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1

Tafazzin knockdown causes hypertrophy of neonatal ventricular myocytes.  

UK PubMed Central (United Kingdom)

Mutation of the mitochondrial protein tafazzin causes dilated cardiomyopathy in Barth syndrome. We employed an adenovirus as a vector to transfer tafazzin small hairpin RNA (shRNA) into neonatal ventricular myocytes (NVMs) to investigate the effects of tafazzin knockdown. The tafazzin shRNA adenovirus consistently knocked down tafazzin mRNA and lowered cardiolipin while significantly decreasing the production of ATP by the mitochondria. The phosphorylation of AMP-activated protein kinase and mitochondrial density were both increased in tafazzin knockdown NVMs compared with scrambled shRNA controls. When we tested whether tafazzin knockdown causes hypertrophy in vitro, we found that the surface area of NVMs infected with tafazzin shRNA adenovirus was significantly increased, as were the protein synthesis and expression of the hypertrophic marker gene, brain natriuretic peptide. Taken together, our data support the concept that a decreased tafazzin expression causes cardiomyocyte hypertrophy in vitro.

He Q

2010-07-01

2

Ventricular adrenomedullin is associated with myocyte hypertrophy in human transplanted heart.  

Science.gov (United States)

Adrenomedullin (ADM) is a vasoactive and natriuretic peptide. While it is known that ADM is increased in failing human ventricles, the expression of ADM in human ventricular allografts remains unknown. The present study was designed to investigate tissue localization and intensity of ADM expression in ventricular biopsy specimens and to characterize ventricular ADM in human cardiac allografts. Thirty-three post-transplant endomyocardial biopsy specimens were examined immunohistochemically. The average score (range: 0-4) of ADM immunoreactivity (IR) was 2.4+/-0.9 (mean+/-standard deviation). Right ventricular (RV) systolic pressure was significantly increased with high ADM-IR (p=0.048) and the ADM-IR positively associated with myocyte size (r(2)=0.23, p=0.010). In contrast, ADM-IR was not associated with systemic blood pressure, serum creatinine, cyclosporine concentration, cardiac fibrosis, or allograft rejection. The present study shows that ADM-IR is present in human ventricular endomyocardium after transplantation, and ADM-IR is associated with the magnitude of RV pressure and myocyte size, suggesting an important role for ventricular ADM in the counteraction against overload as well as in the progress of myocyte hypertrophy after heart transplantation. PMID:12667638

Tsuruda, Toshihiro; Jougasaki, Michihisa; Boerrigter, Guido; Costello-Boerrigter, Lisa C; Cataliotti, Alessandro; Lee, Shang C; Salz-Gilman, Lisa; Nordstrom, Lynda J; McGregor, Christopher G A; Burnett, John C

2003-04-15

3

Left Ventricular Hypertrophy  

Science.gov (United States)

... may be reprinted for personal, noncommercial use only. Left ventricular hypertrophy By Mayo Clinic staff Original Article: http://www.mayoclinic.com/health/left-ventricular-hypertrophy/DS00680 Definition Symptoms Causes Risk factors Complications ...

4

The effect of intermedin on angiotensin II and endothelin-1 induced ventricular myocyte hypertrophy in neonatal rat.  

UK PubMed Central (United Kingdom)

BACKGROUND: Intermedin (IMD), a novel peptide related to calcitonin gene-related peptide (CGRP) and adrenomedullin (ADM), may have localized actions as a modulator of cardiac function. The aim of the study is to explore the effect of IMD on angiotensin II (Ang II) and endothelin-1 (ET-1) induced hypertrophy in ventricular myocytes of neonatal rat and to try to elucidate the possible mechanism. METHODS: Neonatal rat cardiomyocytes were cultured in serum-free medium with and without AngII (1 micromol/L) or ET-1 (60 micromol/L) in the presence and absence of IMD (1 micromol/L). Hypertrophic responses (including cell surface area, alpha-actin, and beta-myosin heavy chain mRNA expression) and cardiomyocyte expression of NADPH oxidase gp91phox were determined. RESULTS: Ang II induced increases in cardiomyocyte size to 305 +/- 32 microm2 (n = 198, p < 0.05, at 48 hours), alpha-actin expression to 4 +/- 2.8-fold (n = 6, p < 0.05, at 48 hours) and beta-myosin heavy chain expression to 11 +/- 4.8-fold (n = 6, p < 0.05, at 48 hours), and expression of the gp91phox subunit of NADPH oxidase to 29.4 +/- 12.7-fold (n = 6, p < 0.05, at 48 hours). These effects were all significantly inhibited by IMD; cardiomyocyte size, alpha-actin expression, beta-myosin heavy chain expression, and gp91phox expression were reduced to 265 +/- 32 microm2 (n = 374, p < 0.05), 3.0 +/- 1.7-fold (n = 6, p < 0.05), 8.7 +/- 4.9-fold (n = 6, p < 0.05), 3.9 +/- 3-fold (n = 6, p < 0.05), respectively. IMD also significantly inhibited ET1-induced increases in cardiomyocyte size and superoxide generation. CONCLUSIONS: IMD exerts an antihypertrophic effect on neonatal cardiomyocytes by reduced levels of superoxide, suggesting that an antioxidant action contributes to the antihypertrophic actions of IMD.

Liu K; Deng X; Gong L; Chen X; Wang S; Chen H; Chen X; Amrit B; He S

2013-01-01

5

HYPERTENSIVE LEFT VENTRICULAR HYPERTROPHY  

Directory of Open Access Journals (Sweden)

Full Text Available The left ventricular hypertrophy is sequlae of systemic hypertension. LVH leads to increasedarrhythmias, accelerated coronary atherosclerosis, and heart failure. The Framingham Heart Studyhas shown that LVH is powerful independent risk factor for cardiovascular morbidity andmortality. Therefore, the optimal anti-hypertensive therapy should provide the regression of LVH.Captropril causes regression of left ventricular hypertrophy. The study was done to calculate the thicknessof inter-ventricular septum, posterior wall and left ventricular internal diameter. M-mode echo-cardiographywas used in 20 patients of left ventricular hypertrophy. Captopril was given in the range of 25-150mg perday in patients of left ventricular hypertrophy with hypertension for a period of six weeks. Result on echocardiographyshows regression of IVST 12.45±0.15 to 11±0.24 and LVID (mm) 46.45±1.29 to 46.20±1.25.

Mahboob Ahmad Wagan

2001-01-01

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Impaired beta-adrenergic response and decreased L-type calcium current of hypertrophied left ventricular myocytes in postinfarction heart failure  

Scientific Electronic Library Online (English)

Full Text Available Abstract in english Infarct-induced heart failure is usually associated with cardiac hypertrophy and decreased ß-adrenergic responsiveness. However, conflicting results have been reported concerning the density of L-type calcium current (I Ca(L)), and the mechanisms underlying the decreased ß-adrenergic inotropic response. We determined I Ca(L) density, cytoplasmic calcium ([Ca2+]i) transients, and the effects of ß-adrenergic stimulation (isoproterenol) in a model of postinfarction heart (more) failure in rats. Left ventricular myocytes were obtained by enzymatic digestion 8-10 weeks after infarction. Electrophysiological recordings were obtained using the patch-clamp technique. [Ca2+]i transients were investigated via fura-2 fluorescence. ß-Adrenergic receptor density was determined by [³H]-dihydroalprenolol binding to left ventricle homogenates. Postinfarction myocytes showed a significant 25% reduction in mean I Ca(L) density (5.7 ± 0.28 vs 7.6 ± 0.32 pA/pF) and a 19% reduction in mean peak [Ca2+]i transients (0.13 ± 0.007 vs 0.16 ± 0.009) compared to sham myocytes. The isoproterenol-stimulated increase in I Ca(L) was significantly smaller in postinfarction myocytes (Emax: 63.6 ± 4.3 vs 123.3 ± 0.9% in sham myocytes), but EC50 was not altered. The isoproterenol-stimulated peak amplitude of [Ca2+]i transients was also blunted in postinfarction myocytes. Adenylate cyclase activation through forskolin produced similar I Ca(L) increases in both groups. ß-Adrenergic receptor density was significantly reduced in homogenates from infarcted hearts (Bmax: 93.89 ± 20.22 vs 271.5 ± 31.43 fmol/mg protein in sham myocytes), while Kd values were similar. We conclude that postinfarction myocytes from large infarcts display reduced I Ca(L) density and peak [Ca2+]i transients. The response to ß-adrenergic stimulation was also reduced and was probably related to ß-adrenergic receptor down-regulation and not to changes in adenylate cyclase activity.

Saraiva, R.M.; Chedid, N.G.B.; Quintero H., C.C.; Díaz G., L.E.; Masuda, M.O.

2003-05-01

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Impaired beta-adrenergic response and decreased L-type calcium current of hypertrophied left ventricular myocytes in postinfarction heart failure  

Directory of Open Access Journals (Sweden)

Full Text Available Infarct-induced heart failure is usually associated with cardiac hypertrophy and decreased ß-adrenergic responsiveness. However, conflicting results have been reported concerning the density of L-type calcium current (I Ca(L)), and the mechanisms underlying the decreased ß-adrenergic inotropic response. We determined I Ca(L) density, cytoplasmic calcium ([Ca2+]i) transients, and the effects of ß-adrenergic stimulation (isoproterenol) in a model of postinfarction heart failure in rats. Left ventricular myocytes were obtained by enzymatic digestion 8-10 weeks after infarction. Electrophysiological recordings were obtained using the patch-clamp technique. [Ca2+]i transients were investigated via fura-2 fluorescence. ß-Adrenergic receptor density was determined by [³H]-dihydroalprenolol binding to left ventricle homogenates. Postinfarction myocytes showed a significant 25% reduction in mean I Ca(L) density (5.7 ± 0.28 vs 7.6 ± 0.32 pA/pF) and a 19% reduction in mean peak [Ca2+]i transients (0.13 ± 0.007 vs 0.16 ± 0.009) compared to sham myocytes. The isoproterenol-stimulated increase in I Ca(L) was significantly smaller in postinfarction myocytes (Emax: 63.6 ± 4.3 vs 123.3 ± 0.9% in sham myocytes), but EC50 was not altered. The isoproterenol-stimulated peak amplitude of [Ca2+]i transients was also blunted in postinfarction myocytes. Adenylate cyclase activation through forskolin produced similar I Ca(L) increases in both groups. ß-Adrenergic receptor density was significantly reduced in homogenates from infarcted hearts (Bmax: 93.89 ± 20.22 vs 271.5 ± 31.43 fmol/mg protein in sham myocytes), while Kd values were similar. We conclude that postinfarction myocytes from large infarcts display reduced I Ca(L) density and peak [Ca2+]i transients. The response to ß-adrenergic stimulation was also reduced and was probably related to ß-adrenergic receptor down-regulation and not to changes in adenylate cyclase activity.

Saraiva R.M.; Chedid N.G.B.; Quintero H. C.C.; Díaz G. L.E.; Masuda M.O.

2003-01-01

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Left ventricular hypertrophy in patients treated with regular hemodialyses  

Directory of Open Access Journals (Sweden)

Full Text Available Left ventricular hypertrophy is the main risk factor for development of cardiovascular morbidity and mortality in patients on hemodialysis. Left ventricular hypertrophy is found in 75% of the patients treated with hemodialysis. Risk factors for left ventricular hypertrophy in patients on hemodialysis include: blood flow through arterial-venous fistula, anemia, hypertension, increased extracellular fluid volume, oxidative stress, microinflammation, hyperhomocysteinemia, secondary hyperpara- thyroidism, and disturbed calcium and phosphate homeostasis. Left ventricular pressure overload leads to parallel placement of new sarcomeres and development of concentric hypertrophy of left ventricle. Left ventricular hypertrophy advances in two stages. In the stage of adaptation, left ventricular hypertrophy occurs as a response to increased tension stress of the left ventricular wall and its action is protective. When volume and pressure overload the left ventricle chronically and without control, adaptive hypertrophy becomes maladaptive hypertrophy of the left ventricle, where myocytes are lost, systolic function is deranged and heart insufficiency is developed. Left ventricular mass index-LVMi greater than 131 g/m2 in men and greater than 100 g/m2 in women, and relative wall thickness of the left ventricle above 0.45 indicate concentric hypertrophy of the left ventricle. Eccentric hypertrophy of the left ventricle is defined echocardiographically as LVMi above 131 g/m2 in men and greater than 100 g/m2 in women, with RWT ?0.45. Identification of patients with increased risk for development of left ventricular hypertrophy and application of appropriate therapy to attain target values of risk factors lead to regression of left ventricular hypertrophy, reduced cardiovascular morbidity and mortality rates and improved quality of life in patients treated with regular hemodialyses.

Petrovi? Dejan; Stojimirovi? Biljana

2008-01-01

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Overexpression of insulin-like growth factor-1 in mice protects from myocyte death after infarction, attenuating ventricular dilation, wall stress, and cardiac hypertrophy.  

Digital Repository Infrastructure Vision for European Research (DRIVER)

To determine whether IGF-1 opposes the stimulation of myocyte death in the surviving myocardium after infarction, transgenic mice overexpressing human IGF-1B in myocytes (FVB.Igf+/-) and wild-type littermates at 1.5 and 2.5 mo of age were subjected to coronary ligation and killed 7 d later. Myocardi...

Li, Q; Li, B; Wang, X; Leri, A; Jana, K P; Liu, Y; Kajstura, J; Baserga, R; Anversa, P

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Reversibility of left ventricular hypertrophy.  

UK PubMed Central (United Kingdom)

Left ventricular hypertrophy (LVH) is a powerful independent risk factor for coronary artery disease. This overview of 104 studies examines the ability of various types of antihypertensive therapies to reverse LVH as assessed by echocardiography. Combination therapy, angiotensin converting enzyme (ACE) inhibitors, and methyldopa were the most effective in reversing LV mass; vasodilators such as minoxidil and hydralazine had no effect on LVH. These differences were independent of the degree of fall in blood pressure and duration of therapy. beta-blockers were as effective as ACE inhibitors in decreasing LV wall thickness. Possible reasons for drug differences in reversing LVH are discussed. Preliminary evidence suggests that reversing LVH by antihypertensive drug therapy is associated with a reduction in cardiovascular complications.

Cruickshank JM

1992-01-01

11

Integrative modeling of the cardiac ventricular myocyte.  

Science.gov (United States)

Cardiac electrophysiology is a discipline with a rich 50-year history of experimental research coupled with integrative modeling which has enabled us to achieve a quantitative understanding of the relationships between molecular function and the integrated behavior of the cardiac myocyte in health and disease. In this paper, we review the development of integrative computational models of the cardiac myocyte. We begin with a historical overview of key cardiac cell models that helped shape the field. We then narrow our focus to models of the cardiac ventricular myocyte and describe these models in the context of their subcellular functional systems including dynamic models of voltage-gated ion channels, mitochondrial energy production, ATP-dependent and electrogenic membrane transporters, intracellular Ca dynamics, mechanical contraction, and regulatory signal transduction pathways. We describe key advances and limitations of the models as well as point to new directions for future modeling research. WIREs Syst Biol Med 2011 3 392-413 DOI: 10.1002/wsbm.122 PMID:20865780

Winslow, Raimond L; Cortassa, Sonia; O'Rourke, Brian; Hashambhoy, Yasmin L; Rice, John Jeremy; Greenstein, Joseph L

2010-09-23

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Intense myocyte formation from cardiac stem cells in human cardiac hypertrophy  

Science.gov (United States)

It is generally believed that increase in adult contractile cardiac mass can be accomplished only by hypertrophy of existing myocytes. Documentation of myocardial regeneration in acute stress has challenged this dogma and led to the proposition that myocyte renewal is fundamental to cardiac homeostasis. Here we report that in human aortic stenosis, increased cardiac mass results from a combination of myocyte hypertrophy and hyperplasia. Intense new myocyte formation results from the differentiation of stem-like cells committed to the myocyte lineage. These cells express stem cell markers and telomerase. Their number increased >13-fold in aortic stenosis. The finding of cell clusters with stem cells making the transition to cardiogenic and myocyte precursors, as well as very primitive myocytes that turn into terminally differentiated myocytes, provides a link between cardiac stem cells and myocyte differentiation. Growth and differentiation of these primitive cells was markedly enhanced in hypertrophy, consistent with activation of a restricted number of stem cells that, through symmetrical cell division, generate asynchronously differentiating progeny. These clusters strongly support the existence of cardiac stem cells that amplify and commit to the myocyte lineage in response to increased workload. Their presence is consistent with the notion that myocyte hyperplasia significantly contributes to cardiac hypertrophy and accounts for the subpopulation of cycling myocytes.

Urbanek, Konrad; Quaini, Federico; Tasca, Giordano; Torella, Daniele; Castaldo, Clotilde; Nadal-Ginard, Bernardo; Leri, Annarosa; Kajstura, Jan; Quaini, Eugenio; Anversa, Piero

2003-01-01

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REGRESSION OF LEFT VENTRICULAR HYPERTROPHY (LVH)  

Directory of Open Access Journals (Sweden)

Full Text Available Left ventricular hypertrophy is an independent risk factor for cardiovascular diseases. Thereforeoptimal anti-hypertensive therapy should provide the regression of LVH. There are certain group of drugs which causeregression of LVH, such as angiotensin converting enzyme inhibitors and diuretics. Objectives: To assess themagnitude regression induced by captopril and indapamide when patients are treated for equal duration of time.Patients & Methods: We gave captopril (25–150 mg) to eleven patients with left ventricular hypertrophy for six monthsand another eight patients, indapamide 2.5 mg (Diuretic) was given for six months. Results: There was an overallreduction of left ventricular mass index (LVMI) by 12.5% in patients taking captopril, while left ventricular mass index(LVMI) decreased by 7.5% in patients taking indapamide. The LVMI decreased from 157.2±12.6 to 137.5±8.7g/m2(Mean±SEM) and from 156.1±9.5 to 141.3± 8.5g/m (Mean±SEM) in patients taking captopril and indapamide 2respectively. The mean blood pressure in both the groups decreased, systolic blood pressure decreased from 172 to146 mm Hg and diastolic blood pressure from 101 to 82 mm Hg. Conclusions: ACE inhibitors induce more regressionthen diuretics when patients are treated for equal duration of time.

SHAHEEN SHAH

2005-01-01

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Echocardiographic evidence of left ventricular hypertrophy in obese dogs.  

UK PubMed Central (United Kingdom)

BACKGROUND: Cardiomyopathy of obesity occurs in humans, but the gross and cellular myocardial response to obesity in dogs is not well defined. OBJECTIVES: To characterize in vivo myocardial morphology and function in normotensive obese dogs, and quantitate collagen, triglyceride and myocyte cross-sectional area (CSA) in postmortem tissues from obese dogs. ANIMALS: Echocardiographic-Doppler measurements of normotensive obese dogs (n = 19) without historical or physical examination evidence of disease, and lean healthy dogs (n = 19) matched for age and ideal weight. Postmortem data were obtained from a separate population of 4 obese and 12 lean dogs without evidence of cardiac disease. METHODS: A prospective, observational study of myocardial morphology and function was conducted by echocardiographic-Doppler measurement. Left ventricular (LV) tissue was collected for quantitation of triglyceride, collagen, and myocyte CSA. RESULTS: Compared with lean control dogs, obese dogs had increased systolic blood pressure (obese 153 ± 19 mm Hg; lean 133 ± 20 mm Hg; P = .003), and increased LV free wall thickness at end-diastole (obese 9.9 ± 1.8 mm, lean 8.7 ± 1.5 mm; P = .03) and end-systole (obese 15.2 ± 2.3 mm, lean 12.9 ± 2.3 mm; P = .004). Isovolumic relaxation time was prolonged in 7/19 (37%) of obese dogs, compared with normal ranges. Myocardial triglyceride and collagen content and myocyte CSA were similar between groups. CONCLUSIONS AND CLINICAL IMPORTANCE: As in humans, LV hypertrophy and diastolic dysfunction can be an early myocardial change in some obese dogs.

Mehlman E; Bright JM; Jeckel K; Porsche C; Veeramachaneni DN; Frye M

2013-01-01

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Left ventricular diastolic performance of left ventricular hypertrophy  

International Nuclear Information System (INIS)

[en] To study left ventricular diastolic performance in different forms of left ventricular hypertrophy, ECG gated cardiac blood pool scan was performed in 11 patients with hypertrophic nonobstructive cardiomyopathy (HCM) and in 19 patients with hypertension (HT), and left ventricular volume curve (LVVC) was analyzed and compared with those of 13 normal subjects (N). Ejection fraction (EF) and early filling volume ratio (the ratio of volume increment of 100 msec later than the zero point in the first derivative of LVVC to the end diastolic volume) (%EFV) were computed from LVVC. Peak ejection rate (PER) and peak filling rate (PFR) were obtained from the first derivative of LVVC. Peak ejection acceleration (PEA) and peak filling acceleration (PFA) were calculated from the second derivative of LVVC. EF, PER and PEA did not show any difference between these 3 groups. PFR was lower in HT (2.6 ± 0.5) compared with those in HCM (3.0 ± 0.5) (p

1987-01-01

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FGF23 induces left ventricular hypertrophy  

Science.gov (United States)

Chronic kidney disease (CKD) is a public health epidemic that increases risk of death due to cardiovascular disease. Left ventricular hypertrophy (LVH) is an important mechanism of cardiovascular disease in individuals with CKD. Elevated levels of FGF23 have been linked to greater risks of LVH and mortality in patients with CKD, but whether these risks represent causal effects of FGF23 is unknown. Here, we report that elevated FGF23 levels are independently associated with LVH in a large, racially diverse CKD cohort. FGF23 caused pathological hypertrophy of isolated rat cardiomyocytes via FGF receptor–dependent activation of the calcineurin-NFAT signaling pathway, but this effect was independent of klotho, the coreceptor for FGF23 in the kidney and parathyroid glands. Intramyocardial or intravenous injection of FGF23 in wild-type mice resulted in LVH, and klotho-deficient mice demonstrated elevated FGF23 levels and LVH. In an established animal model of CKD, treatment with an FGF–receptor blocker attenuated LVH, although no change in blood pressure was observed. These results unveil a klotho-independent, causal role for FGF23 in the pathogenesis of LVH and suggest that chronically elevated FGF23 levels contribute directly to high rates of LVH and mortality in individuals with CKD.

Faul, Christian; Amaral, Ansel P.; Oskouei, Behzad; Hu, Ming-Chang; Sloan, Alexis; Isakova, Tamara; Gutierrez, Orlando M.; Aguillon-Prada, Robier; Lincoln, Joy; Hare, Joshua M.; Mundel, Peter; Morales, Azorides; Scialla, Julia; Fischer, Michael; Soliman, Elsayed Z.; Chen, Jing; Go, Alan S.; Rosas, Sylvia E.; Nessel, Lisa; Townsend, Raymond R.; Feldman, Harold I.; St. John Sutton, Martin; Ojo, Akinlolu; Gadegbeku, Crystal; Di Marco, Giovana Seno; Reuter, Stefan; Kentrup, Dominik; Tiemann, Klaus; Brand, Marcus; Hill, Joseph A.; Moe, Orson W.; Kuro-o, Makoto; Kusek, John W.; Keane, Martin G.; Wolf, Myles

2011-01-01

17

FGF23 induces left ventricular hypertrophy.  

UK PubMed Central (United Kingdom)

Chronic kidney disease (CKD) is a public health epidemic that increases risk of death due to cardiovascular disease. Left ventricular hypertrophy (LVH) is an important mechanism of cardiovascular disease in individuals with CKD. Elevated levels of FGF23 have been linked to greater risks of LVH and mortality in patients with CKD, but whether these risks represent causal effects of FGF23 is unknown. Here, we report that elevated FGF23 levels are independently associated with LVH in a large, racially diverse CKD cohort. FGF23 caused pathological hypertrophy of isolated rat cardiomyocytes via FGF receptor-dependent activation of the calcineurin-NFAT signaling pathway, but this effect was independent of klotho, the coreceptor for FGF23 in the kidney and parathyroid glands. Intramyocardial or intravenous injection of FGF23 in wild-type mice resulted in LVH, and klotho-deficient mice demonstrated elevated FGF23 levels and LVH. In an established animal model of CKD, treatment with an FGF-receptor blocker attenuated LVH, although no change in blood pressure was observed. These results unveil a klotho-independent, causal role for FGF23 in the pathogenesis of LVH and suggest that chronically elevated FGF23 levels contribute directly to high rates of LVH and mortality in individuals with CKD.

Faul C; Amaral AP; Oskouei B; Hu MC; Sloan A; Isakova T; Gutiérrez OM; Aguillon-Prada R; Lincoln J; Hare JM; Mundel P; Morales A; Scialla J; Fischer M; Soliman EZ; Chen J; Go AS; Rosas SE; Nessel L; Townsend RR; Feldman HI; St John Sutton M; Ojo A; Gadegbeku C; Di Marco GS; Reuter S; Kentrup D; Tiemann K; Brand M; Hill JA; Moe OW; Kuro-O M; Kusek JW; Keane MG; Wolf M

2011-11-01

18

Ventricular arrhythmias and left ventricular hypertrophy in hypertrophic cardiomyopathy.  

UK PubMed Central (United Kingdom)

BACKGROUND: In hypertrophic cardiomyopathy (HCM), the degree of left ventricular hypertrophy (LVH) could influence the development of ventricular arrhythmias. OBJECTIVE: In HCM, analyze the association between the occurrence of ventricular arrhythmias determined by Holter electrocardiogram (ECG-Holter) and the degree of LVH determined by maximum wall thickness (MWT) in echocardiography and body mass index (BMI). METHODS: Fifty-four consecutive patients with HCM underwent 24-hour ECG-Holter and echocardiography for assessment of level of LVH through MWT and BMI. Two levels were established for the occurrence of Ventricular Arrhythmias: I - alone or paired extrasystoles and II - Non- Sustained Ventricular Tachycardia (NSVT). RESULTS: In 13 patients (24%) with NSVT (level II), there was a higher frequency of MWT of the left ventricle (LV) > 21 mm (n = 10, 77%, 25 ± 4 mm) and LLLV = 144 g/m² (n = 10, 77%, 200 ± 30 g/m²), in comparison with those presenting with extrasystole arrhythmias (level I) (n = 41, 76%), in which these measures were identified in, respectively, 37 % (n= 15, 23 ± 1 mm), p = 0.023, and 39% (n = 16, 192 ± 53 g / m²) of the cases (p = 0.026). The cut-off values mentioned were determined by the ROC curve with a confidence interval of 95%. NSVT was more common in patients with MWTLV > 21 mm and LLLV > 144 g/m² (8 of 13, 62%) than in those with (4 of 13, 31%) or without (1 of 13; 8%) echocardiographic variables above cut-off values (p = 0.04). CONCLUSION: In HCM, occurrence of ventricular arrhythmias by Holter was associated with the degree of LVH assessed by echocardiography through MWT and BMI.

Piva e Mattos B; Torres MA; Freitas VC; Scolari FL; Loreto MS

2013-05-01

19

Magnetocardiographic indices of left ventricular hypertrophy.  

UK PubMed Central (United Kingdom)

OBJECTIVE: We tested the hypothesis that multichannel magnetocardiographic (MCG) mapping can detect and quantify the degree of left ventricular hypertrophy (LVH). DESIGN: A cross-sectional study. SETTING: Helsinki University Central Hospital, a tertiary referral center. PARTICIPANTS: Forty-two patients with pressure overload induced LVH by gender-specific echocardiographic criteria (LVH group), and 12 healthy middle-aged controls. MAIN OUTCOME MEASURES: MCG QRS-T area integrals and QRS-T angle in magnetic field maps in relation to echocardiographic LVH as well as left ventricular (LV) mass and structure. Conventional 12-lead electrocardiographic (ECG) LVH indices (Sokolow-Lyon voltage, Cornell voltage, Cornell voltage duration product) were assessed for comparison. RESULTS: MCG QRS- and T-wave integrals provided complementary information of echocardiographic LV mass. Their combination, the QRS-T integral, and the QRS-T angle were increased in patients with LVH and, in those patients, correlated significantly with LV mass indexed to body surface area (r = 0.455;P = 0.002 and r= 0.379; P= 0.013, respectively). A QRS-T integral 16000 fT.s had identical sensitivity of 62% at 92% specificity as the gender-adjusted Cornell voltage duration product of 240 micro V.s for the detection of LVH. CONCLUSIONS: The MCG method can detect patients with LVH and also quantify the degree of LVH in patients with increased LV mass.

Karvonen M; Oikarinen L; Takala P; Kaartinen M; Rossinen J; Hänninen H; Montonen J; Nenonen J; Mäkijärvi M; Keto P; Toivonen L; Nieminen MS; Katila T

2002-11-01

20

Ionic currents in ventricular myocytes isolated from the heart of a patient with idiopathic cardiomyopathy.  

UK PubMed Central (United Kingdom)

Whole-cell configuration of the patch-clamp technique was applied to record ionic currents from human ventricular myocytes isolated from a cardiac transplant patient with idiopathic cardiomyopathy. Inward calcium current, transient outward current, and inward rectifier potassium current were recorded, while no discernible delayed rectifier potassium current was observed. Thus the currents that underlie electrical activity in human ventricular myocytes appear to resemble those reported earlier in canine and rabbit ventricular myocytes.

Nánási PP; Varró A; Lathrop DA

1992-06-01

 
 
 
 
21

Ionic currents in ventricular myocytes isolated from the heart of a patient with idiopathic cardiomyopathy.  

Science.gov (United States)

Whole-cell configuration of the patch-clamp technique was applied to record ionic currents from human ventricular myocytes isolated from a cardiac transplant patient with idiopathic cardiomyopathy. Inward calcium current, transient outward current, and inward rectifier potassium current were recorded, while no discernible delayed rectifier potassium current was observed. Thus the currents that underlie electrical activity in human ventricular myocytes appear to resemble those reported earlier in canine and rabbit ventricular myocytes. PMID:1379481

Nánási, P P; Varró, A; Lathrop, D A

1992-06-01

22

Focal Adhesion Kinase and p130Cas Mediate Both Sarcomeric Organization and Activation of Genes Associated with Cardiac Myocyte Hypertrophy  

Digital Repository Infrastructure Vision for European Research (DRIVER)

Hypertrophic terminally differentiated cardiac myocytes show increased sarcomeric organization and altered gene expression. Previously, we established a role for the nonreceptor tyrosine kinase Src in signaling cardiac myocyte hypertrophy. Here we report evidence that p130Cas (Cas) and focal adh...

Kovac?ic?-Milivojevi?, Branka; Roediger, Frederick; Almeida, Eduardo A.C.; Damsky, Caroline H.; Gardner, David G.

23

Enhancement of polydatin on inward rectifier potassium channel current in rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

The aim of this study was to investigate the effect of polydatin on transient outward potassium channel current (Ito), steady-state outward potassium channel current (Iss) and inward rectifier potassium channel current (IK1) in ventricular myocytes of rat using the whole-cell patch clamp technique. The results showed: (1) Polydatin (above 10 µmol/L) increased IK1 of ventricular myocytes in a non-concentration dependent manner. (2) Polydatin neither had any effect on Ito peak current of ventricular myocytes, nor changed activation, inactivation and recovery kinetics of Ito. (3) Polydatin had no effect on Iss of ventricular myocytes. These results suggest that polydatin enhances IK1 channel activity, but has no effect on Ito and Iss channels in rat ventricular myocytes, which might be one of the ionic mechanisms for antiarrhythmic effect of polydatin.

Wei Y; Zhou JJ; Yang J; Zhang J; Zhang LP; Zhang Y

2013-06-01

24

Skeletal myocyte hypertrophy requires mTOR kinase activity and S6K1  

International Nuclear Information System (INIS)

The protein kinase mammalian target of rapamycin (mTOR) is a central regulator of cell proliferation and growth, with the ribosomal subunit S6 kinase 1 (S6K1) as one of the key downstream signaling effectors. A critical role of mTOR signaling in skeletal muscle differentiation has been identified recently, and an unusual regulatory mechanism independent of mTOR kinase activity and S6K1 is revealed. An mTOR pathway has also been reported to regulate skeletal muscle hypertrophy, but the regulatory mechanism is not completely understood. Here, we report the investigation of mTOR's function in insulin growth factor I (IGF-I)-induced C2C12 myotube hypertrophy. Added at a later stage when rapamycin no longer had any effect on normal myocyte differentiation, rapamycin completely blocked myocyte hypertrophy as measured by myotube diameter. Importantly, a concerted increase of average myonuclei per myotube was observed in IGF-I-stimulated myotubes, which was also inhibited by rapamycin added at a time when it no longer affected normal differentiation. The mTOR protein level, its catalytic activity, its phosphorylation on Ser2448, and the activity of S6K1 were all found increased in IGF-I-stimulated myotubes compared to unstimulated myotubes. Using C2C12 cells stably expressing rapamycin-resistant forms of mTOR and S6K1, we provide genetic evidence for the requirement of mTOR and its downstream effector S6K1 in the regulation of myotube hypertrophy. Our results suggest distinct mTOR signaling mechanisms in different stages of skeletal muscle development: While mTOR regulates the initial myoblast differentiation in a kinase-independent and S6K1-independent manner, the hypertrophic function of mTOR requires its kinase activity and employs S6K1 as a downstream effector.

2005-09-10

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Overexpression of ornithine decarboxylase decreases ventricular systolic function during induction of cardiac hypertrophy.  

Science.gov (United States)

Ornithine decarboxylase (ODC), the first enzyme of polyamine metabolism, is rapidly upregulated in response to agents that induce a pathological cardiac hypertrophy. Transgenic mice overexpressing ODC in the heart (MHC-ODC mice) experience a much more dramatic left ventricular hypertrophy in response to ?-adrenergic stimulation with isoproterenol (ISO) compared to wild-type (WT) controls. ISO also induced arginase activity in transgenic hearts but not in controls. The current work studies the cooperation between the cardiac polyamines and L-arginine (L-Arg) availability in MHC-ODC mice. Although ISO-induced hypertrophy is well-compensated, MHC-ODC mice administered L-Arg along with ISO showed a rapid onset of systolic dysfunction and died within 48 h. Myocytes isolated from MHC-ODC mice administered L-Arg/ISO exhibited reduced contractility and altered calcium transients, suggesting an alteration in [Ca(2+)] homeostasis, and abbreviated action potential duration, which may contribute to arrhythmogenesis. The already elevated levels of spermidine and spermine were not further altered in MHC-ODC hearts by L-Arg/ISO treatment, suggesting alternative L-Arg utilization pathways lead to dysregulation of intracellular calcium. MHC-ODC mice administered an arginase inhibitor (Nor-NOHA) along with ISO died almost as rapidly as L-Arg/ISO-treated mice, while the iNOS inhibitor S-methyl-isothiourea (SMT) was strongly protective against L-Arg/ISO. These results point to the induction of arginase as a protective response to ?-adrenergic stimulation in the setting of high polyamines. Further, NO generated by exogenously supplied L-Arg may contribute to the lethal consequences of L-Arg/ISO treatment. Since considerable variations in human cardiac polyamine and L-Arg content are likely, it is possible that alterations in these factors may influence myocyte contractility. PMID:21814794

Giordano, Emanuele; Hillary, Rebecca A; Vary, Thomas C; Pegg, Anthony E; Sumner, Andrew D; Caldarera, Claudio M; Zhang, Xue-Qian; Song, Jianliang; Wang, JuFang; Cheung, Joseph Y; Shantz, Lisa M

2011-08-04

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An analysis of electrocardiographic criteria for determining left ventricular hypertrophy  

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Full Text Available OBJECTIVE: To determine the most sensitive criterion for the detection of left ventricular hypertrophy according to echocardiographically defined left ventricular mass. METHODS: The Sokolow-Lyon voltage, Sokolow-Lyon-Rappaport, Cornell voltage duration product, White-Bock, and Romhilt-Estes point scoring criteria were compared with left ventricular mass index, corrected for body surface, obtained from the echocardiograms of 306 outpatients (176 females, 130 males), of all age groups. RESULTS: The Cornell voltage duration product criteria index had the greatest sensitivity in women (54.90%), and the Sokolow-Lyon-Rappaport index was most sensitive in men (73.53%). When applied to men at the same voltage amplitude (20mm) as that in women, the Cornell index showed increased sensitivity relative to the conventional index (28mm) of 67.65% (P<=0.01) and a sensitivity similar to that of the Sokolow-Lyon-Rappaport index, with higher specificity (P<=0.01). The White-Bock and Romhilt-Estes criteria were the least sensitive in men and women, despite their high specificity. The electrocardiographic criteria were more efficient when dilatation predominated over left ventricular hypertrophy. CONCLUSION: The Cornell index had greater sensitivity in women, and the Sokolow-Lyon-Rappaport index was more sensitive in men. When applied to men at the same voltage amplitude as that of women, the Cornell index had an increase in sensitivity similar to that of the Sokolow-Lyon-Rappaport index.

Carlos Alberto Gasperin; Helio Germiniani; Carlos Roberto Facin; Admar Moraes de Souza; Cláudio Leinig Pereira da Cunha

2002-01-01

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Modification of left ventricular hypertrophy by chronic etomixir treatment.  

UK PubMed Central (United Kingdom)

1. Etomoxir (2[6(4-chlorophenoxy)hexyl]oxirane-2-carboxylate), an irreversible carnitine palmitoyl-transferase 1 inhibitor, reduces the expression of the myocardial foetal gene programme and the functional deterioration during heart adaption to a pressure-overload. Etomoxir may, however, also improve the depressed myocardial function of hypertrophied ventricles after a prolonged pressure overload. 2. To test this hypothesis, we administered racemic etomoxir (15 mg kg(-1) day(-1) for 6 weeks) to rats with ascending aortic constriction beginning 6 weeks after imposing the pressure overload. 3. The right ventricular/body weight ratio increased (P<0.05) by 20% in etomoxir treated rats (n = 10) versus untreated rats with ascending aortic constriction (n = 10). Left ventricular weight was increased (P<0.05) by 8%. Etomoxir blunted the increase in left ventricular chamber volume. Etomoxir raised the proportion of V1 isomyosin (35+/-4% versus 24+/-2%; P<0.05) and decreased the percentage of V3 isomyosin (36+/-4% versus 48+/-3%; P<0.05). 4. Maximum isovolumically developed pressure was higher in etomoxir treated rats than in untreated pressure overloaded rats (371+/-22 versus 315+/-23 mmHg; P<0.05). Maximum rates of ventricular pressure development (14,800+/-1310 versus 12,340+/-1030mmHg s(-1); P<0.05) and decline (6440+/-750 versus 5040+/-710 mmHg s(-1); P<0.05) were increased as well. Transformation of pressure values to ventricular wall stress data revealed an improved myocardial function which could partially account for the enhanced function of the whole left ventricle. 5. The co-ordinated action of etomoxir on ventricular mass, geometry and myocardial phenotype enhanced thus the pressure generating capacity of hypertrophied pressure-overloaded left ventricles and delayed the deleterious dilative remodelling.

Turcani M; Rupp H

1999-01-01

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The bcl-2 gene product prevents programmed cell death of ventricular myocytes.  

UK PubMed Central (United Kingdom)

BACKGROUND: To formally test whether the antiapoptotic protein bcl-2 would prevent programmed cell death in cardiac muscle cells provoked by p53, a known trigger of apoptosis in a variety of different cell types, we used replication defective adenovirus encoding either the bcl-2 and p53 genes to deliver bcl-2 and p53 to ventricular myocytes with high efficiency and uniformity. METHODS AND RESULTS: Vital staining of ventricular myocytes revealed a significant (7-fold, P<.05) increase in myocyte cell death in the presence of p53 in contrast to uninfected cells or those infected with a control virus. In addition, in the presence of p53, nucleosomal DNA fragmentation observed by Hoescht 33258 staining and terminal transferase deoxynucleotide end labeling indicated a significant increase in apoptotic cardiac nuclei compared with control cells, confirming the hypothesis that p53 alone is sufficient to trigger apoptosis of ventricular myocytes. Moreover, a significant increase in transcription of the bax promoter was seen in the presence but not in the absence of p53 compared with control cells. Expression of the antiapoptotic gene bcl-2 in ventricular myocytes was sufficient to prevent ventricular myocyte death and apoptosis provoked by p53. Importantly, the antiapoptotic effects of bcl-2 were independent of altered p53 expression or localization of p53 to cardiac nuclei. However, p53 dependent transcription of bax was repressed 4-fold (P<.05) by bcl-2, suggesting a tentative link between p53-mediated apoptosis and the protective properties conferred by bcl-2 in ventricular myocytes. CONCLUSIONS: To our knowledge, the data provide the first indication for the operation of bcl-2 in ventricular myocytes as an antiapoptotic factor.

Kirshenbaum LA; de Moissac D

1997-09-01

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[Prevalence of left ventricular hypertrophy in diabetic patients].  

UK PubMed Central (United Kingdom)

In order to establish the prevalence of left ventricular hypertrophy (LVH) in patients with type 2 diabetes mellitus, (DM) a cross-sectional study was conducted in these patients studying their anthropometric characteristics, blood pressure and metabolic control. To evaluate the presence of LVH, a trans-thoracic echocardiogram was used. The study included 91 patients, finding a 63.7% prevalence of HVI, with women being more affected than men (p=0.001). Additionally, 46.2% of patients were found to have diastolic dysfunction of the left ventricle. We conclude that there is an important prevalence of LVH in diabetic patients without defined causes of hypertrophy. There was no association with sex, metabolic control, BMI and time of diagnosis.

Valarezo-Sevilla D; Pazmiño-Martínez A; Morales-Mora N

2013-03-01

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Bidirectional regulation of nuclear factor-?B and mammalian target of rapamycin signaling functionally links Bnip3 gene repression and cell survival of ventricular myocytes.  

UK PubMed Central (United Kingdom)

BACKGROUND: Tumor necrosis factor-? and other proinflammatory cytokines activate the canonical nuclear factor (NF)-?B pathway through the kinase IKK?. Previously, we established that IKK? is also critical for Akt-mediated NF-?B activation in ventricular myocytes. Akt activates the kinase mammalian target of rapamycin (mTOR), which mediates important processes such as cardiac hypertrophy. However, whether mTOR regulates cardiac myocyte cell survival is unknown. METHODS AND RESULTS: Herein, we demonstrate bidirectional regulation between NF-?B signaling and mTOR, the balance which determines ventricular myocyte survival. Overexpression of IKK? resulted in mTOR activation and conversely overexpression of mTOR lead to NF-?B activation. Loss of function approaches demonstrated that endogenous levels of IKK? and mTOR also signal through this pathway. NF-?B activation by mTOR was mediated by phosphorylation of the NF-?B p65 subunit increasing p65 nuclear translocation and activation of gene transcription. This circuit was also important for NF-?B activation by the canonical tumor necrosis factor-? pathway. Our previous work has shown that NF-?B signaling suppresses transcription of the death gene Bnip3 resulting in ventricular myocyte survival. Inhibition of mTOR with rapamycin decreased NF-?B activation resulting in increased Bnip3 expression and cell death. Conversely, mTOR overexpression suppressed Bnip3 levels and cell death of ventricular myocytes in response to hypoxia. CONCLUSIONS: To our knowledge, these data provide the first evidence for a bidirectional link between NF-?B signaling and mTOR that is critical in the regulation of Bnip3 expression and cardiac myocyte death. Hence, modulation of this axis may be cardioprotective during ischemia.

Dhingra R; Gang H; Wang Y; Biala AK; Aviv Y; Margulets V; Tee A; Kirshenbaum LA

2013-03-01

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Sexual dimorphism in obesity-mediated left ventricular hypertrophy.  

Science.gov (United States)

In the present study we investigated the influence of sex difference on the development of left ventricular hypertrophy (LVH) during obesity. Male and female C57BL/6J mice were fed for 15 and 25 wk with a high-fat diet (HFD) or low-fat control diet (LFD). Analysis of body composition, monitoring of body weight (BW), and echocardiographic analysis were performed, as well as analysis of expression of different adipocytokines in epicardial adipose tissue. The increment in left ventricular mass (LVM) after HFD (25 wk) was significantly stronger in male mice compared with female mice [LVM: male, 116.9 ± 2.9 (LFD) vs. 142.2 ± 9.3 mg (HFD); female, 84.3 ± 3.3 (LFD) vs. 93.9 ± 1.7 mg (HFD), Psex epicardial adipose tissue. PMID:23666673

Böhm, Christian; Benz, Verena; Clemenz, Markus; Sprang, Christiane; Höft, Beata; Kintscher, Ulrich; Foryst-Ludwig, Anna

2013-05-10

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Differential effects of the peroxynitrite donor, SIN-1, on atrial and ventricular myocyte electrophysiology.  

UK PubMed Central (United Kingdom)

Oxidative stress has been implicated in the pathogenesis of heart failure and atrial fibrillation and can result in increased peroxynitrite production in the myocardium. Atrial and ventricular canine cardiac myocytes were superfused with 3-morpholinosydnonimine-N-ethylcarbamide (SIN-1), a peroxynitrite donor, to evaluate the acute electrophysiologic effects of peroxynitrite. Perforated whole-cell patch clamp techniques were used to record action potentials. SIN-1 (200 µM) increased the action potential duration (APD) in atrial and ventricular myocytes; however, in the atria, APD prolongation was rate independent, whereas in the ventricle APD, prolongation was rate dependent. In addition to prolongation of the action potential, beat-to-beat variability of repolarization was significantly increased in ventricular but not in atrial myocytes. We examined the contribution of intracellular calcium cycling to the effects of SIN-1 by treating myocytes with the SERCA blocker, thapsigargin (5-10 µM). Inhibition of calcium cycling prevented APD prolongation in the atrial and ventricular myocytes, and prevented the SIN-1-induced increase in ventricular beat-to-beat APD variability. Collectively, these data demonstrate that peroxynitrite affects atrial and ventricular electrophysiology differentially. A detailed understanding of oxidative modulation of electrophysiology in specific chambers is critical to optimize therapeutic approaches for cardiac diseases.

