gadolinium-based contrast agents. © 2017 American Heart Association, Inc.

  12. Myocardial motion and deformation patterns in an experimental swine model of acute LBBB/CRT and chronic infarct.

    Science.gov (United States)

    Duchateau, Nicolas; Sitges, Marta; Doltra, Adelina; Fernández-Armenta, Juan; Solanes, Nuria; Rigol, Montserrat; Gabrielli, Luigi; Silva, Etelvino; Barceló, Aina; Berruezo, Antonio; Mont, Lluís; Brugada, Josep; Bijnens, Bart

    2014-06-01

    In cardiac resynchronization therapy (CRT), specific changes in motion/deformation happen with left-bundle-branch-block (LBBB) and following treatment. However, they remain sub-optimally studied. We propose a two-fold improvement of their characterization. This includes controlling them through an experimental model and using more suitable quantification techniques. We used a swine model of acute LBBB and CRT with/without chronic infarct (pure-LBBB: N = 11; LBBB + left-anterior-descending infarct: N = 11). Myocardial displacement, velocity and strain were extracted from short-axis echocardiographic sequences using 2D speckle-tracking. The data was transformed to a single spatiotemporal system of coordinates to perform subject comparisons and quantify pattern changes at similar locations and instants. Pure-LBBB animals showed a specific intra-ventricular dyssynchrony pattern with LBBB (11/11 animals), and the recovery towards a normal pattern with CRT (10/11 animals). Pattern variability was low within the pure-LBBB population, as quantified by our method. This was not correctly assessed by more conventional measurements. Infarct presence affected the pattern distribution and CRT efficiency (improvements in 6/11 animals). Pattern changes correlated with global cardiac function (global circumferential strain) changes in all the animals (corrected: (pLBBBvsBaseline) < 0.001, (pCRTvsBaseline) = NS; non-corrected: (pLBBBvsBaseline) = NS, (pCRTvsBaseline) = 0.028). Our LBBB/CRT experimental model allowed controlling specific factors responsible for changes in mechanical dyssynchrony and therapy. We illustrated the importance of our quantification method to study these changes and their variability. Our findings confirm the importance of myocardial viability and of specific LBBB-related mechanical dyssynchrony patterns.

  13. Myocardial Bridge

    Science.gov (United States)

    ... Sudden Cardiac Arrest Valve Disease Vulnerable Plaque Myocardial Bridge Related terms: myocardium, coronary arteries, myocardial ischemia Your ... surface of the heart. What is a myocardial bridge? A myocardial bridge is a band of heart ...

  14. [Effect of coenzyme Q10 on the expression of tumor necrosis factor-α and interleukin-10 in gingival tissue of experimental periodontitis in rats].

    Science.gov (United States)

    Jin, Hui-jiao; Xue, Yi; Chen, Guang; Wu, Zhong-yin

    2013-11-01

    To investigate the effect of coenzyme Q10 on the levels of tumor necrosis factor-α(TNF-α) and interleukin-10 (IL-10) in gingival tissue of experimental periodontitis in rats. A total of 48 healthy Wistar rats were divided into 3 groups of 16 randomly, normal group, coenzyme Q10 treatment group (Q10 group) and periodontitis group.Normal group was fed with normal diet and water. Periodontitis models were established in other two groups.Q10 group received coenzyme Q10 for 12 weeks and periodontitis group was fed with the same dose of normal saline.Four rats in each group were sacrified before administration and 4, 8 and 12 weeks after administration. Gingival tissue samples from mandiblar first permanent molar were taken. The levels of TNF-α and IL-10 were detected by immunohistochemistry. The expression of TNF-α in periodontitis group [54.9% (52.9%, 57.3%)] was significantly higher than that in Q10 group [15.1% (12.7%, 17.5%)] at 12 weeks (P Q10 group [38.9% (38.0%, 40.4%)] (P Q10 group at 12th weeks (P Q10 group (P Coenzyme Q10 inhibits the expression of TNF-α and promotes the expression of IL-10 in periodontal tissues of experimental periodontitis rats. Coenzyme Q10 may play a role in treating periodontitis.

  15. MRI Findings of Pericardial Fat Necrosis: Case Report

    Energy Technology Data Exchange (ETDEWEB)

    Lee, Hyo Hyeok; Ryu, Dae Shick; Jung, Sang Sig; Jung, Seung Mun; Choi, Soo Jung; Shin, Dae Hee [Gangneung Asan Hospital, Ulsan University College of Medicine, Gangneung (Korea, Republic of)

    2011-06-15

    Pericardial fat necrosis is an infrequent cause of acute chest pain and this can mimic acute myocardial infarction and acute pericarditis. We describe here a patient with the magnetic resonance imaging (MRI) findings of pericardial fat necrosis and this was correlated with the computed tomography (CT) findings. The MRI findings may be helpful for distinguishing pericardial fat necrosis from other causes of acute chest pain and from the fat-containing tumors in the cardiophrenic space of the anterior mediastinum.

  16. Oxygen-Generating Photo-Cross-Linkable Hydrogels Support Cardiac Progenitor Cell Survival by Reducing Hypoxia-Induced Necrosis

    NARCIS (Netherlands)

    Alemdar, N.; Leijten, Jeroen Christianus Hermanus; Camci-Unal, G.; Hjortnaes, J.; Ribas, J.; Paul, A.; Mostafalu, P.; Gaharwar, A.K.; Qiu, Y.; Sonkusale, S.; Liao, R.; Khademhosseini, A.

    2016-01-01

    Oxygen is essential to cell survival and tissue function. Not surprisingly, ischemia resulting from myocardial infarction induces cell death and tissue necrosis. Attempts to regenerate myocardial tissue with cell based therapies exacerbate the hypoxic stress by further increasing the metabolic

  17. Effects of the tumour necrosis factor-alpha inhibitors pentoxifylline and thalidomide in short-term experimental oral mucositis in hamsters.

    Science.gov (United States)

    Lima, V; Brito, G A C; Cunha, F Q; Rebouças, C G; Falcão, B A A; Augusto, R F; Souza, M L P; Leitão, B T; Ribeiro, R A

    2005-06-01

    Oral mucositis is a frequent side-effect of cancer therapy. A definitive method of prophylaxis or treatment is not yet available. As pentoxifylline (PTX) and thalidomide (TLD) have been shown to inhibit cytokine synthesis, we studied the effects of these cytokine inhibitors in an experimental oral mucositis model. Oral mucositis was induced in Golden hamsters by the administration of 5-fluorouracil (5-FU) followed by mechanical trauma of the cheek pouch. On days 4, 5, 10, 12, 14 and 16, lesions induced by 5-FU were examined macroscopically and microscopically, and the presence and intensity of hyperemia, erythema, edema, inflammatory cell infiltration, hemorrhagic areas, ulcers and abscesses were recorded. Saline (control), PTX (5, 15, 45 mg kg(-1)) or TLD (10, 30, 90 mg kg(-1)) were administered daily and animals were killed on day 10 for macroscopic and histological analysis and assay of myeloperoxidase (MPO) activity. Animals were weighed daily, and total and differential leukocyte counts were performed on peripheral blood. PTX and TLD were found to reduce the macroscopic and histological parameters of oral mucositis and MPO activity. PTX and TLD also reversed peripheral neutrophilia, but only PTX prevented weight loss. The results indicate a protective effect of PTX and TLD, suggesting an important role for tumour necrosis factor-alpha (TNF-alpha) in the pathophysiology of 5-FU induced-oral mucositis in hamsters. (c) Eur J Oral Sci, 2005

  18. Experimental study of cerebrospinal fluid tumor necrosis factor-alpha release in penicillin- and cephalosporin-resistant pneumococcal meningitis treated with different antibiotic schedules.

    Science.gov (United States)

    Vivas, M; Force, E; El Haj, C; Tubau, F; Ariza, J; Cabellos, C

    2017-08-01

    To measure the inflammatory response in terms of tumor necrosis factor-alpha (TNF-α) levels in cerebrospinal fluid (CSF), using bacteriolytic versus nonbacteriolytic antibiotic therapy and adjunctive treatment with dexamethasone in an experimental rabbit model of pneumococcal meningitis. In a rabbit model of pneumococcal meningitis, we tested CSF TNF-α levels in several samples from rabbits infected with the HUB 2349 strain and treated with ceftriaxone 100 mg/kg/d, ceftriaxone plus vancomycin 30 mg/kg/d, or daptomycin at 15 mg/kg or 25 mg/kg. Daptomycin schedules were compared with the same doses in combination with dexamethasone at 0.125 mg/kg every 12 hours over a 26-hour period. The ceftriaxone group had the highest levels of TNF-α. TNF-α levels were significantly higher after ceftriaxone administration than in both daptomycin groups. The high-dose daptomycin group presented the lowest inflammatory levels in CSF samples. Adjunctive treatment with dexamethasone in this group modulated the inflammatory response, bringing down CSF TNF-α levels. CSF TNF-α levels were significantly lower in rabbits treated with daptomycin than in rabbits treated with ceftriaxone. Daptomycin avoided the inflammatory peak after administration observed in ceftriaxone-treated rabbits. The use of daptomycin plus dexamethasone achieved a significantly larger reduction in CSF TNF-α levels. Copyright © 2015. Published by Elsevier B.V.

  19. Experimental pain ratings and reactivity of cortisol and soluble tumor necrosis factor-α receptor II following a trial of hypnosis: results of a randomized controlled pilot study.

    Science.gov (United States)

    Goodin, Burel R; Quinn, Noel B; Kronfli, Tarek; King, Christopher D; Page, Gayle G; Haythornthwaite, Jennifer A; Edwards, Robert R; Stapleton, Laura M; McGuire, Lynanne

    2012-01-01

    Current evidence supports the efficacy of hypnosis for reducing the pain associated with experimental stimulation and various acute and chronic conditions; however, the mechanisms explaining how hypnosis exerts its effects remain less clear. The hypothalamic-pituitary-adrenal (HPA) axis and pro-inflammatory cytokines represent potential targets for investigation given their purported roles in the perpetuation of painful conditions; yet, no clinical trials have thus far examined the influence of hypnosis on these mechanisms. Healthy participants, highly susceptible to the effects of hypnosis, were randomized to either a hypnosis intervention or a no-intervention control. Using a cold pressor task, assessments of pain intensity and pain unpleasantness were collected prior to the intervention (Pre) and following the intervention (Post) along with pain-provoked changes in salivary cortisol and the soluble tumor necrosis factor-α receptor II (sTNFαRII). Compared with the no-intervention control, data analyses revealed that hypnosis significantly reduced pain intensity and pain unpleasantness. Hypnosis was not significantly associated with suppression of cortisol or sTNFαRII reactivity to acute pain from Pre to Post; however, the effect sizes for these associations were medium-sized. Overall, the findings from this randomized controlled pilot study support the importance of a future large-scale study on the effects of hypnosis for modulating pain-related changes of the HPA axis and pro-inflammatory cytokines. Wiley Periodicals, Inc.

  20. Diosmin prevents left ventricular hypertrophy, adenosine triphosphatases dysfunction and electrolyte imbalance in experimentally induced myocardial infarcted rats.

    Science.gov (United States)

    Sabarimuthu, Sharmila Queenthy; Ponnian, Stanely Mainzen Prince; John, Babu

    2017-11-05

    Currently, there has been an increased interest globally to identify natural compounds that are pharmacologically potent and have low or no adverse effects for use in preventive medicine. Myocardial infarction is a vital pathological feature resulting in high levels of mortality and morbidity. Left ventricular hypertrophy (LVH), adenosine triphosphatases (ATPases) dysfunction and electrolyte imbalance play a vital role in the pathogenesis of myocardial infarction. This study aims to evaluate the preventive effects of diosmin on LVH, ATPases dysfunction and electrolyte imbalance in isoproterenol induced myocardial infarcted rats. Male albino Wistar rats were pretreated orally with diosmin (10mg/kg body weight) daily for a period of 10 days. After pretreatment, isoproterenol (100mg/kg body weight) was injected subcutaneously into the rats twice at an interval of 24h to induce myocardial infarction. Isoproterenol induced myocardial infarcted rats showed increased LVH, altered levels/ concentrations of serum cardiac troponin-T, heart ATPases, heart sodium ion, calcium ion and potassium ion, and increased myocardial infarct size. Pretreatment with diosmin revealed preventive effects on LVH, and all the above mentioned biochemical parameters evaluated in isoproterenol induced myocardial infarcted rats. The 2, 3, 5-triphenyl tetrazolium chloride staining on myocardial infarct size confirmed the prevention of myocardial infarction. Further, the 1, 1 diphenyl-2- picryl-hydrazyl (DPPH) radical in vitro study revealed a potent DPPH free radical scavenging action of diosmin. Thus, the observed effects of diosmin are due to its antihypertrophic and free radical scavenging activities in isoproterenol induced myocardial infarcted rats. Copyright © 2017 Elsevier B.V. All rights reserved.

  1. Delayed administration of allogeneic cardiac stem cell therapy for acute myocardial infarction could ameliorate adverse remodeling: experimental study in swine.

    Science.gov (United States)

    Crisostomo, Veronica; Baez-Diaz, Claudia; Maestre, Juan; Garcia-Lindo, Monica; Sun, Fei; Casado, Javier G; Blazquez, Rebeca; Abad, Jose L; Palacios, Itziar; Rodriguez-Borlado, Luis; Sanchez-Margallo, Francisco M

    2015-05-12

    .019) higher amount of larger, more mature vessels at the infarct border. The intracoronary injection of 25x10(6) allogeneic cardiac stem cells is generally safe, both early and 7 days after experimental infarction, and alleviates myocardial dysfunction, with a greater limitation of left ventricular remodeling when performed at one week.

  2. Evaluating intramural virtual electrodes in the myocardial wedge preparation: simulations of experimental conditions.

    Science.gov (United States)

    Plank, G; Prassl, A; Hofer, E; Trayanova, N A

    2008-03-01

    While defibrillation is the only means for prevention of sudden cardiac death, key aspects of the process, such as the intramural virtual electrodes (VEs), remain controversial. Experimental studies had attempted to assess intramural VEs by using wedge preparations and recording activity from the cut surface; however, applicability of this approach remains unclear. These studies found, surprisingly, that for strong shocks, the entire cut surface was negatively polarized, regardless of boundary conditions. The goal of this study is to examine, by means of bidomain simulations, whether VEs on the cut surface represent a good approximation to VEs in depth of the intact wall. Furthermore, we aim to explore mechanisms that could give rise to negative polarization on the cut surface. A model of wedge preparation was used, in which fiber orientation could be changed, and where the cut surface was subjected to permeable and impermeable boundary conditions. Small-scale mechanisms for polarization were also considered. To determine whether any distortions in the recorded VEs arise from averaging during optical mapping, a model of fluorescent recording was employed. The results indicate that, when an applied field is spatially uniform and impermeable boundary conditions are enforced, regardless of the fiber orientation VEs on the cut surface faithfully represent those intramurally, provided tissue properties are not altered by dissection. Results also demonstrate that VEs are sensitive to the conductive layer thickness above the cut surface. Finally, averaging during fluorescent recordings results in large negative VEs on the cut surface, but these do not arise from small-scale heterogeneities.

  3. Evaluating Intramural Virtual Electrodes in the Myocardial Wedge Preparation: Simulations of Experimental Conditions☆

    Science.gov (United States)

    Plank, G.; Prassl, A.; Hofer, E.; Trayanova, N.A.

    2008-01-01

    While defibrillation is the only means for prevention of sudden cardiac death, key aspects of the process, such as the intramural virtual electrodes (VEs), remain controversial. Experimental studies had attempted to assess intramural VEs by using wedge preparations and recording activity from the cut surface; however, applicability of this approach remains unclear. These studies found, surprisingly, that for strong shocks, the entire cut surface was negatively polarized, regardless of boundary conditions. The goal of this study is to examine, by means of bidomain simulations, whether VEs on the cut surface represent a good approximation to VEs in depth of the intact wall. Furthermore, we aim to explore mechanisms that could give rise to negative polarization on the cut surface. A model of wedge preparation was used, in which fiber orientation could be changed, and where the cut surface was subjected to permeable and impermeable boundary conditions. Small-scale mechanisms for polarization were also considered. To determine whether any distortions in the recorded VEs arise from averaging during optical mapping, a model of fluorescent recording was employed. The results indicate that, when an applied field is spatially uniform and impermeable boundary conditions are enforced, regardless of the fiber orientation VEs on the cut surface faithfully represent those intramurally, provided tissue properties are not altered by dissection. Results also demonstrate that VEs are sensitive to the conductive layer thickness above the cut surface. Finally, averaging during fluorescent recordings results in large negative VEs on the cut surface, but these do not arise from small-scale heterogeneities. PMID:17993491

  4. Roles of myocardial blood volume and flow in coronary artery disease: an experimental MRI study at rest and during hyperemia

    Energy Technology Data Exchange (ETDEWEB)

    McCommis, Kyle S.; Goldstein, Thomas A.; Pilgram, Thomas [Washington University School of Medicine, Mallinckrodt Institute of Radiology, St. Louis, MO (United States); Abendschein, Dana R. [Washington University School of Medicine, Center for Cardiovascular Research, St. Louis, MO (United States); Misselwitz, Bernd [Bayer Schering Pharma AG, Berlin (Germany); Gropler, Robert J. [Washington University School of Medicine, Mallinckrodt Institute of Radiology, St. Louis, MO (United States); Washington University School of Medicine, Center for Cardiovascular Research, St. Louis, MO (United States); Zheng, Jie [Washington University School of Medicine, Mallinckrodt Institute of Radiology, St. Louis, MO (United States); Cardiovascular Imaging Lab, St. Louis, MO (United States)

    2010-08-15

    To validate fast perfusion mapping techniques in a setting of coronary artery stenosis, and to further assess the relationship of absolute myocardial blood volume (MBV) and blood flow (MBF) to global myocardial oxygen demand. A group of 27 mongrel dogs were divided into 10 controls and 17 with acute coronary stenosis. On 1.5-T MRI, first-pass perfusion imaging with a bolus injection of a blood-pool contrast agent was performed to determine myocardial perfusion both at rest and during either dipyridamole-induced vasodilation or dobutamine-induced stress. Regional values of MBF and MBV were quantified by using a fast mapping technique. Color microspheres and {sup 99m}Tc-labeled red blood cells were injected to obtain respective gold standards. Microsphere-measured MBF and {sup 99m}Tc-measured MBV reference values correlated well with the MR results. Given the same changes in MBF, changes in MBV are twofold greater with dobutamine than with dipyridamole. Under dobutamine stress, MBV shows better association with total myocardial oxygen demand than MBF. Coronary stenosis progressively reduced this association in the presence of increased stenosis severity. MR first-pass perfusion can rapidly estimate regional MBF and MBV. Absolute quantification of MBV may add additional information on stenosis severity and myocardial viability compared with standard qualitative clinical evaluations of myocardial perfusion. (orig.)

  5. Breathing Maneuvers as a Vasoactive Stimulus for Detecting Inducible Myocardial Ischemia - An Experimental Cardiovascular Magnetic Resonance Study.

    Directory of Open Access Journals (Sweden)

    Kady Fischer

    Full Text Available Breathing maneuvers can elicit a similar vascular response as vasodilatory agents like adenosine; yet, their potential diagnostic utility in the presence of coronary artery stenosis is unknown. The objective of the study is to investigate if breathing maneuvers can non-invasively detect inducible ischemia in an experimental animal model when the myocardium is imaged with oxygenation-sensitive cardiovascular magnetic resonance (OS-CMR.In 11 anesthetised swine with experimentally induced significant stenosis (fractional flow reserve <0.75 of the left anterior descending coronary artery (LAD and 9 control animals, OS-CMR at 3T was performed during two different breathing maneuvers, a long breath-hold; and a combined maneuver of 60s of hyperventilation followed by a long breath-hold. The resulting change of myocardial oxygenation was compared to the invasive measurements of coronary blood flow, blood gases, and oxygen extraction. In control animals, all breathing maneuvers could significantly alter coronary blood flow as hyperventilation decreased coronary blood flow by 34±23%. A long breath-hold alone led to an increase of 97±88%, while the increase was 346±327% (p<0.001, when the long breath-hold was performed after hyperventilation. In stenosis animals, the coronary blood flow response was attenuated after both hyperventilation and the following breath-hold. This was matched by the observed oxygenation response as breath-holds following hyperventilation consistently yielded a significant difference in the signal of the MRI images between the perfusion territory of the stenosis LAD and remote myocardium. There was no difference between the coronary territories during the other breathing maneuvers or in the control group at any point.In an experimental animal model, the response to a combined breathing maneuver of hyperventilation with subsequent breath-holding is blunted in myocardium subject to significant coronary artery stenosis. This

  6. The Impact of Different Plasma Glucose Levels on Heart Rate in Experimental Rats With Acute Myocardial Infarction.

    Science.gov (United States)

    Pan, Guo-Zhong; Xie, Jing; Tian, Xiao-Fang; Yang, Shi-Wei; Zhou, Yu-Jie

    2016-08-01

    The aim of the study was to evaluate the impact of different plasma glucose levels on heart rate (HR) in experimental rats with acute myocardial infarction (AMI). One hundred and twenty-one male Wistar rats were randomly divided into AMI group (n = 70) and sham-operation group (n = 51). Both groups had low, normal and high glucose levels, respectively. In the former group, hypertonic glucose was injected into the rats to make their blood glucose levels above 16 mmol/L and insulin below 3.3 mmol/L; then, the left anterior descending artery was ligated. In the later group, the models of different blood glucose levels were the same as the former ones, but false operations, thread without ligating, were given to the rats. Electrocardiogram and troponin I (TnI) confirmed that the models were prepared successfully. Electrocardiogram expression of AMI was the formation of Q-wave in over three adjacent leads and abnormal elevation of TnI. The HR of the rats in the hypoglycemic group is higher than that of the hyperglycemic group and normal blood glucose group before AMI (P < 0.05). The HR of the hyperglycemic rats is higher than that of the hypoglycemic group and normal blood glucose group after AMI (P < 0.05). In the hypoglycemic group, the HR of the rats who suffered from AMI was lower than that of the rats of the sham group (P < 0.05). Hypoglycemia allows faster HR and the HR in the rats with hyperglycemia is higher than that in the rats with hypoglycemia among the AMI rats.

  7. Bioeffects of albumin-encapsulated microbubbles and real-time myocardial contrast echocardiography in an experimental canine model

    Directory of Open Access Journals (Sweden)

    P.M.M. Dourado

    2006-06-01

    Full Text Available Myocardial contrast echocardiography has been used for assessing myocardial perfusion. Some concerns regarding its safety still remain, mainly regarding the induction of microvascular alterations. We sought to determine the bioeffects of microbubbles and real-time myocardial contrast echocardiography (RTMCE in a closed-chest canine model. Eighteen mongrel dogs were randomly assigned to two groups. Nine were submitted to continuous intravenous infusion of perfluorocarbon-exposed sonicated dextrose albumin (PESDA plus continuous imaging using power pulse inversion RTMCE for 180 min, associated with manually deflagrated high-mechanical index impulses. The control group consisted of 3 dogs submitted to continuous imaging using RTMCE without PESDA, 3 dogs received PESDA alone, and 3 dogs were sham-operated. Hemodynamics and cardiac rhythm were monitored continuously. Histological analysis was performed on cardiac and pulmonary tissues. No hemodynamic changes or cardiac arrhythmias were observed in any group. Normal left ventricular ejection fraction and myocardial perfusion were maintained throughout the protocol. Frequency of mild and focal microhemorrhage areas in myocardial and pulmonary tissue was similar in PESDA plus RTMCE and control groups. The percentages of positive microscopical fields in the myocardium were 0.4 and 0.7% (P = NS in the PESDA plus RTMCE and control groups, respectively, and in the lungs they were 2.1 and 1.1%, respectively (P = NS. In this canine model, myocardial perfusion imaging obtained with PESDA and RTMCE was safe, with no alteration in cardiac rhythm or left ventricular function. Mild and focal myocardial and pulmonary microhemorrhages were observed in both groups, and may be attributed to surgical tissue manipulation.

  8. Experimental studies on myocardial glucose metabolism of rats with /sup 18/F-2-fluoro-2-deoxy-D-glucose

    Energy Technology Data Exchange (ETDEWEB)

    Yamada, K.; Endo, S.; Fukuda, H.; Abe, Y.; Yoshioka, S.; Itoh, M.; Kubota, K.; Hatazawa, J.; Satoh, T.; Matsuzawa, T.

    1985-04-01

    The myocardial uptake of /sup 18/F-FDG was investigated under various conditions, and compared with brain and tumour uptake as a function of blood glucose level. The uptake by the heart of normal feeding rats was rapid and remained essentially unchanged up to 2h after /sup 18/F-FDG injection, approximately 3%-4% dose/g tissue. On the other hand, the myocardial uptake of fasted rats was significantly lower than that of control rats throughout the course of the study, and it was about 0.3%-0.4% dose/g tissue. Myocardial uptake of /sup 18/F-FDG was relatively constant at glucose levels under about 120mg/100ml and increased steeply at higher blood glucose levels. In contrast, brain uptake decreased linearly with increasing levels of blood glucose, revealing a strong negative correlation between brain uptake of /sup 18/F-FDG and blood glucose levels. The tumor uptake pattern remained relatively unchanged, irrespective of blood glucose levels. It was revealed that the glucose demands of brain, heart, and tumor were entirely different. After a glucose load, the myocardial uptake of fasted rats increased only slightly from 0.4% to 0.6% dose/g tissue, in spite of transitional hyperglycemia. In contrast, insulin caused myocardial uptake to increase extraordinarily, although it caused a decrease in blood glucose levels.

  9. Effect of melatonin on myocardial oxidative stress induced by experimental obstructive jaundice Efecto de la melatonina en el estrés oxidativo del miocardio en un modelo experimental de obstrucción biliar

    Directory of Open Access Journals (Sweden)

    A. Cruz

    2009-07-01

    Full Text Available Objective: melatonin has been demonstrated to have active antioxidant properties in different tissues during experimental cholestasis. The aim of this research was to study myocardial oxidative stress on obstructive jaundice, and to analyze the effect of melatonin on myocardial oxidative lesions. Material and methods: we achieved cholestasis by ligature and sectioning of the main bile duct. Melatonin was administered intraperitoneally (500 µg/kg/day. We measured malondialdehyde (MDA, reduced glutathione (GSH, catalase (CAT, superoxide dismutase (SOD and glutathione peroxydase (GPx antioxidant enzyme levels in the heart tissue. Results: obstructive cholestasis increased MDA and decreased GSH as well as all antioxidant enzymes. Melatonin administration significantly decreased MDA values, and increased GSH and antioxidant enzymes on the icteric animal myocardium. Conclusions: melatonin treatment prevents oxidative stress in the cardiac tissue as induced by experimental cholestasis.

  10. Reperfusion therapy for acute myocardial infarction: Concepts and controversies from inception to acceptance.

    Science.gov (United States)

    Rentrop, Klaus Peter; Feit, Frederick

    2015-11-01

    More than 20 years of misconceptions derailed acceptance of reperfusion therapy for acute myocardial infarction (AMI). Cardiologists abandoned reperfusion for AMI using fibrinolytic therapy, explored in 1958, because they no longer attributed myocardial infarction to coronary thrombosis. Emergent aortocoronary bypass surgery, pioneered in 1968, remained controversial because of the misconception that hemorrhage into reperfused myocardium would result in infarct extension. Attempts to limit infarct size by pharmacotherapy without reperfusion dominated research in the 1970s. Myocardial necrosis was assumed to progress slowly, in a lateral direction. At least 18 hours was believed to be available for myocardial salvage. Afterload reduction and improvement of the microcirculation, but not reperfusion, were thought to provide the benefit of streptokinase therapy. Finally, coronary vasospasm was hypothesized to be the central mechanism in the pathogenesis of AMI. These misconceptions unraveled in the late 1970s. Myocardial necrosis was shown to progress in a transmural direction, as a "wave front," beginning with the subendocardium. Reperfusion within 6 hours salvaged a subepicardial ischemic zone in experimental animals. Acute angiography provided in vivo evidence of the high incidence of total coronary occlusion in the first hours of AMI. In 1978, early reperfusion by transluminal recanalization was shown to be feasible. The pathogenetic role of coronary thrombosis was definitively established in 1979 by demonstrating that intracoronary streptokinase rapidly restored flow in occluded infarct-related arteries, in contrast to intracoronary nitroglycerine which rarely did. The modern reperfusion era had dawned. Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.

  11. p53-dependent programmed necrosis controls germ cell homeostasis during spermatogenesis.

    Science.gov (United States)

    Napoletano, Francesco; Gibert, Benjamin; Yacobi-Sharon, Keren; Vincent, Stéphane; Favrot, Clémentine; Mehlen, Patrick; Girard, Victor; Teil, Margaux; Chatelain, Gilles; Walter, Ludivine; Arama, Eli; Mollereau, Bertrand

    2017-09-01

    The importance of regulated necrosis in pathologies such as cerebral stroke and myocardial infarction is now fully recognized. However, the physiological relevance of regulated necrosis remains unclear. Here, we report a conserved role for p53 in regulating necrosis in Drosophila and mammalian spermatogenesis. We found that Drosophila p53 is required for the programmed necrosis that occurs spontaneously in mitotic germ cells during spermatogenesis. This form of necrosis involved an atypical function of the initiator caspase Dronc/Caspase 9, independent of its catalytic activity. Prevention of p53-dependent necrosis resulted in testicular hyperplasia, which was reversed by restoring necrosis in spermatogonia. In mouse testes, p53 was required for heat-induced germ cell necrosis, indicating that regulation of necrosis is a primordial function of p53 conserved from invertebrates to vertebrates. Drosophila and mouse spermatogenesis will thus be useful models to identify inducers of necrosis to treat cancers that are refractory to apoptosis.

  12. Generation of small molecules to interfere with regulated necrosis.

    Science.gov (United States)

    Degterev, Alexei; Linkermann, Andreas

    2016-06-01

    Interference with regulated necrosis for clinical purposes carries broad therapeutic relevance and, if successfully achieved, has a potential to revolutionize everyday clinical routine. Necrosis was interpreted as something that no clinician might ever be able to prevent due to the unregulated nature of this form of cell death. However, given our growing understanding of the existence of regulated forms of necrosis and the roles of key enzymes of these pathways, e.g., kinases, peroxidases, etc., the possibility emerges to identify efficient and selective small molecule inhibitors of pathologic necrosis. Here, we review the published literature on small molecule inhibition of regulated necrosis and provide an outlook on how combination therapy may be most effective in treatment of necrosis-associated clinical situations like stroke, myocardial infarction, sepsis, cancer and solid organ transplantation.

  13. Non-invasive technology that improves cardiac function after experimental myocardial infarction: Whole Body Periodic Acceleration (pGz.

    Directory of Open Access Journals (Sweden)

    Arkady Uryash

    Full Text Available Myocardial infarction (MI may produce significant inflammatory changes and adverse ventricular remodeling leading to heart failure and premature death. Pharmacologic, stem cell transplantation, and exercise have not halted the inexorable rise in the prevalence and great economic costs of heart failure despite extensive investigations of such treatments. New therapeutic modalities are needed. Whole Body Periodic Acceleration (pGz is a non-invasive technology that increases pulsatile shear stress to the endothelium thereby producing several beneficial cardiovascular effects as demonstrated in animal models, normal humans and patients with heart disease. pGz upregulates endothelial derived nitric oxide synthase (eNOS and its phosphorylation (p-eNOS to improve myocardial function in models of myocardial stunning and preconditioning. Here we test whether pGz applied chronically after focal myocardial infarction in rats improves functional outcomes from MI. Focal MI was produced by left coronary artery ligation. One day after ligation animals were randomized to receive daily treatments of pGz for four weeks (MI-pGz or serve as controls (MI-CONT, with an additional group as non-infarction controls (Sham. Echocardiograms and invasive pressure volume loop analysis were carried out. Infarct transmurality, myocardial fibrosis, and markers of inflammatory and anti-inflammatory cytokines were determined along with protein analysis of eNOS, p-eNOS and inducible nitric oxide synthase (iNOS.At four weeks, survival was 80% in MI-pGz vs 50% in MI-CONT (p< 0.01. Ejection fraction and fractional shortening and invasive pressure volume relation indices of afterload and contractility were significantly better in MI-pGz. The latter where associated with decreased infarct transmurality and decreased fibrosis along with increased eNOS, p-eNOS. Additionally, MI-pGz had significantly lower levels of iNOS, inflammatory cytokines (IL-6, TNF-α, and higher level of anti

  14. Ressonância magnética vs cintilografia com pirofosfato marcado com tecnécio-99m para a detecção de necrose miocárdica perioperatória Magnetic resonance vs technetium-99m pyrophosphate scintigraphy in the detection of perioperative myocardial necrosis

    Directory of Open Access Journals (Sweden)

    Guilherme Urpia Monte

    2008-08-01

    used in the diagnosis of POMI; however it shows a limited sensitivity for subendocardial lesions. Cardiovascular magnetic resonance imaging (CMRI, in turn, has a high accuracy in the detection of myocardial necrosis. OBJECTIVE: To compare CMRI and MS for the detection of POMI after CABG. METHODS: A total of 24 patients with chronic coronary artery disease were studied using the delayed contrast enhanced CMRI and MS before and after CABG by analyzing the development of areas of perioperative myocardial necrosis (POMI. Biochemical markers of myocardial injury (CKMB and troponin I were also determined before and after surgery. RESULTS: Nineteen patients completed the study. Of these, 6 (32% presented POMI on CMRI and 4 (21% on MS (p = NS. Of the 323 left ventricular segments assessed, 17 (5.3% showed perioperative necrosis on CMRI and 7 (2.2% on MS (p = 0.013. Moderate agreement was observed between the methods (kappa = 0.46. There was disagreement regarding the diagnosis of POMI in 4 (21% cases, most of them with small areas of perioperative necrosis on CMRI which were not visualized on MS. In all cases with POMI on CMRI, significant CKMB and troponin I elevations were observed. CONCLUSION: Moderate diagnostic agreement was observed between the methods for the detection of POMI, but CMRI enabled visualization of small areas of perioperative myocardial necrosis which were not identified on MS and were associated with elevation of biochemical markers of myocardial injury.

  15. Mycobacterium avium subsp. paratuberculosis Infection Causes Suppression of RANTES, Monocyte Chemoattractant Protein 1, and Tumor Necrosis Factor Alpha Expression in Peripheral Blood of Experimentally Infected Cattle

    Science.gov (United States)

    Buza, Joram J.; Mori, Yasuyuki; Bari, Abusaleh M.; Hikono Aodon-geril, Hirokazu; Hirayama, Sachiyo; Shu, Yujing; Momotani, Eiichi

    2003-01-01

    Blood from cattle with subclinical Mycobacterium avium subsp. paratuberculosis infection was stimulated with M. avium subsp. paratuberculosis antigens, and expression of interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α), RANTES, monocyte chemoattractant protein 1 (MCP-1), and IL-8 was measured. Expression of TNF-α, RANTES, and MCP-1 was lower in infected than in uninfected cattle. The reduced response may weaken protective immunity and perpetuate infection. PMID:14638822

  16. Intervertebral disc cells produce tumor necrosis factor alpha, interleukin-1beta, and monocyte chemoattractant protein-1 immediately after herniation: an experimental study using a new hernia model.

    Science.gov (United States)

    Yoshida, Masakazu; Nakamura, Takafumi; Sei, Akira; Kikuchi, Taro; Takagi, Katsumasa; Matsukawa, Akihiro

    2005-01-01

    A new hernia model that simulates human disc herniations was developed in rabbits. The herniated discs were examined by gross appearance and histology and production of tumor necrosis factor alpha, interleukin-1beta, and monocyte chemoattractant protein-1 was investigated. To clarify the early mechanism of spontaneous herniated disc resorption. Macrophage infiltration in herniated discs is essential for disc resorption. However, surgically removed human herniated disc tissues and existing animal hernia models are not suitable for analyzing the mechanism of macrophage infiltration. Recently, we have demonstrated that intervertebral disc cells are capable of producing monocyte chemoattractant protein-1, a potent macrophage chemoattractant, after stimulation with tumor necrosis factor alpha and interleukin-1beta. Intervertebral disc herniations were surgically developed in rabbits using a new technique. The herniated discs were excised at appropriate time intervals after the surgery, and the size and histologic findings were examined. Expressions of tumor necrosis factor alpha, interleukin-1beta, and monocyte chemoattractant protein-1 in herniated discs were investigated immunohistochemically. A new rabbit model of disc herniation was established. The herniated discs spontaneously reduced in size by 12 weeks postsurgery. Infiltrating cells, mainly composed of macrophages, were observed from day 3. Immunohistochemically, intervertebral disc cells in the herniated discs produced tumor necrosis factor alpha and interleukin-1beta on day 1, followed by monocyte chemoattractant protein-1 on day 3. The new hernia model appears to be very useful for studying herniated disc resorption. Intervertebral disc cells may produce inflammatory cytokines/chemokine immediately after the onset of disc herniation, possibly triggering subsequent macrophage infiltration that leads to disc resorption.

  17. Protective and Therapeutic Effects of Chinese Medicine Formula Jiajian Yunvjian on Experimental Cardiac Remodeling after Myocardial Infarction Induced by Coronary Artery Ligation.

    Science.gov (United States)

    Du, Jun; Gu, Wei-Liang; Chen, Chang-Xun; Wang, Ying; Lv, Jian

    2015-01-01

    Introduction. This study was designed to explore the effect and mechanism of a classic Chinese medicine formula Jiajian Yunvjian (JJYNJ) on cardiac remodeling. Cardiac remodeling after myocardial infarction (MI) model was achieved by coronary artery ligation (CAL). Methodology. When dosed orally once daily, the effects of JJYNJ on hemodynamics, left ventricular weight index (LVWI), heart weight index (HWI), concentration, and gene expression of neuroendocrine factors as well as the histomorphological observation were determined. Results. After 4 weeks, mild cardiac remodeling in CAL group was characterized compared with sham group, but after 4 weeks of treatment of JJYNJ, hemodynamics improved, HWI reduced, and circulating angiotensin II (Ang II), endothelin-1 (ET-1), tumor necrosis factor-α (TNF-α), and hydroxyproline (Hyp) concentrations as well as Ang II receptor type 1 (AT1R) mRNA, transforming growth factor β 1 (TGF-β 1) mRNA, and TNF-α mRNA levels in myocardium were lower than in CAL group. Decreased plasma aldosterone (ALD) concentration, cross-sectional area of cardiomyocyte, collagen volume fraction (CVF), collagen types I and III, perivascular collagen area (PVCA), and upregulated nitric oxide (NO) levels were observed at the same time. Conclusions. These findings suggest that JJYNJ may have a protective and therapeutic function on cardiac remodeling related to MI.

  18. Experimental Study of the Effects of EIPA, Losartan, and BQ-123 on Electrophysiological Changes Induced by Myocardial Stretch.

    Science.gov (United States)

    Chorro, Francisco J; Canto, Irene Del; Brines, Laia; Such-Miquel, Luis; Calvo, Conrado; Soler, Carlos; Zarzoso, Manuel; Trapero, Isabel; Tormos, Álvaro; Such, Luis

    2015-12-01

    Mechanical response to myocardial stretch has been explained by various mechanisms, which include Na(+)/H(+) exchanger activation by autocrine-paracrine system activity. Drug-induced changes were analyzed to investigate the role of these mechanisms in the electrophysiological responses to acute myocardial stretch. Multiple epicardial electrodes and mapping techniques were used to analyze changes in ventricular fibrillation induced by acute myocardial stretch in isolated perfused rabbit hearts. Four series were studied: control (n = 9); during perfusion with the angiotensin receptor blocker losartan (1 μM, n = 8); during perfusion with the endothelin A receptor blocker BQ-123 (0.1 μM, n = 9), and during perfusion with the Na(+)/H(+) exchanger inhibitor EIPA (5-[N-ethyl-N-isopropyl]-amiloride) (1 μM, n = 9). EIPA attenuated the increase in the dominant frequency of stretch-induced fibrillation (control=40.4%; losartan=36% [not significant]; BQ-123=46% [not significant]; and EIPA=22% [P<.001]). During stretch, the activation maps were less complex (P<.0001) and the spectral concentration of the arrhythmia was greater (greater regularity) in the EIPA series: control=18 (3%); EIPA = 26 (9%) (P < .02); losartan=18 (5%) (not significant); and BQ-123=18 (4%) (not significant). The Na(+)/H(+) exchanger inhibitor EIPA attenuated the electrophysiological effects responsible for the acceleration and increased complexity of ventricular fibrillation induced by acute myocardial stretch. The angiotensin II receptor antagonist losartan and the endothelin A receptor blocker BQ-123 did not modify these effects. Copyright © 2014 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.

  19. Myocardial Ischemia

    Science.gov (United States)

    ... pectoris: Chest pain caused by myocardial ischemia. www.uptodate.com/home. Accessed June 1, 2015. Deedwania PC. Silent myocardial ischemia: Epidemiology and pathogenesis. www.uptodate.com/home. Accessed June 1, 2015. Mann DL, ...

  20. Increase in experimental infarct size with digoxin in a canine model of myocardial ischemia-reperfusion injury.

    Science.gov (United States)

    Lynch, J J; Simpson, P J; Gallagher, K P; McClanahan, T B; Lee, K A; Lucchesi, B R

    1988-06-01

    In the present study, dogs were pretreated with intravenous digoxin, 0.0125 mg/kg/day, for 6 to 7 consecutive days to achieve clinically relevant serum concentrations; untreated animals were used as control subjects. After pretreatment, nine digoxin-pretreated dogs and nine control dogs were anesthetized and subjected to a 60-minute occlusion of the left circumflex coronary artery, followed by 6 hours of reperfusion. Anatomic myocardial infarct size, expressed as a percentage of the areas at risk of infarction and as a percentage of the total left ventricle were: 20.2 +/- 3.3% control vs 35.4 +/- 6.2% digoxin-pretreated (p less than 0.05) and 8.6 +/- 1.3% control vs 14.7 +/- 2.5% digoxin-pretreated (p less than 0.05), respectively (2.04 +/- 0.37 ng/ml serum digoxin). Regional myocardial blood flow in the nonischemic and ischemic zones tended to be lower in digoxin-pretreated than in control animals at baseline testing and were significantly reduced in the anterior subendocardial sites of digoxin-pretreated dogs during ischemia and reperfusion. These data suggest that an exacerbation or enhancement of myocardial ischemia-reperfusion injury may occur in the presence of clinically observable serum digoxin concentrations.

  1. Neutrophils recruited to the myocardium after acute experimental myocardial infarct generate hypochlorous acid that oxidizes cardiac myoglobin.

    Science.gov (United States)

    Wang, Xiao Suo; Kim, Hyun Bo; Szuchman-Sapir, Andrea; McMahon, Aisling; Dennis, Joanne M; Witting, Paul K

    2016-12-15

    Myocardial inflammation following acute myocardial infarct (AMI) is associated with risk of congestive heart failure. Pro-inflammatory neutrophils were recruited to the damaged myocardium 24 h after permanent coronary ligation in rats to induce AMI as judged by the presence of immune-positive myeloperoxidase (MPO) in the tissues; MPO generates the oxidant hypochlorous acid (HOCl). Neutrophils were absent in hearts from Control (untreated) and surgical Sham. Similarly, rats exposed to 1 h coronary ligation (Ischemia) showed no neutrophil infiltrate. Concomitantly, MPO activity increased in left ventricular (LV) homogenates prepared from the AMI group and this was inhibited by paracetamol and the nitroxide TEMPO. The same LV-homogenates showed increased 3-chlorotyrosine/tyrosine ratios (biomarker for MPO-activity). Combined 2D gel/Western blot indicated cardiac myoglobin (Mb) was modified after AMI. Subsequent MALDI-TOF and LC-MS/MS analysis of isolated protein spots revealed increased Mb oxidation in hearts from the AMI group relative to Control, Sham and Ischemia groups. Peptide mass mapping revealed oxidation of Met9 and Met132 to the corresponding sulfoxides yet Cys67 remained unmodified. Therefore, neutrophil-generated HOCl can oxidize cardiac Mb after AMI and this may impact on its function within the affected myocardium: oxidized Mb maybe a useful marker of myocardial inflammation. Crown Copyright © 2016. Published by Elsevier Inc. All rights reserved.

  2. Cytokine production in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis: dynamics of mRNA expression for interleukin-10, interleukin-12, cytolysin, tumor necrosis factor alpha and tumor necrosis factor beta

    DEFF Research Database (Denmark)

    Issazadeh-Navikas, Shohreh; Ljungdahl, A; Höjeberg, B

    1995-01-01

    The kinetics of mRNA expression in the central nervous system (CNS) for a series of putatively disease-promoting and disease-limiting cytokines during the course of experimental autoimmune encephalomyelitis (EAE) in Lewis rats were studied. Cytokine mRNA-expressing cells were detected...... proliferation and activation of T helper 1 (Th1) type cells producing IFN-gamma. The TNF-beta mRNA expression prior to onset of clinical signs favours a role for this cytokine in disease initiation. A pathogenic effector role of TNF-alpha was suggested from these observations that TNF-alpha mRNA expression...... of putative disease-promoting and -limiting cytokines in the CNS during acute monophasic EAE....

  3. Myocardial scar imaging by standard single-energy and dual-energy late enhancement CT: Comparison with pathology and electroanatomic map in an experimental chronic infarct porcine model.

    Science.gov (United States)

    Truong, Quynh A; Thai, Wai-Ee; Wai, Bryan; Cordaro, Kevin; Cheng, Teresa; Beaudoin, Jonathan; Xiong, Guanglei; Cheung, Jim W; Altman, Robert; Min, James K; Singh, Jagmeet P; Barrett, Conor D; Danik, Stephan

    2015-01-01

    Myocardial scar is a substrate for ventricular tachycardia and sudden cardiac death. Late enhancement CT imaging can detect scar, but it remains unclear whether newer late enhancement dual-energy (LE-DECT) acquisition has benefit over standard single-energy late enhancement (LE-CT). We aim to compare late enhancement CT using newer LE-DECT acquisition and single-energy LE-CT acquisitions with pathology and electroanatomic map (EAM) in an experimental chronic myocardial infarction (MI) porcine study. In 8 pigs with chronic myocardial infarction (59 ± 5 kg), we performed dual-source CT, EAM, and pathology. For CT imaging, we performed 3 acquisitions at 10 minutes after contrast administration: LE-CT 80 kV, LE-CT 100 kV, and LE-DECT with 2 postprocessing software settings. Of the sequences, LE-CT 100 kV provided the best contrast-to-noise ratio (all P ≤ .03) and correlation to pathology for scar (ρ = 0.88). LE-DECT overestimated scar (both P = .02), whereas LE-CT images did not (both P = .08). On a segment basis (n = 136), all CT sequences had high specificity (87%-93%) and modest sensitivity (50%-67%), with LE-CT 100 kV having the highest specificity of 93% for scar detection compared to pathology and agreement with EAM (κ = 0.69). Standard single-energy LE-CT, particularly 100 kV, matched better to pathology and EAM than dual-energy LE-DECT for scar detection. Larger human trials as well as more technical studies that optimize varying different energies with newer hardware and software are warranted. Copyright © 2015 Society of Cardiovascular Computed Tomography. Published by Elsevier Inc. All rights reserved.

  4. Modelo experimental de infarto do miocárdio induzido por isoproterenol em ratos Experimental model of myocardial infarction induced by isoproterenol in rats

    Directory of Open Access Journals (Sweden)

    Heraldo Guedis Lobo Filho

    2011-09-01

    Full Text Available OBJETIVO: Avaliar e validar, em nosso meio, o modelo de infarto do miocárdio induzido por isoproterenol em ratos por meio de análises de parâmetros hematológicos, bioquímicos, de marcadores do estresse oxidativo e histopatológicos. MÉTODOS: Trinta ratos jovens, machos, da linhagem Wistar (145 a 230 g, foram alocados aleatoriamente em dois grupos: grupo Simulado, submetido à falsa indução de infarto do miocárdio, e grupo Infarto, submetido à indução do infarto do miocárdio com isoproterenol. As aplicações, para indução do infarto, foram realizadas durante dois dias consecutivos, com intervalo de 24 horas entre elas. Após 24 horas da última aplicação, os ratos de ambos os grupos foram anestesiados e sacrificados para realização de coleta de sangue para hemograma e análise bioquímica (TGO, TGP, troponina I, ureia e creatinina e coleta de fragmento do miocárdio para avaliação de marcadores do estresse oxidativo (atividade da catalase e concentração de glutationa e exame histopatológico. RESULTADOS: Não houve mortalidade no grupo Simulado, enquanto a mortalidade no grupo Infarto foi de 25%. A indução do infarto do miocárdio com isoproterenol causou elevação das contagens de leucócitos e neutrófilos, dos níveis de TGO, troponina I e ureia, reduziu a atividade da catalase e os níveis teciduais de glutationa e causou alterações histopatológicas. Não acarretou alterações nas concentrações de hemoglobina, TGP e creatinina. CONCLUSÕES: O modelo de infarto do miocárdio induzido por isoproterenol em ratos foi adequadamente reproduzido em nosso laboratório, acarretando alterações em parâmetros hematológicos, bioquímicos, de marcadores de estresse oxidativo e histopatológicos.OBJECTIVE: To evaluate and validate, in our laboratory, the essay of myocardial infarction induced by isoproterenol in rats by means of analysis of hematological, biochemical, oxidative stress markers and histopathological

  5. Evaluation of a metalloporphyrin (THPPMnCl) for necrosis-affinity in rat models of necrosis.

    Science.gov (United States)

    Li, Yue; Liu, Xuejiao; Zhang, Dongjian; Lou, Bin; Peng, Fei; Wang, Xiaoning; Shan, Xin; Jiang, Cuihua; Gao, Meng; Sun, Ziping; Ni, Yicheng; Huang, Dejian; Zhang, Jian

    2015-12-01

    The combination of an (13I)I-labeled necrosis-targeting agent (NTA) with a vascular disrupting agent is a novel and potentially powerful technique for tumor necrosis treatment (TNT). The purpose of this study was to evaluate a NTA candidate, THPPMnCl, using (131)I isotope for tracing its biodistribution and necrosis affinity. (131)I-THPPMnCl was intravenously injected in rat models with liver, muscle, and tumor necrosis and myocardial infarction (MI), followed by investigations with macroscopic autoradiography, triphenyltetrazolium chloride (TTC) histochemical staining, fluorescence microscopy and H&E stained histology for up to 9 days. (131)I-THPPMnCl displayed a long-term affinity for all types of necrosis and accumulation in the mononuclear phagocytic system especially in the liver. Autoradiograms and TTC staining showed a good targetability of (131)I-THPPMnCl for MI. These findings indicate the potential of THPPMnCl for non-invasive imaging assessment of necrosis, such as in MI. However, (13I)I-THPPMnCl is unlikely suitable for TNT due to its long-term retention in normal tissues.

  6. Scintigraphic findings in myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Schuemichen, C.; Krause, T.

    1988-09-01

    Radioisotope studies are currently used mainly to assess the individual risk before and after myocardial infarction (MI). Scintigraphy will be used increasingly to diagnose and localize acute myocardial infarction (AMI), to measure the infarct size and to detect reperfusion, whether spontaneous or after lysis, in the infarct area. High sensitivity and specificity are obtained by using tomographic imaging modalities and by the combined and simultaneous use of markers for perfusion and necrosis. This technique allows recognition even of nontransmural infarctions, involvement of the right ventricle, subendocardial necroses, and ischemic injuries in unstable angina pectoris.

  7. Effect of Cardiac Resynchronization Therapy on Myocardial Fibrosis and Relevant Cytokines in a Canine Model With Experimental Heart Failure.

    Science.gov (United States)

    Wang, Jingfeng; Gong, Xue; Chen, Haiyan; Qin, Shengmei; Zhou, Nianwei; Su, Yangang; Ge, Junbo

    2017-04-01

    Though cardiac resynchronization therapy (CRT) has now proved to be effective on cardiac reverse remodeling, data on the underlying molecular changes are limited. The present study aims to investigate the expression of cytokines concerning myocardial fibrosis in dyssynchronous heart failure (HF) and the potential benefits of CRT. Left bundle branch ablation and rapid pacing was performed to induce a canine model of asynchronous HF. Animals were randomly divided into sham group, HF control group, and CRT group. Echocardiographic data including septum-to-posterior wall motion delay (SPWMD) and standard deviation of the time to peak systolic velocity (Ts-SD) were collected. Histologic samples from lateral left ventricular (LV) and right ventricular (RV) free wall were analyzed and compared among different groups. Serum concentrations of NT-proBNP, TGF-β1 , and osteopontin (OPN) were measured using enzyme-linked immunosorbent assay (ELISA). Protein and mRNA expressions of TGF-β1 /Smad and OPN from myocardial tissues were also detected and compared. CRT improved cardiac function and corrected intraventricular dyssynchrony with increased LV ejection fraction (LVEF) and decreased SPWMD and Ts-SD (P < 0.05). Histological analysis showed that CRT restored cardiomyocyte diameter (from 4.50 to 6.08 μm) and collagen volume fraction (from 19.33% to 11.21%) of LV (P < 0.01), but had little effect on RV. Serum TGF-β1 and OPN level were also reversed toward normal level after CRT (P < 0.05). Compared with sham group, a significantly higher protein and mRNA expressions of TGF-β1 /Smad and OPN were observed in HF control group, which were significantly downregulated in CRT group (P < 0.01). By means of coordinating LV dyssynchrony, cellular and molecular reverse remodeling relevant to fibrosis inhibition could also be invoked by CRT. © 2017 Wiley Periodicals, Inc.

  8. Myocardial Bridging

    Directory of Open Access Journals (Sweden)

    Shi-Min Yuan

    2016-02-01

    Full Text Available Abstract Myocardial bridging is rare. Myocardial bridges are most commonly localized in the middle segment of the left anterior descending coronary artery. The anatomic features of the bridges vary significantly. Alterations of the endothelial morphology and the vasoactive agents impact on the progression of atherosclerosis of myocardial bridging. Patients may present with chest pain, myocardial infarction, arrhythmia and even sudden death. Patients who respond poorly to the medical treatment with β-blockers warrant a surgical intervention. Myotomy is a preferred surgical procedure for the symptomatic patients. Coronary stent deployment has been in limited use due to the unsatisfactory long-term results.

  9. Transauricular embolization of the rabbit coronary artery for experimental myocardial infarction: comparison of a minimally invasive closed-chest model with open-chest surgery

    Directory of Open Access Journals (Sweden)

    Katsanos Konstantinos

    2012-02-01

    Full Text Available Abstract Introduction To date, most animal studies of myocardial ischemia have used open-chest models with direct surgical coronary artery ligation. We aimed to develop a novel, percutaneous, minimally-invasive, closed-chest model of experimental myocardial infarction (EMI in the New Zealand White rabbit and compare it with the standard open-chest surgical model in order to minimize local and systemic side-effects of major surgery. Methods New Zealand White rabbits were handled in conformity with the "Guide for the Care and Use of Laboratory Animals" and underwent EMI under intravenous anesthesia. Group A underwent EMI with an open-chest method involving surgical tracheostomy, a mini median sternotomy incision and left anterior descending (LAD coronary artery ligation with a plain suture, whereas Group B underwent EMI with a closed-chest method involving fluoroscopy-guided percutaneous transauricular intra-arterial access, superselective LAD catheterization and distal coronary embolization with a micro-coil. Electrocardiography (ECG, cardiac enzymes and transcatheter left ventricular end-diastolic pressure (LVEDP measurements were recorded. Surviving animals were euthanized after 4 weeks and the hearts were harvested for Hematoxylin-eosin and Masson-trichrome staining. Results In total, 38 subjects underwent EMI with a surgical (n = 17 or endovascular (n = 21 approach. ST-segment elevation (1.90 ± 0.71 mm occurred sharply after surgical LAD ligation compared to progressive ST elevation (2.01 ± 0.84 mm;p = 0.68 within 15-20 min after LAD micro-coil embolization. Increase of troponin and other cardiac enzymes, abnormal ischemic Q waves and LVEDP changes were recorded in both groups without any significant differences (p > 0.05. Infarct area was similar in both models (0.86 ± 0.35 cm in the surgical group vs. 0.92 ± 0.54 cm in the percutaneous group;p = 0.68. Conclusion The proposed model of transauricular coronary coil embolization avoids

  10. Experimental evidence of metabolic disturbance in the white shrimp Penaeus vannamei induced by the Infectious Hypodermal and Hematopoietic Necrosis Virus (IHHNV).

    Science.gov (United States)

    Galván-Alvarez, Diego; Mendoza-Cano, Fernando; Hernández-López, Jorge; Sánchez-Paz, Arturo

    2012-09-15

    The Infectious Hypodermal and Hematopoietic Necrosis Virus (IHHNV) is a single-stranded DNA virus that infects several penaeid shrimp species, provoking economic losses in farmed shrimp populations estimated at several million of dollars. Furthermore, IHHNV has historically been considered an important threat for wild shrimp populations, but its real measurable impact remains unknown. Currently no treatments are available against IHHNV, and research to develop potential antiviral strategies depends on a detailed understanding of the viral life cycle. However, the exact pathophysiological events underlying the development of metabolic changes in IHHNV-infected shrimp are still unknown. Thus, the biochemical changes caused by the IHHNV infection in plasma and hepatopancreas of the economically important shrimp species Penaeus vannamei were evaluated. Glucose, lactate, total protein, glycogen, triacylglycerides, cholesterol, and total lipids were measured in healthy and IHHNV-infected shrimp. Significant changes were observed in energy substrates (glucose, lactate, triacylglycerides and cholesterol), in plasma and hepatopancreas. These changes may indicate a temporal sequestration of the host-cell metabolic pathways by the virus to maximize its replication and propagation. Copyright © 2012 Elsevier Inc. All rights reserved.

  11. Disruption of Tumor Necrosis Factor Receptor-Associated Factor 5 Exacerbates Murine Experimental Colitis via Regulating T Helper Cell-Mediated Inflammation.

    Science.gov (United States)

    Shang, Jian; Li, Lixia; Wang, Xiaobing; Pan, Huaqin; Liu, Shi; He, Ruohang; Li, Jin; Zhao, Qiu

    2016-01-01

    Tumor necrosis factor (TNF) receptor-associated factor 5 (TRAF5) is a key mediator of TNF receptor superfamily members and is important in both T helper (Th) cell immunity and the regulation of multiple signaling pathways. To clarify TRAF5's influence on inflammatory bowel diseases (IBDs), we investigated TRAF5 deficiency's effect on dextran sulfate sodium- (DSS-) induced colitis. Colitis was induced in TRAF5 knockout (KO) mice and their wild-type (WT) littermates by administering 3% DSS orally for 7 days. The mice were then sacrificed, and their colons were removed. Our data suggested that KO mice were more susceptible to DSS-induced colitis. TRAF5 deficiency significantly enhanced IFN-γ, IL-4, and IL-17a mRNA and protein levels in the colons of DSS-fed mice, and the mRNA expression of T-bet and GATA-3 was also markedly elevated. However, ROR-α and ROR-γt mRNA levels did not differ between DSS-induced KO and WT mice. Flow cytometry showed increased frequencies of Th2 and IFN-γ/IL-17a-coproducing CD4(+) T cells in the colons of DSS-induced KO mice. Additionally, TRAF5 deficiency significantly enhanced the activation of NF-κB in CD4(+) T cells after DSS administration. These results indicated that TRAF5 deficiency significantly aggravated DSS-induced colitis, most likely by regulating Th cell-mediated inflammation.

  12. A quantitative histopathological study of right bundle branch block complicating acute anteroseptal myocardial infarction.

    OpenAIRE

    Okabe, M; Fukuda, K; Nakashima, Y; Hiroki, T; Arakawa, K; Kikuchi, M

    1991-01-01

    The aim of the present study was to evaluate whether necrosis of the right bundle branch is responsible for development of right bundle branch block in acute myocardial infarction. Twenty patients with acute anteroseptal myocardial infarction were studied--10 with right bundle branch block (group A) and 10 without (group B)--to evaluate by serial sectioning the pathological extent of myocardial infarction surrounding the right bundle branch and also that of right bundle branch necrosis. Myoca...

  13. Aborted myocardial infarction: a new target for reperfusion therapy.

    NARCIS (Netherlands)

    Verheugt, F.W.A.; Gersh, B.J.; Armstrong, P.W.

    2006-01-01

    Reperfusion therapy for ST-elevation acute coronary syndromes aims at early and complete recanalization of the infarct-related artery in order to salvage myocardium and improve both early and late clinical outcomes. Myocardial necrosis is usually confirmed and quantified by myocardial enzyme release

  14. Protective effect of catalpol on isoproterenol-induced myocardial ...

    African Journals Online (AJOL)

    hope&shola

    2012-05-10

    May 10, 2012 ... This study was designed to explore whether catalpol protected myocardium against isoproterenol (ISO)-induced myocardial injury ... expressions of tumor necrosis factor-a (TNF-a) and interleukin-1β (IL-1β) caused by ISO. In conclusion, .... muscle fibres without any necrosis (Figure 1A). The morphology of ...

  15. Renal papillary necrosis

    Directory of Open Access Journals (Sweden)

    Stephen A. Geller

    2013-12-01

    Full Text Available In 1877, Dr. Nikolaus Friedreich (1825-1882; student of Virchow who became Professor of Pathology at Heidelberg and who also described Friedreich’s ataxia first described renal papillary necrosis (RPN in patients with prostatic hypertrophy and secondary hydronephrosis. Thereafter in 1937, Froboese and Günther emphasized the association of this entity with diabetes mellitus. These authors also observed renal papillary necrosis in cases of urinary tract obstruction even in the absence of diabetes mellitus.

  16. Myocardial Ischemia

    Science.gov (United States)

    ... occurs when blood flow to the heart muscle (myocardium) is obstructed by a partial or complete blockage of a coronary artery by a buildup of plaques (atherosclerosis). If the plaques rupture, you can have a heart attack (myocardial infarction). Myocardial ischemia occurs when blood flow ...

  17. Experimental study on inhibitory effect of niacinamide on tumor necrosis factor-alpha-induced matrix degradation of annulus fibrous tissue in vitro.

    Science.gov (United States)

    Xu, Runbing; Shao, Zengwu; Xiong, Liming

    2008-10-01

    The inhibitory effect of niacinamide on tumor necrosis factor-alpha (TNF-alpha) induced annulus fibrous (AF) degradation was assessed, and the mechanism of the inhibition was investigated. Chiba's intervertebral disc (IVD) culture model was established. Forty-eight IVDs from 12 adult Japanese white rabbits were randomly divided into 4 groups (12 IVDs in each group), and various concentrations of niacinamide and TNF-alpha were added to the medium for intervention: negative control group, niacinamide control group (0.5 mg/mL niacinamide), degeneration group (10 ng/mL TNF-alpha), and treatment group (0.5 mg/mL niacinamide and 10 ng/mL TNF-alpha). After one week's culture, AFs were collected for glycosaminoglycan (GS) content measurement, safranin O-fast green staining, and immunohistochemical staining for type I, II collagen and cysteine containing aspartate specific protease-3 (Caspase-3). It was found that the GS content in treatment group was increased by about 48% as compared with degeneration group (t=16.93, Pniacinamide control group (t=0.71, P=0.667). Safranine O-fast green staining exhibited higher staining density and better histological structure of AF in the treatment group as compared with the degeneration group. Immunohistochemical staining for both Type I and II collagen demonstrated that lamellar structure and continuity of collagen in treatment group were better reserved than in degeneration group. Positive staining rate of Caspase-3 in AFs of negative control group, niacinamide control group, degeneration group and treatment group was 3.4%, 4.3%, 17.9% and 10.3% respectively. The positive rate in treatment group was significantly lower than in degeneration group (Pniacinamide could effectively alleviate TNF-alpha induced destruction and synthesis inhibition of matrix ingredients in AFs. The inhibition may be related with reduction of expression of Caspase-3. Thus, niacinamide is of potential for IVD degeneration clinical treatment.

  18. Disruption of Tumor Necrosis Factor Receptor-Associated Factor 5 Exacerbates Murine Experimental Colitis via Regulating T Helper Cell-Mediated Inflammation

    Directory of Open Access Journals (Sweden)

    Jian Shang

    2016-01-01

    Full Text Available Tumor necrosis factor (TNF receptor-associated factor 5 (TRAF5 is a key mediator of TNF receptor superfamily members and is important in both T helper (Th cell immunity and the regulation of multiple signaling pathways. To clarify TRAF5’s influence on inflammatory bowel diseases (IBDs, we investigated TRAF5 deficiency’s effect on dextran sulfate sodium- (DSS- induced colitis. Colitis was induced in TRAF5 knockout (KO mice and their wild-type (WT littermates by administering 3% DSS orally for 7 days. The mice were then sacrificed, and their colons were removed. Our data suggested that KO mice were more susceptible to DSS-induced colitis. TRAF5 deficiency significantly enhanced IFN-γ, IL-4, and IL-17a mRNA and protein levels in the colons of DSS-fed mice, and the mRNA expression of T-bet and GATA-3 was also markedly elevated. However, ROR-α and ROR-γt mRNA levels did not differ between DSS-induced KO and WT mice. Flow cytometry showed increased frequencies of Th2 and IFN-γ/IL-17a-coproducing CD4+ T cells in the colons of DSS-induced KO mice. Additionally, TRAF5 deficiency significantly enhanced the activation of NF-κB in CD4+ T cells after DSS administration. These results indicated that TRAF5 deficiency significantly aggravated DSS-induced colitis, most likely by regulating Th cell-mediated inflammation.

  19. Inflammation as a therapeutic target in myocardial infarction: learning from past failures to meet future challenges

    Science.gov (United States)

    Saxena, Amit; Russo, Ilaria; Frangogiannis, Nikolaos G

    2015-01-01

    In the infarcted myocardium, necrotic cardiomyocytes release danger signals, activating an intense inflammatory response. Inflammatory pathways play a crucial role in regulation of a wide range of cellular processes involved in injury, repair and remodeling of the infarcted heart. Pro-inflammatory cytokines, such as tumor necrosis factor-a and interleukin (IL)-1, are markedly upregulated in the infarcted myocardium and promote adhesive interactions between endothelial cells and leukocytes, by stimulating chemokine and adhesion molecule expression. Distinct chemokine/chemokine receptor pairs are implicated in recruitment of various leukocyte subpopulations in the infarcted myocardium. Over the last 30 years, extensive experimental work has explored the role of inflammatory signals and the contributions of leukocyte subpopulations, in myocardial infarction. Robust evidence derived from experimental models of myocardial infarction has identified inflammatory targets that may attenuate cardiomyocyte injury, or protect from adverse remodeling. Unfortunately, attempts to translate the promising experimental findings to clinical therapy have failed. This review manuscript discusses the biology of the inflammatory response following myocardial infarction, attempts to identify the causes for the translational failures of the past, and proposes promising new therapeutic directions. Because of their potential involvement in injurious, reparative and regenerative responses, inflammatory cells may hold the key for design of new therapies in myocardial infarction. PMID:26241027

  20. Increased expression of dermatopontin mRNA in the infarct zone of experimentally induced myocardial infarction in rats: comparison with decorin and type I collagen mRNAs.

    Science.gov (United States)

    Takemoto, Syunji; Murakami, Takashi; Kusachi, Shozo; Iwabu, Akihiro; Hirohata, Satoshi; Nakamura, Keigo; Sezaki, Satoshi; Havashi, Junichi; Suezawa, Chisato; Ninomiya, Yoshifumi; Tsuji, Takao

    2002-11-01

    Dermatopontin, a 22 kDa extracellular matrix (ECM) protein, has been shown to interact with other ECM components, especially decorin, and to regulate ECM formation. We examined dermatopontin mRNA expression in the myocardial infarct zone. The cDNA encoding the rat dermatopontin was cloned by RT-PCR based on screening results from the Expressed Sequence Tag database. The dermatopontin mRNA expression was examined in the infarct zone after experimentally induced myocardial infarction in rats by the methods of Northern blotting and in situ hybridization. The expression of dermatopontin mRNA was compared to that of decorin and type I collagen mRNAs. The isolated clone contained a 609 bp cDNA insert containing a complete open reading frame encoding 202 amino acids. The rat dermatopontin cDNA showed high homology to human and mouse counterparts (>96 %). Northern blotting demonstrated that dermatopontin mRNA expression did not markedly increase on day 2, but was increased on days 7, 14 and 28 by 2.4-, 4.1- and 4.2-fold, respectively, compared to that in preligation hearts. Dermatopontin mRNA expression was regulated almost in parallel with decorin mRNA expression. In situ hybridization demonstrated mRNA signals for dermatopontin in macrophages and spindle-shaped mesenchymal cells (fibroblasts and myofibroblasts) located in the infarct interior zone around infarcted necrotic tissue on day 7. Coexpression of dermatopontin mRNA with decorin and type I collagen mRNAs was observed in spindle-shaped mesenchymal cells. The present results demonstrated the time-dependent increase in the expression of dermatopontin mRNA in parallel with that of decorin mRNA in the infarct zone. Coexpression of dermatopontin mRNA with decorin and type I collagen mRNAs suggests that dermatopontin plays a role in ECM (fibrillar collagen matrix) reformation in the infarct along with decorin and type I collagen.

  1. Assessment of the prophylactic role of aspirin and/or clopidogrel on experimentally induced acute myocardial infarction in hypercholesterolemic rats.

    Science.gov (United States)

    Mohamed, Adham R; El-Hadidy, Wessam F; Mannaa, Hazem F

    2014-12-01

    Hyperlipidemia is a risk factor for cardiovascular diseases such as acute infarction. Inflammation and platelet activation are critical phenomena in acute myocardial infarction (AMI). The aim of the study was to assess potential protective effects of aspirin and/or clopidogrel on AMI in hypercholesterolemic rats. Forty adult male Wistar rats were divided into five groups (eight rats in each). Group I included normal healthy rats. The other 32 rats were subjected to induction of hypercholesterolemia by high-fat diet for 3 weeks, followed by induction of AMI by subcutaneous injections of isoproterenol (85 mg/kg/day, for 2 days). Rats were divided into the following groups: group II, rats with induced hypercholesterolemia and AMI; group III, hypercholesterolemic rats that received aspirin 30 mg/kg/day orally for 7 days before induction of AMI; group IV, hypercholesterolemic rats that received clopidogrel 10 mg/kg/day orally for 7 days before induction of AMI; and group V, hypercholesterolemic rats treated with both aspirin and clopidogrel in the same doses for 7 days before induction of AMI. Serum levels of pentraxin 3 (PTX3), transforming growth factor-β1 (TGF-β1), creatine kinase (CK), lactate dehydrogenase (LDH), total cholesterol and triglycerides were estimated in all rats. Isoproterenol-induced AMI in hypercholesterolemic rats was associated with an increase in serum levels of PTX3, TGF-β1, CK and LDH. Aspirin and/or clopidogrel pretreatment for 1 week led to a reduction of their levels as compared with non-treated rats. However, the reduction caused by combination of aspirin and clopidogrel was more than that caused by each drug separately. Combination of aspirin and clopidogrel could be a therapeutic option for hypercholesterolemic patients to attenuate the complex vascular inflammatory process which is a key step in the setting of AMI.

  2. Remodelação miocárdica após infarto agudo do miocárdio experimental em ratos: efeito do bloqueio do sistema renina angiotensina aldosterona Myocardial remodeling after experimental acute myocardial infarction in rats: effect of renin-angiotensin-aldosterone system blockade

    Directory of Open Access Journals (Sweden)

    Hindalis Ballesteros Epifanio

    2005-01-01

    Full Text Available OBJETIVO: Verificar a ação do lisinopril e do losartan sobre a remodelação miocárdica no infarto experimental em ratos. MÉTODOS: Ratos machos Wistar foram submetidos a infarto e tratados com lisinopril 20 mg/kg/dia (LIS, n=13 ou losartan 20 mg/kg/dia (LOS, n=11, ou mantidos sem tratamento (NT, n=11, por três meses e os resultados comparados com grupo controle (CONT, n=11 de ratos sem infarto. Após a eutanásia, o ventrículo esquerdo foi separado e pesado. Foram medidas a área seccional dos miócitos (AC, fração de colágeno intersticial (CVF e a hidroxiprolina (HOP miocárdica. As variáveis foram comparadas pela ANOVA de uma via, para nível de significância de pOBJECTIVE: To assess the effect of lisinopril and losartan on myocardial remodeling in experimental infarction in rats. METHODS: Male Wistar rats underwent myocardial infarction and were either treated with lisinopril [20 mg/kg/day (LIS, n=13] or losartan [20 mg/kg/day (LOS, n=11], or kept without any treatment (NT, n=11 for 3 months. Their results were compared with those of a control group (CONT, n=11 comprising noninfarcted rats. After euthanasia, the left ventricle was isolated and weighed. The following measurements were taken: the sectional area of myocytes (AC, interstitial collagen fraction (CVF, and myocardial hydroxyproline (HOP. The variables were compared by using 1-way ANOVA, with a significance level of P<0.05. RESULTS: Acute myocardial infarction caused left ventricular hypertrophy. The treatments with lisinopril or losartan could prevent hypertrophy, which was quantified by use of left ventricular weight (LOS=1.06±0.12g, LIS=0.97±0.18g, NT=1.26±0.17g, CONT=1.02±0.09g; P<0.05, of left ventricular weight-to-body weight ratio LV/BW (LOS=2.37± 0.21mg/g, LIS=2.41±0.38mg/g, NT=2.82±0.37mg/g, CONT=2.27± 0.15mg/g, and of left ventricular AC measure-ment (LOS=210±39µ², LIS=217±35µ², NT=256±35µ², CONT=158±06 µ²; P<0.05. The CVF was significantly

  3. Genetic ablation of soluble tumor necrosis factor with preservation of membrane tumor necrosis factor is associated with neuroprotection after focal cerebral ischemia

    DEFF Research Database (Denmark)

    Madsen, Pernille M; Clausen, Bettina H; Degn, Matilda

    2016-01-01

    Microglia respond to focal cerebral ischemia by increasing their production of the neuromodulatory cytokine tumor necrosis factor, which exists both as membrane-anchored tumor necrosis factor and as cleaved soluble tumor necrosis factor forms. We previously demonstrated that tumor necrosis factor...... knockout mice display increased lesion volume after focal cerebral ischemia, suggesting that tumor necrosis factor is neuroprotective in experimental stroke. Here, we extend our studies to show that mice with intact membrane-anchored tumor necrosis factor, but no soluble tumor necrosis factor, display...... reduced infarct volumes at one and five days after stroke. This was associated with improved functional outcome after experimental stroke. No changes were found in the mRNA levels of tumor necrosis factor and tumor necrosis factor-related genes (TNFR1, TNFR2, TACE), pro-inflammatory cytokines (IL-1β, IL-6...

  4. Subcutaneous encapsulated fat necrosis

    DEFF Research Database (Denmark)

    Aydin, Dogu; Berg, Jais O

    2016-01-01

    We have described subcutaneous encapsulated fat necrosis, which is benign, usually asymptomatic and underreported. Images have only been published on two earlier occasions, in which the necrotic nodules appear "pearly" than the cloudy yellow surface in present case. The presented image may help...

  5. Peroxisome proliferator-activated receptors (PPAR) downregulate the expression of pro-inflammatory molecules in an experimental model of myocardial infarction.

    Science.gov (United States)

    Ibarra-Lara, María de la Luz; Sánchez-Aguilar, María; Soria, Elizabeth; Torres-Narváez, Juan Carlos; Del Valle-Mondragón, Leonardo; Cervantes-Pérez, Luz Graciela; Pérez-Severiano, Francisca; Ramírez-Ortega, Margarita Del Carmen; Pastelín-Hernández, Gustavo; Oidor-Chan, Víctor Hugo; Sánchez-Mendoza, Alicia

    2016-06-01

    Myocardial infarction (MI) has been associated with an inflammatory response and a rise in TNF-α, interleukin (IL)-1β, and IL-6. Peroxisome proliferator-activated receptors (PPARs) promote a decreased expression of inflammatory molecules. We aimed to study whether PPAR stimulation by clofibrate decreases inflammation and reduces infarct size in rats with MI. Male Wistar rats were randomized into 3 groups: control, MI + vehicle, and MI + clofibrate (100 mg/kg). Treatment was administered for 3 consecutive days, previous to 2 h of MI. MI induced an increase in protein expression, mRNA content, and enzymatic activity of inducible nitric oxide synthase (iNOS). Additionally, MI incited an increased expression of matrix metalloproteinase (MMP)-2 and MMP-9, intercellular adhesion molecule (ICAM)-1, and IL-6. MI also elevated the nuclear content of nuclear factor-κB (NF-κB) and decreased IκB, both in myocyte nuclei and cytosol. Clofibrate treatment prevented MI-induced changes in iNOS, MMP-2 and MMP-9, ICAM-1, IL-6, NF-κB, and IκB. Infarct size was smaller in clofibrate-treated rats compared to MI-vehicle animals. In silico analysis exhibited 3 motifs shared by genes from renin-angiotensin system, PPARα, iNOS, MMP-2 and MMP-9, ICAM-1, and VCAM-1, suggesting a cross regulation. In conclusion, PPARα-stimulation prevents overexpression of pro-inflammatory molecules and preserves viability in an experimental model of acute MI.

  6. Necrosis Avidity: A Newly Discovered Feature of Hypericin and its Preclinical Applications in Necrosis Imaging

    Science.gov (United States)

    Jiang, Binghu; Wang, Jichen; Ni, Yicheng; Chen, Feng

    2013-01-01

    Hypericin has been widely studied as a potent photosensitizer for photodynamic therapy in both preclinical and clinical settings. Recently, hypericin has also been discovered to have a specific avidity for necrotic tissue. This affinity is also observed in a series of radiolabeled derivatives of hypericin, including [123I]iodohypericin, [124I]iodohypericin, and [131I]iodohypericin. Hypericin, along with other necrosis-avid contrast agents, has been investigated for use in noninvasively targeting necrotic tissues in numerous disorders. Potential clinical applications of hypericin include the identification of acute myocardial infarction, evaluation of tissue viability, assessment of therapeutic responses to treatments, and interventional procedures for solid tumors. The mechanisms of necrosis avidity in hypericin remain to be fully elucidated, although several hypotheses have been suggested. In particular, it has been proposed that the necrosis avidity of hypericin is compound specific; for instance, cholesterol, phosphatidylserine, or phosphatidylethanolamine components in the phospholipid bilayer of cellular membranes may be the major targets for its observed selectivity. Further investigations are needed to identify the specific binding moiety that is responsible for the necrosis avidity of hypericin. PMID:24052807

  7. Scintigraphic myocardial imaging with sup(99m)Tc-labelled gluconate of experimentally produced cardiomyopathy in dogs

    Energy Technology Data Exchange (ETDEWEB)

    Duska, F.; Novak, J.; Mazurova, Y.; Kubicek, J.; Vizda, J.; Kafka, P.

    1983-02-01

    In 10 dogs experimental cardiomyopathy was produced using high intravenous doses of adrenaline and theophylline. The possibility of scintigraphic detection of this non-ischaemic damage was tested by means of sup(99m)Tc-gluconate. In 5 dogs the scintigraphic examination was carried out 4 hrs following the production of the damage. In all 5 cases a marked positivity of the heart scan was observed. The finding was confirmed by the radioactivity of tissue samples from all sections of the heart. In 3 out of 5 dogs the histological examination of the myocardium (PAS and HBFP staining) was positive. In the remaining 5 dogs the scan was performed 24 hrs following the development of the damage. A positive scintigraphic finding was observed in 4 cases, the degree of accumulation being lower than at 4 hrs. The radioactivities of tissue samples were also significantly lower as compared with the 4-hr values. In contrast, the histological findings were markedly positive in all 5 dogs. It follows that sup(99m)Tc-gluconate is capable of detecting in addition to infarctions non-ischaemic damages to the myocardium, too. The normalization of the finding is very quick. This experimental finding appears to be of importance in clinical practice.

  8. Linking surface-fire behavior, stem heating, and tissue necrosis

    Science.gov (United States)

    A.S. Bova; M.B. Dickinson; M.B. Dickinson

    2005-01-01

    Data from 69 experimental, small-plot fires are used to describe relationships among fire intensity, barksurface heat flux, and depth of necrosis in stem tissue for red maple (Acer rubrum L.) and chestnut oak (Quercus prinus L.j. A tetrazolium staining technique was used to determine the depth of necrosis in tree boles subjected to fires with intensities of 20 to 2000...

  9. Experimental blunt chest trauma-induced myocardial inflammation and alteration of gap-junction protein connexin 43.

    Directory of Open Access Journals (Sweden)

    Miriam Kalbitz

    Full Text Available Severe blunt chest trauma in humans is associated with high mortality rates. Whereas lung tissue damage and lung inflammation after blunt chest trauma have extensively been investigated, the traumatic and posttraumatic effects on the heart remain poorly understood. Therefore, the purpose of this study was to define cardiac injury patterns in an experimental blunt chest trauma model in rats.Experimental blunt chest trauma was induced by a blast wave in rats, with subsequent analysis of its effects on the heart. The animals were subjected either to a sham or trauma procedure. Systemic markers for cardiac injury were determined after 24 h and 5 days. Postmortem analysis of heart tissue addressed structural injury and inflammation 24 h and 5 days after trauma.Plasma levels of extracellular histones were elevated 24 h and 5 days after blunt chest trauma compared to sham-treated animals. In the heart, up-regulation of interleukin-1β 24 h after trauma and increased myeloperoxidase activity 24 h and 5 days after trauma were accompanied by reduced complement C5a receptor-1 expression 24 h after trauma. Histological analysis revealed extravasation of erythrocytes and immunohistochemical analysis alteration of the pattern of the gap-junction protein connexin 43. Furthermore, a slight reduction of α-actinin and desmin expression in cardiac tissue was found after trauma together with a minor increase in sarcoplasmatic/endoplasmatic reticlulum calcium-ATPase (SERCA expression.The clinically highly relevant rat model of blast wave-induced blunt chest trauma is associated with cardiac inflammation and structural alterations in cardiac tissue.

  10. Experimental blunt chest trauma-induced myocardial inflammation and alteration of gap-junction protein connexin 43.

    Science.gov (United States)

    Kalbitz, Miriam; Amann, Elisa Maria; Bosch, Belinda; Palmer, Annette; Schultze, Anke; Pressmar, Jochen; Weber, Birte; Wepler, Martin; Gebhard, Florian; Schrezenmeier, Hubert; Brenner, Rolf; Huber-Lang, Markus

    2017-01-01

    Severe blunt chest trauma in humans is associated with high mortality rates. Whereas lung tissue damage and lung inflammation after blunt chest trauma have extensively been investigated, the traumatic and posttraumatic effects on the heart remain poorly understood. Therefore, the purpose of this study was to define cardiac injury patterns in an experimental blunt chest trauma model in rats. Experimental blunt chest trauma was induced by a blast wave in rats, with subsequent analysis of its effects on the heart. The animals were subjected either to a sham or trauma procedure. Systemic markers for cardiac injury were determined after 24 h and 5 days. Postmortem analysis of heart tissue addressed structural injury and inflammation 24 h and 5 days after trauma. Plasma levels of extracellular histones were elevated 24 h and 5 days after blunt chest trauma compared to sham-treated animals. In the heart, up-regulation of interleukin-1β 24 h after trauma and increased myeloperoxidase activity 24 h and 5 days after trauma were accompanied by reduced complement C5a receptor-1 expression 24 h after trauma. Histological analysis revealed extravasation of erythrocytes and immunohistochemical analysis alteration of the pattern of the gap-junction protein connexin 43. Furthermore, a slight reduction of α-actinin and desmin expression in cardiac tissue was found after trauma together with a minor increase in sarcoplasmatic/endoplasmatic reticlulum calcium-ATPase (SERCA) expression. The clinically highly relevant rat model of blast wave-induced blunt chest trauma is associated with cardiac inflammation and structural alterations in cardiac tissue.

  11. Secondary prevention with calcium antagonists after acute myocardial infarction

    DEFF Research Database (Denmark)

    Hansen, J F

    1992-01-01

    Experimental studies have demonstrated that the 3 calcium antagonists nifedipine, diltiazem, and verapamil have a comparable effect in the prevention of myocardial damage during ischaemia. Secondary prevention trials after acute myocardial infarction, which aimed at improving survival...

  12. Elastic image registration to quantify 3-D regional myocardial deformation from volumetric ultrasound: experimental validation in an animal model.

    Science.gov (United States)

    Heyde, Brecht; Bouchez, Stefaan; Thieren, Sabine; Vandenheuvel, Michael; Jasaityte, Ruta; Barbosa, Daniel; Claus, Piet; Maes, Frederik; Wouters, Patrick; D'Hooge, Jan

    2013-09-01

    Although real-time 3-D echocardiography has the potential to allow more accurate assessment of global and regional ventricular dynamics compared with more traditional 2-D ultrasound examinations, it still requires rigorous testing and validation should it break through as a standard examination in routine clinical practice. However, only a limited number of studies have validated 3-D strain algorithms in an in vivo experimental setting. The aim of the present study, therefore, was to validate a registration-based strain estimation methodology in an animal model. Volumetric images were acquired in 14 open-chest sheep instrumented with ultrasonic microcrystals. Radial strain (ɛRR), longitudinal strain (ɛLL) and circumferential strain (ɛCC) were estimated during different stages: at rest, during reduced and increased cardiac inotropy induced by esmolol and dobutamine infusion, respectively, and during acute ischemia. Agreement between image-based and microcrystal-based strain estimates was evaluated by their linear correlation, indicating that all strain components could be estimated with acceptable accuracy (r = 0.69 for ɛRR, r = 0.64 for ɛLL and r = 0.62 for ɛCC). These findings are comparable to the performance of the current state-of-the-art commercial 3-D speckle tracking methods. Furthermore, shape of the strain curves, timing of peak values and location of dysfunctional regions were identified well. Whether 3-D elastic registration performs better than 3-D block matching-based methodologies still remains to be proven. Copyright © 2013 World Federation for Ultrasound in Medicine & Biology. Published by Elsevier Inc. All rights reserved.

  13. Novel adjunctive treatments of myocardial infarction

    DEFF Research Database (Denmark)

    Schmidt, Michael Rahbek; Pryds, Kasper; Bøtker, Hans Erik

    2014-01-01

    Myocardial infarction is a major cause of death and disability worldwide and myocardial infarct size is a major determinant of prognosis. Early and successful restoration of myocardial reperfusion following an ischemic event is the most effective strategy to reduce final infarct size and improve...... by endovascular infusion of cold saline all reduce infarct size and may confer clinical benefit for patients admitted with acute myocardial infarcts. Equally promising, three follow-up studies of the effect of remote ischemic conditioning (RIC) show clinical prognostic benefit in patients undergoing coronary...... clinical outcome, but reperfusion may induce further myocardial damage itself. Development of adjunctive therapies to limit myocardial reperfusion injury beyond opening of the coronary artery gains increasing attention. A vast number of experimental studies have shown cardioprotective effects of ischemic...

  14. Focal necrosis mimicking breast cancer following coronary bypass grafting.

    Science.gov (United States)

    Coufal, Oldřich; Ostřížek, Tomáš; Krsička, Petr; Lžičařová, Eva; Nenutil, Rudolf; Procházková, Monika; Bencsiková, Beatrix; Grell, Peter; Šefr, Roman

    2017-05-30

    Breast cancer can be diagnosed easily in most cases. However, occasionally, we are faced with some conditions that can mimic it. These may include inflammations, benign tumors, cysts, hematomas, or, more rarely, focal necrosis. This report presents a case of focal breast necrosis following myocardial revascularization with the left internal mammary artery, which is a very rare condition, with only few cases described in the literature. The necrosis becomes usually apparent a few days or weeks after the surgery and is often coincidental with the dehiscence of sternotomy with necrosis of wound edges. As it mostly affects the skin, it can be easily recognized. Also, our patient developed a dehisced sternotomy shortly after the surgery but there were no obvious objective changes on the breast. The condition was first dominated only by non-specific subjective symptom-pain. Later, a lump in the breast occurred, when the sternotomy had already healed. Moreover, an enlarged lymph node was palpable in the axilla. Because of non-typical symptoms, the condition was suggestive of breast cancer for a relatively long time. The patient had suffered from a very strong pain until she was treated by mastectomy with a good clinical result. Mammary necrosis following the coronary artery bypass is rare. In most cases, it manifests on the skin shortly after the surgery concurrently with dehisced sternotomy, so it can be easily diagnosed. However, in sporadic cases, the symptoms may occur later and may mimic breast cancer. Our objective is to raise awareness of this rare condition.

  15. IL-6 signalling in patients with acute ST-elevation myocardial infarction

    Directory of Open Access Journals (Sweden)

    Vibeke N. Ritschel

    2014-01-01

    In conclusion, circulating levels of IL-6 and CRP, but not the soluble forms of the receptor (sIL-6R or the receptor signalling subunit (sgp130 were associated with the extent of myocardial necrosis. The biological importance of the IL-6/gp130-mediated signalling pathways in patients with acute myocardial infarction and dysglycemia should be further elucidated.

  16. Comparison of the temporal release pattern of copeptin with conventional biomarkers in acute myocardial infarction

    NARCIS (Netherlands)

    Gu, Youlan L.; Voors, Adriaan A.; Zijlstra, Felix; Hillege, Hans L.; Struck, Joachim; Masson, Serge; Vago, Tarcisio; Anker, Stefan D.; van den Heuvel, Ad F. M.; van Veldhuisen, Dirk J.; de Smet, Bart J. G. L.

    2011-01-01

    Background Early detection of acute myocardial infarction (AMI) using cardiac biomarkers of myocardial necrosis remains limited since these biomarkers do not rise within the first hours from onset of AMI. We aimed to compare the temporal release pattern of the C-terminal portion of provasopressin

  17. Comparison of the temporal release pattern of copeptin with conventional biomarkers in acute myocardial infarction

    NARCIS (Netherlands)

    Y.L. Gu (Youlan); A.A. Voors (Adriaan); F. Zijlstra (Felix); H.L. Hillege (Hans); J. Struck (Joachim); S. Masson (Serge); T. Vago (Tarcisio); S.D. Anker (Stefan); A.F.M. van den Heuvel (Ad); D.J. van Veldhuisen (Dirk); B.J.G.L. de Smet (Bart)

    2011-01-01

    textabstractBackground Early detection of acute myocardial infarction (AMI) using cardiac biomarkers of myocardial necrosis remains limited since these biomarkers do not rise within the first hours from onset of AMI. We aimed to compare the temporal release pattern of the C-terminal portion of

  18. Value of serum tenascin-C in patients with acute myocardial infarction

    African Journals Online (AJOL)

    Rania Gaber

    2015-10-09

    Oct 9, 2015 ... Abstract Background: Myocardial infarction (MI) is defined as myocardial cell necrosis due to significant and sustained ischemia. TN-C is an extracellular matrix glycoprotein that is expressed in several important steps during the very early stage of cardiogenesis. TN-C is not normally expressed in the adult ...

  19. Value of serum tenascin-C in patients with acute myocardial infarction

    African Journals Online (AJOL)

    Background: Myocardial infarction (MI) is defined as myocardial cell necrosis due to significant and sustained ischemia. TN-C is an extracellular matrix glycoprotein that is expressed in several important steps during the very early stage of cardiogenesis. TN-C is not normally expressed in the adult heart, but transiently ...

  20. Myocardial infarct expansion, infarct extension, and reinfarction: pathophysiologic concepts.

    Science.gov (United States)

    Weisman, H F; Healy, B

    1987-01-01

    Infarct expansion and infarct extension are events early in the course of myocardial infarction with serious short- and long-term consequences. Infarct expansion, disproportionate thinning, and dilatation of the infarct segment probably begin within hours of acute infarction and usually reach peak extent within seven to 14 days. Clinical data suggest that infarct expansion occurs in approximately 35% to 45% of anterior transmural myocardial infarctions and to a lesser extent in infarctions at other sites. Although expansion usually develops in large infarcts, the extent of transmural necrosis rather than absolute infarct size predicts its occurrence. Expansion has an adverse effect on infarct structure and function for several reasons. Functional infarct size is increased because of infarct segment lengthening, and expansion results in over-all ventricular dilatation. Thus, patients with expansion of an infarct have poorer exercise tolerance, more congestive heart failure symptoms, and greater early and late mortality than those without expansion. Infarct rupture and late aneurysm formation are two additional structural consequences of infarct expansion. Experimental and clinical data suggest that the incidence and severity of expansion can be modified by interventions. Increased ventricular loading conditions and steroidal and nonsteroidal antiinflammatory agents make expansion more severe. Reperfusion of the infarct segment and pharmacologic interventions that decrease ventricular afterload lessen the severity of expansion. Previous myocardial infarction and preexisting ventricular hypertrophy may also limit the development of infarct expansion. Infarct extension is defined clinically as early in-hospital reinfarction after a myocardial infarction. The pathologic finding of infarct extension is necrotic and healing myocardium of several different recent ages within the same vascular territory. Although this pathologic criterion usually cannot be verified, studies

  1. Type 2 myocardial infarction due to supply-demand mismatch.

    Science.gov (United States)

    Mihatov, Nino; Januzzi, James L; Gaggin, Hanna K

    2017-08-01

    The best-accepted definition of myocardial infarction (MI) is provided by statements from the Universal Definition of MI Global Task force. This article, now in its third iteration, defines MI as myocardial cell death due to prolonged myocardial ischemia. It further delineates an increasingly incident subclassification of MI known as type 2 MI (T2MI). T2MI identifies instances of myocardial necrosis in which an imbalance between myocardial oxygen supply and/or demand occurs for reasons other than atherosclerotic plaque disruption. While associated with considerable risk (comparable to that of type 1 MI, which has well-defined management strategies), the spectrum of potential etiologies for T2MI makes development of precise diagnostic criteria and therapeutic implications of the diagnosis challenging. Copyright © 2017 Elsevier Inc. All rights reserved.

  2. Treatment with oestrogen-receptor agonists or oxytocin in conjunction with exercise protects against myocardial infarction in ovariectomized rats.

    Science.gov (United States)

    Bulut, Erman Caner; Abueid, Leyla; Ercan, Feriha; Süleymanoğlu, Selami; Ağırbaşlı, Mehmet; Yeğen, Berrak Ç

    2016-05-01

    What is the central question of this study? Could the activation of oxytocin or oestrogen receptors be protective against myocardial injury after ovariectomy? If so, would exercising have an additional ameliorating effect? What is the main finding and its importance? The results revealed that when accompanied by exercise, both oestrogen receptor agonists and oxytocin improved cardiac dysfunction, inhibited the generation of pro-inflammatory cytokines and reduced myocardial injury in ovariectomized female rats, suggesting a new approach for protecting postmenopausal women against ischaemia-induced myocardial injury. To investigate the putative protective effects of oxytocin or oestrogen receptor agonists against myocardial injury of ovariectomized sedentary or exercised rats, female Sprague-Dawley rats assigned to sham-operated control and ovariectomized (OVX) groups were kept sedentary or undertook swimming exercise for 4 weeks and were treated with saline, an oestrogen receptor (ER) β (DPN) or ERα agonist (PPT) or oxytocin. Ovariectomy increased weight gain and anxiety in sedentary rats, whereas exercise prevented weight gain. When accompanied by exercise, both ER agonists and oxytocin inhibited weight gain and anxiety; oxytocin, in the absence or presence of exercise, increased the left ventricular diastolic dimensions and ejection fraction, whereas ER agonists also increased left ventricular diameter when given to exercised rats. Upon the induction of myocardial ischaemia-reperfusion in the OVX rats, plasma creatine kinase-(muscle-brain) was depressed by PPT and oxytocin, whereas DPN, PPT and OT reduced plasminogen activator inhibitor-1 concentrations. The increased tumour necrosis factor-α concentration in OVX rats was also suppressed by exercise or DPN, PPT or oxytocin treatments, whereas the interleukin-6 concentration was diminished by all the treatments when given in conjunction with exercise. Disorganization of cardiac muscle fibres was reduced in all

  3. Blood PGC-1α Concentration Predicts Myocardial Salvage and Ventricular Remodeling After ST-segment Elevation Acute Myocardial Infarction.

    Science.gov (United States)

    Fabregat-Andrés, Óscar; Ridocci-Soriano, Francisco; Estornell-Erill, Jordi; Corbí-Pascual, Miguel; Valle-Muñoz, Alfonso; Berenguer-Jofresa, Alberto; Barrabés, José A; Mata, Manuel; Monsalve, María

    2015-05-01

    Peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) is a metabolic regulator induced during ischemia that prevents cardiac remodeling in animal models. The activity of PGC-1α can be estimated in patients with ST-segment elevation acute myocardial infarction. The aim of the present study was to evaluate the value of blood PGC-1α levels in predicting the extent of necrosis and ventricular remodeling after infarction. In this prospective study of 31 patients with a first myocardial infarction in an anterior location and successful reperfusion, PGC-1α expression in peripheral blood on admission and at 72 hours was correlated with myocardial injury, ventricular volume, and systolic function at 6 months. Edema and myocardial necrosis were estimated using cardiac magnetic resonance imaging during the first week. At 6 months, infarct size and ventricular remodeling, defined as an increase > 10% of the left ventricular end-diastolic volume, was evaluated by follow-up magnetic resonance imaging. Myocardial salvage was defined as the difference between the edema and necrosis areas. Greater myocardial salvage was seen in patients with detectable PGC-1α levels at admission (mean [standard deviation (SD)], 18.3% [5.3%] vs 4.5% [3.9%]; P = .04). Induction of PGC-1α at 72 hours correlated with greater ventricular remodeling (change in left ventricular end-diastolic volume at 6 months, 29.7% [11.2%] vs 1.2% [5.8%]; P = .04). Baseline PGC-1α expression and an attenuated systemic response after acute myocardial infarction are associated with greater myocardial salvage and predict less ventricular remodeling. Copyright © 2014 Sociedad Española de Cardiología. Published by Elsevier España, S.L.U. All rights reserved.

  4. Sensitivity of {sup 99m}Tc-pyrophosphate scintigraphy in diagnosis of acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Seong Hee; Park, Tai Que; Chae, Yoo Soon; Kim, Yang Sook [Maryknoll Hospital, Busan (Korea, Republic of)

    1991-01-15

    To assess the difference of the diagnostic sensitivity of {sup 99m}Tc-Pyrophosphate (PYP) myocardial scintigraphy in acute transmural infarction and acute subendocardial infarction, we analyzed 38 patients with a confirmed transmural infarct, 10 with a subendocardial infarct, 2 with old myocardial infarct, and 10 with other cardiovascular disease (2 unstable angina, 6 stable angina, 1 Prinzmetal angina, and 1 atrial fibrillation) according to Berman's criteria for scintigraphic assessment and then come to conclusion; When only focal myocardial uptake wa used as a criteria for positivity, the diagnostic sensitivity of {sup 99m}Tc-PYP scintigraphy in acute subendocardial myocardial infarction was only 40% (4/10) compared with 86.8% (33/38) of acute transmural myocardial infarction. There was no case that was interpreted as focal myocardial uptake in 2 old myocardial infarction and 10 other cardiovascular disease. The incidence of complication was higher in doughnut pattern of myocardial uptake 50% (3/6) than in non-doughnut focal patterns 19.4% (6/31). It is concluded that focal myocardial uptake is a sensitive indicator suggesting acute myocardial necrosis and that {sup 99m}Tc-PYP myocardial scintigraphy is a sensitive technique for diagnosing acute transmural myocardial infarction, but a insensitive method in acute subendocardial infarction, and that the doughnut pattern of myocardial uptake an provide clues to the patient's future course.

  5. Assessment and classification of patients with myocardial injury and infarction in clinical practice

    Science.gov (United States)

    Chapman, Andrew R; Adamson, Philip D

    2017-01-01

    Myocardial injury is common in patients without acute coronary syndrome, and international guidelines recommend patients with myocardial infarction are classified by aetiology. The universal definition differentiates patients with myocardial infarction due to plaque rupture (type 1) from those due to myocardial oxygen supply-demand imbalance (type 2) secondary to other acute illnesses. Patients with myocardial necrosis, but no symptoms or signs of myocardial ischaemia, are classified as acute or chronic myocardial injury. This classification has not been widely adopted in practice, because the diagnostic criteria for type 2 myocardial infarction encompass a wide range of presentations, and the implications of the diagnosis are uncertain. However, both myocardial injury and type 2 myocardial infarction are common, occurring in more than one-third of all hospitalised patients. These patients have poor short-term and long-term outcomes with two-thirds dead in 5 years. The classification of patients with myocardial infarction continues to evolve, and future guidelines are likely to recognise the importance of identifying coronary artery disease in type 2 myocardial infarction. Clinicians should consider whether coronary artery disease has contributed to myocardial injury, as selected patients are likely to benefit from further investigation and in these patients targeted secondary prevention has the potential to improve outcomes. PMID:27806987

  6. Correlation of myocardial p-(123)I-iodophenylpentadecanoic acid retention with (18)F-FDG accumulation during experimental low-flow ischemia.

    Science.gov (United States)

    Shi, Cindy Q; Young, Lawrence H; Daher, Edouard; DiBella, Edward V R; Liu, Yi-Hwa; Heller, Eliot N; Zoghbi, Sami; Wackers, Frans J Th; Soufer, Robert; Sinusas, Albert J

    2002-03-01

    Myocardial ischemia is associated with reduced free fatty acid (FFA) beta-oxidation and increased glucose utilization. This study evaluated the potential of dynamic SPECT imaging of a FFA analog, p-(123)I-iodophenylpentadecanoic acid (IPPA), for detection of ischemia and compares retention of IPPA with (18)F-FDG accumulation. In a canine model of regional low-flow ischemia (n = 9), serial IPPA SPECT images (2 min per image) were acquired over 52--90 min. In a subset of dogs (n = 6), (18)F-FDG was injected after completing SPECT imaging and allowed to accumulate for 40 min before killing the animals. Flow was assessed with radiolabeled microspheres. Myocardial metabolism was evaluated independently by selective coronary arterial and venous sampling. Serial IPPA SPECT images showed an initial defect in the ischemic region (0.70% plus minus 0.03% ischemic-to-nonischemic ratio), which normalized within 48 min because of the slower IPPA clearance from the ischemic region (t(1/2) = 54.2 plus minus 3.3 min) relative to the nonischemic region (t(1/2) = 36.7 plus minus 5.6 min) (P IPPA and (18)F-FDG activities were correlated (r = 0.70; n = 576 segments), and both were maximally increased in segments with a moderate flow reduction (IPPA, 151% of nonischemic; (18)F-FDG, 450% of nonischemic; P IPPA in ischemic regions with moderate flow reduction, which lead to increased late myocardial retention of IPPA. Retention of IPPA correlated with (18)F-FDG accumulation, supporting the potential of IPPA as a noninvasive marker of ischemic myocardium.

  7. Early imaging of experimental myocardial infarction by intracoronary administration of /sup 131/I-labelled anticardiac myosin (Fab')/sub 2/ fragments. [Dogs

    Energy Technology Data Exchange (ETDEWEB)

    Khaw, B.A.; Gold, H.K.; Leinbach, R.C.; Fallon, J.T.; Strauss, W.; Pohost, G.M.; Haber, E.

    1978-12-01

    The feasibility of early imaging of myocardial infarcts by intracoronary injection of /sup 131/I-labelled cardiac myosin-specific antibody (Fab')/sub 2/ was examined. The left anterior descending coronary artery was occluded for 5 hs by a balloon catheter introduced through the carotid artery in 12 dogs. The catheter was withdrawn and 1 mCi /sup 201/Tl was injected intravenously and 500 ..mu..Ci of /sup 131/I antibody were injected into the main left coronary artery. Six of these animals demonstrated evidence of myocardial infarction by ECG and subsequent triphenyl-tetrazolium chloride staining, while the others did not. In each of the infarcted animals, in vivo scintograms one-half h after injection of isotope showed uptake of /sup 131/I in the anteroapical region of the heart corresponding to the region of absent /sup 201/Tl uptake. This relationship was confirmed in the excized hearts and in heart slices. In slices, /sup 131/I uptake corresponded to regions that did not stain with triphenyltetrazolium chloride. In the six animals that did not show evidence for infarction after coronary occlusion, uptake of /sup 131/I was not demonstrated, either in vivo or in excized specimens. In four additional dogs subjected to the same procedure, /sup 125/I-labelled (Fab')/sub 2/ from nonimmune IgG was injected simultaneously into the left main coronary artery with /sup 131/I-labelled canine myosin-specific antibody (Fab')/sub 2/. The ratio of uptake between infarct center and normal tissue was 34.3 +- 1.5 (mean +- SEM) for the specific antibody fragment as contrasted to 6.6 +- 0.4 for the nonimmune IgG fragment, indicating that intracoronary injection does not favor nonspecific sequestration of protein in regions of infarction. Thus the intracoronary administration of myosin-specific antibody fragments leads to early and specific one-half h imaging of myocardial infarcts.

  8. Endothelial necrosis at 1h post-burn predicts progression of tissue injury

    Science.gov (United States)

    Hirth, Douglas; McClain, Steve A.; Singer, Adam J.; Clark, Richard A.F.

    2013-01-01

    Burn injury progression has not been well characterized at the cellular level. To define burn injury progression in terms of cell death, histopathologic spatiotemporal relationships of cellular necrosis and apoptosis were investigated in a validated porcine model of vertical burn injury progression. Cell necrosis was identified by High Mobility Group Box 1 protein and apoptosis by Caspase 3a staining of tissue samples taken 1h, 24h and 7 days post-burn. Level of endothelial cell necrosis at 1h was predictive of level of apoptosis at 24h (Pearson's r=0.87) and of level of tissue necrosis at 7 days (Pearson's r=0.87). Furthermore, endothelial cell necrosis was deeper than interstitial cell necrosis at 1h (pnecrosis at 1h divided the zone of injury progression (Jackson's zone of stasis) into an upper subzone with necrotic endothelial cells and initially viable adnexal and interstitial cells at 1h that progressed to necrosis by 24h, and a lower zone with initially viable endothelial cells at 1h, but necrosis and apoptosis of all cell types by 24h. Importantly, this spatiotemporal series of events and rapid progression resembles myocardial infarction and stroke, and implicates mechanisms of these injuries, ischemia, ischemia reperfusion, and programmed cell death, in burn progression. PMID:23627744

  9. Metformin in non-Diabetic Patients Presenting with ST Elevation Myocardial Infarction : Rationale and Design of the Glycometabolic Intervention as Adjunct to Primary Percutaneous Intervention in ST Elevation Myocardial Infarction (GIPS)-III Trial

    NARCIS (Netherlands)

    Lexis, Chris P. H.; van der Horst, Iwan C. C.; Lipsic, Erik; van der Harst, Pim; Horst-Schrivers, van der Anouk N. A.; Wolffenbuttel, Bruce H. R.; de Boer, Rudolf A.; van Rossum, Albert C.; van Veldhuisen, Dirk J.; de Smet, Bart J. G. L.

    2012-01-01

    Left ventricular dysfunction and the development of heart failure is a frequent and serious complication of myocardial infarction. Recent animal experimental studies suggested that metformin treatment reduces myocardial injury and preserves cardiac function in non-diabetic rats after experimental

  10. The stability of myocardial area at risk estimated electrocardiographically in patients with ST elevation myocardial infarction

    DEFF Research Database (Denmark)

    Carlsen, Esben A; Hassell, Mariëlla E C J; van Hellemond, Irene E G

    2014-01-01

    In patients with ST-elevation myocardial infarction (STEMI) the amount of myocardial area at risk (MaR) indicates the maximal potential loss of myocardium if the coronary artery remains occluded. During the time course of infarct evolution ischemic MaR is replaced by necrosis, which results...... and Selvester score, indicating MaR, is stable until myocardial reperfusion therapy. In a retrospective analysis of a study population of 114 patients, 33 patients were included. The combined Aldrich and Selvester score was determined in ECGs recorded in the ambulance (ECG1) and in the hospital before...... (12 patients) of the combined Aldrich and Selvester score. In conclusion, the ECG estimated MaR was stable between the earliest recording time and initiation of reperfusion treatment only in a subgroup of the patients with STEMI. The findings of this study may suggest heterogeneity in regards...

  11. Pregnancy associated plasma protein A, a novel, quick, and sensitive marker in ST-elevation myocardial infarction

    DEFF Research Database (Denmark)

    Iversen, K.K.; Teisner, A.S.; Teisner, B.

    2008-01-01

    Traditional biomarkers in acute coronary syndromes reflect myocardial necrosis but not the underlying arteriosclerotic disease. Pregnancy-associated plasma protein A (PAPP-A) is a new biomarker in acute coronary syndromes that detects vulnerable plaques in arteriosclerotic disease and identifies......%). In conclusion, PAPP-A levels are elevated in >90% of patients presenting with STEMIs if measured marker of myocardial infarction than CKMB...

  12. [A case report of progressive penile necrosis].

    Science.gov (United States)

    Haba, Tomomi; Koike, Hiroshi

    2014-05-01

    The penis is provided with blood by multiple arteries. Penile necrosis is uncommon. Penile necrosis sporadically occurs in patients with progressive diabetes mellitus and/or end stage renal failure. Penile necrosis is often considered a poor prognostic feature. We present a case of penile necrosis in a patient with mild diabetes mellitus.

  13. Determination of perfusion defect area in experimental myocardial infarction. A comparison between 201-thallium and sup 99m Tc methoxy-isobutyl-isonitril (MIBI)

    Energy Technology Data Exchange (ETDEWEB)

    Mueller, K.D.; Rohmann, S.; Bahavar, H.; Grebe, S.F.; Schaper, W.; Schlepper, M. (Kerckhoff-Klinik, Bad Nauheim (Germany))

    1991-08-01

    To assess the accuracy of two myocardial perfusion markers in quantifying defect size, the left anterior descending coronary artery (LAD) was occluded in 13 porcine hearts. Fourty minutes later 55 MBq {sup 201}TI and 370 MBq {sup 99m}Tc-MIBI were simultaneously injected i.v. in 10 animals. After injection and in vivo double nuclide SPECT acquisition, the risk area was demarcated with fluorescein (FI) dye in 5 animals. The in vitro defect area determined by {sup 201}TI was significant larger (15.8 {+-} 27%) than those of {sup 99m}Tc-MIBI, while FI compared to Tc showed no statistical difference. Thus, in a pig model Tc-MIBI was more accurate with ex vivo imaging. With SPECT thallium imaging defect size was overestimated. In vivo there was a distinct trend with Tc-MIBI studies to underestimate the defect size up to 16%. (orig.).

  14. Stem cell therapy for myocardial infarction

    OpenAIRE

    Moelker, Amber

    2007-01-01

    textabstractCoronary heart disease and heart failure continue to be significant burdens to healthcare systems in the Western world and are predicted to become so in emerging economies. Despite mixed results in both experimental and clinical studies, stem cell therapy is a promising option for patients suffering from myocardial infarction or patients with chronic heart failure after myocardial infarction. However, many issues in the field of cellular cardiomyoplasty still need to be resolved. ...

  15. Warfarin-Induced Skin Necrosis

    Science.gov (United States)

    Papanas, Nikolaos; Karadimas, Efthimios; Polychronidis, Alexandros

    2014-01-01

    Warfarin-induced skin necrosis is an infrequent complication occurring in individuals under warfarin treatment who have a thrombophilic history or after administration of large loading doses of warfarin particularly without simultaneous initial use of heparin. A 62-year-old lady developed skin necrosis 4 days after initiating warfarin therapy of 5 mg daily without initial co-administration of heparin. The patient had a normal clotting profile. Skin necrosis progressed to eschar formation after cessation of warfarin and heparinization stopped expanding. Warfarin was reintroduced at 2 mg daily, initially together with low molecular weight heparin. Autolytic debridement of the necrotic tissue was followed by healing of the cutaneous deficit by secondary intention. Prompt diagnosis and discontinuation of warfarin are crucial for the prognosis. PMID:24648693

  16. Classification of myocardial infarction

    DEFF Research Database (Denmark)

    Saaby, Lotte; Poulsen, Tina Svenstrup; Hosbond, Susanne Elisabeth

    2013-01-01

    The classification of myocardial infarction into 5 types was introduced in 2007 as an important component of the universal definition. In contrast to the plaque rupture-related type 1 myocardial infarction, type 2 myocardial infarction is considered to be caused by an imbalance between demand...... and supply of oxygen in the myocardium. However, no specific criteria for type 2 myocardial infarction have been established....

  17. Transient myocardial ischemia after myocardial infarction

    DEFF Research Database (Denmark)

    Mickley, H

    1995-01-01

    Ambulatory ST-segment monitoring is a relatively new device in the evaluation of myocardial ischemia. The method is unique in allowing us to continuously examine the patient over an extended period of time in a changing environmental milieu. In survivors of acute myocardial infarction the prevale...

  18. Warfarin-induced skin necrosis.

    Science.gov (United States)

    Gelwix, T J; Beeson, M S

    1998-09-01

    Skin necrosis is an uncommon complication of warfarin (Coumadin; Dupont Pharma, Wilmington, DE) therapy. The presentation may mimic other disorders. This article reports a case of a 72-year-old woman who presented to the emergency department complaining of swelling and ecchymosis to her left breast and right foot. The patient had been hospitalized for coronary artery bypass grafting, and had been discharged from the hospital earlier that day. This article reviews the pathophysiology and clinical features of warfarin-induced skin necrosis.

  19. ST segment elevations: Always a marker of acute myocardial infarction?

    Directory of Open Access Journals (Sweden)

    G. Coppola

    2013-07-01

    Full Text Available Chest pain is one of the chief presenting complaints among patients attending Emergency department. The diagnosis of acute myocardial infarction may be a challenge. Various tools such as anamnesis, blood sample (with evaluation of markers of myocardial necrosis, ultrasound techniques and coronary computed tomography could be useful. However, the interpretation of electrocardiograms of these patients may be a real concern. The earliest manifestations of myocardial ischemia typically interest T waves and ST segment. Despite the high sensitivity, ST segment deviation has however poor specificity since it may be observed in many other cardiac and non-cardiac conditions. Therefore, when ST–T abnormalities are detected the physicians should take into account many other parameters (such as risk factors, symptoms and anamnesis and all the other differential diagnoses. The aim of our review is to overview of the main conditions that may mimic a ST segment Elevation Myocardial Infarction (STEMI.

  20. Cardioprotective potential of annexin-A1 mimetics in myocardial infarction.

    Science.gov (United States)

    Qin, Chengxue; Yang, Yuan H; May, Lauren; Gao, Xiaoming; Stewart, Alastair G; Tu, Yan; Woodman, Owen L; Ritchie, Rebecca H

    2015-04-01

    Myocardial infarction (MI) and its resultant heart failure remains a major cause of death in the world. The current treatments for patients with MI are revascularization with thrombolytic agents or interventional procedures. These treatments have focused on restoring blood flow to the ischemic tissue to prevent tissue necrosis and preserve organ function. The restoration of blood flow after a period of ischemia, however, may elicit further myocardial damage, called reperfusion injury. Pharmacological interventions, such as antioxidant and Ca(2+) channel blockers, have shown premises in experimental settings; however, clinical studies have shown limited success. Thus, there is a need for the development of novel therapies to treat reperfusion injury. The therapeutic potential of glucocorticoid-regulated anti-inflammatory mediator annexin-A1 (ANX-A1) has recently been recognized in a range of systemic inflammatory disorders. ANX-A1 binds to and activates the family of formyl peptide receptors (G protein-coupled receptor family) to inhibit neutrophil activation, migration and infiltration. Until recently, studies on the cardioprotective actions of ANX-A1 and its peptide mimetics (Ac2-26, CGEN-855A) have largely focused on its anti-inflammatory effects as a mechanism of preserving myocardial viability following I-R injury. Our laboratory provided the first evidence of the direct protective action of ANX-A1 on myocardium, independent of inflammatory cells in vitro. We now review the potential for ANX-A1 based therapeutics to be seen as a "triple shield" therapy against myocardial I-R injury, limiting neutrophil infiltration and preserving both cardiomyocyte viability and contractile function. This novel therapy may thus represent a valuable clinical approach to improve outcome after MI. Copyright © 2014 Elsevier Inc. All rights reserved.

  1. Defining the transmurality of a chronic myocardial infarction by ultrasonic strain-rate imaging: implications for identifying intramural viability: an experimental study.

    Science.gov (United States)

    Weidemann, Frank; Dommke, Christoph; Bijnens, Bart; Claus, Piet; D'hooge, Jan; Mertens, Paul; Verbeken, Eric; Maes, Alex; Van de Werf, Frans; De Scheerder, Ivan; Sutherland, George R

    2003-02-18

    In a correlative functional/histopathologic study, we investigated the regional deformation characteristics of both chronic nontransmural and transmural infarctions before and after a dobutamine challenge. After stenosing copper-coated stent implantation to produce circumflex artery endothelial proliferation, 18 pigs were followed up for 5 weeks. Posteuthanasia histology showed 10 to have a nontransmural and 8 a transmural infarction. Eight nonstented animals served as controls. Regional radial function was monitored by measuring ultrasound-derived peak systolic strain rates (SR(SYS)) and systolic strains (epsilon(SYS)) (1) before stent implantation and (2) at 5 weeks, at baseline (bs) and during an incremental dobutamine infusion. In controls, dobutamine induced a linear increase in SR(SYS) (dobutamine: bs, 4.8+/-0.4 s(-1); 20 microg x kg(-1) x min(-1), 9.9+/-0.7 s(-1); Ptransmural scar extension correlated closely with epsilon(SYS) at bs (r=0.88). For transmural infarctions, SR(SYS) at bs was significantly reduced and epsilon(SYS) was almost not measurable (SR(SYS), 1.8+/-0.3 s(-1); epsilon(SYS), 3+/-4%). Both deformation parameters showed no further change during the incremental dobutamine infusion. Ultrasonic deformation values could clearly differentiate chronic nontransmural from transmural myocardial infarction. The transmural extension of the scar could be defined by the regional deformation response.

  2. Double-contrast MR imaging of reperfused porcine myocardial infarction. An experimental study using Gd-DTPA-BMA and Dy-DTPA-BMA

    Energy Technology Data Exchange (ETDEWEB)

    Nilsson, S. [Dept. of Diagnostic Radiology, Akademiska Sjukhuset, Univ. Uppsala (Sweden); Wikstroem, G. [Dept. of Internal Medicine, Akademiska Sjukhuset, Univ. Uppsala (Sweden); Ericsson, A. [Dept. of Diagnostic Radiology, Akademiska Sjukhuset, Univ. Uppsala (Sweden); Wikstroem, M. [Dept. of Diagnostic Radiology, Akademiska Sjukhuset, Univ. Uppsala (Sweden); Oeksendal, A. [Nycomed Imaging AS, Oslo (Norway); Waldenstroem, A. [Dept. of Internal Medicine, Umeaa Univ. Hospital (Sweden); Hemmingsson, A. [Dept. of Internal Medicine, Akademiska Sjukhuset, Univ. Uppsala (Sweden)

    1996-01-01

    Purpose: Myocardinal infarctions were induced in 12 pigs to investigate whether a double-contrast method, combining a positive and a negative MR contast agent, could improve the visualization of reperfused myocardial infarctions. Material and Methods: All 12 pigs were subjected to 80 min of occlusion followed by repertusion. In the double-contrast group (6 pigs), Gd-DTPA-BMA (0.3 mmol/kg b.w.) and Dy-DTPA-BMA (1.0 mmol/kg b.w.) were administered i.v. after 30 min of reperfusion. In the remaining 6 pigs, a single injection of Gd-DTPA-BMA (0.3 mmol/kg b.w.) was given after 30 min of reperfusion. All pigs were sacrificed 10 min postcontrast injection, corresponding to a reperfusion time of 40 min. The hearts were excised and imaged with MR. The concentrations of Gd and Dy were measured in infarcted and nonischaemic myocardium using ICP-AES. Results and Conclusion: Contrast media concentrations were more than 4-fold higher in infarcted compared with nonischaemic myocardium. The infarctions were best shown on T1-weighted images, and there were no differences between the double and single contrast groups. In the T2-weighted images, the infarctions were significantly better visualized in the double-contrast group, due to a Dy-induced signal intensity loss in nonischaemic myocardium. (orig.).