Bonilla IM; Sridhar A; Nishijima Y; Györke S; Cardounel AJ; Carnes CA

2013-05-01

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Blood pressure control and left ventricular hypertrophy in hypertensive Nigerians  

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Full Text Available Background : Hypertension is a disease characterized by end-organ complications, leading to high morbidity and mortality in many cases. People with untreated or uncontrolled hypertension often run the risk of developing complications directly associated with the disease. Left ventricular hypertrophy (LVH) has been shown to be a significant risk factor for adverse outcomes both in patients with hypertension and in the general population. We investigated the prevalence and pattern of LVH in a treated hypertensive population at the University College Hospital, Ibadan, Nigeria, using non-hypertensive subjects as control. Design and Setting : A prospective observational study performed at the University College Hospital, Ibadan, Nigeria. Methods : Patients had 6 visits, when at least one blood pressure measurement was recorded for each hypertensive subject and average calculated for systolic blood pressure (SBP) and diastolic blood pressure (DBP) separately. The values obtained were used for stratification of the subjects into controlled and uncontrolled hypertension. Subjects also had echocardiograms to determine their left ventricular mass. Results : LVH was found in 14 (18.2%) of the normotensive group, 40 (20.8%) of the uncontrolled hypertensive group and 14 (24.1%) of the controlled hypertensive group when left ventricular mass (LVM) was indexed to body surface area (BSA). When LVM was indexed to height, left ventricular hypertrophy was found in none of the subjects of the normotensive group, while it was found present in 43 (22.4%) and 14 (24.1%) subjects of the uncontrolled and controlled hypertensive groups, respectively. Significant difference in the prevalence of LVH was detected only when LVM was indexed to height alone. Conclusion : Clinic blood pressure is an ineffective way of assessing BP control. Thus in apparently controlled hypertensive subjects, based on office blood pressure, cardiac structural changes do remain despite antihypertensive therapy. This population is still at risk of cardiovascular events.

Salako Babatunde; Ogah Okechukwu; Adebiyi Adewole; Oladapo Olulola; Aje Akinyemi; Adebayo Adedeji; Ojji Dike; Ipadeola Arinola; Nwafor Chibuike

2009-01-01

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Modeling CICR in rat ventricular myocytes: voltage clamp studies  

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Full Text Available Abstract Background The past thirty-five years have seen an intense search for the molecular mechanisms underlying calcium-induced calcium-release (CICR) in cardiac myocytes, with voltage clamp (VC) studies being the leading tool employed. Several VC protocols including lowering of extracellular calcium to affect Ca2+ loading of the sarcoplasmic reticulum (SR), and administration of blockers caffeine and thapsigargin have been utilized to probe the phenomena surrounding SR Ca2+ release. Here, we develop a deterministic mathematical model of a rat ventricular myocyte under VC conditions, to better understand mechanisms underlying the response of an isolated cell to calcium perturbation. Motivation for the study was to pinpoint key control variables influencing CICR and examine the role of CICR in the context of a physiological control system regulating cytosolic Ca2+ concentration ([Ca2+]myo). Methods The cell model consists of an electrical-equivalent model for the cell membrane and a fluid-compartment model describing the flux of ionic species between the extracellular and several intracellular compartments (cell cytosol, SR and the dyadic coupling unit (DCU), in which resides the mechanistic basis of CICR). The DCU is described as a controller-actuator mechanism, internally stabilized by negative feedback control of the unit's two diametrically-opposed Ca2+ channels (trigger-channel and release-channel). It releases Ca2+ flux into the cyto-plasm and is in turn enclosed within a negative feedback loop involving the SERCA pump, regulating[Ca2+]myo. Results Our model reproduces measured VC data published by several laboratories, and generates graded Ca2+ release at high Ca2+ gain in a homeostatically-controlled environment where [Ca2+]myo is precisely regulated. We elucidate the importance of the DCU elements in this process, particularly the role of the ryanodine receptor in controlling SR Ca2+ release, its activation by trigger Ca2+, and its refractory characteristics mediated by the luminal SR Ca2+ sensor. Proper functioning of the DCU, sodium-calcium exchangers and SERCA pump are important in achieving negative feedback control and hence Ca2+ homeostasis. Conclusions We examine the role of the above Ca2+ regulating mechanisms in handling various types of induced disturbances in Ca2+ levels by quantifying cellular Ca2+ balance. Our model provides biophysically-based explanations of phenomena associated with CICR generating useful and testable hypotheses.

Krishna Abhilash; Sun Liang; Valderrábano Miguel; Palade Philip T; Clark John W

2010-01-01

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Left Ventricular Hypertrophy and Microalbuminuria in Patients With Essential Hypertension  

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Full Text Available Introduction. Microalbuminuria and left ventricular hypertrophy (LVH) have both been shown to predict increased cardiovascular morbidity and mortality, especially in diabetic patients. The present study investigated the relationship between microalbuminuria and LVH in patients with essential hypertension. Materials and Methods. After a primary workup to rule out secondary hypertension, 110 essential hypertensive patients with LVH (mean age, 62.97 ± 11.02 years) and 10 essential hypertensive patients without LVH (mean age, 65.13 ± 10.15 years) were enrolled in this case-control study. Spot urine sample was collected for the assessment of microalbuminuria and creatinine concentrations in the two groups. Smoking status, blood pressure, and serum levels of total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and creatinine were evaluated.  Results. Patients with LVH had significantly higher microalbuminuria level compared with those without LVH (mean urine albumin-creatinine ratio, 54.4 ± 39.48 ?g/mg versus 33.56 ± 21.73 ?g/mg; P P Conclusions. Left ventricular hypertrophy is associated with microalbuminuria in patients with essential hypertension. These data are strengthening the role of microalbuminuria as an indicator of high cardiovascular risk.

Ali Monfared; Arsalan Salari; Fardin Mirbolok; Maryam Momeni; Shora Shafighnia; Maryam Shakiba; Amir Sheikholeslami

2013-01-01

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Calcium dysregulation in ventricular myocytes from mice expressing constitutively active Rac1.  

UK PubMed Central (United Kingdom)

Increased Rac1 activity and its concomitant elevation of reactive oxygen species (ROS) levels is believed to be involved in the development of cardiac diseases such as hypertrophy and arrhythmia. To study the effects of activated Rac1 on the properties of isolated ventricular myocytes we used a transgenic mouse model (RacET) expressing constitutively active Rac1. Concurrent with dilated cardiomyopathy global Ca(2+) handling as well as single cell contractility was substantially decreased. Cellular ROS levels were assessed with two independent assays and unexpectedly depicted decreased ROS production in RacET that was uncoupled from hormonal stimulation. Western blot analysis illustrated a massive increase in cellular Rac1 activity concomitant with a reduction in NADPH-oxidase activity. Analysis of the Ca(2+) current, the ryanodine receptor and fractional Ca(2+) release uncovered defective excitation-contraction (ec) coupling and a substantial increase in sarcoplasmic reticulum Ca(2+) leak together with a larger Ca(2+) spark amplitude and frequency. We conclude that Rac1 activity plays an important role for cardiac diseases but can be uncoupled from NADPH-oxidase activity. Rac1-mediated partial uncoupling of the ec-coupling machinery results in a ROS-independent disarrayed cellular Ca(2+) handling, contractility and impaired cardiac function.

Oberhofer M; Tian Q; Ruppenthal S; Wegener S; Reil JC; Körbel C; Hammer K; Menger M; Neuberger HR; Kaestner L; Lipp P

2013-07-01

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The Association of Growth Differentiation Factor-15 with Left Ventricular Hypertrophy in Hypertensive Patients  

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Growth differentiation factor-15 (GDF-15) has been identified as an endogenous anti-hypertrophy effect. However, the association of plasma GDF-15 levels with left ventricular hypertrophy (LVH) in hypertension is poorly understood. We investigate the effect of plasma GDF-15 levels on left ventricular...

Xue, Hao; Fu, Zhenhong; Chen, Yundai; Xing, Youhong; Liu, Jie; Zhu, Hang; Zhou, Xiao

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Cardiac steatosis and left ventricular hypertrophy in patients with generalized lipodystrophy as determined by magnetic resonance spectroscopy and imaging.  

Science.gov (United States)

Generalized lipodystrophy is a rare disorder characterized by marked loss of adipose tissue with reduced triglyceride storage capacity, leading to a severe form of metabolic syndrome including hypertriglyceridemia, insulin resistance, type 2 diabetes mellitus, and hepatic steatosis. Recent echocardiographic studies suggest that concentric left ventricular (LV) hypertrophy is another characteristic feature of this syndrome, but the mechanism remains unknown. It has recently been hypothesized that the LV hypertrophy could be an extreme clinical example of "lipotoxic cardiomyopathy": excessive myocyte accumulation of triglyceride leading to adverse hypertrophic signaling. To test this hypothesis, the first cardiac magnetic resonance study of patients with generalized lipodystrophy was performed, using magnetic resonance imaging and localized proton spectroscopy to detect excessive triglyceride content in the hypertrophied myocytes. Six patients with generalized lipodystrophy and 6 healthy controls matched for age, gender, and body mass index were studied. As hypothesized, myocardial triglyceride content was threefold higher in patients than controls: 0.6 ± 0.2% versus 0.2 ± 0.1% (p = 0.004). The presence of pericardial fat was also found, representing a previously undescribed adipose depot in generalized lipodystrophy. Patients with generalized lipodystrophy, compared with controls, also had a striking degree of concentric LV hypertrophy, independent of blood pressure: LV mass index 101.0 ± 18.3 versus 69.0 ± 17.7 g/m(2), respectively (p = 0.02), and LV concentricity 1.3 ± 0.3 versus 0.99 ± 0.1 g/ml, respectively (p = 0.04). In conclusion, these findings advance the lipotoxicity hypothesis as a putative underlying mechanism for the dramatic concentric LV hypertrophy found in generalized lipodystrophy. PMID:23800548

Nelson, Michael D; Victor, Ronald G; Szczepaniak, Edward W; Simha, Vinaya; Garg, Abhimanyu; Szczepaniak, Lidia S

2013-06-22

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Geometry and pump function in cardiac ventricular hypertrophy.  

UK PubMed Central (United Kingdom)

Ventricular pump function can be quantified by the inverse relation between pressure and output, i.e., the pump function graph, which is obtained by varying arterial load without changing end-diastolic volume, inotropic state and heart rate. The ratio of pressure and output, i.e., the peripheral resistance, can be represented in the same graph by a line through the origin. The 2 pressure-output relations intersect in the working point, i.e., the pressure and flow at the prevailing steady state. In normal, anesthetized cats the ventricle appears to be matched to the arterial load in the sense that the working point is found at the optimal power, i.e., the optimal value of the product of pressure and output along the pump function graph. To maintain this matching criterion during pressure overload, the ventricular volume has to remain the same while thickening of the wall takes place: concentric hypertrophy. With volume overload, matching would be preserved with eccentric hypertrophy. Because volume and pressure overloads typically lead to eccentric and concentric hypertrophy, respectively, the matching criterion may be a valuable predictor of the geometric changes found with changes in load. This idea was further investigated experimentally by determining the position of the working point in the perinephritic cat that had 1 kidney removed and the other wrapped in cellophane for 15 to 26 weeks. The working point was no longer found at the optimal power, indicating that either matching was permanently comprised or that the ventricle was still trying to restore matching.

Elzinga G; Toorop GP; Gross DR; Westerhof N

1990-04-01

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Cardiac arrhythmias and left ventricular hypertrophy in systemic hypertension  

International Nuclear Information System (INIS)

Background: Hypertensive left ventricular hypertrophy (LVH) is associated with increased risk of arrhythmias and mortality. Objective was to investigate the prevalence of cardiac arrhythmias and LVH in systemic hypertension. Methods: In all subjects blood pressure was measured, electrocardiography and echocardiography was done. Holter monitoring and exercise test perform in certain cases. There were 500 hypertensive patients, 156 (31.2%) men and 344 (69%) women >30 years of age in the study. Among them 177 (35.4%) were diabetic, 224 (45%) were dyslipidemia, 188 (37.6%) were smokers, and 14 (3%) had homocysteinemia. Mean systolic BP (SBP) was 180 +- 20 mm Hg and diastolic BP (DBP) was 95 +- 12 in male and female patients. Left ventricular mass index (LVMI) was 119.2 +- 30 2 2gm/m in male while 103 +- 22 gm/m in female patients. Palpitation was seen in 126 (25%) male and 299 (59.8%) female patients. Atrial fibrillation was noted in 108 (21.6%) male and 125 (25%) female patients, 30 (6%) male and 82 (16.4%) female patients had atrial flutter. Ventricular tachycardia was noted in 37 (7.4%) male and 59 (11.8%) female patients. Holter monitoring showed significant premature ventricular contractions (PVC'S) in 109 (21.8%) male and 128 (25.69%) female patients while Holter showed atrial arrhythmias (APC'S) in 89 (17.8%) males and 119 (23.8%) females. Angiography findings diagnosed coronary artery disease in 119 (23.8%) with CAD male and 225 (45%) without CAD while 47 (9.4%) females presented with CAD and 109 (21.8%) without CAD. Conclusion: A significant association has been demonstrated between hypertension and arrhythmias. Diastolic dysfunction of the left ventricle, left atrial size and function, as well as LVH have been suggested as the underlying risk factors for supraventricular, ventricular arrhythmias and sudden death in hypertensives with LVH. (author)

2010-01-01

 
 
 
 
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Measurement of Cardiac Mechanical Function in Isolated Ventricular Myocytes from Rats and Mice by Computerized Video-Based Imaging  

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Full Text Available Isolated adult cardiac ventricular myocytes have been a useful model for cardiovascular research for more than 20 years. With the recent advances in cellular physiology and transgenic techniques, direct measurement of isolated ventricular myocyte mechanics is becoming an increasingly important technique in cardiac physiology that provides fundamental information on excitation-contraction coupling of the heart, either in drug intervention or pathological states. The goal of this article is to describe the isolation of ventricular myocytes from both rats and mice, and the use of real-time beat-to-beat simultaneous recording of both myocyte contraction and intracellular Ca2+ transient.

Ren Jun; Wold Loren

2001-01-01

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Left ventricular hypertrophy, geometric patterns and clinical correlates among treated hypertensive Nigerians  

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Full Text Available BACKGROUND: Left ventricular hypertrophy can be due to various reasons including hypertension. It constitutes an increased cardiovascular risk . Various left ventricular geometric patterns occur in hypertension and may affect the cardiovascular risk profile of hypertensive subjects. METHODS: One hundred and eighty eight hypertensive subjects participated in this study. Left ventricular hypertrophy was diagnosed by echocardiography. Relative wall thickness was derived by 2 x PWTLVIDd. Subjects were arbitrarily categorized according to the duration of hypertension. Statistical analysis was done using SPSS 15.0. RESULTS:The mean age of the study population was 55.95 plus or minus 10.71 years. Subjects who had hypertension for more than 5 years were more likely to be older and had a lower ejection fraction , larger left ventricular diastolic internal dimension than those with duration of hypertension less than 5 years. Concentric remodelling was the commonest left ventricular geometric pattern among the hypertensive subjects closely followed by normal left ventricular geometry. Concentric hypertrophy and eccentric hypertrophy were rare among the study population.Left ventricular geometry was associated mainly with left ventricular chamber and wall dimensions. CONCLUSION: Concentric remodelling is the commonest pattern of left ventricular geometric pattern of the left ventricle among hypertensive subjects. Left ventricular geometry is associated with the chamber and wall dimensions. Eccentric hypertrophy is associated with the lowest left ventricular systolic function and therefore possibly an herald to progressive systolic impairment

Adeseye Akintunde; Olayinka Akinwusi; George Opadijo

2010-01-01

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[Age-related changes in transient outward potassium current of rat ventricular myocyte].  

UK PubMed Central (United Kingdom)

The study aimed to investigate the age-related changes and drug reactions of transient outward potassium current (Ito) of ventricular myocytes. Twenty-eight Sprague Dawley rats were divided into young (3-5 months), adult (13-15 months) and aged (22-24 months) groups, and Ito currents of isolated myocytes from each group were recorded respectively by patch-clamp. The perfusion of 2.0 mmol/L 4-AP or 1.0 ?mol/L isoproterenol was added respectively in each group, and the changes of Ito were observed. In comparison with young and adult groups, Ito densities of ventricular myocytes in aged group was significantly increased, the curve of steady-state activation of Ito shifted to the left, the close-state inactivation rate significantly decreased, and recovery rate from the steady-state inactivation became quicker. However, no significant changes could be detected for the Ito steady-state inactivation of ventricular myocytes in aged group. The similar responsiveness to 4-AP was observed in all three groups, but the responsiveness to isoproterenol was weaker in the aged group (55.9%) than in the other two groups (127.5% and 125.8%). In conclusion, the results show that Ito of rat ventricular myocyte of aging heart has increased current density and decreased response to isoproterenol.

Fu YC; Chen R; Chen MY; Chen Y; Wang YL; Xu B; Yang J; Yin T; Li Y

2013-04-01

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Metabolites of MDMA induce oxidative stress and contractile dysfunction in adult rat left ventricular myocytes  

Science.gov (United States)

Repeated administration of MDMA (ecstasy) produces eccentric left ventricular (LV) dilation and diastolic dysfunction. While the mechanism(s) underlying this toxicity are unknown; oxidative stress plays an important role. MDMA is metabolized into redox cycling metabolites that produce superoxide. In this study, we demonstrated that metabolites of MDMA induce oxidative stress and contractile dysfunction in adult rat left ventricular myocytes. Metabolites of MDMA used in this study included: alpha-methyl dopamine, N-methyl alpha-methyl dopamine and 2,5- bis(glutathion- S-yl)-alpha-MeDA. Dihydroethidium was used to detect drug-induced increases in reactive oxygen species (ROS) production in ventricular myocytes. Contractile function and changes in intracellular calcium transients were measured in paced (1Hz), Fura-2 AM loaded, myocytes using the IonOptix system. Production of ROS in ventricular myocytes treated with MDMA was not different from control. In contrast, all three metabolites of MDMA exhibited time- and concentration-dependent increases in ROS that were prevented by N-acetyl-cysteine (NAC). The metabolites of MDMA, but not MDMA alone, significantly decreased contractility and impaired relaxation in myocytes stimulated at 1Hz. These effects were prevented by NAC. Together, these data suggest that MDMA-induced oxidative stress in the left ventricle can be due, at least in part, to the metabolism of MDMA to redox active metabolites.

Shenouda, Sylvia K.; Varner, Kurt J.; Carvalho, Felix; Lucchesi, Pamela A.

2010-01-01

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[Variants of left ventricular hypertrophy in patients on programmed hemodialysis  

UK PubMed Central (United Kingdom)

Programmed hemodialysis (PHD) was successfully used in 189 of 207 patients with chronic renal failure (CRF) treated in Ulyanovsk Regional Hemodialysis Center for 10 years. To improve PHD results and prevent fatal complications, a search for objective prognostic indices of cardiovascular disease function was initiated. Left ventricular hypertrophy (LVH) development was compared in two groups of patients of different age (group 1--69 young patients aged 18-40 years; group 2--48 elderly patients aged 55-73 years. Concentric LVH transformed into excentric or mixed one in parallel to an increase of the patients' "dialysis age". This trend was prognostically unfavourable in both groups of patients especially in older patients.

Il'in AP; Bogoiavlenski? VF; Gazitov RM; Poletaev IV

2002-01-01

46

[Variants of left ventricular hypertrophy in patients on programmed hemodialysis].  

Science.gov (United States)

Programmed hemodialysis (PHD) was successfully used in 189 of 207 patients with chronic renal failure (CRF) treated in Ulyanovsk Regional Hemodialysis Center for 10 years. To improve PHD results and prevent fatal complications, a search for objective prognostic indices of cardiovascular disease function was initiated. Left ventricular hypertrophy (LVH) development was compared in two groups of patients of different age (group 1--69 young patients aged 18-40 years; group 2--48 elderly patients aged 55-73 years. Concentric LVH transformed into excentric or mixed one in parallel to an increase of the patients' "dialysis age". This trend was prognostically unfavourable in both groups of patients especially in older patients. PMID:12471833

Il'in, A P; Bogoiavlenski?, V F; Gazitov, R M; Poletaev, I V

2002-01-01

47

Left ventricular hypertrophy and microalbuminuria in patients with essential hypertension.  

UK PubMed Central (United Kingdom)

INTRODUCTION: Microalbuminuria and left ventricular hypertrophy (LVH) have both been shown to predict increased cardiovascular morbidity and mortality, especially in diabetic patients. The present study investigated the relationship between microalbuminuria and LVH in patients with essential hypertension. MATERIALS AND METHODS: After a primary workup to rule out secondary hypertension, 110 essential hypertensive patients with LVH (mean age, 62.97 ± 11.02 years) and 10 essential hypertensive patients without LVH (mean age, 65.13 ± 10.15 years) were enrolled in this case-control study. Spot urine sample was collected for the assessment of microalbuminuria and creatinine concentrations in the two groups. Smoking status, blood pressure, and serum levels of total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and creatinine were evaluated. RESULTS: Patients with LVH had significantly higher microalbuminuria level compared with those without LVH (mean urine albumin-creatinine ratio, 54.4 ± 39.48 ?g/mg versus 33.56 ± 21.73 ?g/mg; P < .001). Multivariable regression analysis showed that the patients with a higher urine albumin-creatinine ratio were more likely to have LVH (OR, 1.028; 95% CI, 1.015 to 1.041; P < .001). Other significant predictive factors for LVH in the model were diastolic blood pressure, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and serum creatinine. CONCLUSIONS: Left ventricular hypertrophy is associated with microalbuminuria in patients with essential hypertension. These data are strengthening the role of microalbuminuria as an indicator of high cardiovascular risk.

Monfared A; Salari A; Mirbolok F; Momeni M; Shafighnia S; Shakiba M; Sheikholeslami A

2013-05-01

48

Echocardiographic partition values and prevalence of left ventricular hypertrophy in hypertensive Nigerians  

Digital Repository Infrastructure Vision for European Research (DRIVER)

Abstract Background Left ventricular hypertrophy (LVH) is a well known independent risk factor for cardiovascular events. It has been shown that combination of left ventricular mass (LVM) and relative wall thickness (RWT) can be used to identify different forms of left ventricular (...

Adebiyi Adewole A; Ogah Okechukwu S; Aje Akinyemi; Ojji Dike B; Adebayo Adedeji K; Oladapo Olulola O; Falase Ayodele O

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Arritmias ventriculares e hipertrofia ventricular esquerda na cardiomiopatia hipertrófica/ Ventricular arrhythmias and left ventricular hypertrophy in hypertrophic cardiomyopathy  

Scientific Electronic Library Online (English)

Full Text Available Abstract in portuguese FUNDAMENTO: Na Cardiomiopatia Hipertrófica (CMH), o grau de Hipertrofia Ventricular Esquerda (HVE) poderia influenciar o desenvolvimento de arritmias ventriculares. OBJETIVO: Analisar, na CMH, a associação entre a ocorrência de arritmias ventriculares no eletrocardiograma-Holter (ECG-Holter) e o grau de HVE determinado ao ecocardiograma pela espessura parietal máxima (EPM) e Índice de Massa (IM). MÉTODOS: Cinquenta e quatro pacientes consecutivos com CMH realizaram (more) ECG-Holter de 24 horas e ecocardiograma para avaliação do grau de HVE através da EPM e IM. Foram estabelecidos dois níveis para a ocorrência de arritmias ventriculares: I - extrassístoles isoladas ou pareadas e II - Taquicardia Ventricular Não Sustentada (TVNS). RESULTADOS: Nos 13 pacientes (24%) com TVNS (nível II), houve maior frequência de EPM do ventrículo esquerdo (VE) > 21 mm (n = 10, 77%; 25 ± 4 mm) e IMVE > 144 g/m² (n = 10, 77%; 200 ± 30 g/m²), em relação àqueles que apresentavam apenas arritmia extrassistólica (nível I) (n = 41, 76%), em que essas medidas foram identificadas em, respectivamente, 37% (n = 15, 23 ± 1 mm), p = 0,023, e 39% (n = 16, 192 ± 53 g/m²) dos casos, p = 0,026. Os citados valores de corte foram determinados por curva ROC com intervalo de confiança de 95%. O registro de TVNS foi mais comum em pacientes com EPMVE > 21 mm e IMVE > 144 g/m² (8 de 13; 62%), do que naqueles com uma (4 de 13; 31%) ou nenhuma (1 de 13; 8%) variável ecocardiográfica acima dos valores de corte, p = 0,04. CONCLUSÃO: A ocorrência de arritmias ventriculares no Holter associou-se, na CMH, ao grau de HVE, avaliado pelo ecocardiograma através da respectiva EPM e IM. Abstract in english BACKGROUND: In hypertrophic cardiomyopathy (HCM), the degree of left ventricular hypertrophy (LVH) could influence the development of ventricular arrhythmias. OBJECTIVE: In HCM, analyze the association between the occurrence of ventricular arrhythmias determined by Holter electrocardiogram (ECG-Holter) and the degree of LVH determined by maximum wall thickness (MWT) in echocardiography and body mass index (BMI). METHODS: Fifty-four consecutive patients with HCM underwent (more) 24-hour ECG-Holter and echocardiography for assessment of level of LVH through MWT and BMI. Two levels were established for the occurrence of Ventricular Arrhythmias: I - alone or paired extrasystoles and II - Non- Sustained Ventricular Tachycardia (NSVT). RESULTS: In 13 patients (24%) with NSVT (level II), there was a higher frequency of MWT of the left ventricle (LV) > 21 mm (n = 10, 77%, 25 ± 4 mm) and LLLV = 144 g/m² (n = 10, 77%, 200 ± 30 g/m²), in comparison with those presenting with extrasystole arrhythmias (level I) (n = 41, 76%), in which these measures were identified in, respectively, 37 % (n= 15, 23 ± 1 mm), p = 0.023, and 39% (n = 16, 192 ± 53 g / m²) of the cases (p = 0.026). The cut-off values mentioned were determined by the ROC curve with a confidence interval of 95%. NSVT was more common in patients with MWTLV > 21 mm and LLLV > 144 g/m² (8 of 13, 62%) than in those with (4 of 13, 31%) or without (1 of 13; 8%) echocardiographic variables above cut-off values (p = 0.04). CONCLUSION: In HCM, occurrence of ventricular arrhythmias by Holter was associated with the degree of LVH assessed by echocardiography through MWT and BMI.

Mattos, Beatriz Piva e; Torres, Marco Antonio Rodrigues; Freitas, Valéria Centeno de; Scolari, Fernando Luís; Loreto, Melina Silva de

2013-01-01

50

Arritmias ventriculares e hipertrofia ventricular esquerda na cardiomiopatia hipertrófica Ventricular arrhythmias and left ventricular hypertrophy in hypertrophic cardiomyopathy  

Directory of Open Access Journals (Sweden)

Full Text Available FUNDAMENTO: Na Cardiomiopatia Hipertrófica (CMH), o grau de Hipertrofia Ventricular Esquerda (HVE) poderia influenciar o desenvolvimento de arritmias ventriculares. OBJETIVO: Analisar, na CMH, a associação entre a ocorrência de arritmias ventriculares no eletrocardiograma-Holter (ECG-Holter) e o grau de HVE determinado ao ecocardiograma pela espessura parietal máxima (EPM) e Índice de Massa (IM). MÉTODOS: Cinquenta e quatro pacientes consecutivos com CMH realizaram ECG-Holter de 24 horas e ecocardiograma para avaliação do grau de HVE através da EPM e IM. Foram estabelecidos dois níveis para a ocorrência de arritmias ventriculares: I - extrassístoles isoladas ou pareadas e II - Taquicardia Ventricular Não Sustentada (TVNS). RESULTADOS: Nos 13 pacientes (24%) com TVNS (nível II), houve maior frequência de EPM do ventrículo esquerdo (VE) > 21 mm (n = 10, 77%; 25 ± 4 mm) e IMVE > 144 g/m² (n = 10, 77%; 200 ± 30 g/m²), em relação àqueles que apresentavam apenas arritmia extrassistólica (nível I) (n = 41, 76%), em que essas medidas foram identificadas em, respectivamente, 37% (n = 15, 23 ± 1 mm), p = 0,023, e 39% (n = 16, 192 ± 53 g/m²) dos casos, p = 0,026. Os citados valores de corte foram determinados por curva ROC com intervalo de confiança de 95%. O registro de TVNS foi mais comum em pacientes com EPMVE > 21 mm e IMVE > 144 g/m² (8 de 13; 62%), do que naqueles com uma (4 de 13; 31%) ou nenhuma (1 de 13; 8%) variável ecocardiográfica acima dos valores de corte, p = 0,04. CONCLUSÃO: A ocorrência de arritmias ventriculares no Holter associou-se, na CMH, ao grau de HVE, avaliado pelo ecocardiograma através da respectiva EPM e IM.BACKGROUND: In hypertrophic cardiomyopathy (HCM), the degree of left ventricular hypertrophy (LVH) could influence the development of ventricular arrhythmias. OBJECTIVE: In HCM, analyze the association between the occurrence of ventricular arrhythmias determined by Holter electrocardiogram (ECG-Holter) and the degree of LVH determined by maximum wall thickness (MWT) in echocardiography and body mass index (BMI). METHODS: Fifty-four consecutive patients with HCM underwent 24-hour ECG-Holter and echocardiography for assessment of level of LVH through MWT and BMI. Two levels were established for the occurrence of Ventricular Arrhythmias: I - alone or paired extrasystoles and II - Non- Sustained Ventricular Tachycardia (NSVT). RESULTS: In 13 patients (24%) with NSVT (level II), there was a higher frequency of MWT of the left ventricle (LV) > 21 mm (n = 10, 77%, 25 ± 4 mm) and LLLV = 144 g/m² (n = 10, 77%, 200 ± 30 g/m²), in comparison with those presenting with extrasystole arrhythmias (level I) (n = 41, 76%), in which these measures were identified in, respectively, 37 % (n= 15, 23 ± 1 mm), p = 0.023, and 39% (n = 16, 192 ± 53 g / m²) of the cases (p = 0.026). The cut-off values mentioned were determined by the ROC curve with a confidence interval of 95%. NSVT was more common in patients with MWTLV > 21 mm and LLLV > 144 g/m² (8 of 13, 62%) than in those with (4 of 13, 31%) or without (1 of 13; 8%) echocardiographic variables above cut-off values (p = 0.04). CONCLUSION: In HCM, occurrence of ventricular arrhythmias by Holter was associated with the degree of LVH assessed by echocardiography through MWT and BMI.

Beatriz Piva e Mattos; Marco Antonio Rodrigues Torres; Valéria Centeno de Freitas; Fernando Luís Scolari; Melina Silva de Loreto

2013-01-01

51

Genetic background of left ventricular hypertrophy in Uzbek hypertensive men.  

UK PubMed Central (United Kingdom)

OBJECTIVES: We evaluated the prevalences of ACE/ID, AGT/M235T, AT1R/A1166C, and CYP11B2/C344T genetic polymorphisms and their association with left ventricular hypertrophy (LVH) in Uzbek hypertensive men. STUDY DESIGN: The study included 172 Uzbek men (mean age 47±10 years) with untreated essential hypertension (EH) of grade 1-2 and 60 normotensive subjects (mean age 41±10 years). All subjects underwent complete M-mode echocardiography to determine left ventricular mass (LVM) and LVM index (LVMI). Genomic DNA was extracted from peripheral blood and was analyzed using polymerase chain reaction-restriction fragment length polymorphism assays. RESULTS: Left ventricular hypertrophy was detected in 148 hypertensive patients (86.1%). The frequencies of the D-allele of the ACE gene and T-allele of the CYP11B2 gene were higher among hypertensive patients than in the controls. There was a significant association between the AGT/M235T polymorphism and LVH. The 235T-allele of the AGT gene, the D-allele of the ACE gene, and the 344T-allele of the CYP11B2 gene were identified as "damaging" alleles. All the patients had "damaging" alleles, the number being one in only seven patients (4.1%), two in 52 patients (30.2%), and three in 89 patients (51.7%). The severity of LVH significantly increased with the number of "damaging" alleles. Among paired carriage of "damaging" alleles, the combination of the D+235T-alleles was found as the most unfavorable pair associated with the degree of LVH. CONCLUSION: There is an association between EH and ACE/ID and CYP11B2/C344T gene polymorphisms in Uzbek males, with higher frequencies of the D-allele of the ACE gene and T-allele of the CYP11B2 gene. Our findings provide evidence for the association of AGT/M235T polymorphism with LVH in Uzbek males, combination of the D+235T-alleles being the most unfavorable pair associated with LVH.

Kurbanova D; Eliseyeva M

2010-10-01

52

Expression and distribution of Src in the nucleus of myocytes in cardiac hypertrophy.  

Science.gov (United States)

The Src kinase is involved in signaling events leading to cardiac hypertrophy. The exact effects of tyrosine phosphorylation and subnuclear distribution on cardiac hypertrophy and failure remain to be investigated. In this study, we examined the intranuclear expression and distribution of c-Src, Src phosphorylated at tyrosine 529 (Src[pY529]), Src phosphorylated at tyrosine 418 (Src[pY418]) and Src phosphorylated at tyrosine 215 (Src[pY215]) in the myocardial nuclei of the left ventricle (LV) from 2-, 6-, 12- and 18-month-old spontaneously hypertensive heart failure (SHHF) rats and age-matched Wistar-Kyoto (WKY) rats as normotensive controls by western blot analysis, immunofluorescent labeling and immunoprecipitation. Cellular Src (c-Src) expression in the myocardial nuclei of the LV of the 2-, 6-, 12- and 18-month-old SHHF rats was not significantly different from that in the myocardial nuclei of the LV of the age-matched WKY rats. Although there were no significant differences observed between the levels of Src[pY529] and Src[pY418] in the myocardial nuclei of the LV of the 2-month-old SHHF and WKY rats, the expression of Src[pY529] significantly decreased, while that of Src[pY418] significantly increased in the myocardial nuclei of the LV of the 6-, 12- and 18-month-old SHHF rats compared to the age-matched WKY controls. Furthermore, as demonstrated by double labeling with antibodies against fibrillarin and Src-associated in mitosis 68 kDa (Sam68), c-Src was co-localized with both Sam68 and fibrillarin in the nuclei; Src[pY529] co-localized with fibrillarin, but Src[pY418] co-localized with Sam68. The results from the present study suggest that the dephosphorylation of Src tyrosine kinase 529, the phosphorylation of tyrosine 418 and their subnuclear redistribution are involved in endonuclear signal transduction in cardiac myocytes, which regulates the development and progression of LV eccentric hypertrophy induced by hypertension. PMID:23673471

Chen, Ping; Li, Faqian; Xu, Zeqing; Li, Zhanyu; Yi, Xian Ping

2013-05-14

53

L-type calcium current in right ventricular outflow tract myocytes of rabbit heart.  

UK PubMed Central (United Kingdom)

The mechanism of idiopathic ventricular tachycardia originating from the right ventricular outflow tract (RVOT) is not clear. Many clinical reports have suggested a mechanism of triggered activity. However, there are few studies investigating this because of the technical difficulties associated with examining this theory. The L-type calcium current (I (Ca-L)), an important inward current of the action potential (AP), plays an important role in arrhythmogenesis. The aim of this study was to explore differences in the APs of right ventricular (RV) and RVOT cardiomyocytes, and differences in electrophysiological characteristics of the ICa-L in these myocytes. Rabbit RVOT and RV myocytes were isolated and their AP and I (Ca-L) were investigated using the patch-clamp technique. RVOT cardiomyocytes had a wider range of AP duration (APD) than RV cardiomyocytes, with some markedly prolonged APDs and markedly shortened APDs. The markedly shortened APDs in RVOT myocytes were abolished by treatment with 4-AP, an inhibitor of the transient outward potassium current, but the markedly prolonged APDs remained, with some myocytes with a long AP plateau not repolarizing to resting potential. In addition, early afterdepolarization (EAD) and second plateau responses were seen in RVOT myocytes but not in RV myocytes. RVOT myocytes had a higher current density for I (Ca-L) than RV myocytes (RVOT (13.16±0.87) pA pF(-1), RV (8.59±1.97) pA pF(-1); P<0.05). The I (Ca-L) and the prolonged APD were reduced, and the EAD and second plateau response disappeared, after treatment with nifedipine (10 ?mol L(-1)), which blocks the I (Ca-L). In conclusion, there was a wider range of APDs in RVOT myocytes than in RV myocytes, which is one of the basic factors involved in arrhythmogenesis. The higher current density for I (Ca-L) is one of the factors causing prolongation of the APD in RVOT myocytes. The combination of EAD with prolonged APD may be one of the mechanisms of RVOT-VT generation.

Liang S; Lin C; Li Y; Liu T; Wang Y

2012-01-01

54

Effects of propafenone on calcium current in guinea-pig ventricular myocytes.  

Digital Repository Infrastructure Vision for European Research (DRIVER)

1. The modulation of L-type voltage-sensitive calcium channels in guinea-pig isolated ventricular myocytes by propafenone was examined by the whole cell voltage-clamp technique. 2. Propafenone, 10(-7) -5 x 10(-5) M, produced a concentration-dependent inhibition of Ca current (ICa) without any signif...

Delgado, C.; Tamargo, J.; Henzel, D.; Lorente, P.

55

Effects of propafenone on calcium currents in single ventricular myocytes of guinea-pig.  

Digital Repository Infrastructure Vision for European Research (DRIVER)

1. The effects of propafenone on the inward calcium current (ICa) were investigated in isolated single ventricular myocytes of the guinea-pig by the whole-cell clamp method. Propafenone inhibited ICa in a dose-dependent manner at concentrations of propafenone ranging from 1 x 10(-8) to 1 x 10(-3) M ...

Fei, L.; Gill, J. S.; McKenna, W. J.; Camm, A. J.

56

Effect of ethanol on action potential and ionic membrane currents in rat ventricular myocytes.  

Czech Academy of Sciences Publication Activity Database

rat ventricular myocyteKód oboru RIV: BO - BiofyzikaImpakt faktor: 3.138, rok: 2010http://apps.isiknowledge.com/full_record.do?product=UA&search_mode=GeneralSearch&qid=15&SID=Y1pmpi@7k2HPEc8ehEE&page=1&doc=1&colname=WOS

Bébarová, M.; Matejovi?, P.; Pásek, MichalG; Ohlídalová, D.; Jansová, D.; Šimurdová, M.; Šimurda, J.

57

Effect of SIN-1 in rat ventricular myocytes: Interference with ?-adrenergic stimulation  

Digital Repository Infrastructure Vision for European Research (DRIVER)

We have examined the effects of the nitric oxide (NO) donor, 3-morpholino-sydnonimine (SIN-1), on Ca 2+ transients, L-type Ca 2+ current (I Ca,L), and cGMP/cAMP content in electrically-stimulated rat ventricular myocytes in the absence and presence of the ?-adrenergic stimulation with isoproterenol....

Yin, X; Shan, Q; Deng, C; Bourreau, JP

58

Metal particulate matter components affect gene expression and beat frequency of neonatal rat ventricular myocytes.  

Digital Repository Infrastructure Vision for European Research (DRIVER)

Soluble particulate matter (PM) components (e.g., metals) have the potential to be absorbed into the bloodstream and transported to the heart where they might induce the expression of inflammatory cytokines and remodel electrical properties. We exposed cultured rat ventricular myocytes to similar co...

Graff, Donald W; Cascio, Wayne E; Brackhan, Joseph A; Devlin, Robert B

59

Effects of trimetazidine on pHi regulation in the rat isolated ventricular myocyte.  

Digital Repository Infrastructure Vision for European Research (DRIVER)

1. We have examined the effects of trimetazidine (TMZ) on intracellular pH (pHi) regulation in rat isolated ventricular myocytes. pHi was recorded ratiometrically by use of the pH-sensitive fluoroprobe, carboxy-SNARF-1 (carboxy-seminaphtorhodafluor). 2. Following an intracellular acid load (induced ...

Lagadic-Gossmann, D.; Le Prigent, K.; Feuvray, D.

60

Left ventricular hypertrophy screening using a hand-held ultrasound device  

Digital Repository Infrastructure Vision for European Research (DRIVER)

AIMS: To test the diagnostic potential of a hand-held ultrasound device for screening for left ventricular hypertrophy in a hypertensive population using a standard echocardiographic system as a reference. METHODS: One hundred consecutive hypertensive patients were enrolled. An ...

Vourvouri, E.C.; Poldermans, D.; Schinkel, A.F.; Koroleva, L.Y.; Sozzi, F.A.M.A.; Parharidis, G.E.; Bax, J.J.; Roelandt, J.R.T.C.

 
 
 
 
61

Risk and management of hypertension-related left ventricular hypertrophy.  

UK PubMed Central (United Kingdom)

Knowledge gained from epidemiological studies and clinical trials on hypertension has led to impressive reductions in morbidity and mortality, particularly from stroke and coronary heart disease (CHD) as complications of end-organ damage from untreated, prolonged systemic hypertension. Data on reductions in stroke when hypertension is treated have been clear and convincing from individual clinical trials. Most of these trials, however, have consistently shown only trends towards a reduction in CHD, and few have individually reported statistically significant reductions. A recent meta-analysis, however, suggests that a significant beneficial reduction in CHD exists when the overall data are examined, although at a lower magnitude of benefit and lesser degree of certainty than for stroke. The presence of left ventricular hypertrophy (LVH) increases the risk of subsequent cardiovascular disease events, cardiovascular mortality and all-cause mortality in hypertensive patients. Although echocardiography appears more sensitive than electrocardiography in diagnosing LVH, much of the information demonstrating risks from LVH is from electrocardiography data, and it is not clear how echocardiography will change the risk prediction. Some data from large clinical trials and populations studies suggest that LVH regresses, particularly if the hypertension is adequately treated. A meta-analysis of a large number of small clinical studies in hypertensive patients suggests that the 4 commonly used antihypertensive drug classes, beta-blockers, diuretics, calcium channel antagonists and ACE inhibitors, are all associated with significant reductions in left ventricular mass. While the primary indication for treatment is clearly the hypertension and not the LVH, the presence of the latter necessitates careful treatment and follow-up of these hypertensive individuals.

Teo KK

1995-12-01

62

BP Control and Left Ventricular Hypertrophy Regression in Children with CKD.  

UK PubMed Central (United Kingdom)

In adult patients with CKD, hypertension is linked to the development of left ventricular hypertrophy, but whether this association exists in children with CKD has not been determined conclusively. To assess the relationship between BP and left ventricular hypertrophy, we prospectively analyzed data from the Chronic Kidney Disease in Children cohort. In total, 478 subjects were enrolled, and 435, 321, and 142 subjects remained enrolled at years 1, 3, and 5, respectively. Echocardiograms were obtained 1 year after study entry and then every 2 years; BP was measured annually. A linear mixed model was used to assess the effect of BP on left ventricular mass index, which was measured at three different visits, and a mixed logistic model was used to assess left ventricular hypertrophy. These models were part of a joint longitudinal and survival model to adjust for informative dropout. Predictors of left ventricular mass index included systolic BP, anemia, and use of antihypertensive medications other than angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Predictors of left ventricular hypertrophy included systolic BP, female sex, anemia, and use of other antihypertensive medications. Over 4 years, the adjusted prevalence of left ventricular hypertrophy decreased from 15.3% to 12.6% in a systolic BP model and from 15.1% to 12.6% in a diastolic BP model. These results indicate that a decline in BP may predict a decline in left ventricular hypertrophy in children with CKD and suggest additional factors that warrant additional investigation as predictors of left ventricular hypertrophy in these patients.

Kupferman JC; Aronson Friedman L; Cox C; Flynn J; Furth S; Warady B; Mitsnefes M

2013-09-01

63

Left Ventricular Hypertrophy Evaluation in Obese Hypertensive Patients: Effect of Left Ventricular Mass Index Criteria  

Directory of Open Access Journals (Sweden)

Full Text Available PURPOSE: To evaluate left ventricular mass (LVM) index in hypertensive and normotensive obese individuals. METHODS: Using M mode echocardiography, 544 essential hypertensive and 106 normotensive patients were evaluated, and LVM was indexed for body surface area (LVM/BSA) and for height² (LVM/h²). The 2 indexes were then compared in both populations, in subgroups stratified according to body mass index (BMI): or = 30kg/m². RESULTS: The BSA index does not allow identification of significant differences between BMI subgroups. Indexing by height² provides significantly increased values for high BMI subgroups in normotensive and hypertensive populations. CONCLUSION: Left ventricular hypertrophy (LVH) has been underestimated in the obese with the use of LVM/BSA because this index considers obesity as a physiological variable. Indexing by height² allows differences between BMI subgroups to become apparent and seems to be more appropriate for detecting LVH in obese populations.

Eduardo Cantoni Rosa; Valdir Ambrósio Moysés; Ricardo Cintra Sesso; Frida Liane Plavnik; Fernando Flexa Ribeiro; Nárcia E. B. Kohlmann; Artur Beltrame Ribeiro; Maria Tereza Zanella; Osvaldo Kohlmann Jr.

2002-01-01

64

Standard electrocardiographic criteria for left ventricular hypertrophy in Nigerian hypertensives.  

UK PubMed Central (United Kingdom)

OBJECTIVES: Left ventricular hypertrophy (LVH) is a major risk factor for cardiovascular morbidity and mortality. Various electrocardiographic criteria for LVH have differing sensitivities and specificities. Most of the available electrocardiographic criteria for LVH have not been evaluated in the African populace. METHODS: Electrocardiograms (ECGs) and echocardiograms were obtained from 100 hypertensive subjects and 60 controls. Electrocardiogram (ECG) LVH was determined by the Sokolow-Lyon, Sokolow-Lyon-Rappaport, Cornell voltage, Romhilt-Estes point score, and the Perugia score criteria. Echocardiographic LVH was defined by LV mass indexed for height at 97.5 percentile of the controls (126 g/m and 130 g/m in females and males respectively). RESULTS: The prevalence of echocardiographic LVH indexed for height was 34% and 1.67% in the hypertensive patients and controls respectively. The prevalence of ECG LVH obtained in the hypertensive patients with the various ECG criteria were 56% for Sokolow-Lyon-Rappaport voltage, 48% for Sokolow-Lyon voltage, 41% for Perugia score, 22% for Cornell sex specific voltage, and 18% for Romhilt-Estes score. Sokolow-Lyon-Rappaport voltage criteria had the best sensitivity (80%) and area under the receiver operating characteristic (ROC) curve while the Romhilt-Estes score had the best specificity (93%). CONCLUSION: Sokolow-Lyon and Sokolow-Lyon-Rappaport voltage criteria combine the best sensitivity and specificity values and would seem better suited for the diagnosis of ECG LVH in Nigerians.