  3. Myocardial Scar Imaging by Standard Single-Energy and Dual-Energy Late Enhancement Computed Tomography: Comparison to Pathology and Electroanatomical Map in an Experimental Chronic Infarct Porcine Model

    Science.gov (United States)

    Truong, Quynh A.; Thai, Wai-ee; Wai, Bryan; Cordaro, Kevin; Cheng, Teresa; Beaudoin, Jonathan; Xiong, Guanglei; Cheung, Jim W.; Altman, Robert; Min, James K.; Singh, Jagmeet P.; Barrett, Conor D.; Danik, Stephan

    2015-01-01

    Background Myocardial scar is a substrate for ventricular tachycardia and sudden cardiac death. Late enhancement computed tomography (CT) imaging can detect scar, but it remains unclear whether newer late enhancement dual-energy (LE-DECT) acquisition has benefit over standard single-energy late enhancement (LE-CT). Objective We aim to compare late enhancement CT using newer LE-DECT acquisition and single-energy LE-CT acquisitions to pathology and electroanatomical map (EAM) in an experimental chronic myocardial infarction (MI) porcine study. Methods In 8 chronic MI pigs (59±5 kg), we performed dual-source CT, EAM, and pathology. For CT imaging, we performed 3 acquisitions at 10 minutes post-contrast: LE-CT 80 kV, LE-CT 100 kV, and LE-DECT with two post-processing software settings. Results Of the sequences, LE-CT 100 kV provided the best contrast-to-noise ratio (all p≤0.03) and correlation to pathology for scar (ρ=0.88). While LE-DECT overestimated scar (both p=0.02), LE-CT images did not (both p=0.08). On a segment basis (n=136), all CT sequences had high specificity (87–93%) and modest sensitivity (50–67%), with LE-CT 100 kV having the highest specificity of 93% for scar detection compared to pathology and agreement with EAM (κ 0.69). Conclusions Standard single-energy LE-CT, particularly 100kV, matched better to pathology and EAM than dual-energy LE-DECT for scar detection. Larger human trials as well as more technical-based studies that optimize varying different energies with newer hardware and software are warranted. PMID:25977115

  4. Prediction and measurement of thermally induced cambial tissue necrosis in tree stems

    Science.gov (United States)

    Joshua L. Jones; Brent W. Webb; Bret W. Butler; Matthew B. Dickinson; Daniel Jimenez; James Reardon; Anthony S. Bova

    2006-01-01

    A model for fire-induced heating in tree stems is linked to a recently reported model for tissue necrosis. The combined model produces cambial tissue necrosis predictions in a tree stem as a function of heating rate, heating time, tree species, and stem diameter. Model accuracy is evaluated by comparison with experimental measurements in two hardwood and two softwood...

  5. Experimental myocardial infarct imaging following intravenous administration of iodine-131 labeled antibody (Fab')/sub 2/ fragments specific for cardiac myosin. [/sup 141/Ce scintiscanning

    Energy Technology Data Exchange (ETDEWEB)

    Khaw, B.A.; Beller, G.A.; Harber, E.

    1978-04-01

    Canine myocardial infarcts resulting from ligation of the left anterior descending coronary artery were localized in vivo by gamma scintigraphy following the intravenous injection of /sup 131/I anticardiac myosin antibody (Fab')/sub 2/. The anteroapical location of the image was confirmed by demonstration of the blood pool with /sup 99m/Tc sulfur colloid, and by subsequent imaging of the excised heart. The scintigram of the excised heart, following prior in vivo injection of /sup 141/Ce-microspheres, showed a region of diminished radioactivity near the apex which corresponded precisely to the region of /sup 131/I antibody (Fab')/sub 2/ uptake. Well defined areas of /sup 131/I antibody (Fab')/sub 2/ activity in the region of infarction were consistently imaged at 48 hours in animals in which the ligature occluding the coronary artery was released at 5 hours; 72 hours were at times required when coronary occlusion persisted throughout the experiment. In both reflow and persistent occlusion models, the concentration of /sup 131/I antibody (Fab')/sub 2/ was inversely related to blood flow as determined from microsphere distribution in the region of infarction; though in areas of equivalent flow (0 to 20% of normal) the mean concentration ratio of antibody uptake to normal tissue was 20.7 +- 2.2 in the reflow model as compared to 11.4 +- 0.7 in the persistent occlusion model. A reduction in blood flow to the affected area of <50% of normal did not result in the production of a localized scintigraphic image.

  6. Sterile Necrosis of the Sternum: A Rare Complication Following Coronary Artery Bypass Surgery

    Directory of Open Access Journals (Sweden)

    Emmanouel Papadakis

    2017-12-01

    Full Text Available We herein present the unique case of a 68-year-old male diabetic patient who developed sterile necrosis of the sternum 1 month after myocardial revascularization with the use of bilateral internal thoracic artery grafts. The sternum had been closed by the bilateral Robicsek wiring technique. The sternum was removed, and bilateral pectoralis major flaps were used to cover the defect. The patient had an uneventful recovery.

  7. Sterile Necrosis of the Sternum: A Rare Complication Following Coronary Artery Bypass Surgery.

    Science.gov (United States)

    Papadakis, Emmanouel; Konstantinidou, Maria Kalliopi; Kanakis, Meletios A

    2017-12-01

    We herein present the unique case of a 68-year-old male diabetic patient who developed sterile necrosis of the sternum 1 month after myocardial revascularization with the use of bilateral internal thoracic artery grafts. The sternum had been closed by the bilateral Robicsek wiring technique. The sternum was removed, and bilateral pectoralis major flaps were used to cover the defect. The patient had an uneventful recovery.

  8. Ischemia and reperfusion in skin flaps: effects of mannitol and vitamin C in reducing necrosis area in a rat experimental model Isquemia e reperfusão de retalhos cutâneos: efeitos do manitol e vitamina C na redução de áreas de necrose em modelo experimental no rato

    Directory of Open Access Journals (Sweden)

    Winston Bonetti Yoshida

    2005-10-01

    Full Text Available PURPOSE: The aim of the present study was to develop an experimental model of ischemia-reperfusion injury in rat skin flap and to verify the effect of mannitol and vitamin C on reducing necrosis area. METHODS: A 6-x 3-cm groin skin flap was raised and submitted to 8 hours of ischemia by clamping the vascular pedicle and to 7 days of reperfusion. The animals were divided in four groups: S1 and S2 (10 animals each and C and T (14 animals each. In groups S1 and S2 skin flaps were not submitted to ischemia and animals received lactated Ringer's solution (S1 and antioxidant solution (S2 . In groups C and T, flaps were subjected to 8 hours of warm ischemia and animals received Lactated Ringer's solution (Group C and antioxidant solution immediately before reperfusion, (Group T. Flap survival was evaluated on the seventh day using a paper template technique and computer-assistant imaging analysis of necrotic and normal areas. RESULTS: Statistical analysis showed no area differences between groups C and T. CONCLUSION: The experimental model provided consistent necrotic area in control groups and drugs used were not effective in improving skin flap survival.OBJETIVO: Neste trabalho foi padronizado modelo experimental de isquemia e reperfusão em retalho cutâneo em ratos no qual estudou-se possibilidade de uma solução antioxidante, composta por Ringer lactato, vitamina C e manitol de reduzir a área de necrose. MÉTODOS: O modelo consistiu de levantamento de retalho cutâneo axial de 6,0 x 3,0cm, submetido à isquemia de 8 horas e reperfusão de 7 dias. Os animais foram divididos em quatro grupos: grupos S1, S2 (10 animais cada, C e T (14 animais cada. Nos grupos S1 e S2 todos os procedimentos dos demais grupos foram efetuados, exceto a isquemia e reperfusão: S1 recebeu apenas Ringer lactato e S2 a solução antioxidante. Os grupos C e T foram submetidos à isquemia. O grupo C recebeu somente Ringer lactato e o grupo T a solução antioxidante. No 7

  9. Neonatal scalp haematoma and necrosis.

    Science.gov (United States)

    Schönmeyr, Björn; Becker, Magnus; Svensson, Henry

    2014-12-01

    Birth trauma after prolonged deliveries and instrument-assisted extractions can result in skin lesions and reduced viability of the scalp. In these instances, scalp swellings and haematomas are often also seen. The classification and inter-relationship between these conditions might not, however, always be clear. This report describes three cases of neonates with scalp swellings and necrosis. Nomenclature, underlying causes, work up, treatment options, and outcomes are presented and discussed. The first case consisted of a newborn with a subgaleal haematoma and occipital pressure necrosis that healed by secondary intention. In the second case, an infected scalp haematoma led to scarring and alopecia that required secondary reconstruction with tissue expansion. The third neonate suffered from a subgaleal haematoma and a scalp lesion that required split skin grafting and secondary reconstruction with tissue expansion.

  10. Necrosis

    Science.gov (United States)

    ... Aster JC. Cellular responses to stress and toxic insults: adaptation, injury, and death. In: Kumar V, Abbas ... the first to achieve this important distinction for online health information and services. Learn more about A. ...

  11. Cardiolipin plays a role in KCN-induced necrosis.

    Science.gov (United States)

    Tsesin, Natalia; Khalfin, Boris; Nathan, Ilana; Parola, Abraham H

    2014-10-01

    Cardiolipin (CL) is a unique anionic, dimeric phospholipid found almost exclusively in the inner mitochondrial membrane and is essential for the function of numerous enzymes that are involved in mitochondrial energy metabolism. While the role of cardiolipin in apoptosis is well established, its involvement in necrosis is enigmatic. In the present study, KCN-induced necrosis in U937 cells was used as an experimental model to assess the role of CL in necrosis. KCN addition to U937 cells induced reactive oxygen species (ROS) formation, while the antioxidants inhibited necrosis, indicating that ROS play a role in KCN-induced cell death. Further, CL oxidation was confirmed by the monomer green fluorescence of 10-N-nonyl acridine orange (NAO) and by TLC. Utilizing the red fluorescence of the dimeric NAO, redistribution of CL in mitochondrial membrane during necrosis was revealed. We also showed that the catalytic activity of purified adenosine triphosphate (ATP) synthase complex, known to be modulated by cardiolipin, decreased following KCN treatment. All these events occurred at an early phase of the necrotic process prior to rupture of the cell membrane. Furthermore, CL-deficient HeLa cells were found to be resistant to KCN-induced necrosis as compared with the wild type cells. We suggest that KCN, an effective reversible inhibitor of cytochrome oxidase and thereby of the respiratory chain leads to ROS increase, which in turn oxidizes CL (amongst other membrane phospholipids) and leads to mitochondrial membrane lipid reorganization and loss of CL symmetry. Finally, the resistance of CL-deficient cells to necrosis further supports the notion that CL, which undergoes oxidation during necrotic cell death, is an integral part of the milieu of events taking place in mitochondria leading to membrane disorganization and mitochondrial dysfunction. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

  12. Acute Esophageal Necrosis: An Update

    Science.gov (United States)

    Inayat, Faisal; Hurairah, Abu; Virk, Hafeez Ul Hassan

    2016-01-01

    Acute esophageal necrosis (AEN) or “black esophagus” is a rare clinical entity with an unclear etiology. It is diagnosed at upper gastrointestinal endoscopy with the presence of strikingly black necrotic esophagus. The treatment is primarily medical, but the prognosis is generally poor due to advanced age and comorbid illnesses in patients who develop AEN. Herein, we discussed the implications of poor glycemic control in regards with AEN and undertook a literature review of this rare diagnosis. PMID:27583242

  13. Targeting of regulated necrosis in kidney disease.

    Science.gov (United States)

    Martin-Sanchez, Diego; Poveda, Jonay; Fontecha-Barriuso, Miguel; Ruiz-Andres, Olga; Sanchez-Niño, María Dolores; Ruiz-Ortega, Marta; Ortiz, Alberto; Sanz, Ana Belén

    2017-06-21

    The term acute tubular necrosis was thought to represent a misnomer derived from morphological studies of human necropsies and necrosis was thought to represent an unregulated passive form of cell death which was not amenable to therapeutic manipulation. Recent advances have improved our understanding of cell death in acute kidney injury. First, apoptosis results in cell loss, but does not trigger an inflammatory response. However, clumsy attempts at interfering with apoptosis (e.g. certain caspase inhibitors) may trigger necrosis and, thus, inflammation-mediated kidney injury. Second, and most revolutionary, the concept of regulated necrosis emerged. Several modalities of regulated necrosis were described, such as necroptosis, ferroptosis, pyroptosis and mitochondria permeability transition regulated necrosis. Similar to apoptosis, regulated necrosis is modulated by specific molecules that behave as therapeutic targets. Contrary to apoptosis, regulated necrosis may be extremely pro-inflammatory and, importantly for kidney transplantation, immunogenic. Furthermore, regulated necrosis may trigger synchronized necrosis, in which all cells within a given tubule die in a synchronized manner. We now review the different modalities of regulated necrosis, the evidence for a role in diverse forms of kidney injury and the new opportunities for therapeutic intervention. Copyright © 2017 Sociedad Española de Nefrología. Published by Elsevier España, S.L.U. All rights reserved.

  14. Ultrasonographic findings of epipericardial fat necrosis: A case report

    Energy Technology Data Exchange (ETDEWEB)

    Park, Chan Yeong; Hwang, Hye Jeon; Lee, Kwan Seop; Lee, In Jae; Park, Kyoung Ha [Dept. of Internal Medicine, Hallym University College of Medicine, Hallym University Sacred Heart Hospital, Anyang (Korea, Republic of)

    2016-04-15

    Epipericardial fat necrosis (EFN) is an infrequent cause of acute chest pain. In rare cases like these, conservative treatment is necessary. Clinically, EFN may mimic emergent cardiopulmonary conditions, such as acute myocardial infarction. Computed tomography (CT) and magnetic resonance imaging characteristics of EFN is well described as encapsulated fatty lesion with perilesional soft tissue strands and thickening of adjacent pericardium in the epipericardial area. For confirmation of the diagnosis, involution of this lesion on follow-up is important. We present a case of EFN observed with ultrasonography (USG). This lesion was shown as a well-defined ovoid shaped mass with heterogeneous echogenicity in the left side of cardiophrenic space on USG. There was no color flow on Doppler USG. Follow-up USG and CT revealed decrease in the size of the lesion.

  15. Acute Retinal Necrosis in Childhood

    Directory of Open Access Journals (Sweden)

    Yoav Y. Pikkel

    2014-05-01

    Full Text Available Background: Acute retinal necrosis (ARN is a viral syndrome consisting of uveitis/vitritis, occlusive vasculitis and peripheral necrosis. Few incidents are reported in children. The etiology is reactivated herpes simplex virus (HSV or varicella-zoster virus (VZV. Treatment with acyclovir is often used. The administration of oral glucocorticosteroids is of unproven benefit. Prognosis is variable but poor. Methods: Three weeks after contracting mild chickenpox, a healthy 4-year-old girl developed blurred vision in her right eye. Severely reduced visual acuity was noted, together with anterior uveitis, ‘mutton-fat' precipitates and vitral flare. Retinal vasculitis with necrosis was present. Serology for toxoplasma, cytomegalovirus and HIV was negative, while HSV and VZV IgG antibodies were positive. She was treated with 30 mg/kg of intravenous methylprednisolone (3 days, 30 mg of oral prednisone (3 days, and tapering for 8 weeks. Intravenous acyclovir was given for 10 days, followed by oral acyclovir for 4 months. Aspirin (100 mg/day was given for 4 months. Results: At 12 months, the girl felt good. Her right eye acuity was 6/9, with an intraocular pressure of 17 mm Hg. The peripheral retina showed scarring but no detachment. Conclusions: This is the first report of a once-daily high-dose methylprednisolone pulse therapy in one of the youngest known ARN cases. Pulsed steroid therapy was based on its known effectiveness in vasculitis, which is the main pathophysiology in ARN. There was no evidence of steroid-related viral over-replication. Our case achieved an excellent clinical and ophthalmic recovery in spite of the poor prognosis. The positive result of this case report provides a basis for further evaluation of high-dose steroid pulse therapy in ARN.

  16. Cardiac MRI for myocardial ischemia.

    LENUS (Irish Health Repository)

    Daly, Caroline

    2013-01-01

    Proper assessment of the physiologic impact of coronary artery stenosis on the LV myocardium can affect patient prognosis and treatment decisions. Cardiac magnetic resonance imaging (CMR) assesses myocardial perfusion by imaging the myocardium during a first-pass transit of an intravenous gadolinium bolus, with spatial and temporal resolution substantially higher than nuclear myocardial perfusion imaging. Coupled with late gadolinium enhancement (LGE) imaging for infarction during the same imaging session, CMR with vasodilating stress perfusion imaging can qualitatively and quantitatively assess the myocardial extent of hypoperfusion from coronary stenosis independent of infarcted myocardium. This approach has been validated experimentally, and multiple clinical trials have established its diagnostic robustness when compared to stress single-photon emission computed tomography. In specialized centers, dobutamine stress CMR has been shown to have incremental diagnostic value above stress echocardiography due to its high imaging quality and ability to image the heart with no restriction of imaging window. This paper reviews the technical aspects, diagnostic utility, prognostic values, challenges to clinical adaptation, and future developments of stress CMR imaging.

  17. Real-time magnetic resonance imaging texture characterization of necrosis during laser interstitital thermotherapy procedures

    Science.gov (United States)

    Betrouni, N.; Lopes, R.; Colin, P.; Mordon, S.

    2010-02-01

    This paper aims to describe the development of a method to monitor laser interstitial thermo therapy by MR images. The method is based on the texture analysis using fractal geometry features of the images to estimate the size of the induced necrosis. The method was validated by comparing the results to macroscopic measurements. It demonstrates the ability to achieve good estimation of the necrosis in ex-vivo experimentations involving pig liver and in vivo experimentations done on tumors grown on Copenhagen rats.

  18. Myocardial Fibrosis in Athletes.

    NARCIS (Netherlands)

    Schoor, F.R. van de; Aengevaeren, V.L.; Hopman, M.T.E.; Oxborough, D.L.; George, K.P.; Thompson, P.D.; Eijsvogels, T.M.H.

    2016-01-01

    Myocardial fibrosis (MF) is a common phenomenon in the late stages of diverse cardiac diseases and is a predictive factor for sudden cardiac death. Myocardial fibrosis detected by magnetic resonance imaging has also been reported in athletes. Regular exercise improves cardiovascular health, but

  19. The spectrum of myocardial homeostasis mechanisms in the settings of cardiac surgery procedures (Review).

    Science.gov (United States)

    Papadakis, Emmanuel; Kanakis, Meletios; Kataki, Agapi; Spandidos, Demetrios A

    2018-02-01

    Classic cardiac surgery, determined through the function of cardiopulmonary bypass machine and myocardial cardioplegic arrest, represents the most controlled scenario for cardiomyocyte homeostatic disturbances due to systemic inflammatory response and myocardial reperfusion injury. An increasing number of studies have demonstrated that myocardial cell homeostasis in cardiac surgery procedures is a sequence of molecularly interrelated and overlapping mechanisms in the form of apoptosis, autophagy and necrosis, which are activated by a plethora of induced inflammatory mediators and gene‑related signaling pathways. In this study, we outline the molecular mechanisms of the cardiomyocyte adaptive homeostatic process and the associated clinical implications, in the settings of classic cardiac surgery procedures.

  20. Acute myocardial infarction.

    Science.gov (United States)

    Reed, Grant W; Rossi, Jeffrey E; Cannon, Christopher P

    2017-01-14

    Acute myocardial infarction has traditionally been divided into ST elevation or non-ST elevation myocardial infarction; however, therapies are similar between the two, and the overall management of acute myocardial infarction can be reviewed for simplicity. Acute myocardial infarction remains a leading cause of morbidity and mortality worldwide, despite substantial improvements in prognosis over the past decade. The progress is a result of several major trends, including improvements in risk stratification, more widespread use of an invasive strategy, implementation of care delivery systems prioritising immediate revascularisation through percutaneous coronary intervention (or fibrinolysis), advances in antiplatelet agents and anticoagulants, and greater use of secondary prevention strategies such as statins. This seminar discusses the important topics of the pathophysiology, epidemiological trends, and modern management of acute myocardial infarction, focusing on the recent advances in reperfusion strategies and pharmacological treatment approaches. Copyright © 2017 Elsevier Ltd. All rights reserved.

  1. Myocardial Viability: From Proof of Concept to Clinical Practice

    Directory of Open Access Journals (Sweden)

    Aditya Bhat

    2016-01-01

    Full Text Available Ischaemic left ventricular (LV dysfunction can arise from myocardial stunning, hibernation, or necrosis. Imaging modalities have become front-line methods in the assessment of viable myocardial tissue, with the aim to stratify patients into optimal treatment pathways. Initial studies, although favorable, lacked sufficient power and sample size to provide conclusive outcomes of viability assessment. Recent trials, including the STICH and HEART studies, have failed to confer prognostic benefits of revascularisation therapy over standard medical management in ischaemic cardiomyopathy. In lieu of these recent findings, assessment of myocardial viability therefore should not be the sole factor for therapy choice. Optimization of medical therapy is paramount, and physicians should feel comfortable in deferring coronary revascularisation in patients with coronary artery disease with reduced LV systolic function. Newer trials are currently underway and will hopefully provide a more complete understanding of the pathos and management of ischaemic cardiomyopathy.

  2. Review Paper: Myocardial Rupture After Acute Myocardial Infarction ...

    African Journals Online (AJOL)

    Myocardial rupture complications after acute myocardial infarction are infrequent but lethal. They mainly involve rupture of the ventricular free wall, ventricular septum, papillary muscle, or combined. We compare features of different kinds of myocardial ruptures after acute myocardial infarction by reviewing the clinical ...

  3. Periodontitis and myocardial hypertrophy.

    Science.gov (United States)

    Suzuki, Jun-Ichi; Sato, Hiroki; Kaneko, Makoto; Yoshida, Asuka; Aoyama, Norio; Akimoto, Shouta; Wakayama, Kouji; Kumagai, Hidetoshi; Ikeda, Yuichi; Akazawa, Hiroshi; Izumi, Yuichi; Isobe, Mitsuaki; Komuro, Issei

    2017-04-01

    There is a deep relationship between cardiovascular disease and periodontitis. It has been reported that myocardial hypertrophy may be affected by periodontitis in clinical settings. Although these clinical observations had some study limitations, they strongly suggest a direct association between severity of periodontitis and left ventricular hypertrophy. However, the detailed mechanisms between myocardial hypertrophy and periodontitis have not yet been elucidated. Recently, we demonstrated that periodontal bacteria infection is closely related to myocardial hypertrophy. In murine transverse aortic constriction models, a periodontal pathogen, Aggregatibacter actinomycetemcomitans markedly enhanced cardiac hypertrophy with matrix metalloproteinase-2 activation, while another pathogen Porphyromonas gingivalis (P.g.) did not accelerate these pathological changes. In the isoproterenol-induced myocardial hypertrophy model, P.g. induced myocardial hypertrophy through Toll-like receptor-2 signaling. From our results and other reports, regulation of chronic inflammation induced by periodontitis may have a key role in the treatment of myocardial hypertrophy. In this article, we review the pathophysiological mechanism between myocardial hypertrophy and periodontitis.

  4. Infectious haematopoietic necrosis virus: Chapter 2

    Science.gov (United States)

    Leong, Jo-Ann; Kurath, Gael

    2017-01-01

    Infectious haematopoietic necrosis virus (IHNV) is a Rhabdovirus that causes significant disease in Pacific salmon (Oncorhynchus spp.), Atlantic salmon (Salmo salar), and rainbow and steelhead trout (O. mykiss). IHNV causes necrosis of the haematopoietic tissues, and consequently it was named infectious haematopoietic necrosis. This virus is waterborne and may transmit horizontally and vertically through virus associated with seminal and ovarian fluids. The clinical signs of disease and diagnosis; pathology; pathophysiology; and control strategies against IHNV are discussed.

  5. Reversible myocardial dysfunction after cardiopulmonary resuscitation.

    Science.gov (United States)

    Ruiz-Bailén, Manuel; Aguayo de Hoyos, Eduardo; Ruiz-Navarro, Silvia; Díaz-Castellanos, Miguel Angel; Rucabado-Aguilar, Luis; Gómez-Jiménez, Francisco Javier; Martínez-Escobar, Sergio; Moreno, Rafael Melgares; Fierro-Rosón, Javier

    2005-08-01

    Myocardial stunning frequently has been described in patients with an acute coronary syndrome. Recently, it has also been described in critically ill patients without ischaemic heart disease. It is possible that the most severe form of any syndrome, leading to cardio-respiratory arrest, may cause myocardial stunning. Myocardial stunning appears to have been demonstrated in experimental studies, though this phenomenon has not been sufficiently studied in human models. The aim of the present work has been to study and describe the possible development of myocardial dysfunction in patients resuscitated after cardio-respiratory arrest, in the absence of acute or previous coronary artery disease. Descriptive study of a case series. The intensive care unit (ICU) of a provincial hospital. The study period was from April 1999 to June 2001. All patients admitted to the ICU with critical, non-coronary artery pathology, with no past history of cardiac disease, and those who were resuscitated after cardio-respiratory arrest, were included in the study. Transthoracic and transoesophageal echocardiography was used to assess left ventricular ejection fraction (LVEF) and disturbances of segmental contractility. This study was carried out within the first 24h after admission, during the first week, during the second or third week, after 1 month, and between 3 and 6 months. Twenty-nine patients with a median age of 65 years (range 24--76) were included in the study. Twelve patients died. Twenty patients developed myocardial dysfunction; the initial LVEF in these patients was 0.28 (0.12--0.51), showing improvement over time in the patients who survived. All of these patients presented disturbances of segmental contractility which also became normal over time. After successful CPR, reversible myocardial dysfunction, consisting of systolic myocardial dysfunction and disturbances of segmental contractility, may occur.

  6. El factor de necrosis de los tumores o caquectina

    Directory of Open Access Journals (Sweden)

    Jorge Eliécer Ossa Londoño

    1988-02-01

    Full Text Available

    Se presenta una revisión de la literatura sobre el Factor de Necrosis de los Tumores o Caquectina, con base en artículos publicados durante los anos 1986-1987, haciendo hincapié en las diferencias funcionales y moleculares entre el FNT Alfa, la Linfotoxina o FNT Beta y la Caquectina. Se enfatizan los mecanismos del shock, de la necrosis tumoral y de la caquexia; se Indican las propiedades antitumorales del FNT in vivo e in vitro y se esbozan esquemas terapéuticos experimentales que permiten colegir que el FNT tendrá un papel Importante en la Inmunoterapia del cáncer en el hombre.

    This is a review of the 1986-1987 Literature on the Tumor Necrosis Factor (TNF or Cachectin, emphasizing functional and molecular differences among TNF alpha, Iymphotoxin or TNF beta and Cachectin. Mechanisms of shock, tumor necrosis and cachexia are discussed. In vivo and ín vítro antitumoral properties of TNF are indicated, as well as some experimental therapeutic regimens. These facts allow the suggestion that TNF might become an Important aid for Immunotherapy of cancer In humans.

  7. Cardioprotective Role of Tumor Necrosis Factor Receptor-Associated Factor 2 by Suppressing Apoptosis and Necroptosis.

    Science.gov (United States)

    Guo, Xiaoyun; Yin, Haifeng; Li, Lei; Chen, Yi; Li, Jing; Doan, Jessica; Steinmetz, Rachel; Liu, Qinghang

    2017-08-22

    Programmed cell death, including apoptosis, mitochondria-mediated necrosis, and necroptosis, is critically involved in ischemic cardiac injury, pathological cardiac remodeling, and heart failure progression. Whereas apoptosis and mitochondria-mediated necrosis signaling is well established, the regulatory mechanisms of necroptosis and its significance in the pathogenesis of heart failure remain elusive. We examined the role of tumor necrosis factor receptor-associated factor 2 (Traf2) in regulating myocardial necroptosis and remodeling using genetic mouse models. We also performed molecular and cellular biology studies to elucidate the mechanisms by which Traf2 regulates necroptosis signaling. We identified a critical role for Traf2 in myocardial survival and homeostasis by suppressing necroptosis. Cardiac-specific deletion of Traf2 in mice triggered necroptotic cardiac cell death, pathological remodeling, and heart failure. Plasma tumor necrosis factor α level was significantly elevated in Traf2-deficient mice, and genetic ablation of TNFR1 largely abrogated pathological cardiac remodeling and dysfunction associated with Traf2 deletion. Mechanistically, Traf2 critically regulates receptor-interacting proteins 1 and 3 and mixed lineage kinase domain-like protein necroptotic signaling with the adaptor protein tumor necrosis factor receptor-associated protein with death domain as an upstream regulator and transforming growth factor β-activated kinase 1 as a downstream effector. It is important to note that genetic deletion of RIP3 largely rescued the cardiac phenotype triggered by Traf2 deletion, validating a critical role of necroptosis in regulating pathological remodeling and heart failure propensity. These results identify an important Traf2-mediated, NFκB-independent, prosurvival pathway in the heart by suppressing necroptotic signaling, which may serve as a new therapeutic target for pathological remodeling and heart failure. © 2017 American Heart

  8. Subendocardial ischemic myocardial lesions associated with severe coronary atherosclerosis.

    Science.gov (United States)

    Geer, J. C.; Crago, C. A.; Little, W. C.; Gardner, L. L.; Bishop, S. P.

    1980-01-01

    Morphologic changes in the subendocardial myocardium that appeared to be caused by severe, chronic subendocardial ischemia were studied in patients with fatal ischemic heart disease admitted to the Specialized Center of Research for Ischemic Heart Disease at the University of Alabama in Birmingham in the period 1970--1977. Thirteen patients were selected for this report on the basis that they had the lesions in the subendocardial myocardium we believe to have been caused by subendocardial ischemia and had no evidence of acute or remote myocardial infarction or other conditions that may have contributed to their terminal illness or death. Clinical findings were unstable angina, congestive heart failure, usually no increase in plasma enzymes indicative of myocardial damage, and electrocardiographic changes consistent with subendocardial ischemia. All 13 patients had 75% or greater stenosis of the three major coronary arteries; none had acute thrombotic or embolic coronary artery occlusion. The left ventricle in all cases was hypertrophied. The subendocardial myocardium showed circumferential pallor, hyperemia, or focal fibrosis without perceptible loss of volume in papillary muscles or trabeculae carneae. Microscopically, acute lesions showed one to two layers of preserved myofibers adjacent to the endocardium, vacuolar change in the deeper fibers, and focal areas of coagulation necrosis of variable size in the myocardium external to the fibers with vacuolar change. Coagulation necrosis was extensive in some cases and usually was not associated with infiltration of neutrophils. The repair reaction involved removal of necrotic sarcoplasm by mononuclear phagocytes, resulting in a reticular-appearing tissue without evidence of stromal collapse. Granulation tissue was not seen. Collagen fibers appeared to be deposited within the area of previous sarcolemmal sheaths. The distribution and morphology of subendocardial myocardial lesions associated with severe coronary

  9. Thermal inactivation of infectious hematopoietic necrosis and infectious pancreatic necrosis virus

    Science.gov (United States)

    Gosting, L.; Gould, R.W.

    1981-01-01

    A plaque assay was used to follow the inactivation kinetics of infectious hematopoietic necrosis virus and infectious pancreatic necrosis virus in cell culture media at various temperatures. Inactivation of infectious hematopoietic necrosis virus in a visceral organ slurry was compared with that in culture media.

  10. Mastectomy skin necrosis after microsurgical breast reconstruction.

    Science.gov (United States)

    Vargas, Christina R; Koolen, Pieter G; Anderson, Katarina E; Paul, Marek A; Tobias, Adam M; Lin, Samuel J; Lee, Bernard T

    2015-10-01

    Mastectomy skin necrosis represents a significant clinical morbidity after immediate breast reconstruction. In addition to aesthetic deformity, necrosis of the native mastectomy skin may require debridement, additional reconstruction, or prolonged wound care and potentially delay oncologic treatment. This study aims to evaluate patient and procedural characteristics to identify predictors of mastectomy skin necrosis after microsurgical breast reconstruction. A retrospective review was performed of all immediate microsurgical breast reconstructions performed at a single academic center. Patient records were queried for age, diabetes, active smoking, previous breast surgery, preoperative radiation, preoperative chemotherapy, body mass index, mastectomy type, mastectomy weight, flap type, autologous flap type, and postoperative mastectomy skin flap necrosis. There were 746 immediate autologous microsurgical flaps performed by three plastic surgeons at our institution during the study period. The incidence of mastectomy skin flap necrosis was 13.4%. Univariate analysis revealed a significantly higher incidence of mastectomy skin necrosis in patients with higher mastectomy weight (P necrosis and both increasing mastectomy weight (odds ratio 1.348 per quartile increase, P = 0.009) and diabetes (odds ratio 2.356, P = 0.011). Increasing mastectomy weight and coexisting diabetes are significantly associated with postoperative mastectomy skin necrosis after microsurgical reconstruction. These characteristics should be considered during patient counseling, procedure selection, operative planning, and intraoperative tissue viability assessment. Copyright © 2015 Elsevier Inc. All rights reserved.

  11. Transmural heterogeneity of myocardial contraction and ischemia. Diagnosis and clinical implications.

    Science.gov (United States)

    Colonna, P; Cadeddu, C; Montisci, R; Chen, L; Meloni, L; Iliceto, S

    2000-03-01

    Myocardial contraction behaves heterogeneously, being greater in subendocardial than in subepicardial layers. Similarly, during acute myocardial ischemia or infarction, the subendocardium is the first myocardial layer to suffer. Conventional two-dimensional echocardiography cannot distinguish the transmural extension of myocardial ischemia or infarction, showing akinesia also when only the subendocardium is affected. Novel ultrasonographic techniques (like tissue characterization with integrated backscatter or Doppler tissue imaging) and nuclear magnetic resonance tagging can investigate myocardial contraction in different transmural layers and distinguish subendocardial from transmural ischemia or infarction. With the advent of thrombolysis and primary angioplasty in the acute phase of myocardial infarction a correct diagnosis of the extension of myocardial necrosis cannot ignore its transmural wavefront development. The salvage of the subepicardial layer does not give direct information on overall myocardial thickening but is one of the major determinants of overall left ventricular dysfunction and size. Although it is still necessary to investigate this phenomenon, new ultrasonographic techniques give us important information and more opportunities to appropriate diagnosis and future treatment of cardiac patients.

  12. Relation of plasma lipoprotein(a) with myocardial viability and left ventricular performance in survivors of myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Aksoy, M.; Goktekin, O.; Gursurer, M.; Emre, A.; Bilge, M.; Yesilcimen, K.; Ersek, B. [Siyami Ersek Thoracic and Cardiovascular Surgery Centre, Istanbul (Turkey); Kepekci, Y.; Akdemir, I.

    1999-11-01

    Previous studies have reported that high serum lipoprotein(a) levels may be responsible for total occlusion of the infarct-related artery via inhibition of intrinsic fibrinolysis during acute myocardial infarction. We evaluated whether this would result in a greater extent of myocardial necrosis and impaired left ventricular function in patients with high lipoprotein(a) levels. Sixty-eight patients with prior myocardial infarction, who were not receiving thrombolytic therapy underwent coronary angiography and stress-redistribution-reinjection Tl-201 scintigraphy. Antegrade TIMI flow in the infarct-related artery was lower (1.54{+-}1.14 vs 2.15{+-}1.05; p=0.03) and the collateral index was higher (1.3{+-}1.0 vs 0.8{+-}0.9; p=0.07) in patients with high lipoprotein(a) levels (>30 mg/dl) compared to those with low lipoprotein(a) levels ({<=}30 mg/dl). Regional wall motion score index was lower (0.8{+-}0.8 vs 1.4{+-}0.5; p=0.008) and global ejection fraction was higher (46{+-}10% vs 40{+-}11%; p=0.03) in patients with low lipoprotein(a) levels. On SPECT images, the number of nonviable defects was higher in patients with high lipoprotein(a) levels (4.0{+-}2.5 vs 1.9{+-}1.3; p=0.0002), whereas the number of viable defects was higher in those with low lipoprotein(a) levels (2.5{+-}1.8 vs 1.5{+-}1.3; p=0.02). We conclude, that high lipoprotein(a) levels may prolong the occlusion of infarct-related artery during acute myocardial infarction and lead to a greater extent of myocardial necrosis and impaired left ventricular function. (author)

  13. Regulation of Tumor Progression by Programmed Necrosis

    Directory of Open Access Journals (Sweden)

    Su Yeon Lee

    2018-01-01

    Full Text Available Rapidly growing malignant tumors frequently encounter hypoxia and nutrient (e.g., glucose deprivation, which occurs because of insufficient blood supply. This results in necrotic cell death in the core region of solid tumors. Necrotic cells release their cellular cytoplasmic contents into the extracellular space, such as high mobility group box 1 (HMGB1, which is a nonhistone nuclear protein, but acts as a proinflammatory and tumor-promoting cytokine when released by necrotic cells. These released molecules recruit immune and inflammatory cells, which exert tumor-promoting activity by inducing angiogenesis, proliferation, and invasion. Development of a necrotic core in cancer patients is also associated with poor prognosis. Conventionally, necrosis has been thought of as an unregulated process, unlike programmed cell death processes like apoptosis and autophagy. Recently, necrosis has been recognized as a programmed cell death, encompassing processes such as oncosis, necroptosis, and others. Metabolic stress-induced necrosis and its regulatory mechanisms have been poorly investigated until recently. Snail and Dlx-2, EMT-inducing transcription factors, are responsible for metabolic stress-induced necrosis in tumors. Snail and Dlx-2 contribute to tumor progression by promoting necrosis and inducing EMT and oncogenic metabolism. Oncogenic metabolism has been shown to play a role(s in initiating necrosis. Here, we discuss the molecular mechanisms underlying metabolic stress-induced programmed necrosis that promote tumor progression and aggressiveness.

  14. [Programmed necrosis and necroptosis - molecular mechanisms].

    Science.gov (United States)

    Giżycka, Agata; Chorostowska-Wynimko, Joanna

    2015-12-16

    Programmed necrosis has been proven vital for organism development and homeostasis maintenance. Its regulatory effects on functional activity of the immune system, as well as on pathways regulating the death mechanisms in cells with diminished apoptotic activity, including malignant cells, have been confirmed. There is also increasing evidence indicating necrosis involvement in many human pathologies. Contrary to previous beliefs, necrosis is not only a passive, pathological, gene-independent process. However, the current knowledge regarding molecular regulation of programmed necrosis is scarce. In part this is due to the multiplicity and complexity of signaling pathways involved in programmed necrosis, as well as the absence of specific cellular markers identifying this process, but also the ambiguous and imprecise international terminology. This review presents the current state of the art on molecular mechanisms of programmed necrosis. In particular, its specific and frequent form, necroptosis, is discussed. The role of RIP1 and RIP3 kinases in this process is presented, as well as the diverse pathways induced by ligation of tumor necrosis factor α, to its receptor, TNFR1, i.e. cell survival, apoptosis or necroptosis.

  15. Comparative study of body surface isopotential map, left ventriculogram and thallium-201 myocardial scintigram in patients with old lateral myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Matsumoto, Naoyuki

    1988-01-01

    In 16 patients with old lateral myocardial infarction, body surface isopotential maps and 12 lead electrocardiograms were compared with left ventriculographic findings. In addition 8 of these subjects were performed thallium-201 myocardial scintigraphy in order to determine the location and extent of myocardial necrosis. Common 12 lead electrocardiographic findings of the subjects were initial Q waves more than 30 msec and inverted T waves in only aVL lead. The patients were classified into 4 groups according to the location and extent of ventricular wall motion abnormalities group I (6 cases) showed hypokinesis in the anterior segment, group II (5 cases): akinesis in the anterior segment and hypokinesis in the seg. 6, group III (4 cases): hypokinesis in the anterior segment and seg. 7, group IV (1 case): hypokinesis in the anterior segment and seg. 4, 7. And each of the 4 groups demonstrated characteristic findings of surface isopotential maps. Group II with coexisting hypokinesis in the seg. 6 showed surface isopotential maps additional pattern of anterior myocardial infarction, and group III with coexisting hypokinesis in the seg. 7 showed additional patterns of posterior myocardial infarction. The classification according to the abnormality of ventricular wall motion was also conformed with the thallium-201 myocardial scintigraphic findings except one case. These results suggest that body surface isopotential map is more useful than the 12 lead electrocardiogram in detecting the location and extent of left ventricular wall motion abnormality in patients with old lateral myocardial infarction. (author) 53 refs.

  16. Myocardial reverse remodeling.

    Science.gov (United States)

    Hellawell, Jennifer L; Margulies, Kenneth B

    2012-06-01

    Despite an extensive literature defining the mechanisms and significance of pathological myocardial remodeling, there has been no comprehensive review of the inverse process, often labeled reverse remodeling. Accordingly, the goal of this review is to overview the varied settings in which clinically significant reverse remodeling has been well documented. When available, we reviewed relevant randomized, controlled clinical trials, and meta-analyses with sufficient cardiac imaging data to permit conclusions about reverse remodeling. When these types of studies were not available, relevant case-control studies and case series that employed appropriate methodology were reviewed. Regression of pathological myocardial hypertrophy, chamber shape distortions, and dysfunction occurs in a wide variety of settings. Although reverse remodeling occurs spontaneously in some etiologies of myocardial dysfunction and failure, remodeling is more commonly observed in response to medical, device-based, or surgical therapies, including β-blockers, revascularization, cardiac resynchronization therapy, and valve surgery. Indeed, reverse remodeling following pathophysiologically targeted interventions helps validate that the targeted mechanisms are propelling and/or sustaining pathological remodeling. The diverse clinical settings in which reverse remodeling has been observed demonstrates that myocardial remodeling is bidirectional and occurs across the full spectrum of myocardial disease severity, duration, and etiology. Observations in several settings suggest that recovered hearts are not truly normal despite parallel improvements at organ, tissue, and cellular level. Nevertheless, the link between reverse remodeling and improved outcomes should inspire further research to better understand the mechanisms responsible for both reverse remodeling and persistent deviations from normalcy. © 2010 Blackwell Publishing Ltd.

  17. Myocardial tissue engineering.

    Science.gov (United States)

    Jawad, Hedeer; Lyon, Alex R; Harding, Sian E; Ali, Nadire N; Boccaccini, Aldo R

    2008-01-01

    Regeneration of the infarcted myocardium after a heart attack is one of the most challenging aspects in tissue engineering. Suitable cell sources and optimized biocompatible materials must be identified. In this review, we briefly discuss the current therapeutic options available to patients with heart failure post-myocardial infarction. We describe the various strategies currently proposed to encourage myocardial regeneration, with focus on the achievements in myocardial tissue engineering (MTE). We report on the current cell types, materials and methods being investigated for developing a tissue-engineered myocardial construct. Generally, there is agreement that a 'vehicle' is required to transport cells to the infarcted heart to help myocardial repair and regeneration. Suitable cell source, biomaterials, cell environment and implantation time post-infarction remain obstacles in the field of MTE. Research is being focused on optimizing natural and synthetic biomaterials for tissue engineering. The type of cell and its origin (autologous or derived from embryonic stem cells), cell density and method of cell delivery are also being explored. The possibility is being explored that materials may not only act as a support for the delivered cell implants, but may also add value by changing cell survival, maturation or integration, or by prevention of mechanical and electrical remodelling of the failing heart.

  18. Acute Necrotizing Esophagitis Followed by Duodenal Necrosis

    Science.gov (United States)

    del Hierro, Piedad Magdalena

    2011-01-01

    Acute Necrotizing Esophagitis is an uncommon pathology, characterized by endoscopic finding of diffuse black coloration in esophageal mucosa and histological presence of necrosis in patients with upper gastrointestinal bleeding. The first case of acute necrotizing esophagitis followed by duodenal necrosis, in 81 years old woman with a positive history of Type 2 Diabetes Mellitus, Hypertension, and usual intake of Nonsteroidal Anti-inflammatory drugs, is reported. Although its etiology remains unknown, the duodenal necrosis suggests that ischemia could be the main cause given that the branches off the celiac axis provide common blood supply to the distal esophageal and duodenal tissue. The massive gastroesophagic reflux and NSAID intake could be involved. PMID:27957030

  19. ROLE OF THE MITOCHONDRION IN PROGRAMMED NECROSIS

    Directory of Open Access Journals (Sweden)

    Christopher eBaines

    2010-11-01

    Full Text Available In contrast to the programmed nature of apoptosis and autophagy, necrotic cell death has always been believed to be a random, uncontrolled process that leads to the accidental death of the cell. This dogma, however, is being challenged and the concept of necrosis also being programmed is gaining ground. In particular, mitochondria appear to play a pivotal role in the mediation of programmed necrosis. The purpose of this review, therefore, is to appraise the current concepts regarding the signaling mechanisms of programmed necrosis, with specific attention to the contribution of mitochondria to this process.

  20. Toll-like receptor 3 plays a role in myocardial infarction and ischemia/reperfusion injury.

    Science.gov (United States)

    Lu, Chen; Ren, Danyang; Wang, Xiaohui; Ha, Tuanzhu; Liu, Li; Lee, Eric J; Hu, Jing; Kalbfleisch, John; Gao, Xiang; Kao, Race; Williams, David; Li, Chuanfu

    2014-01-01

    Innate immune and inflammatory responses mediated by Toll like receptors (TLRs) have been implicated in myocardial ischemia/reperfusion (I/R) injury. This study examined the role of TLR3 in myocardial injury induced by two models, namely, myocardial infarction (MI) and I/R. First, we examined the role of TLR3 in MI. TLR3 deficient (TLR3(-/-)) and wild type (WT) mice were subjected to MI induced by permanent ligation of the left anterior descending (LAD) coronary artery for 21days. Cardiac function was measured by echocardiography. Next, we examined whether TLR3 contributes to myocardial I/R injury. TLR3(-/-) and WT mice were subjected to myocardial ischemia (45min) followed by reperfusion for up to 3days. Cardiac function and myocardial infarct size were examined. We also examined the effect of TLR3 deficiency on I/R-induced myocardial apoptosis and inflammatory cytokine production. TLR3(-/-) mice showed significant attenuation of cardiac dysfunction after MI or I/R. Myocardial infarct size and myocardial apoptosis induced by I/R injury were significantly attenuated in TLR3(-/-) mice. TLR3 deficiency increases B-cell lymphoma 2 (BCL2) levels and attenuates I/R-increased Fas, Fas ligand or CD95L (FasL), Fas-Associated protein with Death Domain (FADD), Bax and Bak levels in the myocardium. TLR3 deficiency also attenuates I/R-induced myocardial nuclear factor KappaB (NF-κB) binding activity, Tumor necrosis factor alpha (TNF-α) and Interleukin-1 beta (IL-1β) production as well as I/R-induced infiltration of neutrophils and macrophages into the myocardium. TLR3 plays an important role in myocardial injury induced by MI or I/R. The mechanisms involve activation of apoptotic signaling and NF-κB binding activity. Modulation of TLR3 may be an effective approach for ameliorating heart injury in heart attack patients. © 2013.

  1. Myocardial Lineage Development

    Science.gov (United States)

    Evans, Sylvia M.; Yelon, Deborah; Conlon, Frank L.; Kirby, Margaret L.

    2010-01-01

    The myocardium of the heart is composed of multiple highly specialized myocardial lineages, including those of the ventricular and atrial myocardium, and the specialized conduction system. Specification and maturation of each of these lineages during heart development is a highly ordered, ongoing process involving multiple signaling pathways and their intersection with transcriptional regulatory networks. Here, we attempt to summarize and compare much of what we know about specification and maturation of myocardial lineages from studies in several different vertebrate model systems. To date, most research has focused on early specification, and while there is still more to learn, less is known about factors that promote subsequent maturation of myocardial lineages required to build the functioning adult heart. PMID:21148449

  2. Biomarkers of cellular apoptosis and necrosis in donor myocardium are not predictive of primary graft dysfunction.

    Science.gov (United States)

    Szarszoi, O; Besik, J; Smetana, M; Maly, J; Urban, M; Maluskova, J; Lodererova, A; Hoskova, L; Tucanova, Z; Pirk, J; Netuka, I

    2016-06-20

    Primary graft dysfunction (PGD) is a life-threatening complication among heart transplant recipients and a major cause of early mortality. Although the pathogenesis of PGD is still unclear, ischemia/reperfusion injury has been identified as a predominant factor. Both necrosis and apoptosis contribute to the loss of cardiomyocytes during ischemia/reperfusion injury, and this loss of cells can ultimately lead to PGD. The aim of our prospective study was to find out whether cell death, necrosis and apoptosis markers present in the donor myocardium can predict PGD. The prospective study involved 64 consecutive patients who underwent orthotopic heart transplantation at our institute between September 2010 and January 2013. High-sensitive cardiac troponin T (hs-cTnT) as a marker of minor myocardial necrosis was detected from arterial blood samples before the donor's pericardium was opened. Apoptosis (caspase-3, active + pro-caspase-3, bcl-2, TUNEL) was assessed from bioptic samples taken from the right ventricle prior graft harvesting. In our study, 14 % of transplant recipients developed PGD classified according to the standardized definition proposed by the ISHLT Working Group. We did not find differences between the groups in regard to hs-cTnT serum levels. The mean hs-cTnT value for the PGD group was 57.4+/-22.9 ng/l, compared to 68.4+/-10.8 ng/l in the group without PGD. The presence and severity of apoptosis in grafted hearts did not differ between grafts without PGD and hearts that subsequently developed PGD. In conclusion, our findings did not demonstrate any association between measured myocardial cell death, necrosis or apoptosis markers in donor myocardium and PGD in allograft recipients. More detailed investigations of cell death signaling pathways in transplanted hearts are required.

  3. Effect of decellularized tissue powders on a rat model of acute myocardial infarction.

    Science.gov (United States)

    Tabuchi, Masaki; Negishi, Jun; Yamashita, Akitatsu; Higami, Tetsuya; Kishida, Akio; Funamoto, Seiichi

    2015-11-01

    Many research groups are currently investigating new treatment modalities for myocardial infarction. Numerous aspects need to be considered for the clinical application of these therapies, such as low cell integration and engraftment rates of cell injection techniques. Decellularized tissues are considered good materials for promoting regeneration of traumatic tissues. The properties of the decellularized tissues are sustained after processing to powder form. In this study, we examined the use of decellularized tissue powder in a rat model of acute myocardial infarction. The decellularized tissue powders, especially liver powder, promoted cell integration and neovascularization both in vitro and in vivo. Decellularized liver powder induced neovascularization in the infarct area, resulting in the suppression of myocardial necrosis. The results of this study suggest that decellularized liver powder has good potential for application as a blood supply material for the treatment of myocardial infarction. Copyright © 2015 Elsevier B.V. All rights reserved.

  4. Measuring myocardial perfusion

    DEFF Research Database (Denmark)

    Qayyum, A A; Kastrup, J

    2015-01-01

    Recently, focus has changed from anatomical assessment of coronary arteries towards functional testing to evaluate the effect of stenosis on the myocardium before intervention. Besides positron-emission tomography (PET), cardiac MRI (CMR), and cardiac CT are able to measure myocardial perfusion......-known and is used in routine clinical practice. However, PET uses radioactive tracers and has a lower spatial resolution compared to CMR and CT. CMR and CT are emerging techniques in the field of myocardial perfusion imaging. CMR uses magnetic resonance to obtain images, whereas CT uses x-rays during first...

  5. Regional left ventricular myocardial contractility and stress in a finite element model of posterobasal myocardial infarction.

    Science.gov (United States)

    Wenk, Jonathan F; Sun, Kay; Zhang, Zhihong; Soleimani, Mehrdad; Ge, Liang; Saloner, David; Wallace, Arthur W; Ratcliffe, Mark B; Guccione, Julius M

    2011-04-01

    Recently, a noninvasive method for determining regional myocardial contractility, using an animal-specific finite element (FE) model-based optimization, was developed to study a sheep with anteroapical infarction (Sun et al., 2009, "A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm," ASME J. Biomech. Eng., 131(11), p. 111001). Using the methodology developed in the previous study (Sun et al., 2009, "A Computationally Efficient Formal Optimization of Regional Myocardial Contractility in a Sheep With Left Ventricular Aneurysm," ASME J. Biomech. Eng., 131(11), p. 111001), which incorporates tagged magnetic resonance images, three-dimensional myocardial strains, left ventricular (LV) volumes, and LV cardiac catheterization pressures, the regional myocardial contractility and stress distribution of a sheep with posterobasal infarction were investigated. Active material parameters in the noninfarcted border zone (BZ) myocardium adjacent to the infarct (T(max_B)), in the myocardium remote from the infarct (T(max_R)), and in the infarct (T(max_I)) were estimated by minimizing the errors between FE model-predicted and experimentally measured systolic strains and LV volumes using the previously developed optimization scheme. The optimized T(max_B) was found to be significantly depressed relative to T(max_R), while T(max_I) was found to be zero. The myofiber stress in the BZ was found to be elevated, relative to the remote region. This could cause further damage to the contracting myocytes, leading to heart failure.

  6. [Antagonistic effect and mechanism of Rosuvastatin on myocardial apoptosis in rats with acute myocardial infarction].

    Science.gov (United States)

    Song, Zhanchun; Bai, Jinghui; Wang, Qi; Chen, Liang; Guo, Qunping; Zhang, Di

    2015-12-01

    To investigate the protective effect of Rosuvastatin on myocardial cells in rats with acute myocardial infarction and its possible mechanism. Rats were randomly assigned to four groups: Control group, Sham group, AMI and Rosuvastatin group. The levels of lactate dehydrogenase (LDH) and creatine jubase (CK), the vitality of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were detected by assay kits and the levels of C-reactive protein (CRP), tumor necrosis factor (TNF) alpha and interleukin (IL)-6 expression were detected by enzyme linked immunosorbent assay (ELISA). TTC/Evans blue staining was used to determine the relative myocardial infarction area, HE staining was used to detect pathologic changes and myocardial apoptosis was detected by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL). What's more, Western blot was used to detect the protein expression of B-cell lymphoma-2 (Bcl-2), Bax, cleaved-Caspase-3, Rock1, Rock2, I-κB and NF-κBp65. The model of acute myocardial infarction rats was established. Compared with Sham group, the myocardial pathological changes were more severe, and the apoptosis number, the production of inflammatory factors and oxidative damage were significantly increased in AMI group. Compared with AMI group, the relative area of infarction myocardium (43% ± 4% vs 31% ± 8%, P=0.004 3) was dramatically reduced, the levels of LDH (2 545.45 ± 613.67 U/L vs 1 573.43 ± 373.72 U/L, P=0.02) and CK (7.49 ± 1.75 U/ml vs 4.42 ± 1.28 U/ml, P=0.04) in serum were significantly lower (Pmyocardial pathological damage degree was relieved, the apoptosis number (41% ± 8% vs 23% ± 6%, P=0.014 7) was significantly decreased, the expression of Bax (1.17 ± 0.10 vs 0.57 ± 0.08, P=0.003) and cleaved-Caspase-3 (1.31 ± 0.07 vs 0.70 ± 0.01, P=0.004) were dramatically reduced, and the expression of Bcl-2 (0.19 ± 0.01 vs 0.32 ± 0.01, P=0.003) was enhanced in Rosuvastatin group. Furthermore, the production of

  7. Tissue Doppler imaging differentiates transmural from nontransmural acute myocardial infarction after reperfusion therapy.

    Science.gov (United States)

    Derumeaux, G; Loufoua, J; Pontier, G; Cribier, A; Ovize, M

    2001-01-30

    The evaluation of transmural extent of necrosis after acute myocardial infarction remains a major problem in clinical practice. We sought to determine whether color M-mode tissue Doppler imaging (TDI) could differentiate transmural from nontransmural myocardial infarction. Twenty-one anesthetized open-chest dogs underwent 90 or 120 minutes of left anterior descending coronary artery occlusion followed by 180 minutes of reperfusion. The transmural extension of infarct was measured by triphenyltetrazolium chloride (TTC) staining. Segment shortening in the endocardium and epicardium of the anterior and posterior walls was assessed by sonomicrometry. Regional myocardial blood flow was measured by radioactive microspheres. TDI was obtained from an epicardial short-axis view. We calculated systolic and diastolic velocities within the endocardium and epicardium of myocardial walls and the subsequent myocardial velocity gradient (MVG). TTC staining could identify 2 groups according to the transmural extent of necrosis: 15 dogs had a nontransmural (NT) necrosis (42+/-3% of wall thickness), and 6 dogs developed a transmural (T) infarct (81+/-4% of wall thickness). In both groups, ischemia resulted in a significant and similar reduction in endocardial and epicardial velocities, with a resulting low systolic MVG in the anterior wall (0.10+/-0.07 in NT and 0.10+/-0.08 s(-1) in T). At 60 minutes of reperfusion, systolic MVG failed to change significantly in the transmural group (-0.20+/-0.09 s(-1)). In contrast, it increased significantly after reflow in the NT group compared with ischemic values (-0.99+/-0.20 versus 0.10+/-0.07 s(-1), P:transmural from nontransmural myocardial infarction early after reperfusion.

  8. Pregnancy associated plasma protein A, a novel, quick, and sensitive marker in ST-elevation myocardial infarction

    DEFF Research Database (Denmark)

    Iversen, Kasper K; Teisner, Ane S; Teisner, Børge

    2008-01-01

    Traditional biomarkers in acute coronary syndromes reflect myocardial necrosis but not the underlying arteriosclerotic disease. Pregnancy-associated plasma protein A (PAPP-A) is a new biomarker in acute coronary syndromes that detects vulnerable plaques in arteriosclerotic disease and identifies...

  9. Myocardial ultrasonic backscatter in hypertension: relation to aldosterone and endothelin.

    Science.gov (United States)

    Kozàkovà, Michaela; Buralli, Simona; Palombo, Carlo; Bernini, Giampaolo; Moretti, Angelica; Favilla, Stefania; Taddei, Stefano; Salvetti, Antonio

    2003-02-01

    A disproportionate accumulation of fibrillar collagen is a characteristic feature of hypertensive heart disease, but the extent of myocardial fibrosis may differ in different models of hypertension. In experimental studies, aldosterone and endothelins emerge as important determinants of myocardial fibrosis. Changes in myocardial extracellular matrix and collagen deposition can be estimated noninvasively by analysis of the ultrasonic backscatter signal, which arises from tissue heterogeneity within the myocardium and describes myocardial texture. This study was designed to investigate the relations between myocardial integrated backscatter and circulating aldosterone and immunoreactive endothelin in human hypertension. The study population consisted of 56 subjects: 14 healthy normotensive volunteers and 42 hypertensive patients (14 with primary aldosteronism, 7 with renovascular hypertension, and 21 with essential hypertension). The patients with essential and secondary hypertension were matched for age, gender, body mass index, and blood pressure. Myocardial integrated backscatter at diastole was 19.8+/-2.0 and 20.8+/-2.9 decibels in normotensive control subjects and patients with essential hypertension and significantly higher in patients with primary aldosteronism (27.4+/-3.8 decibels, P<0.01) and renovascular hypertension (26.8+/-4.8 decibels, P<0.01). In the population as a whole, as well as in the hypertensive subpopulation, myocardial integrated backscatter was directly related to plasma aldosterone (r=0.73 and 0.71, P<0.01 for both) and immunoreactive endothelin (r=0.60 and 0.56, P<0.01 for both). The data of this study suggest that in human hypertension, circulating aldosterone and immunoreactive endothelin may induce alterations in left ventricular myocardial texture, possibly related to increased myocardial collagen content.

  10. [Transient apical dysfunction syndrome (Tako-Tsubo) simulating acute myocardial infarction].

    Science.gov (United States)

    Carrero Lérida, M J; Mariscal Cerrato, M C; Dávila Arias, C; López Ruiz, A; Caballero Güeto, J

    2011-01-01

    Transient apical dysfunction syndrome (TADS) is frequently misdiagnosed as an acute coronary syndrome (ACS). It is characterized by electrocardiographic alterations and elevated myocardial necrosis markers, accompanied by hypokinesia, akinesia or anteroapical dyskinesia, in absence of significant coronary disorders. It generally resolves in days or weeks with individualized support measures. We present the case of a female patient referred to our service for a myocardial perfusion imaging study due to a history suggestive of an acute coronary syndrome after a stressful event. Copyright © 2010 Elsevier España, S.L. y SEMNIM. All rights reserved.

  11. Bilateral acute retinal necrosis after herpetic meningitis

    Directory of Open Access Journals (Sweden)

    Katsura T

    2012-04-01

    Full Text Available Keisho Hirota1,2, Masayuki Akimoto1,3, Toshiaki Katsura21Department of Ophthalmology, Kyoto Medical Center, National Hospital Organization, 2Internal Medicine, Kyoto Medical Center, 3Clinical Research Center, Kyoto Medical Center, Kyoto, JapanPurpose: The report of a case of bilateral acute retinal necrosis after herpetic meningitis.Case report: A 47-year-old man was admitted with the chief complaint of persistent high fever and transient loss of consciousness. Although his general condition improved after intravenous acyclovir administration, the patient presented with visual loss in both eyes 4 days after admission. Visual acuity in his right eye was 20/200 and his left eye had light perception alone. Both eyes showed panretinal arteritis diagnosed as acute retinal necrosis. Panretinal photocoagulation was performed for both eyes. Progression of retinal detachment was prevented in both eyes; however, visual acuity of the left eye was totally lost because of neovascular glaucoma. Visual acuity of the right eye recovered to 20/20.Conclusion: Although cases of bilateral acute retinal necrosis have been reported after herpetic encephalitis, this condition is rare after herpetic meningitis. Prophylactic acyclovir therapy and early panretinal photocoagulation may prevent retinal detachment and improve the prognosis. Neurologists and ophthalmologists should be aware that not only herpetic encephalitis but also herpetic meningitis can lead to acute retinal necrosis within a very short interval.Keywords: acute retinal necrosis, herpetic meningitis, herpes simplex, varicella zoster virus

  12. Hyperglycemia Increases Susceptibility to Ischemic Necrosis

    Directory of Open Access Journals (Sweden)

    D. Lévigne

    2013-01-01

    Full Text Available Diabetic patients are at risk for spontaneous foot ulcers, chronic wounds, infections, and tissue necrosis. Current theories suggest that the development and progression of diabetic foot ulcers are mainly caused by arteriosclerosis and peripheral neuropathy. Tissue necrosis plays a primordial role in the progression of diabetic foot ulcers but the underlying mechanisms are poorly understood. The aim of the present study was to investigate the effects of hyperglycemia per se on the susceptibility of ischemic tissue to necrosis, using a critical ischemic hind limb animal model. We inflicted the same degree of ischemia in both euglycemic and streptozotocin-induced hyperglycemic rats by resecting the external iliac, the femoral, and the saphenous arteries. Postoperative laser Doppler flowmetry of the ischemic feet showed the same degree of reduction in skin perfusion in both hyperglycemic and euglycemic animals. Nevertheless, we found a significantly higher rate of limb necrosis in hyperglycemic rats compared to euglycemic rats (71% versus 29%, resp.. In this study, we revealed that hyperglycemia per se increases the susceptibility to limb necrosis in ischemic conditions. Our results may help to better understand the physiopathology of progressive diabetic wounds and underline the importance of strict glycemic control in patients with critical limb ischemia.

  13. Extrapancreatic necrosis without pancreatic parenchymal necrosis : a separate entity in necrotising pancreatitis?

    NARCIS (Netherlands)

    Bakker, Olaf J.; van Santvoort, Hjalmar; Besselink, Marc G. H.; Boermeester, Marja A.; van Eijck, Casper; Dejong, Kees; van Goor, Harry; Hofker, Hendrik; Ali, Usama Ahmed; Gooszen, Hein G.; Bollen, Thomas L.

    2013-01-01

    Objective In the revised Atlanta classification of acute pancreatitis, the term necrotising pancreatitis also refers to patients with only extrapancreatic fat necrosis without pancreatic parenchymal necrosis (EXPN), as determined on contrast-enhanced CT (CECT). Patients with EXPN are thought to have

  14. Extrapancreatic necrosis without pancreatic parenchymal necrosis: a separate entity in necrotising pancreatitis?

    NARCIS (Netherlands)

    Bakker, O.J.; Santvoort, H. van; Besselink, M.G.; Boermeester, M.A.; Eijck, C. van; Dejong, K.; Goor, H. van; Hofker, S.; Ali, U. Ahmed; Gooszen, H.G.; Bollen, T.L.; Study, G.

    2013-01-01

    OBJECTIVE: In the revised Atlanta classification of acute pancreatitis, the term necrotising pancreatitis also refers to patients with only extrapancreatic fat necrosis without pancreatic parenchymal necrosis (EXPN), as determined on contrast-enhanced CT (CECT). Patients with EXPN are thought to

  15. Tracheal stoma necrosis: a case repor

    Directory of Open Access Journals (Sweden)

    Pak S

    2017-04-01

    Full Text Available Acute tracheal dilatation, due to an overinflated cuff, has been reported early in the course of mechanical ventilation through an endotracheal tube. Tracheal stoma necrosis is a rare complication, but such can accompany acute tracheal dilation. Herein, we report a case of tracheal necrosis 9 days following tracheostomy placement in a 71-year old woman associated with overinflation of the tracheal tube cuff. This case report aims to 1 add to the scant body of knowledge about the diagnosis and management for the patients with tracheal stoma necrosis and 2 raise awareness for error-traps in interpreting diagnostic images, specifically satisfaction of search error, inattentional blindness error, and alliterative error.

  16. [Bonsai induced acute myocardial infarction].

    Science.gov (United States)

    Ayhan, Hüseyin; Aslan, Abdullah Nabi; Süygün, Hakan; Durmaz, Tahir

    2014-09-01

    Incidences of drug abuse and cannabis have increased in young adults, recently. Cannabis induced myocardial infarction has rarely been reported in these people. There is no any literature about a synthetic cannabinoid, being recently most popular Bonsai, to cause myocardial infarction. In this case report we presented a 33-year-old male patient who developed acute myocardial infarction after taking high doses of Bonsai.

  17. Anti-VEGF antibodies mitigate the development of radiation necrosis in mouse brain

    Science.gov (United States)

    Jiang, Xiaoyu; Engelbach, John A; Yuan, Liya; Cates, Jeremy; Gao, Feng; Drzymala, Robert E; Hallahan, Dennis E; Rich, Keith M; Schmidt, Robert E; Ackerman, Joseph JH; Garbow, Joel R

    2014-01-01

    Purpose To quantify the effectiveness of anti-VEGF antibodies (bevacizumab and B20-4.1.1) as mitigators of radiation-induced, CNS (brain) necrosis in a mouse model. Experimental Design Cohorts of mice were irradiated with single-fraction 50- or 60-Gy doses of radiation targeted to the left hemisphere (brain) using the Leksell Perfexion Gamma Knife. The onset and progression of radiation necrosis were monitored longitudinally by in vivo, small-animal MRI, beginning four weeks post-irradiation. MRI-derived necrotic volumes for antibody (Ab)-treated and untreated mice were compared. MRI results were supported by correlative histology. Results Hematoxylin and eosin stained sections of brains from irradiated, non-Ab-treated mice confirmed profound tissue damage, including regions of fibrinoid vascular necrosis, vascular telangiectasia, hemorrhage, loss of neurons, and edema. Treatment with the murine anti-VEGF antibody B20-4.1.1 mitigated radiation-induced changes in an extraordinary, highly statistically-significant manner. The development of radiation necrosis in mice under treatment with bevacizumab (a humanized anti-VEGF antibody) was intermediate between that for B20-4.1.1-treated and non-Ab-treated animals. MRI findings were validated by histologic assessment, which confirmed that anti-VEGF-antibody treatment dramatically reduced late-onset necrosis in irradiated brain. Conclusions The single-hemispheric-irradiation mouse model, with longitudinal MRI monitoring, provides a powerful platform for studying the onset and progression of radiation necrosis and for developing and testing new therapies. The observation that anti-VEGF antibodies are effective mitigants of necrosis in our mouse model will enable a wide variety of studies aimed at dose optimization and timing and mechanism of action with direct relevance to ongoing clinical trials of bevacizumab as a treatment for radiation necrosis. PMID:24647570

  18. Tramadol Alleviates Myocardial Injury Induced by Acute Hindlimb Ischemia Reperfusion in Rats

    Energy Technology Data Exchange (ETDEWEB)

    Takhtfooladi, Hamed Ashrafzadeh; Asl, Adel Haghighi Khiabanian [Department of Pathobiology, Science and Research Branch, Islamic Azad University, Tehran (Iran, Islamic Republic of); Shahzamani, Mehran [Department of Cardiovascular Surgery, Isfahan University of Medical Sciences, Tehran (Iran, Islamic Republic of); Takhtfooladi, Mohammad Ashrafzadeh, E-mail: dr-ashrafzadeh@yahoo.com [Young Researchers and Elites Club, Science and Research Branch, Islamic Azad University, Tehran (Iran, Islamic Republic of); Allahverdi, Amin [Department of Surgery, Science and Research Branch, Islamic Azad University, Tehran (Iran, Islamic Republic of); Khansari, Mohammadreza [Department of Physiology, Science and Research Branch, Islamic Azad University, Tehran (Iran, Islamic Republic of)

    2015-08-15

    Organ injury occurs not only during periods of ischemia but also during reperfusion. It is known that ischemia reperfusion (IR) causes both remote organ and local injuries. This study evaluated the effects of tramadol on the heart as a remote organ after acute hindlimb IR. Thirty healthy mature male Wistar rats were allocated randomly into three groups: Group I (sham), Group II (IR), and Group III (IR + tramadol). Ischemia was induced in anesthetized rats by left femoral artery clamping for 3 h, followed by 3 h of reperfusion. Tramadol (20 mg/kg, intravenous) was administered immediately prior to reperfusion. At the end of the reperfusion, animals were euthanized, and hearts were harvested for histological and biochemical examination. The levels of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were higher in Groups I and III than those in Group II (p < 0.05). In comparison with other groups, tissue malondialdehyde (MDA) levels in Group II were significantly increased (p < 0.05), and this increase was prevented by tramadol. Histopathological changes, including microscopic bleeding, edema, neutrophil infiltration, and necrosis, were scored. The total injuryscore in Group III was significantly decreased (p < 0.05) compared with Group II. From the histological and biochemical perspectives, treatment with tramadol alleviated the myocardial injuries induced by skeletal muscle IR in this experimental model.

  19. Myocardial Calcinosis a Case Report

    Directory of Open Access Journals (Sweden)

    Naciye Özeren

    2014-07-01

    Full Text Available Myocardial calcification (myocardial calcinosis is a rare condition in the literature. Meta-static or dystrophic calcification can be seen in two types. Chronic renal failure, hemodialysis, sec-ondary hyperparathyroidism, hypercalcemia, the blood calcium level as high phenomena that are associated with metastatic calcification. In dystrophic calcification, normal blood calcium levels, normal kidney functions, normal coronary artery are observed. Myocardial calcification as a result of congestive heart failure, fatal arrhythmias, heart valve dysfunction, myocardial infarction may occur. Case: 35 years old Syrian male. In the civil war in Syria bombing injured as a result, nearly two months in various hospitals and treated for renal failure developing died. Evaluated within the scope of forensic autopsy has been decided. At autopsy; scar tissue due to previous operations, in-ternal examination in both kidneys logy was found the abse formation. Microscopy: Lobular pneu-monia, atelectasis, edema in the lung. Retroperitoneal active chronic inflammation, inflammatory exudate, bleeding, abscesses and abscess wall was detected. The coronary arteries were normal. myocardial more pericardial and myocardial tissue including tissue calcification was found in the common. Renal failure caused by a lack of calcium in blood as myocardial calcinosis was evaluat-ed. These deposits often may actually on the whole body, generally, vessels, kidneys, lungs, interstitial tissues of gastric mucosa holds. Pericardium and in myocardial tissue is extremely rare, interesting case is presented here. Key Words: Hypercalcemia, Calcification, Myocardial.

  20. Role of cytokines in myocardial ischemia and reperfusion

    Directory of Open Access Journals (Sweden)

    H. S. Sharma

    1997-01-01

    Full Text Available Mediators of myocardial inflammation, predominantly cytokines, have for many years been implicated in the healing processes after infarction. In recent years, however, more attention has been paid to the possibility that the inflammation may result in deleterious complications for myocardial infarction. The proinflammatory cytokines may mediate myocardial dysfunction associated with myocardial infarction, severe congestive heart failure, and sepsis. A growing body of literature suggests that inflammatory mediators could play a crucial role in ischemia–reperfusion injury. Furthermore, ischemia–reperfusion not only results in the local transcriptional and translational upregulation of cytokines but also leads to tissue infiltration by inflammatory cells. These inflammatory cells are a ready source of a variety of cytokines which could be lethal for the cardiomyocytes. At the cellular level it has been shown that hypoxia causes a series of well documented changes in cardiomyocytes that includes loss of contractility, changes in lipid metabolism and subsequent irreversible cell membrane damage leading to cell death. For instance, hypoxic cardiomyocytes produce interleukin-6 (IL-6 which could contribute to the myocardial dysfunction observed in ischemia reperfusion injury. Ischemia followed by reperfusion induces a number of other multi-potent cytokines, such as IL-1, IL-8, tumor necrosis factor-α (TNF-α, transforming growth factor-β1 (TGF-β1 as well as an angiogenic cytokine/ growth factor, vascular endothelial growth factor (VEGF, in the heart. Intrestingly, these multipotent cytokines (e.g. TNF-α may induce an adaptive cytoprotective response in the reperfused myocardium. In this review, we have included a number of cytokines that may contribute to ventricular dysfunction and/or to the cytoprotective and adaptive changes in the reperfused heart.

  1. Avascular necrosis ofbone following renal transplantation

    African Journals Online (AJOL)

    3. Stanl TE, Marchioro TL, Porter KA, Moore CA, Rifkind D, . Waddell \\'\\'R. Renal homotransplantation: late function and com- plications. Ann [m.em Med 1964: 61: 470-477. 4. Pauon PR, Pfaff \\'\\TW. Aseptic bone necrosis after renal transplan- tation. Surgery 1987; 103: 63-69. 5. Huffer WE, Kuzela D, Popovrzer MNi, Stanl TE.

  2. Myocardial contrast echocardiography in mice: Technical and physiological aspects.

    Science.gov (United States)

    Verkaik, Melissa; van Poelgeest, Erik; Kwekkeboom, Rick F J; Ter Wee, Piet M; van den Brom, Charissa E; Vervloet, Marc G; Eringa, Etto C

    2017-11-03

    Myocardial contrast echocardiography (MCE) offers the opportunity to study myocardial perfusion defects in mice in detail. The value of MCE compared to SPECT, PET and CT consists of high spatial resolution, the possibility of quantification of blood volume and relatively low costs. Nevertheless, a number of technical and physiological aspects should be considered to ensure reproducibility among research groups. The aim of this overview is to describe technical aspects of MCE and the physiological parameters that influence myocardial perfusion data obtained with this technique. First, technical aspects of MCE discussed in this technical review are logarithmic compression of ultrasound data by ultrasound systems, saturation of the contrast signal and acquisition of images during different phases of the cardiac cycle. Second, physiological aspects of myocardial perfusion that are affected by the experimental design are discussed, including the anesthesia regimen, systemic cardiovascular effects of vasoactive agents used and fluctuations in body temperature that alter myocardial perfusion. When these technical and physiological aspects of MCE are taken into account and adequately standardized, MCE is an easily accessible technique for mice that can be used to study the control of myocardial perfusion by a wide range of factors. Copyright © 2017, American Journal of Physiology-Heart and Circulatory Physiology.

  3. Reciprocal ST segment changes in acute inferior myocardial infarction: Clinical, hemodynamic and angiographic implications

    Directory of Open Access Journals (Sweden)

    Hatem El Atroush

    2012-09-01

    Conclusion: The significance of reciprocal ST depression on the electrocardiogram during the course of inferior MI remains uncertain, opinion is divided as to whether it is a benign electrical phenomenon or a sign of a greater myocardial necrosis and more frequent left coronary artery disease, from our study we support the latter opinion. This simple ECG finding may be used to differentiate high risk patients for a more aggressive approach.

  4. Myocyte necrosis underlies progressive myocardial dystrophy in mouse dsg2-related arrhythmogenic right ventricular cardiomyopathy

    NARCIS (Netherlands)

    Pilichou, K.; Remme, C.A.; Basso, C.; Campian, M.E.; Rizzo, S.; Barnett, P.; Scicluna, B.P.; Bauce, B.; van den Hoff, M.J.B.; de Bakker, J.M.T.; Tan, H.L.; Valente, M.; Nava, A.; Wilde, A.A.M.; Moorman, A.F.M.; Thiene, G.; Bezzina, C.R.

    2009-01-01

    Mutations in the cardiac desmosomal protein desmoglein-2 (DSG2) are associated with arrhythmogenic right ventricular cardiomyopathy (ARVC). We studied the explanted heart of a proband carrying the DSG2-N266S mutation as well as transgenic mice (Tg-NS) with cardiac overexpression of the mouse

  5. GSAO-based molecular targeting of myocardial necrosis in acute ischemic insult

    NARCIS (Netherlands)

    Hans De Haas, H.J.; Zandbergen, H.R.; Tahara, N.; Petrov, A.D.; Slart, R.H.J.A.; Boersma, H.H.; Reutelingsperger, C.P.; Narula, J.

    2013-01-01

    Purpose: GSAO has an arsenic group that binds to dithiols on various intracellular proteins that are upregulated during cellular stress including HSP90, PDI, which plays a role in the unfolded protein response and apoptosis, and Beclin-1, which drives autophagy. Extracellular dithiols are uncommon.

  6. A computational and functional study elicits the ameliorating effect of the Chinese herbal formula Huo Luo Xiao Ling Dan on experimental ischemia-induced myocardial injury in rats via inhibition of apoptosis

    Directory of Open Access Journals (Sweden)

    Han XD

    2015-02-01

    Full Text Available Xiang-Dong Han,1 Zhi-Wei Zhou,2–4 Wei Yang,1 Hang-Cheng Ye,1 Ying-Zi Xu,1 Yun-Feng Huang,1 Tong Zhang,1 Shu-Feng Zhou2 1School of Pharmacy, Shanghai University of Traditional Chinese Medicine, Shanghai, People’s Republic of China; 2Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL, USA; 3Guizhou Provincial Key Laboratory for Regenerative Medicine, 4Stem Cell and Tissue Engineering Research Center and Sino-US Joint Laboratory for Medical Sciences, Guizhou Medical University, Guiyang, People’s Republic of China Abstract: Ischemic heart disease (IHD is the leading cause of death worldwide and remains a major life-threatening factor in humans. Apoptosis has been implicated in the pathogenesis of IHD. The Chinese herbal formula Huo Luo Xiao Ling Dan (HLXLD, one of the commonly used Chinese herbal formulas, consists of Salviae miltiorrhizae, Angelica sinensis, Gummi olibanum, and Commiphora myrrha, with a wide spectrum of pharmacological activity. However, the mechanism of action and molecular targets of HLXLD in the treatment of IHD are unclear. This study aimed to computationally predict the molecular interactions between the major active components of HLXLD and key regulators of apoptosis and then examine the effect of HLXLD on coronary artery ligation-induced acute myocardial ischemia in rats. The molecular interactions between the major active components of HLXLD, including ferulic acid, ligustilide, succinic acid, vanillic acid, tanshinone IIA, tanshinone IIB, danshensu, salvianolic acid A, salvianolic acid C, protocatechuic aldehyde, and β-boswellic acid and human protein molecules including B cell lymphoma-extra large (Bcl-xl, B cell lymphoma 2 antagonist/killer 1 (Bak1, B cell lymphoma 2 (Bcl-2, procaspase 3, and caspase 9 with regard to hydrogen bond formation, charge interaction, and π-π stacking using Discovery Studio® program 3.1. The 12 HLXLD components were predicted by

  7. [Effect of electroacupuncture on morphological changes and myocardial metabolism in rats undergoing simulated weightlessness].

    Science.gov (United States)

    Zhang, He; Ji, Bo; Wang, De-sheng; Song, Yan; Xu, Yong-si; Zhang, Ping; Liu, Ya-li; Zhao, Bai-xiao

    2014-12-01

    To observe the effect of electroacupuncture (EA) stimulation of "Neiguan" (PC 6) and "Sanyinjiao" (SP 6) on morphological changes, myocardial energy metabolism in rats undergoing simulated weightlessness. A total of 40 male Wistar rats were randomly divided into normal control, weightlessness model, Neiguan (PC 6) and Sanyinjiao (SP 6) groups (10 rats/group). EA was applied to PC 6 and SP 6 acupoints for 30 min, once every other day. The morphological changes were observed by light microscopy after H. E. staining. Lactate dehydrogenase (LDH), succinate dehydrogenase (SDH) and ATPase activities in the left ventricular myocardium were measured by colorimetry. In weightlessness rats, myocardial pathological changes as loose arrangement, breakage and lytic necrosis of myocardial fibers were found, these changes were obviously improved in rats of both PC 6 and SP 6 groups. Compared with the control group, the ATPase activity was significantly decreased, while the LDH activity was significantly increased in the model group (Pchanges were found in myocardial SDH activity after modeling and EA of the two acupoints (P>0. 05). EA intervention has functions in up-regulating ATP activity and suppressing the myocardial LDH activity in weightlessness rats, which may be related to its effect in improving myocardial pathological changes.

  8. Multiparametric approach to diagnosis of non-Q-wave acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Carpeggiani, C.; L' Abbate, A.; Marzullo, P.; Buzzigoli, G.; Parodi, O.; Sambuceti, G.; Marcassa, C.; Boni, C.; Moscarelli, E.; Distante, A.

    1989-02-15

    The present study investigated whether the lack of enzyme increase is reason enough to exclude necrosis in patients with ischemic heart disease who develop electrocardiographic sustained ST-T changes in the absence of Q waves. In 15 consecutive patients with angina who developed sustained ST-T changes during hospitalization, the presence of myocardial necrosis was investigated by a prospective multiparametric approach. Serum enzymes and myoglobin, pyrophosphate uptake, 2-dimensional echocardiography, perfusion scintigraphy, left ventriculography and coronary angiography were evaluated. According to creatine kinase and creatine kinase-MB peak at twice the upper normal value, the diagnosis of acute myocardial infarction applied only to 40% of patients. However, myoglobin was positive in 80% and a perfusion defect could be documented by an electrocardiographic gated microsphere technique in 100% of patients. The positivity of myoglobin increased to 100% and of creatine kinase and creatine kinase-MB to 87 and 60%, respectively, when a peak value twice the individual lowest value was considered for positivity. The 100% presence of perfusion defects associated with the high prevalence of both positive pyrophosphate uptake (87%) and regional dyssynergies (87 and 73%, respectively, by left ventriculography and echocardiography) strongly suggest that sustained (greater than or equal to 7 days) ST-T changes in this population were indicative of myocardial necrosis. Thus, by conventional enzymatic approach, diagnosis of non-Q-wave infarction can be missed in a sizable number of patients and present important clinical implications.

  9. A prospective study of the incidence of asymptomatic pulp necrosis following crown preparation.

    Science.gov (United States)

    Kontakiotis, E G; Filippatos, C G; Stefopoulos, S; Tzanetakis, G N

    2015-06-01

    To determine the incidence of asymptomatic pulp necrosis following crown preparation as well as the positive predictive value of the electric pulp testing. A total of 120 teeth with healthy pulps scheduled to receive fixed crowns (experimental teeth) were included. Teeth were divided into two groups according to the preoperative crown condition (intact teeth and teeth with preoperative caries, restorations or crowns) and into four groups according to tooth type (maxillary anterior teeth, maxillary posterior teeth, mandibular anterior teeth and mandibular posterior teeth). Experimental and control teeth were submitted to electric pulp testing on three different occasions before treatment commencement (stage 0), at the impression making session (stage 1) and just before the final cementation of the crown (stage 2). Teeth that were considered to contain necrotic pulps were submitted to root canal treatment. Upon access, absence of bleeding was considered as a confirmation of pulp necrosis. Data were analysed using bivariate (chi-square) and multivariate analysis (logistic regression). All reported probability values (P-values) were based on two-sided tests and compared to a significance level of 5%. The overall incidence of pulp necrosis was 9%. Intact teeth had a significantly lower incidence of pulp necrosis (5%) compared with preoperatively structurally compromised teeth (13%) [(OR: 9.113, P = 0.035)]. No significant differences were found amongst the four groups with regard to tooth type (P = 0.923). The positive predictive value of the electric pulp testing was 1.00. The incidence of asymptomatic pulp necrosis of teeth following crown preparation is noteworthy. The presence of preoperative caries, restorations or crowns of experimental teeth correlated with a significantly higher incidence of pulp necrosis. Electric pulp testing remains a useful diagnostic instrument for determining the pulp condition. © 2014 International Endodontic Journal. Published by

  10. Myocardial perfusion modeling using MRI

    DEFF Research Database (Denmark)

    Larsson, H B; Fritz-Hansen, T; Rostrup, Egill

    1996-01-01

    In the present study, it is shown that it is possible to quantify myocardial perfusion using magnetic resonance imaging in combination with gadolinium diethylenetriaminopentaacetic acid (Gd-DTPA). Previously, a simple model and method for measuring myocardial perfusion using an inversion recovery...

  11. Diurnal variations in myocardial metabolism

    Science.gov (United States)

    The heart is challenged by a plethora of extracellular stimuli over the course of a normal day, each of which distinctly influences myocardial contractile function. It is therefore not surprising that myocardial metabolism also oscillates in a time-of-day dependent manner. What is becoming increasin...

  12. Biphasic thallium 201 SPECT-imaging for the noninvasive diagnosis of myocardial perfusion abnormalities in a child with Kawasaki disease--a case report

    Energy Technology Data Exchange (ETDEWEB)

    Hausdorf, G.; Nienaber, C.A.; Spielman, R.P.

    1988-02-01

    The mucocutaneous lymph node syndrome (Kawasaki disease) is of increasing importance for the pediatric cardiologist, for coronary aneurysms with the potential of thrombosis and subsequent stenosis can develop in the course of the disease. The authors report a 2 1/2-year-old female child in whom, fourteen months after the acute phase of Kawasaki disease, myocardial infarction occurred. Biphasic thallium 201 SPECT-imaging using dipyridamole depicted anterior wall ischemia and inferolateral infarction. This case demonstrates that noninvasive vasodilation-redistribution thallium 201 SPECT-imaging has the potential to predict reversible myocardial perfusion defects and myocardial necrosis, even in small infants with Kawasaki disease.

  13. Invasive surgery reduces infarct size and preserves cardiac function in a porcine model of myocardial infarction

    NARCIS (Netherlands)

    van Hout, Gerardus P J; Teuben, Michel P J; Heeres, Marjolein; de Maat, Steven; de Jong, Renate; Maas, Coen; Kouwenberg, Lisanne H J A; Koenderman, Leo; van Solinge, Wouter W; de Jager, Saskia C A; Pasterkamp, Gerard; Höfer, IE

    2015-01-01

    Reperfusion injury following myocardial infarction (MI) increases infarct size (IS) and deteriorates cardiac function. Cardioprotective strategies in large animal MI models often failed in clinical trials, suggesting translational failure. Experimentally, MI is induced artificially and the effect of

  14. Long-term prognostic value of a comprehensive assessment of cardiac magnetic resonance indexes after an ST-segment elevation myocardial infarction.

    Science.gov (United States)

    Merlos, Pilar; López-Lereu, Maria P; Monmeneu, Jose V; Sanchis, Juan; Núñez, Julio; Bonanad, Clara; Valero, Ernesto; Miñana, Gema; Chaustre, Fabián; Gómez, Cristina; Oltra, Ricardo; Palacios, Lorena; Bosch, Maria J; Navarro, Vicente; Llácer, Angel; Chorro, Francisco J; Bodí, Vicente

    2013-08-01

    A variety of cardiac magnetic resonance indexes predict mid-term prognosis in ST-segment elevation myocardial infarction patients. The extent of transmural necrosis permits simple and accurate prediction of systolic recovery. However, its long-term prognostic value beyond a comprehensive clinical and cardiac magnetic resonance evaluation is unknown. We hypothesized that a simple semiquantitative assessment of the extent of transmural necrosis is the best resonance index to predict long-term outcome soon after a first ST-segment elevation myocardial infarction. One week after a first ST-segment elevation myocardial infarction we carried out a comprehensive quantification of several resonance parameters in 206 consecutive patients. A semiquantitative assessment (altered number of segments in the 17-segment model) of edema, baseline and post-dobutamine wall motion abnormalities, first pass perfusion, microvascular obstruction, and the extent of transmural necrosis was also performed. During follow-up (median 51 months), 29 patients suffered a major adverse cardiac event (8 cardiac deaths, 11 nonfatal myocardial infarctions, and 10 readmissions for heart failure). Major cardiac events were associated with more severely altered quantitative and semiquantitative resonance indexes. After a comprehensive multivariate adjustment, the extent of transmural necrosis was the only resonance index independently related to the major cardiac event rate (hazard ratio=1.34 [1.19-1.51] per each additional segment displaying>50% transmural necrosis, P<.001). A simple and non-time consuming semiquantitative analysis of the extent of transmural necrosis is the most powerful cardiac magnetic resonance index to predict long-term outcome soon after a first ST-segment elevation myocardial infarction. Copyright © 2013 Sociedad Española de Cardiología. Published by Elsevier Espana. All rights reserved.

  15. Myocardial triglycerides : magnetic resonance spectroscopy in health and diabetes

    NARCIS (Netherlands)

    Hammer, Sebastiaan

    2008-01-01

    In this thesis we focused on the functional and metabolic consequences of myocardial triglyceride (TG) accumulation in healthy subjects and in patients with diabetes mellitus. Ectopic accumulation of TGs is associated with organ dysfunction in metabolic disease in experimental animal studies. These

  16. Stem Cell Therapy for Myocardial Infarction: Are We Missing Time?

    NARCIS (Netherlands)

    ter Horst, Kasper W.

    2010-01-01

    The success of stem cell therapy in myocardial infarction (MI) is modest, and for stem cell therapy to be clinically effective fine-tuning in regard to timing, dosing, and the route of administration is required. Experimental studies suggest the existence of a temporal window of opportunity bound by

  17. Complement and Dilated Cardiomyopathy: A Role of Sublytic Terminal Complement Complex-Induced Tumor Necrosis Factor-α Synthesis in Cardiac Myocytes

    OpenAIRE

    Zwaka, Thomas P.; Manolov, Dimitar; Özdemir, Cüneyt; Marx, Nikolaus; Kaya, Ziya; Kochs, Matthias; Höher, Martin; Hombach, Vinzenz; Torzewski, Jan

    2002-01-01

    Dilated cardiomyopathy is a syndrome characterized by cardiac enlargement and impaired systolic function of the heart. Tumor necrosis factor (TNF)-α, a pleiotropic cytokine, seems to play a central role in the progression of dilated cardiomyopathy. Recent data suggest that ongoing inflammation in the myocardium may, in many cases, contribute to the development of disease. Chronic generation of autoantibodies to myocardial antigens or, in some cases, viral infection are pathobiologically invol...

  18. Serine racemase: a key player in apoptosis and necrosis

    Directory of Open Access Journals (Sweden)

    Nadia eCanu

    2014-04-01

    Full Text Available A fine balance between cell survival and cell death is required to sculpt the nervous system during development. However, an excess of cell death can occur following trauma, exposure to neurotoxins or alcohol, and some developmental and neurodegenerative diseases, such as Alzheimer’s disease (AD. N-Methyl-D-aspartate receptors (NMDARs support synaptic plasticity and survival of many neuronal populations whereas inappropriate activation may promote various forms of cell death, apoptosis and necrosis representing the two extremes of a continuum of cell death processes both in vitro and in vivo. Hence, by identifying the switches controlling pro-survival vs. apoptosis and apoptosis vs. pro-excitotoxic outcome of NMDAR stimulation, NMDAR modulators could be developed that selectively block the cell death enhancing pro-survival signaling or synaptic plasticity mediated by NMDAR. Among these modulators, a role is emerging for the enzyme serine racemase (SR that synthesizes D-serine, a key co-agonist with glutamate at NMDAR. This review summarizes the experimental evidence from in vitro neuronal cultures -- with special emphasis on cerebellar granule neurons (CGNs -- and in vivo models of neurodegeneration, where the dual role of the SR/D-serine pathway as a master regulator of apoptosis and the apoptosis-necrosis shift will be discussed.

  19. Risk factors for tracheal necrosis after total pharyngolaryngectomy.

    Science.gov (United States)

    Fujiki, Masahide; Miyamoto, Shimpei; Sakuraba, Minoru; Nagamatsu, Shogo; Hayashi, Ryuichi

    2015-08-01

    Tracheal necrosis is a severe complication of total pharyngolaryngectomy (TPL). The purpose of this retrospective study was to identify risk factors for tracheal necrosis after TPL. We performed a retrospective chart review of 177 patients who had undergone TPL. The preoperative, operative, and postoperative variables were examined, and possible risk factors for tracheal necrosis were subjected to univariate analysis and multivariate logistic regression. Tracheal necrosis occurred in 35 patients (19.8%), and tracheoesophageal fistula subsequently developed in 3 of these patients. Multivariate logistic regression analysis identified total esophagectomy and diabetes mellitus as significant risk factors for tracheal necrosis after TPL. The findings of this study will be useful for assessing the risk of tracheal necrosis after TPL. In patients at high risk for tracheal necrosis, efforts should be made to preserve the tracheal circulation and to prevent life-threatening sequelae if tracheal necrosis occurs. © 2014 Wiley Periodicals, Inc.

  20. Regulated necrosis and its implications in toxicology.

    Science.gov (United States)

    Aki, Toshihiko; Funakoshi, Takeshi; Uemura, Koichi

    2015-07-03

    Recent research developments have revealed that caspase-dependent apoptosis is not the sole form of regulated cell death. Caspase-independent, but genetically regulated, forms of cell death include pyroptosis, necroptosis, parthanatos, and the recently discovered ferroptosis and autosis. Importantly, regulated necrosis can be modulated by small molecule inhibitors/activators, confirming the cell autonomous mechanism of these forms of cell death. The success of small molecule-mediated manipulation of regulated necrosis has produced great changes in the field of cell death research, and has also brought about significant changes in the fields of pharmacology as well as toxicology. In this review, we intend to summarize the modes of regulated cell death other than apoptosis, and discuss their implications in toxicology. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

  1. A Case of Unresectable Rectal Necrosis

    Directory of Open Access Journals (Sweden)

    Mohammed Nassif

    2011-01-01

    Full Text Available Introduction. Necrosis of the rectum is an uncommon finding due to abundant collateral vasculature. Its management remains challenging, without clear consensus in the literature. Case Report. We describe a case of a 53-year-old woman with multiple medical comorbidities that presented in septic shock and hematochezia. Colonoscopy revealed ischemic colitis. Conservative management was instituted. At two weeks, she presented evidence of peritonitis. Exploratory laparotomy revealed extensive necrosis of the left colon and rectum. Due to dense inflammation, resection was deemed unsafe. Therefore, a transverse ostomy with mucosal fistula was preformed. Multiple drains were left in place. The patient healed uneventfully. Conclusion. This case illustrates that, if extensive dissection of the distal colon and rectum is unsafe due to the patient's critical condition or technical feasibility, then a diverting ostomy of the proximal viable bowel along with a mucus fistula and good drainage of the abdomen represents an acceptable alternative.

  2. Endoscopic management of pancreatic pseudocysts and necrosis.

    Science.gov (United States)

    Law, Ryan; Baron, Todd H

    2015-02-01

    Over the last several years, there have been refinements in the understanding and nomenclature regarding the natural history of acute pancreatitis. Patients with acute pancreatitis frequently develop acute pancreatic collections that, over time, may evolve into pancreatic pseudocysts or walled-off necrosis. Endoscopic management of these local complications of acute pancreatitis continues to evolve. Treatment strategies range from simple drainage of liquefied contents to repeated direct endoscopic necrosectomy of a complex necrotic collection. In patients with chronic pancreatitis, pancreatic pseudocysts may arise as a consequence of pancreatic ductal obstruction that then leads to pancreatic ductal disruption. In this review, we focus on the indications, techniques and outcomes for endoscopic therapy of pancreatic pseudocysts and walled-off necrosis.

  3. Bilateral Renal Cortical Necrosis in Meningococcal Meningitis

    Directory of Open Access Journals (Sweden)

    C. Kennedy

    2011-01-01

    Full Text Available Bacterial meningitis is a relatively common infection of the cerebrospinal fluid (CSF and leptomeninges. The clinical picture evolves rapidly and, if treatment is delayed, can result in a variety of long-term sequelae, including death. Acute kidney injury in the setting of bacterial meningitis usually results from hypotension and volume depletion and resolves with appropriate treatment. Meningococcaemia with profound hypotension, and/or disseminated intravascular coagulopathy (DIC may very rarely lead to bilateral renal cortical necrosis. In this context, renal recovery is extremely unlikely. We present two cases of meningococcaemia complicated by bilateral renal cortical necrosis and, ultimately, end stage kidney disease. We also present a review of the literature on the subject. The cases outline the importance of early aggressive intervention by a multidisciplinary team.

  4. Therapeutic approaches for tumor necrosis factor inhibition

    OpenAIRE

    Barbosa, Maria Letícia de Castro; Fumian, Milla Machado; Miranda, Ana Luísa Palhares de; Barreiro, Eliezer J.; Lima, Lídia Moreira

    2011-01-01

    Tumor necrosis factor (TNF) consists of an inflammatory cytokine essential for homeostasis and organism defense. Despite its physiological relevance, both increased biosynthesis and release of TNF lead to the exacerbation of inflammatory and oxidative responses, which are related to the pathogenesis of a host of diseases of an inflammatory, autoimmune and/or infectious nature. In this context, effective therapeutic approaches for the modulation of TNF have been the focus of research efforts. ...

  5. Bilateral putaminal necrosis and bronopol toxicity

    OpenAIRE

    Trivisano, Marina; Carapelle, Elena; Martino, Tommaso; Specchio, Luigi Maria

    2015-01-01

    Among alcohols, methanol intoxication is the most frequently associated with cerebral toxicity, causing retinal damage and putaminal necrosis. This consequence is believed to be due to the transformation of methanol into formic acid. We describe the case of a patient who presented with acute impairment of consciousness and tetraparesis after she had been drinking several bottles of a topical antiseptic solution (Lysoform Medical) containing 2-bromo-2-nitro-1,3-propandiol (bronopol) among exci...

  6. Paraneoplastic digital necrosis associated with rectum carcinoma

    Directory of Open Access Journals (Sweden)

    Ali Alkan

    2015-12-01

    Full Text Available Paraneoplastic vascular pathologies are rare in daily practice. There is limited data about this phenomenon. Patient with a diagnosis of metastatic rectum carcinoma presented with digital necrosis. The work up for vascular and rheumatological pathology was inconclusive. Lesions progressively improved with steroid therapy. Paraneoplastic vascular lesions are rare in oncology practice. Our case points out important parts of a rare clinical entity. J Clin Exp Invest 2015; 6 (4: 391-392

  7. [Total prosthesis arthroplasty in femur head necrosis].

    Science.gov (United States)

    Elke, R; Morscher, E

    1990-08-01

    In young patients with advanced necrosis of the femoral head, the short- and medium-term results of total prosthesis arthroplasty are the most satisfactory. However, the prospect of aseptic loosening hangs over such arthroplasties like Damocles' sword. Reports from the literature suggest that, in addition to the age of the patient, there is also an endogenous factor that can be responsible not only for the etiology and pathogenesis of the necrosis, but also for the early loosening of the prosthesis. We have followed up 54 patients (73 hip joints) who had total hip replacement as a result of necrosis of the femoral head between 1976 and 1988. Altogether, 3 acetabular and 5 femoral shafts had to be replaced (7 patients). This corresponds to a loosening rate of 10% after an average of 4.9 years. Hence, the prosthesis changing rate is lower than that reported by other authors, but is still higher than in patients with coxarthrosis. Only 2 of 52 cemented shaft prostheses had to be replaced; the average age of these patients was 61.4 years. Of the 21 cement-free shaft implantations, 3 had to be replaced, the average age of these patients being 42.9 years. The fact that the average age of the latter patients was lower may be the reason for the revision rate not being significantly higher for the non-cemented shafts. In view of the fact that necrosis of the femoral head can rapidly result in the patient becoming an invalid if it is allowed to follow its natural course, hip joint prostheses should also be offered to younger patients.

  8. Maxillary Necrosis: A Sequelae of Fungal Osteomyelitis

    Directory of Open Access Journals (Sweden)

    K Anbarasi

    2010-01-01

    Full Text Available Osteomyelitis is designated to a variety of bone diseases having inflammation as a common denominator. Persistent infection progresses to inflammation of marrow space, haversian system and periostium of affected region. Thrombosis of endothelial vessels cause necrosis and sequestrum formation. Both pyogenic and nonpyogenic infections of jaw lead to this condition. Immunosuppressed patients are more prone to mycelial infections, whereas their occurrence in immunocompetent individuals are highly unusual.

  9. Integrated management of sunflower necrosis disease

    OpenAIRE

    Shirshikar S.P.

    2008-01-01

    Sunflower necrosis disease (SND) is a new threat for sunflower cultivation in India. The disease was observed during 1997 in Karnataka, a major sunflower growing state of India. Later, its occurrence was reported from almost all sunflower growing states of India, posing threat to sunflower cultivation. Presently no reliable resistant sources are available. The disease being viral in nature is very much difficult to combat by single approach. At Oilseeds Research Station, Latur (M.S.), India, ...

  10. Quantification of myocardium at risk in myocardial perfusion SPECT by co-registration and fusion with delayed contrast-enhanced magnetic resonance imaging--an experimental ex vivo study.

    Science.gov (United States)

    Ugander, Martin; Soneson, Helen; Engblom, Henrik; van der Pals, Jesper; Erlinge, David; Heiberg, Einar; Arheden, Håkan

    2012-01-01

    Myocardial perfusion single-photon emission computed tomography (MPS) can be used to assess myocardium at risk in occlusive coronary ischaemia. The aim was to develop a method to quantify myocardium at risk as perfusion defect size on ex vivo MPS using co-registration and fusion with ex vivo magnetic resonance imaging (MRI). Pigs (n = 19) were injected 99mTc-tetrofosmin prior to concluding 40 min of coronary artery occlusion, followed by reperfusion and MRI contrast injection. The excised heart was imaged with T1-weighted MRI and MPS, and images were co-registered using freely available software (Segment v1.8, http://segment.heiberg.se). The left ventricle was semi-automatically delineated in MRI and copied to MPS. The threshold for a MPS perfusion defect was defined as the mean counts in the MPS image at the MRI-determined border between remote myocardium and air. The threshold was measured using count maxima set to the 100th-95th percentile of counts within the myocardium. The count maximum that gave the lowest threshold variability (SD) was considered the most robust. A count maximum using the 100th percentile yielded a threshold of (mean ± SD) 55 ± 6·2%. This method showed the lowest SD compared to 99th-95th percentile count maxima (6·6-7·2%). We describe a method for objective quantification of myocardium at risk as perfusion defect size on MPS using knowledge of the anatomy of the myocardium from co-registered MRI. This enables simultaneous quantification of myocardium at risk by MPS and infarct size by MRI for the evaluation of treatments for myocardial infarction. © 2011 The Authors. Clinical Physiology and Functional Imaging © 2011 Scandinavian Society of Clinical Physiology and Nuclear Medicine.

  11. Chronic Metformin Treatment is Associated with Reduced Myocardial Infarct Size in Diabetic Patients with ST-segment Elevation Myocardial Infarction

    NARCIS (Netherlands)

    Lexis, Chris P. H.; Wieringa, Wouter G.; Hiemstra, Bart; van Deursen, Vincent M.; Lipsic, Erik; van der Harst, Pim; van Veldhuisen, Dirk J.; van der Horst, Iwan C. C.

    Increased myocardial infarct (MI) size is associated with higher risk of developing left ventricular dysfunction, heart failure and mortality. Experimental studies have suggested that metformin treatment reduces MI size after induced ischaemia but human data is lacking. We aimed to investigate the

  12. Increased fetal myocardial sensitivity to insulin-stimulated glucose metabolism during ovine fetal growth restriction.

    Science.gov (United States)

    Barry, James S; Rozance, Paul J; Brown, Laura D; Anthony, Russell V; Thornburg, Kent L; Hay, William W

    2016-04-01

    myocardial function and growth. © 2016 by the Society for Experimental Biology and Medicine.

  13. Bladder necrosis: 'A man without a bladder'.

    Science.gov (United States)

    Bosschieter, Judith; Oudshoorn, Frederik H K; Meuleman, Eric J H; Nieuwenhuijzen, Jakko A

    2018-02-17

    Since the use of antibiotics, bladder necrosis has become a rare condition. We report a case of bladder necrosis in a 90-year-old man following urinary retention. After insertion of a transurethral catheter (TUC), 2 L of urine was evacuated. In the following days, the TUC became intermittently blocked. Adequate bladder drainage could not be obtained despite intensive rinsing and placement of a suprapubic catheter. On surgical exploration necrosis of almost the entire bladder wall, except for the trigone, was encountered. Surgical debridement of the non-viable bladder wall without opening the abdominal cavity was conducted, and a TUC was placed in the Retzius cavity to ensure evacuation of urine. Since the patient was haemodynamically unstable, construction of a urinary diversion was waived and urinary drainage of the Retzius cavity by the TUC was accepted, resulting in adequate urinary drainage without compromising renal function. © BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

  14. Acute myocardial infarction: estimation of at-risk and salvaged myocardium at myocardial perfusion SPECT 1 month after infarction.

    Science.gov (United States)

    Romero-Farina, Guillermo; Aguadé-Bruix, Santiago; Candell-Riera, Jaume; Pizzi, M Nazarena; Pineda, Victor; Figueras, Jaume; Cuberas, Gemma; de León, Gustavo; Castell-Conesa, Joan; García-Dorado, David

    2013-11-01

    To estimate at-risk and salvaged myocardium by using gated single photon emission computed tomography (SPECT) myocardial perfusion imaging after acute myocardial infarction (AMI). The study was approved by the hospital's Ethical Committee on Clinical Trials (trial register number, PR(HG)36/2000), and all patients gave informed consent. Forty patients (mean age, 61.78 years; eight women) with a first AMI underwent two gated SPECT examinations--one before percutaneous coronary intervention (PCI) and one 4-5 weeks after PCI. Myocardium at risk was estimated by assessing the perfusion defect at the first gated SPECT examination, and salvaged myocardium was estimated by assessing the risk area minus necrosis at the second examination. Myocardium at risk was estimated by determining the discordance between the areas of left ventricular (LV) wall motion and perfusion at the second examination. Concordance between tests was analyzed by means of linear regression analysis, the Pearson correlation, the intraclass correlation coefficient, and Bland-Altman analysis. An improvement in perfusion, wall motion, wall thickening, and LV ejection fraction (P Myocardial perfusion gated SPECT performed 1 month after early PCI in a first AMI provides potentially useful information on at-risk and salvaged myocardium. http://radiology.rsna.org/lookup/suppl/doi:10.1148/radiol.13122324/-/DC1. RSNA, 2013

  15. Cardiac MRI. T2-mapping versus T2-weighted dark-blood TSE imaging for myocardial edema visualization in acute myocardial infarction

    Energy Technology Data Exchange (ETDEWEB)

    Nassenstein, K.; Nensa, F.; Schlosser, T.; Umutlu, L.; Lauenstein, T. [University Hospital Essen (Germany). Dept. of Diagnostic and Interventional Radiology and Neuroradiology; Bruder, O. [Elisabeth Hospital, Essen (Germany). Dept. of Cardiology and Angiology; Maderwald, S.; Ladd, M.E. [Duisburg-Essen Univ., Essen (Germany). Erwin L. Hahn Institute for Magnetic Resonance Imaging

    2014-02-15

    Purpose: To assess the diagnostic accuracy of T2 mapping for the detection of myocardial edema in acute myocardial infarction (AMI), and to compare this diagnostic accuracy with that of the current standard for myocardial edema imaging, which is T2w dark-blood TSE imaging. Materials and Methods: 29 patients with AMI were examined at 1.5 T. For the visualization of myocardial edema, T2 maps, calculated from three T2w SSFP images, and T2w dark-blood TSE images were acquired in standard short- and long-axis views. Cine SSFP images were acquired for the analysis of left ventricular (LV) function and late gadolinium enhancement images (LGE) for the visualization of myocardial necrosis. The T2 maps as well as the T2w dark-blood TSE images were evaluated twice independently from the cine SSFP and LGE images. The presence or absence of myocardial edema was rated visually for each LV segment. As the standard of reference, the infarct zone was defined based on the cine SSFP and the LGE images. Results: In this segment-based analysis, T2 mapping showed a sensitivity of 82 % and a specificity of 94 % for the detection of edema in the infarct zone. T2w dark-blood TSE imaging revealed a sensitivity of 50 % and a specificity of 98 %. T2 mapping showed a higher intra-rater agreement compared to T2w dark-blood TSE imaging ({kappa}: 0.87 vs. 0.76). Conclusions: T2 mapping allows for the visualization of myocardial edema in AMI with a high sensitivity and specificity, and features better diagnostic accuracy in terms of a higher sensitivity compared to T2w dark-blood TSE imaging. (orig.)

  16. Dose-dependent effects of alpha-naphthylisothiocyanate disconnect biliary fibrosis from hepatocellular necrosis.

    Science.gov (United States)

    Joshi, Nikita; Ray, Jessica L; Kopec, Anna K; Luyendyk, James P

    2017-01-01

    Exposure of rodents to the xenobiotic α-naphthylisothiocyanate (ANIT) is an established model of experimental intrahepatic bile duct injury. Administration of ANIT to mice causes neutrophil-mediated hepatocellular necrosis. Prolonged exposure of mice to ANIT also produces bile duct hyperplasia and liver fibrosis. However, the mechanistic connection between ANIT-induced hepatocellular necrosis and bile duct hyperplasia and fibrosis is not well characterized. We examined impact of two different doses of ANIT, by feeding chow containing ANIT (0.05%, 0.1%), on the severity of various liver pathologies in a model of chronic ANIT exposure. ANIT-elicited increases in liver inflammation and hepatocellular necrosis increased with dose. Remarkably, there was no connection between increased hepatocellular necrosis and bile duct hyperplasia and peribiliary fibrosis, as these pathologies increased similarly in mice exposed to either dose of ANIT. The results indicate that the severity of hepatocellular necrosis does not dictate the extent of bile duct hyperplasia/fibrosis in ANIT-exposed mice. © 2016 Wiley Periodicals, Inc.

  17. Laser-induced fluorescence spectroscopy in tissue local necrosis detection

    Science.gov (United States)

    Cip, Ondrej; Buchta, Zdenek; Lesundak, Adam; Randula, Antonin; Mikel, Bretislav; Lazar, Josef; Veverkova, Lenka

    2014-03-01

    The recent effort leads to reliable imaging techniques which can help to a surgeon during operations. The fluorescence spectroscopy was selected as very useful online in vivo imaging method to organics and biological materials analysis. The presented work scopes to a laser induced fluorescence spectroscopy technique to detect tissue local necrosis in small intestine surgery. In first experiments, we tested tissue auto-fluorescence technique but a signal-to-noise ratio didn't express significant results. Then we applied a contrast dye - IndoCyanine Green (ICG) which absorbs and emits wavelengths in the near IR. We arranged the pilot experimental setup based on highly coherent extended cavity diode laser (ECDL) used for stimulating of some critical areas of the small intestine tissue with injected ICG dye. We demonstrated the distribution of the ICG exciter with the first file of shots of small intestine tissue of a rabbit that was captured by high sensitivity fluorescent cam.

  18. Myocardial perfusion modeling using MRI

    DEFF Research Database (Denmark)

    Larsson, H B; Fritz-Hansen, T; Rostrup, Egill

    1996-01-01

    In the present study, it is shown that it is possible to quantify myocardial perfusion using magnetic resonance imaging in combination with gadolinium diethylenetriaminopentaacetic acid (Gd-DTPA). Previously, a simple model and method for measuring myocardial perfusion using an inversion recovery...... in the anterior myocardial wall were (mean +/- SD) Ki = 54 +/- 10 ml/100 g/min, lambda = 30 +/- 3 ml/100 g, Vb = 9 +/- 2 ml/100 g, delta T = 3.2 +/- 1.1 s. These results are in good agreement with similar results obtained by other methods....

  19. [A case of rupture of the left ventricle free wall with papillary muscle dysfunction following acute myocardial infarction, operated on successfully].

    Science.gov (United States)

    de Lima, R; Perdigão, C; Neves, L; Cravino, J; Dantas, M; Bordalo, A; Pais, F; Diogo, A N; Ferreira, R; Ribeiro, C

    1990-09-01

    The authors present a case of left ventricular free wall rupture post acute myocardial infarction, associated with mitral papillary posterior muscle necrosis, operated by infartectomy and mitral valvular protesis replacement. They refer the various complications occurred during the hospital staying, and discuss its medical and surgical approach. The patient was discharged alive and six months after the infarction keeps a moderate activity.

  20. Impact of ischemic time on post-infarction left ventricular function in ST-elevation myocardial infarction treated with primary percutaneous coronary intervention

    NARCIS (Netherlands)

    Ng, S.; Ottervanger, J.P.; Hof, A.W. van 't; Boer, M.J. de; Reiffers, S.; Dambrink, J.H.; Hoorntje, J.C.A.; Gosselink, A.T.M.; Suryapranata, H.

    2013-01-01

    BACKGROUND: Myocardial necrosis is a time-dependent event. Nevertheless, clinical studies on association between ischemic time and left ventricle function showed inconsistent findings. Aim of current study is to evaluate the association between ischemic time and the post-infarction left ventricular

  1. Depression following myocardial infarction

    DEFF Research Database (Denmark)

    Larsen, Karen Kjær

    2013-01-01

    Myocardial infarction (MI) is a severe life event that is accompanied by an increased risk of depression. Mounting evidence suggests that post-MI depression is associated with adverse outcomes, but the underlying mechanisms of this association remain unclear, and no previous studies have examined...... whether the mental burden of MI is so heavy that it increases the risk of suicide. Although post-MI depression is common and burdensome, the condition remains under-recognised and under-treated. The development of new strategies to improve the quality of care for people with post-MI depression requires...... thorough understanding of the mechanisms that influence the prognosis as well as knowledge of the present care provided. The purpose of this PhD thesis is accordingly subdivided into four specific aims: 1. To estimate the prevalence of depression in people with MI after three months, and to estimate...

  2. Unusual arrhythmogenic myocardial disease

    Directory of Open Access Journals (Sweden)

    Christer Backman

    2014-01-01

    Full Text Available A twenty-two-year-old lady, with a 2-year history of recurrent tachyarrhythmia, presented with an episode of arrhythmia preceded by sore throat followed by chills, cough and exertional breathlessness, while abroad. She was commenced on penicillin V for 10 days with no improvement and because of worsening cough with purulent sputum she was prescribed broad-spectrum antibiotics and her chills disappeared. Two months later she had a relapse when she felt extremely tired, when a casualty ECG showed right bundle branch block and anterior T-wave inversion. An echocardiogram showed normal size cardiac chambers but the left ventricular basal posterior wall was hypokinetic with a bright echodense 2x3 cm subendocardial segment suggestive of localized fibrosis (Figure 1. The same finding was confirmed with Gadolinium enhanced CMR scan (Figure 2 which suggested a prior myocardial injury. The ejection fraction was normal at the time of CMR.

  3. Myocardial contusion: diagnostic value of cardiac scanning and echocardiography

    Energy Technology Data Exchange (ETDEWEB)

    Coleman, J.; Gonzalez, A.; Harlaftis, N.; Symbas, P.N.

    1976-01-01

    The increase of vehicular high-speed travel has resulted in an increase of blunt trauma, including contusion of the heart. Presently, the only available test to diagnose this form of cardiac injury is a 12-lead electrocardiogram. Some of the electrocardiographic findings, however, which have been considered indicative of myocardial contusion are nonspecific. We have previously shown that supravalvular aortic injection of microspheres of albumin labeled with radioactive technetium (/sup 99m/Tc) outlined the experimentally produced myocardial contusion in eight of the ten dogs. The present study was undertaken to define the value of less invasive techniques, such as echocardiography and cardiac scanning with radionuclides which could be administered intravenously in diagnosing myocardial contusion.

  4. Biomarkers in acute myocardial infarction

    National Research Council Canada - National Science Library

    Chan, Daniel; Ng, Leong L

    2010-01-01

    .... Biomarkers have been used to assist with timely diagnosis, while an increasing number of novel markers have been identified to predict outcome following an acute myocardial infarction or acute coronary syndrome...

  5. Apoptosis and Necrosis in the Liver

    Science.gov (United States)

    Guicciardi, Maria Eugenia; Malhi, Harmeet; Mott, Justin L.; Gores, Gregory J.

    2013-01-01

    Because of its unique function and anatomical location, the liver is exposed to a multitude of toxins and xenobiotics, including medications and alcohol, as well as to infection by hepatotropic viruses, and therefore, is highly susceptible to tissue injury. Cell death in the liver occurs mainly by apoptosis or necrosis, with apoptosis also being the physiologic route to eliminate damaged or infected cells and to maintain tissue homeostasis. Liver cells, especially hepatocytes and cholangiocytes, are particularly susceptible to death receptor-mediated apoptosis, given the ubiquitous expression of the death receptors in the organ. In a quite unique way, death receptor-induced apoptosis in these cells is mediated by both mitochondrial and lysosomal permeabilization. Signaling between the endoplasmic reticulum and the mitochondria promotes hepatocyte apoptosis in response to excessive free fatty acid generation during the metabolic syndrome. These cell death pathways are partially regulated by microRNAs. Necrosis in the liver is generally associated with acute injury (i.e., ischemia/reperfusion injury) and has been long considered an unregulated process. Recently, a new form of “programmed” necrosis (named necroptosis) has been described: the role of necroptosis in the liver has yet to be explored. However, the minimal expression of a key player in this process in the liver suggests this form of cell death may be uncommon in liver diseases. Because apoptosis is a key feature of so many diseases of the liver, therapeutic modulation of liver cell death holds promise. An updated overview of these concepts is given in this article. PMID:23720337

  6. Acute necrosis of oesophagus: clinical case

    OpenAIRE

    Vaio, Teresa; Garcia, Rui; Terrível, Miguel; Alves, Susana; Filipe, Carlos; Reis, Conceição

    2006-01-01

    A necrose aguda do esófago (NAE) é uma situação clínica rara, de etiopatogenia desconhecida, caracterizada pela presença de esófago negro na endoscopia digestiva alta (EDA). Os autores apresentam o caso clínico de um doente de 79 anos de idade, internado por icterícia obstrutiva com 3 semanas de evolução. Ao sétimo dia de internamento, apresentou hematemeses, com descida de hemoglobina de 3 g/dl e esófago negro na EDA. Acute necrosis of oesophagus is a rare disease of unknow...

  7. Frequency of myocardial indium-111 antimyosin uptake after uncomplicated coronary artery bypass grafting

    Energy Technology Data Exchange (ETDEWEB)

    van Vlies, B.; van Royen, E.A.; Visser, C.A.; Meyne, N.G.; van Buul, M.M.; Peters, R.J.; Dunning, A.J. (Academic Medical Center, Amsterdam (Netherlands))

    1990-11-15

    The reported incidence of myocardial damage after coronary artery bypass grafting (CABG) is highly related to the methods used. Since indium-111 monoclonal antimyosin antibody scintigraphy has been shown to be highly specific and sensitive for myocardial necrosis, even in small lesions, uptake of this radiotracer was evaluated after CABG. In 23 consecutive patients without previous myocardial infarction who underwent CABG for stable angina, 80 MBq indium-111 antimyosin was injected on the third postoperative day. Planar images were obtained 48 hours later and analyzed for myocardial uptake of indium-111 antimyosin. Scintigraphic results were related to creatine kinase MB levels, duration of both aortic cross-clamping and cardiopulmonary bypass, and electrocardiographic changes. In all patients surgical procedure and postoperative course was uncomplicated. Indium-111 antimyosin uptake was present in 19 of 23 patients (82%). It was diffused in 7 patients and localized in 12. No pathologic Q waves occurred postoperatively. Fourteen patients exhibited ST-segment changes. No good relation was found among indium-111 antimyosin uptake and creatine kinase MB levels, duration of cross-clamping or bypass, and ST-T changes. It is concluded that some degree of myocardial damage, though silent, is common after CABG.