Dada A; Adebiyi AA; Aje A; Oladapo OO; Falase AO

2005-01-01

65

Prevalencia de hipertrofia ventricular izquierda en pacientes diabéticos Prevalence of left ventricular hypertrophy in diabetic patients  

Directory of Open Access Journals (Sweden)

Full Text Available Con el objetivo de establecer la prevalencia de hipertrofia ventricular izquierda (HVI) en pacientes con diabetes mellitus tipo 2 (DM), se realizó un estudio transversal en estos pacientes, estableciendo sus características antropométricas, presión arterial y control metabólico. Para evaluar la presencia de HVI se empleó ecocardiografía transtorácica. El estudio incluyó 91 pacientes, en los cuales la prevalencia de HVI fue de 63,7%, siendo más frecuente en mujeres que en varones (p=0,001). Adicionalmente, se encontró un 46,2% de pacientes con disfunción diastólica del ventrículo izquierdo. Se concluye que existe una importante prevalencia de HVI en pacientes diabéticos sin antecedentes de causas definidas de hipertrofia. No se encontró relación con sexo, control metabólico, IMC y tiempo de diagnósticoIn order to establish the prevalence of left ventricular hypertrophy (LVH) in patients with type 2 diabetes mellitus, (DM) a cross-sectional study was conducted in these patients studying their anthropometric characteristics, blood pressure and metabolic control. To evaluate the presence of LVH, a trans-thoracic echocardiogram was used. The study included 91 patients, finding a 63.7% prevalence of HVI, with women being more affected than men (p=0.001). Additionally, 46.2% of patients were found to have diastolic dysfunction of the left ventricle. We conclude that there is an important prevalence of LVH in diabetic patients without defined causes of hypertrophy. There was no association with sex, metabolic control, BMI and time of diagnosis

Diego Valarezo-Sevilla; Armín Pazmiño-Martínez; Nidya Morales-Mora

2013-01-01

66

Two cases of reversible left ventricular hypertrophy during recovery from takotsubo cardiomyopathy.  

UK PubMed Central (United Kingdom)

We report 2 cases of reversible ventricular hypertrophy in patients with takotsubo cardiomyopathy (stress-induced cardiomyopathy) during recovery of cardiac function. The first case involved a 72-year-old woman who presented with cerebral infarction. On admission, an elevated troponin I and decreased apical wall motion were observed with normal myocardial perfusion imaging. The second case involved a 79-year-old woman who presented with angina, anxiety resulting from emotional stress, slightly decreased apical wall motion, and normal epicardial arteries. In both cases, apical hypertrophy of the left ventricle was observed at approximately 3 weeks after onset, when the wall motion had improved. The ventricular wall gradually became thinner over time. To our knowledge, this is the first report of reversible ventricular hypertrophy in patients with takotsubo cardiomyopathy. We hypothesize the hypertrophic signaling in the myocardium was stimulated by catecholamines, which are the suggested etiology of takotsubo cardiomyopathy, and the hypertrophied myocardium gradually returned to normal as the syndrome receded.

Kato T; Ban Y; Kuruma S; Ishida S; Doi C; Iura T; Terawaki H; Inoko M; Nohara R

2013-04-01

67

Right ventricular hypertrophy in systemic hypertension: an updated review of clinical studies.  

UK PubMed Central (United Kingdom)

AIM: Experimental and clinical evidence supports the view that right ventricular hypertrophy (RVH) may parallel left ventricular hypertrophy in systemic hypertension; a comprehensive analysis of this issue, however, is lacking. Thus, we analyzed the literature in order to provide an updated information on the right ventricular structural changes associated to systemic hypertension. DESIGN: A literature search using the key words 'right ventricle' 'right ventricular hypertrophy', 'biventricular hypertrophy' 'right and left ventricular hypertrophy'. 'hypertension', 'echocardiography' was performed in order to identify relevant articles. Full articles published in English language in the last three decades reporting studies in adult hypertensive individuals were considered. RESULTS: A total of 13 studies, including 1290 untreated (45%) and treated hypertensive patients and 259 normotensive controls, were considered. Overall, in hypertensive individuals right ventricular wall was thicker than in normotensive counterparts (standardized difference 1.3 mm, P?

Cuspidi C; Sala C; Muiesan ML; De Luca N; Schillaci G

2013-05-01

68

[The usefulness of the electrocardiogram in the diagnosis of left ventricular hypertrophy in essential arterial hypertension  

UK PubMed Central (United Kingdom)

The aim of the study is to analyse the usefulness of electrocardiographic criteria of left ventricular hypertrophy in essential hypertension. Seventy four patients (27 males, 47 females), 49 +/- 11 years--old with mild--moderate systemic hypertension (blood pressure greater than or equal to 140/90 mmHg) have been prospectively studied. A 12-lead electrocardiogram and an echocardiogram (M and 2D mode) have been performed after the basic clinical study. A left ventricular mass index (Devereux's method) greater than 131 g/square meters (males) or greater than 110 g/square meters (females) has been considered as left ventricular hypertrophy. Sensitivity, specificity and accuracy of 11 current electrocardiographic criteria of left ventricular hypertrophy have been determined. Sensitivity of these criteria was very low (0-0.35), while specificity was high (0.71-1). Total QRS voltage showed the best accuracy (0.51), while V5 or V6 R wave amplitude greater than 26 mm showed the best sensitivity (0.35). Current electrocardiographic criteria of left ventricular hypertrophy are not very useful in the diagnosis of left ventricular hypertrophy in essential hypertension.

Rodríguez Padial L; Navarro Lima A; Sánchez Domínguez J

1991-06-01

69

Sexual dimorphism in obesity-mediated left ventricular hypertrophy.  

UK PubMed Central (United Kingdom)

In the present study we investigated the influence of sex difference on the development of left ventricular hypertrophy (LVH) during obesity. Male and female C57BL/6J mice were fed for 15 and 25 wk with a high-fat diet (HFD) or low-fat control diet (LFD). Analysis of body composition, monitoring of body weight (BW), and echocardiographic analysis were performed, as well as analysis of expression of different adipocytokines in epicardial adipose tissue. The increment in left ventricular mass (LVM) after HFD (25 wk) was significantly stronger in male mice compared with female mice [LVM: male, 116.9 ± 2.9 (LFD) vs. 142.2 ± 9.3 mg (HFD); female, 84.3 ± 3.3 (LFD) vs. 93.9 ± 1.7 mg (HFD), Psex < 0.01]. In parallel, males developed a higher BW and fat mass after 25 wk HFD than female mice [BW: male, 33 ± 0.9 (LFD) vs. 53 ± 0.8 g (HFD); fat mass: male, 8.8 ± 0.9 (LFD) vs. 22.8 ± 0.7 g (HFD); BW: female, 22.5 ± 0.4 (LFD) vs. 33.7 ± 1.3 g (HFD); fat mass: female, 4.0 ± 0.2 (LFD) vs. 13.2 ± 1.2 g (HFD)] (P < 0.01 for BW+ fat mass female vs. male). The mRNA expression of adipocytokines in epicardial fat after 25 wk of diet showed higher levels of adiponectin (2.8-fold), leptin (4.2-fold), and vaspin (11.9-fold) in male mice compared with female mice (P < 0.05). To identify new adipose-derived molecular mediators of LVH, we further elucidated the cardiac impact of vaspin. Murine primary cardiac fibroblast proliferation was significantly induced by vaspin (1.8-fold, vaspin 1 ?g/l, P < 0.05 vs. control) compared with 1.9-fold induction by angiotensin II (10 ?M). The present study demonstrates a sex-dependent regulation of diet-induced LVH associated with sexual dimorphic expression of adipocytokines in epicardial adipose tissue.

Böhm C; Benz V; Clemenz M; Sprang C; Höft B; Kintscher U; Foryst-Ludwig A

2013-07-01

70

Cardiac developmental defects and eccentric right ventricular hypertrophy in cardiomyocyte focal adhesion kinase (FAK) conditional knockout mice.  

Science.gov (United States)

Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase that plays an important role in integrin-mediated signal transduction. To explore the role and mechanisms of FAK in cardiac development, we inactivated FAK in embryonic cardiomyocytes by crossing the floxed FAK mice with myosin light chain-2a (MLC2a) Cre mice, which expressed Cre as early as embryonic day 9.5 in the heart. The majority of conditional FAK knockout mice generated from MLC2a-Cre (CFKO-2a) died in the embryonic stage with thin ventricular wall and ventricular septal defects. A small fraction of CFKO-2a mice survived to adulthood with spontaneous eccentric right ventricle hypertrophy. Transmission electron microscopy analysis displayed swelling in the rough endoplasmic reticulum in CFKO-2a embryonic cardiomyocytes. We found that decreased cell proliferation, but not increased cell apoptosis or differentiation, is the reason for the thin ventricular wall in CFKO-2a mice. Microarray analysis suggests that myocyte enhancer factor 2a (MEF2a) can be regulated by FAK and that inactivation of FAK in the embryonic heart compromised MEF2a expression. Last, we found that Src, but not PI3K, is important in mediating signal transduction for the regulation of MEF2a by FAK. Together, these results identified the role and mechanisms of FAK in embryonic cardiac development. PMID:18448675

Peng, Xu; Wu, Xiaoyang; Druso, Joseph E; Wei, Huijun; Park, Ann Yong-Jin; Kraus, Marc S; Alcaraz, Ana; Chen, Ju; Chien, Shu; Cerione, Richard A; Guan, Jun-Lin

2008-04-30

71

The adult heart responds to increased workload with physiologic hypertrophy, cardiac stem cell activation, and new myocyte formation.  

UK PubMed Central (United Kingdom)

AimsIt is a dogma of cardiovascular pathophysiology that the increased cardiac mass in response to increased workload is produced by the hypertrophy of the pre-existing myocytes. The role, if any, of adult-resident endogenous cardiac stem/progenitor cells (eCSCs) and new cardiomyocyte formation in physiological cardiac remodelling remains unexplored.Methods and resultsIn response to regular, intensity-controlled exercise training, adult rats respond with hypertrophy of the pre-existing myocytes. In addition, a significant number (?7%) of smaller newly formed BrdU-positive cardiomyocytes are produced by the exercised animals. Capillary density significantly increased in exercised animals, balancing cardiomyogenesis with neo-angiogenesis. c-kit(pos) eCSCs increased their number and activated state in exercising vs. sedentary animals. c-kit(pos) eCSCs in exercised hearts showed an increased expression of transcription factors, indicative of their commitment to either the cardiomyocyte (Nkx2.5(pos)) or capillary (Ets-1(pos)) lineages. These adaptations were dependent on exercise duration and intensity. Insulin-like growth factor-1, transforming growth factor-?1, neuregulin-1, bone morphogenetic protein-10, and periostin were significantly up-regulated in cardiomyocytes of exercised vs. sedentary animals. These factors differentially stimulated c-kit(pos) eCSC proliferation and commitment in vitro, pointing to a similar role in vivo.ConclusionIntensity-controlled exercise training initiates myocardial remodelling through increased cardiomyocyte growth factor expression leading to cardiomyocyte hypertrophy and to activation and ensuing differentiation of c-kit(pos) eCSCs. This leads to the generation of new myocardial cells. These findings highlight the endogenous regenerative capacity of the adult heart, represented by the eCSCs, and the fact that the physiological cardiac adaptation to exercise stress is a combination of cardiomyocyte hypertrophy and hyperplasia (cardiomyocytes and capillaries).

Waring CD; Vicinanza C; Papalamprou A; Smith AJ; Purushothaman S; Goldspink DF; Nadal-Ginard B; Torella D; Ellison GM

2012-10-01

72

The adult heart responds to increased workload with physiologic hypertrophy, cardiac stem cell activation, and new myocyte formation.  

Science.gov (United States)

AimsIt is a dogma of cardiovascular pathophysiology that the increased cardiac mass in response to increased workload is produced by the hypertrophy of the pre-existing myocytes. The role, if any, of adult-resident endogenous cardiac stem/progenitor cells (eCSCs) and new cardiomyocyte formation in physiological cardiac remodelling remains unexplored.Methods and resultsIn response to regular, intensity-controlled exercise training, adult rats respond with hypertrophy of the pre-existing myocytes. In addition, a significant number (?7%) of smaller newly formed BrdU-positive cardiomyocytes are produced by the exercised animals. Capillary density significantly increased in exercised animals, balancing cardiomyogenesis with neo-angiogenesis. c-kit(pos) eCSCs increased their number and activated state in exercising vs. sedentary animals. c-kit(pos) eCSCs in exercised hearts showed an increased expression of transcription factors, indicative of their commitment to either the cardiomyocyte (Nkx2.5(pos)) or capillary (Ets-1(pos)) lineages. These adaptations were dependent on exercise duration and intensity. Insulin-like growth factor-1, transforming growth factor-?1, neuregulin-1, bone morphogenetic protein-10, and periostin were significantly up-regulated in cardiomyocytes of exercised vs. sedentary animals. These factors differentially stimulated c-kit(pos) eCSC proliferation and commitment in vitro, pointing to a similar role in vivo.ConclusionIntensity-controlled exercise training initiates myocardial remodelling through increased cardiomyocyte growth factor expression leading to cardiomyocyte hypertrophy and to activation and ensuing differentiation of c-kit(pos) eCSCs. This leads to the generation of new myocardial cells. These findings highlight the endogenous regenerative capacity of the adult heart, represented by the eCSCs, and the fact that the physiological cardiac adaptation to exercise stress is a combination of cardiomyocyte hypertrophy and hyperplasia (cardiomyocytes and capillaries). PMID:23100284

Waring, Cheryl D; Vicinanza, Carla; Papalamprou, Angela; Smith, Andrew J; Purushothaman, Saranya; Goldspink, David F; Nadal-Ginard, Bernardo; Torella, Daniele; Ellison, Georgina M

2012-10-25

73

Association between electrocardiographic left ventricular hypertrophy with strain pattern and left ventricular structure and function.  

UK PubMed Central (United Kingdom)

BACKGROUND AND PURPOSE: Electrocardiographic left ventricular hypertrophy (LVH) with strain pattern has been documented as a marker for LVH. Its presence on the ECG of hypertensive patients is associated with poor prognosis. The study was carried out to assess the association of the electrocardiographic strain with left ventricular mass (LVM) and function in hypertensive Nigerians. MATERIAL AND METHODS: ECG as well as echocardiograms were performed in 64 hypertensive patients with ECG-LVH and strain pattern, 65 patients with ECG-LVH by Sokolow-Lyon (SL) voltage criteria and 62 normal controls. RESULTS: The study showed that electrocardiographic left ventricular (LV) strain pattern is associated with dilated left atrium, larger LV internal dimensions and greater absolute and indexed LVM in hypertensive Nigerians compared with ECG-LVH by SL voltage criteria alone or normal controls. CONCLUSION: The findings of this study support the fact that the ECG strain pattern is associated with increased LVM and an increased risk of developing abnormal LV geometry.

Ogah OS; Adebiyi AA; Oladapo OO; Aje A; Ojji DB; Adebayo AK; Salako BL; Falase AO

2006-01-01

74

Prevalencia de hipertrofia ventricular izquierda en pacientes diabéticos/ Prevalence of left ventricular hypertrophy in diabetic patients  

Scientific Electronic Library Online (English)

Full Text Available Abstract in spanish Con el objetivo de establecer la prevalencia de hipertrofia ventricular izquierda (HVI) en pacientes con diabetes mellitus tipo 2 (DM), se realizó un estudio transversal en estos pacientes, estableciendo sus características antropométricas, presión arterial y control metabólico. Para evaluar la presencia de HVI se empleó ecocardiografía transtorácica. El estudio incluyó 91 pacientes, en los cuales la prevalencia de HVI fue de 63,7%, siendo más frecuente en mujer (more) es que en varones (p=0,001). Adicionalmente, se encontró un 46,2% de pacientes con disfunción diastólica del ventrículo izquierdo. Se concluye que existe una importante prevalencia de HVI en pacientes diabéticos sin antecedentes de causas definidas de hipertrofia. No se encontró relación con sexo, control metabólico, IMC y tiempo de diagnóstico Abstract in english In order to establish the prevalence of left ventricular hypertrophy (LVH) in patients with type 2 diabetes mellitus, (DM) a cross-sectional study was conducted in these patients studying their anthropometric characteristics, blood pressure and metabolic control. To evaluate the presence of LVH, a trans-thoracic echocardiogram was used. The study included 91 patients, finding a 63.7% prevalence of HVI, with women being more affected than men (p=0.001). Additionally, 46.2% (more) of patients were found to have diastolic dysfunction of the left ventricle. We conclude that there is an important prevalence of LVH in diabetic patients without defined causes of hypertrophy. There was no association with sex, metabolic control, BMI and time of diagnosis

Valarezo-Sevilla, Diego; Pazmiño-Martínez, Armín; Morales-Mora, Nidya

2013-03-01

75

Non-invasive electrical markers in patients with left ventricular hypertrophy.  

Directory of Open Access Journals (Sweden)

Full Text Available Introduction The left ventricular hypertrophy is related with the genesis of ventricular arrhythmiasand sudden death. Depending of the cause, different histologycalmodifications that generate different arrhythmogenic substrates, takesplace. However, few bibliographical evidences exist about the characterizationof these, with non-invasive electrical markers.Objetive To determine the presence of non-invasive electrical markers in patients withleft ventricular hypertrophy of different causes, and to relate the magnitude,of the same one, with the presence of non-invasive electrical markers.Method In the descriptive study 107 patients, with ecocardiographic diagnosis ofleft ventricular hypertrophy were included. They were assisted at the Institutode Cardiología y Cirugía Cardiovascular, between January 2005 andDecember 2007. They were classified in groups according to the ethiologyof the left ventricular hypertrophy: Pathological left ventricular hypertrophy?that included the patients with left ventricular hypertrophy generated byhigh blood pressure, aortic stenosis and hypertrophic cardiomyopathy?,and physiologic left ventricular hypertrophy ?group formed by athletesfrom the national teams of oar and swimming. They were also included, 35seemingly healthy fellows without left ventricular hypertrophy as controlgroup. We obtained a high resolution electrocardiogram at rest of twelvesimultaneous derivations to determine: the late potentials, the QTc interval,the QT special dispersion, the Tp-Te interval and the Tp-Te dispersion; also,the correlation between these markers and the magnitude of left ventricularhypertrophy was stablished.Results The non-invasive electrical markers prevailed in the group of patients withleft ventricular hypertrophy of pathological cause: the late potentials werepositive in the 37,8% and the abnormal QT space dispersion in 18,3% bothwere statistically significant, the prolonged QTc interval was present in21,9% and the mean Tp-Te dispersion was 48,7±24,9ms, in a non significantway, when comparing them with the group of physiologic cause andthe control group. In the group of pathological left ventricular hypertrophythere was a prevalence of all markers, in patients with hypertrophic cardiomyopathy:the late potentials were positive in 57,1%, the QT space dispersionwas abnormal in 28,6% and the mean Tp-Te interval133,6±37,4ms in a significant manner, when comparing with those thatpresent, aortic stenosis and high blood pressure. The prolonged QTc interval38,1% and the mean of the Tp-Te dispersion were bigger in thegroup of hypertrophic cardiomyopathy 57,1±32,2 ms, although it was notsignificant in relation with the groups of patients who suffer from aorticstenosis and high blood pressure. All markers had a weak correlation withthe magnitude of left ventricular hypertrophy (r=0,179-0,292; p <0,05).Conclusions We concluded that the studied non-invasive electrical markers were morefrequent in the group of patients with pathological left ventricular hypertrophy,and inside this, in the patients with hypertrophic cardiomyopathy andthat a weak correlation exists between the magnitude of hypertrophy andthe presence of these markers.

Nadia Sánchez Torres; Juan A. Álvarez Gómez; Margarita Dorantes Sánchez; Jesús Castro Hevia; Geovedy Martínez García; Irma Fernández Madero

2011-01-01

76

Left ventricular hypertrophy in hypertensive children and adolescents: predictors and prevalence.  

Science.gov (United States)

Left ventricular hypertrophy is an independent predictor of cardiovascular morbidity and mortality in adults. In children, the primary correlate of left ventricular mass (LVM) is lean body mass, but fat mass, gender and systolic blood pressure are also contributors. LVM can be estimated from echocardiographic measurements, and by indexing this allometrically to height to the 2.7 power, the left ventricular mass index (LVMI) can be calculated. LVMI optimizes detection of left ventricular hypertrophy with established normal curves for children from birth to 18 years. In children with sustained hypertension, 8-41 % have LVMI above the 95th percentile and in 10-15.5 % of these, LVMI is elevated above levels associated with increased mortality in adults. The presence of obesity is associated with higher LVMI than is found in children with hypertension alone. In children with chronic kidney disease, left ventricular hypertrophy develops relatively early and becomes more prevalent as kidney function decreases. In summary, left ventricular hypertrophy is a sensitive marker of target organ damage in children with BP elevation, obesity and chronic kidney disease providing important management information. PMID:23893038

Kavey, Rae-Ellen W

2013-10-01

77

Left ventricular hypertrophy in hypertensive children and adolescents: predictors and prevalence.  

UK PubMed Central (United Kingdom)

Left ventricular hypertrophy is an independent predictor of cardiovascular morbidity and mortality in adults. In children, the primary correlate of left ventricular mass (LVM) is lean body mass, but fat mass, gender and systolic blood pressure are also contributors. LVM can be estimated from echocardiographic measurements, and by indexing this allometrically to height to the 2.7 power, the left ventricular mass index (LVMI) can be calculated. LVMI optimizes detection of left ventricular hypertrophy with established normal curves for children from birth to 18 years. In children with sustained hypertension, 8-41 % have LVMI above the 95th percentile and in 10-15.5 % of these, LVMI is elevated above levels associated with increased mortality in adults. The presence of obesity is associated with higher LVMI than is found in children with hypertension alone. In children with chronic kidney disease, left ventricular hypertrophy develops relatively early and becomes more prevalent as kidney function decreases. In summary, left ventricular hypertrophy is a sensitive marker of target organ damage in children with BP elevation, obesity and chronic kidney disease providing important management information.

Kavey RE

2013-10-01

78

Genetic variants predicting left ventricular hypertrophy in a diabetic population: a Go-DARTS study including meta-analysis.  

UK PubMed Central (United Kingdom)

BACKGROUND: Left ventricular hypertrophy has multiple aetiologies including diabetes and genetic factors. We aimed to identify genetic variants predicting left ventricular hypertrophy in diabetic individuals. METHODS: Demographic, echocardiographic, prescribing, morbidity, mortality and genotyping databases connected with the Genetics of Diabetes Audit and Research in Tayside, Scotland project were accurately linked using a patient-specific identifier. Left ventricular hypertrophy cases were identified using echocardiographic data.Genotyping data from 973 cases and 1443 non-left ventricular hypertrophy controls were analysed, investigating whether single nucleotide polymorphisms associated with left ventricular hypertrophy in previous Genome Wide Association Studies predicted left ventricular hypertrophy in our population of individuals with type 2 diabetes. Meta-analysis assessed overall significance of these single nucleotide polymorphisms, which were also used to create gene scores. Logistic regression assessed whether these scores predicted left ventricular hypertrophy. RESULTS: Two single nucleotide polymorphisms previously associated with left ventricular hypertrophy were significant: rs17132261: OR 2.03, 95%?CI 1.10-3.73, p-value 0.02 and rs2292462: OR 0.82, 95% CI 0.73-0.93 and p-value 2.26x10-3. Meta-analysis confirmed rs17132261 and rs2292462 were associated with left ventricular hypertrophy (p=1.03x10-8 and p=5.86x10-10 respectively) and one single nucleotide polymorphisms in IGF1R (rs4966014) became genome wide significant upon meta-analysis although was not significant in our study. Gene scoring based on published single nucleotide polymorphisms also predicted left ventricular hypertrophy in our study.Rs17132261, within SLC25A46, encodes a mitochondrial phosphate transporter, implying abnormal myocardial energetics contribute to left ventricular hypertrophy development. Rs2292462 lies within the obesity-implicated neuromedin B gene. Rs4966014 lies within the IGF1R1 gene. IGF1 signalling is an established factor in cardiac hypertrophy. CONCLUSIONS: We created a resource to study genetics of left ventricular hypertrophy in diabetes and validated our left ventricular hypertrophy phenotype in replicating single nucleotide polymorphisms identified by previous genome wide association studies investigating left ventricular hypertrophy.

Parry HM; Donnelly LA; Van Zuydam N; Doney AS; Elder DH; Morris AD; Struthers AD; Palmer CN; Lang CC

2013-01-01

79

Inhibition of L-type calcium currents by salusin-beta in rat cardiac ventricular myocytes.  

UK PubMed Central (United Kingdom)

Salusin-beta is a new regulatory peptide relevant to the cardiovascular system and exerts negative inotropic effect on ventricular muscle. The purpose of the present study was to determine whether salusin-beta can inhibit cardiac L-type calcium channel current (I(Ca,L)). Using whole-cell voltage-clamp techniques, I(Ca,L) was measured in ventricular myocytes isolated from 12 to 16 weeks rats. Salusin-beta dose-dependently and reversibly reduced the magnitude of I(Ca,L) in rat ventricular myocytes. Neither threshold potential nor the peak potential of current-voltage relationship was affected. Salusin-beta increased the rate of I(Ca,L) inactivation without altering its gating properties. These results suggest salusin-beta inhibited I(Ca,L) by increasing the rate of I(Ca,L) inactivation and the inhibition of L-type Ca(2+) channels induced by salusin-beta may contribute to its negative inotropic effect on ventricular muscle.

Shi JS; Li D; Li N; Lin L; Yang YJ; Tang Y; Sun T; Yuan WJ; Ren AJ

2010-06-01

80

Inhibition of L-type calcium currents by salusin-beta in rat cardiac ventricular myocytes.  

Science.gov (United States)

Salusin-beta is a new regulatory peptide relevant to the cardiovascular system and exerts negative inotropic effect on ventricular muscle. The purpose of the present study was to determine whether salusin-beta can inhibit cardiac L-type calcium channel current (I(Ca,L)). Using whole-cell voltage-clamp techniques, I(Ca,L) was measured in ventricular myocytes isolated from 12 to 16 weeks rats. Salusin-beta dose-dependently and reversibly reduced the magnitude of I(Ca,L) in rat ventricular myocytes. Neither threshold potential nor the peak potential of current-voltage relationship was affected. Salusin-beta increased the rate of I(Ca,L) inactivation without altering its gating properties. These results suggest salusin-beta inhibited I(Ca,L) by increasing the rate of I(Ca,L) inactivation and the inhibition of L-type Ca(2+) channels induced by salusin-beta may contribute to its negative inotropic effect on ventricular muscle. PMID:20307603

Shi, Jing-Song; Li, Dong; Li, Ning; Lin, Li; Yang, Yong-Ji; Tang, Ying; Sun, Tao; Yuan, Wen-Jun; Ren, An-Jing

2010-03-20

 
 
 
 
81

Impact of left ventricular geometry on prognosis in hypertensive patients with left ventricular hypertrophy (the LIFE study)  

DEFF Research Database (Denmark)

AIMS: Less is known about the relation between in-treatment left ventricular (LV) geometry and risk of cardiovascular events. We assessed LV geometric patterns on baseline and annual echocardiograms as time-varying predictors of the primary composite endpoint (cardiovascular death, stroke, and myocardial infarction) in 937 hypertensive patients with LV hypertrophy during 4.8 years losartan- or atenolol-based treatment in the Losartan Intervention for Endpoint reduction in hypertension (LIFE) echocardiography substudy. METHODS AND RESULTS: LV geometry was determined from LV mass/body surface area and relative wall thickness in combination. At end of the study, 52% of patients with initial LV hypertrophy had normal geometry (P < 0.001). In particular, concentric remodelling was reduced by 82% and concentric LV hypertrophy by 84%. Development of LV hypertrophy was seen in <5%. In Cox regression analyses including LV geometric patterns as time-varying variables and adjusting for treatment, Framingham risk score, race, and time-varying systolic blood pressure, the patterns independently predicted higher risk of primary composite endpoints [HR 2.99 (1.16-7.71) for concentric remodelling, HR 1.79 (1.17-2.73) for eccentric hypertrophy, and HR 2.71 (1.13-6.45) for concentric hypertrophy; all P < 0.05]. CONCLUSION: In hypertensive patients with ECG LV hypertrophy, in-treatment LV geometry by echocardiography adds information on risk of cardiovascular events Udgivelsesdato: 2008/11

Gerdts, E.; Cramariuc, D.

2008-01-01

82

Relationship between serum leptin levels and left ventricular hypertrophy  

Directory of Open Access Journals (Sweden)

Full Text Available Objective: Previous studies showed relation between elevated serum leptin levels (SLL) and hypertension. The aim of this study was to evaluate relationship between SLL and left ventricular hypertrophy (LVH) and body mass index (BMI) in obese hypertensive patients.Methods: Eighty patients with newly diagnosed essential hypertension were included in this cross-sectional, case-controlled study. Hypertensive patients were classified as; level-I or level-II according to JNC-VII classification and as normal weighted (18-24.99 kg/m2), over weighted (25-26.99 kg/m2) and obese (27 kg/m2 and above) according to BMI’s. All the patients were evaluated by echocardiography and blood samples were withdrawn for determination SLL. Statistical analysis was performed using Wilcoxon sign rank, Mann Whitney U and Kruskal Wallis tests. Logistic regression analysis was applied for the evaluation of relationship between SLL and clinical variables.Results: Mean levels of arterial blood pressure (ABP) of total 80 patients (36 males and 44 females) was 155±1.1/95.1±0.7 mmHg and the mean age was 48.9±1.3 years. Patients with level I hypertension (n=32) had mean ABP of 149.7±0.5/90.9±0.6 mmHg and with level-II hypertension (n=48) - mean ABP 168.5±1.6/102.9±0.9 mmHg. The mean BMI in normal weighted group (n=26) was 22.7±0.3 kg/m2, over weighted group (n=19)-26.1±0.2 kg/m2 and obese group (n=35)-30.9±0.5 kg/m2. There were no differences in LVH incidence between hypertension level groups and BMI groups (p>0.05). Serum leptin levels were similar in patients with level I and level II hypertension (33.5±2.9 ng/ml and 37.3±3.6ng/ml, respectively, p>0.05). However, leptin levels were higher in obese patients as compared with normal and over weighted patients (40.9±3.2 ng/ml versus 28.5±3.6 ng/ml and 32.8 ± 4.9 ng/ml, p<0.01). Patients with LVH had significantly higher levels of leptin as compared with patients without LVH (51.40±5.1 ng/ml versus 28.30±4.20 ng/ml, p<0.05). Logistic regression analysis demonstrated that SLL independently of blood pressure and BMI is related with LVH (OR - 1.7, %95 CI - 1.2-1.9, p<0.05).Conclusion: Our study showed that elevated serum leptin levels are significantly related with LVH independently of body mass index and level of blood pressure. Thus, elevated SLLs, independently of hypertension level and BMI classification, coexist with LVH. Sympathetic activation or direct cardiac receptor activation or proliferative effects of leptin may be responsible for this coexistence.

Ozgur Kartal; Volkan Inal; Oben Baysan; Kenan Saglam

2008-01-01

83

Does Contractile Ca2+ Control Calcineurin-NFAT Signaling and Pathological Hypertrophy in Cardiac Myocytes?  

Science.gov (United States)

In noncontractile cells, a sustained increase in total cytoplasmic Ca2+ concentration is typically needed to activate the intracellular protein phosphatase calcineurin, leading to dephosphorylation of the transcription factor nuclear factor of activated T cells (NFAT), its nuclear translocation, and induction of gene expression. It remains a mystery exactly how Ca2+-dependent signaling pathways, such as that mediated by calcineurin-NFAT, are regulated in contracting cardiac myocytes given the highly specialized manner in which Ca2+ concentration rhythmically cycles in excitation-contraction coupling. Here, we critically review evidence that supports the hypothesis that calcineurin-NFAT signaling is regulated by contractile Ca2+ transients in cardiac myocytes.

Steven R. Houser (Temple University School of Medicine;Department of Physiology REV); Jeffery D. Molkentin (University of Cincinnati;Cincinnati Department of Pediatrics REV)

2008-06-24

84

Impaired left ventricular filling in hypertensive left ventricular hypertrophy as a marker of the presence of an arrhythmogenic substrate.  

UK PubMed Central (United Kingdom)

OBJECTIVE: To assess the prevalence of ventricular late potentials and ventricular tachycardia in hypertensive subjects with left ventricular hypertrophy and to study their relation to clinical characteristics. SETTING: Teaching and general hospital in Padua. METHODS: 107 hypertensive subjects with echocardiographic signs of left ventricular hypertrophy were studied with signal averaged electrocardiography and 24 hour Holter monitoring. Signal averaged electrocardiogram analysis was performed with high pass filters of 25 Hz, 40 Hz, and 80 Hz. Ventricular late potentials were considered to be present if at least two determinants of the signal averaged electrocardiogram were abnormal in one of the three filters. 70 normotensive subjects served as age matched controls. RESULTS: 25% (27) of the hypertensive subjects and 6% (four) of the controls showed late potentials on signal averaged electrocardiography (P < 0.0001). The hypertensive subjects with late potentials had a higher prevalence of ventricular tachycardia (33%, 9/27) than those without late potentials (13%, 10/80; P = 0.035). Twenty nine per cent (31/107) of the hypertensive subjects had an inversion of the early to atrial filling velocity (E/A ratio < 1) on Doppler analysis of transmitral flow. Within this group the percentage of subjects with late potentials (55%, 17/31) and ventricular tachycardia (42%, 13/31) was much greater than that within the group of subjects without an inverted E/A ratio (13%, 10/76 (P < 0.0001) and 12%, 9/76 (P = 0.001) respectively). In a multivariate analysis only the E/A ratio was related to the presence or absence of either late potentials (P = 0.0001) or ventricular tachycardia (P = 0.0008). Both late potentials and ventricular tachycardia were unrelated to left ventricular mass, geometry, and systolic performance. CONCLUSIONS: A relation was found between the occurrence of ventricular tachycardia and the presence of late potentials in hypertensive subjects with left ventricular hypertrophy. Impaired left ventricular filling was the main marker for the arrhythmogenic substrate present in this disease.

Palatini P; Maraglino G; Accurso V; Sturaro M; Toniolo G; Dovigo P; Baccillieri S

1995-03-01

85

Raloxifene acutely suppresses ventricular myocyte contractility through inhibition of the L-type calcium current  

Science.gov (United States)

The selective oestrogen (ER) receptor modulator, raloxifene, is widely used in the treatment of postmenopausal osteoporosis, but may also possess cardioprotective properties. We investigated whether it directly suppresses myocyte contractility through Ca2+ channel antagonism in a similar way to 17?-oestradiol. Cell shortening and Ca2+ transients were measured in single guinea-pig ventricular myocytes field-stimulated (1 Hz, 37°C) in a superfusion chamber. Electrophysiological recordings were performed using single electrode voltage-clamp. Raloxifene decreased cell shortening (EC50 2.4 ?M) and the Ca2+ transient amplitude (EC50 6.4 ?M) in a concentration-dependent manner. At a concentration of 1 ?M, raloxifene produced a 33±2% (mean±s.e.m) and 24±2% reduction, respectively (P<0.001, n=14 for both parameters). These inhibitory actions were not observed in myocytes that had been incubated with the specific antagonist, ICI 182,780 (10 ?M) (n=11). Raloxifene (1 ?M) shortened action potential durations at 50 and 90% repolarisation (P<0.05 and <0.001, respectively; n=27) and decreased peak L-type Ca2+ current by 45%, from ?5.1±0.5 pA/pF to ?2.8±0.3 pA/pF (P<0.001, n=18). Raloxifene did not significantly alter sarcoplasmic reticulum Ca2+ content, as assessed by integrating the Na+/Ca2+ exchanger currents following rapid caffeine application. The present study provides evidence for direct inhibitory actions of raloxifene on ventricular myocyte contractility, mediated through Ca2+ channel antagonism.

Liew, Reginald; Stagg, Mark A; MacLeod, Kenneth T; Collins, Peter

2004-01-01

86

Mechanisms of the negative inotropic effects of sphingosine-1-phosphate on adult mouse ventricular myocytes.  

Science.gov (United States)

Sphingosine-1-phosphate (S1P) induces a transient bradycardia in mammalian hearts through activation of an inwardly rectifying K(+) current (I(K(ACh))) in the atrium that shortens action potential duration (APD) in the atrium. We have investigated probable mechanisms and receptor-subtype specificity for S1P-induced negative inotropy in isolated adult mouse ventricular myocytes. Activation of S1P receptors by S1P (100 nM) reduced cell shortening by approximately 25% (vs. untreated controls) in field-stimulated myocytes. S1P(1) was shown to be involved by using the S1P(1)-selective agonist SEW2871 on myocytes isolated from S1P(3)-null mice. However, in these myocytes, S1P(3) can modulate a somewhat similar negative inotropy, as judged by the effects of the S1P(1) antagonist VPC23019. Since S1P(1) activates G(i) exclusively, whereas S1P(3) activates both G(i) and G(q), these results strongly implicate the involvement of mainly G(i). Additional experiments using the I(K(ACh)) blocker tertiapin demonstrated that I(K(ACh)) can contribute to the negative inotropy following S1P activation of S1P(1) (perhaps through G(ibetagamma) subunits). Mathematical modeling of the effects of S1P on APD in the mouse ventricle suggests that shortening of APD (e.g., as induced by I(K(ACh))) can reduce L-type calcium current and thus can decrease the intracellular Ca(2+) concentration ([Ca(2+)](i)) transient. Both effects can contribute to the observed negative inotropic effects of S1P. In summary, these findings suggest that the negative inotropy observed in S1P-treated adult mouse ventricular myocytes may consist of two distinctive components: 1) one pathway that acts via G(i) to reduce L-type calcium channel current, blunt calcium-induced calcium release, and decrease [Ca(2+)](i); and 2) a second pathway that acts via G(i) to activate I(K(ACh)) and reduce APD. This decrease in APD is expected to decrease Ca(2+) influx and reduce [Ca(2+)](i) and myocyte contractility. PMID:18024550

Landeen, Lee K; Dederko, Dorothy A; Kondo, Colleen S; Hu, Betty S; Aroonsakool, Nakon; Haga, Jason H; Giles, Wayne R

2007-11-16

87

Calcium current restitution in mammalian ventricular myocytes is modulated by intracellular calcium.  

Science.gov (United States)

Restitution of the conventional L-type calcium current (ICa) was studied in dog or guinea pig ventricular myocytes to understand its time course and regulation. Whole-cell ICa free of other overlapping currents was recorded with a suction pipette. The intracellular environment was varied by intracellular dialysis. The properties of ICa were similar in dog and guinea pig ventricular myocytes, except that the amplitude of ICa was larger in the latter (2.2 +/- 0.5 nA in guinea pig cells and 0.9 +/- 0.2 nA in dog cells, n = 8 for both). In both types of cells during restitution a holding voltage (Vh) negative to -50 mV induced a transient increase in ICa above the control level (ICa overshoot). This overshoot was inhibited by substituting barium for calcium, lowering [Ca]0, increasing intracellular calcium buffering capacity, ryanodine (1-2 microM), or caffeine (10 mM). The overshoot peaked 30-100 msec after repolarization from the conditioning depolarization and gradually declined over the following 2-3 seconds. During the overshoot, although the amplitude of ICa was larger its half-time of decay was longer than the control. The maximum overshoot occurred following a conditioning step to plateau voltages and it was decreased by prolonging the conditioning step from 50 to 100 or 500 msec. It is concluded that intracellular calcium regulates restitution of the L-type calcium channels in mammalian ventricular myocytes and that the sarcoplasmic reticulum is involved in this process. PMID:2456166

Tseng, G N

1988-08-01

88

Calcium current restitution in mammalian ventricular myocytes is modulated by intracellular calcium.  

UK PubMed Central (United Kingdom)

Restitution of the conventional L-type calcium current (ICa) was studied in dog or guinea pig ventricular myocytes to understand its time course and regulation. Whole-cell ICa free of other overlapping currents was recorded with a suction pipette. The intracellular environment was varied by intracellular dialysis. The properties of ICa were similar in dog and guinea pig ventricular myocytes, except that the amplitude of ICa was larger in the latter (2.2 +/- 0.5 nA in guinea pig cells and 0.9 +/- 0.2 nA in dog cells, n = 8 for both). In both types of cells during restitution a holding voltage (Vh) negative to -50 mV induced a transient increase in ICa above the control level (ICa overshoot). This overshoot was inhibited by substituting barium for calcium, lowering [Ca]0, increasing intracellular calcium buffering capacity, ryanodine (1-2 microM), or caffeine (10 mM). The overshoot peaked 30-100 msec after repolarization from the conditioning depolarization and gradually declined over the following 2-3 seconds. During the overshoot, although the amplitude of ICa was larger its half-time of decay was longer than the control. The maximum overshoot occurred following a conditioning step to plateau voltages and it was decreased by prolonging the conditioning step from 50 to 100 or 500 msec. It is concluded that intracellular calcium regulates restitution of the L-type calcium channels in mammalian ventricular myocytes and that the sarcoplasmic reticulum is involved in this process.

Tseng GN

1988-08-01

89

Left ventricular filling patterns in patients with systemic hypertension and left ventricular hypertrophy (the LIFE study). Losartan Intervention For Endpoint  

DEFF Research Database (Denmark)

Abnormal left ventricular (LV) filling may exist in early stages of hypertension. Whether this finding is related to LV hypertrophy is currently controversial. This study was undertaken to assess relations between abnormal diastolic LV filling and LV geometry in a large series of hypertensive patients with electrocardiographic LV hypertrophy. M-mode, 2-dimensional, and pulsed Doppler echocardiographic recordings of mitral inflow velocity and isovolumetric relaxation time (IVRT) were obtained in 750 patients with stage I to III hypertension and LV hypertrophy determined by electrocardiography (sex-adjusted Cornell voltage duration criteria or Sokolow-Lyon voltage criteria) after 14 days of placebo treatment. The patients' mean age was 67+/-7 years and 44% were women. One hundred forty patients (19%) had normal LV geometric pattern, 79 (11%) had concentric remodeling, 342 (45%) had eccentric LV hypertrophy, and 189 (25%) had concentric LV hypertrophy. A normal LV filling pattern was found in 116 patients (16%),abnormal relaxation in 519 (69%), "pseudonormal" filling was found in 83 (11%), and a restrictive filling pattern in 32 (4%). Prolonged IVRT was associated with LV hypertrophy (p

Wachtell, K; Smith, G

2000-01-01

90

Calcium current in isolated neonatal rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

1. Calcium currents (ICa) from neonatal rat ventricular heart muscle cells grown in primary culture were examined using the 'whole-cell' voltage-clamp technique (Hamill, Marty, Neher, Sakmann & Sigworth, 1981). Examination of ICa was limited to one calcium channel type, 'L' type (Nilius, Hess, Lansman & Tsien, 1985), by appropriate voltage protocols. 2. We measured transient and steady-state components of ICa, and could generally describe ICa in terms of the steady-state activation (d infinity) and inactivation (f infinity) parameters. 3. We observed that the reduction of ICa by the calcium channel antagonist D600 can be explained by both a shift of d infinity to more positive potentials as well as a slight reduction of ICa conductance. D600 did not significantly alter either the rate of inactivation of ICa or the voltage dependence of f infinity. 4. The calcium channel modulator BAY K8644 shifted both d infinity and f infinity to more negative potentials. Additionally, BAY K8644 increased the rate of inactivation at potentials between +5 and +55 mV. Furthermore, BAY K8644 also increased ICa conductance, a change consistent with a promotion of 'mode 2' calcium channel activity (Hess, Lansman & Tsien, 1984). 5. We conclude that, as predicted by d infinity and f infinity, there is a significant steady-state component of ICa ('window current') at plateau potentials in neonatal rat heart cells. Modulation of the steady-state and transient components of ICa by various agents can be attributed both to specific alterations in d infinity and f infinity and to more complicated alterations in the mode of calcium channel activity.

Cohen NM; Lederer WJ

1987-10-01

91

Protective effect of left ventricular hypertrophy in right coronary artery occlusions  

Scientific Electronic Library Online (English)

Full Text Available Abstract in english OBJECTIVE: To test the hypothesis that left ventricular hypertrophy (LVH) reduces the electrocardiographic and functional effects of right coronary artery occlusion. METHODS: We analysed 215 patients (166 males and 49 women,age of 58.9±10.6 years), with occlusion of the right coronary artery without other associated lesions. There was no significant difference (p>0.05) in age and gender distribution between the 78 patients with LVH (left ventricular mass >100g/m²) (Grou (more) p A) when compared with the 137 patients without LVH (left ventricular mass

Gomes, Marne de Freitas; Gottschall, Carlos Antônio Mascia

1999-02-01

92

Left ventricular hypertrophy in Turner syndrome : a prospective echocardiographic study  

DEFF Research Database (Denmark)

Cardiovascular risk stratification in Turner syndrome (TS) is difficult. Increased left ventricular mass associates with an adverse prognosis in several settings, and this study aimed to elucidate this risk marker in relation to metabolic and cardiovascular status in TS.