  8. Post myocardial infarction of the left ventricle: the course ahead seen by cardiac MRI

    Science.gov (United States)

    Masci, Pier Giorgio

    2012-01-01

    In the last decades, cardiac magnetic resonance imaging (MRI) has gained acceptance in cardiology community as an accurate and reproducible diagnostic imaging modality in patients with ischemic heart disease (IHD). In particular, in patients with acute myocardial infarction (MI) cardiac MRI study allows a comprehensive assessment of the pattern of ischemic injury in term of reversible and irreversible damage, myocardial hemorrhage and microvascular obstruction (MVO). Myocardial salvage index, derived by quantification of myocardium (area) at risk and infarction, has become a promising surrogate end-point increasingly used in clinical trials testing novel or adjunctive reperfusion strategies. Early post-infarction, the accurate and reproducible quantification of myocardial necrosis, along with the characterization of ischemic myocardial damage in its diverse components, provides important information to predict post-infarction left ventricular (LV) remodeling, being useful for patients stratification and management. Considering its non-invasive nature, cardiac MRI suits well for investigating the time course of infarct healing and the changes occurring in peri-infarcted (adjacent) and remote myocardium, which ultimately promote the geometrical, morphological and functional abnormalities of the entire left ventricle (global LV remodeling). The current review will focus on the cardiac MRI utility for a comprehensive evaluation of patients with acute and chronic IHD with particular regard to post-infarction remodeling. PMID:24282705

  9. Melatonin Does Not Affect Oxidative/Inflammatory Biomarkers in a Closed-Chest Porcine Model of Acute Myocardial Infarction

    DEFF Research Database (Denmark)

    Løvland Halladin, Natalie; Ekeløf, Sarah; Jensen, Svend Eggert

    2014-01-01

    Aim: To test whether melatonin reduces oxidative and inflammatory biomarkers in a closed-chest porcine model of acute myocardial infarction. Materials and Methods: Twenty pigs were randomized to receive a total dosage of 200 mg (0.4 mg/ml) of melatonin, or placebo immediately prior to reperfusion...... or oxidative stress markers after experimental myocardial infarction compared to placebo....

  10. Melatonin does not affect oxidative/inflammatory biomarkers in a closed-chest porcine model of acute myocardial infarction

    DEFF Research Database (Denmark)

    Halladin, Natalie L.; Busch, Sarah Victoria Ekeløf; Jensen, Svend Eggert

    2014-01-01

    AIM: To test whether melatonin reduces oxidative and inflammatory biomarkers in a closed-chest porcine model of acute myocardial infarction. MATERIALS AND METHODS: Twenty pigs were randomized to receive a total dosage of 200 mg (0.4 mg/ml) of melatonin, or placebo immediately prior to reperfusion...... or oxidative stress markers after experimental myocardial infarction compared to placebo....

  11. Type 2 myocardial infarction: A descriptive analysis and comparison with type 1 myocardial infarction.

    Science.gov (United States)

    Landes, Uri; Bental, Tamir; Orvin, Katia; Vaknin-Assa, Hana; Rechavia, Eldad; Iakobishvili, Zaza; Lev, Eli; Assali, Abid; Kornowski, Ran

    2016-01-01

    While 'plaque rupture' is the paradigm of type 1 myocardial infarction (T1MI), T2MI is myocardial necrosis secondary to oxygen supply-demand mismatch. Being a heterogeneous and rather newly defined group, data are lacking about T2MI. A retrospective review of medical records of patients diagnosed with T2MI in the Rabin Cardiology Center, Israel between the years 2007 and 2012 was performed. Following a descriptive analysis, we used multivariate time dependent models to estimate the association of T2MI with the risk for 30-day, 1-year, and 5-year all-cause-mortality and major adverse cardiovascular events (MACE), and compared it to a T1MI group matched for age, gender and electrocardiographic changes. The study included 107 T2MI (and 107 T1MI) patients. Sepsis, anemia, and atrial fibrillation were the most common etiologies. Triple anti-thrombotic therapy was given to 22% of T2MI patients (vs. 82% of T1MI patients, p<0.001). Twenty-five percent were managed using urgent percutaneous coronary intervention. Angiography unmasked acute plaque rupture in 29% of T2MI patients group. Compared to T1MI, T2MI was associated with higher all-cause-mortality rate: adjusted-hazard-ratio 7.14 (1.31-38.9) at 30 days, 3.42 (1.51-7.75) at 1 year, and 2.08 (1.14-3.81) at 5 years follow-up. MACE risk was consistent between T2 and T1MI patients. The most common T2MI triggers are sepsis, anemia, and atrial fibrillation. Compared to a T1MI population, T2MI is associated with higher short- and long-term mortality rates but equal cardiovascular mortality and MACE risk. As many as 30% may harbor plaque rupture and in fact have T1MI. Copyright © 2015. Published by Elsevier Ltd.

  12. Bilateral putaminal necrosis and bronopol toxicity

    Science.gov (United States)

    Trivisano, Marina; Carapelle, Elena; Martino, Tommaso; Specchio, Luigi Maria

    2015-01-01

    Among alcohols, methanol intoxication is the most frequently associated with cerebral toxicity, causing retinal damage and putaminal necrosis. This consequence is believed to be due to the transformation of methanol into formic acid. We describe the case of a patient who presented with acute impairment of consciousness and tetraparesis after she had been drinking several bottles of a topical antiseptic solution (Lysoform Medical) containing 2-bromo-2-nitro-1,3-propandiol (bronopol) among excipients, in order to lose weight during previous months. Moreover, she had been on a strict slimming diet. Soon after admission, a severe respiratory and metabolic impairment became rapidly evident, requiring an intensive care unit admission. Cerebral MRI showed the presence of bilateral putaminal necrosis. She recovered in 10 days, surprisingly, without any evident clinical neurological signs. Methanol, also bronopol, when diluted in aqueous solution, at warm temperature and/or higher pH, may release formaldehyde, which is converted into formic acid, a basal ganglia toxic compound. PMID:25697297

  13. Mastectomy skin flap necrosis: challenges and solutions

    Science.gov (United States)

    Robertson, Stuart A; Jeevaratnam, Johann A; Agrawal, Avi; Cutress, Ramsey I

    2017-01-01

    Introduction Mastectomy skin flap necrosis (MSFN) has a reported incidence of 5%–30% in the literature. It is often a significant and underappreciated problem. The aim of this article was to review the associated challenges and possible solutions. Methods A MEDLINE search was performed using the search term “mastectomy skin flap necrosis”. Titles and abstracts from peer-reviewed publications were screened for relevance. Results MSFN is a common complication and may present as partial- or full-thickness necrosis. Predictive patient risk factors include smoking, diabetes, obesity, radiotherapy, previous scars and severe medical comorbidity. MSFN leads to a number of challenges, including wound management problems, delays to adjuvant therapy, esthetic compromise, implant extrusion, patient distress and financial loss. Careful preoperative planning and meticulous surgical technique may reduce the incidence of MSFN. A number of intraoperative techniques are available to try and predict skin flaps at risk of MSFN. MSFN may be managed operatively or nonoperatively. Early intervention may reduce the morbidity of MSFN in selected cases. Topical nitroglycerin ointment may be beneficial in reducing MSFN following immediate reconstruction, but the evidence base is still limited. Conclusion MSFN can result in considerable challenges for the patient and the health care service. This review discusses the management options for this problem. PMID:28331365

  14. Mechanisms of Acetaminophen-Induced Liver Necrosis

    Science.gov (United States)

    Roberts, Dean W.; James, Laura P.

    2010-01-01

    Although considered safe at therapeutic doses, at higher doses, acetaminophen produces a centrilobular hepatic necrosis that can be fatal. Acetaminophen poisoning accounts for approximately one-half of all cases of acute liver failure in the United States and Great Britain today. The mechanism occurs by a complex sequence of events. These events include: (1) CYP metabolism to a reactive metabolite which depletes glutathione and covalently binds to proteins; (2) loss of glutathione with an increased formation of reactive oxygen and nitrogen species in hepatocytes undergoing necrotic changes; (3) increased oxidative stress, associated with alterations in calcium homeostasis and initiation of signal transduction responses, causing mitochondrial permeability transition; (4) mitochondrial permeability transition occurring with additional oxidative stress, loss of mitochondrial membrane potential, and loss of the ability of the mitochondria to synthesize ATP; and (5) loss of ATP which leads to necrosis. Associated with these essential events there appear to be a number of inflammatory mediators such as certain cytokines and chemokines that can modify the toxicity. Some have been shown to alter oxidative stress, but the relationship of these modulators to other critical mechanistic events has not been well delineated. In addition, existing data support the involvement of cytokines, chemokines, and growth factors in the initiation of regenerative processes leading to the reestablishment of hepatic structure and function. PMID:20020268

  15. Acute fatal acetaminophen overdose without liver necrosis.

    Science.gov (United States)

    Singer, Peter P; Jones, Graham R; Bannach, Bernard G; Denmark, Lloyd

    2007-07-01

    Two unusual cases of suicidal overdose of acetaminophen (paracetamol) without the usual extensive centrilobular necrosis of the liver are reported. Both cases were subjected to comprehensive drug screening by immunoassay, and a combination of gas chromatography with mass spectrometry, nitrogen detection, and electron capture detection. Acetaminophen was detected in both cases. No other drugs were detected in case #1, and only a small amount of olanzapine (<0.1 mg/L) was detected in case #2. No anatomical cause of death was identified in either case. If untreated, the normal outcome of a large acetaminophen overdose would be massive hepatic necrosis with delayed death and low blood and tissue acetaminophen concentrations. In contrast, particularly high postmortem acetaminophen concentrations were measured in both our cases with little hepatic tissue damage. For case #1, femoral blood acetaminophen 1280 mg/L, vitreous 878 mg/L, and liver 729 mg/kg; in case #2, cardiac blood 1220 mg/L, vitreous 779 mg/L, liver 3260 mg/kg, and gastric 11,500 mg/500 g. Acetaminophen was measured using high performance liquid chromatography with UV detection (254 nm) using 3-hydroxyacetanilide as the internal standard. The very high concentrations of acetaminophen is these cases but relatively little hepatic damage suggests an alternative, possibly cardiac, mechanism of death.

  16. Brief Myocardial Ischemia Produces Cardiac Troponin I Release and Focal Myocyte Apoptosis in the Absence of Pathological Infarction in Swine

    Directory of Open Access Journals (Sweden)

    Brian R. Weil, PhD

    2017-04-01

    Full Text Available Summary: In a porcine model of brief ischemia leading to reversible stunning in the absence of tissue necrosis, we demonstrated delayed release of cardiac troponin I (cTnI that exceeded the 99th percentile for normal animals 60 min after reperfusion and rose to readily detectable levels 24 h later. Although tissue analysis at 60 min showed no evidence of infarction, TUNEL staining demonstrated isolated myocytes undergoing apoptosis, which was absent after 24 h. These results demonstrate that cTnI elevations occur after ischemia of a duration that is insufficient to produce myocyte necrosis and reflect myocyte injury associated with apoptosis in the absence of pathological evidence of infarction. Key Words: cardiac troponin I, cardiomyocyte apoptosis, myocardial ischemia, myocardial stunning

  17. Myocardial scintigraphy in the diagnosis of myocardial contusion

    Energy Technology Data Exchange (ETDEWEB)

    Terashima, Masayoshi; Shinoda, Mitsutaka; Iwama, Hiroshi; Hirama, Hisao; Hoshino, Toshiaki; Urabe, Shinpei [Central Aizu General Hospital, Fukushima (Japan); Meguro, Taiichiroh

    1996-04-01

    To assess the clinical value of a new fatty acid imaging tracer, {sup 123}I-{beta}-methyl iodophenyl pentadecanoic acid (BMIPP), I-BMIPP and thallium-201 (Tl) dual imaging was performed at rest in fifteen patients with mild blunt chest trauma (mean AIS thoracic 1.4{+-}0.51, mean ISS 6.47{+-}3.50, mean RTS 7.69{+-}0.43). All patients were prospectively evaluated on the basis of serial electrocardiograms (ECG) and cardiac enzyme studies (total CPK). Tl and BMIPP dual scintigrams were performed within 10 days following admission. SPECT images were divided into seven segments, and the segmental images were visually scored according to tracer uptake on a 3 (severely decreased tracer uptake) to 0 (normal) scale. Nine patients had scintigraphic defects and were considered to have a myocardial contusion. ECG findings, AIS, ISS, and CPK levels failed to distinguish between scintigraphically positive patients and scintigraphically negative patients. Five of the 14 hypoperfused segments on BMIPP imaging, showed normal Tl uptake, one showed lower BMIPP uptake than Tl, and the remaining eight showed similar distribution of both tracers. The mismatch between tracer uptake on BMIPP images and Tl images was thought to reflect impaired myocardial fatty acid metabolism. Thus, mild blunt chest trauma results in a higher frequency of traumatic myocardial injury than previously recognized, and BMIPP is a promising radio-pharmaceutical for evaluating impaired myocardial fatty acid metabolism in patients with myocardial contusion. (author).

  18. PMWS: Experimental model and co-infections

    DEFF Research Database (Denmark)

    Allan, G. M.; McNeilly, F.; Ellis, J

    2004-01-01

    and pneumonia and typical histological lesions include lymphocytic depletion and multinucleated giant cell formation in lymph nodes, degeneration and necrosis of hepatocytes, and multifocal lymphohistocytic interstitial pneumonia. This communication will review the results of experimental infections...

  19. [Changes of myocardial enzymes related to glycolysis and fatty acid metabolism in chronic myocardial ischemia: experiment with pigs].

    Science.gov (United States)

    Gong, Jing; Wang, Hong-yue; Pu, Jie-lin; Zheng, Ying-li; Shen, Rui; Yang, Min-fu; He, Zuo-xiang

    2008-08-12

    To investigate the changes myocardial enzymes related to glycolysis and fatty acid metabolism in chronic myocardial ischemia and to evaluate the relationship between the gene expression of glycolytic metabolism related enzymes and myocardial viability. Fourteen Chinese experimental pigs underwent placement of arterial ring into the left anterior descending coronary artery so as to establish models of myocardial ischemia and infarction. (18)F-2-deoxy-2-fluoro-D-glucose single photon emission computed tomography was conducted to observe the viability of the myocardium. One week later the pigs were killed with their hearts taken out. Specimens of ischemic zone, infarction zone, and non-ischemic zone were obtained. RT-PCR was used to detect the mRNA expression of glucose transporter (GLUT) 1, GLUT4, medium-chain acyl-CoA dehydrogenase (MCAD), and heart-fatty acid binding protein (H-FABP). Immunohistochemistry was used to examine the protein expression of Glut1 and Glut4. Periodic Acid Schiff-hematoxylin staining was conducted to detect the glycogen. Pathological examination showed 5 pigs with myocardial infarction and 5 pigs with ischemia. In the pigs with ischemia, the mRNA expression levels of GLUT1 and GLUT4 in the ischemic zone were 9466 +/- 9033 and 60 398 +/- 64 699 respectively, both significantly higher than those in the control zone (5854 +/- 5287 and 34 188 +/- 44 714 respectively, P = 0.043, P = 0.043). the RNA expression of H-FABP in the ischemic zone was 18 123 +/- 15 925, significantly lower than that in the control zone (50 718 +/- 62 412, P = 0.043), and there was no significant difference in the mRNA expression level of MCAD. In the pigs with infarction the mRNA expression of level of H-FABP in the infarction zone was 21 919 +/- 15 224, significantly lower than that in the control zone (87 545 +/- 92 990, P = 0.043), and there were not significant differences in the mRNA expression levels of the GLUT1, GLUT4, and MCAD genes (all P > 0.05). The m

  20. Cardiac MRI: T2-Mapping Versus T2-Weighted Dark-Blood TSE Imaging for Myocardial Edema Visualization in Acute Myocardial Infarction.

    Science.gov (United States)

    Naßenstein, K; Nensa, F; Schlosser, T; Bruder, O; Umutlu, L; Lauenstein, T; Maderwald, S; Ladd, M E

    2014-02-01

    To assess the diagnostic accuracy of T2 mapping for the detection of myocardial edema in acute myocardial infarction (AMI), and to compare this diagnostic accuracy with that of the current standard for myocardial edema imaging, which is T2w dark-blood TSE imaging. 29 patients with AMI were examined at 1.5 T. For the visualization of myocardial edema, T2 maps, calculated from three T2w SSFP images, and T2w dark-blood TSE images were acquired in standard short- and long-axis views. Cine SSFP images were acquired for the analysis of left ventricular (LV) function and late gadolinium enhancement images (LGE) for the visualization of myocardial necrosis. The T2 maps as well as the T2w dark-blood TSE images were evaluated twice independently from the cine SSFP and LGE images. The presence or absence of myocardial edema was rated visually for each LV segment. As the standard of reference, the infarct zone was defined based on the cine SSFP and the LGE images. In this segment-based analysis, T2 mapping showed a sensitivity of 82 % and a specificity of 94 % for the detection of edema in the infarct zone. T2w dark-blood TSE imaging revealed a sensitivity of 50 % and a specificity of 98 %. T2 mapping showed a higher intra-rater agreement compared to T2w dark-blood TSE imaging (κ: 0.87 vs. 0.76). T2 mapping allows for the visualization of myocardial edema in AMI with a high sensitivity and specificity, and features better diagnostic accuracy in terms of a higher sensitivity compared to T2w dark-blood TSE imaging. Citation Format: • Naßenstein K, Nensa F, Schlosser T et al. Cardiac MRI: T2-Mapping Versus T2-Weighted Dark-Blood TSE Imaging for Myocardial Edema Visualization in Acute Myocardial Infarction. Fortschr Röntgenstr 2014; 186: 166 - 172. © Georg Thieme Verlag KG Stuttgart · New York.

  1. Exenatide reduces reperfusion injury in patients with ST-segment elevation myocardial infarction

    DEFF Research Database (Denmark)

    Lønborg, Jacob; Vejlstrup, Niels Grove; Kelbæk, Henning Skov

    2011-01-01

    Aims Exenatide, a glucagon-like-peptide-1 analogue, increases myocardial salvage in experimental settings with coronary occlusion and subsequent reperfusion. We evaluated the cardioprotective effect of exenatide at the time of reperfusion in patients with ST-segment elevation myocardial infarction...... and maintained for 6 h after the procedure. The primary endpoint was salvage index calculated from myocardial area at risk (AAR), measured in the acute phase, and final infarct size measured 90 ± 21 days after pPCI by cardiac magnetic resonance (CMR). In 105 patients evaluated with CMR, a significantly larger...

  2. Dense motion field estimation from myocardial boundary displacements.

    Science.gov (United States)

    Morais, Pedro; Queirós, Sandro; Ferreira, Adriano; Rodrigues, Nuno F; Baptista, Maria J; D'hooge, Jan; Vilaça, João L; Barbosa, Daniel

    2016-09-01

    Minimally invasive cardiovascular interventions guided by multiple imaging modalities are rapidly gaining clinical acceptance for the treatment of several cardiovascular diseases. These images are typically fused with richly detailed pre-operative scans through registration techniques, enhancing the intra-operative clinical data and easing the image-guided procedures. Nonetheless, rigid models have been used to align the different modalities, not taking into account the anatomical variations of the cardiac muscle throughout the cardiac cycle. In the current study, we present a novel strategy to compensate the beat-to-beat physiological adaptation of the myocardium. Hereto, we intend to prove that a complete myocardial motion field can be quickly recovered from the displacement field at the myocardial boundaries, therefore being an efficient strategy to locally deform the cardiac muscle. We address this hypothesis by comparing three different strategies to recover a dense myocardial motion field from a sparse one, namely, a diffusion-based approach, thin-plate splines, and multiquadric radial basis functions. Two experimental setups were used to validate the proposed strategy. First, an in silico validation was carried out on synthetic motion fields obtained from two realistic simulated ultrasound sequences. Then, 45 mid-ventricular 2D sequences of cine magnetic resonance imaging were processed to further evaluate the different approaches. The results showed that accurate boundary tracking combined with dense myocardial recovery via interpolation/diffusion is a potentially viable solution to speed up dense myocardial motion field estimation and, consequently, to deform/compensate the myocardial wall throughout the cardiac cycle. Copyright © 2015 John Wiley & Sons, Ltd. Copyright © 2015 John Wiley & Sons, Ltd.

  3. Emergency coronary bypass grafting for evolving myocardial infarction. Effects on infarct size and left ventricular function

    Energy Technology Data Exchange (ETDEWEB)

    Flameng, W.; Sergeant, P.; Vanhaecke, J.; Suy, R.

    1987-07-01

    Emergency aorta-coronary bypass grafting was performed early in the course of evolving myocardial infarction in 48 patients. The time interval between the onset of symptoms and reperfusion was 169 +/- 80 minutes. Quantitative assessment of postoperative thallium 201 myocardial scans in 19 patients revealed a significant salvage of myocardium after surgical reperfusion: The size of the residual infarction was less than 50% of that in a matched, medically treated, prospective control group (n = 39) (p less than 0.05). Postoperative equilibrium-gated radionuclide blood pool studies (technetium 99m) showed an enhanced recovery of regional and global ejection fraction after operation as compared to after medical treatment (p less than 0.05). Ultrastructural evaluation of biopsy specimens obtained during the operation delineated subendocardial necrosis in the majority of cases (72%), but subepicardial necrosis was found in only 6% of instances. Q-wave abnormalities were observed on the postoperative electrocardiogram in 50% of cases. Operative mortality was 0% in low-risk patients (i.e., hemodynamically stable condition, n = 26) and 18% in high-risk patients (i.e., cardiogenic shock including total electromechanical dysfunction, n = 22). Survival rate at 18 months was 92% +/- 4%, and 95% +/- 4% of the survivors were event free. It is concluded that early surgical reperfusion of evolving myocardial infarction limits infarct size significantly, enhances functional recovery, and may be a lifesaving operation in patients having cardiogenic shock associated with unsuccessful resuscitation.

  4. Anti-Inflammatory Effects of the Chinese Herbal Formula Sini Tang in Myocardial Infarction Rats

    Directory of Open Access Journals (Sweden)

    Jiangang Liu

    2014-01-01

    Full Text Available The aim of this study was to evaluate the anti-inflammatory profiling of the Chinese herbal formula Sini Tang (SNT in myocardial infarction (MI rats. SNT, a decoction consisting of four herbs: Aconitum carmichaelii, Cinnamomum cassia, Zingiber officinale, and Glycyrrhiza uralensis, was characterized as a remedy to treat syndromes corresponding to heart failure and MI in China. Potential biomarkers, which reflect the extent of myocardial necrosis and correlate with cardiac outcomes following MI, such as atrial natriuretic peptide (ANP, high sensitivity C-reactive protein (hs-CRP, and proinflammatory cytokines such as tumor necrosis factor-α, interleukin-6, and interleukin-1β (TNF-α, IL-6, and IL-1β were determined in plasma, serum, and in myocardial tissue of MI rats after treatment with SNT. Our data indicate that SNT decreased significantly the levels of hs-CRP, TNF-α, IL-6, and IL-1β in MI rats. SNT decreased the expression of ANP levels in plasma and increased the vascular active marker nitric oxide, which limits vascular inflammation. In addition, SNT could decrease the expression of endothelin-1 levels in rat plasma post-MI. Our data suggest that the Chinese herbal formula SNT has the potential to improve cardiac function after MI. SNT may be a candidate for treating MI and its associated inflammatory responses.

  5. Effects of single-dose atorvastatin on interleukin-6, interferon gamma, and myocardial no-reflow in a rabbit model of acute myocardial infarction and reperfusion

    Energy Technology Data Exchange (ETDEWEB)

    Zhao, X.J. [Affiliated Hospital of Binzhou Medical University, Department of Cardiology, Binzhou, China, Department of Cardiology, Affiliated Hospital of Binzhou Medical University, Binzhou (China); Liu, X.L. [Qilu Hospital, Shandong University, Department of Cardiology, Jinan, China, Department of Cardiology, Qilu Hospital, Shandong University, Jinan (China); He, G.X. [Third Military Medical University, Southwest Hospital, Department of Cardiology, Chongqing, China, Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing (China); Xu, H.P. [Affiliated Hospital of Binzhou Medical University, Department of Cardiology, Binzhou, China, Department of Cardiology, Affiliated Hospital of Binzhou Medical University, Binzhou (China)

    2014-03-03

    The mechanisms of statins relieving the no-reflow phenomenon and the effects of single-dose statins on it are not well known. This study sought to investigate the effects of inflammation on the no-reflow phenomenon in a rabbit model of acute myocardial infarction and reperfusion (AMI/R) and to evaluate the effects of single-dose atorvastatin on inflammation and myocardial no-reflow. Twenty-four New Zealand white male rabbits (5-6 months old) were randomized to three groups of eight: a sham-operated group, an AMI/R group, and an atorvastatin-treated group (10 mg/kg). Animals in the latter two groups were subjected to 4 h of coronary occlusion followed by 2 h of reperfusion. Serum levels of interleukin (IL)-6 were measured by enzyme-linked immunosorbent assay. The expression of interferon gamma (IFN-γ) in normal and infarcted (reflow and no-reflow) myocardial tissue was determined by immunohistochemical methods. The area of no-reflow and necrosis was evaluated pathologically. Levels of serum IL-6 were significantly lower in the atorvastatin group than in the AMI/R group (P<0.01). Expression of IFN-γ in infarcted reflow and no-reflow myocardial tissue was also significantly lower in the atorvastatin group than in the AMI/R group. The mean area of no-reflow [47.01% of ligation area (LA)] was significantly smaller in the atorvastatin group than in the AMI/R group (85.67% of LA; P<0.01). The necrosis area was also significantly smaller in the atorvastatin group (85.94% of LA) than in the AMI/R group (96.56% of LA; P<0.01). In a secondary analysis, rabbits in the atorvastatin and AMI/R groups were divided into two groups based on necrosis area (90% of LA): a small group (<90% of LA) and a large group (>90% of LA). There was no significant difference in the area of no-reflow between the small (61.40% of LA) and large groups (69.87% of LA; P>0.05). Single-dose atorvastatin protected against inflammation and myocardial no-reflow and reduced infarct size during AMI/R in

  6. Gemcitabine-Induced Extensive Skin Necrosis

    Directory of Open Access Journals (Sweden)

    Sara D'epiro

    2012-01-01

    Full Text Available An 82-year-old woman presented with oedema and extensive necrotic ulcerative lesions on the back side of her lower limbs, emerging after the second cycle of chemotherapy consisting of Gemcitabine for metastatic pancreatic cancer. The absence of any convincing argument in favor of cardiovascular or autoimmune disease led us to attribute the onset of skin necrosis to chemotherapy administration. Although skin ischemia has also been described as a paraneoplastic syndrome, in this case we could observe a temporal and causal relationship to Gemcitabine infusion. Recently, this drug has been associated with important vascular side effects; its vascular toxicity is in fact higher than previously estimated. To our knowledge, careful attention should be reserved to neoplastic patients candidated to Gemcitabine administration, especially if previously affected by arterial vascular disease, venous thromboembolism, or collagenoses.

  7. Angiographic assessment of reperfusion in acute myocardial infarction by myocardial blush grade

    NARCIS (Netherlands)

    Henriques, JPS; Zijlstra, F; van 't Hof, AWJ; de Boer, MJ; Gosselink, M; Hoorntje, JCA; Suryapranata, H; Dambrink, Jan Hendrik Everwijn

    2003-01-01

    Background-Angiographic successful reperfusion in acute myocardial infarction has been defined as TIMI 3 flow. However, TIMI 3 flow does not always result in effective myocardial reperfusion. Myocardial blush grade (MBG) is an angiographic measure of myocardial perfusion. We hypothesized that

  8. Angiographic assessment of reperfusion in acute myocardial infarction by myocardial blush grade

    NARCIS (Netherlands)

    Henriques, Jose P. S.; Zijlstra, Felix; van 't Hof, Arnoud W. J.; de Boer, Menko-Jan; Dambrink, Jan-Henk E.; Gosselink, Marcel; Hoorntje, Jan C. A.; Suryapranata, Harry

    2003-01-01

    Angiographic successful reperfusion in acute myocardial infarction has been defined as TIMI 3 flow. However, TIMI 3 flow does not always result in effective myocardial reperfusion. Myocardial blush grade (MBG) is an angiographic measure of myocardial perfusion. We hypothesized that optimal

  9. Activation of complement factor B contributes to murine and human myocardial ischemia/reperfusion injury

    OpenAIRE

    Nicholas Chun; Haddadin, Ala S.; Junying Liu; Yunfang Hou; Wong, Karen A.; Daniel Lee; Rushbrook, Julie I.; Karan Gulaya; Roberta Hines; Tamika Hollis; Beatriz Nistal Nuno; Mangi, Abeel A.; Sabet Hashim; Marcela Pekna; Amy Catalfamo

    2017-01-01

    The pathophysiology of myocardial injury that results from cardiac ischemia and reperfusion (I/R) is incompletely understood. Experimental evidence from murine models indicates that innate immune mechanisms including complement activation via the classical and lectin pathways are crucial. Whether factor B (fB), a component of the alternative complement pathway required for amplification of complement cascade activation, participates in the pathophysiology of myocardial I/R injury has not been...

  10. Myocardial infarction in children: Two interesting cases

    Directory of Open Access Journals (Sweden)

    Suryawanshi Suresh

    2011-01-01

    Full Text Available Myocardial infarction in children is extremely rare and can have various etiologies. The following two case reports highlight rare but important causes of myocardial infarction in children.

  11. Dynamic CT myocardial perfusion imaging

    Energy Technology Data Exchange (ETDEWEB)

    Caruso, Damiano [Division of Cardiovascular Imaging, Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, SC (United States); Department of Radiological Sciences, Oncological and Pathological Sciences, University of Rome “Sapienza”, Latina (Italy); Eid, Marwen [Division of Cardiovascular Imaging, Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, SC (United States); Schoepf, U. Joseph, E-mail: schoepf@musc.edu [Division of Cardiovascular Imaging, Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, SC (United States); Division of Cardiology, Department of Medicine, Medical University of South Carolina, Charleston, SC (United States); Jin, Kwang Nam [Division of Cardiovascular Imaging, Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, SC (United States); Department of Radiology, Seoul Metropolitan Government-Seoul National University Boramae Medical Center, Seoul (Korea, Republic of); Varga-Szemes, Akos [Division of Cardiovascular Imaging, Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, SC (United States); Tesche, Christian [Division of Cardiovascular Imaging, Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, SC (United States); Department of Cardiology and Intensive Care Medicine, Heart Center Munich-Bogenhausen, Munich (Germany); Mangold, Stefanie [Division of Cardiovascular Imaging, Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, SC (United States); Department of Diagnostic and Interventional Radiology, University Hospital of Tuebingen, Tuebingen (Germany); and others

    2016-10-15

    Highlights: • CT myocardial perfusion provides functional assessment of the myocardium. • CCTA is limited in determining the hemodynamic significance of coronary stenosis. • CT-MPI can accurately detect hemodynamically significant coronary artery stenosis. - Abstract: Non-invasive cardiac imaging has rapidly evolved during the last decade due to advancements in CT based technologies. Coronary CT angiography has been shown to reliably assess coronary anatomy and detect high risk coronary artery disease. However, this technique is limited to anatomical assessment, thus non-invasive techniques for functional assessment of the heart are necessary. CT myocardial perfusion is a new CT based technique that provides functional assessment of the myocardium and allows for a comprehensive assessment of coronary artery disease with a single modality when combined with CTA. This review aims to discuss dynamic CT myocardial perfusion as a new technique in the assessment of CAD.

  12. Endotoxemic myocardial dysfunction: subendocardial collagen deposition related to coronary driving pressure.

    Science.gov (United States)

    Soriano, Francisco Garcia; Guido, Maria Carolina; Barbeiro, Hermes Vieira; Caldini, Elia Garcia; Lorigados, Clara Batista; Nogueira, Antonio Carlos

    2014-11-01

    Sepsis impairs the autoregulation of myocardial microcirculatory blood flow, but whether this impairment is correlated with myocardial remodeling is unknown. This study investigated the role of coronary driving pressure (CDP) as a determinant of microcirculatory blood flow and myocardial fibrosis in endotoxemia and sepsis. The study is composed of two parts: a prospective experimental study and an observational clinical study. The experimental study was performed on male Wistar rats weighing 300 to 320 g. Endotoxemia was induced in rats by lipopolysaccharide (LPS) injection (10 mg·kg intraperitoneally). Hemodynamic evaluation was performed 1.5 to 24 h after LPS injection by measuring the mean arterial pressure, CDP, left ventricular end-diastolic pressure, dP/dtmax, and dP/dtmin. Microspheres were also infused into the left ventricle to measure myocardial blood flow, and myocardial tissue was histologically assessed to analyze collagen deposition. The CDP, mean arterial pressure, and myocardial blood flow were reduced by 55%, 30%, and 70%, respectively, in rats 1.5 h after LPS injection compared with phosphate buffer saline injection (P subendocardial blood flow (r = 0.73) and fibrosis (r = 0.8). Left ventricular function was significantly impaired in the LPS-treated rats, as demonstrated by dP/dtmax (6,155 ± 455 vs. 3,746 ± 406 mmHg·s, baseline vs. LPS; P subendocardial blood flow was positively correlated with CDP, and higher CDP was negatively correlated with myocardial collagen deposition. Thus, early reductions in myocardial blood flow and CDP facilitate late myocardial fibrosis in rats and likely in humans.

  13. Cardiac metabolism in myocardial ischemia.

    Science.gov (United States)

    Rosano, Giuseppe M C; Fini, Massimo; Caminiti, Giuseppe; Barbaro, Giuseppe

    2008-01-01

    Myocardial ischemia occurs for a mismatch between blood flow and metabolic requirements, when the rate of oxygen and metabolic substrates delivery to the myocardium is insufficient to meet the myocardial energy requirements for a given myocardial workload. During ischemia, substantial changes occur in cardiac energy metabolism, as a consequence of the reduced oxygen availability. Some of these metabolic changes are beneficial and may help the heart adapt to the ischemic condition. However, most of the changes are maladaptive and contribute to the severity of the ischemic injury leading stunned or hibernating myocardium, cell death and ultimately to contractile disfunction. Dramatic changes in cardiac metabolism and contractile function, also occur during myocardial reperfusion as a consequence of the generation of oxygen free radicals, loss of cation homeostasis, depletion of energy stores, and changes in subcellular activities. The reperfusion injury may cause in the death of cardiac myocytes that were still viable immediately before myocardial reperfusion. This form of myocardial injury, by itself can induce cardiomyocyte death and increase infarct size. During acute ischemia the relative substrate concentration is the prime factor defining preference and utilization rate. Allosteric enzyme regulation and protein phosphorylation cascades, partially controlled by hormones such as insulin, modulate the concentration effect; together they provide short-term adjustments of cardiac energy metabolism. The expression of metabolic genes is also dynamically regulated in response to developmental and (patho)physiological conditions, leading to long-term adjustments. Specific nuclear receptor transcription factors and co-activators regulate the expression of these genes. Understanding the functional role of these changes is critical for developing the concept of metabolic intervention for heart disease. The paper will review the alterations in energy metabolism that occur

  14. Morphological aspects of myocardial bridges

    Directory of Open Access Journals (Sweden)

    Almira Lujinović

    2013-11-01

    Full Text Available Although some myocardial bridges can be asymptomatic, their presence often causes coronary disease either through direct compression of the “tunnel” segment or through stimulation and accelerated development of atherosclerosis in the segment proximally to the myocardial bridge. The studied material contained 30 human hearts received from the Department of Anatomy. The hearts were preserved 3 to 5 days in 10% formalin solution. Thereafter, the fatty tissue was removed and arterial blood vessels prepared by careful dissection with special reference to the presence of the myocardial bridges. Length and thickness of the bridges were measured by the precise electronic caliper. The angle between the myocardial bridge fibre axis and other axis of the crossed blood vessel was measured by a goniometer. The presence of the bridges was confirmed in 53.33% of the researched material, most frequently (43.33% above the anterior interventricular branch. The mean length of the bridges was 14.64±9.03 mm and the mean thickness was 1.23±1.32 mm. Myocardial bridge fibres pass over the descending blood vessel at the angle of 10-90 degrees. The results obtained on a limited sample suggest that the muscular index of myocardial bridge is the highest for bridges located on RIA, but that the difference is not significant in relation to bridges located on other branches. The results obtained suggest that bridges located on other branches, not only those on RIA, could have a great contractive power and, consequently, a great compressive force, which would be exerted on the wall of a crossed blood vessel.

  15. Magnetic Resonance Imaging in Myocardial Fibrosis Related to Ischemic Events

    Directory of Open Access Journals (Sweden)

    Himcinschi Elisabeta

    2017-09-01

    Full Text Available Given the higher amount of detail it offers, the use of magnetic resonance (MR in the field of cardiology has increased, thus leading to a decrease in the use of invasive and irradiating methods for diagnosing various cardiovascular disorders. The only precautions for MR imaging are metallic implants and advanced-stage chronic kidney disease. For the acquisition of clear and dynamic myocardial images, methods such as spin echo imaging for anatomical description, steady-state free precession imaging for the assessment of ventricular cavity size and function, flow velocity encoding for blood flow measurements, radiofrequency tagging for dynamics, and even spectroscopy for metabolism evaluation are used. Cardiac magnetic resonance (CMR is considered the gold standard imaging method for the anatomical characterization of the heart and obtaining information related to myocardial dynamics. In case of ischemic events, CMR is used for a detailed description of the necrotic area and the complications, and for tracking the ventricular remodeling. By administrating a contrast agent (gadolinium, the difference between sub-endothelial and transmural infarctions can be distinguished, highlighting even microvascular lesions responsible for the extension of the necrosis. The assessment of the dynamics of ventricular remodeling and viability through late gadolinium enhancement (LGE technology highlights the area of fibrosis and the occurrence of late complications.

  16. Sequential thallium-201 myocardial scintigraphy after acute infarction in man

    Energy Technology Data Exchange (ETDEWEB)

    Fletcher, J.W.; Mueller, H.S.; Rao, P.S.

    1980-07-01

    Three sequential Tl-201 myocardial perfusion studies were performed in 21 patients (18 men, 3 women) with first acute transmural myocardia infarction. The Tl-201 image defect size was determined with a semiquantitative visual scoring method and temporal changes in image defect size were compared to CK-MB infarct size and enzymatic evidence of progressive myocardial necrosis and infarct extension. Progressive decreases in Tl-201 image defect size were observed and the visual score in all 21 patients decreased significantly from 6.5 +- 3.7 (mean +- SD) on day 1 to 4.9 +- 3.5 on day 12. Eleven patients without evidence of infarct extension had significantly lower infarct size, a significant decrease in visual score by the 12th day and had significantly smaller Tl-201 defects at all three study times compared to 10 patients with infarct extension. Seven of 10 (70%) with extension had an initial visual score greater than or equal to 7 compared to only 2/11 (18%) without extension. The temporal behavior of Tl-201 image defects is related to the size of the infarction and presence or absence of extension. Sequential studies comparing early initial and subsequent defect size may assist in evaluating the behavior of ischemic and infarcted myocardium in the postinfarction period.

  17. Fibroblasts in myocardial infarction: a role in inflammation and repair

    Science.gov (United States)

    Shinde, Arti V.; Frangogiannis, Nikolaos G.

    2014-01-01

    Fibroblasts do not only serve as matrix-producing reparative cells, but exhibit a wide range of functions in inflammatory and immune responses, angiogenesis and neoplasia. The adult mammalian myocardium contains abundant fibroblasts enmeshed within the interstitial and perivascular extracellular matrix. The current review manuscript discusses the dynamic phenotypic and functional alterations of cardiac fibroblasts following myocardial infarction. Extensive necrosis of cardiomyocytes in the infarcted heart triggers an intense inflammatory reaction. In the early stages of infarct healing, fibroblasts become pro-inflammatory cells, activating the inflammasome and producing cytokines, chemokines and proteases. Pro-inflammatory cytokines (such as Interleukin-1) delay myofibroblast transformation, until the wound is cleared from dead cells and matrix debris. Resolution of the inflammatory infiltrate is associated with fibroblast migration, proliferation, matrix protein synthesis and myofibroblast conversion. Growth factors and matricellular proteins play an important role in myofibroblast activation during the proliferative phase of healing. Formation of a mature cross-linked scar is associated with clearance of fibroblasts, as poorly-understood inhibitory signals restrain the fibrotic response. However, in the non-infarcted remodeling myocardium, local fibroblasts may remain activated in response to volume and pressure overload and may promote interstitial fibrosis. Considering their abundance, their crucial role in cardiac inflammation and repair, and their involvement in myocardial dysfunction and arrhythmogenesis, cardiac fibroblasts may be key therapeutic targets in cardiac remodeling. PMID:24321195

  18. Effects of relaxing music on cardiac autonomic balance and anxiety after acute myocardial infarction.

    Science.gov (United States)

    White, J M

    1999-07-01

    Acute myocardial infarction places additional demands on an already compromised myocardium. Relaxing music can induce a relaxation response, thereby reversing the deleterious effects of the stress response. To compare the effects of relaxing music; quiet, uninterrupted rest; and "treatment as usual" on anxiety levels and physiological indicators of cardiac autonomic function. A 3-group repeated measures experimental design was used. Forty-five patients, 15 per group, with acute myocardial infarction were assigned randomly to 20 minutes of (1) music in a quiet, restful environment (experimental group); (2) quiet, restful environment without music (attention); or (3) treatment as usual (control). Anxiety levels and physiological indicators were measured. Immediately after the intervention, reductions in heart rate, respiratory rate, and myocardial oxygen demand were significantly greater in the experimental group than in the control group. The reductions in heart rate and respiratory rate remained significantly greater 1 hour later. Changes in heart rate, respiratory rate, and myocardial oxygen demand in the attention group did not differ significantly from changes in the other 2 groups. The 3 groups did not differ with respect to systolic blood pressure. Increases in high-frequency heart rate variability were significantly greater in the experimental and attention groups than in the control group immediately after the intervention. State anxiety was reduced in the experimental group only; the reduction was significant immediately and 1 hour after the intervention. Patients recovering from acute myocardial infarction may benefit from music therapy in a quiet, restful environment.

  19. Estimation of myocardial volume at risk from CT angiography

    Science.gov (United States)

    Zhu, Liangjia; Gao, Yi; Mohan, Vandana; Stillman, Arthur; Faber, Tracy; Tannenbaum, Allen

    2011-03-01

    The determination of myocardial volume at risk distal to coronary stenosis provides important information for prognosis and treatment of coronary artery disease. In this paper, we present a novel computational framework for estimating the myocardial volume at risk in computed tomography angiography (CTA) imagery. Initially, epicardial and endocardial surfaces, and coronary arteries are extracted using an active contour method. Then, the extracted coronary arteries are projected onto the epicardial surface, and each point on this surface is associated with its closest coronary artery using the geodesic distance measurement. The likely myocardial region at risk on the epicardial surface caused by a stenosis is approximated by the region in which all its inner points are associated with the sub-branches distal to the stenosis on the coronary artery tree. Finally, the likely myocardial volume at risk is approximated by the volume in between the region at risk on the epicardial surface and its projection on the endocardial surface, which is expected to yield computational savings over risk volume estimation using the entire image volume. Furthermore, we expect increased accuracy since, as compared to prior work using the Euclidean distance, we employ the geodesic distance in this work. The experimental results demonstrate the effectiveness of the proposed approach on pig heart CTA datasets.

  20. Acute esophageal necrosis: a case report and review | Lahbabi ...

    African Journals Online (AJOL)

    Acute esophageal necrosis, commonly referred to as "black esophagus" or "acute necrotizing esophagitis", is a rare clinical disorder with an unclear etiology. The definition excludes patients with a history of recent caustic ingestion. Oesophageal necrosis can be diagnosed at endoscopy by the presence of black necroting ...

  1. Avascular necrosis of bone following renal transplantation | Naiker ...

    African Journals Online (AJOL)

    Alcohol conswnption and radiological evidence of osteoporosis were more prevalent in the avascular necrosis group (42,8% v. 29,0% and 28,5% v. 7,2% respectively). Avascular necrosis did not correlate with age, sex, renal function at 1 year or severe secondary hyperparathyroidism. This study suggests that corticosteroid ...

  2. Tumor necrosis after preventive embolization of large renal angiomyolipomas.

    Science.gov (United States)

    El Rafei, M; Renard, B; Puech, P; Devos, P; Gaillard, V; Lemaître, L

    2015-06-01

    The purpose of this study was to retrospectively evaluate tumor necrosis following preventive embolization in patients with renal angiomyolipoma (RAML) at high risk of bleeding. Arterial embolization was performed in 24 patients (22 women, 2 men; mean age, 43±13 years) with a total of 30 RAMLs (mean volume, 137 cm(3)±163) between 1996 and 2012. Two sub-groups of patients were identified and further compared based on the presence or not of necrosis following arterial embolization. The technical and clinical success rates of arterial embolization of RAMLs were 97% and 87%, respectively. The mean initial volume of RAMLs differed between the two sub-groups with 331 cm(3) in the group with tumor necrosis and 88 cm(3) in the group without tumor necrosis (P=0.0047). High-fat content RAMLs were predominantly observed in the necrosis group and the mean volume reduction observed for high-fat RAMLs was 65% whereas it was 36% for low-fat content RAMLs. The six patients who developed RAML necrosis had arterial embolization using microspheres (one patient with microspheres alone and five with a combination of microspheres and metallic coils). All necrotic RAMLs displayed arterial dysplasia. The risk of tumor necrosis is higher for larger RAMLs. The role of distal arterial embolization with microspheres in tumor necrosis in RAML is suggested by the results of our study but could not be definitely demonstrated statistically due to the limited sample size. Copyright © 2015. Published by Elsevier Masson SAS.

  3. Subcutaneous Fat Necrosis of the Newborn: A Case Report

    Energy Technology Data Exchange (ETDEWEB)

    Yi, Kyung Sik; Cho, Bum Sang; Bae, Il Hun; Lee, Seung Young; Jeon, Min Hee; Lee, Ok Jun; Kim, Mi Jung [Chungbuk National University College of Medicine, Cheongju (Korea, Republic of)

    2007-09-15

    Subcutaneous fat necrosis in the newborn is an uncommon transient disorder of the subcutaneous adipose tissue that develops after birth. We describe the characteristic ultrasonography and CT findings of a case of pathologically confirmed subcutaneous fat necrosis located at the subcutaneous fat layer of the neck, back, and shoulders with a review of the literature

  4. Total gastric necrosis: A case report and literature review | Huang ...

    African Journals Online (AJOL)

    Total gastric necrosis is a rare disease and easy to misdiagnose. Here we report a rare case of total gastric necrosis. The patient, an 89-year-old male, had epigastric pain for 5 days. He was transferred to our hospital because of intraperitoneal hemorrhage and hypovolemic shock. We performed an emergency laparotomy.

  5. Hypercalcemia in Association With Subcutaneous Fat Necrosis of ...

    African Journals Online (AJOL)

    The case of a four weeks-old girl with subcutaneous fat necrosis and associated hypercalcemia is presented. Subcutaneous Fat Necrosis of the New born (SCFN) is an uncommon disorder which is rarely complicated with life threatening hypercalcemia. Though it is reported from many parts of the world this is the first case ...

  6. Therapeutic approaches for tumor necrosis factor inhibition

    Directory of Open Access Journals (Sweden)

    Maria Letícia de Castro Barbosa

    2011-09-01

    Full Text Available Tumor necrosis factor (TNF consists of an inflammatory cytokine essential for homeostasis and organism defense. Despite its physiological relevance, both increased biosynthesis and release of TNF lead to the exacerbation of inflammatory and oxidative responses, which are related to the pathogenesis of a host of diseases of an inflammatory, autoimmune and/or infectious nature. In this context, effective therapeutic approaches for the modulation of TNF have been the focus of research efforts. Approximately one million individuals worldwide have been treated with biotechnological inhibitors of this cytokine, the so-called anti-TNF biopharmaceuticals. However, given the high risk of infection and the limitations related to cost and administration routes, new therapeutic approaches aimed at biological targets that directly or indirectly modulate the production and/or activation of TNF appear promising alternatives for the discovery of new anti-inflammatory and immunomodulatory orally active drugs and are therefore discussed in this paper.O fator de necrose tumoral (do inglês, tumor necrosis factor - TNF consiste em uma citocina inflamatória essencial para a homeostase e defesa do organismo. A despeito de sua relevância fisiológica, o aumento da biossíntese e liberação do TNF conduzem à exacerbação das respostas inflamatória e oxidativa, as quais estão relacionadas à patogênese de várias doenças de natureza inflamatória, auto-imune e/ou infecciosa. A busca por abordagens terapêuticas eficientes na modulação do TNF tem sido alvo de diversos esforços de pesquisa. Aproximadamente um milhão de pessoas ao redor do mundo já foi tratado com inibidores biotecnológicos desta citocina, os chamados biofármacos anti-TNF. Entretanto, em face ao elevado risco de infecções e as limitações relacionadas ao custo e a via de administração, novas abordagens terapêuticas com foco em alvos que modulem, de forma direta ou indireta, a produ

  7. Clinical study on myocardial imaging with. beta. -methyl-p-( sup 123 I)-iodophenyl-pentadecanoic acid in patients with mitochondrial myopathy

    Energy Technology Data Exchange (ETDEWEB)

    Kihara, Koichi; Nakajo, Masayuki; Shono, Hirohisa (Kagoshima Univ. (Japan). Faculty of Medicine) (and others)

    1992-04-01

    Myocardial imaging with {beta}-methyl-p-({sup 123}I)-iodophenyl-pentadecanoic acid ({sup 123}I-BMIPP), a new radiopharmaceutical designed to evaluate myocardial fatty acid metabolism, was performed in 7 patients with mitochondrial myopathy to detect their myocardial damages in comparison with {sup 201}Tl myocardial imaging. These patients were divided into 4 chronic progressive external ophthalmoplegia (CPEO) cases, 2 mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) cases and 1 myoclonus epilepsy with ragged-red fibers (MERRF). In visual assessment, we observed more myocardial segments with decreased uptake of {sup 123}I-BMIPP compared to {sup 201}Tl in MELAS cases than in CPEO cases. The mean myocardial uptake of {sup 123}I-BMIPP was higher than that of {sup 201}Tl in CPEO cases. On the other hand, in MELAS and MERRF cases, the mean myocardial uptake of {sup 123}I-BMIPP was lower than that of {sup 201}Tl. Abnormal findings suggesting myocardial damages were observed in echocardiogram and/or in electrocardiogram in MELAS and MERRF cases, while no such abnormal findings were observed in CPEO cases. Along with the previously reported experimental result that the impairment of rat myocardial mitochondria decreased myocardial uptake of {sup 123}I-BMIPP, these results suggest that {sup 123}I-BMIPP may be useful to detect myocardial damages in patients with mitochondrial myopathy. (author)

  8. Myocardial Fibrosis in Congenital Heart Disease.

    Science.gov (United States)

    Rathod, Rahul H; Powell, Andrew J; Geva, Tal

    2016-05-25

    Myocardial fibrosis is common in patients with congenital heart disease (CHD) and has been associated with arrhythmias, decreased functional status, and adverse ventricular mechanics. There are multiple types of myocardial fibrosis that occur in response to different pathophysiologic stimuli. Recent advances in imaging technology have made detection and quantification of the types of myocardial fibrosis possible. In this review, we describe the pathophysiology of myocardial fibrosis, examine the imaging techniques used to evaluate fibrosis, and discuss the relationship between myocardial fibrosis and clinical outcomes in CHD. (Circ J 2016; 80: 1300-1307).

  9. Diabetic Inhibition of Preconditioning- and Postconditioning-Mediated Myocardial Protection against Ischemia/Reperfusion Injury

    Directory of Open Access Journals (Sweden)

    Xia Yin

    2012-01-01

    Full Text Available Ischemic preconditioning (IPC or postconditioning (Ipost is proved to efficiently prevent ischemia/reperfusion injuries. Mortality of diabetic patients with acute myocardial infarction was found to be 2–6 folds higher than that of non-diabetic patients with same myocardial infarction, which may be in part due to diabetic inhibition of IPC- and Ipost-mediated protective mechanisms. Both IPC- and Ipost-mediated myocardial protection is predominantly mediated by stimulating PI3K/Akt and associated GSK-3β pathway while diabetes-mediated pathogenic effects are found to be mediated by inhibiting PI3K/Akt and associated GSK-3β pathway. Therefore, this review briefly introduced the general features of IPC- and Ipost-mediated myocardial protection and the general pathogenic effects of diabetes on the myocardium. We have collected experimental evidence that indicates the diabetic inhibition of IPC- and Ipost-mediated myocardial protection. Increasing evidence implies that diabetic inhibition of IPC- and Ipost-mediated myocardial protection may be mediated by inhibiting PI3K/Akt and associated GSK-3β pathway. Therefore any strategy to activate PI3K/Akt and associated GSK-3β pathway to release the diabetic inhibition of both IPC and Ipost-mediated myocardial protection may provide the protective effect against ischemia/reperfusion injuries.

  10. Maxillary necrosis by mucormycosis. a case report and literature review.

    Science.gov (United States)

    Auluck, Ajit

    2007-09-01

    The maxilla rarely undergoes necrosis due to its rich vascularity. Maxillary necrosis can occur due to bacterial infections such as osteomyelitis, viral infections such as herpes zoster or fungal infections such as mucormycosis, aspergillosis etc. Mucormycosis is an opportunistic fulminant fungal infection, which mainly infects immunocompromised patients. The infection begins in the nose and paranasal sinuses due to inhalation of fungal spores. The infection can spread to orbital and intracranial structures either by direct invasion or through the blood vessels. The fungus invades the arteries leading to thrombosis that subsequently causes necrosis of hard and soft tissues. We report a case of maxillary necrosis by mucormycosis in an uncontrolled diabetic patient to emphasize early diagnosis of this potentially fatal fungal infection. We briefly discuss different diseases which can lead to maxillary necrosis and review the current concepts in management of mucormycosis. Early diagnosis and prompt treatment can reduce the mortality and morbidity of this lethal fungal infection.

  11. Pathophysiology, Diagnosis, and Treatment of Radiation Necrosis in the Brain

    Science.gov (United States)

    MIYATAKE, Shin-Ichi; NONOGUCHI, Noasuke; FURUSE, Motomasa; YORITSUNE, Erina; MIYATA, Tomo; KAWABATA, Shinji; KUROIWA, Toshihiko

    2015-01-01

    New radiation modalities have made it possible to prolong the survival of individuals with malignant brain tumors, but symptomatic radiation necrosis becomes a serious problem that can negatively affect a patient’s quality of life through severe and lifelong effects. Here we review the relevant literature and introduce our original concept of the pathophysiology of brain radiation necrosis following the treatment of brain, head, and neck tumors. Regarding the pathophysiology of radiation necrosis, we introduce two major hypotheses: glial cell damage or vascular damage. For the differential diagnosis of radiation necrosis and tumor recurrence, we focus on the role of positron emission tomography. Finally, in accord with our hypothesis regarding the pathophysiology, we describe the promising effects of the anti-vascular endothelial growth factor antibody bevacizumab on symptomatic radiation necrosis in the brain. PMID:25744350

  12. Molecular mechanisms of liver injury: apoptosis or necrosis.

    Science.gov (United States)

    Wang, Kewei

    2014-10-01

    Hepatic apoptosis is thought of as a prevalent mechanism in most forms of liver injury. However, the role of hepatic apoptosis is often intermixed with the cellular necrosis. It remains unknown how apoptosis is relevant to the progression of the liver injury. This review summarizes the characteristics of both hepatic apoptosis and necrosis in pathogenesis of liver diseases. Apoptosis and necrosis represent alternative outcomes of different etiology during liver injury. Apoptosis is a main mode of cell death in chronic viral hepatitis, but is intermingled with necrosis in cholestatic livers. Necrosis is the principal type of liver cell killing in acetaminophen-induced hepatotoxicity. Anti-apoptosis as a strategy is beneficial to liver repair response. Therapeutic options of liver disease depend on the understanding toward pathogenic mechanisms of different etiology. Copyright © 2014 Elsevier GmbH. All rights reserved.

  13. NecroQuant: quantitative assessment of radiological necrosis

    Science.gov (United States)

    Hwang, Darryl H.; Mohamed, Passant; Varghese, Bino A.; Cen, Steven Y.; Duddalwar, Vinay

    2017-11-01

    Clinicians can now objectively quantify tumor necrosis by Hounsfield units and enhancement characteristics from multiphase contrast enhanced CT imaging. NecroQuant has been designed to work as part of a radiomics pipelines. The software is a departure from the conventional qualitative assessment of tumor necrosis, as it provides the user (radiologists and researchers) a simple interface to precisely and interactively define and measure necrosis in contrast-enhanced CT images. Although, the software is tested here on renal masses, it can be re-configured to assess tumor necrosis across variety of tumors from different body sites, providing a generalized, open, portable, and extensible quantitative analysis platform that is widely applicable across cancer types to quantify tumor necrosis.

  14. Myocardial Structural and Biological Anomalies Induced by High Fat Diet in Psammomys obesus Gerbils.

    Directory of Open Access Journals (Sweden)

    Abdelhamid Sahraoui

    Full Text Available Psammomys obesus gerbils are particularly prone to develop diabetes and obesity after brief period of abundant food intake. A hypercaloric high fat diet has been shown to affect cardiac function. Here, we sought to determine whether a short period of high fat feeding might alter myocardial structure and expression of calcium handling proteins in this particular strain of gerbils.Twenty Psammomys obesus gerbils were randomly assigned to receive a normal plant diet (controls or a high fat diet. At baseline and 16-week later, body weight, plasma biochemical parameters (including lipid and carbohydrate levels were evaluated. Myocardial samples were collected for pathobiological evaluation.Sixteen-week high fat dieting resulted in body weight gain and hyperlipidemia, while levels of carbohydrates remained unchanged. At myocardial level, high fat diet induced structural disorganization, including cardiomyocyte hypertrophy, lipid accumulation, interstitial and perivascular fibrosis and increased number of infiltrating neutrophils. Myocardial expressions of pro-apoptotic Bax-to-Bcl-2 ratio, pro-inflammatory cytokines [interleukin (IL-1β and tumor necrosis factor (TNF-α], intercellular (ICAM1 and vascular adhesion molecules (VCAM1 increased, while gene encoding cardiac muscle protein, the alpha myosin heavy polypeptide (MYH6, was downregulated. Myocardial expressions of sarco(endoplasmic calcium-ATPase (SERCA2 and voltage-dependent calcium channel (Cacna1c decreased, while protein kinase A (PKA and calcium-calmodulin-dependent protein kinase (CaMK2D expressions increased. Myocardial expressions of ryanodine receptor, phospholamban and sodium/calcium exchanger (Slc8a1 did not change.We conclude that a relative short period of high fat diet in Psammomys obesus results in severe alterations of cardiac structure, activation of inflammatory and apoptotic processes, and altered expression of calcium-cycling determinants.

  15. Circulating cytochrome c as potential biomarker of impaired reperfusion in ST-segment elevation acute myocardial infarction.

    Science.gov (United States)

    Marenzi, Giancarlo; Giorgio, Marco; Trinei, Mirella; Moltrasio, Marco; Ravagnani, Paolo; Cardinale, Daniela; Ciceri, Fabio; Cavallero, Annalisa; Veglia, Fabrizio; Fiorentini, Cesare; Cipolla, Carlo M; Bartorelli, Antonio L; Pelicci, Piergiuseppe

    2010-11-15

    In patients with ST-segment elevation acute myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI), abrupt reperfusion can induce myocardial injury and apoptotic cell death. Reperfusion-induced myocardial damage, however, cannot be easily evaluated in clinical practice because of the lack of specific biomarkers. Cytochrome c, a mitochondrial protein, is released on reperfusion into the cytosol, where it triggers the apoptotic process. It can reach the external fluid and circulating blood when cell rupture occurs. We measured the cytochrome c circulating levels in patients with STEMI undergoing pPCI, and correlated them with the clinical signs of myocardial necrosis and reperfusion. The plasma creatine kinase-MB mass and serum cytochrome c (enzyme-linked immunosorbent assay method) were serially measured in 55 patients with STEMI undergoing pPCI. The angiographic and electrocardiographic signs of myocardial reperfusion were also assessed. Cytochrome c transiently increased in all patients with STEMI, with a curve that paralleled that of creatine kinase-MB. A significant relation was found between the peak values of the 2 biomarkers (R = 0.35, p = 0.01) and between the areas under the 2 curves (R = 0.33, p = 0.02). The creatine kinase-MB peak value correlated significantly with the clinical features of infarct extension. In contrast, the cytochrome c peak value correlated inversely with the myocardial blush grade. Patients with clinical signs of myocardial reperfusion injury had a significantly greater cytochrome c peak value than patients without reperfusion injury (median 1.65 ng/ml, interquartile range 1.20 to 2.20, vs 1.1 ng/ml, interquartile range 0.65 to 1.55; p = 0.04). In conclusion, serum cytochrome c is detectable in the early phase of STEMI treated with pPCI and is associated with clinical signs of impaired myocardial reperfusion. Copyright © 2010 Elsevier Inc. All rights reserved.