Mortensen, Kristian Havmand; Gravholt, Claus HØjbjerg

2012-01-01

93

Left atrial systolic force in hypertensive patients with left ventricular hypertrophy: the LIFE study  

DEFF Research Database (Denmark)

In hypertensive patients without prevalent cardiovascular disease, enhanced left atrial systolic force is associated with left ventricular hypertrophy and increased preload. It also predicts cardiovascular events in a population with high prevalence of obesity. Relations between left atrial systolic force and left ventricular geometry and function have not been investigated in high-risk hypertrophic hypertensive patients. Participants in the Losartan Intervention For Endpoint reduction in hypertension echocardiography substudy without prevalent cardiovascular disease or atrial fibrillation (n = 567) underwent standard Doppler echocardiography. Left atrial systolic force was obtained from the mitral orifice area and Doppler mitral peak A velocity. Patients were divided into groups with normal or increased left atrial systolic force (>14.33 kdyn). Left atrial systolic force was high in 297 patients (52.3%), who were older and had higher body mass index and heart rate (all P < 0.01) but similar systolic and diastolic blood pressure, in comparison with patients with normal left atrial systolic force. After controlling for confounders, increased left atrial systolic force was associated with larger left ventricular diameter and higher left ventricular mass index (both P < 0.01). Prevalence of left ventricular hypertrophy was greater (84 vs. 64%; P < 0.001). Participants with increased left atrial systolic force exhibited normal ejection fraction; higher stroke volume, cardiac output, transmitral peak E velocities and peak A velocities; and lower E/A ratio (all P < 0.01). Enhanced left atrial systolic force identifies hypertensive patients with greater left ventricular mass and prevalence of left ventricular hypertrophy, but normal left ventricular chamber systolic function with increased transmitral flow gradient occurring during early filling, consistent with increased preload Udgivelsesdato: 2008/7

Chinali, M.; Simone, G. de

2008-01-01

94

Pressure mediated hypertrophy and mechanical stretch up-regulate expression of the long form of leptin receptor (ob-Rb) in rat cardiac myocytes  

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Full Text Available Abstract Background Hyperleptinemia is known to participate in cardiac hypertrophy and hypertension, but the relationship between pressure overload and leptin is poorly understood. We therefore examined the expression of leptin (ob) and the leptin receptor (ob-R) in the pressure-overloaded rat heart. We also examined gene expressions in culture cardiac myocytes to clarify which hypertension-related stimulus induces these genes. Results Pressure overload was produced by ligation of the rat abdominal aorta, and ob and ob-R isoform mRNAs were measured using a real-time polymerase chain reaction (PCR). We also measured these gene expressions in neonatal rat cardiac myocytes treated with angiotensin II (ANGII), endothelin-1 (ET-1), or cyclic mechanical stretch. Leptin and the long form of the leptin receptor (ob-Rb) gene were significantly increased 4?weeks after banding, but expression of the short form of the leptin receptor (ob-Ra) was unchanged. ob-Rb protein expression was also detected by immunohistochemistry in hypertrophied cardiac myocytes after banding. Meanwhile, plasma leptin concentrations were not different between the control and banding groups. In cultured myocytes, ANGII and ET-1 increased only ob mRNA expression. However, mechanical stretch activated both ob and ob-Rb mRNA expression in a time-dependent manner, but ob-Ra mRNA was unchanged by any stress. Conclusions We first demonstrated that both pressure mediated hypertrophy and mechanical stretch up-regulate ob-Rb gene expression in heart and cardiac myocytes, which are thought to be important for leptin action in cardiac myocytes. These results suggest a new local mechanism by which leptin affects cardiac remodeling in pressure-overloaded hearts.

Matsui Hiroki; Yokoyama Tomoyuki; Tanaka Chie; Sunaga Hiroaki; Koitabashi Norimichi; Takizawa Takako; Arai Masashi; Kurabayashi Masahiko

2012-01-01

95

Influence of left ventricular hypertrophy on infarct size and left ventricular ejection fraction in ST-elevation myocardial infarction  

International Nuclear Information System (INIS)

[en] Background: Left ventricular hypertrophy (LVH) predisposes to larger infarct size, which may be underestimated by the left ventricular ejection fraction (LVEF) due to supranormal systolic performance often present in patients with LVH. The aim of the study was to compare infarct size and LVEF in patients with ST-segment elevation myocardial infarction (STEMI) and increased left ventricular mass on cardiac magnetic resonance (CMR). Methods: The study included unselected group of 52 patients (61 ± 11 years, 69% male) with first STEMI who had CMR after median 5 days from the onset of the event. Left ventricular hypertrophy (LVH) was defined as left ventricular mass index exceeding 95th percentile of references values for age and gender. Infarct size was assessed with means of late gadolinium enhancement (LGE). Results: LVH was found in 16 patients (31%). In comparison to the rest of the group, patients with LVH had higher absolute and relative infarct mass (p = 0.002 and p = 0.02, respectively). LVH was related to higher prevalence of microvascular obstruction and myocardial haemorrhage and higher number of LV segments with transmural necrosis (p = 0.02, p = 0.01 and p = 0.01, respectively). Despite marked difference in the infarct size between both studied subgroups there was no difference in LVEF and mean number of dysfunctional LV segments. Conclusions: Patients with LVH undergoing STEMI have larger infarct size underestimated by the LV systolic performance in comparison to patients without LVH.

2012-01-01

96

Evaluation of myocardial function in the presence of left ventricular hypertrophy in athletes and hypertensive patients  

Directory of Open Access Journals (Sweden)

Full Text Available Introduction Myocardial hypertrophy of the left ventricle may be of physiological or pathological nature. Distinction of these two types of hypertrophy is sometimes not easy and represents a diagnostic challenge. The aim of the study was to assess global diastolic and regional systolic and diastolic myocardial function in the presence of left ventricular hypertrophy in athletes and hypertensive patients. Material and methods In 18 male hypertensive patients and 14 male athletes global diastolic left ventriclar function and regional systolic and diastolic myocardial function of septum and posterior wall were investigated by pulsed wave tissue Doppler imaging. Results Ejection fraction and left ventricle mass index did not differ significantly between two groups. Hypertensive patients were found to have diastolic dysfunction while athletes had normal left ventricular diastolic function (the difference between the groups was P<0.00001). Index of regional diastolic function of septum as well as of the posterior wall was significantly less in hypertensive patients than in athletes (P<0.00001 for both). In spite of the normal global systolic function the regional systolic function of septum and posterior wall was significantly less in hypertensive patients than in athletes (P<0.02for both). Conclusion The present results show significantly less global and regional diastolic function of hypertrophied myocardium in hypertensive patients than in athletes. In the presence of preserved left ventricular systolic function, the quantification of myocardial velocity revealed significantly lower regional systolic function of septum and posterior wall in hypertensive patients than in athletes.

Deljanin-Ili? Marina; Ili? Stevan; ?or?evi? Dragan; Zdravkovi? Marija; Ili? Vladimir

2008-01-01

97

Functional cross-talk between aldosterone and angiotensin-(1-7) in ventricular myocytes.  

UK PubMed Central (United Kingdom)

High serum levels of aldosterone have been linked to the development of cardiac disease. In contrast, angiotensin (Ang)-(1-7) was extensively shown to possess cardioprotective effects, including the attenuation of cardiac dysfunction induced by excessive mineralocorticoid activation in vivo, suggesting possible interactions between these 2 molecules. Here, we investigated whether there is cross-talk between aldosterone and Ang-(1-7) and its functional consequences for calcium (Ca(2+)) signaling in ventricular myocytes. Short-term effects of aldosterone on Ca(2+) transient were assessed in Fluo-4/AM-loaded myocytes. Confocal images showed that Ang-(1-7) had no effect on Ca(2+) transient parameters, whereas aldosterone increased the magnitude of the Ca(2+) transient. Quite unexpectedly, addition of Ang-(1-7) to aldosterone-treated myocytes further enhanced the amplitude of the Ca(2+) transient suggesting a synergistic effect of these molecules. Aldosterone action on Ca(2+) transient amplitude was mediated by protein kinase A, and was related to an increase in Ca(2+) current (I(Ca)) density. Both changes were not altered by Ang-(1-7). When cardiomyocytes were exposed to aldosterone, increased Ca(2+) spark rate was measured. Ang-(1-7) prevented this change. In addition, a NO synthase inhibitor restored the effect of aldosterone on Ca(2+) spark rate in Ang-(1-7)-treated myocytes and attenuated the synergistic effect of these 2 molecules on Ca(2+) transient. These results indicate that NO plays an important role in this cross-talk. Our results bring new perspectives in the understanding of how 2 prominent molecules with supposedly antagonist cardiac actions cross-talk to synergistically amplify Ca(2+) signals in cardiomyocytes.

de Almeida PW; de Freitas Lima R; de Morais Gomes ER; Rocha-Resende C; Roman-Campos D; Gondim AN; Gavioli M; Lara A; Parreira A; de Azevedo Nunes SL; Alves MN; Santos SL; Alenina N; Bader M; Resende RR; dos Santos Cruz J; Souza dos Santos RA; Guatimosim S

2013-02-01

98

Effects of astragaloside IV on action potentials and ionic currents in guinea-pig ventricular myocytes.  

UK PubMed Central (United Kingdom)

Astragaloside IV (AS-IV) is one of the main active constituents of Astragalus membranaceus, which has various actions on the cardiovascular system. However, its electrophysiological mechanisms are not clear. In the present study, we investigated the effects of AS-IV on action potentials and membrane currents using the whole-cell patch clamp technique in isolated guinea-pig ventricular myocytes. AS-IV prolonged the action potential duration (APD) at all three tested concentrations. The peak effect was achieved with 1×10(-6) M, at which concentration AS-IV significantly prolonged the APD at 95% repolarization from 313.1±38.9 to 785.3±83.7 ms. AS-IV at 1×10(-6) M also enhanced the inward rectifier K(+) currents (I(K1)) and inhibited the delayed rectifier K(+) currents (I(K)). AS-IV (1×10(-6) M) strongly depressed the peak of voltage-dependent Ca(2+) channel current (I(CaL)) from -607.3±37.5 to -321.1±38.3 pA. However, AS-IV was not found to affect the Na(+) currents. Taken together, AS-IV prolonged APD of guinea-pig ventricular myocytes, which might be explained by its inhibition of I(K). AS-IV also influences Ca(2+) signaling through suppressing ICaL.

Zhao M; Zhao J; He G; Sun X; Huang X; Hao L

2013-01-01

99

Propafenone and its metabolites preferentially inhibit IKr in rabbit ventricular myocytes.  

UK PubMed Central (United Kingdom)

Propafenone is an antiarrhythmic agent with recognized cardiac myocyte repolarizing K+ current inhibitory effects. It has two known electropharmacologically active metabolites, 5-hydroxy- and N-depropylpropafenone, whose K+ current inhibitory effects are less thoroughly elucidated than those of the parent compound. This study characterizes and directly compares the pharmacologic interaction of all three compounds with two key repolarizing K+ currents, the rapidly activating delayed rectifier IKr and the transient outward current Ito, using the whole-cell patch-clamp technique in isolated rabbit ventricular myocytes. All three agents potently inhibited IKr with IC50 values of 0.80 +/-0.14, 1.88 +/-0.21, and 5.78 +/-1.24 microM for propafenone, 5-hydroxypropafenone, and N-depropylpropafenone, respectively, based on reduction of peak tail current amplitude following repolarization from +50 mV to -30 mV. IKr inhibition was concentration- and weakly voltage-dependent, with a time course from channel activation that was well described by a single exponential model and consistent with open channel block. Propafenone and its 5-hydroxy and N-depropyl metabolites also blocked Ito with IC50 values of 7.27 +/-0.53, 40.29 +/-7.55, and 44.26 +/-5.73 microM, respectively, at +50 mV. No significant drug effects were observed with respect to Ito voltage dependence of steady-state inactivation or time course of recovery from inactivation. The preferential interaction of propafenone and its metabolites with IKr relative to Ito in ventricular myocytes sheds new light on the anti- and proarrhythmic activity of propafenone in vivo.

Cahill SA; Gross GJ

2004-01-01

100

Exogenous and endogenous ceramides elicit volume-sensitive chloride current in ventricular myocytes.  

UK PubMed Central (United Kingdom)

AIMS: Because ceramide accumulates in several forms of cardiovascular disease and ceramide-induced apoptosis may involve the volume-sensitive Cl(-) current, I(Cl,swell), we assessed whether ceramide activates I(Cl,swell). METHODS AND RESULTS: I(Cl,swell) was measured in rabbit ventricular myocytes by whole-cell patch clamp after isolating anion currents. Exogenous C(2)-ceramide (C(2)-Cer), a membrane-permeant short-chain ceramide, elicited an outwardly rectifying Cl(-) current in both physiological and symmetrical Cl(-) solutions that was fully inhibited by DCPIB, a specific I(Cl,swell) blocker. In contrast, the metabolically inactive C(2)-Cer analogue C(2)-dihydroceramide (C(2)-H(2)Cer) failed to activate Cl(-) current. Bacterial sphingomyelinase (SMase), which generates endogenous long-chain ceramides as was confirmed by tandem mass spectrometry, also elicited an outwardly rectifying Cl(-) current that was inhibited by DCPIB and tamoxifen, another I(Cl,swell) blocker. Bacterial SMase-induced current was partially reversed by osmotic shrinkage and fully suppressed by ebselen, a scavenger of reactive oxygen species. Outward rectification with physiological and symmetrical Cl(-) gradients, block by DCPIB and tamoxifen, and volume sensitivity are characteristics that identify I(Cl,swell). Insensitivity to C(2)-H(2)Cer and block by ebselen suggest involvement of ceramide signalling rather than direct lipid-channel interaction. CONCLUSION: Exogenous and endogenous ceramide elicited I(Cl,swell) in ventricular myocytes. This may contribute to persistent activation of I(Cl,swell) and aspects of altered myocyte function in cardiovascular diseases associated with by ceramide accumulation.

Raucci FJ Jr; Wijesinghe DS; Chalfant CE; Baumgarten CM

2010-04-01

 
 
 
 
101

Effects of nifedipine on left ventricular systolic and diastolic functions in patients with left ventricular hypertrophy  

International Nuclear Information System (INIS)

[en] The effect of nifedpine on left ventricular (LV) systolic and diastolic function was studied in 10 patients with hypertrophic cadiomyopathy(HCM), 8 patients with hypertensive hypertrophy(HT) and 9 normal subjects. Multigated cardiac blood pool imaging with Tc-99m were obtained at 40-degree left anterior oblique position before and after nifedipine administration (10 mg, sublingually). As systolic indices, we obtained LV ejection fraction and mean first third ejection rate. And as diastolic indices, mean filling rate during first third of diastole (1/3 FRsub(mean)) and diastolic maximal filling rate were calculated. Before nifedipine, systolic indices were significantly superior in HCM group than in other 2 groups, and diastolic indices were significantly lower in HCM and HT groups than in normal. After nifedipine, systolic indices improved in HT group but they did not change in other 2 groups. Diastolic indices improved significantly in HCM and HT groups after nifedpine. In HCM group, 1/3 FRsub(mean) improved more markedly in symptomatic patients than in asymptomatic patients. The ratio of diastolic function to systolic function (1/3 FRsub(mean)/1/3 ERsub(mean)) did not change in normal and HT groups but it increased significantly in HCM group. There we a slight increase in heart rate (HR) and decrease in systemic arterial pressure (BP). The increase in HR was similar among 3 groups but the decrease in BP was significantly greater in HT group in whom control BP was significantly higher than other groups. LV end-diastolic volume did not change in 3 groups by nifedipine administration. These data suggested that abnormal diastolic function in HCM and HT was faborably modified by nifedipine, but their mechanisms were different. In HT, it was considered to relate with improved systolic function due to LV afterload reduction, while in HCM, it was not related to the peripheral hemodynamic effects nor improved systolic function. (author)

1984-01-01

102

Effects of nifedipine on left ventricular systolic and diastolic functions in patients with left ventricular hypertrophy  

Energy Technology Data Exchange (ETDEWEB)

The effect of nifedpine on left ventricular (LV) systolic and diastolic function was studied in 10 patients with hypertrophic cadiomyopathy(HCM), 8 patients with hypertensive hypertrophy(HT) and 9 normal subjects. Multigated cardiac blood pool imaging with Tc-99m were obtained at 40-degree left anterior oblique position before and after nifedipine administration (10 mg, sublingually). As systolic indices, we obtained LV ejection fraction and mean first third ejection rate. And as diastolic indices, mean filling rate during first third of diastole (1/3 FRsub(mean)) and diastolic maximal filling rate were calculated. Before nifedipine, systolic indices were significantly superior in HCM group than in other 2 groups, and diastolic indices were significantly lower in HCM and HT groups than in normal. After nifedipine, systolic indices improved in HT group but they did not change in other 2 groups. Diastolic indices improved significantly in HCM and HT groups after nifedpine. In HCM group, 1/3 FRsub(mean) improved more markedly in symptomatic patients than in asymptomatic patients. The ratio of diastolic function to systolic function (1/3 FRsub(mean)/1/3 ERsub(mean)) did not change in normal and HT groups but it increased significantly in HCM group. There we a slight increase in heart rate (HR) and decrease in systemic arterial pressure (BP). The increase in HR was similar among 3 groups but the decrease in BP was significantly greater in HT group in whom control BP was significantly higher than other groups. LV end-diastolic volume did not change in 3 groups by nifedipine administration. These data suggested that abnormal diastolic function in HCM and HT was faborably modified by nifedipine, but their mechanisms were different. In HT, it was considered to relate with improved systolic function due to LV afterload reduction, while in HCM, it was not related to the peripheral hemodynamic effects nor improved systolic function.

Narita, Michihiro; Kurihara, Tadashi; Murano, Kenichi; Usami, Masahisa; Honda, Minoru; Kanao, Keisuke (Sumitomo Hospital, Osaka (Japan))

1984-10-01

103

[Vector-echocardiographic correlations in type B right ventricular hypertrophy  

UK PubMed Central (United Kingdom)

The correlation between the right posterior surface of the QRS complex in the horizontal plane and the various parameters characterizing the right ventricle on TM and 2D echocardiography on left parasternal longitudinal sections and subcostal sections was investigated by the Chi-square independence test and Student's t test in 185 cases of heart disease due to various aetiologies. The right posterior surface (Octant III) of the QRS complex in the horizontal plane is independent of the diastolic thickness of the right ventricular posterior wall (RVPW); the diastolic thickness of the right ventricular anterior wall (RVAW); the right ventricular ejection fraction (RVEF); the systolic diameter and diastolic diameter of the right ventricle; the percentage thickening of the RVPW and the RVAW; and, finally, there is no significant relationship between the diastolic thickness of the RVPW and that of the RVAW. Its variance according to the presence or absence and the nature of an associated conduction disorder (RBBB, RIBBB, RBBB + LAHB, LAHB, LBBB, LIBBB or Kent) was not significant for a risk of error of 5% and 1%. The right posterior surface (Octant III) of the QRS complex in the horizontal plane is significantly correlated with the right ventricular mass (RVM), calculated from the diastolic thickness of the right ventricular posterior wall (RVPW): alpha < 0.001; according to a simplified formula: RVM g/m2 = (RVDD + 2 RVPW)3. The correlation between these last two quantitative parameters is borderline significant r = 0.11 t = 1.25, 0.20 < alpha < 0.30 according to a linear regression equation: y = 55.15-34.71 x; Po = 549 t = 1.48, increasing from 0 to 0.137 and decreasing beyond 0.137, linearity hypothesis: admissible, p = 0.04.

Hayat JC

1996-05-01

104

[Vector-echocardiographic correlations in type B right ventricular hypertrophy].  

Science.gov (United States)

The correlation between the right posterior surface of the QRS complex in the horizontal plane and the various parameters characterizing the right ventricle on TM and 2D echocardiography on left parasternal longitudinal sections and subcostal sections was investigated by the Chi-square independence test and Student's t test in 185 cases of heart disease due to various aetiologies. The right posterior surface (Octant III) of the QRS complex in the horizontal plane is independent of the diastolic thickness of the right ventricular posterior wall (RVPW); the diastolic thickness of the right ventricular anterior wall (RVAW); the right ventricular ejection fraction (RVEF); the systolic diameter and diastolic diameter of the right ventricle; the percentage thickening of the RVPW and the RVAW; and, finally, there is no significant relationship between the diastolic thickness of the RVPW and that of the RVAW. Its variance according to the presence or absence and the nature of an associated conduction disorder (RBBB, RIBBB, RBBB + LAHB, LAHB, LBBB, LIBBB or Kent) was not significant for a risk of error of 5% and 1%. The right posterior surface (Octant III) of the QRS complex in the horizontal plane is significantly correlated with the right ventricular mass (RVM), calculated from the diastolic thickness of the right ventricular posterior wall (RVPW): alpha RVDD + 2 RVPW)3. The correlation between these last two quantitative parameters is borderline significant r = 0.11 t = 1.25, 0.20 < alpha < 0.30 according to a linear regression equation: y = 55.15-34.71 x; Po = 549 t = 1.48, increasing from 0 to 0.137 and decreasing beyond 0.137, linearity hypothesis: admissible, p = 0.04. PMID:8763647

Hayat, J C

1996-05-01

105

Acetylcholine and adenosine activate the G protein-gated muscarinic K+ channel in ferret ventricular myocytes.  

UK PubMed Central (United Kingdom)

The properties of the K+ channel activated by acetylcholine (ACh) and adenosine (Ado) were examined in single ferret ventricular myocytes using patch-clamp techniques. In the whole-cell configuration, ACh and Ado induced an inwardly rectifying K+ current and shortened the action potential duration. The effect of ACh was blocked by atropine, while the Ado effect was interrupted by 8-cyclopentyl,1,2-dipropyl xanthine, a specific Ado A1 receptor antagonist. In cell-attached recordings, ACh and Ado added to the pipette solution activated a single population of inwardly rectifying K+ channels, distinct from the iK1 channel. The channel had a slope conductance of approximately 40 pS in symmetrical 150 mM K+ solutions and a mean open time of 0.8 ms. Excision of the patch into the inside-out patch configuration in guanosine triphosphate (GTP)-free solution abolished the channel activity. The channel was reversibly reactivated by adding GTP to the intracellular side of the patch. GTP gamma S activated the channel irreversibly. When the inside-out patch was treated with the A protomer of pertussis toxin (PTX), intracellular GTP no longer activated the K+ channel. The results show that ferret ventricular myocytes possess a K+ channel activated by both muscarinic and Ado A1 receptors. Its electrophysiological properties and the gating by a PTX-sensitive G protein in a membrane-delimited fashion are identical with those of the muscarinic K+ channels in nodal and atrial tissues of other species. In conclusion, the G protein-gated muscarinic K+ channel is expressed in ferret ventricular myocardium and may underlie the direct negative inotropism of ACh and Ado in this tissue.

Ito H; Hosoya Y; Inanobe A; Tomoike H; Endoh M

1995-06-01

106

Laminar arrangement of ventricular myocytes influences electrical behavior of the heart.  

Science.gov (United States)

The response of the heart to electrical shock, electrical propagation in sinus rhythm, and the spatiotemporal dynamics of ventricular fibrillation all depend critically on the electrical anisotropy of cardiac tissue. A long-held view of cardiac electrical anisotropy is that electrical conductivity is greatest along the myocyte axis allowing most rapid propagation of electrical activation in this direction, and that conductivity is isotropic transverse to the myocyte axis supporting a slower uniform spread of activation in this plane. In this context, knowledge of conductivity in two directions, parallel and transverse to the myofiber axis, is sufficient to characterize the electrical action of the heart. Here we present new experimental data that challenge this view. We have used a novel combination of intramural electrical mapping, and experiment-specific computer modeling, to demonstrate that left ventricular myocardium has unique bulk conductivities associated with three microstructurally-defined axes. We show that voltage fields induced by intramural current injection are influenced by not only myofiber direction, but also the transmural arrangement of muscle layers or myolaminae. Computer models of these experiments, in which measured 3D tissue structure was reconstructed in-silico, best matched recorded voltages with conductivities in the myofiber direction, and parallel and normal to myolaminae, set in the ratio 4:2:1, respectively. These findings redefine cardiac tissue as an electrically orthotropic substrate and enhance our understanding of how external shocks may act to successfully reset the fibrillating heart into a uniform electrical state. More generally, the mechanisms governing the destabilization of coordinated electrical propagation into ventricular arrhythmia need to be evaluated in the light of this discovery. PMID:17947797

Hooks, Darren A; Trew, Mark L; Caldwell, Bryan J; Sands, Gregory B; LeGrice, Ian J; Smaill, Bruce H

2007-10-18

107

Retrograde hot-shot cardioplegia in patients with left ventricular hypertrophy undergoing aortic valve replacement.  

UK PubMed Central (United Kingdom)

BACKGROUND: Intermittent antegrade cold-blood cardioplegia followed by terminal warm-blood cardioplegic reperfusion or hot-shot is reported to reduce myocardial injury in the setting of coronary surgery. The efficacy of this cardioplegic technique in patients with left ventricular hypertrophy secondary to aortic stenosis remains uncertain. METHODS: Thirty-six patients with left ventricular hypertrophy undergoing aortic valve replacement were prospectively randomized to cold-blood cardioplegia either alone (cold-blood cardioplegia group) or with retrograde hot-shot (hot-shot group). Reperfusion injury was assessed by measuring myocardial levels of adenosine triphosphate and lactate in left and right ventricular biopsies taken 5 minutes after institution of cardiopulmonary bypass and 20 minutes after removal of cross-clamp using high-performance liquid chromatography and enzymatic techniques. Myocardial injury was assessed by serial release of troponin I up to 48 hours postoperatively. Overall clinical outcome was prospectively collected. RESULTS: Baseline and intraoperative characteristics were similar between groups. In the hot-shot group, there were no significant changes in the myocardial concentration of adenosine triphosphate and lactate in both left and right ventricular biopsies after reperfusion. In the cold-blood cardioplegia group, there was a trend to a fall in adenosine triphosphate levels in the left and right ventricular biopsies after reperfusion, but this reached statistical significance only in the right ventricle. Troponin I release was raised in both groups at 4 and 12 hours after surgery (p < 0.05), but did not reach levels of myocardial infarction. CONCLUSIONS: The terminal retrograde hot-shot reperfusion does not add any extra benefit to antegrade cold-blood cardioplegia in preventing myocardial injury in patients with left ventricular hypertrophy undergoing aortic valve replacement. Nevertheless, it appears to reduce ischemic stress in the right ventricle. There was no difference in clinical outcome between groups.

Ascione R; Suleiman SM; Angelini GD

2008-02-01

108

Caffeine-induced decreases in the inward rectifier potassium and the inward calcium currents in rat ventricular myocytes.  

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The effects of high (20 mM) concentrations of caffeine were studied on the transmembrane voltage and currents in rat single ventricular myocytes by the whole cell configuration of the patch clamp technique. Rapid application of caffeine released Ca2+ from the sarcoplasmic reticulum and induced a Ni(...

Varro, A.; Hester, S.; Papp, J. G.

109

Effects of propafenone on electrical and mechanical activities of single ventricular myocytes isolated from guinea-pig hearts.  

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1. The effects of propafenone on the transmembrane action potential and sarcomere shortening during twitch contraction were investigated in single ventricular myocytes isolated from guinea-pig hearts. 2. Propafenone at low concentrations (3-5 x 10(-7) M) slightly lengthened action potential duration...

Honjo, H.; Watanabe, T.; Kamiya, K.; Kodama, I.; Toyama, J.

110

Effect of N-feruloyl tyramine (an analogue of tyramine) on inwardly rectifying potassium channel in frog ventricular myocytes ???????N-????????????????????????????????????????  

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Electrophysiological effects of N-feruloyl tyramine (NFT), an analogue of tyramine, on potassium currents in frog ventricular myocytes were examined using single-channel recording and whole-cell voltage clamp technique. Extracellular application of NFT induced a concentration-dependent decrease of m...

??, ?; ????, ???; Munemori, Makoto

111

Ca Sparks Do Not Explain all Ryanodine Receptor-Mediated SR Ca Leak in Mouse Ventricular Myocytes  

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Diastolic Ca leak from the sarcoplasmic reticulum (SR) of ventricular myocytes reduces the SR Ca content, stabilizing the activity of the SR Ca release channel ryanodine receptor for the next beat. SR Ca leak has been visualized globally using whole-cell fluorescence, or locally using confocal micro...

Santiago, Demetrio J.; Curran, Jerald W.; Bers, Donald M.; Lederer, W.J.; Stern, Michael D.; Ríos, Eduardo; Shannon, Thomas R.

112

Echocardiographic Partition Values and Prevalence of Left Ventricular Hypertrophy in Hypertensive Jamaicans  

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Full Text Available Left ventricular hypertrophy (LVH) detected by either electrocardiography or echo- cardiography has been shown to be an extremely strong predictor of morbidity and mortality in patients with essential hypertension and in members of the general population. Alternative to LVH, left ventricular geometrical patterns offer incremental prognostic value beyond that provided by the other cardiovascular risk factors including left ventricular mass (LVM). Combination of LVM and relative wall thickness (RWT) can be used to identify different left ventricular geometrical patterns. Various indexation methods normalised for LVM have been shown to offer prognostic significance. There was no prior study on the prevalence of LVH and geometric patterns in hypertensive patients in Jamaica using multiple partition values. Our study was designed to estimate the prevalence of LVH and geometrical patterns in a hypertensive Caribbean population in Jamaica using 10 different published cut-off values.

Chiranjivi Potu; Edwin Tulloch-Reid; Dainia Baugh; Olusegun A Ismail; Ernest C. Madu

2012-01-01

113

Voltage-dependent properties of macroscopic and elementary calcium channel currents in guinea pig ventricular myocytes.  

UK PubMed Central (United Kingdom)

Whole-cell Ca channel currents were recorded from guinea pig ventricular myocytes that were internally perfused with Cs solution and bathed in solutions containing 3.6 mM Ca, 3.6 mM Ba or 90 mM Ba (34 degrees C). Single Ca channel currents were recorded from cell-attached membrane patches of similar myocytes; the patch pipettes contained a 90 mM Ba solution. 1. Although the shape of the whole-cell I-V relation was independent of the bathing solution, this was not the case with the location of the inward current maximum (Vpeak); Vpeak in 90 mM Ba was about 30 mV positive to Vpeak in 3.6 mM Ba. 2. The activation and inactivation of whole-cell currents were voltage dependent. Compared to the voltage dependencies in 3.6 mM Ba, those in 90 mM Ba were shifted by about 30 mV to the right, suggesting a neutralization of surface charges. 3. Observations compatible with the ion permeation model proposed by Hess and Tsien (1984) included (a) a depression of current during Ca/Ba solution exchange, (b) a high divalent to monovalent ion permeability, and (c) rectification of the outward limb of the I-V relation. 4. Estimated current densities at Vpeak were similar for myocytes in 3.6 mM Ca and 3.6 mM Ba, and about 10 times larger in 90 mM Ba. 5. Average currents (I) calculated from ensembles of records of single Ca channel current had voltage-dependent time courses resembling those of whole-cell IBa (90 mM). 6. Single-channel I-V relations were superimposable on whole-cell I-V curves suggesting that voltage-dependent single-channel parameters (probability of opening, elementary current amplitude) can be related to the voltage-dependent macroscopic current parameters (activation, instantaneous I-V relation) when scaled by channel number. 7. The density of Ca channels in myocytes was calculated from whole-cell IBa (90 mM) and average current through single channels. The outcome, 3-5 channels/micron 2, agrees with two other recent estimates (Tsien et al. 1983; Lux and Brown 1984). However, it is difficult to reconcile with the much lower density that one would forecast from the frequency of functional channel observation in myocyte membrane patches (Pelzer et al. 1985c).

McDonald TF; Cavalié A; Trautwein W; Pelzer D

1986-05-01

114

A high-fructose diet worsens eccentric left ventricular hypertrophy in experimental volume overload.  

UK PubMed Central (United Kingdom)

The development of left ventricular (LV) hypertrophy (LVH) can be affected by diet manipulation. Concentric LVH resulting from pressure overload can be worsened by feeding rats with a high-fructose diet. Eccentric LVH is a different type of hypertrophy and is associated with volume overload (VO) diseases. The impact of an abnormal diet on the development of eccentric LVH and on ventricular function in chronic VO is unknown. This study therefore examined the effects of a fructose-rich diet on LV eccentric hypertrophy, ventricular function, and myocardial metabolic enzymes in rats with chronic VO caused by severe aortic valve regurgitation (AR). Wistar rats were divided in four groups: sham-operated on control diet (SC; n = 13) or fructose-rich diet (SF; n = 13) and severe aortic regurgitation fed with the same diets [aortic regurgitation on control diet (ARC), n = 16, and aortic regurgitation on fructose-rich diet (ARF), n = 13]. Fructose-rich diet was started 1 wk before surgery, and the animals were euthanized 9 wk later. SF and ARF had high circulating triglycerides. ARC and ARF developed significant LV eccentric hypertrophy after 8 wk as expected. However, ARF developed more LVH than ARC. LV ejection fraction was slightly lower in the ARF compared with ARC. The increased LVH and decreased ejection fraction could not be explained by differences in hemodynamic load. SF, ARC, and ARF had lower phosphorylation levels of the AMP kinase compared with SC. A fructose-rich diet worsened LV eccentric hypertrophy and decreased LV function in a model of chronic VO caused by AR in rats. Normal animals fed the same diet did not develop these abnormalities. Hypertriglyceridemia may play a central role in this phenomenon as well as AMP kinase activity.

Bouchard-Thomassin AA; Lachance D; Drolet MC; Couet J; Arsenault M

2011-01-01

115

Nampt secreted from cardiomyocytes promotes development of cardiac hypertrophy and adverse ventricular remodeling.  

Science.gov (United States)

Nicotinamide phosphoribosyltransferase (Nampt) is an important coenzyme involved in cellular redox reactions. Inside the cell, Nampt (iNampt) functions as a rate-limiting enzyme in the NAD salvage pathway, and outside the cell (eNampt), it acts as a proinflammatory cytokine. High-circulating levels of Nampt are reported in different pathological conditions. This study was designed to examine the role of Nampt in the development of cardiac hypertrophy and ventricular remodeling. We studied the hypertrophic response in Nampt heterozygous (+/-) knockout and cardiac-specific overexpressing Nampt transgenic mice. Whereas Nampt(+/-) mice were protected against agonist (isoproterenol and angiotensin II)-induced hypertrophy, Nampt transgenic mice spontaneously developed cardiac hypertrophy at 6 mo of age. Experiments conducted to gain insight into the mechanism revealed that treatment of cardiomyocytes with recombinant (eNampt) or overexpression with Nampt-synthesizing adenovirus vector (Ad.Nampt) induced cardiomyocyte hypertrophy. The prohypertrophic effects of eNampt and Ad.Nampt were blocked by the addition of a Nampt-blocking antibody into cultures, thus suggesting that Nampt was in fact invoking hypertrophic response of cardiomyocytes by acting on the cell surface receptors. We also found increased Nampt levels in the supernatant of cardiomyocyte cultures subjected to stress by either serum starvation or H(2)O(2) treatment. Exploration of signaling pathways in Nampt-induced cardiac hypertrophy and fibrosis revealed increased activation of mitogen-activated protein kinases, namely, JNK1, p38, and ERK. This was also associated with increased calcineurin levels and nuclear factor of activated T-cell localization into the nucleus. From these studies we conclude that cardiomyocytes are capable of secreting Nampt during stress, and exogenous Nampt is a positive regulator of cardiac hypertrophy and adverse ventricular remodeling. PMID:23203961

Pillai, Vinodkumar B; Sundaresan, Nagalingam R; Kim, Gene; Samant, Sadhana; Moreno-Vinasco, Liliana; Garcia, Joe G N; Gupta, Mahesh P

2012-11-30

116

Nampt secreted from cardiomyocytes promotes development of cardiac hypertrophy and adverse ventricular remodeling.  

UK PubMed Central (United Kingdom)

Nicotinamide phosphoribosyltransferase (Nampt) is an important coenzyme involved in cellular redox reactions. Inside the cell, Nampt (iNampt) functions as a rate-limiting enzyme in the NAD salvage pathway, and outside the cell (eNampt), it acts as a proinflammatory cytokine. High-circulating levels of Nampt are reported in different pathological conditions. This study was designed to examine the role of Nampt in the development of cardiac hypertrophy and ventricular remodeling. We studied the hypertrophic response in Nampt heterozygous (+/-) knockout and cardiac-specific overexpressing Nampt transgenic mice. Whereas Nampt(+/-) mice were protected against agonist (isoproterenol and angiotensin II)-induced hypertrophy, Nampt transgenic mice spontaneously developed cardiac hypertrophy at 6 mo of age. Experiments conducted to gain insight into the mechanism revealed that treatment of cardiomyocytes with recombinant (eNampt) or overexpression with Nampt-synthesizing adenovirus vector (Ad.Nampt) induced cardiomyocyte hypertrophy. The prohypertrophic effects of eNampt and Ad.Nampt were blocked by the addition of a Nampt-blocking antibody into cultures, thus suggesting that Nampt was in fact invoking hypertrophic response of cardiomyocytes by acting on the cell surface receptors. We also found increased Nampt levels in the supernatant of cardiomyocyte cultures subjected to stress by either serum starvation or H(2)O(2) treatment. Exploration of signaling pathways in Nampt-induced cardiac hypertrophy and fibrosis revealed increased activation of mitogen-activated protein kinases, namely, JNK1, p38, and ERK. This was also associated with increased calcineurin levels and nuclear factor of activated T-cell localization into the nucleus. From these studies we conclude that cardiomyocytes are capable of secreting Nampt during stress, and exogenous Nampt is a positive regulator of cardiac hypertrophy and adverse ventricular remodeling.

Pillai VB; Sundaresan NR; Kim G; Samant S; Moreno-Vinasco L; Garcia JG; Gupta MP

2013-02-01

117

Electrocardiographic left ventricular hypertrophy with strain pattern: prevalence, mechanisms and prognostic implications.  

UK PubMed Central (United Kingdom)

BACKGROUND: Electrocardiographic left ventricular hypertrophy with strain pattern has been documented as a marker for left ventricular hypertrophy. Its presence on the ECG of hypertensive patients is associated with a poor prognosis. This review was undertaken to report the prevalence, mechanism and prognostic implications of this ECG abnormality. MATERIALS AND METHODS: We conducted a comprehensive search of electronic databases to identify studies relating to the title of this review. The search criteria were related to the title. Two of the reviewers independently screened the searches. RESULTS: Results were described qualitatively. The data were not pooled because there were no randomised studies on the topic. The prevalence of ECG strain pattern ranged from 2.1 to 36%. The highest prevalence was reported before the era of good antihypertensive therapy. The sensitivity as a measure of left ventricular hypertrophy ranged from 3.8 to 50%, while the specificity was in the range of 89.8 to 100%. Strain pattern was associated with adverse cardiovascular risk factors as well as increased all-cause and CV morbidity and mortality. ST-segment depression and T-wave inversion on the ECG was recognised as the strongest marker of morbidity and mortality when ECG-LVH criteria were utilised for risk stratification in hypertensive subjects. CONCLUSION: Electrocardiographic strain pattern identifies cardiac patients at higher risk of cardiovascular-related as well as all-cause morbidity and mortality.

Ogah OS; Oladapo OO; Adebiyi AA; Adebayo AK; Aje A; Ojji DB; Salako BL; Falase AO

2008-01-01

118

[The assessment of left ventricular hypertrophy in patients with the primary hypertension with the use of Cardiac Magnetic Resonance].  

UK PubMed Central (United Kingdom)

The aim of the study is to present usefulness of Cardiac Magnetic Resonance (CMR) to assess left ventricular hypertrophy in hypertensive patients. 48 patients were examined (24 females and 24 males) from 37 to 75 years of age (mean age was 56 years) with diagnosed cardiac hypertrophy in the course of 2nd and 3rd degree primary hypertension. All patients from this group underwent Cardio MR examination using MR 1.5 T Signa Excite (GE) system. Dedicated software was used for post-processing (MASS, Medis). We assessed left ventricular functional parameters such as: Ejection Fraction (EF), End-Diastolic Volume(EDV) and End-Systolic Volume (ESV). We also assessed left ventricular diameters as well as left ventricular posterior wall (PWD) and interventricular septum (IVSD) thickness. We also calculated left ventricular mass (LVM) and left ventricular mass index (LVMI). In most cases (66.7%) patients had significant increase of LVM. On the base of LVMI hypertrophy of the left ventricle was found in 6.2% patients. We affirmed statistically significant changes of left ventricular's morphological and functional parameters. The significant correlation was found between posterior wall diameter (PWD) and LVM, as well as between interventricular septum (IVSD) and LVM. The significant correlation was found between posterior wall diameter (PWD) and left ventricular Ejection Fraction (EF) and End-Systolic Volume (ESV). Cardio MR is an effective method to detect left ventricular hypertrophy (LVH) in hypertensive patients.

Brzozowska-Czarnek A; Bryll A

2013-01-01

119

Anti-hypertensive drugs have different effects on ventricular hypertrophy regression  

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Full Text Available OBJECTIVES: There is a direct relationship between the regression of left ventricular hypertrophy (LVH) and a decreased risk of mortality. This investigation aimed to describe the effects of anti-hypertensive drugs on cardiac hypertrophy through a meta-analysis of the literature. METHODS: The Medline (via PubMed), Lilacs and Scielo databases were searched using the subject keywords cardiac hypertrophy, antihypertensive and mortality. We aimed to analyze the effect of anti-hypertensive drugs on ventricle hypertrophy. RESULTS: The main drugs we described were enalapril, verapamil, nifedipine, indapamina, losartan, angiotensin-converting enzyme inhibitors and atenolol. These drugs are usually used in follow up programs, however, the studies we investigated used different protocols. Enalapril (angiotensin-converting enzyme inhibitor) and verapamil (Ca++ channel blocker) caused hypertrophy to regress in LVH rats. The effects of enalapril and nifedipine (Ca++ channel blocker) were similar. Indapamina (diuretic) had a stronger effect than enalapril, and losartan (angiotensin II receptor type 1 (AT1) receptor antagonist) produced better results than atenolol (selective ?1 receptor antagonist) with respect to LVH regression. CONCLUSION: The anti-hypertensive drugs induced various degrees of hypertrophic regression.

Celso Ferreira Filho; Luiz Carlos de Abreu; Vitor E. Valenti; Marcelo Ferreira; Adriano Meneghini; José Alexandre Silveira; Andrés R. Pérez Riera; Eduardo Colombari; Neif Murad; Paulo Roberto Santos-Silva; Lovian José Henrique Pereira da Silva; Luiz Carlos Marques Vanderlei; Tatiana D. Carvalho; Celso Ferreira

2010-01-01

120

Effects of extracellular ATP on ICa, [Ca2+]i, and contraction in isolated ferret ventricular myocytes.  

UK PubMed Central (United Kingdom)

The effects of extracellular ATP on the voltage-activated "L-type" Ca current (ICa), action potential, resting and transient intracellular Ca2+ levels, and cell contraction were examined in enzymatically isolated myocytes from the right ventricles of ferrets. With the use of the whole cell patch-clamp technique, extracellular ATP (10(-7) to 10(-3) M) inhibited ICa in a time- and concentration-dependent manner. ATP decreased the peak amplitude of ICa without altering the residual current at the end of 500-ms clamp steps. The concentration-response relationship for ATP inhibition of ICa was well described by a conventional Michaelis-Menten relationship with a half-maximal inhibitory concentration of 1 microM and a maximal effect of 50%. Consistent with its inhibitory effect on ICa, ATP hyperpolarized the plateau phase and shortened the action potential duration. In fura-2-loaded myocytes, extracellular ATP did not change the resting myoplasmic Ca2+ levels; however, when current was elicited under voltage-clamp conditions, ATP both decreased the myoplasmic intracellular Ca2+ transient and inhibited the degree of cell shortening. Our results suggest that ATP could be a genuine and potent extracellular modulator of cardiac function in ferret ventricular myocardium.

Qu Y; Himmel HM; Campbell DL; Strauss HC

1993-03-01

 
 
 
 
121

Isoproterenol increases the fraction of spark-dependent RyR-mediated leak in ventricular myocytes.  

UK PubMed Central (United Kingdom)

Recent research suggests that the diastolic ryanodine-receptor-mediated release of Ca(2+) (J(leak)) from the sarcoplasmic reticulum of ventricular myocytes occurs in spark and nonspark forms. Further information about the role(s) of these release manifestations is scarce, however. This study addresses whether the fraction of spark-mediated J(leak) increases due to ?-adrenergic stimulation. Confocal microscopy was used to simultaneously image Ca(2+) sparks and quantify J(leak) in intact rabbit myocytes, either in the absence or in the presence of 125 nM isoproterenol. It was found that isoproterenol treatment shifts the spark-frequency-J(leak) relationship toward an increased sensitivity to a [Ca(2+)] trigger. In agreement, a small but significant increase in spark width was found for cells with matched baseline [Ca(2+)] and total SR [Ca(2+)]. The reconstruction of release fluxes, when applied to the average sparks from those selected cells, yielded a wider release source in the isoproterenol event, indicating the recruitment of peripheral ryanodine receptors. Overall, the results presented here indicate that ?-adrenergic stimulation increases the spark-dependent fraction of J(leak). Working together, the increased Ca(2+) sensitivity and the greater spark width found during isoproterenol treatment may increase the probability of Ca(2+) wave generation.

Santiago DJ; Ríos E; Shannon TR

2013-03-01

122

Study of Huoxue Qianyang Granules in revising the left ventricular hypertrophy of spontaneous hypertension rats  

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Full Text Available Objective: To study the mechanism of Huoxue Qianyang Granule (HXQYG), a traditional Chinese compound medicine, in revising the left ventricular hypertrophy of hypertension. Methods: Spontaneous hypertension rats (SHR) were randomly divided into seven groups: untreated group, Songling Xuemaikang (SLXMK)-treated group, captopril-treated group, high-, medium- and low-dose HXQYG-treated groups, and normal control group. The systolic blood pressure (SBP) and left ventricular mass index (LVMI) were measured. The content of angiotensin ? (Ang?) in left ventricular tissue was determined by radioimmunoassay. The expressions of angiotensin converting enzyme (ACE) protein and mRNA in left ventricular tissue were analyzed separately by immunohistochemical method and RT-PCR. Results: (1) SBP and LVMI were higher in the untreated group than those in the normal control group, and they were lower in the high- and medium-dose HXQYG-treated groups than those in the untreated group, but higher than those in the captopril-treated group, and without significant difference as compared to those in the SLXMK-treated group. (2) The content of Ang? and expressions of ACE protein and mRNA in the left ventricular tissue in the untreated group were higher than those in the normal control group, and they were lower in the HXQYG-treated groups than those in the untreated group, but higher than those in the captopril-treated group, and without significant difference as compared to those in the SLXMK-treated group. Conclusion: HXQYG can reverse the left ventricular hypertrophy of SHR, which may be due to decreasing the amount of Ang? and expressions of ACE protein and mRNA in the left ventricular tissue.

Duan ZHOU; Mei-Fang XIAO

2006-01-01

123

Influence of infrasound exposure on the whole L-type calcium currents in rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

This study was designed to examine the effect of infrasound exposure (5 Hz at 130 dB) on whole-cell L-type Ca2+ currents (WLCC) in rat ventricular myocytes and the underlying mechanism(s) involved. Thirty-two adult Sprague-Dawley rats were randomly assigned to infrasound exposure and control groups. [Ca2+](i), WLCC, mRNA expression of the a(1c) subunit of L-type Ca2+ channels (LCC), and SERCA2 protein were examined on day 1, 7, and 14 after initiation of infrasound exposure. Fluo-3/AM fluorescence and the laser scanning confocal microscope techniques were used to measure [Ca2+](i) in freshly isolated ventricular myocytes. The Ca2+ fluorescence intensity (FI), denoting [Ca2+](i) in cardiomyocytes, was significantly elevated in a time-dependent manner in the exposure groups. There was a significant increase in WLCC in the 1-day group and a further significant increase in the 7- and 14-day groups. LCC mRNA expression measured by RT-PCR revealed a significant rise in the 1-day group and a significant additional rise in the 7- and 14-day groups compared with control group. SERCA2 expression was significantly upregulated in the 1-day group followed by an overt decrease in the 7- and 14-day groups. Prolonged exposure of infrasound altered WLCC in rat cardiomyocytes by shifting the steady-state inactivation curves to the right (more depolarized direction) without altering the slope and biophysical properties of I (Ca,L). Taken together, our data suggest that changes in [Ca2+](I) levels as well as expression of LCC and SERCA2 may contribute to the infrasound exposure-elicited cardiac response.

Pei Z; Zhuang Z; Xiao P; Chen J; Sang H; Ren J; Wu Z; Yan G

2009-06-01

124

Influence of infrasound exposure on the whole L-type calcium currents in rat ventricular myocytes.  

Science.gov (United States)

This study was designed to examine the effect of infrasound exposure (5 Hz at 130 dB) on whole-cell L-type Ca2+ currents (WLCC) in rat ventricular myocytes and the underlying mechanism(s) involved. Thirty-two adult Sprague-Dawley rats were randomly assigned to infrasound exposure and control groups. [Ca2+](i), WLCC, mRNA expression of the a(1c) subunit of L-type Ca2+ channels (LCC), and SERCA2 protein were examined on day 1, 7, and 14 after initiation of infrasound exposure. Fluo-3/AM fluorescence and the laser scanning confocal microscope techniques were used to measure [Ca2+](i) in freshly isolated ventricular myocytes. The Ca2+ fluorescence intensity (FI), denoting [Ca2+](i) in cardiomyocytes, was significantly elevated in a time-dependent manner in the exposure groups. There was a significant increase in WLCC in the 1-day group and a further significant increase in the 7- and 14-day groups. LCC mRNA expression measured by RT-PCR revealed a significant rise in the 1-day group and a significant additional rise in the 7- and 14-day groups compared with control group. SERCA2 expression was significantly upregulated in the 1-day group followed by an overt decrease in the 7- and 14-day groups. Prolonged exposure of infrasound altered WLCC in rat cardiomyocytes by shifting the steady-state inactivation curves to the right (more depolarized direction) without altering the slope and biophysical properties of I (Ca,L). Taken together, our data suggest that changes in [Ca2+](I) levels as well as expression of LCC and SERCA2 may contribute to the infrasound exposure-elicited cardiac response. PMID:19387569

Pei, Zhaohui; Zhuang, Zhiqiang; Xiao, Pingxi; Chen, Jingzao; Sang, Hanfei; Ren, Jun; Wu, Zhenbiao; Yan, Guangmei

2009-04-22

125

Accumulation of slowly activating delayed rectifier potassium current (IKs) in canine ventricular myocytes  

DEFF Research Database (Denmark)

In guinea-pig ventricular myocytes, in which the deactivation of slowly activating delayed rectifier potassium current (IKs) is slow, IKs can be increased by rapid pacing as a result of incomplete deactivation and subsequent current accumulation. Whether accumulation of IKs occurs in dogs, in which the deactivation is much faster, is still unclear. In this study the conditions under which accumulation occurs in canine ventricular myocytes were studied with regard to its physiological relevance in controlling action potential duration (APD). At baseline, square pulse voltage clamp experiments revealed that the accumulation of canine IKs could occur, but only at rather short interpulse intervals (<100 ms). With action potential (AP) clamp commands of constant duration (originally recorded at rate of 2 Hz), an accumulation was only found at interpulse intervals close to 0 ms. Transmembrane potential recordings with high-resistance microelectrodes revealed, however, that at the fastest stimulation rates with normally captured APs (5 Hz) the interpulse interval exceeded 50 ms. This suggested that no IKs accumulation occurs, which was supported by the lack of effect of an IKs blocker, HMR 1556 (500 nM), on APD. In the presence of the beta-adrenergic receptor agonist isoproterenol (isoprenaline, 100 nM) the accumulation with AP clamp commands of constant duration was much more pronounced and a significant accumulating current was found at a relevant interpulse interval of 100 ms. HMR 1556 prolonged APD, but this lengthening was reverse rate dependent. AP clamp experiments in a physiologically relevant setting (short, high rate APs delivered at a corresponding rate) revealed a limited accumulation of IKs in the presence of isoproterenol. In conclusion, a physiologically relevant accumulation of IKs was only observed in the presence of isoproterenol. Block of IKs, however, led to a reverse rate-dependent prolongation of APD indicating that IKs does not have a dominant role at short cycle lengths.

Stengl, Milan; Volders, Paul G A

2003-01-01

126

Modulation of impact of high fat diet in pathological and physiological left ventricular cardiac hypertrophy by fluvastatin.  

UK PubMed Central (United Kingdom)

The male Wistar rats were kept at high fat diet for 90 days and subjected to partial abdominal aortic constriction (PAAC) at 62nd and continued up to 90th day. Similarly, rats were kept at high fat diet for 90 days and subjected to chronic swimming training (CST) at 46th day and continued up to 90th day. Obesity was assessed by % age change in body weight, WHR ratio and adiposity index whereas cardiac hypertrophy was assessed by using index of cardiac hypertrophy, i.e., left ventricular weight, left ventricular weight to body weight, (LVW/BW), left ventricular wall thickness (LVWT), cardiomyocyte diameter, LV, protein content and collagen content. Further, mean arterial blood pressure (MABP) was also recorded. Oxidative stress was assessed by measuring the levels of thiobarbituric acid reactive species (TBARS), levels of superoxide anion generation and levels of reduced glutathione in left ventricular tissue. The PAAC and CST increased the index of cardiac hypertrophy. Moreover, PAAC has significantly increased MABP. Fluvastatin, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, significantly attenuated PAAC induced left ventricular cardiac hypertrophy and MABP whereas no significant change was observed in CST-induced cardiac hypertrophy. Furthermore, fluvastatin significantly attenuated the oxidative stress by decreasing the levels of TBARS and superoxide anion generation and increasing the levels of reduced glutathione. These results suggest that fluvastatin prevented the PAAC-induced cardiac hypertrophy.

Singh R; Krishan P

2010-03-01

127

Modulation of impact of high fat diet in pathological and physiological left ventricular cardiac hypertrophy by fluvastatin.  

Science.gov (United States)

The male Wistar rats were kept at high fat diet for 90 days and subjected to partial abdominal aortic constriction (PAAC) at 62nd and continued up to 90th day. Similarly, rats were kept at high fat diet for 90 days and subjected to chronic swimming training (CST) at 46th day and continued up to 90th day. Obesity was assessed by % age change in body weight, WHR ratio and adiposity index whereas cardiac hypertrophy was assessed by using index of cardiac hypertrophy, i.e., left ventricular weight, left ventricular weight to body weight, (LVW/BW), left ventricular wall thickness (LVWT), cardiomyocyte diameter, LV, protein content and collagen content. Further, mean arterial blood pressure (MABP) was also recorded. Oxidative stress was assessed by measuring the levels of thiobarbituric acid reactive species (TBARS), levels of superoxide anion generation and levels of reduced glutathione in left ventricular tissue. The PAAC and CST increased the index of cardiac hypertrophy. Moreover, PAAC has significantly increased MABP. Fluvastatin, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, significantly attenuated PAAC induced left ventricular cardiac hypertrophy and MABP whereas no significant change was observed in CST-induced cardiac hypertrophy. Furthermore, fluvastatin significantly attenuated the oxidative stress by decreasing the levels of TBARS and superoxide anion generation and increasing the levels of reduced glutathione. These results suggest that fluvastatin prevented the PAAC-induced cardiac hypertrophy. PMID:20053524

Singh, Randhir; Krishan, Pawan

2009-10-24

128

End-stage cardiac failure in humans is coupled with the induction of proliferating cell nuclear antigen and nuclear mitotic division in ventricular myocytes.  

UK PubMed Central (United Kingdom)

Proliferating cell nuclear antigen (PCNA) is a late growth-regulated gene that is expressed at the G1-S boundary of the cell cycle and is required for DNA synthesis and cell proliferation. Since quantitative results suggest that myocyte hyperplasia occurs in the decompensated human heart, we postulated that induction of the PCNA gene may be present in the failing heart in humans. PCNA protein was detected in myocardial samples obtained from the left and right ventricles of patients with congestive heart failure. Endomyocardial biopsies collected from donor subjects were used as control tissue. The percentage of positively stained myocyte nuclei in the ventricles was established by using PCNA monoclonal antibody and the immunoperoxidase technique. The localization of PCNA in myocytes was confirmed by alpha-sarcomeric actin antibody staining. PCNA labeling was present in left ventricular myocytes of 29 of the 32 hearts examined. In the right ventricle, 24 of the 29 samples showed positive staining. In a subset of 25 patients, the percentage of PCNA-labeled myocyte nuclei was measured and found to constitute 49 +/- 22% of left ventricular myocytes. A similar analysis for the right ventricle, conducted in 21 patients, showed that 49 +/- 19% of the myocyte nuclei exhibited PCNA protein. In addition, mitotic figures in myocytes were documented. A quantitative analysis of this cellular process revealed that 11 myocyte nuclei per 1 million cells exhibited mitotic images in chronic heart failure. Immediately after myocardial infarction, two cells per million showed mitotic division, and this phenomenon was restricted to the region adjacent to the necrotic tissue. No PCNA labeling or nuclear mitotic images were detected in the ventricular myocardium of control subjects. Thus, the observation that diffuse PCNA labeling and myocyte mitotic division are present in hearts with end-stage failure strongly suggests that adult ventricular myocytes are not terminally differentiated cells and that myocyte cellular hyperplasia may constitute a growth reserve mechanism of the diseased heart.

Quaini F; Cigola E; Lagrasta C; Saccani G; Quaini E; Rossi C; Olivetti G; Anversa P

1994-12-01

129

Swelling-activated Gd3+-sensitive cation current and cell volume regulation in rabbit ventricular myocytes.  

Science.gov (United States)

The role of swelling-activated currents in cell volume regulation is unclear. Currents elicited by swelling rabbit ventricular myocytes in solutions with 0.6-0.9x normal osmolarity were studied using amphotericin perforated patch clamp techniques, and cell volume was examined concurrently by digital video microscopy. Graded swelling caused graded activation of an inwardly rectifying, time-independent cation current (ICir,swell) that was reversibly blocked by Gd3+, but ICir,swell was not detected in isotonic or hypertonic media. This current was not related to IK1 because it was insensitive to Ba2+. The PK/PNa ratio for ICir,swell was 5.9 +/- 0.3, implying that inward current is largely Na+ under physiological conditions. Increasing bath K+ increased gCir,swell but decreased rectification. Gd3+ block was fitted with a K0.5 of 1.7 +/- 0.3 microM and Hill coefficient, n, of 1.7 +/- 0.4. Exposure to Gd3+ also reduced hypotonic swelling by up to approximately 30%, and block of current preceded the volume change by approximately 1 min. Gd3+-induced cell shrinkage was proportional to ICir,swell when ICir,swell was varied by graded swelling or Gd3+ concentration and was voltage dependent, reflecting the voltage dependence of ICir,swell. Integrating the blocked ion flux and calculating the resulting change in osmolarity suggested that ICir,swell was sufficient to explain the majority of the volume change at -80 mV. In addition, swelling activated an outwardly rectifying Cl- current, ICl,swell. This current was absent after Cl- replacement, reversed at ECl, and was blocked by 1 mM 9-anthracene carboxylic acid. Block of ICl,swell provoked a 28% increase in swelling in hypotonic media. Thus, both cation and anion swelling-activated currents modulated the volume of ventricular myocytes. Besides its effects on cell volume, ICir,swell is expected to cause diastolic depolarization. Activation of ICir, swell also is likely to affect contraction and other physiological processes in myocytes. PMID:9276755

Clemo, H F; Baumgarten, C M

1997-09-01

130

Swelling-activated Gd3+-sensitive cation current and cell volume regulation in rabbit ventricular myocytes.  

UK PubMed Central (United Kingdom)

The role of swelling-activated currents in cell volume regulation is unclear. Currents elicited by swelling rabbit ventricular myocytes in solutions with 0.6-0.9x normal osmolarity were studied using amphotericin perforated patch clamp techniques, and cell volume was examined concurrently by digital video microscopy. Graded swelling caused graded activation of an inwardly rectifying, time-independent cation current (ICir,swell) that was reversibly blocked by Gd3+, but ICir,swell was not detected in isotonic or hypertonic media. This current was not related to IK1 because it was insensitive to Ba2+. The PK/PNa ratio for ICir,swell was 5.9 +/- 0.3, implying that inward current is largely Na+ under physiological conditions. Increasing bath K+ increased gCir,swell but decreased rectification. Gd3+ block was fitted with a K0.5 of 1.7 +/- 0.3 microM and Hill coefficient, n, of 1.7 +/- 0.4. Exposure to Gd3+ also reduced hypotonic swelling by up to approximately 30%, and block of current preceded the volume change by approximately 1 min. Gd3+-induced cell shrinkage was proportional to ICir,swell when ICir,swell was varied by graded swelling or Gd3+ concentration and was voltage dependent, reflecting the voltage dependence of ICir,swell. Integrating the blocked ion flux and calculating the resulting change in osmolarity suggested that ICir,swell was sufficient to explain the majority of the volume change at -80 mV. In addition, swelling activated an outwardly rectifying Cl- current, ICl,swell. This current was absent after Cl- replacement, reversed at ECl, and was blocked by 1 mM 9-anthracene carboxylic acid. Block of ICl,swell provoked a 28% increase in swelling in hypotonic media. Thus, both cation and anion swelling-activated currents modulated the volume of ventricular myocytes. Besides its effects on cell volume, ICir,swell is expected to cause diastolic depolarization. Activation of ICir, swell also is likely to affect contraction and other physiological processes in myocytes.

Clemo HF; Baumgarten CM

1997-09-01

131

Left Ventricular Hypertrophy: An allometric comparative analysis of different ECG markers  

International Nuclear Information System (INIS)

Allometry, in general biology, measures the relative growth of a part in relation to the whole living organism. Left ventricular hypertrophy (LVH) is the heart adaptation to excessive load (systolic or diastolic). The increase in left ventricular mass leads to an increase in the electrocardiographic voltages. Based on clinical data, we compared the allometric behavior of three different ECG markers of LVH. To do this, the allometric fit AECG ? + ? (VM) relating left ventricular mass (estimated from ecocardiographic data) and ECG amplitudes (expressed as the Cornell-Voltage, Sokolow and the ECG overall voltage indexes) were compared. Besides, sensitivity and specificity for each index were analyzed. The more sensitive the ECG criteria, the better the allometric fit. In conclusion: The allometric paradigm should be regarded as the way to design new and more sensitive ECG-based LVH markers.

2011-12-23

132

The association of growth differentiation factor-15 with left ventricular hypertrophy in hypertensive patients.  

UK PubMed Central (United Kingdom)

Growth differentiation factor-15 (GDF-15) has been identified as an endogenous anti-hypertrophy effect. However, the association of plasma GDF-15 levels with left ventricular hypertrophy (LVH) in hypertension is poorly understood. We investigate the effect of plasma GDF-15 levels on left ventricular hypertrophy (LVH) in hypertension. We measured the plasma levels of GDF-15 in 299 untreated hypertensive patients which consisted of 99 with LVH and 200 without LVH using immunoradiometric assay. All subjects were examined by the ultrasonic cardiograph to determine Left ventricular (LV) internal diameters, septal thickness, and posterior wall thickness. The associations of GDF-15 with left ventricular mass index (LVMI), LV end-systolic and -diastolic diameters, LV wall thickness, and LV ejection fraction were evaluated. We found that plasma GDF-15 levels in hypertensive patients with LVH [median 1101, 25th-75th percentiles (879-1344) ng/L] were higher than that in hypertensive patients without LVH [median 516, 25th-75th percentiles (344-640) ng/L] (P<0.001). After adjustment for traditional covariates, plasma GDF-15 levels were independently related to LVMI (R(2) = 0.53; ? = 0.624, P<0.001), LV interventricular septal thickness (R(2) = 0.23; ? = 0.087, P<0.01) and LV posterior wall thickness (R(2) = 0.26; ? = 0.103, P<0.05). Our cross-sectional data on a hospital-based sample indicate that plasma GDF-15 levels are associated with LVH in hypertensive patients.

Xue H; Fu Z; Chen Y; Xing Y; Liu J; Zhu H; Zhou X

2012-01-01

133

Association between diabetes mellitus and left ventricular hypertrophy in a multiethnic population.  

UK PubMed Central (United Kingdom)

It is still controversial whether type 2 diabetes mellitus (T2DM) is associated with increased left ventricular (LV) mass independent of body size. We tested the hypothesis that T2DM is independently associated with LV mass in a multiethnic cohort. In the Northern Manhattan Study (NOMAS) cohort sample, a total of 1,932 subjects (67.9+/-9.6 years, 769 men and 1,163 women, 443 with DM and 1,489 without DM) were studied by transthoracic echocardiography, and LV mass was calculated. LV hypertrophy was defined as the upper quartile of LV mass. Multivariable models were used to assess the association of T2DM with LV mass after adjusting for age, gender, race, body mass index (BMI), systolic blood pressure, education, history of coronary artery disease, physical activity, and alcohol consumption. LV mass (189+/-60 vs 174+/-59 g, p<0.0001), BMI, and systolic blood pressure were higher in the DM group than in the non-DM group, whereas age and gender distributions were similar between groups. In multivariable analysis, T2DM was independently associated with increased LV mass (p=0.03). Presence of T2DM was associated with increased risk of LV hypertrophy (adjusted odds ratio 1.46, 95% confidence interval 1.13 to 1.88, p=0.004). Although no interactions were observed between T2DM and BMI on LV hypertrophy (p=0.6), there was a significant interaction between T2DM and waist circumference on LV hypertrophy (p=0.01). In conclusion, T2DM was independently associated with increased LV hypertrophy independent of various covariates in this multiethnic sample. Presence of T2DM increased the risk of LV hypertrophy by about 1.5-fold, and it possibly interacted with central obesity.

Eguchi K; Boden-Albala B; Jin Z; Rundek T; Sacco RL; Homma S; Di Tullio MR

2008-06-01

134

Effect of ouabain on myocardial ultrastructure and cytoskeleton during the development of ventricular hypertrophy.  

UK PubMed Central (United Kingdom)

The aim of this work is to study cytoskeletal impairment during the development of ouabain-induced ventricular hypertrophy. Male Sprague-Dawley rats were treated with either ouabain or saline. Systolic blood pressure (SBP) was recorded weekly. At the end of the 3rd and 6th week, the rats were killed and cardiac mass index were measured. Hematoxylin-eosin and Sirius red staining were carried out and cardiac ultrastructure were studied using transmission electron microscopy. The mRNA level of Profilin-1, Desmin, PCNA, TGF-?(1) and ET-1 in the left ventricle were measured using real-time quantitative PCR while their protein levels were examined by Western blot or immunohistochemistry. After 3 weeks, there was no significant difference in the mean SBP, cardiac mass index, mRNA and protein expression of PCNA, TGF-?(1) and ET-1 between the two groups. However, ouabain-treated rats showed disorganized cardiac cytoskeleton with abnormal expression of Profilin-1 and Desmin. After 6 weeks, the cardiac mass index remained the same in the two groups while PCNA, TGF-?(1), and ET-1 have been upregulated in ouabain-treated rats. The cardiac cytoskeletal impairment was more severe in ouabain-treated rats with further changes of Profilin-1 and Desmin. Cytoskeletal abnormality is an ultra-early change during ouabain-induced ventricular hypertrophy, before the release of hypertrophic factors. Therapy for prevention of ouabain-induced hypertrophy should start at the early stage by preventing the cytoskeleton from disorganization.

Zhao SH; Gao HQ; Ji X; Wang Y; Liu XJ; You BA; Cui XP; Qiu J

2013-01-01

135

L-364,373 (R-L3) enantiomers have opposite modulating effects on IKs in mammalian ventricular myocytes.  

Science.gov (United States)

Activators of the slow delayed rectifier K? current (IKs) have been suggested as promising tools for suppressing ventricular arrhythmias due to prolongation of repolarization. Recently, L-364,373 (R-L3) was nominated to activate IKs in myocytes from several species; however, in some studies, it failed to activate IKs. One later study suggested opposite modulating effects from the R-L3 enantiomers as a possible explanation for this discrepancy. Therefore, we analyzed the effect of the RL-3 enantiomers on IKs in ventricular mammalian myocytes, by applying standard microelectrode and whole-cell patch-clamp techniques at 37 °C. We synthesized 2 substances, ZS_1270B (right) and ZS_1271B (left), the 2 enantiomers of R-L3. In rabbit myocytes, ZS_1270B enhanced the IKs tail current by approximately 30%, whereas ZS_1271B reduced IKs tails by 45%. In guinea pig right ventricular preparations, ZS_1270B shortened APD90 (action potential duration measured at 90% repolarization) by 12%, whereas ZS_1271B lengthened it by approximately 15%. We concluded that R-L3 enantiomers in the same concentration range indeed have opposite modulating effects on IKs, which may explain why the racemic drug R-L3 previously failed to activate IKs. ZS_1270B is a potent IKs activator, therefore, this substance is appropriate to test whether IKs activators are ideal tools to suppress ventricular arrhythmias originating from prolongation of action potentials. PMID:23889560

Corici, Claudia; Kohajda, Zsófia; Kristóf, Attila; Horváth, András; Virág, László; Szél, Tamás; Nagy, Norbert; Szakonyi, Zsolt; Fülöp, Ferenc; Muntean, Danina M; Varró, András; Jost, Norbert

2013-01-08

136

Distinct Transient Outward Potassium Current (Ito) Phenotypes and Distribution of Fast-inactivating Potassium Channel Alpha Subunits in Ferret Left Ventricular Myocytes  

Digital Repository Infrastructure Vision for European Research (DRIVER)

The biophysical characteristics and ? subunits underlying calcium-independent transient outward potassium current (Ito) phenotypes expressed in ferret left ventricular epicardial (LV epi) and endocardial (LV endo) myocytes were analyzed using patch clamp, fluorescent in situ hybridization (FISH), ...

Brahmajothi, Mulugu V.; Campbell, Donald L.; Rasmusson, Randall L.; Morales, Michael J.; Trimmer, James S.; Nerbonne, Jeanne M.

137

Amiodarone Kyusei Toyo Ga Ieusagi Tanri Shinshitsukin Saibo Ni Oyobosu Denki Seirigakuteki Sayo (Effects of Perfusion of Amiodarone on Electrophysiological Properties in Single Rabbit Ventricular Myocytes).  

Science.gov (United States)

The acute administration of amiodarone, an antiarrhythmic agent, was studied and the data was compared with chronic administration. The ventricular myocytes were isolated from rabbit hearts, perfusated with perfusate containing amiodarone, and action pote...

K. Kamiya J. Cheng I. Kodama J. Toyama

1993-01-01

138

Relation of Leptin to Left Ventricular Hypertrophy (from the Multi-Ethnic Study of Atherosclerosis).  

Science.gov (United States)

Increasing adiposity increases the risk for left ventricular (LV) hypertrophy. Adipokines are hormone-like substances from adipose tissue that influence several metabolic pathways relevant to LV hypertrophy. Data were obtained from participants enrolled in the Multi-Ethnic Study of Atherosclerosis (MESA) who underwent magnetic resonance imaging of the heart and who also had fasting venous blood assayed for 4 distinct adipokines (adiponectin, leptin, tumor necrosis factor-?, and resistin). One-thousand four hundred sixty four MESA participants had complete data. The mean age was 61.5 years, the mean body mass index was 27.6 kg/m(2), and 49% were women. With adjustment for age, gender, race, height, and weight, multivariate linear regression modeling revealed that a 1-SD increment in leptin was significantly associated with smaller LV mass (ß: -4.66% predicted, p leptin are associated with more favorable values of several measures of LV structure and function. PMID:23711806

Allison, Matthew A; Bluemke, David A; McClelland, Robyn; Cushman, Mary; Criqui, Michael H; Polak, Joseph F; Lima, Joao A

2013-05-24

139

Metabolic gene remodeling and mitochondrial dysfunction in failing right ventricular hypertrophy secondary to pulmonary arterial hypertension.  

UK PubMed Central (United Kingdom)

BACKGROUND: Right ventricular (RV) dysfunction (RVD) is the most frequent cause of death in patients with pulmonary arterial hypertension. Although abnormal energy substrate use has been implicated in the development of chronic left heart failure, data describing such metabolic remodeling in RVD remain incomplete. Thus, we sought to characterize metabolic gene expression changes and mitochondrial dysfunction in functional and dysfunctional RV hypertrophy. METHODS AND RESULTS: Two different rat models of RV hypertrophy were studied. The model of RVD (SU5416/hypoxia) exhibited a significantly decreased gene expression of peroxisome proliferator-activated receptor-? coactivator-1?, peroxisome proliferator-activated receptor-? and estrogen-related receptor-?. The expression of multiple peroxisome proliferator-activated receptor-? coactivator-1? target genes required for fatty acid oxidation was similarly decreased. Decreased peroxisome proliferator-activated receptor-? coactivator-1? expression was also associated with a net loss of mitochondrial protein and oxidative capacity. Reduced mitochondrial number was associated with a downregulation of transcription factor A, mitochondrial, and other genes required for mitochondrial biogenesis. Electron microscopy demonstrated that, in RVD tissue, mitochondria had abnormal shape and size. Lastly, respirometric analysis demonstrated that mitochondria isolated from RVD tissue had a significantly reduced ADP-stimulated (state 3) rate for complex I. Conversely, functional RV hypertrophy in the pulmonary artery banding model showed normal expression of peroxisome proliferator-activated receptor-? coactivator-1?, whereas the expression of fatty acid oxidation genes was either preserved or unregulated. Moreover, pulmonary artery banding-RV tissue exhibited preserved transcription factor A mitochondrial expression and mitochondrial respiration despite elevated RV pressure-overload. CONCLUSIONS: Right ventricular dysfunction, but not functional RV hypertrophy in rats, demonstrates a gene expression profile compatible with a multilevel impairment of fatty acid metabolism and significant mitochondrial dysfunction, partially independent of chronic pressure-overload.

Gomez-Arroyo J; Mizuno S; Szczepanek K; Van Tassell B; Natarajan R; dos Remedios CG; Drake JI; Farkas L; Kraskauskas D; Wijesinghe DS; Chalfant CE; Bigbee J; Abbate A; Lesnefsky EJ; Bogaard HJ; Voelkel NF

2013-01-01

140

[Vector-echocardiographic correlations in left ventricular hypertrophy of arterial hypertension  

UK PubMed Central (United Kingdom)

In almost 200 case of left ventricular hypertrophy (LVH) secondary to hypertension (HT), including 75 cases with conduction disorders, 100 cases of normal adults and 20 cases of normal children, segmental (initial horizontal vector, maximal anterior and posterior vector of the QRS) and spatial vectorial parameters were correlated to segmental echocardiographic parameters (septum, anterior and posterior wall of the left ventricle) and mass parameters (left ventricular mass index). The only significant quantitative variables in hypertensive LVH are: on electrocardiography: the AQRS and Sokolow's index: on vectocardiography: the spatial vector: its magnitude, azimuth and elevation, the maximal posterior vector: its amplitude, the maximal anterior vector: its amplitude, the maximal width of the QRS azimuth of the efferent limb of the QRS, the ventricular gradient in the horizontal, frontal and sagittal planes; on echocardiography: the left ventricular mass index, the diastolic thickness of the septum and the VMNES, the diastolic thickness of the posterior wall of the left ventricle and its percentage thickening. The only significant correlations were observed between: the maximal posterior vector of QRS and the diastolic thickness of the posterior wall of the left ventricle: 0.01 < alpha < 0.02; the spatial vector and the left ventricular mass index: 0.01 < alpha < 0.001. The presence of a conduction disorder does not modify these last two qualitative variables but alters their correlation.

Hayat JC

1995-04-01

 
 
 
 
141

Action potential duration determines sarcoplasmic reticulum Ca2+ reloading in mammalian ventricular myocytes.  

Science.gov (United States)

After sarcoplasmic reticulum (SR) Ca2+ depletion in intact ventricular myocytes, electrical activity promotes SR Ca2+ reloading and recovery of twitch amplitude. In ferret, recovery of twitch and caffeine-induced contracture required fewer twitches than in rabbit or rat. In rat, there was no difference in action potential duration at 90% repolarization (APD90) at steady state (SS) versus at the first post-depletion (PD) twitch. The SS APD90 was similar in ferret and rabbit (but longer than in rat). However, compared to SS, the PD APD90 was lengthened in ferret, but shortened in rabbit. When rabbit myocytes were subjected to AP-clamp patterns during SR Ca2+ reloading (ferret- or rabbit-type APs), reloading was much faster using the ferret AP templates. We conclude that the faster SR Ca2+ refilling in ferret is due to the increased Ca2+ influx during the longer PD AP. The PD versus SS APD90 difference was suppressed by thapsigargin in ferret (indicating Ca2+ dependence). In rabbit, the PD AP shortening depended on the preceding diastolic interval (rather than Ca2+), because rest produced the same AP shortening, and SS APD90 increased as a function of frequency (in contrast to ferret). Transient outward current (Ito) was larger and recovered from inactivation much faster in ferret than in rabbit. Moreover, slow Ito recovery (tau approximately 3 s) in rabbit was a much larger fraction of Ito. Our data and a computational model (including two Ito components) suggest that in rabbit the slowly recovering Ito is responsible for short post-rest and PD APs, for the unusual frequency dependence of APD90, and ultimately for the slower post-depletion SR Ca2+ reloading. PMID:15243136

Bassani, Rosana A; Altamirano, Julio; Puglisi, José L; Bers, Donald M

2004-07-08

142

Excitation-contraction coupling in ventricular myocytes is enhanced by paracrine signaling from mesenchymal stem cells.  

UK PubMed Central (United Kingdom)

In clinical trials mesenchymal stem cells (MSCs) are transplanted into cardiac ischemic regions to decrease infarct size and improve contractility. However, the mechanism and time course of MSC-mediated cardioprotection are incompletely understood. We tested the hypothesis that paracrine signaling by MSCs promotes changes in cardiac excitation-contraction (EC) coupling that protects myocytes from cell death and enhances contractility. Isolated mouse ventricular myocytes (VMs) were treated with control tyrode, MSC conditioned-tyrode (ConT) or co-cultured with MSCs. The Ca handling properties of VMs were monitored by laser scanning confocal microscopy and whole cell voltage clamp. ConT superfusion of VMs resulted in a time dependent increase of the Ca transient amplitude (ConT(15min): ?F/F(0)=3.52±0.38, n=14; Ctrl(15min):? ?F/F(0)=2.41±0.35, n=14) and acceleration of the Ca transient decay (?: ConT: 269±18ms n=14; vs. Ctrl: 315±57ms, n=14). Voltage clamp recordings confirmed a ConT induced increase in I(Ca,L) (ConT: -5.9±0.5 pA/pF n=11; vs. Ctrl: -4.04±0.3 pA/pF, n=12). The change of ? resulted from increased SERCA activity. Changes in the Ca transient amplitude and ? were prevented by the PI3K inhibitors Wortmannin (100nmol/L) and LY294002 (10?mol/L) and the Akt inhibitor V (20?mol/L) indicating regulation through PI3K signal transduction and Akt activation which was confirmed by western blotting. A change in ? was also prevented in eNOS(-/-) myocytes or by inhibition of eNOS suggesting an NO mediated regulation of SERCA activity. Since paracrine signaling further resulted in increased survival of VMs we propose that the Akt induced change in Ca signaling is also a mechanism by which MSCs mediate an anti-apoptotic effect.

DeSantiago J; Bare DJ; Semenov I; Minshall RD; Geenen DL; Wolska BM; Banach K

2012-06-01

143

Taurine-magnesium coordination compound attenuates hypoxia/reoxygenation induced ion channel dysfunction in rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

Because of the known anti-arrhythmic effects of taurine-magnesium coordination compound (TMCC), the aim of the present study was to explore the electrophysiological effects of TMCC on hypoxia/reoxygenation (H/R)-induced arrhythmias in rat ventricular myocytes. Sodium current (I Na), the L-type calcium current (I Ca,L), and the transient outward potassium current (I to) were evaluated using whole-cell patch-clamp recordings in rat ventricular myocytes following H/R injury. The H/R group significantly decreased sodium currents, while L-type calcium currents and transient outward potassium currents was significantly increased (all p<0.01). TMCC (200 and 400 ?M) prevented abnormal sodium currents induced by H/R by inhibiting steady-state inactivation. It also counteracted abnormal L-type calcium currents induced by H/R by inhibiting steady-state activation and facilitating steady-state inactivation. In addition, it mitigated abnormal transient outward potassium currents induced by H/R by inhibiting steady-state activation. TMCC prevents H/R-induced arrhythmias in rat ventricular myocytes by modifying ion channel function.

Zhao L; Lou JS; Kang Y

2013-04-01

144

Effects of ropivacaine on membrane potential and voltage-dependent calcium channel current in single guinea-pig ventricular myocytes.  

UK PubMed Central (United Kingdom)

PURPOSE: This study was undertaken to assess the effects of ropivacaine on the membrane action potential and the voltage-dependent L-type calcium channel current ( I(Ca)) in guinea-pig single ventricular myocytes. METHODS: Single ventricular myocytes were prepared by enzymatic dispersion. Whole-cell current and voltage-clamp techniques were used to monitor membrane potentials and I(Ca). RESULTS: Ropivacaine (10(-5) and 10(-4) M) reduced the overshoot and shortened the duration of the action potential. Hyperpolarization of the resting membrane potential was observed in the presence of ropivacaine (10(-4) M). Ropivacaine (10(-5)-10(-3) M) reduced I(Ca) dose-dependently and reversibly, and the 50% inhibitory concentration (IC(50)) of ropivacaine was estimated as 4.3 x 10(-4) M. Furthermore, the inhibition of I(Ca) was not a use-dependent block. CONCLUSION: Ropivacaine has an inhibitory effect on I(Ca) in the guinea-pig single ventricular myocyte. It is concluded that the mild negative inotropic effect induced by ropivacaine can be attributed in part to shortening of the duration of the action potential, which is caused by inhibition of I(Ca).

Hatakeyama N; Yamada M; Shibuya N; Yamazaki M; Yamamura S; Sugaya M; Momose Y

2002-01-01

145

Effect of ajmaline on transient outward current in rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

The mechanism of ajmaline-induced inhibition of the transient outward current (I(to)) has been investigated in right ventricular myocytes of rat using the whole cell patch clamp technique. Ajmaline decreased the amplitude and the time integral of I(to) in a concentration-dependent, but frequency- and use-independent manner. In contrast to the single exponential time course of I(to)-inactivation in control conditions (tau(i) = 37.1 +/- 2.7 ms), the apparent inactivation was fitted by a sum of two exponentials under the effect of ajmaline with concentration-dependent fast and slow components (tau(f) = 11.7 +/- 0.8 ms, tau(s) = 57.6 +/- 2.7 ms at 10 micromol/l) suggesting block development primarily in the open channel state. An improved expression enabling to calculate the association and dissociation rate constants from the concentration dependence of tau(f) and tau(s) was derived and resulted in k(on) = 4.57 x 10(6) +/- 0.32 x 10(6) mol(-1).l.s(-1) and k(off) = 20.12 +/- 5.99 s(-1). The value of K(d) = 4.4 micromol/l calculated as k(off) / k(on) was considerably lower than IC(50) = 25.9 +/- 2.9 micromol/l evaluated from the concentration dependence of the integrals of I(to). Simulations on a simple model combining Hodgkin-Huxley type gating kinetics and drug-channel interaction entirely in open channel state agreed well with the experimental data including the difference between the K(d) and IC(50). According to the model, the fraction of blocked channels increases upon depolarization and declines if depolarization is prolonged. The repolarizing step induces recovery from block with time constant of 52 ms. We conclude that in the rat right ventricular myocytes, ajmaline is an open channel blocker with fast recovery from the block at resting voltage.

Bébarová M; Matejovic P; Pásek M; Simurdová M; Simurda J

2005-03-01

146

[Heart rate variability in patients with hypertension and left ventricular hypertrophy].  

UK PubMed Central (United Kingdom)

The aim of the study was to analyse the heart rate variability (HRV) in patients with moderate essential hypertension complicated by left ventricular hypertrophy (LVH). Forty-two patients with untreated essential hypertension participated in the study group and 45 normotensives (16M, 29F, age 49.8 +/- 5.6 years) served as the controls. The hypertensives were divided into those with LVH (n = 25, 10M, 15F, age 50.1 +/- 5.9 years) and those without LVH (n = 17, 4M, 13F, age 52.0 +/- 3.4 years). HRV was recorded and analysed using the CardioPSA System, Medatec. In each subject, 30 min. of ECG recording was obtained: 15 min. in the supine, position and 15 min. in the upright position. Fast Fourier transform was used to analyse total power, low frequency (LF, 0.04-0.15 Hz) and high frequency components (HF, 0.15-0.40 Hz). Left ventricular mass was calculated from echocardiograms using the Deveraux formula. LVH was defined as a left ventricular mass index (LVM) > 134 g/m2 for men and > 110 g/m2 for women. A T-test was used to test for nter-group differences: p < 0.05 was considered as significant. In hypertensive patients with left ventricular hypertrophy, we observed decreased values of HF component, both in supine and upright positions, as compared to hypertensives without LVH. Components of HRV did not differ between the hypertensives without LVH and the normotensives. In hypertensives with a LVH the high frequency component of HRV was decreased, indicating impaired para-sympathetic activity.

Stolarz K; Olszanecka A; Rajzer M; Lubaszewski W; Kawecka-Jaszcz K

2002-01-01

147

[Heart rate variability in patients with hypertension and left ventricular hypertrophy].  

Science.gov (United States)

The aim of the study was to analyse the heart rate variability (HRV) in patients with moderate essential hypertension complicated by left ventricular hypertrophy (LVH). Forty-two patients with untreated essential hypertension participated in the study group and 45 normotensives (16M, 29F, age 49.8 +/- 5.6 years) served as the controls. The hypertensives were divided into those with LVH (n = 25, 10M, 15F, age 50.1 +/- 5.9 years) and those without LVH (n = 17, 4M, 13F, age 52.0 +/- 3.4 years). HRV was recorded and analysed using the CardioPSA System, Medatec. In each subject, 30 min. of ECG recording was obtained: 15 min. in the supine, position and 15 min. in the upright position. Fast Fourier transform was used to analyse total power, low frequency (LF, 0.04-0.15 Hz) and high frequency components (HF, 0.15-0.40 Hz). Left ventricular mass was calculated from echocardiograms using the Deveraux formula. LVH was defined as a left ventricular mass index (LVM) > 134 g/m2 for men and > 110 g/m2 for women. A T-test was used to test for nter-group differences: p < 0.05 was considered as significant. In hypertensive patients with left ventricular hypertrophy, we observed decreased values of HF component, both in supine and upright positions, as compared to hypertensives without LVH. Components of HRV did not differ between the hypertensives without LVH and the normotensives. In hypertensives with a LVH the high frequency component of HRV was decreased, indicating impaired para-sympathetic activity. PMID:12632890

Stolarz, Katarzyna; Olszanecka, Agnieszka; Rajzer, Marek; Lubaszewski, Wojciech; Kawecka-Jaszcz, Kalina

2002-01-01

148

Reduction of Left Ventricular Hypertrophy by Sirolimus in Kidney Transplant Recipients: A Nonrandomized Clinical Trial  

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Full Text Available Background: Persistence of left ventricular hypertrophy (LVH) in renal transplant recipients is associated with unfavorable outcomes. Calcineurin-inhibitor (CNI) nephrotoxicity is a major cause of morbidity and mortality after kidney transplantation. In this study we compared sirolimus (SRL) with calcineurin-inhibitor as primary immunosuppressants for the attenuation of left ventricular hypertrophy in renal transplantation recipients. Methods: In this prospective cohort study done in Shariati Hospital in 2010, we evaluated the effects of sirolimus and CNI on LVH of 55 renal transplant recipients. The cases (19) received sirolimus while the controls (36) received CNI while being matched for age and duration of transplantation. Data regarding blood pressure (BP), hemoglobin, serum creatinine, uric acid and lipid concentrations were assessed and changes in left ventricular (LV) mass were evaluated by echocardiography over a one-year follow-up. Results: Left ventricular mass significantly decreased (P=0.0001) in the SRL group but blood pressure did not differ between the two groups. LV mass and LV mass index both decreased significantly (P?0.05) but the difference was not associated with changes in BP. The difference in interventricular septal thickness at end diastole (IVSD) and posterior wall diameter (PWD) were significant (P?0.05) in the SRL group but the difference in end diastolic diameter (EDD) was not significant. Conclusion: Conversion from CNI to SRL-based immunosuppressive therapy in RTRs is safe and SRL may decrease LVH. SRL seems to be safe and improve renal function without cardiac compromise in kidney transplant recipients.

Sedghipour M; Tabatabaei SAH; Sadadi F; Kamal Hedayat D; Nikdoost F; Sate H; Ghorbani Yekta B

2012-01-01

149

Comparison of the T-tubule system in adult rat ventricular and atrial myocytes, and its role in excitation-contraction coupling and inotropic stimulation.  

Science.gov (United States)

Narrow, tubular, inward projections of the sarcolemma ('T-tubules') are an established feature of adult mammalian ventricular myocytes that enables them to generate the whole-cell Ca2+ transients and produce coordinated contraction. Loss of T-tubules can occur during ageing and under pathological conditions, leading to altered cardiac excitation-contraction coupling. In contrast to adult ventricular cells, atrial myocytes do not generally express an extensive T-tubule system at any stage of development, and therefore rely on Ca2+ channels around their periphery for the induction of Ca2+ signalling and excitation-contraction coupling. Consequently, the characteristics of systolic Ca2+ signals in adult ventricular and atrial myocytes are temporally and spatially distinct. However, although atrial myocytes do not have the same regularly spaced convoluted T-tubule structures as adult ventricular cells, it has been suggested that a proportion of adult atrial cells have a more rudimentary tubule system. We examined the structure and function of these atrial tubules, and explored their impact on the initiation and recovery of Ca2+ signalling in electrically paced myocytes. The atrial responses were compared to those in adult ventricular cells that had intact T-tubules, or that had been chemically detubulated. We found that tubular structures were present in a significant minority of adult atrial myocytes, and were unlike the T-tubules in adult ventricular cells. In those cells where they were present, the atrial tubules significantly altered the on-set, amplitude, homogeneity and recovery of Ca2+ transients. The properties of adult atrial myocyte Ca2+ signals were different from those in adult ventricular cells, whether intact or detubulated. Excitation-contraction coupling in detubulated adult ventricular myocytes, therefore, does not approximate to atrial signalling, even though Ca2+ signals are initiated in the periphery of the cells in both of these situations. Furthermore, inotropic responses to endothelin-1 were entirely dependent on T-tubules in adult ventricular myocytes, but not in atrial cells. Our data reveal that that the T-tubules in atrial cells impart significant functional properties, but loss of these tubular membranes does not affect Ca2+ signalling as dramatically as detubulation in ventricular myocytes. PMID:20106523

Smyrnias, Ioannis; Mair, Waltraud; Harzheim, Dagmar; Walker, Simon A; Roderick, H Llewelyn; Bootman, Martin D

2010-01-27

150

Comparison of the T-tubule system in adult rat ventricular and atrial myocytes, and its role in excitation-contraction coupling and inotropic stimulation.  

UK PubMed Central (United Kingdom)

Narrow, tubular, inward projections of the sarcolemma ('T-tubules') are an established feature of adult mammalian ventricular myocytes that enables them to generate the whole-cell Ca2+ transients and produce coordinated contraction. Loss of T-tubules can occur during ageing and under pathological conditions, leading to altered cardiac excitation-contraction coupling. In contrast to adult ventricular cells, atrial myocytes do not generally express an extensive T-tubule system at any stage of development, and therefore rely on Ca2+ channels around their periphery for the induction of Ca2+ signalling and excitation-contraction coupling. Consequently, the characteristics of systolic Ca2+ signals in adult ventricular and atrial myocytes are temporally and spatially distinct. However, although atrial myocytes do not have the same regularly spaced convoluted T-tubule structures as adult ventricular cells, it has been suggested that a proportion of adult atrial cells have a more rudimentary tubule system. We examined the structure and function of these atrial tubules, and explored their impact on the initiation and recovery of Ca2+ signalling in electrically paced myocytes. The atrial responses were compared to those in adult ventricular cells that had intact T-tubules, or that had been chemically detubulated. We found that tubular structures were present in a significant minority of adult atrial myocytes, and were unlike the T-tubules in adult ventricular cells. In those cells where they were present, the atrial tubules significantly altered the on-set, amplitude, homogeneity and recovery of Ca2+ transients. The properties of adult atrial myocyte Ca2+ signals were different from those in adult ventricular cells, whether intact or detubulated. Excitation-contraction coupling in detubulated adult ventricular myocytes, therefore, does not approximate to atrial signalling, even though Ca2+ signals are initiated in the periphery of the cells in both of these situations. Furthermore, inotropic responses to endothelin-1 were entirely dependent on T-tubules in adult ventricular myocytes, but not in atrial cells. Our data reveal that that the T-tubules in atrial cells impart significant functional properties, but loss of these tubular membranes does not affect Ca2+ signalling as dramatically as detubulation in ventricular myocytes.

Smyrnias I; Mair W; Harzheim D; Walker SA; Roderick HL; Bootman MD

2010-03-01

151

Asociación de la hipertrofía ventricular izquierda con eventos cardiacos posteriores a intervencionismo coronario percutáneo. Association of left ventricular hypertrophy with cardiac events after percutaneous coronary intervention.  

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Full Text Available Introduction: Left ventricular hypertrophy is not included in the prognostic models of cardiacevents after percutaneous coronary intervention.Objective To determine the association of left ventricular hypertrophy with the presenceof cardiac events during 4 years follow-up after percutaneous coronary intervention.Method 80 hypertensive patients without prior revascularization, undergoing successfulpercutaneous coronary intervention with bare-metal stents at the NationalCardiology and Cardiovascular Surgery Institute between December 2002 andApril 2004, were prospectively included. The demographic, clinical and angiographiccharacteristics were included in our database during the procedure.We made a 4 years follow-up.Results Restenosis (p<0.02) was more frequent in the group of hypertensive patientswith hypertrophy of both anterior and posterior left ventricle walls. Univariateregression analysis showed that left ventricular hypertrophy associates with ahigher restenosis incidence (OR 3.12; CI 95% 1.20-8.14).Conclusions Left ventricular hypertrophy is a risk marker of restenosis after percutaneouscoronary intervention. There was no association with any other cardiac eventduring the long follow-up of hypertensive patients.