  16. TROPONIN T AND HISTOLOGICAL CHARACTERISTICS OF RAT MYOCARDIAL INFARCTION INDUCED BY ISOPROTERENOL

    Science.gov (United States)

    Hasić, Sabaheta; Jadrić, Radivoj; Kiseljaković, Emina; Mornjaković, Zakira; Winterhalter-Jadrić, Mira

    2007-01-01

    Tin our investigation, we used short-time model of myocardial infarction of rats induced by high dose of isoproterenol (ISP). We investigated cardiac troponin T blood level (cTnT) and histologi-cal characteristics of rat myocardium. ISP, single, intraperitoneal dose 250 mg/kg was given to male, adult, Wistar rats (n=12). Rats were distributed depending on their body weight in subgroups: ISP I (BW 260-280g) and ISP II (BW 250-400g). Control group (n=9) was treated with intraperitoneal dose of 0,95% NaCl. Cardiac TnT was measured by electrochemiluminiscence (ECLA) sandwich immunoassay in rat serum 4 hours after ISP application. Rats’ hearts were dissected and examined by qualitative histological method (HE). Statistical significance was set at 0,05. There was significant difference in cTnT of ISP II (p=0,0001) vs. control and ISP I (p<0,05) vs. control. Significant difference was beetween ISP I and ISP II subgroups (p<0.001). The accent of histological changes of myocardium was on nuclei of cell. Cells showed acydophilic changes and nuclei disappearance as signs of coagulative necrosis development. Extensivity of histological changes were different beetween ISP I and ISP II subgroup. Used dose of ISP induced development of myocardial necrosis in rats. Suben-docardial portion of myocardium was more vulnerability than subepicardial portion. Rats of ISP II had more extensive histological changes than these in ISP I. Administered doses of ISP enabled cTnT utilization as a marker of myocardial necrosis. PMID:17848144

  17. Perceived stress in myocardial infarction

    NARCIS (Netherlands)

    Arnold, Suzanne V.; Smolderen, K.G.E.; Buchanan, Donna M.; Li, Yan; Spertus, John A.

    2012-01-01

    Objectives This study sought to determine the association of chronic stress with long-term adverse outcomes after acute myocardial infarction (AMI).BackgroundChronic stress has been shown to be associated with the development of cardiovascular disease and, in the case of particular types of stress

  18. Neonatal Myocardial Infarction or Myocarditis?

    NARCIS (Netherlands)

    de Vetten, Leanne; Bergman, Klasien A.; Elzenga, Nynke J.; van Melle, Joost P.; Timmer, Albertus; Bartelds, Beatrijs

    We report a 29 week-gestation preterm infant who presented during his second week of life with cardiogenic shock. Clinical presentation and first diagnostics suggested myocardial infarction, but echocardiographic features during follow-up pointed to a diagnosis of enteroviral myocarditis. The child

  19. Myocardial perfusion at fatal infarction

    DEFF Research Database (Denmark)

    Hvid-Jacobsen, K; Møller, J T; Kjøller, E

    1992-01-01

    In a consecutive study of myocardial scintigraphy in acute ischemic syndrome, four patients had 99mTc-hexamibi injected intravenously before they developed fatal cardiogenic shock. Planar scintigraphy was performed after death. Slices of the hearts after autopsy were analyzed for scintigraphic...

  20. Dosimetry in myocardial perfusion imaging

    Energy Technology Data Exchange (ETDEWEB)

    Toledo, Janine M.; Trindade, Bruno; Ribeiro, Tarcisio P.C. [Universidade Federal de Minas Gerais (DEN/UFMG), Belo Horizonte (Brazil). Dept. de Engenharia Nuclear. Programa de Pos-Graduacao em Ciencias e Tecnicas Nucleares

    2011-07-01

    This paper conducts a dosimetric investigation on the myocardial perfusion image protocol, together with a literature reviewing, motivated by the significant statistic increasing on mortality, morbidity and disability associated with cardiovascular disease, surpassing infectious diseases. Nuclear Cardiology plays a role n the diagnostic functional evaluation of the heart and in the prognostic of patients with suspected or known cardiac ischemia. In the context of unstable myocardial ischemic syndrome, myocardial perfusion scintigraphy is a non-invasive procedure performed by administering a radiopharmaceutical targeted to the heart. As tool for this study are that the images obtained by thoracic angiotomography and abdominal aorta as a anatomic and functional information for model reproduction in SISCODES - System of Codes for Absorbed Dose Calculations based on Stochastic Methods. Data were manipulated in order to create a voxel computational model of the heart to be running in MCNP - Monte Carlo Neutron Particle Code. . It was assumed a homogeneous distribution of Tl-201 in cardiac muscle. Simulations of the transport of particles through the voxel and the interaction with the heart tissue were performed. As a result, the isodose curves in the heart model are displayed as well as the dose versus volume histogram of the heart muscle. We conclude that the present computational tools can generate doses distributed in myocardial perfusion. (author)

  1. Regional myocardial perfusion and performance

    NARCIS (Netherlands)

    H.C. Schamhardt (Henk)

    1980-01-01

    textabstractThe function of the heart is to pump blood from the veins into the arteries in response to the need of the tissues for oxygen and substrates. During its action the heart itself needs these nutrients. Factors that mainly determine the myocardial oxygen demand are (fig.0.1): heart rate,

  2. The Orchestra of Myocardial Regeneration

    NARCIS (Netherlands)

    Siddiqi, S.

    2014-01-01

    A glimpse on previous and current literature ignites the recognition of the luxurious era that cardiac science has reached. In particular, the past fifteen years have provided tremendous advancements in the field of myocardial biology with the characterization of cardiac stem cells, reprogramming of

  3. Pregnancy-related myocardial infarction

    NARCIS (Netherlands)

    Lameijer, H.; Lont, M. C.; Buter, H.; van Boven, A. J.; Boonstra, P. W.; Pieper, P. G.

    Introduction The risk of acute myocardial infarction in young women is low, but increases during pregnancy due to the physiological changes in pregnancy, including hypercoagulability. Ischaemic heart disease during pregnancy is not only associated with increased maternal morbidity and mortality, but

  4. Spousal Adjustment to Myocardial Infarction.

    Science.gov (United States)

    Ziglar, Elisa J.

    This paper reviews the literature on the stresses and coping strategies of spouses of patients with myocardial infarction (MI). It attempts to identify specific problem areas of adjustment for the spouse and to explore the effects of spousal adjustment on patient recovery. Chapter one provides an overview of the importance in examining the…

  5. Biomarkers in acute myocardial infarction

    Directory of Open Access Journals (Sweden)

    Ng Leong L

    2010-06-01

    Full Text Available Abstract Myocardial infarction causes significant mortality and morbidity. Timely diagnosis allows clinicians to risk stratify their patients and select appropriate treatment. Biomarkers have been used to assist with timely diagnosis, while an increasing number of novel markers have been identified to predict outcome following an acute myocardial infarction or acute coronary syndrome. This may facilitate tailoring of appropriate therapy to high-risk patients. This review focuses on a variety of promising biomarkers which provide diagnostic and prognostic information. Heart-type Fatty Acid Binding Protein and copeptin in combination with cardiac troponin help diagnose myocardial infarction or acute coronary syndrome in the early hours following symptoms. An elevated N-Terminal Pro-B-type Natriuretic Peptide has been well validated to predict death and heart failure following a myocardial infarction. Similarly other biomarkers such as Mid-regional pro-Atrial Natriuretic Peptide, ST2, C-Terminal pro-endothelin 1, Mid-regional pro-Adrenomedullin and copeptin all provide incremental information in predicting death and heart failure. Growth differentiation factor-15 and high-sensitivity C-reactive protein predict death following an acute coronary syndrome. Pregnancy associated plasma protein A levels following chest pain predicts risk of myocardial infarction and revascularisation. Some biomarkers such as myeloperoxidase and high-sensitivity C-reactive protein in an apparently healthy population predicts risk of coronary disease and allows clinicians to initiate early preventative treatment. In addition to biomarkers, various well-validated scoring systems based on clinical characteristics are available to help clinicians predict mortality risk, such as the Thrombolysis In Myocardial Infarction score and Global Registry of Acute Coronary Events score. A multimarker approach incorporating biomarkers and clinical scores will increase the prognostic

  6. Molecular Mechanism of Apoptosis and Necrosis

    Directory of Open Access Journals (Sweden)

    Gulfidan Coskun

    2011-06-01

    Full Text Available Organismal homeostasis depends on an intricate balance between cell death and renewal. Apoptosis is a process of programmed cell death that plays a critical role in some normal and pathologic conditions beginning from embryologic development and ends at death. Apoptosis is initiated by morphological changes at the cell membrane, surface organels and nucleus. Apoptosis starts with death signals coming from outside or inside of the cell and continue to activate the mechanisms of apoptosis via cell death receptor or mitochondrial pathways. During apoptosis a group proteases are activated which cause DNA fragmentation, cytoplasmic shrinkage and membrane blebbing. Apoptotic cells divide into apoptotic bodies and then these apoptotic bodies are removed from tissue by phagocytes and adjacent cells In contrast to the “programmed” nature of apoptosis, necrotic cell death has always been believed to be a random, uncontrolled process that leads to death of the cell. Also necrosis, which is an other type of cell death, came to be used to describe pathologic cell death which cause inflamation. [Archives Medical Review Journal 2011; 20(3.000: 145-158

  7. Immunization with viral antigens: Infectious haematopoietic necrosis

    Science.gov (United States)

    Winton, J.R.; Midtlyng, Paul J.; Brown, F.

    1997-01-01

    Infectious haematopoietic necrosis (IHN) is one of the most important viral diseases of salmonids, especially among juvenile fish where losses can be high. For over 20 years, researchers have tested a variety of preparations for control of IHN. Early vaccines consisted of killed virus and were effective when delivered by injection, but too costly to be practical on a large scale. Attenuated vaccines were developed by serial passage in cell culture and by monoclonal antibody selection. These offered excellent protection and were cost-effective, but residual virulence and uncertainty about their effects on other aquatic species made them poor candidates for licensing. Subunit vaccines using part of the IHNV glycoprotein gene cloned into E. coli or into an attenuated strain of A. salmonicida have been tested, appeared safe and were inexpensive. These vaccines were reported to provide some protection when delivered by immersion. Information on the location of antigenic sites on the glycoprotein led to trials using synthetic peptides, but these did not seem to be economically viable. Recently, plasmid vectors encoding the glycoprotein gene under control of a cytomegalovirus promoter were developed for genetic immunization. The constructs were highly protective when delivered by injection, but a more practical delivery system is needed. Thus, while several vaccine strategies have been tried in order to stimulate specific immunity against IHN, more research is needed to develop a commercially viable product for control of this important disease.

  8. Mortality rate in type 2 myocardial infarction

    DEFF Research Database (Denmark)

    Saaby, Lotte; Poulsen, Tina Svenstrup; Diederichsen, Axel Cosmus Pyndt

    2014-01-01

    2 myocardial infarction. CONCLUSIONS: Mortality in patients with type 2 myocardial infarction is high, reaching approximately 50% after 2 years. Further descriptive and survival studies are needed to improve the scientific evidence on which treatment of type 2 myocardial infarction is based.......BACKGROUND: The classification of myocardial infarction into 5 types was introduced in 2007. The prognostic impact of this universal definition, with particular focus on type 2 myocardial infarction, has not been studied prospectively in unselected hospital patients. METHODS: During a 1-year period......, all hospitalized patients having cardiac troponin I measured were considered. The diagnosis of a myocardial infarction was according to the universal definition, and specified criteria were used in the classification of type 2 myocardial infarction. Follow-up was at least 1 year, with mortality...

  9. The effect of levosimendan on myocardial ischemia–reperfusion injury in streptozotocin-induced diabetic rats

    Directory of Open Access Journals (Sweden)

    Hasan Ali Kiraz

    2015-12-01

    indicate that levosimendan may be helpful in reducing myocardial necrosis, myocardial inflammation, and myocardial tissue edema resulting from ischemia–reperfusion injury.

  10. The effect of levosimendan on myocardial ischemia–reperfusion injury in streptozotocin-induced diabetic rats

    Science.gov (United States)

    Kiraz, Hasan Ali; Poyraz, Fatih; Kip, Gülay; Erdem, Özlem; Alkan, Metin; Arslan, Mustafa; Özer, Abdullah; Şivgin, Volkan; Çomu, Faruk Metin

    2015-01-01

    levosimendan may be helpful in reducing myocardial necrosis, myocardial inflammation, and myocardial tissue edema resulting from ischemia–reperfusion injury. PMID:26649830

  11. Necrosis, a regulated mechanism of cell death La necrosis, un mecanismo regulado de muerte celular

    Directory of Open Access Journals (Sweden)

    Mauricio Rojas López

    2010-05-01

    Full Text Available

    Three types of cellular death have been defined by morphological and biochemical criteria: apoptosis, necrosis and autophagy. Apoptosis is a regulated cell death, mainly mediated by caspases; autophagy induces degradation of intracellular damaged organelles through the formation of vesicles that fuse with hydrolytic vacuoles.

     

    Necrosis has been traditionally defined by the rupture the cytoplasmic membrane with subsequent release of intracellular material, triggering localized inflammatory Intrinsic cellular activities and the events preceding cellular collapse are critical to determine the type of tissue damage.

     

    The fact that all three types of cellular death can coexist in any organ and tissue with different availabilities of ATP, suggests that necrosis can be conceived as an active event and that to some extent it may be regulated. Alterations in the structure of proteins and in the

  12. Area at risk can be assessed by iodine-123-meta-iodobenzylguanidine single-photon emission computed tomography after myocardial infarction: a prospective study.

    Science.gov (United States)

    Hedon, Christophe; Huet, Fabien; Ben Bouallegue, Fayçal; Vernhet, Hélène; Macia, Jean-Christophe; Cung, Thien-Tri; Leclercq, Florence; Cade, Stéphane; Cransac, Frédéric; Lattuca, Benoit; Vandenberghe, D'Arcy; Bourdon, Aurélie; Benkiran, Meriem; Vauchot, Fabien; Gervasoni, Richard; D'estanque, Emmanuel; Mariano-Goulart, Denis; Roubille, François

    2018-02-01

    Myocardial salvage is an important surrogate endpoint to estimate the impact of treatments in patients with ST-segment elevation myocardial infarction (STEMI). The aim of this study was to evaluate the correlation between cardiac sympathetic denervation area assessed by single-photon emission computed tomography (SPECT) using iodine-123-meta-iodobenzylguanidine (I-MIBG) and myocardial area at risk (AAR) assessed by cardiac magnetic resonance (CMR) (gold standard). A total of 35 postprimary reperfusion STEMI patients were enrolled prospectively to undergo SPECT using I-MIBG (evaluates cardiac sympathetic denervation) and thallium-201 (evaluates myocardial necrosis), and to undergo CMR imaging using T2-weighted spin-echo turbo inversion recovery for AAR and postgadolinium T1-weighted phase sensitive inversion recovery for scar assessment. I-MIBG imaging showed a wider denervated area (51.1±16.0% of left ventricular area) in comparison with the necrosis area on thallium-201 imaging (16.1±14.4% of left ventricular area, Parea (P=0.23) and was adequately correlated (R=0.56, P=0.0002). Myocardial salvage evaluated by SPECT imaging (mismatch denervated but viable myocardium) was significantly higher than by CMR (P=0.02). In patients with STEMI, I-MIBG SPECT, assessing cardiac sympathetic denervation may precisely evaluate the AAR, providing an alternative to CMR for AAR assessment.

  13. Insulin Like Growth Factor-1 (IGF-1 Causes Overproduction of IL-8, an Angiogenic Cytokine and Stimulates Neovascularization in Isoproterenol-Induced Myocardial Infarction in Rats

    Directory of Open Access Journals (Sweden)

    Nagaraja Haleagrahara

    2011-11-01

    Full Text Available Angiogenesis factors are produced in response to hypoxic or ischemic insult at the site of pathology, which will cause neovascularization. Insulin like growth factor-1 (IGF-1 exerts potent proliferative, angiogenic and anti-apoptotic effects in target tissues. The present study was aimed to evaluate the effects of IGF-1 on circulating level of angiogenic cytokine interleukin-8 (IL-8, in experimentally-induced myocardial ischemia in rats. Male Sprague-Dawley rats were divided into control, IGF-1 treated (2 µg/kg/day subcutaneously, for 5 and 10 days, isoproterenol (ISO treated (85 mg/kg, subcutaneously for two days and ISO with IGF-1 treated (for 5 and 10 days. Heart weight, serum IGF-1, IL-8 and cardiac marker enzymes (CK-MB and LDH were recorded after 5 and 10 days of treatment. Histopathological analyses of the myocardium were also done. There was a significant increase in serum cardiac markers with ISO treatment indicating myocardial infarction in rats. IGF-1 level increased significantly in ISO treated groups and the level of IGF-1 was significantly higher after 10 days of treatment. IL-8 level increased significantly after ISO treatment after 5 and 10 days and IGF-1 concurrent treatment to ISO rats had significantly increased IL-8 levels. Histopathologically, myocyte necrosis and nuclear pyknosis were reduced significantly in IGF-1 treated group and there were numerous areas of capillary sprouting suggestive of neovascularization in the myocardium. Thus, IGF-1 protects the ischemic myocardium with increased production of circulating angiogenic cytokine, IL-8 and increased angiogenesis.

  14. Umbilical necrosis rates after abdominal-based microsurgical breast reconstruction.

    Science.gov (United States)

    Ricci, Joseph A; Kamali, Parisa; Becherer, Babette E; Curiel, Daniel; Wu, Winona; Tobias, Adam M; Lin, Samuel J; Lee, Bernard T

    2017-07-01

    Umbilical stalk necrosis represents a rare, yet important complication after abdominal-based microsurgical breast reconstruction, which is both underrecognized and understudied in the literature. Once identified, umbilical reconstruction can be an extremely challenging problem. All consecutive breast free flaps at a single institution from February 2004 to February 2016 were reviewed, excluding non-abdominal-based flaps. Patients were divided based on the development of umbilical necrosis postoperatively. Demographics, surgical characteristics, and other complications were compared between the groups. A total of 918 patients met the inclusion criteria, with 29 developing umbilical necrosis identified (3.2%). Patients developing necrosis tended to be older (49.4 yrs versus 52.9 yrs; P necrosis was also associated with increased flap weight (830 g versus 656 g; P necrosis was not associated with any concomitant complications. Umbilical stalk necrosis was found to occur in 3.2% of patients and was associated with several preoperative comorbidities and intraoperative characteristics. This information should help influence intraoperative decision-making to prevent the development of this undesirable complication. Copyright © 2017 Elsevier Inc. All rights reserved.

  15. Plaquing procedure for infectious hematopoietic necrosis virus

    Science.gov (United States)

    Burke, J.A.; Mulcahy, D.

    1980-01-01

    A single overlay plaque assay was designed and evaluated for infectious hematopoietic necrosis virus. Epithelioma papillosum carpio cells were grown in normal atmosphere with tris(hydroxymethyl)aminomethane- or HEPES (N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid)-buffered media. Plaques were larger and formed more quickly on 1- to 3-day-old cell monolayers than on older monolayers. Cell culture medium with a 10% addition of fetal calf serum (MEM 10) or without serum (MEM 0) were the most efficient virus diluents. Dilution with phosphate-buffered saline, saline, normal broth, or deionized water reduced plaque numbers. Variations in the pH (7.0 to 8.0) of a MEM 0 diluent did not affect plaque numbers. Increasing the volume of viral inoculum above 0.15 ml (15- by 60-mm plate) decreased plaquing efficiency. Significantly more plaques occurred under gum tragacanth and methylcellulose than under agar or agarose overlays. Varying the pH (6.8 to 7.4) of methylcellulose overlays did not significantly change plaque numbers. More plaques formed under the thicker overlays of both methylcellulose and gum tragacanth. Tris(hydroxymethyl)aminomethane and HEPES performed equally well, buffering either medium or overlay. Plaque numbers were reduced when cells were rinsed after virus adsorption or less than 1 h was allowed for adsorption. Variation in adsorption time between 60 and 180 min did not change plaque numbers. The mean plaque formation time was 7 days at 16 degrees C. The viral dose response was linear when the standardized assay was used.

  16. First report of natural infection of Vigna mungo var. silvestris L. by Groundnut bud necrosis virus, a tospovirus

    Directory of Open Access Journals (Sweden)

    Mohammad AKRAM

    2010-09-01

    Full Text Available In the autumn of 2008, Vigna mungo var. silvestris growing in the experimental field of the Indian Institute of Pulses Research, Kanpur, India, showed chlorosis around some lateral veins and vein branches (mainly near the leaflet margin, downward curling of the leaf margins, necrosis of the stems and petioles, and twisting of the leaflets. Disease incidence was 20%. Symptoms indicated that the cause was Groundnut bud necrosis virus. The virus was identified on the basis of the symptoms on the diagnostic host, and the reverse transcription polymerase chain reaction (RT-PCR using specific primers of the NSm and NP genes. To our knowledge this is the first report of Groundnut bud necrosis virus on V. mungo var. silvestris.

  17. Acute myocardial infarction during regadenoson myocardial perfusion imaging.

    Science.gov (United States)

    Shah, Sachil; Parra, David; Rosenstein, Robert S

    2013-06-01

    Pharmacologic stress testing uses vasodilators to provide objective evidence of myocardial ischemia. Adenosine and dipyridamole are nonselective adenosine receptor agonists that have been associated with myocardial infarction (MI) during intravenous infusion. Mechanisms postulated for this effect include coronary steal, transmural steal, global hypotension, and direct vasoconstriction. Regadenoson, a direct A2A agonist, was approved for use in stress testing in 2008. We describe a 68-year-old man who presented to our institution with typical angina, relieved by nitroglycerin. He did not have electrocardiogram (ECG) changes suggestive of myocardial pathology, and laboratory testing did not reveal a significant rise in troponin-I levels. To further assess the etiology of his symptoms, he underwent a pharmacologic stress test with regadenoson followed by technetium 99 m sestamibi. Six minutes after regadenoson infusion, the patient developed severe retrosternal chest pain accompanied by ST elevations on ECG. Sublingual nitroglycerin was administered that resolved both the pain and ECG changes. The patient subsequently underwent urgent coronary angiography and was found to have a 95% critical stenosis involving the left anterior descending artery. We conclude this case represents a MI secondary to coronary steal phenomenon induced by regadenoson infusion. Clinicians should be aware this adverse effect can occur despite the improved side-effect profile of regadenoson. Continuous monitoring of vital signs and the ECG with regular assessment of symptoms is imperative to identify this rare but potentially devastating adverse event. © 2013 Pharmacotherapy Publications, Inc.

  18. Avascular necrosis of the femoral head presenting as trochanteric bursitis.

    Science.gov (United States)

    Mandell, B F

    1990-01-01

    Five patients are described with avascular necrosis of the femoral head who presented with ipsilateral trochanteric bursitis, in the absence of clearcut hip joint disease. Avascular necrosis was indicated by magnetic resonance imaging. It is suggested that clinical trochanteric bursitis, especially when refractory to local corticosteroid treatment, may be the initial sign of hip disease. In the patient with risk factor(s) for avascular necrosis that diagnosis should be considered and evaluated with appropriate studies, such as magnetic resonance imaging, to prevent weight bearing at an early stage and permit possible surgical decompression in the hope of postponing or obviating the need for total hip replacement. PMID:2241294

  19. Indomethacin induced avascular necrosis of head of femur

    OpenAIRE

    Prathapkumar, K; Smith, I; Attara, G

    2000-01-01

    Chemically induced avascular necrosis of bone is a well documented entity. Indomethacin is one of the causes of this condition but is often difficult to recognise. Review of the literature shows that only one case of indomethacin induced avascular necrosis has been reported in the English language between 1966 and the present.
The case of a young healthy man, who developed avascular necrosis of head of femur after prolonged administration of indomethacin, is reported here.


Keywords: indomet...

  20. Mandibular bone necrosis after use of paraformaldehyde-containing paste

    Directory of Open Access Journals (Sweden)

    Chi-hwan Lee

    2016-11-01

    Full Text Available Paraformaldehyde has been used in the past as a pulpotomy agent. However, it has a severe cytotoxic effect and may cause alveolar bone necrosis. Depulpin, a devitalizing agent containing 49% paraformaldehyde, is no longer used frequently due to its severe side effects. In the two cases described in the present study, Depulpin was used as a devitalizing agent during root canal treatment. It caused a gradual loss of sensibility in adjacent teeth, gingival necrosis, and osteomyelitis. This case report demonstrates the serious side effects of using a paraformaldehyde-containing paste as a devitalizing agent for pulp, particularly mandibular bone necrosis.

  1. Mandibular bone necrosis after use of paraformaldehyde-containing paste

    Science.gov (United States)

    Lee, Chi-hwan; Choi, Yoorina

    2016-01-01

    Paraformaldehyde has been used in the past as a pulpotomy agent. However, it has a severe cytotoxic effect and may cause alveolar bone necrosis. Depulpin, a devitalizing agent containing 49% paraformaldehyde, is no longer used frequently due to its severe side effects. In the two cases described in the present study, Depulpin was used as a devitalizing agent during root canal treatment. It caused a gradual loss of sensibility in adjacent teeth, gingival necrosis, and osteomyelitis. This case report demonstrates the serious side effects of using a paraformaldehyde-containing paste as a devitalizing agent for pulp, particularly mandibular bone necrosis. PMID:27847756

  2. Challenges With the Diagnosis and Treatment of Cerebral Radiation Necrosis

    Energy Technology Data Exchange (ETDEWEB)

    Chao, Samuel T., E-mail: chaos@ccf.org [Department of Radiation Oncology, Cleveland Clinic, Cleveland, Ohio (United States); Rose Ella Burkhardt Brain Tumor and Neuro-oncology Center, Cleveland Clinic, Cleveland, Ohio (United States); Ahluwalia, Manmeet S. [Department of Medical Oncology, Cleveland Clinic, Cleveland, Ohio (United States); Rose Ella Burkhardt Brain Tumor and Neuro-oncology Center, Cleveland Clinic, Cleveland, Ohio (United States); Barnett, Gene H. [Department of Neurosurgery, Cleveland Clinic, Cleveland, Ohio (United States); Rose Ella Burkhardt Brain Tumor and Neuro-oncology Center, Cleveland Clinic, Cleveland, Ohio (United States); Stevens, Glen H.J. [Department of Neurology, Cleveland Clinic, Cleveland, Ohio (United States); Rose Ella Burkhardt Brain Tumor and Neuro-oncology Center, Cleveland Clinic, Cleveland, Ohio (United States); Murphy, Erin S. [Department of Radiation Oncology, Cleveland Clinic, Cleveland, Ohio (United States); Rose Ella Burkhardt Brain Tumor and Neuro-oncology Center, Cleveland Clinic, Cleveland, Ohio (United States); Stockham, Abigail L. [Department of Radiation Oncology, Cleveland Clinic, Cleveland, Ohio (United States); Shiue, Kevin [Case Western Reserve University School of Medicine, Cleveland, Ohio (United States); Suh, John H. [Department of Radiation Oncology, Cleveland Clinic, Cleveland, Ohio (United States); Rose Ella Burkhardt Brain Tumor and Neuro-oncology Center, Cleveland Clinic, Cleveland, Ohio (United States)

    2013-11-01

    The incidence of radiation necrosis has increased secondary to greater use of combined modality therapy for brain tumors and stereotactic radiosurgery. Given that its characteristics on standard imaging are no different that tumor recurrence, it is difficult to diagnose without use of more sophisticated imaging and nuclear medicine scans, although the accuracy of such scans is controversial. Historically, treatment had been limited to steroids, hyperbaric oxygen, anticoagulants, and surgical resection. A recent prospective randomized study has confirmed the efficacy of bevacizumab in treating radiation necrosis. Novel therapies include using focused interstitial laser thermal therapy. This article will review the diagnosis and treatment of radiation necrosis.

  3. Myocardial infarction and stem cells

    Directory of Open Access Journals (Sweden)

    K Ananda Krishna

    2011-01-01

    Full Text Available Permanent loss of cardiomyocytes and scar tissue formation after myocardial infarction (MI results in an irreversible damage to the cardiac function. Cardiac repair (replacement, restoration, and regeneration is, therefore, essential to restore function of the heart following MI. Existing therapies lower early mortality rates, prevent additional damage to the heart muscle, and reduce the risk of further heart attacks. However, there is need for treatment to improve the infarcted area by replacing the damaged cells after MI. Thus, the cardiac tissue regeneration with the application of stem cells may be an effective therapeutic option. Recently, interest is more inclined toward myocardial regeneration with the application of stem cells. However, the potential benefits and the ability to improve cardiac function with the stem cell-based therapy need to be further addressed. In this review, we focus on the clinical applications of stem cells in the cardiac repair.

  4. Validation of Contrast Enhanced Cine Steady-State Free Precession and T2-Weigthed CMR for Assessment of Ischemic Myocardial Area- At-Risk

    DEFF Research Database (Denmark)

    Søvsø Szocska Hansen, Esben; Pedersen, Steen Fjord; Pedersen, Steen Bønløkke

    2017-01-01

    Measuring myocardial salvage is important to evaluate the possible cardioprotective effects of adjunctive cardioprotective intervention in patients with myocardial infarction undergoing primary percutaneous intervention. Contrast-enhanced steady-state free precession magnetic resonance imaging (CE-CINE......) has recently been used to quantify AAR and validated against myocardial perfusion SPECT. In this study we sought to determine how well T2-STIR and CE-CINE depicts AAR in an experimental porcine model of myocardial ischemia-reperfusion injury using histopathology as the reference for infarct size...

  5. Myocardial infarction and subsequent pregnancy

    Directory of Open Access Journals (Sweden)

    Tedoldi Citânia Lúcia

    2000-01-01

    Full Text Available We report the case of a 40-year-old woman with 2 previous myocardial infarctions, revascularization surgery, and an ongoing pregnancy complicated with preeclampsia and fetal hypoxia. Her follow-up performed by a multidisciplinary team made possible the birth through cesarean section of a premature infant of the female sex with a very low birth weight, but without severe respiratory distress of the hyaline membrane disease type. Three months after the delivery, mother and daughter were healthy.

  6. Using Feily's method prevented scalp necrosis in three patients incline to the scalp recipient necrosis; what is new in prevention of scalp necrosis?

    Science.gov (United States)

    Feily, Amir; Feily, Ahmad

    2017-01-01

    Serious complications arising from surgical hair restoration are relatively uncommon following well-performed and well-planned surgery by skillful surgical techniques, good communication, and postoperative follow-up. Surgical complications often categorized as those which occur in the donor site and the recipient site. In this paper among recipient area complication we focused on recipient area necrosis that arises when an increased number of recipient grafts are utilized and de-vascularization of the scalp occurs as a result of the large wound area due to the dense packing splitting of recipient skin. Recently, Feily et al. explained an interesting method to prevent development of recipient area necrosis following a hair transplant procedure. Herein we reported three cases of dense hair transplantation using the Feilys method that after slitting they troubled by unusual long lasting dark areas on the scalp and they need more than 24 hr's patience for prevention of scalp necrosis. © 2016 Wiley Periodicals, Inc.

  7. Myocardial infarction in the elderly.

    Science.gov (United States)

    Carro, Amelia; Kaski, Juan Carlos

    2011-04-01

    Advances in pharmacological treatment and effective early myocardial revascularization have -in recent years- led to improved clinical outcomes in patients with acute myocardial infarction (AMI). However, it has been suggested that compared to younger subjects, elderly AMI patients are less likely to receive evidence-based treatment, including myocardial revascularization therapy. Several reasons have been postulated to explain this trend, including uncertainty regarding the true benefits of the interventions commonly used in this setting as well as increased risk mainly associated with comorbidities. The diagnosis, management, and post-hospitalization care of elderly patients presenting with an acute coronary syndrome pose many difficulties at present. A complex interplay of variables such as comorbidities, functional and socioeconomic status, side effects associated with multiple drug administration, and individual biologic variability, all contribute to creating a complex clinical scenario. In this complex setting, clinicians are often required to extrapolate evidence-based results obtained in cardiovascular trials from which older patients are often, implicitly or explicitly, excluded. This article reviews current recommendations regarding management of AMI in the elderly.

  8. Myocardial perfusion after marathon running.

    Science.gov (United States)

    Kalliokoski, Kari K; Laaksonen, Marko S; Luotolahti, Matti; Laine, Hanna; Takala, Teemu O; Nuutila, Pirjo; Knuuti, Juhani

    2004-08-01

    We investigated the effects of acute prolonged exercise (marathon running) on cardiac function and myocardial perfusion. Cardiac dimensions and function were measured in seven endurance-trained men using echocardiography before and repeatedly after marathon (42.2 km) running (at 10 min, 150 min, and 20 h). Myocardial perfusion and perfusion resistance were measured using positron emission tomography and 15O-H2O before and 85-115 min after running. Echocardiographic indices showed only mild and clinically non-significant changes in cardiac function after running. Rate-pressure-corrected basal myocardial perfusion (0.89+/-0.13 vs. 1.20+/-0.32 mL min(-1) g(-1), P=0.04) was increased after running. Also, adenosine-stimulated perfusion tended to be higher (3.67+/-0.81 vs. 4.47+/-0.52 mL min(-1) g(-1), P=0.12) and perfusion resistance during adenosine stimulation was significantly lower after running (26+/-6 vs. 18+/-3 mmHg min g mL(-1), P=0.03). Plasma free fatty acid (FFA) concentration was significantly increased after running. These results show that marathon running does not cause marked changes in cardiac function in healthy men. Basal perfusion was increased after exercise, probably reflecting changes in fuel preferences to increased use of FFAs. Strenuous exercise also seems to enhance coronary reactivity, which could thereby serve as a protective mechanism to vascular events after exercise.

  9. Partial cecal necrosis treated by laparoscopic partial cecal resection.

    Science.gov (United States)

    Perko, Zdravko; Bilan, Kanito; Vilović, Katarina; Druzijanić, Nikica; Kraljević, Damir; Juriicić, Josko; Krnić, Dragan; Srsen, Darko; Pogorelić, Zenon; Tomić, Snjezana

    2006-12-01

    Acute colonic ischemia is the common cause of colitis in elderly population. However, isolated ischemic necrosis of cecum is rare entity, often associated with variety of conditions. Here we present a case of a 73-year old woman with a past history of hypertension presented with clinical symptoms of right lower quadrant abdominal pain and tenderness localized to the right lower quadrant, guarding and rebound tenderness. With diagnosis of acute appendicitis, the patient underwent laparoscopy where the cecal partial necrosis was discovered. Necrotic area of cecum was excised using two endoscopic cutters and laparoscopic appendectomy was performed. Pathologist report showed thrombosis of vessels and necrosis of entire cecal wall. The patient completely recovered without any surgical complications. This is the first case of partial cecum necrosis laparoscopicaly managed and with a partial cecal resection only.

  10. Incremental change in acute esophageal necrosis: report of two cases.

    Science.gov (United States)

    Wu, Ming-Ho; Wu, Han-Yun

    2014-02-01

    Acute esophageal necrosis, also called "black esophagus" because of its characteristic appearance on endoscopy, is a life-threatening disease; however, its temporal evolution on endoscopy is not well understood. We describe the serial changes in acute esophageal necrosis in two patients, who underwent four upper endoscopic examinations each. Serial endoscopy demonstrated progressive necrosis extending from the lower esophagus proximally to involve the middle or upper thoracic esophagus in both patients. The first patient was treated with transhiatal esophagectomy, followed by esophageal reconstruction, and medical control of repeated duodenal ulcer bleeding. The second patient died of esophageal perforation, as a complication of Sengstaken-Blakemore tube stent placement to control esophageal bleeding. We report these cases to demonstrate the importance of early detection and prompt surgical treatment of acute esophageal necrosis.

  11. Fueling the Flames: Mammalian Programmed Necrosis in Inflammatory Diseases

    Science.gov (United States)

    Chan, Francis Ka-Ming

    2012-01-01

    Programmed necrosis or necroptosis is an inflammatory form of cell death driven by TNF-like death cytokines, toll-like receptors, and antigen receptors. Unlike necrosis induced by physical trauma, a dedicated pathway is involved in programmed necrosis. In particular, a kinase complex composed of the receptor interacting protein kinase 1 (RIPK1) and RIPK3 is a central step in necrotic cell death. Assembly and activation of this RIPK1–RIPK3 “necrosome” is critically controlled by protein ubiquitination, phosphorylation, and caspase-mediated cleavage events. The molecular signals cumulate in formation of intracellular vacuoles, organelle swelling, internal membrane leakage, and eventually plasma membrane rupture. These morphological changes can result in spillage of intracellular adjuvants to promote inflammation and further exacerbate tissue injury. Because of the inflammatory nature of necrosis, it is an attractive pathway for therapeutic intervention in acute inflammatory diseases. PMID:23125016

  12. Bilateral streptococcal corneoscleritis complicating [beta] irradiation induced scleral necrosis

    Energy Technology Data Exchange (ETDEWEB)

    Moriarty, A.P.; Crawford, G.J.; McAllister, I.L.; Constable, I.J. (Royal Perth Hospital, WA (Australia))

    1993-04-01

    Bacterial corneoscleritis may complicate scleral necrosis induced by [beta] irradiation following pterygium removal. Previous cases have been unilateral. The authors report a case of severe bilateral corneoscleritis caused by Streptococcus pneumoniae. (author).

  13. Renal papillary necrosis and pyelonephritis accompanying fenoprofen therapy.

    Science.gov (United States)

    Husserl, F E; Lange, R K; Kantrow, C M

    1979-10-26

    Renal papillary necrosis occurred after fenoprofen calcium administration in a patient with systemic lupus erythematosus and urinary tract infection. Possible mechanisms of renal damage may be hypersensitivity, decreased blood flow, and decreased production of a prostaglandin E-like substance.

  14. Magnetic resonance imaging of myocardial injury and ventricular torsion after marathon running.

    Science.gov (United States)

    Hanssen, Henner; Keithahn, Alexandra; Hertel, Gernot; Drexel, Verena; Stern, Heiko; Schuster, Tibor; Lorang, Dan; Beer, Ambros J; Schmidt-Trucksäss, Arno; Nickel, Thomas; Weis, Michael; Botnar, Rene; Schwaiger, Markus; Halle, Martin

    2011-02-01

    Recent reports provide indirect evidence of myocardial injury and ventricular dysfunction after prolonged exercise. However, existing data is conflicting and lacks direct verification of functional myocardial alterations by CMR [cardiac MR (magnetic resonance)]. The present study sought to examine structural myocardial damage and modification of LV (left ventricular) wall motion by CMR imaging directly after a marathon. Analysis of cTnT (cardiac troponin T) and NT-proBNP (N-terminal pro-brain natriuretic peptide) serum levels, echocardiography [pulsed-wave and TD (tissue Doppler)] and CMR were performed before and after amateur marathon races in 28 healthy males aged 41 ± 5 years. CMR included LGE (late gadolinium enhancement) and myocardial tagging to assess myocardial injury and ventricular motion patterns. Echocardiography indicated alterations of diastolic filling [decrease in E/A (early transmitral diastolic filling velocity/late transmitral diastolic filling velocity) ratio and E' (tissue Doppler early transmitral diastolic filling velocity)] postmarathon. All participants had a significant increase in NT-proBNP and/or cTnT levels. However, we found no evidence of LV LGE. MR tagging demonstrated unaltered radial shortening, circumferential and longitudinal strain. Myocardial rotation analysis, however, revealed an increase of maximal torsion by 18.3% (13.1 ± 3.8 to 15.5 ± 3.6 °; P=0.002) and maximal torsion velocity by 35% (6.8 ± 1.6 to 9.2 ± 2.5 °·s-1; P<0.001). Apical rotation velocity during diastolic filling was increased by 1.23 ± 0.33 °·s-1 after marathon (P<0.001) in a multivariate analysis adjusted for heart rate, whereas peak untwist rate showed no relevant changes. Although marathon running leads to a transient increase of cardiac biomarkers, no detectable myocardial necrosis was observed as evidenced by LGE MRI (MR imaging). Endurance exercise induces an augmented systolic wringing motion of the myocardium and increased diastolic filling

  15. Leukocytosis: a risk factor for myocardial infarction

    OpenAIRE

    Kotla, Suman

    2012-01-01

    Suman K KotlaDepartment of Internal Medicine, Memorial Medical Center, Johnstown, PA, USAAbstract: Myocardial infarction commonly results from atherosclerotic lesions in the coronary arteries. Approximately 5% of patients with acute myocardial infarction do not have atherosclerotic disease. In this case report, we present an unusual leukostatic complication in a patient with acute myeloblastic leukemia and extreme hyperleukocytosis who presented with an acute myocardial infarction that resolv...

  16. Maxillary necrosis by mucormycosis : a case report and literature review

    OpenAIRE

    Auluck, Ajit

    2007-01-01

    The maxilla rarely undergoes necrosis due to its rich vascularity. Maxillary necrosis can occur due to bacterial infections such as osteomyelitis, viral infections such as herpes zoster or fungal infections such as mucormycosis, aspergillosis etc. Mucormycosis is an opportunistic fulminant fungal infection, which mainly infects immunocompromised patients. The infection begins in the nose and paranasal sinuses due to inhalation of fungal spores. The infection can spread to orbital and intr...

  17. Myocardial bridging as a cause of acute myocardial infarction: a case report

    Directory of Open Access Journals (Sweden)

    Emiroglu Yunus

    2002-09-01

    Full Text Available Abstract Background Systolic compression of a coronary artery by overlying myocardial tissue is termed myocardial bridging. Myocardial bridging usually has a benign prognosis, but some cases resulting in myocardial ischemia, infarction and sudden cardiac death have been reported. We are reporting a case of myocardial bridging which was complicated with acute myocardial infarction associated with inappropriate blood donation. Case presentation A 33 year-old-man was admitted to our emergency with acute anteroseptal myocardial infarction after a blood donation. The electrocardiography showed sinus rhythm and was consistent with an acute anteroseptal myocardial infarction. We decided to perform primary percutanous intervention (PCI. Myocardial bridging was observed in the mid segment of the left anterior descending coronary artery on coronary angiogram. PCI was canceled and medical follow up was decided. Blood transfusion was made because he had a deep anemia. A normal hemaglobin level and clinical reperfusion was achieved after ten hours by blood transfusion. At the one year follow up visit, our patient was healthy and had no cardiac complaints. Conclusions Myocardial bridging may cause acute myocardial infarction in various clinical conditions. Although the condition in this case caused profound anemia related acute myocardial infarction, its treatment and management was unusual.

  18. Increases in myeloperoxidase levels after exercise in myocardial perfusion scintigraphy are not induced by myocardial ischemia

    NARCIS (Netherlands)

    van der Zee, P. M.; Meuwese, M. C.; Verberne, H. J.; de Ruijter, M.; van Straalen, J. P.; Fischer, J. C.; Sturk, A.; van Eck-Smit, B. L. F.; Stroes, E. S. G.; de Winter, R. J.

    2008-01-01

    Background: Increased systemic levels of myeloperoxidase (MPO) have been reported in patients with acute myocardial ischemia. We studied the association between exercise-induced myocardial ischemia measured by myocardial perfusion scintigraphy (MPS) and the magnitude and time course of changes in

  19. Myocardial perfusion scintigraphy: the evidence.

    Science.gov (United States)

    Underwood, S R; Anagnostopoulos, C; Cerqueira, M; Ell, P J; Flint, E J; Harbinson, M; Kelion, A D; Al-Mohammad, A; Prvulovich, E M; Shaw, L J; Tweddel, A C

    2004-02-01

    This review summarises the evidence for the role of myocardial perfusion scintigraphy (MPS) in patients with known or suspected coronary artery disease. It is the product of a consensus conference organised by the British Cardiac Society, the British Nuclear Cardiology Society and the British Nuclear Medicine Society and is endorsed by the Royal College of Physicians of London and the Royal College of Radiologists. It was used to inform the UK National Institute of Clinical Excellence in their appraisal of MPS in patients with chest pain and myocardial infarction. MPS is a well-established, non-invasive imaging technique with a large body of evidence to support its effectiveness in the diagnosis and management of angina and myocardial infarction. It is more accurate than the exercise ECG in detecting myocardial ischaemia and it is the single most powerful technique for predicting future coronary events. The high diagnostic accuracy of MPS allows reliable risk stratification and guides the selection of patients for further interventions, such as revascularisation. This in turn allows more appropriate utilisation of resources, with the potential for both improved clinical outcomes and greater cost-effectiveness. Evidence from modelling and observational studies supports the enhanced cost-effectiveness associated with MPS use. In patients presenting with stable or acute chest pain, strategies of investigation involving MPS are more cost-effective than those not using the technique. MPS also has particular advantages over alternative techniques in the management of a number of patient subgroups, including women, the elderly and those with diabetes, and its use will have a favourable impact on cost-effectiveness in these groups. MPS is already an integral part of many clinical guidelines for the investigation and management of angina and myocardial infarction. However, the technique is underutilised in the UK, as judged by the inappropriately long waiting times and by

  20. Implication of Snail in Metabolic Stress-Induced Necrosis

    Science.gov (United States)

    Ju, Min Kyung; Moon, Ji Young; Park, Hye Gyeong; Yoo, Mi-Ae; Choi, Byung Tae; Yook, Jong In; Lim, Sung-Chul; Han, Song Iy; Kang, Ho Sung

    2011-01-01

    Background Necrosis, a type of cell death accompanied by the rupture of the plasma membrane, promotes tumor progression and aggressiveness by releasing the pro-inflammatory and angiogenic cytokine high mobility group box 1. It is commonly found in the core region of solid tumors due to hypoxia and glucose depletion (GD) resulting from insufficient vascularization. Thus, metabolic stress-induced necrosis has important clinical implications for tumor development; however, its regulatory mechanisms have been poorly investigated. Methodology/Principal Findings Here, we show that the transcription factor Snail, a key regulator of epithelial-mesenchymal transition, is induced in a reactive oxygen species (ROS)-dependent manner in both two-dimensional culture of cancer cells, including A549, HepG2, and MDA-MB-231, in response to GD and the inner regions of a multicellular tumor spheroid system, an in vitro model of solid tumors and of human tumors. Snail short hairpin (sh) RNA inhibited metabolic stress-induced necrosis in two-dimensional cell culture and in multicellular tumor spheroid system. Snail shRNA-mediated necrosis inhibition appeared to be linked to its ability to suppress metabolic stress-induced mitochondrial ROS production, loss of mitochondrial membrane potential, and mitochondrial permeability transition, which are the primary events that trigger necrosis. Conclusions/Significance Taken together, our findings demonstrate that Snail is implicated in metabolic stress-induced necrosis, providing a new function for Snail in tumor progression. PMID:21448462

  1. Moderate elevation of intracellular creatine by targeting the creatine transporter protects mice from acute myocardial infarction

    Science.gov (United States)

    Lygate, Craig A.; Bohl, Steffen; ten Hove, Michiel; Faller, Kiterie M.E.; Ostrowski, Philip J.; Zervou, Sevasti; Medway, Debra J.; Aksentijevic, Dunja; Sebag-Montefiore, Liam; Wallis, Julie; Clarke, Kieran; Watkins, Hugh; Schneider, Jürgen E.; Neubauer, Stefan

    2012-01-01

    Aims Increasing energy storage capacity by elevating creatine and phosphocreatine (PCr) levels to increase ATP availability is an attractive concept for protecting against ischaemia and heart failure. However, testing this hypothesis has not been possible since oral creatine supplementation is ineffectual at elevating myocardial creatine levels. We therefore used mice overexpressing creatine transporter in the heart (CrT-OE) to test for the first time whether elevated creatine is beneficial in clinically relevant disease models of heart failure and ischaemia/reperfusion (I/R) injury. Methods and results CrT-OE mice were selected for left ventricular (LV) creatine 20–100% above wild-type values and subjected to acute and chronic coronary artery ligation. Increasing myocardial creatine up to 100% was not detrimental even in ageing CrT-OE. In chronic heart failure, creatine elevation was neither beneficial nor detrimental, with no effect on survival, LV remodelling or dysfunction. However, CrT-OE hearts were protected against I/R injury in vivo in a dose-dependent manner (average 27% less myocardial necrosis) and exhibited greatly improved functional recovery following ex vivo I/R (59% of baseline vs. 29%). Mechanisms contributing to ischaemic protection in CrT-OE hearts include elevated PCr and glycogen levels and improved energy reserve. Furthermore, creatine loading in HL-1 cells did not alter antioxidant defences, but delayed mitochondrial permeability transition pore opening in response to oxidative stress, suggesting an additional mechanism to prevent reperfusion injury. Conclusion Elevation of myocardial creatine by 20–100% reduced myocardial stunning and I/R injury via pleiotropic mechanisms, suggesting CrT activation as a novel, potentially translatable target for cardiac protection from ischaemia. PMID:22915766

  2. Heart disease induced by AAS abuse, using experimental mice/rats models and the role of exercise-induced cardiotoxicity.

    Science.gov (United States)

    Riezzo, I; De Carlo, D; Neri, M; Nieddu, A; Turillazzi, E; Fineschi, V

    2011-05-01

    The anabolic-androgenic steroids (AAS) are all synthetic derivates of testosterone and are commonly used as sport performance enhancers in athletes. The heart is one of the organs most frequently affected by administration of anabolic steroids. A direct myocardial injury caused by AAS is supposed to determine marked hypertrophy in myocardial cells, extensive regional fibrosis and necrosis. A number of excellent studies, using animal models, were performed to evaluate the cardiac effects of AAS. It is known that exogenous administration induced cardiac hypertrophy in vitro and in vivo, and when combined with exercise, anabolic steroid use has been shown to change exercise-induced physiological cardiac hypertrophy to pathophysiological cardiac hypertrophy. However the molecular mechanisms are still poorly understood. It's described that sudden cardiac death, myocardial infarct; ventricular remodelling and cardiomyopathy do to AAS is related to apoptosis and oxidative stress when associated with exercise. Mechanical stimuli and circulating humoral factors (TNF-α, HSP-70, IL-1β) released by the heart and peripheral organs are responsible. Testosterone and derivates can work through genomic (activation of specific androgen receptor, interaction with coactivators and co-repressors transcription factors, gene regulation) and non-genomic mechanism (membrane-receptor-second messenger cascades). Chronic AAS abuse results in different patterns of pathologic alterations, which depend on type, dose, frequency, and mode of use. The difficulty in interpreting experimental data on animals (mice and rats) lies in the diversity of experiments (the diversity of substances, which show different properties, different mice / rats by sex and age, duration of treatment with AAS, dosages used, type, scope and exercise duration).

  3. Myocardial Expression of Macrophage Migration Inhibitory Factor in Patients with Heart Failure

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    Julia Pohl

    2017-10-01

    Full Text Available Macrophage migration inhibitory factor (MIF is a pleiotropic inflammatory protein and contributes to several different inflammatory and ischemic/hypoxic diseases. MIF was shown to be cardioprotective in experimental myocardial ischemia/reperfusion injury and its expression is regulated by the transcription factor hypoxia-inducible factor (HIF-1α. We here report on MIF expression in the failing human heart and assess myocardial MIF in different types of cardiomyopathy. Myocardial tissue samples from n = 30 patients were analyzed by quantitative Real-Time PCR. MIF and HIF-1α mRNA expression was analyzed in myocardial samples from patients with ischemic (ICM and non-ischemic cardiomyopathy (NICM and from patients after heart transplantation (HTX. MIF expression was elevated in myocardial samples from patients with ICM compared to NICM. Transplanted hearts showed lower MIF levels compared to hearts from patients with ICM. Expression of HIF-1α was analyzed and was shown to be significantly increased in ICM patients compared to patients with NICM. MIF and HIF-1α mRNA is expressed in the human heart. MIF and HIF-1α expression depends on the underlying type of cardiomyopathy. Patients with ICM show increased myocardial MIF and HIF-1α expression.

  4. Effectiveness of calcium chloride in reduction of shoot necrosis incocoa (Theobroma cacao L. in vitro propagation

    Directory of Open Access Journals (Sweden)

    Sulistyani Pancaningtyas

    2012-05-01

    Full Text Available Various efforts have been developed for the optimization of the various stages in vitro micropropagation. The maturation stage and pre-acclimatization plantlets is an important stages that must be considered to produce vigorous plants and ready to be planted in the field. The purpose of this study was to reduced shoot tip necrosis in cocoa planlets to obtaine vigorous planlets from in vitro propagation through the addition of Calcium Chloride (CaCl2. The study used two stages of embryogenic development. The first was embryo maturation stage and the second was the shoot growth development stage. The study was arranged factorially in experiment design of Completely Randomized Design consisting of two factors i.e. concentration of CaCl2 consisted of 0, 50, 100, 150, and 200 mg/l and clones consisted of Sulawesi 1 and Sca 6. Each experiment was repeated three times, so the number of combination trials were 5x2x3=30 experimental units. The parameters observed included shoot growth percentage and vigorous planlets percentage. The results showed that the addition of CaCl2 at a concentration of 150 mg/l during maturition stage increased the embryos performance and percentage of shoot tip. However, it could not prevent the shoot tip necrosis. Whereas, the addition at a concentration of 50 mg/l during the shoot m growth development stage could reduced necrosis, suggested to increase the quality of in vitro planlets.Key words: Cocoa, necrosis, calcium chloride, somatic embryogenesis, embryos, planlets, in vitro.

  5. Regenerative healing following foetal myocardial infarction.

    Science.gov (United States)

    Herdrich, Benjamin J; Danzer, Enrico; Davey, Marcus G; Allukian, Myron; Englefield, Virginia; Gorman, Joseph H; Gorman, Robert C; Liechty, Kenneth W

    2010-12-01

    The adult response to myocardial infarction results in inflammation, scar formation, left ventricular dilatation, and loss of regional and global function. Regenerative scarless healing has been demonstrated in foetal dermis and tendon and is associated with diminished inflammation. We hypothesised that following foetal myocardial infarction, there would be minimal inflammation, regenerative healing, and preservation of function. Anteroapical myocardial infarction encompassing 20% of the left ventricle was created in adult or early gestation foetal sheep. Myocardial function was serially assessed using quantitative echocardiography. Infarct architecture was examined histologically for evidence of scar formation. Cellular inflammation, cellular proliferation, and apoptosis were assessed using immunohistochemistry. In the adult sheep 4 weeks following myocardial infarction, there was a significant decline in ejection fraction (EF) (41±7.4% to 26±7.4%, p<0.05), and the akinetic myocardial segment increased in size (6.9±0.8 cm to 7.9±1.1 cm, p<0.05). By contrast, there was no decline in the foetal EF (53±8.1% to 55±8.8%) and no akinetic foetal myocardial segment 4 weeks post-infarction. The foetal infarcts lacked an inflammatory cell infiltrate and healed with minimal fibrosis, compared with the adults. Foetal infarcts also demonstrated 5-bromo-2'-deoxyuridine (BrdU)+ proliferating cells, including cardiomyocytes, within the infarct. These data demonstrate that the foetal response to myocardial infarction is dramatically different from the adult and is characterised by minimal inflammation, lack of fibrosis, myocardial proliferation and restoration of cardiac function. Diminished inflammation is associated with foetal regenerative cardiac healing following injury. Understanding the mechanisms involved in foetal myocardial regeneration may lead to applications to alter the adult response following myocardial infarction. Copyright © 2010 European Association for

  6. Regenerative healing following fetal myocardial infarction

    Science.gov (United States)

    Herdrich, Benjamin J.; Danzer, Enrico; Davey, Marcus G.; Allukian, Myron; Englefield, Virginia; Gorman, Joseph H.; Gorman, Robert C.; Liechty, Kenneth W.

    2010-01-01

    Objectives The adult response to myocardial infarction results in inflammation, scar formation, left ventricular dilatation, and loss of regional and global function. Regenerative scarless healing has been demonstrated in fetal dermis and tendon and is associated with diminished inflammation. We hypothesized that following fetal myocardial infarction there would be minimal inflammation, regenerative healing, and preservation of function. Methods Anteroapical myocardial infarction encompassing 20% of the left ventricle were created in adult or early gestation fetal sheep. Myocardial function was serially assessed using quantitative echocardiography. Infarct architecture was examined histologically for evidence of scar formation. Cellular inflammation, cellular proliferation, and apoptosis were assessed using immunohistochemistry. Results In the adult sheep 4 weeks following myocardial infarction, there was a significant decline in ejection fraction (41±7.4% to 26±7.4%, p<0.05), and the akinetic myocardial segment increased in size (6.9±0.8 cm to 7.9±1.1 cm, p<0.05). In contrast, there was no decline in the fetal ejection fraction (53±8.1% to 55±8.8%) and no akinetic fetal myocardial segment 4 weeks post-infarction. The fetal infarcts lacked an inflammatory cell infiltrate and healed with minimal fibrosis, compared to the adults. Fetal infarcts also demonstrated BrdU+ proliferating cells, including cardiomyocytes, within the infarct. Conclusions These data demonstrate that the fetal response to myocardial infarction is dramatically different than the adult and is characterized by minimal inflammation, lack of fibrosis, myocardial proliferation, and restoration of cardiac function. Diminished inflammation is associated with fetal regenerative cardiac healing following injury. Understanding the mechanisms involved in fetal myocardial regeneration may lead to applications to alter the adult response following myocardial infarction. PMID:20452780

  7. Thrombolysis significantly reduces transient myocardial ischaemia following first acute myocardial infarction

    DEFF Research Database (Denmark)

    Mickley, H; Pless, P; Nielsen, J R

    1992-01-01

    In order to investigate whether thrombolysis affects residual myocardial ischaemia, we prospectively performed a predischarge maximal exercise test and early out-of-hospital ambulatory ST segment monitoring in 123 consecutive men surviving a first acute myocardial infarction (AMI). Seventy...... less than 0.02). Thrombolysis resulted in a non-significant reduction in exercise-induced ST segment depression: prevalence 43% vs 62% in controls. However, during ambulatory monitoring the duration of transient myocardial ischaemia was significantly reduced in thrombolysed patients: 322 min vs 1144...... myocardial ischaemia. This may explain the improvement in myocardial function during physical activities, which was also observed in this study....

  8. 2000 Volvo Award winner in basic science studies: Exogenous tumor necrosis factor-alpha mimics nucleus pulposus-induced neuropathology. Molecular, histologic, and behavioral comparisons in rats.

    Science.gov (United States)

    Igarashi, T; Kikuchi, S; Shubayev, V; Myers, R R

    2000-12-01

    This study tested the hypothesis that the 17-kDa form of tumor necrosis factor-alpha is the pathophysiologic agent expressed by herniated nucleus pulposus in vivo that is primarily responsible for the histologic and behavioral manifestations of experimental sciatica associated with herniated lumbar discs. The authors determined the molecular weight and concentration of active tumor necrosis factor-alpha in rat herniated disc and used exogenous tumor necrosis factor-alpha at the same molecular weight to study its neuropathologic effect on rat nerve root and dorsal root ganglion preparations in vivo. Expressed by herniated nucleus pulposus in culture, tumor necrosis factor-alpha causes neuropathologic injury in nerve roots and neuropathic pain states in which mechanical allodynia is seen in response to peripheral stimuli. Western blotting was used to identify the molecular weight of the operative tumor necrosis factor-alpha protein form, and measures of optical density were used for semiquantitative determination of concentration. Plastic-embedded nerve roots and dorsal root ganglion were used for neuropathologic evaluation, and von Frey stimulation was used to quantify mechanical allodynia. The 17-kDa form of tumor necrosis factor-alpha is expressed by herniated nucleus pulposus at a concentration of approximately 0.48 ng per herniated rat lumbar disc. Exogenous tumor necrosis factor-alpha applied in vivo to rat nerve roots produced neuropathologic changes and behavior deficits that mimicked experimental studies with herniated nucleus pulposus applied to nerve roots. The data reinforce other evidence that tumor necrosis factor-alpha is involved in mechanisms of neuropathic pain.

  9. Exogenous Nkx2.5- or GATA-4-transfected rabbit bone marrow mesenchymal stem cells and myocardial cell co-culture on the treatment of myocardial infarction in rabbits.

    Science.gov (United States)

    Li, Pu; Zhang, Lei

    2015-08-01

    The present study aimed to investigate the effects of Nkx2.5 or GATA-4 transfection with myocardial extracellular environment co-culture on the transformation of bone marrow mesenchymal stem cells (BMSCs) into differentiated cardiomyocytes. Nkx2.5 or GATA-4 were transfected into myocardial extracellular environment co-cultured BMSCs, and then injected into the periphery of infarcted myocardium of a myocardial infarction rabbit model. The effects of these gene transfections and culture on the infarcted myocardium were observed and the results may provide an experimental basis for the efficient myocardial cell differentiation of BMSCs. The present study also suggested that these cells may provide a source and clinical basis for myocardial injury repair via stem cell transplantation. The present study examined whether Nkx2.5 or GATA-4 exogenous gene transfection with myocardial cell extracellular environment co-culture were able to induce the differentiation of BMSCs into cardiac cells. In addition, the effect of these transfected BMSCs on the repair of the myocardium following myocardial infarction was determined using New Zealand rabbit models. The results demonstrated that myocardial cell differentiation was significantly less effective following exogenous gene transfection of Nkx2.5 or GATA-4 alone compared with that of transfection in combination with extracellular environment co-culture. In addition, the results of the present study showed that exogenous gene transfection of Nkx2.5 or GATA-4 into myocardial cell extracellular environment co-cultured BMSCs was able to significantly enhance the ability to repair, mitigating the death of myocardial cells and activation of the myocardium in rabbits with myocardial infarction compared with those of the rabbits transplanted with untreated BMSCs. In conclusion, the exogenous Nkx2.5 and GATA-4 gene transfection into myocardial extracellular environment co-cultured BMSCs induced increased differentiation into myocardial

  10. T1 mapping in patients with acute myocardial infarction.

    Science.gov (United States)

    Messroghli, Daniel R; Niendorf, Thoralf; Schulz-Menger, Jeanette; Dietz, Rainer; Friedrich, Matthias G

    2003-01-01

    Pixel-by-pixel calculation of T1 values (T1 mapping) has been used in different tissues to focus on T1 changes in a quantitative fashion. The aim of this study was to establish T1 mapping of human myocardium on a 1.5 Tesla system and to examine its diagnostic potential in patients with acute myocardial infarction (AMI). 8 patients with reperfused AMI (day 3 +/- 1) underwent multi-breath-hold MRI in a 1.5 Tesla system. Sets of five images with varying T1 weighting were acquired prior to and after the administration of contrast agent to generate images from calculated T1 values (T1 mapping). Prior to the contrast agent administration, all patients showed T1 prolongation in the area of infarction, which was identified in separate measurements using the delayed enhancement approach. Compared to noninfarcted areas, T1 values in the infarcted areas were increased by 18 +/- 7% (SE, p T1 prolongation was larger than that of the hyper-enhanced areas in conventional contrast-enhanced images. T1 maps obtained after the application of Gadolinium-DTPA revealed a T1 reduction of 27 +/- 4% in infarcted tissue compared to noninfarcted areas (p T1 reduction were in agreement with the hyper-enhanced regions in conventional T1-weighted images. T1 mapping visualizes changes in the longitudinal relaxation time induced by AMI. T1 mapping can detect myocardial necrosis without the use of contrast media. Information that can be extracted from a combination of pre- and postcontrast T1 maps exceeds that from conventional contrast studies.

  11. Different Causes of Death in Patients with Myocardial Infarction Type 1, Type 2 and Myocardial Injury

    DEFF Research Database (Denmark)

    Lambrecht, S; Sarkisian, Laura; Saaby, Lotte

    2017-01-01

    troponin I measured on clinical indication, were prospectively studied. Patients with at least 1 cardiac troponin I value >30 ng/L underwent case ascertainment and individual evaluation by an experienced adjudication committee. Patients were classified as having type 1 myocardial infarction, type 2...... myocardial infarction or myocardial injury according to the criteria of the Universal definition of myocardial infarction. Follow-up was ensured until December 31st 2014. Data on mortality and causes of death were obtained from the Danish Civil Registration System and the Danish Register of Causes of Death....... RESULTS: Overall, 3762 consecutive patients were followed for a mean of 3.2 years (IQR, 1.3-3.6 years). All-cause mortality differed significantly between categories: Type 1 myocardial infarction 32%, type 2 myocardial infarction 62%, myocardial injury 59%, and 22% in patients with non-elevated troponin...

  12. Experimental myocardial stem cell therapy for ST-elevation myocardial infarction

    DEFF Research Database (Denmark)

    Kastrup, Jens; Mygind, Naja D; Qayyum, Abbas A

    2016-01-01

    ), chronic IHD and heart failure. The patients suffer from chest pain (angina), dyspnea and a reduced quality of life. Common for all these conditions is loss of functional cardiomyocytes and endothelial cells. Stem cell therapy to regenerate injured myocardium is a new treatment option which has gained much...... interest in the last 10-15 years especially after STEMI. Many preclinical and clinical studies have shown encouraging results but also very diverse clinical outcomes after stem cell treatment. This diversity in results may be explained by different factors, such as cell isolation technique, infarct...... location, timing and route of delivery, cell dosage, cell type etc. The present review will try to elaborate and clarify the present status for stem cell therapy in STEMI....

  13. Myocardial infarction and nocturnal hypoxaemia

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    Penčić Biljana

    2007-01-01

    Full Text Available Introduction: There is an increased risk of cardiovascular morbidity and mortality in patients with nocturnal intermittent hypoxaemia. Objecive. The aim of this study was to evalute the influence of nocturnal hypoxaemia on ventricular arrhythmias and myocardial ischaemia in patients with myocardial infarction (MI. Method. We studied 77 patients (55.8±7.9 years with MI free of complications, chronic pulmonary diseases, abnormal awake blood gases tension. All patients underwent overnight pulse oximetry and 24-hour electrocardiography. Patients were divided into two groups according to nocturnal hypoxaemia. Total number of ventricular premature complex (VPC; maximal VPC/h; incidence of VPC Lown class>2 and occurrence of ST-segment depression were analyzed for nocturnal (10 PM to 6 AM, daytime (6 AM to 22 PM periods and for the entire 24 hours. Results. Both groups were similar in age, gender, standard risk factors, myocardial infarction size and did not differ in VPC during the analyzed periods. The number of nocturnal maximal VPC/h was insignificantly greater in group 1 (with hypoxaemia compared to group 2 (without hypoxaemia, (p=0.084. Maximal VPC/h did not differ significantly either for daytime or for 24 hours among the groups. Nocturnal VPC Lown>2 were significantly more frequent in group 1 (25% vs 0%, p=0.002. The incidence of VPC Lown>2 was similar during the daytime, and during 24 hrs in both groups. Occurrence of ST-segment depression did not differ between groups 1 and 2. Conclusion. Nocturnal hypoxaemia was associated with complex nocturnal ventricular arrhythmias in patients with MI. .

  14. Protocols of myocardial perfusion SPECT

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    Kim, Seong Min [College of Medicine, Chungnam National University, Daejeon (Korea, Republic of)

    2005-02-15

    In myocardial perfusion scintigraphy, the results of this evaluation now confront the practitioner of nuclear medicine with methodological options. Most nuclear cardiologic studies are performed using thallium-201, Tc-99m sestamibi and Tc-99m tertrofosmin. Some part of these studies use some form of pharmacologic stress test. While tailoring each test to the individual is ideal, this may be impractical for a busy department. Accordingly, established protocols to be used for patients with similar clinical presentations will be helpful. The following review presents methodology of various imaging protocols mainly according to the guidelines of nuclear cardiology procedures in American Society of Nuclear Cardiology.

  15. Perinatal changes in myocardial metabolism in lambs

    NARCIS (Netherlands)

    Bartelds, B; Knoester, H; Smid, GB; Takens, J; Visser, GH; Penninga, L; van der Leij, FR; Beaufort-Krol, GCM; Zijlstra, WG; Heymans, HSA; Kuipers, JRG

    2000-01-01

    Background-Lactate accounts for a third of myocardial oxygen consumption before and in the first 2 weeks after birth. It is unknown how the remainder of myocardial oxygen is consumed. Glucose is thought to be important before birth, whereas long-chain fatty acids (LC-FA) are the prime substrate for

  16. Ambulatory ST segment monitoring after myocardial infarction

    DEFF Research Database (Denmark)

    Mickley, H

    1994-01-01

    The prevalence of transient myocardial ischaemia after myocardial infarction seems to be lower than in other subgroups with coronary artery disease. In postinfarction patients, however, a greater proportion of ischaemic episodes are silent. At present there is substantial evidence that transient ...

  17. An unusual case of myocardial infarction.

    Science.gov (United States)

    Rovetta, Riccardo; Vizzardi, Enrico; D'Aloia, Antonio; Bonadei, Ivano; Sciatti, Edoardo; Metra, Marco

    2014-06-01

    Myocardial infarction may be the result of embolism of calcified material from the aortic valve or thrombotic formations adhering to the same. We report a case of late myocardial infarction secondary to embolization from a thrombus adherent to the aortic valve jutting out in the ostium of the left main coronary artery.

  18. MYOCARDIAL FIBROSIS IN PATIENTS WITH DIABETES MELLITUS

    Directory of Open Access Journals (Sweden)

    O. M. Drapkina

    2013-01-01

    Full Text Available The mechanism of myocardial damage in diabetes mellitus is considered. The pathogenesis of myocardial fibrosis, leading to diabetic cardiomyopathy, is described in details. Management tactics aimed at the prevention of heart failure in patients with diabetes is proposed.

  19. Do episodes of anger trigger myocardial infarction?

    DEFF Research Database (Denmark)

    Möller, J; Hallqvist, J; Diderichsen, Finn

    1999-01-01

    Our objectives were to study anger as a trigger of acute myocardial infarction (MI) and to explore potential effect modification by usual behavioral patterns related to hostility.......Our objectives were to study anger as a trigger of acute myocardial infarction (MI) and to explore potential effect modification by usual behavioral patterns related to hostility....

  20. Myocardial infarction : early diagnosis and cardioprotective strategies

    NARCIS (Netherlands)

    Oerlemans, M.I.F.J.

    2012-01-01

    In this thesis, we have investigated novel diagnostic and cardioprotective strategies to limit myocardial cell death and improve cardiac function after myocardial infarction. We demonstrated a new way to speed up the diagnosis of acute MI by using very small pieces of RNA (microRNAs). Using these

  1. [How to treat fat necrosis after lipofilling into the breast?].

    Science.gov (United States)

    Ho Quoc, C; Delay, E

    2015-06-01

    Fat necrosis is a phenomenon that has been known for a long time in surgery. The fat necrosis is produced because of tissue ischemia and it is also known as cytosteatonecrosis. These lesions can appear with different manifestations: indurations or cysts. Fat necrosis develops in breast aesthetic surgery (breast reduction) or reconstructive breast surgery (after abdominal flaps like TRAM or DIEP). In our department we have been using fat grafting into the breast since 1998 and it has really improved the aesthetic results in breast surgery. Also the fat necrosis lesions can appear after fat grafting, and they should be identified in order to avoid worrying the patient and other doctors that are treating her. The purpose of this article is to present different aspects of fat necrosis after surgery and therapeutic approaches to these problems. The two authors have noticed the frequency of fat necrosis in the breast after fat grafting into the breast in aesthetic surgery (asymmetry, deformity, lipoaugmentation, improvement of aesthetic sequelae) and reconstructive surgery (after total mastectomy or to improve the aspect of sequelae after conservative surgery). A retrospective study was performed including a homogenous series of consecutive cases that needed breast lipofilling, operated by the two authors. Fat was harvested with cannula after infiltration. The adipose tissue was preparated with a short centrifugation. Fat grafting was realized as backward injections. The tolerance of the performed technique has been studied with the discovery of the fat necrosis lesions after surgery up to one-year follow-up evaluation. Between 1998 and 2013, 2236 fat transfers have been performed by the two authors and were included in a series of consecutive homogenous cases treated by using the same surgical technique. The fat necrosis incidence after lipofilling in the breast shows two frequency curves: the first one with a frequency of 15% (the first 50 cases) and then decreases

  2. Management of infected pancreatic necrosis: state of the art

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    Roberto Rasslan

    Full Text Available ABSTRACT Pancreatic necrosis occurs in 15% of acute pancreatitis. The presence of infection is the most important factor in the evolution of pancreatitis. The diagnosis of infection is still challenging. Mortality in infected necrosis is 20%; in the presence of organic dysfunction, mortality reaches 60%. In the last three decades, there has been a real revolution in the treatment of infected pancreatic necrosis. However, the challenges persist and there are many unsolved questions: antibiotic treatment alone, tomography-guided percutaneous drainage, endoscopic drainage, video-assisted extraperitoneal debridement, extraperitoneal access, open necrosectomy? A step up approach has been proposed, beginning with less invasive procedures and reserving the operative intervention for patients in which the previous procedure did not solve the problem definitively. Indication and timing of the intervention should be determined by the clinical course. Ideally, the intervention should be done only after the fourth week of evolution, when it is observed a better delimitation of necrosis. Treatment should be individualized. There is no procedure that should be the first and best option for all patients. The objective of this work is to critically review the current state of the art of the treatment of infected pancreatic necrosis.

  3. The Extracellular Matrix Regulates Granuloma Necrosis in Tuberculosis.

    Science.gov (United States)

    Al Shammari, Basim; Shiomi, Takayuki; Tezera, Liku; Bielecka, Magdalena K; Workman, Victoria; Sathyamoorthy, Tarangini; Mauri, Francesco; Jayasinghe, Suwan N; Robertson, Brian D; D'Armiento, Jeanine; Friedland, Jon S; Elkington, Paul T

    2015-08-01

    A central tenet of tuberculosis pathogenesis is that caseous necrosis leads to extracellular matrix destruction and bacterial transmission. We reconsider the underlying mechanism of tuberculosis pathology and demonstrate that collagen destruction may be a critical initial event, causing caseous necrosis as opposed to resulting from it. In human tuberculosis granulomas, regions of extracellular matrix destruction map to areas of caseous necrosis. In mice, transgenic expression of human matrix metalloproteinase 1 causes caseous necrosis, the pathological hallmark of human tuberculosis. Collagen destruction is the principal pathological difference between humanised mice and wild-type mice with tuberculosis, whereas the release of proinflammatory cytokines does not differ, demonstrating that collagen breakdown may lead to cell death and caseation. To investigate this hypothesis, we developed a 3-dimensional cell culture model of tuberculosis granuloma formation, using bioelectrospray technology. Collagen improved survival of Mycobacterium tuberculosis-infected cells analyzed on the basis of a lactate dehydrogenase release assay, propidium iodide staining, and measurement of the total number of viable cells. Taken together, these findings suggest that collagen destruction is an initial event in tuberculosis immunopathology, leading to caseous necrosis and compromising the immune response, revealing a previously unappreciated role for the extracellular matrix in regulating the host-pathogen interaction. © The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

  4. Myocardial ultrasonic tissue characterization in patients with thyroid dysfunction

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    Schmidt André

    2010-04-01

    Full Text Available Abstract Background Structural myocardial abnormalities have been extensively documented in hypothyroidism. Experimental studies in animal models have also shown involvement of thyroid hormones in gene expression of myocardial collagen. This study was planned to investigate the ability of ultrasonic tissue characterization, as evaluated by integrated backscatter (IBS, to early identify myocardial involvement in thyroid dysfunction. Patients and Methods We studied 15 patients with hyperthyroidism (HYPER, 8 patients with hypothyroidism (HYPO, 14 patients with subclinical hypothyroidism (SCH and 19 normal (N subjects, who had normal LV systolic function. After treatment, 10 HYPER, 6 HYPO, and 8 SCH patients were reevaluated. IBS images were obtained and analyzed in parasternal short axis (papillary muscle level view, at left ventricular (LV posterior wall. The following IBS variables were analyzed: 1 the corrected coefficient (CC of IBS, obtained by dividing IBS intensity by IBS intensity measured in a rubber phantom, using the same equipment adjustments, at the same depth; 2 cardiac cyclic variation (CV of IBS - peak-to-peak difference between maximal and minimal values of IBS during cardiac cycle; 3 cardiac cyclic variation index (CVI of IBS - percentual relationship between the cyclic variation (CV and the mean value of IBS intensity. Results CC of IBS was significantly larger (p Conclusions CC of IBS was able to differentiate cardiac involvement in patients with overt HYPO and HYPER who had normal LV systolic function. These early myocardial structural abnormalities were partially reversed by drug therapy in HYPER group. On the other hand, although mean IBS intensity tended to be slightly larger in patients with SCH as compared to N, this difference was not statistical significant.

  5. Risk stratification after myocardial infarction. Clinical overview

    Energy Technology Data Exchange (ETDEWEB)

    O' Rourke, R.A. (Department of Medicine, University of Texas Health Science Center, San Antonio (United States))

    1991-09-01

    Many patients with an acute myocardial infarction can be stratified into subgroups that are at high risk for morbidity and mortality on the basis of clinical characteristics that indicate recurrent myocardial ischemia, persistent left ventricular dysfunction, and/or recurrent cardiac arrhythmias. In patients with uncomplicated myocardial infarction the assessment of symptoms, physical findings, and ECG changes during predischarge exercise testing often identifies patients at increased risk for further cardiac events. Because of the suboptimum sensitivity and specificity of the exercise ECG for detecting myocardial ischemia, myocardial perfusion imaging with 201Tl and/or assessment of global and segmental ventricular function by two-dimensional echocardiography or radionuclide cineangiography during or immediately after exercise are often added to the predischarge risk stratification.

  6. Acute myocardial infarction following a hornet sting

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    Cvetković-Matić Danica

    2009-01-01

    Full Text Available Background. The occurrence of an acute myocardial infarction following a hornet sting has been very rarely reported in the previous literature. Pathogenetic mechanisms include direct action of the venom components on the coronary endothelium and allergic reaction with mediators released from mast cells. The anaphylactic reaction and venom components can produce acute coronary artery thrombosis. Case report. We reported a 45-year-old man with acute myocardial infarction after a hornet sting in the presence of anaphylaxis. We also discussed clinical implications and pathophysiological mechanisms of acute myocardial infarction caused by hymenoptera sting. Conclusion. A case report of this unusual acute myocardial infarction highlights the potential acute myocardial ischemia associated with hymenoptera sting which requests early diagnosis, thorough cardiovascular evaluation and appropriate treatment.

  7. Biomarkers in patients with myocardial fibrosis

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    An Zhe

    2017-10-01

    Full Text Available Myocardial fibrosis is observed in many cardiovascular diseases including hypertension, heart failure and cardiomyopathy. Myocardial fibrosis has been proved to be reversible and treatable only under timely intervention, which makes early detection and assessment of fibrosis crucial. Aside from tissue biopsy as the gold standard for the diagnosis of myocardial fibrosis, circulating biomarkers have been adopted as noninvasive assessment of this lesion. Dysregulated collagen deposition is thought to be the major cause of myocardial fibrosis. Collagens, procollagens, TGF-β, TIMP, galectin-3, and microRNAs are thought to be indicators of myocardial fibrosis. In this review, we summarize the molecules that are frequently used as biomarkers in diagnosis of cardiac fibrosis. Mechanisms of fibrosis that they take part in are also introduced.

  8. Taxonomy of segmental myocardial systolic dysfunction

    Science.gov (United States)

    McDiarmid, Adam K.; Pellicori, Pierpaolo; Cleland, John G.

    2017-01-01

    The terms used to describe different states of myocardial health and disease are poorly defined. Imprecision and inconsistency in nomenclature can lead to difficulty in interpreting and applying trial outcomes to clinical practice. In particular, the terms ‘viable’ and ‘hibernating’ are commonly applied interchangeably and incorrectly to myocardium that exhibits chronic contractile dysfunction in patients with ischaemic heart disease. The range of inherent differences amongst imaging modalities used to define myocardial health and disease add further challenges to consistent definitions. The results of several large trials have led to renewed discussion about the classification of dysfunctional myocardial segments. This article aims to describe the diverse myocardial pathologies that may affect the myocardium in ischaemic heart disease and cardiomyopathy, and how they may be assessed with non-invasive imaging techniques in order to provide a taxonomy of myocardial dysfunction. PMID:27147609

  9. Acute myocardial infarction with changing axis deviation.

    Science.gov (United States)

    Patanè, Salvatore; Marte, Filippo

    2011-07-01

    Changing axis deviation has been rarely reported also during atrial fibrillation or atrial flutter. Changing axis deviation has been rarely reported also during acute myocardial infarction associated with atrial fibrillation. Isolated left posterior hemiblock is a very rare finding but the evidence of transient right axis deviation with a left posterior hemiblock pattern has been reported during acute anterior myocardial infarction as related with significant right coronary artery obstruction and collateral circulation between the left coronary system and the posterior descending artery. Left anterior hemiblock development during acute inferior myocardial infarction can be an indicator of left anterior descending coronary artery lesions, multivessel coronary artery disease, and impaired left ventricular systolic function. We present a case of changing axis deviation in a 62-year-old Italian man with acute myocardial infarction. Also this case focuses attention on changing axis deviation during acute myocardial infarction. Copyright © 2009 Elsevier Ireland Ltd. All rights reserved.

  10. Cardiac MRI of myocardial salvage at the peri-infarct border zones after primary coronary intervention.

    Science.gov (United States)

    O'Regan, Declan P; Ahmed, Rizwan; Neuwirth, Clare; Tan, Yvonne; Durighel, Giuliana; Hajnal, Joseph V; Nadra, Imad; Corbett, Simon J; Cook, Stuart A

    2009-07-01

    The purpose of this study was to use cardiac MRI to define the morphology of the reversibly injured peri-infarct border zone in patients treated with primary percutaneous coronary intervention (PPCI) for acute ST elevation myocardial infarction. In 15 patients, T2-weighted myocardial edema imaging was used to identify the ischemic bed or area at risk (AAR), and late gadolinium enhancement imaging was used to measure infarct size. Images were coregistered, and the boundaries of edema and necrosis were defined using an edge-detection methodology. We observed that infarction always involved the subendocardium but showed variable transmural extension within the AAR. The mean infarct size was 22 +/- 19% (range: 8-48%), and the mean AAR was 34 +/- 12% (range: 20-57%). The infarcted myocardium was always smaller than the ischemic AAR and involved between 34% and 99% (mean 72 +/- 21%) of the ischemic bed primarily due to variation in transmural infarct extension. Although a lateral border zone of potentially viable myocardium was often present, its extent was limited (range: 0-11 mm, mean: 5 +/- 4 mm). As a result of this, infarcts occupied the majority (range: 70-100%, mean: 82 +/- 13%) of the width of the AAR. The mean fractional wall thickening in the infarcted, peri-infarcted, and remote myocardium was 3.6 +/- 16.0%, 40.5 +/- 26.4%, and 88.2 +/- 39.3%, respectively. These findings demonstrate that myocardial salvage is largely determined by epicardial limitation of the infarct within the ischemic AAR after PPCI. The lateral boundaries of necrosis approximate to the lateral extent of the ischemic bed and systolic wall motion abnormalities extend well beyond the infarct border zone.

  11. Urocortin Treatment Improves Acute Hemodynamic Instability and Reduces Myocardial Damage in Post-Cardiac Arrest Myocardial Dysfunction.

    Science.gov (United States)

    Huang, Chien-Hua; Wang, Chih-Hung; Tsai, Min-Shan; Hsu, Nai-Tan; Chiang, Chih-Yen; Wang, Tzung-Dau; Chang, Wei-Tien; Chen, Huei-Wen; Chen, Wen-Jone

    2016-01-01

    Hemodynamic instability occurs following cardiac arrest and is associated with high mortality during the post-cardiac period. Urocortin is a novel peptide and a member of the corticotrophin-releasing factor family. Urocortin has the potential to improve acute cardiac dysfunction, as well as to reduce the myocardial damage sustained after ischemia reperfusion injury. The effects of urocortin in post-cardiac arrest myocardial dysfunction remain unclear. We developed a preclinical cardiac arrest model and investigated the effects of urocortin. After cardiac arrest induced by 6.5 min asphyxia, male Wistar rats were resuscitated and randomized to either the urocortin treatment group or the control group. Urocortin (10 μg/kg) was administrated intravenously upon onset of resuscitation in the experimental group. The rate of return of spontaneous circulation (ROSC) was similar between the urocortin group (76%) and the control group (72%) after resuscitation. The left ventricular systolic (dP/dt40) and diastolic (maximal negative dP/dt) functions, and cardiac output, were ameliorated within 4 h after ROSC in the urocortin-treated group compared to the control group (Pcardiac arrest myocardial dysfunction.

  12. Protein kinase A-mediated cardioprotection of Tongxinluo relates to the inhibition of myocardial inflammation, apoptosis, and edema in reperfused swine hearts.

    Science.gov (United States)

    Li, Xiang-dong; Yang, Yue-jin; Cheng, Yu-tong; Dou, Ke-fei; Tian, Yi; Meng, Xian-min

    2013-01-01

    Our previous studies have demonstrated that Tongxinluo (TXL), a traditional Chinese medicine, can protect hearts against no-reflow and reperfusion injury in a protein kinase A (PKA)-dependent manner. The present study was to investigate whether the PKA-mediated cardioprotection of TXL against no-reflow and reperfusion injury relates to the inhibition of myocardial inflammation, edema, and apoptosis. In a 90-minute ischemia and 3-hour reperfusion model, minipigs were randomly assigned to sham, control, TXL (0.05 g/kg, gavaged one hour prior to ischemia), and TXL + H-89 (a PKA inhibitor, intravenously and continuously infused at 1.0 µg/kg per minute) groups. Myocardial no-reflow, necrosis, edema, and apoptosis were determined by pathological and histological studies. Myocardial activity of PKA and myeloperoxidase was measured by colorimetric method. The expression of PKA, phosphorylated cAMP response element-binding protein (p-CREB) (Ser(133)), tumor necrosis factor α (TNF-α), P-selectin, apoptotic proteins, and aquaporins was detected by Western blotting analysis. TXL decreased the no-reflow area by 37.4% and reduced the infarct size by 27.0% (P cardioprotection of TXL against no-reflow and reperfusion injury relates to the inhibition of myocardial inflammation, edema, and apoptosis in the reflow and no-reflow myocardium.

  13. Effects of intracoronary melatonin on ischemia-reperfusion injury in ST-elevation myocardial infarction

    DEFF Research Database (Denmark)

    Ekeløf, Sarah V; Halladin, Natalie L; Jensen, Svend E

    2016-01-01

    , an endogenous hormone, acts through antioxidant mechanisms and could potentially minimize the myocardial injury. The aim of the experimental study was to examine the cardioprotective effects of melatonin in a porcine closed-chest reperfused infarction model. A total of 20 landrace pigs were randomized...

  14. Effects of Myocardial Contractility on Microemboli Production by Mechanical Heart Valves in a Bovine Model

    OpenAIRE

    Deklunder, Ghislaine; Lecroart, Jean-Louis; Conger, Jeff L.; Lapeyre, Didier; Gregoric, Igor; Rose, Harris; Tamez, Daniel; Frazier, O. H.

    2000-01-01

    Microemboli caused by mechanical heart valves have the potential to cause cerebrovascular events. We investigated the effects of myocardial contractility and heart rate on microemboli production in association with conventional and experimental mechanical heart valves implanted in the mitral position in a bovine model.

  15. The Role of MicroRNAs in Myocardial Infarction: From Molecular Mechanism to Clinical Application

    Directory of Open Access Journals (Sweden)

    Teng Sun

    2017-03-01

    Full Text Available MicroRNAs (miRNAs are a class of small single-stranded and highly conserved non-coding RNAs, which are closely linked to cardiac disorders such as myocardial infarction (MI, cardiomyocyte hypertrophy, and heart failure. A growing number of studies have demonstrated that miRNAs determine the fate of the heart by regulating cardiac cell death and regeneration after MI. A deep understanding of the pathophysiology of miRNA dependent regulatory pathways in these processes is required. The role of miRNAs as diagnostic, prognostic, and therapeutic targets also needs to be explored in order to utilize them in clinical settings. This review summarizes the role of miRNAs in myocardial infarction and focuses mainly on their influence on cardiomyocyte regeneration and cell death including apoptosis, necrosis, and autophagy. In addition, the targets of pro- and anti-MI miRNAs are comparatively described. In particular, the possibilities of miRNA-based diagnostic and therapeutic strategies for myocardial infarction are discussed in this review.

  16. Salvage assessment with cardiac MRI following acute myocardial infarction underestimates potential for recovery of systolic strain.

    Science.gov (United States)

    O'Regan, Declan P; Ariff, Ben; Baksi, A John; Gordon, Fabiana; Durighel, Giuliana; Cook, Stuart A

    2013-05-01

    Our aim was to evaluate the relationship between the degree of salvage following acute ST elevation myocardial infarction (STEMI) and subsequent reversible contractile dysfunction using cardiac magnetic resonance (CMR) imaging. Thirty-four patients underwent CMR examination 1-7 days after primary percutaneous coronary intervention (PPCI) for acute STEMI with follow-up at 1 year. The ischaemic area-at-risk (AAR) was assessed with T2-weighted imaging and myocardial necrosis with late gadolinium enhancement. Myocardial strain was quantified with complementary spatial modulation of magnetisation (CSPAMM) tagging. Ischaemic segments with poor (myocardium improved between baseline and follow-up (-10.1 % ± 0.5 vs. -16.2 % ± 0.5 %, P myocardium and salvage assessment performed within the first week of revascularisation may underestimate the potential for functional recovery. • MRI can measure how much myocardium is damaged after a heart attack. • Heart muscle that appears initially non-viable may sometimes partially recover. • Enhancement around the edges of infarcts may resolve over time. • Evaluating new cardio-protective treatments with MRI requires appreciation of its limitations.

  17. Cardioprotective Effects of Astragalin against Myocardial Ischemia/Reperfusion Injury in Isolated Rat Heart.

    Science.gov (United States)

    Qu, Daoxu; Han, Jichun; Ren, Huanhuan; Yang, Wenxiao; Zhang, Xinjie; Zheng, Qiusheng; Wang, Dong

    2016-01-01

    This study aims to evaluate the cardioprotective effects of astragalin against myocardial ischemia/reperfusion (I/R) injury in isolated rat heart. The cardioprotective effects of astragalin on myocardial I/R injury were investigated on Langendorff apparatus. Adult male Sprague-Dawley rats were randomly divided into five groups. The results showed that astragalin pretreatment improved myocardial function. Compared with I/R group, lactate dehydrogenase (LDH) and creatine kinase (CK) activities in coronary flow decreased in astragalin pretreatment groups, whereas superoxide dismutase (SOD) activity and glutathione/glutathione disulfide (GSH/GSSG) ratio significantly increased. The levels of malondialdehyde (MDA), intracellular reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) decreased in astragalin-treated groups. The infarct size (IS) and apoptosis rate in hearts from astragalin-treated groups were lower than those in hearts from the I/R group. Western blot analysis also revealed that astragalin preconditioning significantly reduced Bax level, whereas Bcl-2 was increased in the myocardium. Therefore, astragalin exhibited cardioprotective effects via its antioxidative, antiapoptotic, and anti-inflammatory activities.

  18. Dexrazoxane Shows No Protective Effect in the Acute Phase of Reperfusion during Myocardial Infarction in Pigs.

    Science.gov (United States)

    Kamat, Pranitha; Vandenberghe, Stijn; Christen, Stephan; Bongoni, Anjan K; Meier, Bernhard; Rieben, Robert; Khattab, Ahmed A

    2016-01-01

    Calcium and iron overload participate in the mechanisms of ischemia/reperfusion (I/R) injury during myocardial infarction (MI). Calcium overload induces cardiomyocyte death by hypercontraction, while iron catalyses generation of reactive oxygen species (ROS). We therefore hypothesized that dexrazoxane, an intracellular metal chelator, would attenuate I/R injury. MI was induced in pigs by occlusion of the left anterior descending artery for 1 hour followed by 2 hours reperfusion. Thirty minutes before reperfusion either 5 mg/ml dexrazoxane (n = 5) or saline (n = 5) was infused intravenously. Myocardial necrosis as percentage of the area at ischemic risk was found to be similar in both groups (77.2 ± 18% for dexrazoxane and 76.4 ± 14% for saline group) as determined by triphenyl tetrazolium chloride staining of the ischemic myocardium. Also, serum levels of troponin-I were similar in both groups. A conductance catheter was used to measure left ventricular pressure and volume at all times. Markers for tissue damage due to ROS (HNE), endothelial cell activation (CD31) and inflammation (IgG, C3b/c, C5b9, MCP-1) were assessed on tissue and/or in serum. No significant differences were observed between the groups for the parameters analyzed. To conclude, in this clinically relevant model of early reperfusion after acute myocardial ischemia, dexrazoxane lacked attenuating effects on I/R injury as shown by the measured parameters.

  19. Dexrazoxane Shows No Protective Effect in the Acute Phase of Reperfusion during Myocardial Infarction in Pigs.

    Directory of Open Access Journals (Sweden)

    Pranitha Kamat

    Full Text Available Calcium and iron overload participate in the mechanisms of ischemia/reperfusion (I/R injury during myocardial infarction (MI. Calcium overload induces cardiomyocyte death by hypercontraction, while iron catalyses generation of reactive oxygen species (ROS. We therefore hypothesized that dexrazoxane, an intracellular metal chelator, would attenuate I/R injury. MI was induced in pigs by occlusion of the left anterior descending artery for 1 hour followed by 2 hours reperfusion. Thirty minutes before reperfusion either 5 mg/ml dexrazoxane (n = 5 or saline (n = 5 was infused intravenously. Myocardial necrosis as percentage of the area at ischemic risk was found to be similar in both groups (77.2 ± 18% for dexrazoxane and 76.4 ± 14% for saline group as determined by triphenyl tetrazolium chloride staining of the ischemic myocardium. Also, serum levels of troponin-I were similar in both groups. A conductance catheter was used to measure left ventricular pressure and volume at all times. Markers for tissue damage due to ROS (HNE, endothelial cell activation (CD31 and inflammation (IgG, C3b/c, C5b9, MCP-1 were assessed on tissue and/or in serum. No significant differences were observed between the groups for the parameters analyzed. To conclude, in this clinically relevant model of early reperfusion after acute myocardial ischemia, dexrazoxane lacked attenuating effects on I/R injury as shown by the measured parameters.

  20. Mst1 inhibition rescues β1-adrenergic cardiomyopathy by reducing myocyte necrosis and non-myocyte apoptosis rather than myocyte apoptosis

    Science.gov (United States)

    Lee, Grace J.; Yan, Lin; Vatner, Dorothy E.

    2015-01-01

    It is generally held that inhibition of mammalian sterile 20-like kinase 1 (Mst1) protects the heart through reducing myocyte apoptosis. We determined whether inhibition with a dominant-negative Mst1 (DN-Mst1) would protect against the cardiomyopathy induced by chronic β1-adrenergic receptor (β1-AR) stimulation by preventing myocyte apoptosis. DN-Mst1 mice were mated with β1-AR transgenic (Tg) mice and followed for 20 months. β1-AR Tg mice developed cardiomyopathy as they aged, as reflected by premature mortality and depressed cardiac function, which were rescued in β1-AR × DN-Mst1 bigenic mice. Surprisingly, myocyte apoptosis did not significantly decrease with Mst1 inhibition. Instead, Mst1 inhibition predominantly reduced non-myocyte apoptosis, e.g., fibroblasts, macrophages, neutrophils and endothelial cells. Fibrosis in the hearts with cardiomyopathy increased fivefold and this increase was nearly abolished in the bigenic mice with Mst1 inhibition. Regression analysis showed no correlation between myocyte apoptosis and cardiac function or myocyte number, whereas the latter two correlated significantly, p myocyte necrosis, chronic β-AR stimulation with isoproterenol was induced for 24 h and myocyte necrosis was assessed by 1 % Evans blue dye. Compared to WT, DN-Mst1 mice showed significant inhibition, p myocyte necrosis. We confirmed this result in Mst1-knockout mice, which also showed significant protection, p myocyte necrosis compared to WT. These data indicate that Mst1 inhibition rescued cardiac fibrosis and myocardial dysfunction in β1-AR cardiomyopathy. However, this did not occur through Mst1 inhibition of myocyte apoptosis but rather by inhibition of cardiomyocyte necrosis and non-myocyte apoptosis, features of Mst1 not considered previously. PMID:25600225

  1. A Rare Cause of Acute Abdomen: Idiopathic Isolated Cecal Necrosis

    Directory of Open Access Journals (Sweden)

    Ender Özer

    2015-03-01

    Full Text Available Idiopathic isolated cecal necrosis is a clinical problem characterized by right-sided inferior abdominal pain. It is rarely seen, develops due to decreased blood flow to the colon and, imitates acute appendicitis. Its clinical signs are similar to many illnesses causing sensitivity in the right inferior quadrant and, the diagnosis is generally determined during surgery. An 86-year-old male patient presented with the complaints of abdominal pain, trichiniasis, nausea and vomiting. Surgical intervention was decided when physical examination and laboratory results were taken into consideration. After diagnostic laparoscopy, right hemicolectomy was performed because of cecal necrosis. While the mortality and morbidity rates for ischemic bowel disease are high, prognosis for early diagnosed patients with isolated cecal necrosis is better, provided that timely surgical treatment is decided.

  2. Miserable case of total hip replacement caused by postirradiation necrosis

    Energy Technology Data Exchange (ETDEWEB)

    Ihara, Fumitoshi; Okue, Akira; Kumagai, Hiroyuki; Ohzuma, Masakazu; Wada, Fumio (Saga Prefectural Hospital (Japan))

    1983-06-01

    We experienced a miserable case of postirradiation femoral head necrosis. Osteomyelitis due to a screw penetration into the cecum was followed by total hip replacement. The patient is a sixty seven years old woman. As she was injured by inoperable uterus cancer at fifty one years old, /sup 60/Co irradiation therapy was done. As postirradiation necrosis occurred 5 years after irradiation, total hip replacement (Mckee-Farrar type) was done. However, bone necrosis area in iliac bone due to irradiation progressed gradually, and anchoring screw migrated proximally into the cecum. Then the fistula formed at the region of right major trochanter. In fistulography, contrast medium leaked out into the cecum. So after iliocecectomy and anastomosis of colon, removal of prosthesis and local continuous suction irrigation was done twice. Since then, there has been no recurrence.

  3. Elevated serum free pregnancy-associated plasma protein-A independently predicts mortality in haemodialysis patients but is not associated with recurrent haemodialysis-induced ischaemic myocardial injury.

    Science.gov (United States)

    Jefferies, Helen J; Tertti, Risto; Wittfooth, Saara; Burton, James O; Metsärinne, Kaj; Pettersson, Kim; McIntyre, Christopher W

    2015-01-01

    Pregnancy-associated plasma protein-A (PAPP-A) is a putative marker of atheroma instability and ischaemic myocardial stress prior to necrosis. Total PAPP-A (tPAPP-A) levels in acute coronary syndromes predict adverse outcomes. However, free PAPP-A (fPAPP-A) predominates in the circulation. Ischaemic haemodialysis (HD)-induced cardiac injury (myocardial stunning) is common and is associated with markers of myocardial necrosis, inflammation, cardiovascular events and mortality. Coronary plaque instability in pathophysiology of HD-induced myocardial stunning has not been studied. We aimed to investigate the relationship of fPAPP-A with stunning and mortality. 130 prevalent patients from two HD centres (Finland and UK) were studied. Pre-HD free, complexed and total PAPP-A were measured by immunoassay. A subset of 62 patients underwent echocardiography to assess HD-induced myocardial stunning. The mean duration of follow-up was 407 ± 98 days. fPAPP-A was elevated (median: 3.45 mIU/l) and correlated with dialysis vintage (r = 0.391, p PAPP-A was not related to stunning. Dialysis vintage and cTnT independently predicted Ln fPAPP-A (model R = 0.463). fPAPP-A, cTnT and age independently predicted death (Nagelkerke R(2) = 0.362). fPAPP-A, a novel predictor of HD-related mortality, demonstrates better prognostic power than tPAPP-A. Coronary plaque instability may contribute to sub-lethal myocardial injury, but may not be critical in pathogenesis of HD-induced ischaemic cardiac injury.

  4. Myocardial uptake of {sup 99m}Tc-annexin-V and {sup 111}In-antimyosin-antibodies after ischemia-reperfusion in rats

    Energy Technology Data Exchange (ETDEWEB)

    Sarda-Mantel, Laure [Universite Denis Diderot-Paris 7, UMR S773, Paris (France); AP-HP, Groupe Hospitalier Bichat-Beaujon, Service de Medecine Nucleaire, Paris (France); INSERM, U773, Paris (France); Hopital Bichat, Service de Medecine Nucleaire, Paris (France); Hervatin, Florence [Universite Denis Diderot-Paris 7, UMR S773, Paris (France); CEA, DSV/DRM/SHFJ, Orsay (France); Michel, Jean-Baptiste; Louedec, Liliane [INSERM, U698, Paris (France); Martet, Genevieve [Universite Denis Diderot-Paris 7, UMR S773, Paris (France); INSERM, U773, Paris (France); Rouzet, Francois; Lebtahi, Rachida; Merlet, Pascal; Le Guludec, Dominique [Universite Denis Diderot-Paris 7, UMR S773, Paris (France); AP-HP, Groupe Hospitalier Bichat-Beaujon, Service de Medecine Nucleaire, Paris (France); INSERM, U773, Paris (France); Khaw, Ban-An [Bouve College of Pharmacy and Health Sciences, Center for Drug Targeting and Analysis, Boston, MA (United States)

    2008-01-15

    Phosphatidylserin exposure on cell surfaces occurs early during apoptosis and is detected in vivo by using {sup 99m}Tc-annexin-V (ANX). Cardiomyocyte membrane disruption is detected in vivo by using {sup 111}In-antimyosin-antibodies (AM). We aimed to determine if ANX and AM allow evaluation of the time-course of these two distinct cell death events after myocardial ischemia-reperfusion. Coronary tying (20 min) followed by reperfusion (IR) was performed in 31 rats. Twelve of the rats were injected with ANX, 11 with AM, and eight with both tracers. Myocardial uptake of tracers was studied 1-2 h, 4 h, or 24 h after IR by scintigraphy (ANX, n = 14) and autoradiography (all cases), and compared to histology and Apostain staining. Scintigraphy was positive in all rats 2 h after IR and in three of five rats at 24 h. On autoradiography, ANX activity was intense in myocardial lesions as early as 1 h post-IR, whereas AM activity was mild at 2 h then increased at 4 h post-IR. ANX and AM uptakes evolved from mid-myocardium to endocardial and epicardial regions from 2 h to 24 h post-IR. Apostain staining was significant in myocardial lesions (p < 10{sup 6} compared to six sham-operated rats). On histology, myocardial lesion was characterized by interstitial oedema, myocytes necrosis, and dramatic thinning at 24 h. These data suggest that ANX and AM allow temporal and regional evaluations of PS exposure and membrane disruption, respectively, during myocytes death after 20-min myocardial ischemia followed by reperfusion. Also, (i) apoptosis starts very early in injured myocardium, (ii) myocyte necrosis occurs later (3-4 h post-reperfusion), and (iii) most dead cells are removed from mid-myocardium between 6 h and 24 h after reperfusion. (orig.)

  5. Imaging of cavitary necrosis in complicated childhood pneumonia

    Energy Technology Data Exchange (ETDEWEB)

    Hodina, M.; Schnyder, P.; Gudinchet, F. [Department of Diagnostic and Interventional Radiology, University Hospital, CHUV, Lausanne (Switzerland); Hanquinet, S. [HCUG Geneva, Geneva (Switzerland); Cotting, J. [Department of Pediatrics, University Hospital, CHUV, Lausanne (Switzerland)

    2002-02-01

    The aim of this study was to illustrate the chest radiographs (CR) and CT imaging features and sequential findings of cavitary necrosis in complicated childhood pneumonia. Among 30 children admitted in the Pediatric Intensive Care Unit for persistent or progressive pneumonia, respiratory distress or sepsis despite adequate antibiotic therapy, a study group of 9 children (5 girls and 4 boys; mean age 4 years) who had the radiographic features and CT criteria for cavitary necrosis complicated pneumonia was identified. The pathogens identified were Streptococcus pneumoniae (n=4), Aspergillus (n=2), Legionella (n=1), and Staphylococcus aureus (n=1). Sequential CR and CT scans were retrospectively reviewed. Follow-up CR and CT were evaluated for persistent abnormalities. Chest radiographs showed consolidations in 8 of the 9 patients. On CT examination, cavitary necrosis was localized to 1 lobe in 2 patients and 7 patients showed multilobar or bilateral areas of cavitary necrosis. In 3 patients of 9, the cavitary necrosis was initially shown on CT and visualization by CR was delayed by a time span varying from 5 to 9 days. In all patients with cavities, a mean number of five cavities were seen on antero-posterior CR, contrasting with the multiple cavities seen on CT. Parapneumonic effusions were shown by CR in 3 patients and in 5 patients by CT. Bronchopleural fistulae were demonstrated by CT alone (n=3). No purulent pericarditis was demonstrated. The CT scan displayed persistent residual pneumatoceles of the left lower lobe in 2 patients. Computed tomography is able to define a more specific pattern of abnormalities than conventional CR in children with necrotizing pneumonia and allows an earlier diagnosis of this rapidly progressing condition. Lung necrosis and cavitation may also be associated with Aspergillus or Legionella pneumonia in the pediatric population. (orig.)

  6. Direct Evidence that Myocardial Insulin Resistance following Myocardial Ischemia Contributes to Post-Ischemic Heart Failure

    Science.gov (United States)

    Fu, Feng; Zhao, Kun; Li, Jia; Xu, Jie; Zhang, Yuan; Liu, Chengfeng; Yang, Weidong; Gao, Chao; Li, Jun; Zhang, Haifeng; Li, Yan; Cui, Qin; Wang, Haichang; Tao, Ling; Wang, Jing; Quon, Michael J; Gao, Feng

    2015-01-01

    A close link between heart failure (HF) and systemic insulin resistance has been well documented, whereas myocardial insulin resistance and its association with HF are inadequately investigated. This study aims to determine the role of myocardial insulin resistance in ischemic HF and its underlying mechanisms. Male Sprague-Dawley rats subjected to myocardial infarction (MI) developed progressive left ventricular dilation with dysfunction and HF at 4 wk post-MI. Of note, myocardial insulin sensitivity was decreased as early as 1 wk after MI, which was accompanied by increased production of myocardial TNF-α. Overexpression of TNF-α in heart mimicked impaired insulin signaling and cardiac dysfunction leading to HF observed after MI. Treatment of rats with a specific TNF-α inhibitor improved myocardial insulin signaling post-MI. Insulin treatment given immediately following MI suppressed myocardial TNF-α production and improved cardiac insulin sensitivity and opposed cardiac dysfunction/remodeling. Moreover, tamoxifen-induced cardiomyocyte-specific insulin receptor knockout mice exhibited aggravated post-ischemic ventricular remodeling and dysfunction compared with controls. In conclusion, MI induces myocardial insulin resistance (without systemic insulin resistance) mediated partly by ischemia-induced myocardial TNF-α overproduction and promotes the development of HF. Our findings underscore the direct and essential role of myocardial insulin signaling in protection against post-ischemic HF. PMID:26659007

  7. Gastric Rupture and Necrosis in Prader-Willi Syndrome

    Science.gov (United States)

    Stevenson, David A.; Heinemann, Janalee; Angulo, Moris; Butler, Merlin G.; Loker, Jim; Rupe, Norma; Kendell, Patrick; Cassidy, Suzanne B.; Scheimann, Ann

    2011-01-01

    Hyperphagia and obesity are common features in individuals with Prader-Willi syndrome (PWS). Demographic and cause of death data from individuals with PWS were obtained through a national support organization. Four reports of unexpected mortality due to gastric rupture and necrosis were found in 152 reported deaths, accounting for 3% of the causes of mortality. Four additional individuals were suspected to have gastric rupture. Vomiting and abdominal pain, although rare in PWS, were frequent findings in this cohort. The physician should consider an emergent evaluation for gastric rupture and necrosis in individuals with PWS who present with vomiting and abdominal pain. PMID:17667731

  8. Bullous lesions, sweat gland necrosis and rhabdomyolysis in alcoholic coma

    Directory of Open Access Journals (Sweden)

    Neelakandhan Asokan

    2014-01-01

    Full Text Available A 42-year-old male developed hemorrhagic bullae and erosions while in alcohol induced coma. The lesions were limited to areas of the body in prolonged contact with the ground in the comatose state. He developed rhabdomyolysis, progressing to acute renal failure (ARF. Histopathological examination of the skin showed spongiosis, intraepidermal vesicles, and necrosis of eccrine sweat glands with denudation of secretory epithelial lining cells. With supportive treatment and hemodialysis, the patient recovered in 3 weeks time. This is the first reported case of bullous lesions and sweat gland necrosis occurring in alcohol-induced coma complicated by rhabdomyolysis and ARF.

  9. Viral erythrocytic necrosis: Chapter 2.2.7

    Science.gov (United States)

    Winton, James R.; Hershberger, Paul K.

    2014-01-01

    Viral erythrocytic necrosis (VEN), originally termed piscine erythrocytic necrosis, is a condition that has been reported to affect the red blood cells (RBCs) of many species of marine and anadromous fishes in both the Atlantic and Pacific Oceans (Nicholson and Reno 1981; Smail 1982; Wolf 1988; Dannevig and Thorud 1999). Fish with VEN may develop a severe anemia that can reduce their stamina, predispose them to other infections or increase the impact of other stressors (MacMillan et al. 1980; Nicholson and Reno 1981; Meyers et al. 1986; Haney et al. 1992) resulting in population-scale impacts in susceptible species (Hershberger et al. 2009).

  10. RIP3: a molecular switch for necrosis and inflammation

    Science.gov (United States)

    Moriwaki, Kenta; Chan, Francis Ka-Ming

    2013-01-01

    The receptor-interacting protein kinase 3 (RIP3/RIPK3) has emerged as a critical regulator of programmed necrosis/necroptosis, an inflammatory form of cell death with important functions in pathogen-induced and sterile inflammation. RIP3 activation is tightly regulated by phosphorylation, ubiquitination, and caspase-mediated cleavage. These post-translational modifications coordinately regulate the assembly of a macromolecular signaling complex termed the necrosome. Recently, several reports indicate that RIP3 can promote inflammation independent of its pronecrotic activity. Here, we review our current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases. PMID:23913919

  11. Hesperidin blunts streptozotocin-isoproternol induced myocardial toxicity in rats by altering of PPAR-γ receptor.

    Science.gov (United States)

    Agrawal, Yogeeta O; Sharma, Pankaj Kumar; Shrivastava, Birendra; Arya, Dharamvir Singh; Goyal, Sameer N

    2014-08-05

    Hesperidin has been shown to possess cardioprotective and anti-diabetic potential. Hitherto, its molecular mechanism on isoproterenol (ISO)-induced myocardial dysfunction in diabetes is still not explored. Hence, for the first time we sought to investigate whether hesperidin exerts any beneficial effect on the pathophysiology of myocardial infarction (MI) in diabetes through the PPAR-γ pathway by assessing a variety of indices e.g., apoptosis, hemodynamic, biochemical and histoarchitectural changes. Diabetes was induced by a single dose of STZ (50 mg/kg IP). Diabetic rats received either hesperidin (100 mg/kg/day orally), the PPAR-γ antagonist GW9662 (1 mg/kg/day IP), or both for 14 days with concurrent administration of ISO (85 mg/kg SC) on days 13 and 14. ISO-STZ rats resulted in severe myocardial dysfunction (decreased ±LVdP/dt and increased LVEDP). In addition, augmented myocardial thiobarbituric acid-reactive substances and serum troponin-I with a concomitant decrease in level of glutathione and activities of catalase, superoxide dismutase antioxidants with cardiac injury biomarkers creatine kinase-MB isoenzyme, lactate dehydrogenase were seen. Morphological studies of the ISO-STZ challenged myocardium exhibited severe necrosis, edema and inflammatory changes. In Western blot analysis, Bcl-2 and PPAR-γ expression were decreased where as Bax expression was significantly increased, suggesting role of apoptosis in myocardial dysfunction. Interestingly, hesperidin treatment positively modulated these parameters as validated by improved hemodynamic and left ventricular functions, fortified endogenous anti-oxidant defence system and improved structural integrity of the myocardium. However, significant effects were lowered in animals treated with hesperidin plus GW9662. Moreover, down-regulated PPAR-γ and Bcl-2 expressions in myocardial infarcted diabetic hearts were increased by hesperidin treatment. Hence, for the first time the present study suggests that

  12. The aetiology and possible prevention of myocardial infarction ...

    African Journals Online (AJOL)

    The aetiology and possible prevention of myocardial infarction. ... The subjects of this study were 250 cases of myocardial infarction treated personally. ... Until the aetiology of myocardial infarction has been clarified, it would appear reasonable to treat these factors so as to perhaps afford potential myocardial infarction ...

  13. Magnetic resonance imaging for characterizing myocardial diseases.

    Science.gov (United States)

    Saeed, Maythem; Liu, Hui; Liang, Chang-Hong; Wilson, Mark W

    2017-09-01

    The National Institute of Health defined cardiomyopathy as diseases of the heart muscle. These myocardial diseases have different etiology, structure and treatment. This review highlights the key imaging features of different myocardial diseases. It provides information on myocardial structure/orientation, perfusion, function and viability in diseases related to cardiomyopathy. The standard cardiac magnetic resonance imaging (MRI) sequences can reveal insight on left ventricular (LV) mass, volumes and regional contractile function in all types of cardiomyopathy diseases. Contrast enhanced MRI sequences allow visualization of different infarct patterns and sizes. Enhancement of myocardial inflammation and infarct (location, transmurality and pattern) on contrast enhanced MRI have been used to highlight the key differences in myocardial diseases, predict recovery of function and healing. The common feature in many forms of cardiomyopathy is the presence of diffuse-fibrosis. Currently, imaging sequences generating the most interest in cardiomyopathy include myocardial strain analysis, tissue mapping (T1, T2, T2*) and extracellular volume (ECV) estimation techniques. MRI sequences have the potential to decode the etiology by showing various patterns of infarct and diffuse fibrosis in myocarditis, amyloidosis, sarcoidosis, hypertrophic cardiomyopathy due to aortic stenosis, restrictive cardiomyopathy, arrythmogenic right ventricular dysplasia and hypertension. Integrated PET/MRI system may add in the future more information for the diagnosis and progression of cardiomyopathy diseases. With the promise of high spatial/temporal resolution and 3D coverage, MRI will be an indispensible tool in diagnosis and monitoring the benefits of new therapies designed to treat myocardial diseases.

  14. Myocardial perfusion imaging with dual energy CT

    Energy Technology Data Exchange (ETDEWEB)

    Jin, Kwang Nam [Division of Cardiovascular Imaging, Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, SC (United States); Department of Radiology, SMG-SNU Boramae Medical Center, Seoul (Korea, Republic of); De Cecco, Carlo N. [Division of Cardiovascular Imaging, Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, SC (United States); Caruso, Damiano [Division of Cardiovascular Imaging, Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, SC (United States); Department of Radiological Sciences, Oncology and Pathology, University of Rome “Sapienza”, Rome (Italy); Tesche, Christian [Division of Cardiovascular Imaging, Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, SC (United States); Department of Cardiology and Intensive Care Medicine, Heart Center Munich-Bogenhausen, Munich (Germany); Spandorfer, Adam; Varga-Szemes, Akos [Division of Cardiovascular Imaging, Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, SC (United States); Schoepf, U. Joseph, E-mail: schoepf@musc.edu [Division of Cardiovascular Imaging, Department of Radiology and Radiological Science, Medical University of South Carolina, Charleston, SC (United States); Division of Cardiology, Department of Medicine, Medical University of South Carolina, Charleston, SC (United States)

    2016-10-15

    Highlights: • Stress dual-energy sCTMPI offers the possibility to directly detect the presence of myocardial perfusion defects. • Stress dual-energy sCTMPI allows differentiating between reversible and fixed myocardial perfusion defects. • The combination of coronary CT angiography and dual-energy sCTMPI can improve the ability of CT to detect hemodynamically relevant coronary artery disease. - Abstract: Dual-energy CT (DECT) enables simultaneous use of two different tube voltages, thus different x-ray absorption characteristics are acquired in the same anatomic location with two different X-ray spectra. The various DECT techniques allow material decomposition and mapping of the iodine distribution within the myocardium. Static dual-energy myocardial perfusion imaging (sCTMPI) using pharmacological stress agents demonstrate myocardial ischemia by single snapshot images of myocardial iodine distribution. sCTMPI gives incremental values to coronary artery stenosis detected on coronary CT angiography (CCTA) by showing consequent reversible or fixed myocardial perfusion defects. The comprehensive acquisition of CCTA and sCTMPI offers extensive morphological and functional evaluation of coronary artery disease. Recent studies have revealed that dual-energy sCTMPI shows promising diagnostic accuracy for the detection of hemodynamically significant coronary artery disease compared to single-photon emission computed tomography, invasive coronary angiography, and cardiac MRI. The aim of this review is to present currently available DECT techniques for static myocardial perfusion imaging and recent clinical applications and ongoing investigations.

  15. Left ventricular myocardial contractility is depressed in the borderzone after posterolateral myocardial infarction.

    Science.gov (United States)

    Shimkunas, Rafael; Zhang, Zhihong; Wenk, Jonathan F; Soleimani, Mehrdad; Khazalpour, Michael; Acevedo-Bolton, Gabriel; Wang, Guanying; Saloner, David; Mishra, Rakesh; Wallace, Arthur W; Ge, Liang; Baker, Anthony J; Guccione, Julius M; Ratcliffe, Mark B

    2013-05-01

    Contractility in the borderzone (BZ) after anteroapical myocardial infarction (MI) is depressed. We tested the hypothesis that BZ contractility is also decreased after posterolateral MI. Five sheep underwent posterolateral MI. Magnetic resonance imaging (MRI) was performed 2 weeks before and 16 weeks after MI, and left ventricular (LV) volume and regional strain were measured. Finite element (FE) models were constructed, and the systolic material parameter, Tmax, was calculated in the BZ and remote myocardium by minimizing the difference between experimentally measured and calculated LV strain and volume. Sheep were sacrificed 17 weeks after MI, and myocardial muscle fibers were taken from the BZ and remote myocardium. Fibers were chemically demembranated, and isometric developed force, Fmax, was measured at supramaximal [Ca(2+)]. Routine light microscopy was also performed. There was no difference in Tmax in the remote myocardium before and 16 weeks after MI. However, there was a large decrease (63.3%, p = 0.005) in Tmax in the BZ when compared with the remote myocardium 16 weeks after MI. In addition, there was a significant reduction of BZ Fmax for all samples (18.9%, p = 0.0067). Myocyte cross-sectional area increased by 61% (p = 0.021) in the BZ, but there was no increase in fibrosis. Contractility in the BZ is significantly depressed relative to the remote myocardium after posterolateral MI. The reduction in contractility is due at least in part to a decrease in contractile protein function. Copyright © 2013 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.

  16. Mitochondrial DNA‑induced inflammatory damage contributes to myocardial ischemia reperfusion injury in rats: Cardioprotective role of epigallocatechin.

    Science.gov (United States)

    Qin, Chao-Yi; Zhang, Hong-Wei; Gu, Jun; Xu, Fei; Liang, Huai-Min; Fan, Kang-Jun; Shen, Jia-Yu; Xiao, Zheng-Hua; Zhang, Er-Yong; Hu, Jia

    2017-11-01

    Inflammation serves an important role in the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Fragments of endogenous damaged‑associated molecular patterns, recently identified as mitochondrial DNA (mtDNA), have been proven to be a potent pro‑inflammatory mediator. Epigallocatechin‑3‑gallate (EGCG) is able to regulate the expression levels of a series of inflammatory cytokines. However, the involvement of endogenous mtDNA in EGCG‑regulated inflammatory activities in the context of myocardial I/R injury remains to be elucidated. The present study was designed to investigate the role of mtDNA in EGCG‑mediated myocardial protection in a rat I/R model. Significant positive correlations between elevated plasma mtDNA copy numbers and the expression levels of tumor necrosis factor (TNF) and interleukins (IL)‑6 and ‑8 were observed in the myocardial tissue following an I/R injury (Pcardioprotective effects may be achieved by inhibiting the release of mtDNA from damaged mitochondria and that this protection was at least in part dependent on the PI3K/RAC‑α serine/threonine‑protein kinase associated signaling pathway.

  17. Nitrogen-13-labeled ammonia for myocardial imaging

    Energy Technology Data Exchange (ETDEWEB)

    Walsh, W.F.; Fill, H.R.; Harper, P.V.