Amaury Flores Sánchez; María B. Cabalé Vilariño; Luis R. Llerena Rojas

2011-01-01

152

Evaluation of left ventricular hypertrophy using thallium-201 myocardial scintigraphy, echocardiography and vectorcardiography  

International Nuclear Information System (INIS)

Thallium-201 (201Tl) myocardial scintigraphy was performed in 40 patients with left ventricular hypertrophy(LVH). Twelve out of 40 patients had pressure overloading (Aortic stenosis: 5, Hypertension: 7), 14 patients had volume overloading (Aortic regurgitation: 9, Mitral regurgitation: 5) and 14 had idiopathic cardiomyopathy (Hypertrophic type (HCM): 8, Congestive type (CCM): 6), respectively. LV area, LV uptake index and Wall uptake ratio were calculated from left anterior oblique view of 201Tl myocardial images. These three indices of both pressure overloading and volume overloading were significantly higher than those of controls. The degree of LVH was indicated by both LV area and LV uptake index. LV area was significantly larger in volume overloading than in pressure overloading. In idiopathic cardiomyopathy, these three indices of HCM and LV area and LV uptake index of CCM were significantly increased compared with those of controls. LV area of CCM was significantly larger than that of HCM, while Wall uptake ratio of HCM was significantly higher than that of CCM. LV uptake index and Wall uptake ratio of HCM became higher according as left ventricular cavity became smaller. LV area of CCM became larger in proportion as left ventricular cavity became larger and as left ventricular wall thickness became thinner. (author)

1983-01-01

153

Effect of Anemia on Left Ventricular Hypertrophy and Ejection Fraction in Maintenance Hemodialysis Patients  

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Full Text Available The present research aimed to consider the adverse effects of amenia on left venrticular function and structure in dialysis patients due to End-Stage Renal Disease (ESRD) undergoing regular hemodialysis. For patients complete blood count, serum Iron, total iron binding capacity and serum ferritin were measured. On the basis of septal thickness, the patients stratified into, no Left Ventricular Hypertrophy (LVH), mild, moderate and severe LVH. In this study a significant difference of Haemoglobin (Hb) and Haematocryt (Hct ) between males and females with more values in the female group and a significant inverse correlation of serum ferritin with hemoglobin levels were found. A significant inverse correlation of Left Ventricular (LV) ejection fraction with duration of hemodialysis treatment was observed. A near significant inverse correlation of LV ejection fraction with serum ferritin was found, also a significant inverse correlation of LVH with LV ejection fraction was observed too. In present study female dialysis patients had more prominent anemia than males which implies more attention to anemia treatment in this group. We showed an inverse association of LV ejection fraction with serum ferritin. We also showed that duration of hemodialysis treatment have an adverse effect on progression of LVH. We concluded that anemia in conjunction with other important factors like duration of dialysis could aggravate the hypertrophy of LV.

M.D. Azar Baradaran; M.D. Hamid Nasri

2005-01-01

154

Combining stimulus direction and waveform for optimization of threshold stimulation of isolated ventricular myocytes.  

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Electric field stimulation is widely used for heart pacing and arrhythmia reversion. In this study, we analysed the influence of waveform and direction of external stimulating electric field on the excitation threshold of isolated ventricular myocytes. The threshold field (E(T)) was lower when the field was applied longitudinally (E(T,L)) rather than transversally (E(T,T)) to the cell major axis. Rheobase was greater for transversal stimulation, but chronaxie and estimated membrane polarization were similar for both directions. The calculated maximal variation in membrane potential at the threshold (DeltaV(T) approximately 15 mV) was insensitive to field direction. As DeltaV(T) values were similar, we assumed that the E(T,T)/E(T,L) ratio might be described solely as the ratio of the major and minor cell semi-axes. Accordingly, the ratio thus estimated was comparable to that determined experimentally. Stimulus waveform significantly affected both E(T) and DeltaV(T), which were greater for monophasic versus biphasic stimuli. Direction and waveform effects were independent. We conclude that (a) direction affects E(T) by its influence on the ability of a given field intensity to cause threshold membrane polarization and (b) threshold-lowering effects of longitudinal stimulation and biphasic waveforms apparently depend on different mechanisms, are additive and thus may be combined to decrease the energy requirement for myocardial stimulation. PMID:16868351

Bassani, Rosana A; Lima, Katherine A; Gomes, Paulo A P; Oliveira, Pedro X; Bassani, José W M

2006-07-10

155

Contribution of Ca(2+) transporters to relaxation in intact ventricular myocytes from developing rats.  

Science.gov (United States)

The relative contributions of Ca(2+) transporters to intracellular Ca(2+) concentration ([Ca(2+)](i)) decline associated with twitch relaxation were analyzed in intact ventricular myocytes from developing and adult rats. This was accomplished by estimation of individual integrated Ca(2+) fluxes with the use of kinetic parameters calculated from [Ca(2+)](i) measurements during twitches and caffeine-evoked contractures, and from myocardial passive Ca(2+) buffering data. Our main findings were the following: 1) twitch relaxation and [Ca(2+)](i) decline were significantly slower during the first postnatal week than in adults, 2) inhibition of sarcoplasmic reticulum (SR) Ca(2+) accumulation resulted in faster [Ca(2+)](i) decline in young cells than in adult cells, 3) the contributions of the SR Ca(2+) uptake and Na(+)/Ca(2+) exchange (NCX) to twitch relaxation increased from ~75 to 92%, and decreased from 24 to 5%, respectively, from birth to adulthood, and 4) Ca(2+) transport by the sarcolemmal Ca(2+)-ATPase was apparently increased in neonates. Our data indicate that despite a marked increase in NCX contribution to cell relaxation in immature rats, the SR Ca(2+)-ATPase appears to be the predominant transporter responsible for relaxation-associated [Ca(2+)](i) decline from birth to adulthood. PMID:12003852

Bassani, Rosana A; Bassani, José W M

2002-06-01

156

Optical action potential screening on adult ventricular myocytes as an alternative QT-screen.  

UK PubMed Central (United Kingdom)

BACKGROUND/AIMS: QT-interval screens are increasingly important for cardiac safety on all new medications. So far, investigations rely on animal experiments or cell-based screens solely probing for conductance alterations in heterologously expressed hERG-channels in cell lines allowing for a high degree of automation. Adult cardiomyocytes can not be handled by automated patch-clamp setups. Therefore optical screening of primary isolated ventricular myocytes is regarded as an alternative. Several optical voltage sensors have been reported for ratiometric measurements, but they all influenced the naïve action potential. The aim of the present study was to explore the recording conditions and define settings that allow optical QT-interval screens. METHODS: Based on an improved optical design, individual action potentials could be recorded with an exceptional signal-to-noise-ratio. The sensors were validated using the patch-clamp technique, confocal microscopy and fluorescence lifetime imaging in combination with global unmixing procedures. RESULTS: We show that the small molecule dye di-8-ANEPPS and the novel genetically encoded sensor Mermaid provide quantitative action potential information. When applying such sensors we identified distinctly different pharmacological profiles of action potentials for adult and neonatal rat cardiomyocytes. CONCLUSION: Optical methods can be used for QT-interval investigations based on cellular action potentials using either the small molecule dye di-8-ANEPPS or the genetically encoded sensor Mermaid. Adult cardiomyocytes are superior to neonatal cardiomyocytes for such pharmacological investigations. Optical QT-screens may replace intricate animal experiments.

Tian Q; Oberhofer M; Ruppenthal S; Scholz A; Buschmann V; Tsutsui H; Miyawaki A; Zeug A; Lipp P; Kaestner L

2011-01-01

157

Blocking effect of puerarin on calcium channel in isolated guinea pig ventricular myocytes.  

UK PubMed Central (United Kingdom)

OBJECTIVE: To identify whether Puerarin (Puer) has blocking effects on L-type calcium channel. METHODS: We used whole-cell recording of patch-clamp techniques to analyse calcium channel current in ventricular myocytes isolated from Langendorff guinea pig hearts by collagenase. RESULTS: In control group, peak calcium channel current was decreased by 10.6% and 29.8% at 5, 10 min of recording time, respectively. For the same period, 0.1 mmol/L Puer reduced calcium current by 23.9% and 72.4%. 0.1 and 1 mmol/L Puer inhibited the amplitude of peak Calcium channel current by 40.6% and 63.2% after perfusing for 10 min. Compared with control group in which "rundown" phenomenon was observed, Puer also demonstrated its blocking effect on L-type channel. While washout of Puer with perfusing solution, calcium channel current went down further instead of recovery. Current-voltage (I-V) curves showed that the levels of calcium channel current were obviously decreased by Puer (both 0.1 mmo/L and 1 mmo/L) form -40 mV to +10 mV. CONCLUSION: Puer has blocking effect on L-type calcium channel in a concentration dependent manner.

Qian Y; Li Z; Huang L; Han X; Sun J; Zhou H; Liu Z

1999-09-01

158

Use-dependent features of 4-aminopyridine block of transient outward current in rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

The inhibition of the calcium-independent transient outward current (Ito) by the widely used blocker 4-aminopyridine (4-AP) was studied in adult Wistar rat ventricular myocytes, enzymatically isolated and voltage-clamped in the whole cell configuration using patch-clamp pipettes. 4-AP at 1 mmol/l concentration caused complete steady-state block of Ito at resting or hyperpolarized voltages. The block was partially removed during repeated depolarizations applied at frequencies above 0.25 Hz. Changes in the level of block during a depolarizing pulse (to + 40 mV) and during a following rest period (at -90 mV) were analyzed. On depolarization, the recovery from 4-AP block (at 0.5 mmol/l) started with a delay approximately corresponding to the time constant of Ito inactivation and then followed a monoexponential time course (time constant of about 44 ms). The restoration of block at a holding voltage of -90 mV, after recovery of Ito from inactivation, followed a monoexponential time course (time constant of about 1.2 s). The results are consistent with the hypothesis that the binding site for 4-AP at the Ito channel is available in the closed and open states but not when inactivated. Unblocking of Ito at stimulation intervals shorter than approximately 1 s may occur at 4-AP concentrations below 4 mmol/l.

Christé G; Simurdová M; Simurda J

1995-04-01

159

Use-dependent features of 4-aminopyridine block of transient outward current in rat ventricular myocytes.  

Science.gov (United States)

The inhibition of the calcium-independent transient outward current (Ito) by the widely used blocker 4-aminopyridine (4-AP) was studied in adult Wistar rat ventricular myocytes, enzymatically isolated and voltage-clamped in the whole cell configuration using patch-clamp pipettes. 4-AP at 1 mmol/l concentration caused complete steady-state block of Ito at resting or hyperpolarized voltages. The block was partially removed during repeated depolarizations applied at frequencies above 0.25 Hz. Changes in the level of block during a depolarizing pulse (to + 40 mV) and during a following rest period (at -90 mV) were analyzed. On depolarization, the recovery from 4-AP block (at 0.5 mmol/l) started with a delay approximately corresponding to the time constant of Ito inactivation and then followed a monoexponential time course (time constant of about 44 ms). The restoration of block at a holding voltage of -90 mV, after recovery of Ito from inactivation, followed a monoexponential time course (time constant of about 1.2 s). The results are consistent with the hypothesis that the binding site for 4-AP at the Ito channel is available in the closed and open states but not when inactivated. Unblocking of Ito at stimulation intervals shorter than approximately 1 s may occur at 4-AP concentrations below 4 mmol/l. PMID:8846885

Christé, G; Simurdová, M; Simurda, J

1995-04-01

160

Mechanical deformation of ventricular myocytes modulates both TRPC6 and Kir2.3 channels.  

Science.gov (United States)

Cardiomyocytes respond to mechanical stretch with an increase [Ca2+]i. Here, we analyzed which ion channels could mediate this effect. Murine ventricular myocytes were attached to a glass coverslip and a cell-attached glass stylus sheared the upper cell part versus the attached cell bottom. At negative clamp potentials, stretch induced inward currents that increased with the extent of stretch and reversed within 2 min after relaxation from stretch. Stretch activated a nearly voltage-independent GsMTx-4-sensitive non-selective cation conductance Gns, antibodies against TRPC6 prevented Gns activation. In addition, stretch deactivated a Cs+-sensitive inwardly rectifying potassium conductance GK1, antibodies against Kir2.3 inhibited this effect. Immunolabeling localized TRPC6 and Kir2.3 in T-tubular membranes, and stretch-induced changes in membrane currents were absent in cells whose T-tubules had been removed. In absence of stretch, we could activate Gns and deactivate GK1 by 1-oleoyl-2-acetyl-sn-glycerol (OAG) and other amphipaths. We interpret that the function of TRPC6 and Kir2.3 channels is controlled by both tension and curvature of the surrounding lipid bilayer that are changed by incorporation of amphipaths. Stretch-activation of TRPC6 channels may increase Ca2+ influx directly and indirectly, by membrane depolarization (activation of voltage-gated Ca2+ channels) and by elevated [Na+]i (augmented Na+,Ca2+-exchange). PMID:18635261

Dyachenko, V; Husse, B; Rueckschloss, U; Isenberg, G

2008-07-16

 
 
 
 
161

Mechanical deformation of ventricular myocytes modulates both TRPC6 and Kir2.3 channels.  

UK PubMed Central (United Kingdom)

Cardiomyocytes respond to mechanical stretch with an increase [Ca2+]i. Here, we analyzed which ion channels could mediate this effect. Murine ventricular myocytes were attached to a glass coverslip and a cell-attached glass stylus sheared the upper cell part versus the attached cell bottom. At negative clamp potentials, stretch induced inward currents that increased with the extent of stretch and reversed within 2 min after relaxation from stretch. Stretch activated a nearly voltage-independent GsMTx-4-sensitive non-selective cation conductance Gns, antibodies against TRPC6 prevented Gns activation. In addition, stretch deactivated a Cs+-sensitive inwardly rectifying potassium conductance GK1, antibodies against Kir2.3 inhibited this effect. Immunolabeling localized TRPC6 and Kir2.3 in T-tubular membranes, and stretch-induced changes in membrane currents were absent in cells whose T-tubules had been removed. In absence of stretch, we could activate Gns and deactivate GK1 by 1-oleoyl-2-acetyl-sn-glycerol (OAG) and other amphipaths. We interpret that the function of TRPC6 and Kir2.3 channels is controlled by both tension and curvature of the surrounding lipid bilayer that are changed by incorporation of amphipaths. Stretch-activation of TRPC6 channels may increase Ca2+ influx directly and indirectly, by membrane depolarization (activation of voltage-gated Ca2+ channels) and by elevated [Na+]i (augmented Na+,Ca2+-exchange).

Dyachenko V; Husse B; Rueckschloss U; Isenberg G

2009-01-01

162

Three distinct directions of intramural activation reveal nonuniform side-to-side electrical coupling of ventricular myocytes.  

UK PubMed Central (United Kingdom)

BACKGROUND: The anisotropy of cardiac tissue is a key determinant of 3D electric propagation and the stability of activation wave fronts in the heart. The electric properties of ventricular myocardium are widely assumed to be axially anisotropic, with activation propagating most rapidly in the myofiber direction and at uniform velocity transverse to this. We present new experimental evidence that contradicts this view. METHODS AND RESULTS: For the first time, high-density intramural electric mapping (325 electrodes at approximately 4x4x1-mm spacing) from pig left ventricular tissue was used to reconstruct 3D paced activation surfaces projected directly onto 3D tissue structure imaged throughout the same left ventricular volume. These data from 5 hearts demonstrate that ventricular tissue is electrically orthotropic with 3 distinct propagation directions that coincide with local microstructural axes defined by the laminar arrangement of ventricular myocytes. The maximum conduction velocity of 0.67+/-0.019 ms(-1) was aligned with the myofiber axis. However, transverse to this, the maximum conduction velocity was 0.30+/-0.010 ms(-1), parallel to the myocyte layers and 0.17+/-0.004 ms(-1) normal to them. These orthotropic conduction velocities give rise to preferential activation pathways across the left ventricular free wall that are not captured by structurally detailed computer models, which incorporate axially anisotropic electric properties. CONCLUSIONS: Our findings suggest that current views on uniform side-to-side electric coupling in the heart need to be revised. In particular, nonuniform laminar myocardial architecture and associated electric orthotropy should be included in future models of initiation and maintenance of ventricular arrhythmia.

Caldwell BJ; Trew ML; Sands GB; Hooks DA; LeGrice IJ; Smaill BH

2009-08-01

163

Prognostic significance of left ventricular diastolic dysfunction in patients with left ventricular hypertrophy and systemic hypertension (the LIFE Study)  

DEFF Research Database (Denmark)

Patients with hypertension and left ventricular (LV) hypertrophy commonly have impaired diastolic filling. However, it remains unknown whether changes in LV diastolic filling variables are associated with cardiovascular morbidity and mortality. In this study, 778 patients with hypertension with electrocardiographic LV hypertrophy who underwent echocardiography at baseline and annually thereafter during randomized losartan- or atenolol-based antihypertensive treatment were followed for a mean of 4.6 years. The composite cardiovascular end point was the first occurrence of fatal or nonfatal myocardial infarction, fatal or nonfatal stroke, and cardiovascular mortality. Antihypertensive therapy resulted in an increase in the prevalence of normal transmitral flow pattern from 28% to 46% of patients. Although antihypertensive treatment often resulted in a marked increase in the prevalence of normal mitral valve flow pattern, this was not associated with reduced cardiovascular morbidity and mortality when adjusting for blood pressure, left atrial diameter, LV mass index, and treatment in time-varying Cox analyses. In contrast, lower in-treatment E/A ratios and shorter mitral valve deceleration times were associated with less risk for heart failure. Similarly, normal in-treatment transmitral flow pattern was strongly associated with less risk for heart failure (hazard ratio 0.22, 95% confidence interval 0.05 to 0.98, p = 0.048), even when taking in-treatment left atrial diameter and blood pressure into account. In conclusion, antihypertensive treatment in patients with hypertension with electrocardiographic LV hypertrophy resulted in significant improvement in transmitral flow patterns; this was not associated with reduced cardiovascular morbidity and mortality. However, normal in-treatment LV filling was strongly associated with a reduced risk for hospitalization for heart failure.

Wachtell, Kristian; Palmieri, Vittorio

2010-01-01

164

Nighttime blood pressure and new-onset left ventricular hypertrophy: findings from the Pamela population.  

UK PubMed Central (United Kingdom)

The relationship between circadian blood pressure (BP) variations and the extent of subclinical cardiac organ damage is still debated. In a general population, we investigated the association of night-to-day BP fall, as well as nocturnal BP level (mean and lowest values), with left ventricular (LV) hypertrophy and the value of both BP parameters in predicting new-onset LV hypertrophy. Office BP, 24-hour ambulatory BP values, and laboratory investigations were assessed on entry in 1682 subjects (50.2% men; mean age, 50.2±13.7 years) of the Pressioni Arteriose Monitorate E Loro Associazioni. Echocardiographic LV mass was measured at the initial evaluation and 10 years later. Multiple regression analyses, including daytime systolic BP (SBP), age, sex, and body mass index, showed that the lowest SBP level and the extent of nocturnal SBP decline were independently related to baseline LV mass. After adjustment for several confounders, both mean nocturnal SBP (relative risk for each 10-mm Hg increase in SBP, 1.15; 95% confidence interval, 1.01-1.23; P<0.0001) and the lowest SBP level (relative risk for each 10-mm Hg increase in SBP, 1.10; 95% confidence interval, 1.02-1.19; P=0.01) were independent predictors of new-onset LV hypertrophy. This was not the case for the magnitude of nighttime SBP fall (hazard ratio for each 10% decrease in SBP, 0.91; 95% confidence interval, 0.80-1.04; P=0.18). In a general population, nighttime BP level rather than the nocturnal BP decline may be regarded as a reliable parameter for predicting the development of LV hypertrophy in subjects with normal LV mass. This finding may have important implications for optimizing cardiovascular prevention in the general population.

Cuspidi C; Facchetti R; Bombelli M; Sala C; Negri F; Grassi G; Mancia G

2013-07-01

165

Echocardiographic partition values and prevalence of left ventricular hypertrophy in hypertensive Nigerians.  

UK PubMed Central (United Kingdom)

BACKGROUND: Left ventricular hypertrophy (LVH) is a well known independent risk factor for cardiovascular events. It has been shown that combination of left ventricular mass (LVM) and relative wall thickness (RWT) can be used to identify different forms of left ventricular (LV) geometry. Prospective studies have shown that LV geometric patterns have prognostic implications, with the worst prognosis associated with concentric hypertrophy. The methods for the normalization or indexation of LVM have also recently been shown to confer some prognostic value especially in obese population. We sought to determine the prevalence of echocardiographic lLVH using eight different and published cut-off or threshold values in hypertensive subjects seen in a developing country's tertiary centre. METHODS: Echocardiography was performed in four hundred and eighty consecutive hypertensive subjects attending the cardiology clinic of the University college Hospital Ibadan, Nigeria over a two-year period. RESULTS: Complete data was obtained in 457 (95.2%) of the 480 subjects (48.6% women). The prevalence of LVH ranged between 30.9-56.0%. The highest prevalence was when LVM was indexed to the power of 2.7 with a partition value of 49.2 g/ht2.7 in men and 46.7 g/ht2.7 in women. The lowest prevalence was observed when LVM was indexed to body surface area (BSA) and a partition value of 125 g/m2 was used for both sexes. Abnormal LV geometry was present in 61.1%-74.0% of our subjects and commoner in women. CONCLUSION: The prevalence of LVH hypertensive patients is strongly dependent on the cut-off value used to define it. Large-scale prospective study will be needed to determine the prognostic implications of the different LV geometry in native Africans.

Adebiyi AA; Ogah OS; Aje A; Ojji DB; Adebayo AK; Oladapo OO; Falase AO

2006-01-01

166

Echocardiographic partition values and prevalence of left ventricular hypertrophy in hypertensive Nigerians  

Directory of Open Access Journals (Sweden)

Full Text Available Abstract Background Left ventricular hypertrophy (LVH) is a well known independent risk factor for cardiovascular events. It has been shown that combination of left ventricular mass (LVM) and relative wall thickness (RWT) can be used to identify different forms of left ventricular (LV) geometry. Prospective studies have shown that LV geometric patterns have prognostic implications, with the worst prognosis associated with concentric hypertrophy. The methods for the normalization or indexation of LVM have also recently been shown to confer some prognostic value especially in obese population. We sought to determine the prevalence of echocardiographic lLVH using eight different and published cut-off or threshold values in hypertensive subjects seen in a developing country's tertiary centre. Methods Echocardiography was performed in four hundred and eighty consecutive hypertensive subjects attending the cardiology clinic of the University college Hospital Ibadan, Nigeria over a two-year period. Results Complete data was obtained in 457 (95.2%) of the 480 subjects (48.6% women). The prevalence of LVH ranged between 30.9–56.0%. The highest prevalence was when LVM was indexed to the power of 2.7 with a partition value of 49.2 g/ht2.7 in men and 46.7 g/ht2.7 in women. The lowest prevalence was observed when LVM was indexed to body surface area (BSA) and a partition value of 125 g/m2 was used for both sexes. Abnormal LV geometry was present in 61.1%–74.0% of our subjects and commoner in women. Conclusion The prevalence of LVH hypertensive patients is strongly dependent on the cut-off value used to define it. Large-scale prospective study will be needed to determine the prognostic implications of the different LV geometry in native Africans.

Adebiyi Adewole A; Ogah Okechukwu S; Aje Akinyemi; Ojji Dike B; Adebayo Adedeji K; Oladapo Olulola O; Falase Ayodele O

2006-01-01

167

A model of the guinea-pig ventricular cardiac myocyte incorporating a transverse-axial tubular system.  

Science.gov (United States)

A model of the guinea-pig cardiac ventricular myocyte has been developed that includes a representation of the transverse-axial tubular system (TATS), including heterogeneous distribution of ion flux pathways between the surface and tubular membranes. The model reproduces frequency-dependent changes of action potential shape and intracellular ion concentrations and can replicate experimental data showing ion diffusion between the tubular lumen and external solution in guinea-pig myocytes. The model is stable at rest and during activity and returns to rested state after perturbation. Theoretical analysis and model simulations show that, due to tight electrical coupling, tubular and surface membranes behave as a homogeneous whole during voltage and current clamp (maximum difference 0.9 mV at peak tubular INa of -38 nA). However, during action potentials, restricted diffusion and ionic currents in TATS cause depletion of tubular Ca2+ and accumulation of tubular K+ (up to -19.8% and +3.4%, respectively, of bulk extracellular values, at 6 Hz). These changes, in turn, decrease ion fluxes across the TATS membrane and decrease sarcoplasmic reticulum (SR) Ca2+ load. Thus, the TATS plays a potentially important role in modulating the function of guinea-pig ventricular myocyte in physiological conditions. PMID:17888503

Pásek, Michal; Simurda, Jiri; Orchard, Clive H; Christé, Georges

2007-08-11

168

The effects of implanted valve sizes on ventricular hypertrophy in aortic stenosis  

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Full Text Available Objective: We aimed to study the effects of the valve sizes according to body surface area on aortic gradient and ventricular hypertrophy in the cases of aortic valve replacement due to isolated aortic stenosis.Methods: Between January 2006 and April 2007, patients (12 men, 15 women; totally 27) followed up prospectively with echocardiography fourth and sixth month postoperatively. The patients were divided into two groups according to the prosthetic aortic valve diameters (19-21 mm vs 23-25 mm). The primary endpoints between the two groups (aortic regurgitation, left ventricular mass index and transvalvular gradient measured by color and continuous wave Doppler) were compared. Fischer exact test and Mann-Whitney U test were used for intergroup comparison whereas intragroup analysis was done with Freidman test.Results: Mean systolic gradient and left ventricular mass index were significantly reduced in 23 mm and 25 mm valves (p<0.01) in the postoperative follow-up. In addition, especially, decline in the values of left ventricular mass, left ventricular mass index, peak systolic gradient and the mean systolic gradient were found to be significant. These values associated with regression were detectable at the postoperative 4th month, but actual significant regression was observed at the postoperative 6th month (p<0.01). On the other hand, the values obtained for 19 mm and 21 mm valves also showed significant progress (p<0.05).Conclusion: Factors such as age, gender and activity are important in the selection of appropriate valve sizes in aortic valve replacement. However, the patient's body surface is the most important prognostic factor compared to others.

Hikmet Selçuk Gedik; Kemal Korkmaz; Gökhan Lafç?; Adnan Yalç?nkaya; Kerim Ça?l?

2012-01-01

169

Homeostatic regulation of electrical excitability in physiological cardiac hypertrophy.  

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Pathological biomechanical stresses cause cardiac hypertrophy, which is associated with QT prolongation and arrhythmias. Previous studies have demonstrated that repolarizing K(+) current densities are decreased in pressure overload-induced left ventricular hypertrophy, resulting in action potential and QT prolongation. Cardiac hypertrophy also occurs with exercise training, but this physiological hypertrophy is not associated with electrical abnormalities or increased arrhythmia risk, suggesting that repolarizing K(+) currents are upregulated, in parallel with the increase in myocyte size, to maintain normal cardiac function. To explore this hypothesis directly, electrophysiological recordings were obtained from ventricular myocytes isolated from two mouse models of physiological hypertrophy, one produced by swim-training of wild-type mice and the other by cardiac-specific expression of constitutively active phosphoinositide-3-kinase-p110? (caPI3K?). Whole-cell voltage-clamp recordings revealed that repolarizing K(+) current amplitudes were higher in ventricular myocytes isolated from swim-trained and caPI3K?, compared with wild-type, animals. The increases in K(+) current amplitudes paralleled the observed cellular hypertrophy, resulting in normalized or increased K(+) current densities. Electrocardiographic parameters, including QT intervals, as well as ventricular action potential waveforms in swim-trained animals/myocytes were indistinguishable from controls, demonstrating preserved electrical function. Additional experiments revealed that inward Ca(2+) current amplitudes/densities were also increased in caPI3K?, compared with WT, left ventricular myocytes. The expression of transcripts encoding K(+), Ca(2+) and other ion channel subunits was increased in swim-trained and caPI3K? ventricles, in parallel with the increase in myocyte size and with the global increases in total cellular RNA expression. In contrast to pathological hypertrophy, therefore, the functional expression of repolarizing K(+) (and depolarizing Ca(2+)) channels is increased with physiological hypertrophy, reflecting upregulation of the underlying ion channel subunit transcripts and resulting in increased current amplitudes and the normalization of current densities and action potential waveforms. Taken together, these results suggest that activation of PI3K? signalling preserves normal myocardial electrical functioning and could be protective against the increased risk of arrhythmias and sudden death that are prevalent in pathological cardiac hypertrophy. PMID:20974681

Yang, Kai-Chien; Foeger, Nicholas C; Marionneau, Céline; Jay, Patrick Y; McMullen, Julie R; Nerbonne, Jeanne M

2010-10-25

170

Prevalence and Determinants of Left Ventricular Hypertrophy in Hypertensive Patients at a Primary Care Clinic  

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Full Text Available Left ventricular hypertrophy (LVH) has prognostic significance on cardiovascular mortality and morbidity. However, echocardiography screening for LVH is not routinely done for hypertensive patients in a primary care setting. thus, this quantitative study aims to determine the prevalence and factors associated with LVH in hypertensive patients at a primary care setting. this was a cross-sectional study of 359 consecutive patients with uncomplicated essential hypertension attending a hospital-based clinic in Malaysia. All subjects underwent an echocardiography test. LVH occur when the left ventricular posterior wall thickness together with inter-ventricular septal thickness is ?11 mm. It was found that 24% patients fulfilled the criteria for LVH. the mean age of the study population was 59.2±7.7 years; mean duration of hypertension was 9.7±7.5 years; and mean blood pressure was 136.5/81.5 (±13.7/7.7) mmHg. Using multiple logistic regression analysis, patients who were obese [odds ratio (oR) 8.34, 95% confidence interval (CI) 3.14, 22.22] and male gender (oR 1.96, 95% CI 1.08, 3.16) had significant positive association with LVH. LVH was found in approximately one fourth of the hypertensive patients at a hospital-based primary care setting. there was a significant positive association between LVH and obesity and being male. Guidelines for enhancing use of echocardiography in detecting LVH may be needed.

Ching SM; Chia YC; Wan Azman WA

2012-01-01

171

Association of left ventricular hypertrophy with high-sensitive C-reactive protein in hemodialysis patients.  

UK PubMed Central (United Kingdom)

BACKGROUND: Micro inflammation and cardiovascular disease such as left ventricular hypertrophy (LVH) are common in hemodialysis (HD) patients. Hence, we have evaluated the relationship between high-sensitive C-reactive protein (hs-CRP), as an inflammation marker, and left ventricular mass index (LVMi) and left ventricular mass (LVM) in HD patients. METHODS: An analytical cross-sectional study was performed in 104 HD patients. Serum hs-CRP, LVMi, LVM, and blood pressure were evaluated; demographic data and duration of HD were also recorded. Finally, results were analyzed by using Student's t test, Pearson's correlation coefficient, one-way ANOVA and multiple regression to determine the relationship between LVMi and other variables. RESULTS: A total of 66 male patients (63.46 %) and 38 female patients, with a mean age of 51.75 ± 15.98 years-old, participated in this study. Hypertension was the most common underlying disease (65.4 %). The mean LVMi was 366.98 ± 120.89 g/m(2) and the mean hs-CRP was 8.55 mg/l. Eighty-nine percent of patients had LVH. The hs-CRP level was significantly associated with age and with LVM (P = 0.0001, P = 0.039, respectively). On multivariate analysis, hs-CRP and systolic blood pressure were found to be independent predictors of LVM and LVMi. CONCLUSIONS: This study shows that hs-CRP and systolic BP are independent predictors of LVH in HD patients.

Monfared A; Salari A; Kazemnezhad E; Lebadi M; Khosravi M; Mehrjardi NK; Rahimifar S; Amini N

2013-01-01

172

Variants of tumor necrosis factor-induced protein 3 gene are associated with left ventricular hypertrophy in hypertensive patients.  

UK PubMed Central (United Kingdom)

BACKGROUND: Tumor necrosis factor-induced protein 3 (TNFAIP3) gene has been shown important in cardiac remodeling. The aim of the present study was to investigate whether the variants of TNFAIP3 gene are associated with left ventricular hypertrophy (LVH) in hypertensive patients. METHODS: Four representatives of all the other single nucleotide polymorphisms (SNPs) in TNFAIP3 gene were tested for association with hypertrophy in two independent hypertensive populations (n = 2120 and n = 324). RESULTS: We found that only the tag SNP (rs5029939) was consistently lower in the hypertensives with cardiac hypertrophy than in those without cardiac hypertrophy in the two study populations, indicating a protective effect on LVH (odds ratio (OR) (95% confidence interval (CI)) 0.58 (0.358 - 0.863), P = 0.035; OR (95%CI) = 0.477 (0.225 - 0.815), P < 0.05, respectively). Multiple regression analyses confirmed that the patients with G allele of rs5029939 had less thickness in inter-ventricular septum, left ventricular posterior wall, relative wall thickness and left ventricular mass index than did those with CC allele in the hypertensive patients in both study populations (all P < 0.01). CONCLUSION: These findings indicate that the SNP (rs5029939) in the TNFAIP3 gene may serve as a novel protective genetic marker for the development of LVH in patients with hypertension.

Xue H; Wang SX; Wang XJ; Xin Y; Wang H; Song XD; Sun K; Wang YB; Hui RT

2011-05-01

173

Increased guanylate cyclase activity is associated with an increase in cyclic guanosine 3',5'-monophosphate in left ventricular hypertrophy.  

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Left ventricular hypertrophy (LVH) produced by aortic valve plication leads to increased myocardial cyclic GMP. We tested whether this was a result of increased soluble guanylate cyclase activity or nitric oxide (NO) synthase and its functional consequences. We used the nitric oxide donor 3-morpholi...

Sadoff, J D; Scholz, P M; Tse, J; Weiss, H R

174

Changes in electrocardiographic left ventricular hypertrophy and risk of major cardiovascular events in isolated systolic hypertension: the LIFE study  

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The predictive value of changes in the severity of electrocardiographic left ventricular hypertrophy (ECG-LVH) during antihypertensive therapy remains unclear in isolated systolic hypertension (ISH). In a Losartan Intervention For Endpoint reduction in hypertension substudy, we included 1320 patients aged 54-83 years with systolic blood pressure (BP) of 160-200?mm?Hg, diastolic BP

Larstorp, A C K; Okin, P M

2011-01-01

175

Iodine-123 phenylpentadecanoic acid myocardial scintigraphy in patients with left ventricular hypertrophy: Alterations in left ventricular distribution and utilization  

International Nuclear Information System (INIS)

Regional alterations in myocardial substrate uptake and/or utilization have been demonstrated in rats with hypertension. To determine whether alterations in left ventricular fatty acid uptake and/or utilization are present in patients with left ventricular hypertrophy (LVH), we compared the results of rest and exercise iodine-123 phenylpentadecanoic acid (IPPA) myocardial scintigraphy in 10 patients with hypertension who had concentric LVH without evidence of coronary artery disease and in 15 normal subjects. Patients with LVH had more heterogeneous left ventricular activity of IPPA compared to normal subjects after exercise but not at rest. Although IPPA clearance was similar in both patients with LVH and normal subjects, postexercise washout in segments showing decreased initial IPPA uptake was reduced compared to washout at rest in patients with LVH (11.7 +/- 7.5% versus 21.5 +/- 8.4% at 20 minutes after injection, n = 15; p = 0.005). Exercise thallium-201 (TI-201) scintigraphy was normal in all seven patients with LVH tested. Patients with LVH showed significantly greater heterogeneity in IPPA uptake compared to TI-201 uptake immediately after exercise (25 +/- 5% versus 16 +/- 6%; p = 0.013). We conclude that (1) compared to normal subjects, patients with LVH show heterogeneous myocardial IPPA activity after exercise but not at rest; (2) postexercise washout of IPPA was decreased in segments with reduced uptake after exercise in patients with LVH; and (3) the distribution of IPPA is more heterogeneous than that of TI-201 immediately after exercise in patients with concentric LVH. The postexercise heterogeneity in IPPA uptake and delayed washout in segments with reduced initial uptake is consistent with exercise-induced myocardial ischemia in patients with LVH.

1990-01-01

176

The reduction of left ventricular hypertrophy after renal transplantation is not influenced by the immunosuppressive regimen.  

UK PubMed Central (United Kingdom)

BACKGROUND: Cardiovascular (CV) disease is the first cause of death after kidney transplantation. Left ventricular hypertrophy (LVH) is one of the main CV risk factors. It has been reported that the antiproliferative properties of everolimus (EVE) treatment may decrease left ventricular mass. The aim of this study was to evaluate the evolution of LVH in two groups of kidney transplant recipients receiving immunosuppressive treatment with low-dose calcineurin inhibitor (CNI) + EVE or CNI + mycophenolate mofetil (MMF). METHODS: We evaluated 104 patients of mean age 47.5 ± 13.1 years who underwent kidney transplantation between January 2006 and December 2009 pretransplant by echocardiography, which was repeated every year for 3 years during which all patients continued the initial therapy. Over the 3-year period 76 subjects were treated with MMF, and 28 with EVE. We recorded left ventricular end-diastolic diameter (LVEDD), interventricular septum thickness in diastole (IVSTD), left ventricular posterior wall thickness in diastole (LVPWD), left ventricular end-diastolic volume and end-systolic volume during the follow-up echocardiographic evaluations. RESULTS: No differences in the evolution of the echocardiographic parameters were observed between the two groups-MMF versus EVE group: LVEDD, 50.3 ± 5.1 versus 51.2 ± 6.7 mm; IVSTD, 11.2 ± 1.9 versus 11.3 ± 2 mm; LVPWD, 10.2 ± 1.9 versus 10.5 ± 1.7 mm; relative wall thickness, 0.041 ± 0.08 versus 0.42 ± 0.08; ejection fraction, 63 ± 6% versus 61 ± 5%; and left ventricular mass index, 113 ± 28.9 versus 121.9 ± 39.4 g/m(2), respectively. Compared with pretransplant echocardiographic evaluations, similar reductions in left ventricular mass index were noted in both groups after transplantation. CONCLUSIONS: We observed that after renal transplantation there was a reduction of the LVH respect to the pretransplant dialytic status. The two immunosuppressive regimen did not influence the evolution of post-transplant LVH.

Salerno MP; Rossi E; Favi E; Pedroso JA; Spagnoletti G; Romagnoli J; Citterio F

2013-09-01

177

Urotensin II activates sarcolemmal Na+/H+ exchanger in adult rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

OBJECTIVES: Our aims in the present study were (1) to determine the effects of urotensin II (UT-II) on the sarcolemmal Na/H exchanger (NHE1) activity, and (2) to investigate possible kinase pathways for UT-II-mediated NHE1 stimulation. METHODS: In single rat ventricular myocytes (n = 5-10/group) loaded with the pH-sensitive fluoroprobe carboxy-seminaphthorhodafluor-1, acid efflux rates (JH) were determined as an index of NHE1 activity by rate of recovery of intracellular pH (pHi) from NH4Cl-induced acidosis and the intrinsic buffering power. Phosphorylation of extracellular signal-regulated kinase (ERK), a key kinase of NHE1 activation, was determined by Western blot analysis. RESULTS: JH increased by 31%-71% relative to control in the presence of 100 nmol/L UT-II at pHi range of 6.6-7.0. Stimulation of NHE1 activity by UT-II was abolished by inhibitors of phospholipase C, protein kinase C, and ERK kinase; 2-nitro-4-carboxyphenil-N,N-diphenilcarbamate at 100 micromol/L, GF109203X at 300 nmol/L, and PD98059 at 50 micromol/L, respectively. Moreover, UT-II at 100 nmol/L produced a significant increase in cellular ERK1/2 phosphorylation, which was also inhibited by those inhibitors. CONCLUSIONS: Our study was the first to demonstrate that UT-II activates the cardiac sarcolemmal NHE1 and that the phenomenon may involve, at least in part, the phospholipase C-protein kinase C-ERK pathway.

Kato K; Yasutake M; Jia D; Snabaitis AK; Avkiran M; Kusama Y; Takano T; Mizuno K

2010-02-01

178

Effect of ethanol on action potential and ionic membrane currents in rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

AIM: Even though alcohol intoxication is often linked to arrhythmias, data describing ethanol effect on cardiac ionic channels are rare. In addition, ethanol is used as a solvent of hydrophobic compounds in experimental studies. We investigated changes of the action potential (AP) configuration and main ionic membrane currents in rat cardiomyocytes under 20-1500 m(M) ethanol. Methods:? Experiments were performed on enzymatically isolated rat right ventricular myocytes using the whole cell patch-clamp technique at room temperature. Results:? Ethanol reversibly decelerated the upstroke velocity and decreased AP amplitude and duration at 0.2 and 3 Hz. The fast sodium current I(Na) , l-type calcium current I(Ca) and transient outward potassium current I(to) were reversibly inhibited in a concentration-dependent manner (50% inhibition at 446 ± 12, 553 ± 49 and 1954 ± 234 m(M), respectively, with corresponding Hill coefficients 3.1 ± 0.3, 1.1 ± 0.2 and 0.9 ± 0.1). Suppression of I(Na) and I(Ca) magnitude was slightly voltage dependent. The effect on I(Ca) and I(to) was manifested mainly as an acceleration of their apparent inactivations with a decreased slow and fast time constant respectively. As a consequence of marked differences in n(H) , sensitivity of the currents to ethanol at 10% inhibition decreases in the following order: I(Ca) (75 mm, 3.5‰), I(to) (170 m(M), 7.8‰) and I(Na) (220 m(M), 10.1‰). Conclusion:? Our results suggest a slight inhibition of all the currents at ethanol concentrations relevant to deep alcohol intoxication. The concentration dependence measured over a wide range may serve as a guideline when using ethanol as a solvent.

Bébarová M; Matejovi? P; Pásek M; Ohlídalová D; Jansová D; Simurdová M; Simurda J

2010-12-01

179

ATP counteracts the rundown of gap junctional channels of rat ventricular myocytes by promoting protein phosphorylation.  

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1. The degree of cell-to-cell coupling between ventricular myocytes of neonatal rats appeared well preserved when studied in the perforated version of the patch clamp technique or, in double whole-cell conditions, when ATP was present in the patch pipette solution. In contrast, when ATP was omitted, the amplitude of junctional current rapidly declined (rundown). 2. To examine the mechanism(s) of ATP action, an 'internal perfusion technique' was adapted to dual patch clamp conditions, and reintroduction of ATP partially reversed the rundown of junctional channels. 3. Cell-to-cell communication was not preserved by a non-hydrolysable ATP analogue (5'-adenylimidodiphosphate, AMP-PNP), indicating that the effect most probably did not involve direct interaction of ATP with the channel-forming proteins. 4. An ATP analogue supporting protein phosphorylation but not active transport processes (adenosine 5'-O-(3-thiotriphosphate), ATPgammaS) maintained normal intercellular communication, suggesting that the effect was due to kinase activity rather than to altered intracellular Ca2+. 5. A broad spectrum inhibitor of endogenous serine/threonine protein kinases (H7) reversibly reduced the intercellular coupling. A non-specific exogenous protein phosphatase (alkaline phosphatase) mimicked the effects of ATP deprivation. The non-specific inhibition of endogenous protein phosphatases resulted in the preservation of substantial cell-to-cell communication in ATP-free conditions. 6. The activity of gap junctional channels appears to require both the presence of ATP and protein kinase activity to counteract the tonic activity of endogenous phosphatase(s). PMID:10087344

Verrecchia, F; Duthe, F; Duval, S; Duchatelle, I; Sarrouilhe, D; Herve, J C

1999-04-15

180

ATP counteracts the rundown of gap junctional channels of rat ventricular myocytes by promoting protein phosphorylation.  

UK PubMed Central (United Kingdom)

1. The degree of cell-to-cell coupling between ventricular myocytes of neonatal rats appeared well preserved when studied in the perforated version of the patch clamp technique or, in double whole-cell conditions, when ATP was present in the patch pipette solution. In contrast, when ATP was omitted, the amplitude of junctional current rapidly declined (rundown). 2. To examine the mechanism(s) of ATP action, an 'internal perfusion technique' was adapted to dual patch clamp conditions, and reintroduction of ATP partially reversed the rundown of junctional channels. 3. Cell-to-cell communication was not preserved by a non-hydrolysable ATP analogue (5'-adenylimidodiphosphate, AMP-PNP), indicating that the effect most probably did not involve direct interaction of ATP with the channel-forming proteins. 4. An ATP analogue supporting protein phosphorylation but not active transport processes (adenosine 5'-O-(3-thiotriphosphate), ATPgammaS) maintained normal intercellular communication, suggesting that the effect was due to kinase activity rather than to altered intracellular Ca2+. 5. A broad spectrum inhibitor of endogenous serine/threonine protein kinases (H7) reversibly reduced the intercellular coupling. A non-specific exogenous protein phosphatase (alkaline phosphatase) mimicked the effects of ATP deprivation. The non-specific inhibition of endogenous protein phosphatases resulted in the preservation of substantial cell-to-cell communication in ATP-free conditions. 6. The activity of gap junctional channels appears to require both the presence of ATP and protein kinase activity to counteract the tonic activity of endogenous phosphatase(s).

Verrecchia F; Duthe F; Duval S; Duchatelle I; Sarrouilhe D; Herve JC

1999-04-01

 
 
 
 
181

Reversibility of left ventricular hypertrophy by differing types of antihypertensive therapy.  

UK PubMed Central (United Kingdom)

Left ventricular hypertrophy (LVH), as assessed by ECG or echocardiography, is a powerful independent coronary risk factor. The present overview of 104 studies sets out to compare the ability of various forms of antihypertensive therapy to reverse LVH as assessed by echocardiography. Most observations involved four classes of treatment--combination therapy, ACE inhibitors, beta-blockers and calcium antagonists (mainly dihydropyridines). The former two therapies were significantly more effective than the latter two in reversing LV mass, independently of length of time on treatment and degree of fall in blood pressure. Possible reasons for these differences are discussed. The clinical significance of these results is unclear although preliminary data indicate that regressing LVH is associated with fewer cardiovascular events.

Cruickshank JM; Lewis J; Moore V; Dodd C

1992-04-01

182

The evaluation of left ventricular eccentric hypertrophy by 201Tl-myocardial scintigraphy  

International Nuclear Information System (INIS)

In order to elucidate the mechanism of left ventricular eccentric hypertrophy in conditions of volume overload, Tl-201 myocardial scintigraphy was performed in patients with aortic valve regurgitation and mitral valve regurgitation. There was a good relationship between the severity of Tl-defects, as determined by Tl-201 myocardial scintigraphy, and the changes in the T wave on the ECG on the one hand and the NYHA functional classification of heart diseases. In 17 of 18 patients where LVDd increased with increasing severity of Tl-defects and the defects were moderate to severe, LVDd was 65 mm or larger. There was a significant negative correlation between the washout rate for the whole circumference of the left ventricle, as determined by exercise Tl-201 SPECT, and LVDd (r=-0.603, p

1989-01-01

183

Frequent left ventricular hypertrophy independent of blood pressure in 1851 pre-western Inuit  

DEFF Research Database (Denmark)

BACKGROUND: Elevated blood pressure is a risk factor for cardiovascular disease and may be detected by left ventricular hypertrophy (LVH) in electrocardiogram (ECG). Pre-western Inuit had frequent signs of LVH in ECG predominantly in the 3rd decade while a low occurrence of ischemic heart disease. METHODS: We evaluated the association between blood pressures and ECG signs of LVH, cardiac auscultation, and symptoms related to heart disease in the recently recovered data from the survey of 1851 Inuit conducted in 1962-1964 in East Greenland. RESULTS: The participation rate was 97%. Among the 812 Inuit aged 18years or above blood pressure was unaltered until the age of 39years (systolic, p=76; diastolic, p=0.36) and increased subsequently (both, p140mmHg was more frequent when aged >40years (p90mmHg was more common in men (p40years (p

Andersen, Stig; Kjærgaard, Marie

2011-01-01

184

Hydroxysafflor yellow A attenuates left ventricular remodeling after pressure overload-induced cardiac hypertrophy in rats.  

UK PubMed Central (United Kingdom)

Abstract Context: Hydroxysafflor yellow A (HSYA), the main chemical component of the safflower yellow pigments, is used extensively in traditional Chinese medicine for the treatment of cerebrovascular and cardiovascular diseases. Objective: The present study determined the effects of HSYA on left ventricular hypertrophy after pressure overload and investigated the underlying mechanisms. Materials and methods: Cardiac hypertrophy was induced by the ligation of abdominal aorta in male Wistar rats. The rats were then divided into five groups and treated with captopril (100?mg/kg) or HSYA at different doses (0, 10, 20 and 40?mg/kg). Six weeks after treatment, the weight of left ventricle, LVMI (left ventricular mass index) and pathological changes were measured. MMP-2 (metalloproteinase 2) and MMP-9 (metalloproteinase 9) levels were determined by ELISA. Protein expressions of Bcl-2 and Bax were evaluated by immunohistochemistry. Results: HSYA (20, 40?mg/kg) significantly attenuated the increase of LVMI (ventricular weight/body weight) by 13.04 and 30.43% respectively, when compared with the model group. This was associated with the amelioration of pathological lesion, such as cardiac muscle fibers were smaller and the nuclei of cardiomyocytes were lightly stained in animals treated with HSYA (20, 40?mg/kg). In addition, the administration of HSYA at doses of 20 and 40?mg/kg increased the Bcl-2/Bax ratio (1.17?±?0.08 and 1.39?±?0.07 versus 0.71?±?0.06). In addition, the serum MMP-2 and MMP-9 levels were blocked by the treatment at doses of 20 and 40?mg/kg HSYA (MMP-2, 76.1?±?9.2 and 65.6?±?6.8 versus 82.9?±?6.2, ng/ml; MMP-9, 66.6?±?4.8 and 57.5?±?5.0 versus 83.5?±?6.0, ng/ml). Conclusion: These findings indicated that HSYA has beneficial effects on hypertensive ventricular remodeling, which may involve mechanisms of inhibiting cell apoptosis and suppressing metalloproteinases expression.

Wang J; Zhang Q; Mei X; Zhang X

2013-09-01

185

Clinical importance of coronary perfusion pressure in the hypertensive patient with left ventricular hypertrophy.  

UK PubMed Central (United Kingdom)

In patients with severe left ventricular hypertrophy (LVH), but no significant coronary artery disease (CAD), acute lowering of diastolic blood pressure (DBP) to less than 85 mm Hg is reported to result in a 26% fall in coronary blood flow and an increase in myocardial oxygen demand; S-T segment and T-wave changes in the ECG are observed when DBP is acutely lowered to the 70s in these patients. In the presence of good resting left ventricular function, acute lowering of DBP to the 60s in well-controlled hypertensives on a beta-blocker, with either CAD or LVH, results in a mean increase of about 20% in ventricular ejection fraction. By contrast, patients with a combination of CAD and LVH experience a mean 6% fall in ejection fraction implying poor left ventricular functional reserve. In low risk populations, which exclude patients with severe ischaemia, diabetics and smokers, the lower the DBP the fewer the number of myocardial infarctions. However, in heterogeneous hypertensive populations which include high risk patients, such as ischaemics and diabetics (e.g. the MRFIT population), there is a strong U- or J-curve relationship between DBP and CAD deaths. Meta-analysis of high quality studies involving heterogeneous populations has shown that the U- or J-point is at 84 mm Hg and probably relates to high risk patients with ischaemia and/or LVH. Recent data from the Framingham group indicate that the patients most at risk are those with a combination of CAD and LVH: these patients showed a marked U-shaped curve with the U- or J-point at about 85-89 mm Hg DBP.(ABSTRACT TRUNCATED AT 250 WORDS)

Cruickshank JM

1992-01-01

186

CLINICAL SIGNIFICANCE OF SIGNAL-AVERAGED ELECTROCARDIOGRAM IN PATIENTS WITH ARTERIAL HYPERTENSION AND LEFT VENTRICULAR HYPERTROPHY  

Directory of Open Access Journals (Sweden)

Full Text Available It is still unknown which factors determine the presence of positive signal-averaged electrocardiograms in hypertension and their prognostic powerfor adverse cardiovascular events.The aim of the study was to examine the frequency of late potentialsand spectral turbulence analysis as well as the correlation betweennoninvasive parameters and five-year prognosis of late potentials andspectral turbulence analysis in patients with arterial hypertension and leftventricular hypertrophy.The study included 90 patients with hypertensive left ventricularhypertrophy and 35 healthy subjects. Patients were on regular medicamenttherapy and were followed up for five years.The positive late potentials were found in 17 (18.9%) patients and in 3(8.6%) healthy subjects. The positive spectral turbulence analysis was foundin 14 (15.5%) patients with left ventricular hypertrophy and in 2 (5.7%)healthy subjects. Independent predictor for positive late potentials was bodysurface area (p<0.05) and for positive spectral turbulence analysis was leftventricular mass index (p<0.01). The fifteen (16.7%) patients had cardiovascularand cerebrovascular adverse events. There was no correlationbetween positive late potentials and positive spectral turbulence analysis andbad outcome during the five-year follow-up of hypertensive patients.

Dragan Djordjevic; Branko Lovic; Marina Deljanin Ilic; Ivan Tasic; Stevan Ilic; Bojana Stamenkovic; Dejan Petrovic

2005-01-01

187

Rapamycin attenuates hypoxia-induced pulmonary vascular remodeling and right ventricular hypertrophy in mice  

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Full Text Available Abstract Background Chronic hypoxia induces pulmonary arterial hypertension (PAH). Smooth muscle cell (SMC) proliferation and hypertrophy are important contributors to the remodeling that occurs in chronic hypoxic pulmonary vasculature. We hypothesized that rapamycin (RAPA), a potent cell cycle inhibitor, prevents pulmonary hypertension in chronic hypoxic mice. Methods Mice were held either at normoxia (N; 21% O2) or at hypobaric hypoxia (H; 0.5 atm; ~10% O2). RAPA-treated animals (3 mg/kg*d, i.p.) were compared to animals injected with vehicle alone. Proliferative activity within the pulmonary arteries was quantified by staining for Ki67 (positive nuclei/vessel) and media area was quantified by computer-aided planimetry after immune-labeling for ?-smooth muscle actin (pixel/vessel). The ratio of right ventricle to left ventricle plus septum (RV/[LV+S]) was used to determine right ventricular hypertrophy. Results Proliferative activity increased by 34% at day 4 in mice held under H (median: 0.38) compared to N (median: 0.28, p = 0.028) which was completely blocked by RAPA (median HO+RAPA: 0.23, p = 0.003). H-induced proliferation had leveled off within 3 weeks. At this time point media area had, however, increased by 53% from 91 (N) to 139 (H, p Conclusion Therapy with rapamycin may represent a new strategy for the treatment of pulmonary hypertension.

Paddenberg Renate; Stieger Philipp; von Lilien Anna-Laura; Faulhammer Petra; Goldenberg Anna; Tillmanns Harald H; Kummer Wolfgang; Braun-Dullaeus Ruediger C

2007-01-01

188

Adenylyl cyclase subtype-specific compartmentalization: differential regulation of L-type Ca2+ current in ventricular myocytes.  

UK PubMed Central (United Kingdom)

RATIONALE: Adenylyl cyclase (AC) represents one of the principal molecules in the ?-adrenergic receptor signaling pathway, responsible for the conversion of ATP to the second messenger, cAMP. AC types 5 (ACV) and 6 (ACVI) are the 2 main isoforms in the heart. Although highly homologous in sequence, these 2 proteins play different roles during the development of heart failure. Caveolin-3 is a scaffolding protein, integrating many intracellular signaling molecules in specialized areas called caveolae. In cardiomyocytes, caveolin is located predominantly along invaginations of the cell membrane known as t-tubules. OBJECTIVE: We take advantage of ACV and ACVI knockout mouse models to test the hypothesis that there is distinct compartmentalization of these isoforms in ventricular myocytes. METHODS AND RESULTS: We demonstrate that ACV and ACVI isoforms exhibit distinct subcellular localization. The ACVI isoform is localized in the plasma membrane outside the t-tubular region and is responsible for ?1-adrenergic receptor signaling-mediated enhancement of the L-type Ca(2+) current (ICa,L) in ventricular myocytes. In contrast, the ACV isoform is localized mainly in the t-tubular region where its influence on ICa,L is restricted by phosphodiesterase. We further demonstrate that the interaction between caveolin-3 with ACV and phosphodiesterase is responsible for the compartmentalization of ACV signaling. CONCLUSIONS: Our results provide new insights into the compartmentalization of the 2 AC isoforms in the regulation of ICa,L in ventricular myocytes. Because caveolae are found in most mammalian cells, the mechanism of ?- adrenergic receptor and AC compartmentalization may also be important for ?-adrenergic receptor signaling in other cell types.

Timofeyev V; Myers RE; Kim HJ; Woltz RL; Sirish P; Heiserman JP; Li N; Singapuri A; Tang T; Yarov-Yarovoy V; Yamoah EN; Hammond HK; Chiamvimonvat N

2013-06-01

189

Organic nitrates favor regression of left ventricular hypertrophy in hypertensive patients on chronic peritoneal dialysis.  

Science.gov (United States)

The aim of the study was to evaluate the effect of nitrates on left ventricular hypertrophy (LVH) in hypertensive patients on chronic peritoneal dialysis (PD). Sixty-four PD patients with hypertension were enrolled in this study. All patients accepted antihypertensive drugs at baseline. Thirty-two patients (nitrate group) took isosorbide mononitrate for 24 weeks. The remaining 32 patients (non-nitrate group) took other antihypertensive drugs. Blood pressure (BP), left ventricular mass index (LVMI) and plasma asymmetric dimethylarginine (ADMA) were monitored. Subjects with normal renal function were included as the control group (n = 30). At baseline, plasma ADMA levels in PD patients were significantly higher than the control group, but there was no significant difference in plasma ADMA levels between the two groups. At the end of the 24-week period, BP, LVMI, LVH prevalence and plasma ADMA levels in the nitrate group were significantly lower than those in the non-nitrate group. BP did not show a significant difference between 12 and 24 weeks in the nitrate group with a reduced need for other medication. Logistic regression analysis showed that nitrate supplementation and SBP reduction were independent risk factors of LVMI change in PD patients after adjusting for age, gender, diabetes history and CCB supplementation. It was concluded that organic nitrates favor regression of LVH in hypertensive patients on chronic peritoneal dialysis, and nitrates may be considered for use before employing the five other antihypertensive agents other than nitrates. PMID:23296279

Li, Han; Wang, Shixiang

2013-01-07

190

Organic nitrates favor regression of left ventricular hypertrophy in hypertensive patients on chronic peritoneal dialysis.  

UK PubMed Central (United Kingdom)

The aim of the study was to evaluate the effect of nitrates on left ventricular hypertrophy (LVH) in hypertensive patients on chronic peritoneal dialysis (PD). Sixty-four PD patients with hypertension were enrolled in this study. All patients accepted antihypertensive drugs at baseline. Thirty-two patients (nitrate group) took isosorbide mononitrate for 24 weeks. The remaining 32 patients (non-nitrate group) took other antihypertensive drugs. Blood pressure (BP), left ventricular mass index (LVMI) and plasma asymmetric dimethylarginine (ADMA) were monitored. Subjects with normal renal function were included as the control group (n = 30). At baseline, plasma ADMA levels in PD patients were significantly higher than the control group, but there was no significant difference in plasma ADMA levels between the two groups. At the end of the 24-week period, BP, LVMI, LVH prevalence and plasma ADMA levels in the nitrate group were significantly lower than those in the non-nitrate group. BP did not show a significant difference between 12 and 24 weeks in the nitrate group with a reduced need for other medication. Logistic regression analysis showed that nitrate supplementation and SBP reduction were independent risk factors of LVMI change in PD patients after adjusting for age, gender, diabetes history and CCB supplementation. It was concluded that organic nitrates favor regression of LVH in hypertensive patients on chronic peritoneal dialysis, and nitrates may be considered for use before employing the five other antihypertensive agents other than nitrates.

Li H; Wang S

2013-01-01

191

Impact of electrocardiographic findings for diagnosis of left ventricular hypertrophy in patients with primary aldosteronism.  

UK PubMed Central (United Kingdom)

BACKGROUND: Compared to patients with similar levels of hypertension, patients with primary aldosteronism have a greater left ventricular hypertrophy (LVH). The presence of LVH should be detected as early as possible to prevent cardiovascular complications associated with the condition. We evaluated comparative diagnostic value of electrocardiographic (ECG) indexes for LVH in patients with primary aldosteronism. METHODS: ECG and echocardiographic data were obtained in 88 patients with primary aldosteronism. We analyzed the four most commonly used ECG indexes, including Sokolow-Lyon index, Cornell voltage index, Cornell product index, and Gubner index. RESULTS: Echocardiographic LVH was found in 35 patients (40%). Sensitivity ranged from 0% for Gubner index to 49% for Cornell product index. Specificity ranged from 81% for Sokolow-Lyon index to 100% for Gubner index. Sokolow-Lyon index (r=0.43, p<0.001), Cornell voltage index (r=0.55, p<0.001) and Cornell product index (r=0.52, p<0.001) correlated significantly with left ventricular mass (LVM) index. No significant correlation was found between Gubner index and LVM index. CONCLUSIONS: ECG indexes had a reasonably high specificity, but a low sensitivity for LVH in patients with primary aldosteronism. Cornell voltage index and Cornell product index had a better diagnostic value of LVH, and had a better correlation with LVM index in these patients.

Kurisu S; Iwasaki T; Mitsuba N; Ishibashi K; Dohi Y; Kihara Y

2013-03-01

192

Organic Nitrates Favor Regression of Left Ventricular Hypertrophy in Hypertensive Patients on Chronic Peritoneal Dialysis  

Directory of Open Access Journals (Sweden)

Full Text Available The aim of the study was to evaluate the effect of nitrates on left ventricular hypertrophy (LVH) in hypertensive patients on chronic peritoneal dialysis (PD). Sixty-four PD patients with hypertension were enrolled in this study. All patients accepted antihypertensive drugs at baseline. Thirty-two patients (nitrate group) took isosorbide mononitrate for 24 weeks. The remaining 32 patients (non-nitrate group) took other antihypertensive drugs. Blood pressure (BP), left ventricular mass index (LVMI) and plasma asymmetric dimethylarginine (ADMA) were monitored. Subjects with normal renal function were included as the control group (n = 30). At baseline, plasma ADMA levels in PD patients were significantly higher than the control group, but there was no significant difference in plasma ADMA levels between the two groups. At the end of the 24-week period, BP, LVMI, LVH prevalence and plasma ADMA levels in the nitrate group were significantly lower than those in the non-nitrate group. BP did not show a significant difference between 12 and 24 weeks in the nitrate group with a reduced need for other medication. Logistic regression analysis showed that nitrate supplementation and SBP reduction were independent risk factors of LVMI change in PD patients after adjusting for age, gender, diabetes history and CCB supplementation. It was concluded that organic nitrates favor regression of LVH in hypertensive patients on chronic peritoneal dialysis, and nitrates may be considered for use before employing the five other antihypertensive agents other than nitrates.

Han Li; Shixiang Wang

2013-01-01

193

The role of secondary hyperparathyroidism in left ventricular hypertrophy of patients under chronic hemodialysis  

Directory of Open Access Journals (Sweden)

Full Text Available End-stage renal disease (ESRD) patients frequently develop structural cardiac abnormalities, particularly left ventricular hypertrophy (LVH). The mechanisms involved in these processes are not completely understood. In the present study, we evaluated a possible association between parathyroid hormone (PTH) levels and left ventricular mass (LVM) in patients with ESRD. Stable uremic patients on intermittent hemodialysis treatment were evaluated by standard two-dimensional echocardiography and their sera were analyzed for intact PTH. Forty-one patients (mean age 45 years, range 18 to 61 years), 61% males, who had been on hemodialysis for 3 to 186 months, were evaluated. Patients were stratified into 3 groups according to serum PTH: low levels (280 pg/ml; group III = 21 patients). A positive statistically significant association between LVM index and PTH was identified (r = 0.34; P = 0.03, Pearson's correlation coefficient) in the sample as a whole. In subgroup analyses, we did not observe significant associations in the low and intermediate PTH groups; nevertheless, PTH and LVM index were correlated in patients with high PTH levels (r = 0.62; P = 0.003). LVM index was also inversely associated with hemoglobin (r = -0.34; P = 0.03). In multivariate analysis, after adjustment for age, hemoglobin, body mass index, and blood pressure, the only independent predictor of LVM index was PTH level. Therefore, PTH is an independent predictor of LVH in patients undergoing chronic hemodialysis. Secondary hyperparathyroidism may contribute to the elevated cardiovascular morbidity associated with LVH in ESRD.

R.B. Randon; L.E. Rohde; L. Comerlato; J.P. Ribeiro; R.C. Manfro

2005-01-01

194

Prevalence and severity of echocardiographic left ventricular hypertrophy in hypertensive patients in clinical practice.  

UK PubMed Central (United Kingdom)

BACKGROUND AND AIM: The prevalence of left ventricular hypertrophy (LVH) in human hypertension has been mostly documented in population-based samples and selected hypertensive cohorts. Rather scant data are available from clinical practice. Thus, we examined the prevalence of LVH in a large group of hypertensive patients referred by general practitioners to a routine echocardiographic examination. METHODS: A total of 2249 hypertensive subjects (mean age 62 years, 52.3% men, 84.5% treated) referred by their practitioners to 17 outpatient echocardiographic laboratories across Italy for detection of hypertensive early cardiac damage were included in the study. LVH was defined as left ventricular mass (A) ? 225/163 g, (B) ? 116/96 g/m(2), (C) ? 49/45 g/m(2.7) in men/women, respectively; LVH was graded as mild, moderate and severe according to Lang's report. RESULTS: Overall, patients with LVH were 58%, 58% and 65% by criteria A, B and C, respectively. LVH was mild in 33% (A), 36% (B) and 29% (C), moderate in 31% (A), 28% (B) and 27% (C), and severe in 36% (A), 36% (B) and 44% (C). CONCLUSIONS: Data provided by this multicentre nationwide survey support the view that, despite therapeutic interventions, LVH remains a highly frequent phenotype in human hypertension and that severe LVH is present in a large fraction of hypertensives.

Cuspidi C; Negri F; Muiesan ML; Capra A; Lonati L; Milan A; Sala C; Longo M; Morganti A

2011-02-01

195

[Angiotensin converting enzyme and left ventricular hypertrophy in uremic patients: correlation and therapeutic options].  

UK PubMed Central (United Kingdom)

INTRODUCTION: Anemia has been shown to be a key component of renal failure, as well as of the occurrence of left ventricular hypertrophy (LVH), with special attention paid to the paracrine mechanism of left ventricular remodelling. AIM: The aim of the study was to analyze possible association of serum angiotensin-converting enzyme (ACE) activity and LVH in hemodialysis patients with anemia treated with human recombinant erythropoietin (rHuEpo) during six months. METHOD: LV geometry was determined by echocardiographic analysis in 20 hemodialysis patients before and after erythropoietin treatment. Serum ACE activity was measured by spectrophotometric method using hippyril-l-histidyl-l-leucin as a substrate. RESULTS: Serum ACE activity increased to 47.3% in hemodialysis patients with LVH as compared to patients with normal LV mass. A significant positive correlation was found between the level of ACE activity and LV mass index (p=0.004). Six-month erythropoietin treatment of anemia led to a significant reduction of LV mass index (p<0.008) and serum ACE activity (p=0.003) from the initial values. CONCLUSION: The levels of serum ACE activity are associated with LV geometry. Our findings suggested the possibility of simultaneous and modest modulation of LV mass and serum ACE activity with rHuEpo correction of renal anemia.

Rasi? S; Catovi? A; Huski? J; Haraci? A; Babi? N; Avdagi? N; Uncanin S

2004-01-01

196

The association of ankle brachial index with left ventricular hypertrophy and left ventricular mass index: the Dong-gu study.  

UK PubMed Central (United Kingdom)

BACKGROUND: To investigate the association between ankle-brachial index (ABI), left ventricular hypertrophy (LVH) and left ventricular mass index (LVMI) in a general population. PATIENTS AND METHODS: The study population consisted of 8,246 people aged 50 years and older who participated in the baseline survey of the Dong-gu Study conducted in Korea between 2007 and 2010. Trained research technicians measured LV mass using mode M ultrasound echocardiography and ABI using an oscillometric method. RESULTS: After adjustment for risk factors and common carotid artery intima-media thickness (CCA-IMT) and the number of plaques, higher ABIs (1.10 1.19, 1.20 - 1.29, and ? 1.30) were significantly and linearly associated with high LVMI (1.10 - 1.19 ABI: ?, 3.33; 95 % CI, 1.72 - 4.93; 1.20 - 1.29 ABI: ?, 6.51; 95 % CI, 4.02 - 9.00; ? 1.30 ABI: ?, 14.83; 95 % CI, 6.18 - 23.48). An ABI of 1.10 - 1.19 and 1.20 - 1.29 ABI was significantly associated with LVH (1.10 - 1.19 ABI: OR, 1.35; 95 % CI, 1.19 - 1.53; 1.20 - 1.29 ABI: OR, 1.59; 95 % CI, 1.31 - 1.92) and ABI ? 1.30 was marginally associated with LVH (OR, 1.73; 95 % CI, 0.93 - 3.22, p = 0.078). CONCLUSIONS: After adjustment for other cardiovascular variables and CCA-IMT and the number of plaques, higher ABIs are associated with LVH and LVMI in Koreans aged 50 years and older.

Choi SW; Kim HY; Ahn HR; Lee YH; Kweon SS; Choi JS; Rhee JA; Nam HS; Jeong SK; Park KS; Ryu SY; Shin MH

2013-07-01

197

KS370G, a synthetic caffeamide derivative, improves left ventricular hypertrophy and function in pressure-overload mice heart.  

UK PubMed Central (United Kingdom)

Cardiac hypertrophy is an important compensatory mechanism in response to a pressure overload, but a sustained excessive cardiac workload may deteriorate to maladaptive hypertrophy and to increased risk of heart failure. In this study, we evaluated the effects of KS370G on left ventricular hypertrophy and function. Abdominal aortic banding was performed by constricting the abdominal aorta. Hypertrophied heart was studied at 8 weeks after the operation. After the operation, KS370G 1mg/kg (K1 group) was administered by oral gavage once a day. Left ventricular function was measured by a 1.2F pressure-volume catheter (Scisense, Canada). The levels of protein for ?-SMA (smooth muscle actin), p-AKT (protein kinase B), p-GSK3? (glycogen synthase kinase 3?) and p-ERKs (extracellular signal-regulated kinases) in myocardium were analyzed by Western blot. Plasma levels of angiotensin II, atrial natriuretic peptide and lactate dehydrogenase were analyzed by commercial kits. H.E. staining and M.T. staining methods were also used to observe diameter of cardiomyocytes and collagen accumulation. Chronic oral treatment with 1mg/kg KS370G inhibited cardiac hypertrophy and improved cardiac function induced by pressure overload. KS370G also decreased the plasma levels of atrial natriuretic peptide and lactate dehydrogenase. Besides, pressure overload-induced increase of ?-SMA and phosphorylation of ERK, AKT and GSK3? were significantly reduced by chronic oral treatment with KS370G. We also found that chronic oral treatment with KS370G reduced cardiac collagen accumulation. KS370G improved left ventricular function and inhibited cardiac hypertrophy through the decrease of the phosphorylation of ERK, AKT and GSK3? in pressure-overload mice heart.

Weng YC; Chuang CF; Chuang ST; Chiu HL; Kuo YH; Su MJ

2012-06-01

198

Frequent periodic leg movement during sleep is associated with left ventricular hypertrophy and adverse cardiovascular outcomes.  

UK PubMed Central (United Kingdom)

BACKGROUND: Sleep disturbance caused by obstructive sleep apnea is recognized as a contributing factor to adverse cardiovascular outcomes. However, the effect of restless legs syndrome, another common cause of fragmented sleep, on cardiac structure, function, and long-term outcomes is not known. The aim of this study was to assess the effect of frequent leg movement during sleep on cardiac structure and outcomes in patients with restless legs syndrome. METHODS: In our retrospective study, patients with restless legs syndrome referred for polysomnography were divided into those with frequent (periodic movement index > 35/hour) and infrequent (? 35/hour) leg movement during sleep. Long-term outcomes were determined using Kaplan-Meier and logistic regression models. RESULTS: Of 584 patients, 47% had a periodic movement index > 35/hour. Despite similarly preserved left ventricular ejection fraction, the group with periodic movement index > 35/hour had significantly higher left ventricular mass and mass index, reflective of left ventricular hypertrophy (LVH). There were no significant baseline differences in the proportion of patients with hypertension, diabetes, hyperlipidemia, prior myocardial infarction, stroke or heart failure, or the use of antihypertensive medications between the groups. Patients with frequent periodic movement index were older, predominantly male, and had more prevalent coronary artery disease and atrial fibrillation. However, on multivariate analysis, periodic movement index > 35/hour remained the strongest predictor of LVH (odds ratio, 2.45; 95% confidence interval, 1.67-3.59; P < .001). Advanced age, female sex, and apnea-hypopnea index were other predictors of LVH. Patients with periodic movement index > 35/hour had significantly higher rates of heart failure and mortality over median 33-month follow-up. CONCLUSIONS: Frequent periodic leg movement during sleep is an independent predictor of severe LVH and is associated with increased cardiovascular morbidity and mortality.

Mirza M; Shen WK; Sofi A; Jahangir A; Mori N; Tajik AJ; Jahangir A

2013-07-01

199

Hypertension, fluid overload and micro inflammation are associated with left ventricular hypertrophy in maintenance hemodialysis patients.  

Science.gov (United States)

Abstract This cross-sectional study aims to identify the potential risk factors of left ventricular hypertrophy (LVH) in hemodialysis (HD) patients. Echocardiography, anthropometric measurements and biochemical analyses were performed for 112 HD patients. In univariate analysis, body mass index, systolic blood pressure, diastolic blood pressure, glycosylated hemoglobin, glycated albumin, high sensitivity C-reactive protein (hs-CRP), cardiac troponin T (cTnT), amino-terminal pro-B-natriuretic peptide (NT-proBNP) and carotid artery intima-media thickness were positively correlated with left ventricular mass index (LVMI); pre-albumin, serum creatinine, left ventricular ejection fraction (LVEF) and fractional shortening were negatively correlated with LVMI. Linear regression analysis showed systolic blood pressure, NT-proBNP and LVEF were independently associated with LVMI. According to a binary logistic regression model, higher systolic blood pressure, NT-proBNP and hs-CRP levels showed independent correlation with LVH. Receiver operator characteristic curves analysis showed the associations between NT-proBNP and LVH more closely than hs-CRP and cTnT. The area under the curve for NT-proBNP, hs-CRP and cTnT was 0.762 (95% CI: 0.660-0.864, p?

Xu, Yan; Chen, Yue; Li, Daming; Li, Jiangtao; Liu, Xi; Cui, Chunli; Yu, Chen

2013-08-01

200

DELAYED TREATMENT EFFECTS OF XANTHINE OXIDASE INHIBITION ON SYSTOLIC OVERLOAD-INDUCED LEFT VENTRICULAR HYPERTROPHY AND DYSFUNCTION  

Science.gov (United States)

The nonpurine selective xanthine oxidase (XO) inhibitor febuxostat attenuates development of left ventricular (LV) hypertrophy and dysfunction in mice when treatment is initiated within 1 hour of transverse aortic constriction (TAC). This study investigated whether a 7-day delay of treatment with the XO inhibitors febuxostat or allopurinol would reverse TAC-induced changes after onset of heart failure (HF). Neither treatment significantly affected TAC-induced LV hypertrophy; only febuxostat caused a modest improvement in LV function (?10% increase in LV ejection fraction). However, the purine analog allopurinol tended to increase mortality compared with vehicle or febuxostat in HF mice.

Xu, X.; Zhao, L.; Hu, X.; Zhang, P.; Wessale, J.; Bache, R.; Chen, Y.

2010-01-01

 
 
 
 
201

Left ventricular hypertrophy as a determinant of renal outcome in patients with high cardiovascular risk.  

UK PubMed Central (United Kingdom)

OBJECTIVE: The prognostic importance of left ventricular hypertrophy (LVH) on renal impairment has not been addressed previously. We investigated whether LVH determines renal outcomes in patients with high cardiovascular risk. METHODS: We retrospectively studied 6163 men with high cardiovascular risk (68 ± 13 years, 23% with coronary artery disease, 34% with diabetes, 83% with hypertension and 30% smokers) followed for a period of 14 years. Left ventricular mass index was assessed at baseline, whereas kidney function and blood pressure levels were determined at both baseline and the end of the follow-up period. Renal outcomes were doubling of serum creatinine, estimated glomerular filtration rate (eGFR) below 30 ml/min per 1.73 m and incident hemodialysis. RESULTS: During the follow-up, 5.8% (n = 356), 7% (n = 429) and 2.7% (n = 165) of men fulfilled the above-mentioned three outcomes, respectively. After adjustment, for each 42 g/m (1 SD) increase in left ventricular mass index, there was a rise in risk of all renal outcomes by 45.7% (95% confidence interval 28.5-58.3) for doubling of serum creatinine, 51.9% (95% confidence interval 39.7-65%) for eGFR below 30 ml/min per 1.73 m and 58.3% (95% confidence interval 39.7-79.3) for hemodialysis (P < 0.001 for all). Severe LVH (160 < left ventricular mass index ? 180 g/m) compared with non-LVH predicted a significant increase in: doubling of serum creatinine by 103.8%, eGFR-guided outcome by 109.1% and hemodialysis by 74.1%. In those with LVH and impaired kidney function at baseline (GFR <60 ml/min per 1.73 m) compared with those without such entities, serum creatinine, eGFR and hemodialysis-guided outcomes were increased by four-fold, 15-fold and 16-fold, respectively. CONCLUSION: Increased left ventricular mass is a predictor of subsequent kidney dysfunction and should be considered in renal risk stratification in a broad spectrum of men with high cardiovascular risk.

Tsioufis C; Kokkinos P; Macmanus C; Thomopoulos C; Faselis C; Doumas M; Stefanadis C; Papademetriou V

2010-11-01

202

Nocturnal Blood Pressure Pattern Affects Left Ventricular Remodeling and Late Gadolinium Enhancement in Patients with Hypertension and Left Ventricular Hypertrophy.  

UK PubMed Central (United Kingdom)

BACKGROUND: Left ventricular hypertrophy (LVH) is an independent predictor of cardiac mortality, regardless of its etiology. Previous studies have shown that high nocturnal blood pressure (BP) affects LV geometry in hypertensive patients. It has been suggested that continuous pressure overload affects the development of LVH, but it is unknown whether persistent pressure influences myocardial fibrosis or whether the etiology of LVH is associated with myocardial fibrosis. Comprehensive cardiac magnetic resonance (CMR) including the late gadolinium enhancement (LGE) technique can evaluate both the severity of changes in LV geometry and myocardial fibrosis. We tested the hypothesis that the nocturnal non-dipper BP pattern causes LV remodeling and fibrosis in patients with hypertension and LVH. METHODS: Forty-seven hypertensive patients with LVH evaluated by echocardiography (29 men, age 73.0±10.4 years) were examined by comprehensive CMR and 24-h ambulatory blood pressure monitoring (ABPM). RESULTS AND CONCLUSIONS: Among the 47 patients, twenty-four had nocturnal non-dipper BP patterns. Patients with nocturnal non-dipper BP patterns had larger LV masses and scar volumes independent of etiologies than those in patients with dipper BP patterns (p?=?0.035 and p?=?0.015, respectively). There was no significant difference in mean 24-h systolic BP between patients with and without nocturnal dipper BP patterns (p?=?0.367). Among hypertensive patients with LVH, the nocturnal non-dipper blood pressure pattern is associated with both LV remodeling and myocardial fibrosis independent of LVH etiology.

Yokota H; Imai Y; Tsuboko Y; Tokumaru AM; Fujimoto H; Harada K

2013-01-01

203

Effect of ajmaline on action potential and ionic currents in rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

The effect of ajmaline on action potential (AP) and ionic current components has been investigated in right ventricular myocytes of rat at room temperature using the whole cell patch clamp technique. Ajmaline decreased the upstroke velocity ((dV/dt)max) of AP and the AP amplitude, increased the AP duration measured at 50 and 90% repolarization, and reversibly inhibited most components of membrane ionic current in a concentration-dependent manner. The following values of IC50 and of the Hill coefficient (nH) resulted from approximation of the measured data by the Hill formula: for fast sodium current (INa) IC50=27.8+/-1.14 micromol/l and nH=1.27+/-0.25 at holding potential -75 mV, IC50=47.2+/-1.16 micromol/l and nH=1.16+/-0.21 at holding potential -120 mV; for L-type calcium current (ICa-L) IC50=70.8+/-0.09 micromol/l and n(H)=0.99+/-0.09; for transient outward potassium current (Ito) IC50=25.9+/-2.91 micromol/l and nH=1.07+/-0.15; for ATP-sensitive potassium current (IK(ATP)) IC50=13.3+/-1.1 micromol/l and nH=1.16+/-0.15. The current measured at the end of 300 ms depolarizing impulse was composed of an ajmaline-insensitive component and a component inhibited with IC50=61.0+/-1.1 micromol/l and nH=0.91+/-0.08. At hyperpolarizing voltages, ajmaline at high concentration of 300 micromol/l reduced the inward moiety of time-independent potassium current (IK1) by 36%. The results indicate that the inhibition of INa causes both the decreased rate of rise of depolarizing phase and the lowered amplitude of AP. The inhibition of Ito is responsible for the ajmaline-induced AP prolongation.

Bébarová M; Matejovic P; Pásek M; Simurdová M; Simurda J

2005-09-01

204

Determinants of Beat-to-Beat Variability of Repolarization Duration in the Canine Ventricular Myocyte: A Computational Analysis  

Science.gov (United States)

Beat-to-beat variability of repolarization duration (BVR) is an intrinsic characteristic of cardiac function and a better marker of proarrhythmia than repolarization prolongation alone. The ionic mechanisms underlying baseline BVR in physiological conditions, its rate dependence, and the factors contributing to increased BVR in pathologies remain incompletely understood. Here, we employed computer modeling to provide novel insights into the subcellular mechanisms of BVR under physiological conditions and during simulated drug-induced repolarization prolongation, mimicking long-QT syndromes type 1, 2, and 3. We developed stochastic implementations of 13 major ionic currents and fluxes in a model of canine ventricular-myocyte electrophysiology. Combined stochastic gating of these components resulted in short- and long-term variability, consistent with experimental data from isolated canine ventricular myocytes. The model indicated that the magnitude of stochastic fluctuations is rate dependent due to the rate dependence of action-potential (AP) duration (APD). This process (the “active” component) and the intrinsic nonlinear relationship between membrane current and APD (“intrinsic component”) contribute to the rate dependence of BVR. We identified a major role in physiological BVR for stochastic gating of the persistent Na+ current (INa) and rapidly activating delayed-rectifier K+ current (IKr). Inhibition of IKr or augmentation of INa significantly increased BVR, whereas subsequent ?-adrenergic receptor stimulation reduced it, similar to experimental findings in isolated myocytes. In contrast, ?-adrenergic stimulation increased BVR in simulated long-QT syndrome type 1. In addition to stochastic channel gating, AP morphology, APD, and beat-to-beat variations in Ca2+ were found to modulate single-cell BVR. Cell-to-cell coupling decreased BVR and this was more pronounced when a model cell with increased BVR was coupled to a model cell with normal BVR. In conclusion, our results provide new insights into the ionic mechanisms underlying BVR and suggest that BVR reflects multiple potentially proarrhythmic parameters, including increased ion-channel stochasticity, prolonged APD, and abnormal Ca2+ handling.

Heijman, Jordi; Zaza, Antonio; Johnson, Daniel M.; Rudy, Yoram; Peeters, Ralf L. M.

2013-01-01

205

Determinants of Beat-to-Beat Variability of Repolarization Duration in the Canine Ventricular Myocyte: A Computational Analysis.  

UK PubMed Central (United Kingdom)

Beat-to-beat variability of repolarization duration (BVR) is an intrinsic characteristic of cardiac function and a better marker of proarrhythmia than repolarization prolongation alone. The ionic mechanisms underlying baseline BVR in physiological conditions, its rate dependence, and the factors contributing to increased BVR in pathologies remain incompletely understood. Here, we employed computer modeling to provide novel insights into the subcellular mechanisms of BVR under physiological conditions and during simulated drug-induced repolarization prolongation, mimicking long-QT syndromes type 1, 2, and 3. We developed stochastic implementations of 13 major ionic currents and fluxes in a model of canine ventricular-myocyte electrophysiology. Combined stochastic gating of these components resulted in short- and long-term variability, consistent with experimental data from isolated canine ventricular myocytes. The model indicated that the magnitude of stochastic fluctuations is rate dependent due to the rate dependence of action-potential (AP) duration (APD). This process (the "active" component) and the intrinsic nonlinear relationship between membrane current and APD ("intrinsic component") contribute to the rate dependence of BVR. We identified a major role in physiological BVR for stochastic gating of the persistent Na(+) current (INa) and rapidly activating delayed-rectifier K(+) current (IKr). Inhibition of IKr or augmentation of INa significantly increased BVR, whereas subsequent ?-adrenergic receptor stimulation reduced it, similar to experimental findings in isolated myocytes. In contrast, ?-adrenergic stimulation increased BVR in simulated long-QT syndrome type 1. In addition to stochastic channel gating, AP morphology, APD, and beat-to-beat variations in Ca(2+) were found to modulate single-cell BVR. Cell-to-cell coupling decreased BVR and this was more pronounced when a model cell with increased BVR was coupled to a model cell with normal BVR. In conclusion, our results provide new insights into the ionic mechanisms underlying BVR and suggest that BVR reflects multiple potentially proarrhythmic parameters, including increased ion-channel stochasticity, prolonged APD, and abnormal Ca(2+) handling.

Heijman J; Zaza A; Johnson DM; Rudy Y; Peeters RL; Volders PG; Westra RL

2013-08-01

206

Determinants of Beat-to-Beat Variability of Repolarization Duration in the Canine Ventricular Myocyte: A Computational Analysis.  

Science.gov (United States)

Beat-to-beat variability of repolarization duration (BVR) is an intrinsic characteristic of cardiac function and a better marker of proarrhythmia than repolarization prolongation alone. The ionic mechanisms underlying baseline BVR in physiological conditions, its rate dependence, and the factors contributing to increased BVR in pathologies remain incompletely understood. Here, we employed computer modeling to provide novel insights into the subcellular mechanisms of BVR under physiological conditions and during simulated drug-induced repolarization prolongation, mimicking long-QT syndromes type 1, 2, and 3. We developed stochastic implementations of 13 major ionic currents and fluxes in a model of canine ventricular-myocyte electrophysiology. Combined stochastic gating of these components resulted in short- and long-term variability, consistent with experimental data from isolated canine ventricular myocytes. The model indicated that the magnitude of stochastic fluctuations is rate dependent due to the rate dependence of action-potential (AP) duration (APD). This process (the "active" component) and the intrinsic nonlinear relationship between membrane current and APD ("intrinsic component") contribute to the rate dependence of BVR. We identified a major role in physiological BVR for stochastic gating of the persistent Na(+) current (INa) and rapidly activating delayed-rectifier K(+) current (IKr). Inhibition of IKr or augmentation of INa significantly increased BVR, whereas subsequent ?-adrenergic receptor stimulation reduced it, similar to experimental findings in isolated myocytes. In contrast, ?-adrenergic stimulation increased BVR in simulated long-QT syndrome type 1. In addition to stochastic channel gating, AP morphology, APD, and beat-to-beat variations in Ca(2+) were found to modulate single-cell BVR. Cell-to-cell coupling decreased BVR and this was more pronounced when a model cell with increased BVR was coupled to a model cell with normal BVR. In conclusion, our results provide new insights into the ionic mechanisms underlying BVR and suggest that BVR reflects multiple potentially proarrhythmic parameters, including increased ion-channel stochasticity, prolonged APD, and abnormal Ca(2+) handling. PMID:23990775

Heijman, Jordi; Zaza, Antonio; Johnson, Daniel M; Rudy, Yoram; Peeters, Ralf L M; Volders, Paul G A; Westra, Ronald L

2013-08-22

207

Pressure overload-induced mild cardiac hypertrophy reduces left ventricular transmural differences in mitochondrial respiratory chain activity and increases oxidative stress  

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Objective: Increased mechanical stress and contractility characterizes normal left ventricular (LV) subendocardium (Endo) but whether Endo mitochondrial respiratory chain complex activities is reduced as compared to subepicardium (Epi) and whether pressure overload-induced LV hypertrophy (LVH) might...

Kindo, Michel; Gerelli, Sébastien; Bouitbir, Jamal; Charles, Anne-Laure; Zoll, Joffrey; Hoang Minh, Tam; Monassier, Laurent

208

Protective effect of left ventricular hypertrophy in right coronary artery occlusions  

Directory of Open Access Journals (Sweden)

Full Text Available OBJECTIVE: To test the hypothesis that left ventricular hypertrophy (LVH) reduces the electrocardiographic and functional effects of right coronary artery occlusion. METHODS: We analysed 215 patients (166 males and 49 women,age of 58.9±10.6 years), with occlusion of the right coronary artery without other associated lesions. There was no significant difference (p>0.05) in age and gender distribution between the 78 patients with LVH (left ventricular mass >100g/m²) (Group A) when compared with the 137 patients without LVH (left ventricular mass <100g/m²) (Group B). RESULTS: The electrocardiographic finding of transmural necrosis was more often found in group B patients than in group A patients (56.9% and 30.8%, respectively; p<0.05). The left ventricular function parameters of group A were better than those of group B: the ratio end-diastolic pressure/systolic pressure (EDP/SP) (A: 0.108±0.036; B: 0.121±0.050; p<0.05); the end-diastolic volume index (A: 75.9±31.3ml/m²; B: 88.0±31.0ml/m²; p<0.01); the end-systolic volume index (A: 16.0±10.0ml/m²; B: 27.0 ±20.0ml/m²; p<0.001); the ejection fraction (A 78.6±10.8%; B 67.7±17.9%; p<0.001); the anteroinferior shortening (A: 43.9±10.3%; B: 35.1±12.8%; p<0.001). A higher degree of coronary tortuosity was observed in group A than in group B (78.2% and 24.1%; p<0.001) and also a more frequent absent or minimal diaphragmatic hypokinetic area (A: 80.8%; B: 54.0%; p<0.05). CONCLUSION: LVH reduces the effects of myocardial sequela and protects LV function when right coronary occlusion develops.

Gomes Marne de Freitas; Gottschall Carlos Antônio Mascia

1999-01-01

209

Redox modulation of L-type calcium channels in ferret ventricular myocytes. Dual mechanism regulation by nitric oxide and S-nitrosothiols  

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The effects of NO-related activity and cellular thiol redox state on basal L-type calcium current, ICa,L, in ferret right ventricular myocytes were studied using the patch clamp technique. SIN-1, which generates both NO. and O2-, either inhibited or stimulated ICa,L. In the presence of superoxide di...

210

The calcium-independent transient outward potassium current in isolated ferret right ventricular myocytes. II. Closed state reverse use- dependent block by 4-aminopyridine  

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Block of the calcium-independent transient outward K+ current, I(to), by 4-aminopyridine (4-AP) was studied in ferret right ventricular myocytes using the whole cell patch clamp technique. 4-AP reduces I(to) through a closed state blocking mechanism displaying "reverse use- dependent" behavior that ...

211

The effect of atenolol on NT-proBNP and troponin in asymptomatic cats with severe left ventricular hypertrophy because of hypertrophic cardiomyopathy: a pilot study.  