    1977-01-01

    Cyclotron-produced nitrogen-13 (half-life 10 min), as labeled ammonia (/sup 13/NH/sub 4//sup +/), has been evaluated as a myocardial perfusion imaging agent. The regional myocardial uptake of /sup 13/NH/sub 4//sup +/ has been shown to be proportional to regional tissue perfusion in animal studies. Intravenously administered /sup 13/NH/sub 4//sup +/ is rapidly cleared from the circulation, being extracted by the liver (15 percent), lungs, myocardium (2 percent--4 percent), brain, kidney, and bladder. Myocardial ammonia is metabolized mainly to glutamine via the glutamine synthetase pathway. Pulmonary uptake is substantial, but usually transient, except in smokers where clearance may be delayed. The positron annihilation irradiation (511 keV) of /sup 13/N may be imaged with a scintillation camera, using either a specially designed tungsten collimator or a pinhole collimator. After early technical problems with collimation and the production method of /sup 13/NH/sub 4//sup +/ were overcome, reproducible high quality myocardial images were consistently obtained. The normal myocardial image was established to be of a homogeneous ''doughnut'' configuration. Imaging studies performed in patients with varying manifestations of ischemic and valvular heart disease showed a high incidence of localized perfusion defects, especially in patients with acute myocardial infarction. Sequential studies at short intervals in patients with acute infarction showed correlation between alterations in regional perfusion and the clinical course of the patient. It is concluded that myocardial imaging with /sup 13/NH/sub 4//sup +/ and a scintillation camera provides a valid and noninvasive means of assessing regional myocardial perfusion. This method is especially suitable for sequential studies of acute cardiac patients at short intervals. Coincidence imaging of the 511 keV annihilation irradiation provides a tomographic and potentially quantitative assessment of the

  18. Post-contrast myocardial T(1) and ECV disagree in a longitudinal canine study.

    Science.gov (United States)

    Koopmann, Matthias; Hong, KyungPyo; Kholmovski, Eugene G; Huang, Eric C; Hu, Nan; Ying, Jian; Levenson, Richard; Vijayakumar, Sathya; Dosdall, Derek J; Ranjan, Ravi; Kim, Daniel

    2014-08-01

    Both post-contrast myocardial T1 and extracellular volume (ECV) measurements have been associated with diffuse interstitial fibrosis. The cardiovascular magnetic resonance (CMR) field is migrating towards ECV, because it is largely insensitive to confounders that affect post-contrast myocardial T1 . Despite the theoretical advantages of myocardial ECV over post-contrast myocardial T1 , systematic experimental studies comparing the two measurements are largely lacking. We sought to measure the temporal changes in post-contrast myocardial T1 and ECV in an established canine model with chronic atrial fibrillation. Seventeen mongrel dogs, implanted with a pacemaker to induce chronic atrial fibrillation via rapid atrial pacing, were scanned multiple times for a total of 46 CMR scans at 3T. These dogs with different disease durations (0-22 months) were part of a separate longitudinal study aimed at studying the relationship between AF and pathophysiology. In each animal, we measured native and post-contrast T1 values and hematocrit. Temporal changes in post-contrast myocardial T1 and ECV, as well as other CMR parameters, were modeled with linear mixed effect models to account for repeated measurements over disease duration. In 17 animals, post-contrast myocardial T1 decreased significantly from 872 to 698 ms (p ECV increased from 21.0 to 22.0% (p = 0.38), which corresponds to only a 4.5% relative increase. To partially investigate this discrepancy, we quantified collagen volume fraction (CVF) in post-mortem heart tissues of six canines sacrificed at different disease durations (0-22 months). CVF quantified by histology increased from 0.9 to 1.9% (p = 0.56), which agrees better with ECV than with post-contrast myocardial T1 . This study shows that post-contrast myocardial T1 and ECV may disagree in a longitudinal canine study. A more comprehensive study, including histologic, cardiac, and renal functional analyses, is warranted to test rigorously which CMR parameter (ECV

  19. Computer-assisted myocardial blush quantification after percutaneous coronary angioplasty for acute myocardial infarction : a substudy from the TAPAS trial

    NARCIS (Netherlands)

    Vogelzang, Mathijs; Vlaar, Pieter J.; Svilaas, Tone; Amo, Diny; Nijsten, Maarten W. N.; Zijlstra, Felix

    Myocardial reperfusion after acute myocardial infarction can be angiographically assessed by the myocardial blush grade (MBG) or TIMI Perfusion Grade. These scores are based on subjective human judgement and lead to a score of four categories. A more operator-independent way of scoring myocardial

  20. The end of the unique myocardial band

    DEFF Research Database (Denmark)

    MacIver, David H; Partridge, John B; Agger, Peter

    2018-01-01

    Two of the leading concepts of mural ventricular architecture are the unique myocardial band and the myocardial mesh model. We have described, in an accompanying article published in this journal, how the anatomical, histological and high-resolution computed tomographic studies strongly favour...... the latter concept. We now extend the argument to describe the linkage between mural architecture and ventricular function in both health and disease. We show that clinical imaging by echocardiography and magnetic resonance imaging, and electrophysiological studies, all support the myocardial mesh model. We...

  1. Changing axis deviation during acute myocardial infarction.

    Science.gov (United States)

    Patanè, Salvatore; Marte, Filippo

    2010-07-09

    Changing axis deviation has been reported during acute myocardial infarction also associated with atrial fibrillation. Isolated left posterior hemiblock is a very rare finding but the evidence of transient right axis deviation with a left posterior hemiblock pattern has been reported during acute anterior myocardial infarction as related with significant right coronary artery obstruction and collateral circulation between the left coronary system and the posterior descending artery. We present a case of changing axis deviation in a 70-year-old Italian man with acute myocardial infarction. Copyright (c) 2008 Elsevier Ireland Ltd. All rights reserved.

  2. Myocardial infarction in the young

    Directory of Open Access Journals (Sweden)

    Cengel A

    2009-01-01

    Full Text Available An increasing number of patients under 40 years of age are being hospitalized with the diagnosis of acute myocardial infarction. This is partly due to the increased prevalance of risk factors for atherosclerosis in the younger age group; especially increased incidence of impaired fasting glucose, high triglyceride, low high-density lipoprotein levels and increased waist to hip ratio. However, non-atherosclerotic coronary artery disease or hypercoagulability should also be investigated or at least suspected in the younger patients. The pathophysiology of different clinical conditions and disease states which cause acute coronary syndromes in the young patients are reviewed, and the diagnostic modalities and therapatic options for these conditions are briefly discussed by searching for "premature atherosclerosis", "hypercoagulable states", "risk factors for atherosclerosis in youth", "novel risk factors for atherosclerosis", "non-atherosclerotic coronary artery diseases" in PubMed.

  3. [Cardiac rehabilitation after myocardial infarction].

    Science.gov (United States)

    Ghannem, M; Ghannem, L; Ghannem, L

    2015-12-01

    Although the proofs of the benefits of cardiac rehabilitation accumulate, many patients are not sent to rehabilitation units, especially younger and very elderly patients. As the length of stay in acute care units decreases, rehabilitation offers more time to fully assess the patients' conditions and needs. Meta-analyses of randomised trials suggest that mortality can be improved by as much as 20-30%. In addition, rehabilitation helps managing risk factors, including hyperlipidemia, diabetes, smoking and sedentary behaviours. Physical training also helps improving exercise capacity. Because of all of these effects, cardiac rehabilitation for post-myocardial infarction patients has been given a class IA recommendation in current guidelines. Copyright © 2015 Elsevier Masson SAS. All rights reserved.

  4. Exercise Training Protects Against Acute Myocardial Infarction via Improving Myocardial Energy Metabolism and Mitochondrial Biogenesis

    OpenAIRE

    Lichan Tao; Yihua Bei; Shenghui Lin; Haifeng Zhang; Yanli Zhou; Jingfa Jiang; Ping Chen; Shutong Shen; Junjie Xiao; Xinli Li

    2015-01-01

    Background/Aims: Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Myocardial infarct size was examined with triphenyltetr...

  5. Regadenoson for myocardial perfusion scintigraphy.

    Science.gov (United States)

    Reyes, Eliana; Pennell, Dudley J

    2010-09-01

    Stress myocardial perfusion scintigraphy (MPS) plays a major role in the detection of obstructive coronary artery disease and provides valuable diagnostic and prognostic information to guide clinical decision-making with regard to medical therapy and coronary revascularisation. Current stress techniques for MPS are effective but their use may be limited by reduced tolerability, contraindications and untoward side effects. The recently developed selective adenosine A2A receptor agonists have the potential for improving stress tolerability, hence expanding the indications for functional imaging in the assessment of coronary artery disease. This article reviews the basic principles underlying activation of coronary arteriolar adenosine A2A receptors. It describes the benefits and limitations of current vasodilator stress agents and highlights the effectiveness, side effect profile and tolerability of regadenoson, the only selective adenosine A2A receptor agonist available at present for clinical use. The reader will gain an understanding of the pharmacokinetics and mechanism of action of regadenoson for the assessment of coronary artery disease when combined with myocardial perfusion imaging. The reader will also become aware of the available evidence on the clinical usefulness of regadenoson MPS and its future applications. Selective activation of coronary arteriolar adenosine A2A receptors by regadenoson provides an effective modality of stress for the detection of inducible perfusion abnormality in patients with known or suspected coronary disease. The effectiveness of regadenoson is similar to that of adenosine, but test tolerability is improved with regadenoson. The use of this agent simplifies stress testing and has the potential for expanding the applications of functional imaging to patient populations unsuitable for conventional vasodilator stress with adenosine or dipyridamole.

  6. Phylogeography of infectious haematopoietic necrosis virus in North America

    DEFF Research Database (Denmark)

    Kurath, G.; Garver, K.A.; Troyer, R.M.

    2003-01-01

    Infectious hematopoietic necrosis virus (IHNV) is a rhabdoviral pathogen that infects wild and cultured salmonid fish throughout the Pacific Northwest of North America. IHNV causes severe epidemics in young fish and can cause disease or occur asymptomatically in adults. In a broad survey of 323 I...

  7. Tumour necrosis factor alpha and interleukin 10 gene ...

    Indian Academy of Sciences (India)

    Tumour necrosis factor alpha and interleukin 10 gene polymorphisms and the risk of ischemic stroke in south Indian population. Shehnaz Sultana Venkata K. Kolla Yasovanthi Jeedigunta Pranay K. Penagaluru Sindhu Joshi P. Usha Rani P. P. Reddy. Research Note Volume 90 Issue 2 August 2011 pp 361-364 ...

  8. Total Gastric Necrosis: A Case Report and Literature Review

    African Journals Online (AJOL)

    2017-05-22

    May 22, 2017 ... KEY MESSAGES: Total gastric necrosis is a rare disease with no specific clinical manifestation. When it is suspected, surgical treatment should be carried out immediately. ... causing celiac artery trunk thrombosis. JOP 2008;9:512-4. 10. Han J, Wu MC, Yang T. Challenge of China's rural health. BMJ. 2016 ...

  9. Radiation-induced femoral head necrosis | Abdulkareem | Nigerian ...

    African Journals Online (AJOL)

    There are very few cases of radiation-induced femoral head necrosis described in the literature, therefore, this case will add new knowledge and highlights important aspects in the diagnosis and management of this uncommon condition. Our patient was 74 years old and presented with left hip and groin pain for 8 months, ...

  10. Generation of truncated recombinant form of tumor necrosis factor ...

    African Journals Online (AJOL)

    Generation of truncated recombinant form of tumor necrosis factor receptor-1 to produce cancer vaccine. Hamide Hatamihanza1, Mehrdad Hashemi1*, Azim ..... Saghafi Z. Generation and characterization of chicken egg yolk antibodies (IgY) against TNFR1. Bratisl Med J. 2014; 116: 316-320. 8. Jian J1, Zhao S, Tian Q, ...

  11. Prevalence and associations of symptomatic renal papillary necrosis ...

    African Journals Online (AJOL)

    Aim: To assess the prevalence and associations of symptomatic renal papillary necrosis (RPN) in sickle cell anemia patients. Patients and Methods: The case notes of homozygous hemoglobin (Hb) S patients diagnosed with RPN were retrospectively assessed. Diagnosis was based on microscopic hematuria and positive ...

  12. Prevalence and associations of symptomatic renal papillary necrosis ...

    African Journals Online (AJOL)

    2015-11-12

    Nov 12, 2015 ... Pandya KK, Koshy M, Brown N, Presman D. Renal papillary necrosis in sickle cell hemoglobinopathies. J Urol 1976;115:497-501. 11. Alhwiesh A. An update on sickle cell nephropathy. Saudi J Kidney Dis Transpl. 2014;25:249-65. 12. Breyer MD, Hao C, Qi Z. Cyclooxygenase-2 selective inhibitors and the.

  13. Generation of truncated recombinant form of tumor necrosis factor ...

    African Journals Online (AJOL)

    Conclusion: A truncated form of TNFR-1 has been successfully expressed in a bacterial expression system and purified on affinity column. The purified protein can be used in in vivo experiments to prepare specified agonist antibodies for TNFR-1. Keywords: Tumor necrosis factor receptor 1 (TNFR-1), Cysteine rich domain 2 ...

  14. Intestinal necrosis in young patient due to arterial tumour embolism

    DEFF Research Database (Denmark)

    Dahle, Einar; Gögenur, Ismail; Nørgaard, Peter

    2012-01-01

    of intestinal necrosis. Histological examination showed several arterial tumour emboli, morphologically similar to the primary sarcoma. The patient died 1 year after successful surgery. Because of the improved survival of patients with osteosarcoma, acute mesenteric ischaemia should be considered in acute...

  15. Septum necrosis following CPAP treatment of preterm infant

    DEFF Research Database (Denmark)

    Fjaeldstad, Alexander; Cipliene, Rasa; Ramsgaard-Jensen, Trine

    2014-01-01

    This case describes the complications of intensive respiratory support in a preterm infant. During two months of rigorous nasal continuous positive airway pressure (CPAP) therapy with intermittent use of CPAP-mask and -prongs, an ulcer in the nasal mucus membrane developed into septum necrosis...

  16. The Link Between Oxidative Stress Response and Tumor Necrosis ...

    African Journals Online (AJOL)

    Thyroid hormones are essential for normal organ growth, development and function. They regulate the basal metabolic rate of different types of cells, including hepatocytes. Oxidative stress plays an essential role in the pathogenesis of thyroid disorders and disturbed tissue functions. Tumor necrosis factor-alpha (TNF-α) is a ...

  17. Comparison of Types of Cell Death: Apoptosis and Necrosis.

    Science.gov (United States)

    Manning, Francis; Zuzel, Katherine

    2003-01-01

    Cell death is an essential factor in many biological processes including development. Discusses two types of cell death: (1) necrosis (induced by sodium azide); and (2) apoptosis (induced by sodium chromate). Illustrates key features that differ between these two types of cells death including loss of membrane integrity and internucleosomal DNA…

  18. Correlation Between Tumor Necrosis Factor Alpha and Proteinuria ...

    African Journals Online (AJOL)

    Serum tumor necrosis factor-α (TNF-α), urine TNF-α and C-reactive protein (CRP) levels were measured in all subjects. Correlations between these inflammatory parameters and degree of proteinuria, duration of diabetes and degree of glycemic control were examined. Results: Levels of the three inflammatory parameters ...

  19. Pituitary necrosis and vasospasm following removal of craniopharyngioma

    Directory of Open Access Journals (Sweden)

    Linda Ratanaprasatporn

    2015-03-01

    Full Text Available We report a case of vasospasm complicating delayed pituitary necrosis after craniopharyngioma resection in an 18-year old female. This is the first reported case that utilizes aggressive blood pressure management, fluid optimization, and rheologic doses of mannitol to successfully treat severe symptomatic vasospasm.

  20. Association of cardiotrophin-1 with myocardial fibrosis in hypertensive patients with heart failure.

    Science.gov (United States)

    López, Begoña; González, Arantxa; Querejeta, Ramón; Larman, Mariano; Rábago, Gregorio; Díez, Javier

    2014-03-01

    Cardiotrophin-1 has been shown to be profibrogenic in experimental models. The aim of this study was to analyze whether cardiotrophin-1 is associated with left ventricular end-diastolic stress and myocardial fibrosis in hypertensive patients with heart failure. Endomyocardial biopsies from patients (n=31) and necropsies from 7 control subjects were studied. Myocardial cardiotrophin-1 protein and mRNA and the fraction of myocardial volume occupied by collagen were increased in patients compared with controls (Phypertensive patients with heart failure. It is proposed that exaggerated cardiomyocyte production of cardiotrophin-1 in response to increased left ventricular end-diastolic stress may contribute to fibrosis through stimulation of fibroblasts in heart failure of hypertensive origin.

  1. Effects and Mechanisms of Chinese Herbal Medicine in Ameliorating Myocardial Ischemia-Reperfusion Injury

    Directory of Open Access Journals (Sweden)

    Qing Liu

    2013-01-01

    Full Text Available Myocardial ischemia-reperfusion (MIR injury is a major contributor to the morbidity and mortality associated with coronary artery disease, which accounts for approximately 450,000 deaths a year in the United States alone. Chinese herbal medicine, especially combined herbal formulations, has been widely used in traditional Chinese medicine for the treatment of myocardial infarction for hundreds of years. While the efficacy of Chinese herbal medicine is well documented, the underlying molecular mechanisms remain elusive. In this review, we highlight recent studies which are focused on elucidating the cellular and molecular mechanisms using extracted compounds, single herbs, or herbal formulations in experimental settings. These studies represent recent efforts to bridge the gap between the enigma of ancient Chinese herbal medicine and the concepts of modern cell and molecular biology in the treatment of myocardial infarction.

  2. Fat necrosis of the breast: clinical, mammographic and sonographic features

    Energy Technology Data Exchange (ETDEWEB)

    Bilgen, Isil Guenhan; Ustun, Esin Emin; Memis, Aysenur

    2001-08-01

    Objective: the purpose of this study was to describe and quantitate the clinical, mammographic and sonographic (US) features and to evaluate the evolution of fat necrosis in the breast. Materials and methods: a retrospective review of the clinical, mammographic and US findings of 126 fat necrosis lesions in 94 patients, diagnosed between 1989 and 1999, was done. All the cases included in the study had at least 3 years follow-up mammograms. In addition, 48 patients with a total of 62 fat necrosis lesions, also had an US follow-up. Fat necrosis was diagnosed on the basis of histologic (n=25) and initial or follow-up imaging (n=69) findings. Results: the predominant mammographic features of the 114 lesions apparent on mammograms were radiolucent oil cyst (n=34, 26.9%), round opacity (n=16, 12.6%), asymmetrical opacity or heterogenicity of the subcutaneous tissues (n=20, 15.8%), dystrophic calcifications (n=34, 26.9%), clustered pleomorphic microcalcifications (n=5, 3.9%), and suspicious speculated mass (n=5, 3.9%). In five patients with 12 (9.5%) palpable masses, mammograms were normal. The predominant US features of the 112 lesions apparent on sonograms were solid (n=18, 14.2%), anechoic with posterior acoustic enhancement (n=21, 16.6%), anechoic with posterior acoustic shadowing (n=20, 15.8%), cystic with internal echoes (n=14, 11.1%), cystic with mural nodule (n=5, 3.9%) and increased echogenicity of the subcutaneous tissues (n=34, 26.9%). In five patients with 14 (11.1%) lesions, sonographic examination was normal. Mammographic follow-up showed that five of the radiolucent oil cysts developed curvilinear calcifications, six of the round opacities decreased in size and density, and another two disappeared. Eleven of the dystrophic calcifications became even more coarse. Six of the asymmetrical opacities became vague and one developed an oil cyst and coarse calcifications. The only nonoperated speculated mass developed a typical small radiolucent oil cyst in the

  3. Cardioprotective Effects of Rosmarinic Acid on Isoproterenol-Induced Myocardial Infarction in Rats

    Directory of Open Access Journals (Sweden)

    Negisa Seyed Toutounchi, Arash Afrooziyan, Maryam Rameshrad, Aysa Rezabakhsh, Haleh Vaez, Sanaz Hamedeyazdan, Fatemeh Fathiazad, Alireza Garjani

    2017-06-01

    Full Text Available Background: Rosmarinic acid is a polyphenolic compound with considerable antioxidant activities. We aimed to investigate its cardioprotective effects against isoproterenol-induced myocardial infarction (MI in rats. Methods: Male Wistar rats were assigned to 5 groups of control, isoproterenol, and treatments with 10, 20, 40 mg/kg of rosmarinic acid. Myocardial infarction was induced by subcutaneous injection of isoproterenol (100 mg/kg once daily for 2 days. Rosmarinic acid was injected intraperitoneally once daily for 4 days, from the day of isoproterenol injection. In the fifth day the animals were anesthetized and hemodynamic and electrocardiographic parameters were recorded. After collecting the blood samples, the hearts were removed, weighed immediately to measure the cardiac enlargement, and kept for further histological studies. Lactate dehydrogenase and malondialdehyde were measured in the heart tissues for evaluating the damages and lipid peroxidation, respectively. Results: Rosmarinic acid revealed a considerable antioxidant activity in vitro, with IC50 of 6.43µg/ml. Isoproterenol induced cardiac arrhythmias, myocardial damage and cardiac enlargement. Rosmarinic acid significantly reduced peripheral neutrophil percentage and inhibited isoproterenol-induced ST-segment elevation and R-amplitude depression in the infarcted hearts. It also significantly increased the mean arterial pressure and heart rate and decreased the left ventricular end diastolic pressure. The ventricular contractility was considerably improved by rosmarinic acid. Histopathological evaluations showed that rosmarinic acid significantly diminished the post-MI necrosis and fibrosis in the myocardium and inhibited the cardiac edematous. Conclusion: It is deducible from the results that rosmarinic acid improves the cardiac performance and inhibits post-MI myocardial depression, probably due to its anti-oxidative activity.

  4. Clinical and laboratory peculiarities of acute myocardial infarction after chronic tonsillitis

    Directory of Open Access Journals (Sweden)

    Shvarts Y.G.

    2012-06-01

    Full Text Available Aim: The definition of the relationship of clinical and laboratory features of acute myocardial infarction depending on the suffering of chronic tonsillitis. Materials and methods. The study included 54 patients with acute myocardial infarction suffering for 1-2 days. The collection of the anamnesis, assessment of clinical factors, inspection of the palatine tonsils, clinical and biochemical blood tests have been done. Markers of myocardial necrosis, an electrocardiogram with calculation of a dispersion of interval QT, echocardiogram have been taken into account. Results. 45 of 54 patients reported the symptoms of chronic tonsillitis in their lifetime. At 17 patients the previous diagnosis of chronic tonsillitis has been made, in 6 of them bilateral tonsillectomy was held. All of the patients were divided into 2 groups: 1 with proven chronic tonsillitis (17 patients and 2 — the others (37 patients. At patients with chronic tonsillitis substantially more developed acute heart failure at sick this group glucose of the blood at receipt was higher than in 2 groups (p=0,004, given distinction was independent of presence of diabetes. According to the echocardiography 1 group of patients determined course-diastolic dimensions of the right ventricle increase in comparison with 2 groups (p=0,01. Conclusion. In patients with chronic tonsillitis more severe course of acute myocardial infarction has been determined, which became evident in the relatively high values of blood glucose on admission. The frequent development of congestive heart failure, and increase of the course-diastolic dimensions of the right ventricle have been also revealed.

  5. Transmural distribution of myocardial infarction: difference between the right and left ventricles in a canine model

    Energy Technology Data Exchange (ETDEWEB)

    Ohzono, K.; Koyanagi, S.; Urabe, Y.; Harasawa, Y.; Tomoike, H.; Nakamura, M.

    1986-07-01

    The evolution of myocardial infarction 24 hours after ligating both the right coronary artery and the obtuse marginal branch of the left circumflex coronary artery was examined in 33 anesthetized dogs. Postmortem coronary angiography and a tracer microsphere technique were used to determine risk areas and their collateral blood flows, respectively. The mean weight of the risk areas was 11.3 +/- 0.5 g (mean +/- SEM) in the right ventricle and 10.5 +/- 0.9 g in the left ventricle (NS). The weight of infarcted tissue was 5.7 +/- 0.7 g in the right ventricle and 5.2 +/- 0.9 g in the left ventricle (NS). In both ventricles, infarct weight was linearly related to risk area size, and the percent of risk area necrosis was inversely correlated with the extent of collateral flow at 24 hours of coronary ligation, defined as the mean myocardial blood flow inside the central risk area. Ratios of infarct to risk area between the subendocardial and subepicardial layers were 0.76 +/- 0.06 and 0.28 +/- 0.05 in the right and left ventricles, respectively (p less than 0.01, between ventricles, n = 31), which coincided well with subendocardial-to-subepicardial-flow ratios at 24 hours, ie, 0.86 +/- 0.04 in the right ventricle and 0.32 +/- 0.06 in the left ventricle (p less than 0.01). The regional distribution of myocardial infarction correlated well with flow distribution inside the risk area; the slope of these relations was similar between the subendocardium and subepicardium in the right ventricle, whereas in the left ventricle it was larger in the subendocardium than in the subepicardium. Thus, in the dog, the inherent change in the regional distribution of coronary collateral blood flow is an important modifier in the evolution of myocardial infarction, especially in the left ventricle.

  6. Porphyromonas Gingivalis Elevated High-Mobility Group Box 1 Levels After Myocardial Infarction in Mice.

    Science.gov (United States)

    Srisuwantha, Rungtiwa; Shiheido, Yuka; Aoyama, Norio; Sato, Hiroki; Kure, Keitetsu; Laosrisin, Narongsak; Izumi, Yuichi; Suzuki, Jun-Ichi

    2017-10-21

    High mobility group box 1 (HMGB1) is a nuclear protein released from necrotic cells, inducing inflammatory responses. Epidemiological studies suggested a possible association between periodontitis and cardiovascular diseases (CVDs). Due to tissue damage and necrosis of cardiac cells following myocardial infarction (MI), HMGB1 is released, activating an inflammatory reaction. However, it remains unclear whether periodontitis is also involved in myocardial damage. The purpose of this study was to determine the effect of the periodontal pathogen Porphyromonas gingivalis (P.g.) after MI in mice.C57BL/6J wild type mice in post-MI were inoculated with P.g. in the infected group (P.g.-inoculated MI group) and with phosphate buffer saline (PBS) in the control group (PBS-injected MI group). Plasma samples and twelve tissue samples from mice hearts after MI were obtained. We determined the expression of HMGB1 by ELISA and immunohistochemistry.The level of HMGB1 protein in the P.g.-inoculated MI group was significantly higher than in the PBS-injected MI group on day 5, but not on day 14. Immunohistochemistry analysis revealed that HMGB1 was mainly expressed in cardiomyocytes, immune cells, and vascular endothelial cells in the PBS-injected MI group, while HMGB1 was seen broadly in degenerated cardiomyocytes, extracellular fields, immune cells, and vascular endothelial cells in the P.g.-inoculated MI group. A significant increase in the number of HMGB1 positive cells was observed in the P.g.-inoculated MI group compared to the PBS-injected MI group.Infection with P.g. after MI enhanced myocardial HMGB1 expression. There is a possible relationship between periodontitis and post-infarction myocardial inflammation through HMGB-1.

  7. Clinical Characteristics and Outcomes of Patients with Myocardial Infarction, Myocardial Injury, and Nonelevated Troponins

    DEFF Research Database (Denmark)

    Sarkisian, Laura; Saaby, Lotte; Poulsen, Tina S

    2015-01-01

    was diagnosed in cases of a cardiac troponin I increase or decrease pattern with at least 1 value >30 ng/L (99th percentile) together with myocardial ischemia. Myocardial injury was defined as cardiac troponin I values >30 ng/L, but without signs or symptoms indicating overt cardiac ischemia. Patients with peak...... troponin value is encountered in the absence of obvious myocardial ischemia, a careful search for other clinical conditions is crucial. METHODS: In 2010 to 2011, we prospectively studied hospitalized patients who had cardiac troponin I measured on clinical indication. An acute myocardial infarction...

  8. Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in rats.

    Science.gov (United States)

    Nakagawa, Pablo; Liu, Yunhe; Liao, Tang-Dong; Chen, Xiaojuan; González, Germán E; Bobbitt, Kevin R; Smolarek, Derek; Peterson, Ed L; Kedl, Ross; Yang, Xiao-Ping; Rhaleb, Nour-Eddine; Carretero, Oscar A

    2012-11-01

    Myocarditis is commonly associated with cardiotropic infections and has been linked to development of autoimmunity. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring tetrapeptide that prevents inflammation and fibrosis in hypertension and other cardiovascular diseases; however, its effect on autoimmune-mediated cardiac diseases remains unknown. We studied the effects of Ac-SDKP in experimental autoimmune myocarditis (EAM), a model of T cell-mediated autoimmune disease. This study was conducted to test the hypothesis that Ac-SDKP prevents autoimmune myocardial injury by modulating the immune responses. Lewis rats were immunized with porcine cardiac myosin and treated with Ac-SDKP or vehicle. In EAM, Ac-SDKP prevented both systolic and diastolic cardiac dysfunction, remodeling as shown by hypertrophy and fibrosis, and cell-mediated immune responses without affecting myosin-specific autoantibodies or antigen-specific T cell responses. In addition, Ac-SDKP reduced cardiac infiltration by macrophages, dendritic cells, and T cells, pro-inflammatory cytokines [interleukin (IL)-1α, tumor necrosis factor-α, IL-2, IL-17] and chemokines (cytokine-induced neutrophil chemoattractant-1, interferon-γ-induced protein 10), cell adhesion molecules (intercellular adhesion molecule-1, L-selectin), and matrix metalloproteinases (MMP). Ac-SDKP prevents autoimmune cardiac dysfunction and remodeling without reducing the production of autoantibodies or T cell responses to cardiac myosin. The protective effects of Ac-SDKP in autoimmune myocardial injury are most likely mediated by inhibition of 1) innate and adaptive immune cell infiltration and 2) expression of proinflammatory mediators such as cytokines, chemokines, adhesion molecules, and MMPs.

  9. Estimation of shear stress by using a myocardial bridge-mural coronary artery simulating device.

    Science.gov (United States)

    Ding, Hao; Yang, Qian; Shang, Kun; Lan, Hailian; Lv, Jie; Liu, Zhilin; Liu, Yang; Sheng, Lixing; Zeng, Yanjun

    2017-01-01

    This study was aimed at developing a myocardial bridge-mural coronary artery simulative device and analyzing the relationship between shear stress on the mural coronary artery and atherosclerosis. A myocardial bridge-mural coronary artery simulative device was used to simulate experiments in vitro. In the condition of maintaining any related parameters such as system temperature, average flow rate, and heart rate, we calculated and observed changes in proximal and distal mean values, and oscillatory value of shear stress on the mural coronary artery by regulating the compression level of the myocardial bridge to the mural coronary artery. Under 0% compression, no significant differences were observed in distal and proximal mean values and oscillatory value of the shear stress on the mural coronary artery. With the increase in the degree of compression, the mean shear stress at the distal end was greater than that at the proximal end, but the oscillatory value of the shear stress at the proximal end was greater than that at the distal end. The experimental results of this study indicate that myocardial bridge compression leads to abnormal hemodynamics at the proximal end of the mural coronary artery. This abnormal phenomenon is of great significance in the study of atherosclerosis hemodynamic pathogenesis, which has potential clinical value for pathological effects and treatments of myocardial bridge.

  10. Experimental oleander (Nerium oleander) intoxication in broiler chickens (Gallus gallus).

    Science.gov (United States)

    Omidi, Arash; Razavizadeh, Alireza T; Movassaghi, Ahmad R; Aslani, Mohammad R

    2012-08-01

    Dried leaves of oleander were orally given at a single dose of 500 mg/kg body weight to 20 clinically healthy male chickens. Clinical signs of toxicosis began to appear about 1 h after receiving the oleander and included hypersalivation, vomiting, diarrhea, deep depression, and sudden death. Also, hyperemia in the combs and wattles was obviously seen. Electrocardiograms (ECG) were repeatedly recorded at 30 min intervals. ECGs findings included increasing the QRS duration in some birds and various kinds of arrhythmias. Bradycardia was the most frequently detected finding (30.43%). During necropsy, there were congestion and hemorrhages in the visceral organs particularly in heart, liver, kidney, and lung. Histopathology revealed myocardial cell necrosis with hyperemia and hemorrhage, severe diffuse pulmonary congestion and edema, severe renal congestion and hemorrhage with tubular necrosis, and coagulative necrosis of hepatocytes with hyperemia and hemorrhage. There were also congestion, mild epithelial necrosis and desquamation with infiltration of mononuclear inflammatory cells in the proventriculus of all birds. There was also mild to moderate congestion in the intestines with scattered necrosis of surface enterocytes. The lack of information about the toxicity of oleanders in poultry was the main cause for this study. The results suggest that chickens appear to respond to oleander poisoning in a manner similar to other species.

  11. Regional Mechanics Determine Collagen Fiber Structure in Healing Myocardial Infarcts

    Science.gov (United States)

    Fomovsky, Gregory M.; Rouillard, Andrew D.; Holmes, Jeffrey W.

    2012-01-01

    Following myocardial infarction, the mechanical properties of the healing infarct are an important determinant of heart function and the risk of progression to heart failure. In particular, mechanical anisotropy (having different mechanical properties in different directions) in the healing infarct can preserve pump function of the heart. Based on reports of different collagen structures and mechanical properties in various animal models, we hypothesized that differences in infarct size, shape, and/or location produce different patterns of mechanical stretch that guide evolving collagen fiber structure. We tested the effects of infarct shape and location using a combined experimental and computational approach. We studied mechanics and collagen fiber structure in cryoinfarcts in 53 Sprague-Dawley rats and found that regardless of shape or orientation, cryoinfarcts near the equator of the left ventricle stretched primarily in the circumferential direction and developed circumferentially aligned collagen, while infarcts at the apex stretched similarly in the circumferential and longitudinal direction and developed randomly oriented collagen. In a computational model of infarct healing, an effect of mechanical stretch on fibroblast and collagen alignment was required to reproduce the experimental results. We conclude that mechanical environment determines collagen fiber structure in healing myocardial infarcts. Our results suggest that emerging post-infarction therapies that alter regional mechanics will also alter infarct collagen structure, offering both potential risks and novel therapeutic opportunities. PMID:22418281

  12. Repetitive Myocardial Infarctions Secondary to Delirium Tremens

    Directory of Open Access Journals (Sweden)

    David Schwartzberg

    2014-01-01

    Full Text Available Delirium tremens develops in a minority of patients undergoing acute alcohol withdrawal; however, that minority is vulnerable to significant morbidity and mortality. Historically, benzodiazepines are given intravenously to control withdrawal symptoms, although occasionally a more substantial medication is needed to prevent the devastating effects of delirium tremens, that is, propofol. We report a trauma patient who required propofol sedation for delirium tremens that was refractory to benzodiazepine treatment. Extubed prematurely, he suffered a non-ST segment myocardial infarction followed by an ST segment myocardial infarction requiring multiple interventions by cardiology. We hypothesize that his myocardial ischemia was secondary to an increased myocardial oxygen demand that occurred during his stress-induced catecholamine surge during the time he was undertreated for delirium tremens. This advocates for the use of propofol for refractory benzodiazepine treatment of delirium tremens and adds to the literature on the instability patients experience during withdrawal.

  13. Cardiac biomarkers in acute myocardial infarction

    National Research Council Canada - National Science Library

    Aldous, Sally J

    2013-01-01

    ... (established and novel) assays. Cardiac troponin, our current "gold standard" biomarker criterion for the diagnosis of myocardial infarction has high sensitivity and specificity for this diagnosis and therapies instituted...

  14. Effects of antidepressant treatment following myocardial infarction

    NARCIS (Netherlands)

    Van Melle, Joost P.; De Jonge, Peter; Honig, Adriaan; Schene, Aart H.; Kuyper, Astrid M. G.; Crijns, Harry J. G. M.; Schins, Annique; Tulner, Dorien; Van den Berg, Maarten P.; Ormel, Johan

    Background Depression following myocardial infarction is associated with poor cardiac prognosis. It is unclear whether antidepressant treatment improves long-term depression status and cardiac prognosis. Aims To evaluate the effects of antidepressant treatment compared with usual care in an

  15. Effects of antidepressant treatment following myocardial infarction

    NARCIS (Netherlands)

    van Melle, Joost P.; de Jonge, Peter; Honig, Adriaan; Schene, Aart H.; Kuyper, Astrid M. G.; Crijns, Harry J. G. M.; Schins, Annique; Tulner, Dorien; van den Berg, Maarten P.; Ormel, Johan

    2007-01-01

    BACKGROUND: Depression following myocardial infarction is associated with poor cardiac prognosis. It is unclear whether antidepressant treatment improves long-term depression status and cardiac prognosis. AIMS: To evaluate the effects of antidepressant treatment compared with usual care in an

  16. Biventricular thrombi complicating acute myocardial infarction.

    Science.gov (United States)

    Sanghvi, Sanjeev; Baroopal, Anil; Sarda, Pawan

    2016-09-01

    A rare case of biventricular thrombi complicating acute myocardial infarction detected during echocardiography is described. Copyright © 2016 Cardiological Society of India. Published by Elsevier B.V. All rights reserved.

  17. Diagnosing Myocardial Contusion after Blunt Chest Trauma.

    Science.gov (United States)

    Alborzi, Zahra; Zangouri, Vahid; Paydar, Shahram; Ghahramani, Zahra; Shafa, Masih; Ziaeian, Bizhan; Radpey, Mohammad Reza; Amirian, Armin; Khodaei, Shahin

    2016-04-13

    A myocardial contusion refers to a bruise of the cardiac muscle, the severity of which can vary depending on the severity of the injury and when the injury occurs. It is a major cause of rapid death which happens after blunt chest trauma and should be suspected at triage in the emergency department. We demonstrated that suspected myocardial contusion patients who have normal electrocardiograms (ECGs) and biomarker tests can be safely discharged. However, if the test results are abnormal, the next steps should be echocardiography and more advanced measures. Diagnosing myocardial contusion is very difficult because of its nonspecific symptoms. If a myocardial contusion happens, cardiogenic shock or arrhythmia must be anticipated, and the patient must be carefully monitored.

  18. Mechanisms involved in symptomatic myocardial bridging

    NARCIS (Netherlands)

    Hazenberg, A. J. C.; Jessurun, G. A. J.; Tio, R. A.

    Background. In patients with extensive myocardial bridging, evaluation of its clinical significance remains a challenge. Hypothesis. Sequential invasive testing is feasible and gives more insight into the pathophysiological mechanism of bridging-related angina. Methods. Twelve patients with chest

  19. Myocardial infarction following cannabis induced coronary vasospasm

    National Research Council Canada - National Science Library

    Gunawardena, Mudalige Don Vajira Malin; Rajapakse, Senaka; Herath, Jagath; Amarasena, Naomali

    2014-01-01

    Smoking cannabis is a rare cause of myocardial infarction. We report a 29-year-old man who presented with acute coronary syndrome following consumption of a type of cannabis with the street name 'Kerala Ganja...

  20. Diagnosing Myocardial Contusion after Blunt Chest Trauma

    Directory of Open Access Journals (Sweden)

    Zahra Alborzi

    2016-10-01

    Full Text Available A myocardial contusion refers to a bruise of the cardiac muscle, the severity of which can vary depending on the severity of the injury and when the injury occurs. It is a major cause of rapid death which happens after blunt chest trauma and should be suspected at triage in the emergency department. We demonstrated that suspected myocardial contusion patients who have normal electrocardiograms (ECGs and biomarker tests can be safely discharged. However, if the test results are abnormal, the next steps should be echocardiography and more advanced measures. Diagnosing myocardial contusion is very difficult because of its nonspecific symptoms. If a myocardial contusion happens, cardiogenic shock or arrhythmia must be anticipated, and the patient must be carefully monitored.

  1. Myocardial bridges: a prospective forensic autopsy study

    National Research Council Canada - National Science Library

    Micić-Labudović, Jelena; Atanasijević, Tatjana; Popović, Vesna; Mihailović, Zoran; Nikolić, Slobodan; Puzović, Dragana

    2015-01-01

    ...) in the autopsy material considering the descending branch of the LAD to be the most important one in the nourishment of the myocardium and myocardial bridges to be the most frequent in its area...

  2. Echocardiography diagnosis of myocardial infarction complications

    Directory of Open Access Journals (Sweden)

    N.D. Oryshchyn

    2016-03-01

    Full Text Available Diagnosis and management of myocardial infarction complications are discussed in this article. These complications are associated with high level of mortality and surgery is a main treatment method. High level of suspicion and early diagnosis are essential for appropriate treatment and improvement of prognosis. Echocardiography is a main diagnostic method. Analysis of literature about contemporary management of mechanical complications of myocardial infarction has been performed, case reports are presented.

  3. [Emergency treatment of myocardial infarction in women].

    Science.gov (United States)

    Allonneau, Alexandre; Gonzva, Jonathan; Lovi, Steven; Klein, Isabelle; Lefort, Hugues

    Acute myocardial infarction (MI) affects mainly men. In women, chest pain is less typical, delaying the diagnosis and increasing the time before treatment is delivered. Morbidity-mortality is greater notably due to a modification of the myocardial reperfusion strategy. The acute care of MI is almost identical for men and women. Knowing more about the epidemiology of women with MI enables prevention strategies to be targeted. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

  4. Acute myocardial infarction: 'telomerasing' for cardioprotection

    OpenAIRE

    Sanchís-Gomar, Fabián; Lucía Mulas, Alejandro

    2015-01-01

    Reactivating the telomerase gene through gene therapy after acute myocardial infarction (AMI) has been recently reported to improve survival in mice. Given that regular physical exercise also activates this gene, therapeutic and lifestyle interventions targeting telomerase need to be explored as possible additions to the current armamentarium for myocardial regeneration. 9.292 JCR (2015) Q1, 17/289 Biochemistry & mollecular biology, 17/187 Cell biology, 8/124 Medicine, research & experimen...

  5. Report of Intracerebral Hemorrhage Following Myocardial Infarction

    Directory of Open Access Journals (Sweden)

    Akvan Paymard

    2017-03-01

    Full Text Available Background and Objectives: Stroke is a rare complication of myocardial infarction (AMI. Aspirin, plavix, and enoxaparin are among drug treatments for myocardial infarction, which lead to stroke. The present study is a case report of stroke after myocardial infarction, which discusses patient’s records and clinical history along with paraclinical findings. Case Report: The patient was a 60-year-old man with a history of heart disease and diabetes, presented with severe chest pain and dyspnea to the Emergency Department of Yasuj Sajad Hospital on January 29, 2015, and after taking ECG, it was found that there was no signs of myocardial infarction, but troponin test was positive two times. The diagnosis was myocardial infarction without ST segment elevation. The patient took aspirin and plavix, and after subcutaneous injection of enoxaparin at the dose of 80 mg, his level of consciousness decreased, which caused GCS:5, right-side mydriasis, and motor paralysis in the left half of the body, therefore, CT was performed, and the patient that had about 90 ml hemorrhage in temporoparietal lobe. The patient was transformed to the operating room and 60 ml blood was removed using partial lobectomy and a microscope. After hospitalization in ICU for several days, the patient was extubated under the SIMV mode. Considering the high prevalence of heart disease, especially increasing rate of myocardial infarction in the country, anticoagulants should be more carefully used and after administration of this group of drugs, patients be regularly monitored for side effects.

  6. Silent myocardial ischemia during coronary angioplasty.

    Science.gov (United States)

    Dellborg, M; Emanuelsson, H; Swedberg, K

    1993-01-01

    Silent myocardial ischemia is a marker in patients with coronary artery disease identifying those at high risk for subsequent cardiac events. During provoked myocardial ischemia some patients with angina pectoris do not develop chest pain. Are there clinical, angiographic or electrocardiographic differences between patients with chest pain as compared with patients without chest pain during provoked myocardial ischemia? Coronary angioplasty is a well-established method for the treatment of coronary stenosis, but it is also an interesting model for the study of myocardial ischemia as a result of coronary occlusion. We monitored 114 patients with angina pectoris during coronary angioplasty with dynamic, computerized vectorcardiography. During inflation of the balloon 33 of 114 patients had silent ischemia. Patients with silent myocardial ischemia had similar reasons for terminating the preangioplasty exercise test and where on similar anti-ischemic drug regimes. Silent myocardial ischemia was significantly associated with a history of diabetes, presence of collaterals, a history of less severe previous angina and less ST segment changes during angioplasty as compared with patients with painful ischemia. It is suggested that during coronary angioplasty silent ischemia may be caused by a less severe degree of ischemia, possibly as a result of the protective effect of collaterals.

  7. Myocardial Dysfunction and Shock after Cardiac Arrest

    Science.gov (United States)

    Jentzer, Jacob C.; Chonde, Meshe D.; Dezfulian, Cameron

    2015-01-01

    Postarrest myocardial dysfunction includes the development of low cardiac output or ventricular systolic or diastolic dysfunction after cardiac arrest. Impaired left ventricular systolic function is reported in nearly two-thirds of patients resuscitated after cardiac arrest. Hypotension and shock requiring vasopressor support are similarly common after cardiac arrest. Whereas shock requiring vasopressor support is consistently associated with an adverse outcome after cardiac arrest, the association between myocardial dysfunction and outcomes is less clear. Myocardial dysfunction and shock after cardiac arrest develop as the result of preexisting cardiac pathology with multiple superimposed insults from resuscitation. The pathophysiology involves cardiovascular ischemia/reperfusion injury and cardiovascular toxicity from excessive levels of inflammatory cytokine activation and catecholamines, among other contributing factors. Similar mechanisms occur in myocardial dysfunction after cardiopulmonary bypass, in sepsis, and in stress-induced cardiomyopathy. Hemodynamic stabilization after resuscitation from cardiac arrest involves restoration of preload, vasopressors to support arterial pressure, and inotropic support if needed to reverse the effects of myocardial dysfunction and improve systemic perfusion. Further research is needed to define the role of postarrest myocardial dysfunction on cardiac arrest outcomes and identify therapeutic strategies. PMID:26421284

  8. Assessment of myocardial viability using PET

    Energy Technology Data Exchange (ETDEWEB)

    Yoon, Seok Nam [College of Medicine, Ajou University, Suwon (Korea, Republic of)

    2005-02-15

    The potential for recovery of left ventricular dysfunction after myocardial revascularization represents a practical clinical definition for myocardial viability. The evaluation of viable myocardium in patients with severe global left ventricular dysfunction due to coronary artery disease and with regional dysfunction after acute myocardial infarction is an important issue whether left ventricular dysfunction may be reversible or irreversible after therapy. If the dysfunction is due to stunning or hibernation, functional improvement is observed. But stunned myocardium may recover of dysfunction with no revascularization. Hibernation is chronic process due to chronic reduction in the resting myocardial blood flow. There are two types of myocardial hibernation; 'functional hibernation' with preserved contractile reserve and 'structural hibernation' without contractile reserve in segments with preserved glucose metabolism. This review focus on the application of F-18 FDG and other radionuclides to evaluate myocardial viability. In addition the factors influencing predictive value of FDG imaging for evaluating viability and the different criteria for viability are also reviewed.

  9. Computational modeling of acute myocardial infarction.

    Science.gov (United States)

    Sáez, P; Kuhl, E

    2016-01-01

    Myocardial infarction, commonly known as heart attack, is caused by reduced blood supply and damages the heart muscle because of a lack of oxygen. Myocardial infarction initiates a cascade of biochemical and mechanical events. In the early stages, cardiomyocytes death, wall thinning, collagen degradation, and ventricular dilation are the immediate consequences of myocardial infarction. In the later stages, collagenous scar formation in the infarcted zone and hypertrophy of the non-infarcted zone are auto-regulatory mechanisms to partly correct for these events. Here we propose a computational model for the short-term adaptation after myocardial infarction using the continuum theory of multiplicative growth. Our model captures the effects of cell death initiating wall thinning, and collagen degradation initiating ventricular dilation. Our simulations agree well with clinical observations in early myocardial infarction. They represent a first step toward simulating the progression of myocardial infarction with the ultimate goal to predict the propensity toward heart failure as a function of infarct intensity, location, and size.

  10. Microvascular Resistance Predicts Myocardial Salvage and Infarct Characteristics in ST‐Elevation Myocardial Infarction

    Science.gov (United States)

    Payne, Alexander R.; Berry, Colin; Doolin, Orla; McEntegart, Margaret; Petrie, Mark C.; Lindsay, M. Mitchell; Hood, Stuart; Carrick, David; Tzemos, Niko; Weale, Peter; McComb, Christie; Foster, John; Ford, Ian; Oldroyd, Keith G.

    2012-01-01

    Background The pathophysiology of myocardial injury and repair in patients with ST‐elevation myocardial infarction is incompletely understood. We investigated the relationships among culprit artery microvascular resistance, myocardial salvage, and ventricular function. Methods and Results The index of microvascular resistance (IMR) was measured by means of a pressure‐ and temperature‐sensitive coronary guidewire in 108 patients with ST‐elevation myocardial infarction (83% male) at the end of primary percutaneous coronary intervention. Paired cardiac MRI (cardiac magnetic resonance) scans were performed early (2 days; n=108) and late (3 months; n=96) after myocardial infarction. T2‐weighted‐ and late gadolinium–enhanced cardiac magnetic resonance delineated the ischemic area at risk and infarct size, respectively. Myocardial salvage was calculated by subtracting infarct size from area at risk. Univariable and multivariable models were constructed to determine the impact of IMR on cardiac magnetic resonance–derived surrogate outcomes. The median (interquartile range) IMR was 28 (17–42) mm Hg/s. The median (interquartile range) area at risk was 32% (24%–41%) of left ventricular mass, and the myocardial salvage index was 21% (11%–43%). IMR was a significant multivariable predictor of early myocardial salvage, with a multiplicative effect of 0.87 (95% confidence interval 0.82 to 0.92) per 20% increase in IMR; Pmicrovascular obstruction and myocardial hemorrhage. Conclusion Microvascular resistance measured during primary percutaneous coronary intervention significantly predicts myocardial salvage, infarct characteristics, and left ventricular ejection fraction in patients with ST‐elevation myocardial infarction. (J Am Heart Assoc. 2012;1:e002246 doi: 10.1161/JAHA.112.002246) PMID:23130166

  11. Systemic inflammatory response following acute myocardial infarction

    National Research Council Canada - National Science Library

    Lu FANG Xiao-Lei Moorea Anthony M Dart Le-Min WANG

    2015-01-01

    Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response...

  12. Detection of Myocardial Ischemia-Reperfusion Injury Using a Fluorescent Near-Infrared Zinc(II-Dipicolylamine Probe and 99mTc Glucarate

    Directory of Open Access Journals (Sweden)

    Leonie wyffels

    2012-05-01

    Full Text Available A fluorescent zinc 2,2′-dipicolylamine coordination complex PSVue®794 (probe 1 is known to selectively bind to phosphatidylserine exposed on the surface of apoptotic and necrotic cells. In this study, we investigated the cell death targeting properties of probe 1 in myocardial ischemia-reperfusion injury. A rat heart model of ischemia-reperfusion was used. Probe 1, control dye, or 99mTc glucarate was intravenously injected in rats subjected to 30-minute and 5-minute myocardial ischemia followed by 2-hour reperfusion. At 90 minutes or 20 hours postinjection, myocardial uptake was evaluated ex vivo by fluorescence imaging and autoradiography. Hematoxylin-eosin and cleaved caspase-3 staining was performed on myocardial sections to demonstrate the presence of ischemia-reperfusion injury and apoptosis. Selective accumulation of probe 1 could be detected in the area at risk up to 20 hours postinjection. Similar topography and extent of uptake of probe 1 and 99mTc glucarate were observed at 90 minutes postinjection. Histologic analysis demonstrated the presence of necrosis, but only a few apoptotic cells could be detected. Probe 1 selectively accumulates in myocardial ischemia-reperfusion injury and is a promising cell death imaging tool.

  13. Troponin levels within the normal range and probability of inducible myocardial ischemia and coronary events in patients with acute chest pain.

    Science.gov (United States)

    Bouzas-Mosquera, Alberto; Peteiro, Jesús; Broullón, Francisco J; Constanso, Ignacio P; Rodríguez-Garrido, Jorge L; Martínez, Dolores; Yáñez, Juan C; Bescos, Hildegart; Álvarez-García, Nemesio; Vázquez-Rodríguez, José Manuel

    2016-03-01

    Patients with suspected acute coronary syndromes and negative cardiac troponin (cTn) levels are deemed at low risk. Our aim was to assess the effect of cTn levels on the frequency of inducible myocardial ischemia and subsequent coronary events in patients with acute chest pain and cTn levels within the normal range. We evaluated 4474 patients with suspected acute coronary syndromes, nondiagnostic electrocardiograms and serial cTnI levels below the diagnostic threshold for myocardial necrosis using a conventional or a sensitive cTnI assay. The end points were the probability of inducible myocardial ischemia and coronary events (i.e., coronary death, myocardial infarction or coronary revascularization within 3 months). The probability of inducible myocardial ischemia was significantly higher in patients with detectable peak cTnI levels (25%) than in those with undetectable concentrations (14.6%, pacute coronary syndromes and seemingly negative cTnI. Copyright © 2015 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.

  14. Magnetic resonance imaging (MRI) of inflamed myocardium using iron oxide nanoparticles in patients with acute myocardial infarction - preliminary results.

    Science.gov (United States)

    Yilmaz, Ali; Rösch, Sabine; Klingel, Karin; Kandolf, Reinhard; Helluy, Xavier; Hiller, Karl-Heinz; Jakob, Peter M; Sechtem, Udo

    2013-02-20

    Superparamagnetic iron oxide nanoparticle (SPIO)-based molecular imaging agents targeting macrophages have been developed and successfully applied in animal models of myocardial infarction. The purpose of this clinical trial was to investigate whether magnetic resonance imaging (MRI) of macrophages using ferucarbotran (Resovist®) allows improved visualisation of the myocardial (peri-)infarct zone compared to conventional gadolinium-based necrosis/fibrosis imaging in patients with acute myocardial infarction. The clinical study NIMINI-1 was performed as a prospective, non-randomised, non-blinded, single agent phase III clinical trial (NCT0088644). Twenty patients who had experienced either an acute ST-elevation or non-ST-elevation myocardial infarction (STEMI/NSTEMI) were included to this study. Following coronary angiography, a first baseline cardiovascular magnetic resonance (CMR) study (pre-SPIO) was performed within seven days after onset of cardiac symptoms. A second CMR study (post-SPIO) was performed either 10 min, 4h, 24h or 48h after ferucarbotran administration. The CMR studies comprised cine-CMR, T2-weighted "edema" imaging, T2-weighted cardiac imaging and T1-weighted late-gadolinium-enhancement (LGE) imaging. The median extent of short-axis in-plane LGE was 28% (IQR 19-31%). Following Resovist® administration the median extent of short-axis in-plane T2-weighted hypoenhancement (suggestive of intramyocardial haemorrhage and/or SPIO accumulation) was 0% (IQR 0-9%; p=0.68 compared to pre-SPIO). A significant in-slice increase (>3%) in the extent of T2-weighted "hypoenhancement" (post-SPIO compared to pre-SPIO) was seen in 6/16 patients (38%). However, no patient demonstrated "hypoenhancement" in T2-weighted images following Resovist® administration that exceeded the area of LGE. T2/T2-weighted MRI aiming at non-invasive myocardial macrophage imaging using the approved dose of ferucarbotran does not allow improved visualisation of the myocardial (peri

  15. Prognostic significance of transient myocardial ischaemia after first acute myocardial infarction: five year follow up study

    DEFF Research Database (Denmark)

    Mickley, H; Nielsen, J R; Berning, J

    1995-01-01

    OBJECTIVE: To assess the five year prognostic significance of transient myocardial ischaemia on ambulatory monitoring after a first acute myocardial infarction, and to compare the diagnostic and long term prognostic value of ambulatory ST segment monitoring, maximal exercise testing, and echocard...

  16. The efficacy of nisoldipine on myocardial perfusion in patients with silent myocardial ischemia

    Energy Technology Data Exchange (ETDEWEB)

    Yamazaki, Junichi; Muto, Hiroshi; Naitou, Katsutoshi [Toho University, Tokyo (Japan). Omori Hospital] [and others

    1997-06-01

    Patients who had old myocardial infarction associated with myocardial viability and ischemia were divided into a pain-free group and a pain-positive group of nine patients each. The improvement of myocardial perfusion with nisoldipine therapy was compared between the two groups using exercise-load Tl-201 myocardial SPECT (myocardial SPECT). The exercise time was significantly prolonged from 505 seconds to 607 seconds after administration of nisoldipine in the pain-positive group (p<0.05), but there was no change in the pain-free group. The extent score of the full circumference of the left ventricle, the severity score, and the %Tl uptake of the infarcted region were significantly improved in both groups by administration of nisoldipine. These findings suggested that nisoldipine caused a decrease in the myocardial oxygen requirements associated with reduction of the afterload and coronary artery dilatation in the pain-positive group, but mainly caused coronary dilatation in the pain-free group. Since myocardial perfusion also improved after nisoldipine administration in the pain-free group, the possibility that calcium antagonists can be used for prophylactic treatment of asymptomatic myocardial ischemia was suggested. (author)

  17. Value of the Doppler index of myocardial performance in the early phase of acute myocardial infarction

    DEFF Research Database (Denmark)

    Poulsen, S H; Jensen, S E; Tei, C

    2000-01-01

    Prospective assessment of a nongeometric Doppler-derived index of combined systolic and diastolic myocardial performance was performed in 64 patients with acute myocardial infarction (MI) within 1 hour after their arrival to the hospital and in 39 age-matched healthy subjects. The index is defined...

  18. Myocardial Infarction Area Quantification using High-Resolution SPECT Images in Rats

    Energy Technology Data Exchange (ETDEWEB)

    Oliveira, Luciano Fonseca Lemos de [Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP (Brazil); Mejia, Jorge [Faculdade de Medicina de São José do Rio Preto, São José do Rio Preto, SP (Brazil); Carvalho, Eduardo Elias Vieira de; Lataro, Renata Maria; Frassetto, Sarita Nasbine [Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP (Brazil); Fazan, Rubens Jr.; Salgado, Hélio Cesar [Departamento de Fisiologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP (Brazil); Galvis-Alonso, Orfa Yineth [Faculdade de Medicina de São José do Rio Preto, São José do Rio Preto, SP (Brazil); Simões, Marcus Vinícius, E-mail: msimoes@fmrp.usp.br [Divisão de Cardiologia, Departamento de Clínica Médica, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP (Brazil)

    2013-07-15

    Imaging techniques enable in vivo sequential assessment of the morphology and function of animal organs in experimental models. We developed a device for high-resolution single photon emission computed tomography (SPECT) imaging based on an adapted pinhole collimator. To determine the accuracy of this system for quantification of myocardial infarct area in rats. Thirteen male Wistar rats (250 g) underwent experimental myocardial infarction by occlusion of the left coronary artery. After 4 weeks, SPECT images were acquired 1.5 hours after intravenous injection of 555 MBq of 99mTc-Sestamibi. The tomographic reconstruction was performed by using specially developed software based on the Maximum Likelihood algorithm. The analysis of the data included the correlation between the area of perfusion defects detected by scintigraphy and extent of myocardial fibrosis assessed by histology. The images showed a high target organ/background ratio with adequate visualization of the left ventricular walls and cavity. All animals presenting infarction areas were correctly identified by the perfusion images. There was no difference of the infarct area as measured by SPECT (21.1 ± 21.2%) and by histology (21.7 ± 22.0%; p=0.45). There was a strong correlation between individual values of the area of infarction measured by these two methods. The developed system presented adequate spatial resolution and high accuracy for the detection and quantification of myocardial infarction areas, consisting in a low cost and versatile option for high-resolution SPECT imaging of small rodents.

  19. Prevention, detection, and management of infected necrosis in severe acute pancreatitis

    NARCIS (Netherlands)

    Bakker, Olaf J.; van Santvoort, Hjalmar C.; Besselink, Marc G. H.; van der Harst, Erwin; Hofker, H. Sijbrand; Gooszen, Hein G.

    2009-01-01

    The management of infected peripancreatic or pancreatic necrosis in patients with severe pancreatitis has changed considerably in recent years. This review discusses the recent literature on prevention, detection, and management of infected necrosis. Though antibiotics, probiotics, and enteral

  20. Possible cause underlying gastric necrosis and perforation: Celiac artery thrombosis

    Directory of Open Access Journals (Sweden)

    Ahmet Peker

    2017-12-01

    Full Text Available In this article, we are sharing a case of a 76-year-old woman with known hypertension, atrial fibrillation,diabetes mellitus, coronary artery disease, who is presenting with stomach necrosis and perforation possibly due to celiac artery thrombosis after newly developed abdominal pain and bloody vomiting. In our case, emergency surgery was planned and the patient refused the operation and was lost at 48 hours of clinical follow-up. We aimed to discuss the etiology of celiac artery thrombosis, briefly. We believe that necrosis and perforation of the stomach due to celiac artery thrombosis deserves to be shared because it is a rare and difficult case to manage.