UK PubMed Central (United Kingdom)

BACKGROUND: Atenolol often is used empirically in cats with hypertrophic cardiomyopathy (HCM) before the onset of heart failure, although evidence of efficacy is lacking. Cardiac biomarkers play a critical role in the early detection of subclinical cardiac disease, in the prediction of long-term prognosis, and in monitoring the response to therapy in humans. HYPOTHESIS: Circulating concentrations of the biomarkers N-terminal pro-B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) will decrease after chronic administration of atenolol PO to cats with severe HCM but no signs of heart failure. ANIMALS: Six Maine Coon or Maine Coon cross cats with severe HCM. METHODS: Cats were treated with atenolol (12.5 mg PO q12 h) for 30 days. No cat had left ventricular dynamic outflow tract obstruction caused by systolic anterior motion of the mitral valve. The concentrations of NT-proBNP and cTnI were assayed before and on the last day of drug administration. RESULTS: There was no statistically significant change in NT-proBNP (median before, 394 pmol/L; range, 71-1,500 pmol/L; median after, 439 pmol/L; range, 24-1,500 pmol/L; P = .63) or in cTnI (median before, 0.24?ng/mL; range, 0.10-0.97?ng/mL; median after, 0.28 ng/mL; range, 0.09-1.0 ng/mL; P = .69) after administration of atenolol. CONCLUSIONS: Atenolol administration did not decrease NT-proBNP or cTnI concentrations in cats with severe left ventricular hypertrophy caused by hypertrophic cardiomyopathy. These results suggest that atenolol did not decrease myocardial ischemia and myocyte death in these cats. A larger clinical trial is warranted to verify these findings.

Jung SW; Kittleson MD

2011-09-01

212

QRS Voltage-Duration Product in the Identification of Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats  

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Full Text Available OBJECTIVE - Evaluation of the performance of the QRS voltage-duration product (VDP) for detection of left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHR). METHODS - Orthogonal electrocardiograms (ECG) were recorded in male SHR at the age of 12 and 20 weeks, when systolic blood pressure (sBP) reached the average values of 165±3 mmHg and 195±12 mmHg, respectively. Age- and sex- matched normotensive Wistar Kyoto (WKY) rats were used as controls. VDP was calculated as a product of maximum QRS spatial vector magnitude and QRS duration. Left ventricular mass (LVM) was weighed after rats were sacrificed. RESULTS - LVM in SHR at 12 and 20 weeks of age (0.86±0.05 g and 1.05±0.07 g, respectively) was significantly higher as compared with that in WKY (0.65±0.07 g and 0.70±0.02 g). The increase in LVM closely correlated with the sBP increase. VDP did not reflect the increase in LVM in SHR. VDP was lower in SHR as compared with that in WKY, and the difference was significant at the age of 20 weeks (18.2mVms compared with 10.7mVms, p<0.01). On the contrary, a significant increase in the VDP was observed in the control WKY at the age of 20 weeks without changes in LVM. The changes in VDP were influenced mainly by the changes in QRSmax. CONCLUSION - LVM was not the major determinant of QRS voltage changes and consequently of the VDP. These data point to the importance of the nonspatial determinants of the recorded QRS voltage in terms of the solid angle theory.

Bacharova Ljuba; Kyselovic Jan; Klimas Jan

2002-01-01

213

Etiology, pathophysiology, and treatment of left ventricular hypertrophy: focus on severe hypertension.  

UK PubMed Central (United Kingdom)

Left ventricular hypertrophy (LVH), a common finding in hypertensive patients, has emerged as one of the most potent risk factors for future cardiovascular mortality in patients with hypertension. LVH is associated with multiple physiologic abnormalities, which may account for the increased risk. These include coronary perfusion abnormalities such as reduced coronary flow reserve, altered coronary flow autoregulation, subendocardial hypoperfusion, and abnormal left ventricular (LV) diastolic function. Although abnormalities of LV diastolic function are more common in LVH, they may occur early in the course of the disease. There may be a threshold of average awake ambulatory blood pressure (BP), 130/85 mm Hg, below which neither diastolic abnormalities nor LVH is detected. The reasons for reduced reserve coronary flow reserve are complex and include structural and functional abnormalities of myocardial blood vessels such as reduced capillary density, reduced luminal diameter of intramyocardial small arteries, and increased vascular tone, possibly as a result of factors such as abnormal endothelium-dependent relaxation. Preliminary data suggest that regression of LVH is associated with improved survival. Severe hypertensive patients would be expected to achieve the greatest benefit, because, if left untreated, this group has nearly 20% mortality within 2 years. To evaluate the effect of nifedipine gastrointestinal therapeutic system (GITS) on LV mass, 16 patients with initial diastolic BP > 120 mm Hg were treated for 1 year with either monotherapy or in combination with a thiazide diuretic. Because it has not been unequivocally shown that changes in LV mass have physiologic benefit, associated alterations in LV systolic function, LV filling, plasma renin activity, atrial natriuretic peptide, and catecholamines were also evaluated.(ABSTRACT TRUNCATED AT 250 WORDS)

Phillips RA

1993-01-01

214

Economic benefits of left ventricular hypertrophy regression in patients with arterial hypertension  

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Full Text Available Aim. To evaluate by modelling the economic benefits of left ventricular hypertrophy (LVH) regression in patients with arterial hypertension (HT) due to therapy with fixed combination of valsartan/amlodipine.Material and methods. 20 patients (15 females and 5 males, aged 18 to 70 years) with essential HT accompanied by metabolic syndrome with a history of previous ineffective antihypertensive therapy were included into the study. All patients were treated with fixed combination of amlodipine/valsartan in doses of 5/160 and 10/160 mg depending on blood pressure (BP) level. Treatment duration was 24 weeks. Changes in BP level, LVH regression were assessed. Economic evaluation was performed on the basis of modelling with the specialized software Decision Tree 4.xla.Results. Effect of fixed amlodipine/valsartan combination therapy on LVH was used to estimate treatment effectiveness and to build the model. Patients were distributed according to left ventricular (LV) mass (at baseline and after 24 weeks of therapy). Significant decrease in LV mass from 205.8±50.4 to 181.9±45.1 g (p<0.05) was revealed. The model took into account economic and frequency factors for 10 year prognosis: this therapy prevents 36 deaths, 6 strokes, 24 myocardial infarction per 1000 patients. Absence of need in treatment of these prevented events can save 2 516 772.42 RUR for every 1 000 patients. It would reduce the total costs per patient during 10 years.Conclusion. Treatment with amlodipine/valsartan single pill combination has not only clinical advantages, but also pharmacoeconomic benefits. This combination reduces risk of acute myocardial infarction and death more effectively. Treatment with fixed valsartan/amlodipine combination saves maximum years of life with less cost during 10 years. Despite of higher pharmacotherapy costs, fixed valsartan/amlodipine combination reduces total costs due to prevention of fatal and nonfatal cardiovascular events.

E.I. Tarlovskaya; N.S. Maksimchuk; S.V. Malchicova; M.V. Avksentieva; I.E. Sapozhnikova; Y.A. Balandina

2011-01-01

215

Vitamin D reduces left atrial volume in patients with left ventricular hypertrophy and chronic kidney disease.  

UK PubMed Central (United Kingdom)

BACKGROUND: Left atrial enlargement, a sensitive integrator of left ventricular diastolic function, is associated with increased cardiovascular morbidity and mortality. Vitamin D is linked to lower cardiovascular morbidity, possibly modifying cardiac structure and function; however, firm evidence is lacking. We assessed the effect of an activated vitamin D analog on left atrial volume index (LAVi) in a post hoc analysis of the PRIMO trial (clinicaltrials.gov: NCT00497146). METHODS AND RESULTS: One hundred ninety-six patients with chronic kidney disease (estimated glomerular filtration rate 15-60 mL/min per 1.73 m(2)), mild to moderate left ventricular hypertrophy, and preserved ejection fraction were randomly assigned to 2 ?g of oral paricalcitol or matching placebo for 48 weeks. Two-dimensional echocardiography was obtained at baseline and at 24 and 48 weeks after initiation of therapy. Over the study period, there was a significant decrease in LAVi (-2.79 mL/m(2), 95% CI -4.00 to -1.59 mL/m(2)) in the paricalcitol group compared with the placebo group (-0.70 mL/m(2) [95% CI -1.93 to 0.53 mL/m(2)], P = .002). Paricalcitol also attenuated the rise in levels of brain natriuretic peptide (10.8% in paricalcitol vs 21.3% in placebo, P = .02). For the entire population, the change in brain natriuretic peptide correlated with change in LAVi (r = 0.17, P = .03). CONCLUSIONS: Forty-eight weeks of therapy with an active vitamin D analog reduces LAVi and attenuates the rise of BNP. In a population where only few therapies alter cardiovascular related morbidity and mortality, these post hoc results warrant further confirmation.

Tamez H; Zoccali C; Packham D; Wenger J; Bhan I; Appelbaum E; Pritchett Y; Chang Y; Agarwal R; Wanner C; Lloyd-Jones D; Cannata J; Thompson BT; Andress D; Zhang W; Singh B; Zehnder D; Pachika A; Manning WJ; Shah A; Solomon SD; Thadhani R

2012-12-01

216

Electrocardiographic predictors of sudden cardiac death in patients with left ventricular hypertrophy.  

UK PubMed Central (United Kingdom)

BACKGROUND: Left ventricular hypertrophy (LVH) has been associated with increased risk of sudden cardiac death (SCD), and improvements in risk stratification methodology are warranted. METHODS: We evaluated electrocardiographic intervals as potential markers of SCD risk in LVH. Corrected QT, QRS, and JT intervals were evaluated in consecutive cases with SCD and LVH from the ongoing Oregon Sudden Unexpected Death study who underwent a 12-lead electrocardiogram (EKG) and echocardiogram prior to and unrelated to the SCD event. Comparisons of age, gender, body mass index, LV ejection fraction, and EKG intervals together with clinical conditions (hypertension and diabetes) were conducted with geographically matched controls that had coronary artery disease but no history of ventricular arrhythmias or cardiac arrest. LVH was determined using the modified American Society of Echocardiography equation for LV mass. Independent samples t-test, Pearson's chi-square test, and multiple logistic regression were used for statistical comparisons. RESULTS: Of the 109 cases and 49 controls who met study criteria, age, gender, and comorbidities were similar among cases and controls. The mean LV mass index was not significantly different in cases compared to controls. However mean QTc (470.6 ± 53.6 ms vs 440.7 ± 38.7 ms; P < 0.0001) and QRS duration (113.6 ± 30.0 ms vs 104.9 ± 18.7 ms; P = 0.03) were significantly higher in cases than controls. In logistic regression analysis, prolonged QTc was the only EKG interval significantly associated with SCD (OR 1.72 [1.23-2.40]). CONCLUSION: Prolonged QTc was independently associated with SCD among subjects with LVH and merits further evaluation as a predictor of SCD in LVH.

Panikkath R; Reinier K; Uy-Evanado A; Teodorescu C; Gunson K; Jui J; Chugh SS

2013-05-01

217

Risk factors for increased left ventricular hypertrophy in patients with chronic kidney disease.  

UK PubMed Central (United Kingdom)

BACKGROUND: Although left ventricular hypertrophy (LVH) has been established as a predictor of cardiovascular events in chronic kidney disease (CKD), the relationship between the prevalence of LVH and CKD stage during the predialysis period has not been fully examined. METHODS: We measured left ventricular mass index (LVMI) in a cross-sectional cohort of participants in the Chronic Kidney Disease Japan Cohort (CKD-JAC) study in order to identify factors that are associated with increased LVMI in patients with stage 3-5 CKD. LVH was defined as LVMI > 125 g/m(2) in male patients and >110 g/m(2) in female patients. RESULTS: We analyzed baseline characteristics in 1185 participants (male 63.7 %, female 36.3 %). Diabetes mellitus was the underlying disease in 41.3 % of patients, and mean age was 61.8 ± 11.1 years. LVH was detected in 21.7 % of patients at baseline. By multivariate logistic analysis, independent risk factors for LVH were past history of cardiovascular disease (odds ratio [OR] 0.574; 95 % confidence interval [CI] 0.360-0.916; P = 0.020), systolic blood pressure (OR 1.179; 95 % CI 1.021-1.360; P = 0.025), body mass index (OR 1.135; 95 % CI 1.074-1.200; P < 0.001), and serum calcium level (OR 0.589; 95 % CI 0.396-0.876; P = 0.009). CONCLUSION: Cross-sectional baseline data from the CKD-JAC study shed light on the association between LVH and risk factors in patients with decreased renal function. Further longitudinal analyses of the CKD-JAC cohort are needed to evaluate the prognostic value of LVH in CKD patients.

Nitta K; Iimuro S; Imai E; Matsuo S; Makino H; Akizawa T; Watanabe T; Ohashi Y; Hishida A

2013-01-01

218

Atherosclerosis and vascular calcification are independent predictors of left ventricular hypertrophy in chronic haemodialysis patients.  

UK PubMed Central (United Kingdom)

BACKGROUND: Accelerated atherosclerosis and vascular calcification are common in chronic haemodialysis (HD) patients. In this study, we aimed to investigate the relationship between left ventricular hypertrophy (LVH) in HD patients and atherosclerosis and vascular calcification measured by electron beam computed tomography (EBCT). METHODS: In a cohort of 118 HD patients (52 male, 66 female, mean age: 46+/-13 years), we measured biochemical parameters, including BUN, creatinine, albumin, haemoglobin, C-reactive protein and fibrinogen levels, and performed echocardiography, high-resolution B-mode carotid ultrasonography and EBCT in 85 of them. The degree of stenosis was measured at four different sites (communis, bulbus, interna and externa) in both carotid arteries. Carotid plaque scores were calculated by summing the degrees of stenosis measured at all locations. RESULTS: LVH was detected in 89 of the patients (75%). Plaque-positive patients had higher left ventricular mass index (LVMI) than plaque-negative patients (175+/-59 vs 143+/-46 g/m2, P = 0.003). LVMI was correlated with systolic blood pressure (r = 0.62, P<0.001), pulse pressure (r = 0.58, P<0.001), haemoglobin levels (r = - 0.25, P = 0.008), carotid plaque score (r = 0.32, P = 0.001) and coronary (CACS) and aortic wall calcification score (AWCS) (r = 0.34, P = 0.002 and r = 0.43, P<0.001, respectively). Multiple linear regression analysis (model r = 0.76) showed the independent factors related to LVMI to be systolic blood pressure, pulse pressure, CACS and presence of carotid plaques. CONCLUSION: Extra-coronary atherosclerosis and vascular calcification are associated with LVH in HD patients. Whether the treatment of atherosclerosis or vascular calcification may cause regression of or even prevent LVH in HD patients remains to be seen.

Yildiz A; Memisoglu E; Oflaz H; Yazici H; Pusuroglu H; Akkaya V; Erzengin F; Tepe S

2005-04-01

219

Association between an ANF Gene I/D dimorphism and left ventricular hypertrophy in a Gulf Arab population.  

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Full Text Available BACKGROUND: An association case-controlled study was carried out on a group of 151 United Arab Emirates nationals--62 normotensives with and without left ventricular hypertrophy (LVH) and 89 hypertensives, also with and without LVH--with a view to evaluating the value of an insertion/deletion (I/D) dimorphism located in the second intron of the human atrial natriuretic factor (ANF) gene in relation to left ventricular hypertrophy. Subjects and METHODS: Criteria used for LVH inclusion were: demonstration of Sokoloe and Lyon ECG criteria (sum of S wave in V(1), and tallest R wave in lead V5 or V6 > or =35 mm) and echocardiography findings (interventricular septum > or =1.2 cm; posterior LV wall > or =1.3 cm) in the long axis. ANF gene was obtained according to the usual methods by DNA extraction by means of polymerase chain reactions (PCR). The frequencies of this marker were performed according to the Hardy-Weinberg proportions. RESULTS: Our findings show that there was a significant difference in the distribution of the I and D alleles between the two groups (LVH vs non-LVH), with chi(2) = 12.34, 2df, P=0.002, making this a significant association of the D allele with LVH. CONCLUSION: Our results do suggest that variants of the ANF gene might be involved in the determination of left ventricular hypertrophy.

Obineche Enyioma; Frossard Philippe; Bokhari Awais

2002-01-01

220

Association between an ANF gene I/D dimorphism and left ventricular hypertrophy in a Gulf Arab Population  

International Nuclear Information System (INIS)

[en] An association case-control study was carried out on a group of 151 United Arab Emirates nationals-62 normotensives with and without left ventricular hypertrophy (LVH) and 89 hypertensives, also with and without LVH-with a view to evaluating the value of an intersection/deletion (ID) dimorphism located in the second intron of the human atrial natriuretic factor (ANF) gene in relation to left ventricular hypertrophy. Criteria used for LVH inclusion were: demonstration of Sokoloe and Lyon ECG criteria (sum of S wave in V1 and R wave in lead V5 or V6 > 35 mm) and echocardiography findings (interventricular septum > 1.2 cm; posterior LV wall > 1.3 cm) in the long axis. ANF gene was obtained according to the usual methods by DNA extraction by means of polymerase chain reaction (PCR). The frequencies of this marker were performed according to the Hardy-Weinberg proportions. Our finding show that there was a significant difference in the distribution of the I and D alleles between the two groups (LVH vs non-LVH) with x2 = 12.34, 2df, P=0.002, making this a significant association of the D allele with LVH. Our results do suggest that variants of the ANF gene might be involved in the determination of left ventricular hypertrophy. (author)

2002-01-01

 
 
 
 
221

Aspectos electrocardiográfícos de la hipertrofia ventricular derecha en el cor pulmonale crónico/ Electrocardiographs features of right ventricular hypertrophy in chronic cor pulmonale  

Scientific Electronic Library Online (English)

Full Text Available Abstract in spanish Se exponen los criterios electrofisiológicos para el diagnóstico electrocardiográfico de los crecimientos ventriculares derechos, a la luz de la sucesión del proceso de activación del miocardio ventricular. La hipertrofia ventricular derecha por sobrecarga sistólica sostenida puede ser global o segmentaria. En el primer caso, p. ej. cardiopatía hipertensiva pulmonar crónica de origen vascular, aumentan la magnitud y la manifestación de todos los principales vecto (more) res resultantes de la activación de dicho ventrículo: IIs, IId y IIId. Si la hipertrofia ventricular derecha es de tipo segmentario, p. ej. neumopatía crónica por obstrucción bronquial, aumentan la magnitud y la manifestación sólo de algunos de los vectores resultantes de la activación del ventrículo derecho. En el caso mencionado, aumenta la manifestación del vector basal derecho: IIId. Cuando coexiste isquemia subepicárdica o transmural del ventrículo derecho, la onda T negativa en las derivaciones precordiales derechas y transicionales tiene características de tipo primario y se asocia a prolongación del intervalo Q-Tc en ausencia de acción digitálica. Se presentan dos ejemplos demostrativos de las correlaciones existentes entre datos electrocardiográficos y datos anatómicos en la hipertrofia global y en la segmentaria del ventrículo derecho, respectivamente. Abstract in english The electrophysiological criteria for diagnosing right ventricular hypertrophy, characteristic of chronic cor pulmonale, are described. Right ventricular hypertrophy due to a sustained systolic overload can be global or regional. In the first situation, as for example, an idiopathic pulmonary hypertension, the magnitude and manifestation of all the main vectors resulting from the depolarization of this ventricle are increased: IIs (septal), IIr (parietal), and IIIr (basal (more) ). When the right ventricular hypertrophy is of the segmental (regional) type, as for example, that due to a chronic bronchial obstruction, the magnitude and manifestation of only some right vectors are increased. In this condition, only the magnitude of the right basal vector (IIIr) is augmented. In the presence of subepicardial or transmural ischemia of the right ventricle, negative T waves of primary type are recorded in right precordial and transitional leads, where the Q-Tc interval is prolonged in the absence of digitalis effect. Two demonstrative examples of the correlations existing between the electrocardiographic and anatomical findings in global and regional hypertrophies, respectively, of the right ventricle are presented.

de Micheli, Alfredo; Aranda, Alberto; Medrano, Gustavo A

2006-03-01

222

Depression, cardiometabolic function and left ventricular hypertrophy in African men and women: the SABPA study.  

UK PubMed Central (United Kingdom)

Depressive symptoms are associated with an increased risk for developing cardiovascular diseases, driven by its link to the metabolic syndrome (MetS). This phenomenon, however, still needs to be investigated in the African population. The aim of this study is to investigate the association between left ventricular hypertrophy (LVH) and MetS risk markers in a determined sample. The researchers stratified Black African men and women into with depressive symptoms (D) or without depressive symptoms (ND) group, based on the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria score. Fasting MetS, chronic hyperglycemia (HbA1c), ambulatory blood pressure (BP) and Cornell product-LVH (CP-LVH) in ECG measures were obtained. Depressive symptoms were reported in 45.3% of the sample. Independent of depression status, African men and women revealed a pre-diabetic state (glycated hemoglobin >5.7%). CP-LVH was associated with decreased low high-density lipoprotein cholesterol in D African women. In D African men, systolic BP (P = .001) and HbA1c (P = .08) explained 64% and 31% of the variation in LVH, respectively. In conclusion, depressive symptoms in Black African women were associated with a measure of target end organ damage, CP-LVH, and this association was driven by a metabolic factor. In Black African men, independent of depressive symptoms, LVH, was driven by cardiometabolic factors, namely SBP and HbA1c.

Mashele N; Malan L; van Rooyen JM; Harvey BH; Potgieter JC; Hamer M

2013-01-01

223

Influence of dietary sodium modulation on electrocardiographic voltage criteria for left ventricular hypertrophy in normotensive individuals.  

UK PubMed Central (United Kingdom)

OBJECTIVE: Dietary sodium intake and left ventricular hypertrophy (LVH) on electrocardiogram (ECG) are both independent determinants of cardiovascular risk. Prior studies demonstrated that acute dietary sodium modulation significantly altered LVH-specific ECG voltage in hypertensive individuals, thus modifying cardiovascular risk prediction; but whether this phenomenon exists in normotensive individuals is not known. We evaluated the influence of dietary sodium intake on ECG voltage and ECG criteria for LVH in normotensive individuals. METHODS: Retrospective evaluation of ECGs of healthy normotensive individuals (n = 39) who were prospectively randomized to a dietary study protocol of 1 week of high-sodium diet (>200 mmol of sodium per day) and 1 week of low-sodium diet (<10 mmol/d) was conducted. Electrocardiogram voltage amplitudes and biochemical assessments were performed at the end of each dietary intervention. RESULTS: As expected, blood pressure declined and measures of circulating renin-angiotensin-aldosterone system activity rose significantly with low-sodium diet. No significant changes in specific LVH voltage criteria or overall precordial or limb lead ECG voltage amplitudes were detected between diets. CONCLUSION: Although immediate dietary sodium modulation has been shown to significantly alter LVH-specific ECG voltage and the detection of LVH in hypertensive individuals, dietary sodium intake did not influence ECG voltage in normotensive individuals. Healthy normotensive individuals may exhibit adaptive measures that dampen ECG voltage fluctuations in response to dietary sodium modulation. More specific cardiac imaging studies may provide additional insight into this observation and the influence of dietary sodium in cardiac health.

Larson C; Vaidya A; Sun B; Williams JS

2012-01-01

224

A Computational Model Integrating Electrophysiology, Contraction, and Mitochondrial Bioenergetics in the Ventricular Myocyte  

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An intricate network of reactions is involved in matching energy supply with demand in the heart. This complexity arises because energy production both modulates and is modulated by the electrophysiological and contractile activity of the cardiac myocyte. Here, we present an integrated mathematical ...

Cortassa, Sonia; Aon, Miguel A.; O'Rourke, Brian; Jacques, Robert; Tseng, Hsiang-Jer; Marbán, Eduardo; Winslow, Raimond L.

225

Action Potential Duration Restitution Portraits of Mammalian Ventricular Myocytes: Role of Calcium Current  

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Construction of the action potential duration (APD) restitution portrait allows visualization of multiple aspects of the dynamics of periodically paced myocytes at various basic cycle lengths (BCLs). For the first time, we obtained the restitution portrait of isolated rabbit and guinea pig cardiac v...

Tolkacheva, Elena G.; Anumonwo, Justus M. B.; Jalife, José

226

High-molecular-weight polyethylene glycol protects cardiac myocytes from hypoxia- and reoxygenation-induced cell death and preserves ventricular function.  

UK PubMed Central (United Kingdom)

Apoptosis plays a significant role in maladaptive remodeling and ventricular dysfunction following ischemia-reperfusion injury. There is a critical need for novel approaches to inhibit apoptotic cell death following reperfusion, as this loss of cardiac myocytes can progressively lead to heart failure. We investigated the ability and signaling mechanisms of a high-molecular-weight polyethylene glycol-based copolymer, PEG 15-20, to protect cardiac myocytes from hypoxia-reoxygenation (H-R)-induced cell death and its efficacy in preserving ventricular function following extended hypothermic ischemia and warm reperfusion as relevant to cardiac transplantation. Pretreatment of neonatal rat ventricular myocytes with a 5% PEG solution led to a threefold decline in apoptosis after H-R relative to untreated controls. There was a similar decline in caspase-3 activity in conjunction with inhibition of cytochrome c release from the inner mitochondrial membrane. Treatment with PEG also reduced reactive oxygen species production after H-R, and sarcolemmal lipid-raft architecture was preserved, consistent with membrane stabilization. Cell survival signaling was upregulated after H-R with PEG, as demonstrated by increased phosphorylation of Akt, GSK-3?, and ERK1/2. There was also maintenance of cardiac myocyte ?-adrenergic signaling, which is critical for myocardial function. PEG 15-20 was very effective in preserving left ventricular function following prolonged hypothermic ischemia and warm reperfusion. PEG 15-20 has a potent protective antiapoptotic effect in cardiac myocytes exposed to H-R injury and may represent a novel therapeutic strategy to decrease myocardial cell death and ventricular dysfunction at the time of reperfusion during acute coronary syndrome or following prolonged donor heart preservation.

Malhotra R; Valuckaite V; Staron ML; Theccanat T; D'Souza KM; Alverdy JC; Akhter SA

2011-05-01

227

Effect of delayed intervention with ACE-inhibitor therapy on myocyte hypertrophy and growth of the cardiac interstitium in the rat model of myocardial infarction.  

UK PubMed Central (United Kingdom)

The effectiveness of angiotensin-converting enzyme (ACE)-inhibitor therapy in attenuating ventricular remodeling when initiated immediately following myocardial damage is clearly established. Less information, however, is available on the impact of late therapy on the remodeling process, especially its influence on the cellular components of these structural changes. The purpose of this study was to examine the effects of converting enzyme inhibitor therapy commenced 28 days following infarction in the rat on changes in cardiac myocyte dimension and the interstitium. At 28 days following infarction, myocyte cell length (153.9+/-7.3 v 131.1+/-5.9 micron, P=0.0002) and cell volume in the free wall of the left ventricle (38. 5+/-5.0 x 10(3) v31.4+/-3.1 x 10(3), P=0.009) had increased compared with sham-operated rats. Similar changes were noted in the septum and right ventricle. Captopril therapy administered between 28 and 56 days attenuated a further increase in cell length noted in an untreated group in the left ventricle (153.5+/-15.3 v 167.3+/-13.7 micron, P=0.02), right ventricle (153.8+/-20.5 v 173.8+/-2.3 micron, P=0.01) and septum (158.0+/-20.2 v 179.1+/-16.6 micron, P=0.004). There was an increase in hydroxyproline content in the right ventricle and a similar trend in the left ventricle in the untreated myocardial infarction groups. These changes were not altered by captopril therapy. In summary, even late therapy with captopril attenuates progressive myocyte remodeling, which may contribute to the ability of ACE-inhibitor therapy to slow progressive chamber enlargement following infarction.

McDonald KM; Chu C; Francis GS; Carlyle W; Judd DL; Hauer K; Hartman M; Cohn JN

1997-12-01

228

The aqueous extract, not organic extracts, of Terminalia arjuna bark exerts cardiotonic effect on adult ventricular myocytes.  

Science.gov (United States)

The bark of Terminalia arjuna (TA) has been used for centuries in ayurvedic medicine as cardiotonics for treatment of cardiac disorders. It became recently available as over-the-counter supplements marketed for maintaining a healthy heart. However, the cellular mechanism of its cardiotonic effect remains undefined. The present study was designed to investigate the physicochemical property and inotropic effect of the aqueous extract of TA bark (TA(AqE)) on adult rat ventricular myocytes in comparison with extracts prepared sequentially with organic solvents (organic extracts). The kinetics of myocyte contraction and caffeine-induced contraction were analyzed to assess the effect of TA(AqE) on sarcoplasmic reticular (SR) function. The inotropic effect of TA(AqE) was also compared with that of known cardiotonics, isoproterenol (ISO) and ouabain (Ouab). We found that TA(AqE) decoctions exerted positive inotropy, accelerated myocyte relaxation and increased caffeine-induced contraction concentration-dependently. In contrast, TA organic extracts caused interruption of excitability and arrhythmias without consistent inotropic action. In conclusion, TA(AqE)-induced cardiotonic action via enhancing SR function, a unique action minimizing the occurrence of arrhythmias, makes TA(AqE) a promising and relatively safe cardiotonic beneficial to the healthy heart and the treatment for chronic heart disease. The cardiotonic effect of TA(AqE) is consistent with the therapeutic property of TA bark used in ayurvedic medicine. The method of administration and/or selective omission of hydrophobic components from bark powder could be crucial to the efficacy and safety of TA bark in cardiac therapy and uses as over-the-counter supplements. PMID:21315570

Oberoi, Lalit; Akiyama, Toshiyuki; Lee, Kuo-Hsiung; Liu, Shi J

2011-02-15

229

The aqueous extract, not organic extracts, of Terminalia arjuna bark exerts cardiotonic effect on adult ventricular myocytes.  

UK PubMed Central (United Kingdom)

The bark of Terminalia arjuna (TA) has been used for centuries in ayurvedic medicine as cardiotonics for treatment of cardiac disorders. It became recently available as over-the-counter supplements marketed for maintaining a healthy heart. However, the cellular mechanism of its cardiotonic effect remains undefined. The present study was designed to investigate the physicochemical property and inotropic effect of the aqueous extract of TA bark (TA(AqE)) on adult rat ventricular myocytes in comparison with extracts prepared sequentially with organic solvents (organic extracts). The kinetics of myocyte contraction and caffeine-induced contraction were analyzed to assess the effect of TA(AqE) on sarcoplasmic reticular (SR) function. The inotropic effect of TA(AqE) was also compared with that of known cardiotonics, isoproterenol (ISO) and ouabain (Ouab). We found that TA(AqE) decoctions exerted positive inotropy, accelerated myocyte relaxation and increased caffeine-induced contraction concentration-dependently. In contrast, TA organic extracts caused interruption of excitability and arrhythmias without consistent inotropic action. In conclusion, TA(AqE)-induced cardiotonic action via enhancing SR function, a unique action minimizing the occurrence of arrhythmias, makes TA(AqE) a promising and relatively safe cardiotonic beneficial to the healthy heart and the treatment for chronic heart disease. The cardiotonic effect of TA(AqE) is consistent with the therapeutic property of TA bark used in ayurvedic medicine. The method of administration and/or selective omission of hydrophobic components from bark powder could be crucial to the efficacy and safety of TA bark in cardiac therapy and uses as over-the-counter supplements.

Oberoi L; Akiyama T; Lee KH; Liu SJ

2011-02-01

230

Cardiotrofina-1 circulante puede diferenciar la hipertrofia ventricular fisiológica del atleta de la hipertrofia patológica del paciente hipertenso/ Circulating cardiotrophyn-1 may help differenciate left ventricular hypertrophy seen in athletes from pathologic left ventricular hypertrophy associated to hypertension  

Scientific Electronic Library Online (English)

Full Text Available Abstract in spanish Introducción: Cardiotrofina-1 (CT-1), una citoquina perteneciente a la superfamilia de la interleukina-6, se encuentra elevada en pacientes con hipertensión arterial (HTA) e hipertrofia ventricular izquierda (HVI). Sus niveles se correlacionan con el tamaño auricular izquierdo y con las presiones de llenado del ventrículo izquierdo. Los niveles de CT-1 en atletas con HVI fisiológica no han sido investigados. Métodos: Estudio transversal. Se incluyeron pacientes con (more) HTA esencial con y sin evidencia ecográfica de cardiopatía hipertensiva (CH)(HVI y relación E/E'>10), recientemente diagnosticada y sin tratamiento. Un grupo de atletas normotensos con diagnóstico ecográfico de HVI y un grupo control de sujetos normotensos pareados por edad y sexo. En todos los sujetos se midieron los niveles plasmáticos de CT-1 (ELISA). Se definió HVI mediante diagnóstico ecocargiográfico, utilizando el índice de masa ventricular izquierda usando la fórmula de Devereux (hombres ³115 gramos/m², mujer ³95 gramos/m²). Las presiones de llenado del VI se estimaron con la relación E/E' (doppler tisular en el anillo mitral medial). Resultados: Se incluyeron 10 pacientes por grupo. Los atletas con HVI presentaron una relación E/E' Abstract in english Background: Cardiotrophyn-1 (CT-1), is a cytokine which is increased in patients with hypertension (HT) and left ventricular hypertrophy (LVH). This increase occurs in proportion to left atrial size and left ventricular filling pressures. CT-1 levels in athletes with LVH have not been investigated Methods: Crossectional study. We evaluated: a) hypertensive patients with LVH and E/E' > 10 by echocardiography, recently diagnosed and receiving no medications; b) normotensive (more) athletes with LVH as shown by echocardiography, and c) normotensive subjects, paired by age and sex. Plasma levels of CT-1 (ELISA) were measured in all. LVH was defined as left ventricular mass index > 115 G/m² (males) or > 95 G/m² (females). Results: E/E' was lower in athletes than hypertensive patients with LVH (6.5 ± 1 vs 12.9 ± 1.1, p

Gabrielli, Luigi; Yañez, Fernando; Ocaranza, María Paz; Godoy, Iván; Castro, Pablo; Greig, Douglas; Hernández, Claudia; Llevaneras, Silvana; Jalil, Jorge

2009-04-01

231

CAVEOLIN-3 IS UP-REGULATED IN THE PHYSIOLOGICAL LEFT VENTRICULAR HYPERTROPHY INDUCED BY VOLUNTARY EXERCISE TRAINING IN RATS  

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Full Text Available Various substances have been introduced in relation with cardiac hypertrophy almost always with controversy in their roles in signal transduction. Those controversies may attribute to the diversity of cardiac hypertrophy. We previously showed that calcineurin was activated in physiological left ventricular hypertrophy (LVH) induced by voluntary exercise training, but not in decompensated pressure-overload LVH. In the current study, we advanced our search for the differences between the voluntary exercise-induced LVH and the pressure-overload LVH into several other hypertrophy-related substances including caveolin. Wistar rats were assigned to one of the following three groups: 10 weeks of voluntary exercise (EX), sedentary regimen (SED), and 4 weeks of ascending aortic constriction (AC). The EX rats voluntarily ran 1.6±1.1 km/day in the specially manufactured cages resulting in LVH (24 % increase in left ventricular weight per body weight ratio). Myocardial tissue homogenate of the EX rats revealed different characteristics in signal transduction of hypertrophy from that of the AC. The EX rats had normal sarcoplasmic reticulum (SR) Ca2+ATPase mRNA level and normal myosin heavy chain isozyme pattern assessed by RNA protection assay, while AC rats had decreased SR Ca2+ATPase mRNA level and increased beta myosin heavy chain mRNA level. Myocardial caveolin-3 protein levels assessed by Western blotting increased in the EX rats but decreased in the AC rats. The voluntary exercise-induced LVH differed in signal transduction from the decompensated pressure-overload LVH. Caveolin-3 was induced in the voluntary exercise-induced LVH, while it was decreased in the decompensated pressure-overload LVH

Teruhiko Aoyagi; Yoshihiro Ishikawa; Hitosh Oshikawa; Koichiro Kinugawa; Ikuo Yokoyama; Ryozo Nagai

2002-01-01

232

Simulation of the effect of rogue ryanodine receptors on a calcium wave in ventricular myocytes with heart failure  

Science.gov (United States)

Calcium homeostasis is considered to be one of the most important factors for the contraction and relaxation of the heart muscle. However, under some pathological conditions, such as heart failure (HF), calcium homeostasis is disordered, and spontaneous waves may occur. In this study, we developed a mathematical model of formation and propagation of a calcium wave based upon a governing system of diffusion-reaction equations presented by Izu et al (2001 Biophys. J. 80 103-20) and integrated non-clustered or 'rogue' ryanodine receptors (rogue RyRs) into a two-dimensional (2D) model of ventricular myocytes isolated from failing hearts in which sarcoplasmic reticulum (SR) Ca2+ pools are partially unloaded. The model was then used to simulate the effect of rogue RyRs on initiation and propagation of the calcium wave in ventricular myocytes with HF. Our simulation results show that rogue RyRs can amplify the diastolic SR Ca2+ leak in the form of Ca2+ quarks, increase the probability of occurrence of spontaneous Ca2+ waves even with smaller SR Ca2+ stores, accelerate Ca2+ wave propagation, and hence lead to delayed afterdepolarizations (DADs) and cardiac arrhythmia in the diseased heart. This investigation suggests that incorporating rogue RyRs in the Ca2+ wave model under HF conditions provides a new view of Ca2+ dynamics that could not be mimicked by adjusting traditional parameters involved in Ca2+ release units and other ion channels, and contributes to understanding the underlying mechanism of HF.

Lu, Luyao; Xia, Ling; Ye, Xuesong; Cheng, Heping

2010-06-01

233

SERUM IGF-I AND HORMONAL RESPONSES TO INCREMENTAL EXERCISE IN ATHLETES WITH AND WITHOUT LEFT VENTRICULAR HYPERTROPHY  

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Full Text Available We investigated the response of insulin-like growth factor (IGF- I), insulin-like growth factor binding protein-3 (IGFBP-3) and some hormones, i.e., testosterone (T), growth hormone (GH), cortisol (C), and insulin (I), to maximal exercise in road cyclists with and without diagnosed left ventricular hypertrophy. M-mode and two-dimensional Doppler echocardiography was performed in 30 professional male endurance athletes and a group of 14 healthy untrained subjects using a Hewlett-Packard Image Point HX ultrasound system with standard imaging transducers. Echocardiography and an incremental physical exercise test were performed during the competitive season. Venous blood samples were drawn before and immediately after the maximal cycling exercise test for determination of somatomedin and hormonal concentrations. The basal concentration of IGF-I was statistically higher (p < 0.05) in athletes with left ventricular muscle hypertrophy (LVH) when compared to athletes with a normal upper limit of the left ventricular wall (LVN) (p < 0.05) and to the control group (CG) (p < 0.01). The IGF-I level increased significantly at maximal intensity of incremental exercise in CG (p < 0.01), LVN (p < 0.05) and LVH (p < 0.05) compared to respective values at rest. Long-term endurance training induced an increase in resting (p < 0.01) and post-exercise (p < 0.05) IGF-I/IGFBP-3 ratio in athletes with LVH compared to LVN. The testosterone (T) level was lower in LVH at rest compared to LVN and CG groups (p < 0.05). These results indicate that resting serum IGF-I concentration were higher in trained subjects with LVH compared to athletes without LVH. Serum IGF- I/IGFBP-3 elevation at rest and after exercise might suggest that IGF-I act as a potent stimulant of left ventricular hypertrophy in chronically trained endurance athletes

Aleksandra Zebrowska; Zbigniew Gasior; Józef Langfort

2009-01-01

234

Left ventricular hypertrophy in COPD without hypoxemia: the elephant in the room?  

UK PubMed Central (United Kingdom)

BACKGROUND: COPD is associated with significant cardiovascular mortality. Left ventricular hypertrophy (LVH) is a pivotal cardiovascular risk factor. The prevalence of LVH in COPD is currently unknown. METHODS: We performed a pilot study of 93 normoxemic patients with COPD and 34 control subjects. Patients underwent echocardiography to measure left ventricular (LV) dimensions, ECG, measurement of serum B-type natriuretic peptide (BNP) levels, and 24-h BP recording. Spirometry and oxygen saturations were also recorded. RESULTS: The oxygen saturations of patients with COPD were normal, at 96.5% (95% CI, 96.1%-97.0%), with a mean FEV(1) of 70.0% predicted (95% CI, 65.2%-74.8%). A total of 30.1% of patients with COPD met the echocardiographic criteria for LVH based on LV mass index, with more LVH in female patients than in male patients (43.2% vs 21.4%, P = .02). The LV mass index in patients with COPD was 96.2 g/m(2) (95% CI, 90.1-102.7 g/m(2)) vs 82.9 g/m(2) (95% CI, 75.8-90.6 g/m(2)) in control subjects ( P = .017). The LV mass index remained high in patients with COPD in the absence of a hypertension history (94.5 g/m(2) vs 79.9 g/m(2), P = .015) and with 24-h systolic BP <135 mm Hg (96.7 g/m(2) vs 82.5 g/m(2), P = .024). The LV ejection fraction (mean = 63.4%) and BNP (mean = 28.7 pg/mL) were normal in patients with COPD. The mean 24-h BP was normal in patients with COPD, at 125/72 mm Hg. ECG was less sensitive for detecting LVH than was echocardiography. CONCLUSION: LVH with normal LV ejection fraction and BNP levels was present in a significant proportion of normotensive, normoxemic patients with COPD, especially female patients. Clinical trials are, therefore, indicated to evaluate treatments to regress LVH in patients with COPD.

Anderson WJ; Lipworth BJ; Rekhraj S; Struthers AD; George J

2013-01-01

235

Regression of left ventricular hypertrophy and microalbuminuria changes during antihypertensive treatment.  

UK PubMed Central (United Kingdom)

OBJECTIVE: The objective of the present study was to assess the regression of left ventricular hypertrophy (LVH) during antihypertensive treatment, and its relationship with the changes in microalbuminuria. INDIVIDUALS AND METHODS: One hundred and sixty-eight previously untreated patients with echocardiographic LVH, 46 (27%) with microalbuminuria, were followed during a median period of 13 months (range 6-23 months) and treated with lifestyle changes and antihypertensive drugs. Twenty-four-hour ambulatory blood pressure monitoring, echocardiography and urinary albumin excretion were assessed at the beginning and at the end of the study period. RESULTS: Left ventricular mass index (LVMI) was reduced from 137 [interquartile interval (IQI), 129-154] to 121 (IQI, 104-137) g/m (P?50%) had the same odds of achieving regression of LVH as patients with normoalbuminuria (ORm 1.1; 95% CI 0.38-3.25; P?=?0.85). However, those with microalbuminuria at baseline, who did not regress, had less probability of achieving LVH regression than the normoalbuminuric patients (OR 0.26; 95% CI 0.07-0.90; P?=?0.03) even when adjusted for age, sex, initial LVMI, GFR, blood pressure and angiotensin-converting enzyme inhibitor (ACE-I) or angiotensin receptor blocker (ARB) treatment during the follow-up. CONCLUSION: Patients who do not have a significant reduction in microalbuminuria have less chance of achieving LVH regression, independent of blood pressure reduction.

Rodilla E; Pascual JM; Costa JA; Martin J; Gonzalez C; Redon J

2013-08-01

236

Refinement of total 12-lead QRS voltage criteria for diagnosing left ventricular hypertrophy  

Directory of Open Access Journals (Sweden)

Full Text Available Objective: We sought to test the hypothesis that the total QRS voltage without either set of the limb leads (I, II, III) or (R, L, F) may be a better indicator of LVH as compared to the total QRS voltage. Background: The total 12 lead QRS voltage has been a validated electrocardiographic criterion for left ventricular hypertrophy (LVH), with an upper limit of175 mm. However, there is some redundancy in this measurement as the output of the limb leads is repeated because leads I, II, III, and R, L, F use the same three electrodes. Methods: 43 unselected, consecutive echocardiograms were examined for evidence of LVH by wall thickness. Electrocardiogram (ECG) of these patients within a week of the echocardiogram were then examined for the total 12 leads QRS voltage, minus I, II, III and total minus R, L, F voltages. ECG findings were then compared with corresponding echocardiographic dimensions. Results: A total QRS voltage of123 mmon ECG yielded a sensitivity of 73% and specificity of 67% for diagnosing LVH with 95% CI = 0.59 - 0.89, p = 0.007. Total minus (R, L and F) value of110 mmon ECG appears to give the best sensitivity (73%), specificity (72%), and accuracy (64% negative predictive value and 82% positive predictive value) for LVH. Conclusion: It appears that total QRS voltage minus either set of the limb leads, especially the total minus R, L and F is a better criterion, with110 mmbeing the best specific, sensitive and accurate index for diagnosing LVH.

Deepti Kumar; Rishi Bajaj; Lovely Chhabra; David H. Spodick

2013-01-01

237

T-wave axis deviation and Left Ventricular Hypertrophy interaction in diabetes and hypertension.  

UK PubMed Central (United Kingdom)

Electrocardiographic signs of Left Ventricular Hypertrophy (ECG-LVH) and T-wave axis (TA) deviation are independent predictors of fatal and non fatal events. We assessed the prevalence of ECG-LVH, TA abnormalities and their combination according to the presence or absence of diabetes and/or hypertension in a large sample of the adult general Italian population. Data from 10,184 women (54±11years) and 8775 men (54±11years) were analyzed from the Moli-sani cohort, a database of randomly recruited adults (age >35) from the general population of Molise, a central region of Italy that includes collection of standard 12-lead resting ECG. Subjects with previous myocardial infarction, angina, cerebrovascular disease or left bundle brunch block or missing values for TA or ECG-LVH have been excluded. TA was measured from the standard 12-lead ECG and it was defined as the rotation of the T wave in the frontal plane as computed by a proprietary algorithm (CalECG/Bravo, AMPS-LLC, NY). ECG-LVH was defined as Sokolow Lyon voltage (SLv) >35mm or Cornell voltage duration Product (CP)>=2440 mm*ms. Among subjects with ECG-LVH, prevalence of hypertension was 59.0% and 49.7%, respectively for men and women, whereas that of diabetes was 10.7% and 5.7%. In hypertensives, TA was normal in 72.3% of subjects, borderline in 24.8% and abnormal in 2.9%. In diabetics, TA was normal in 70.4% of subjects, borderline in 26.5% and abnormal in 3.1%. In both hypertensive and diabetic subjects, the prevalence of ECG-LVH, was significantly greater in subjects with borderline or abnormal TA. Hypertension was an independent predictor of abnormal TA (odd ratio: 1.38, P=.025). These results suggest that hypertension might play a relevant role in the pathogenesis of TA deviation.

Assanelli D; Di Castelnuovo A; Rago L; Badilini F; Vinetti G; Gianfagna F; Salvetti M; Zito F; Donati MB; de Gaetano G; Iacoviello L

2013-09-01

238

Increased prevalence of left ventricular hypertrophy in hypertensive women with type 2 diabetes mellitus  

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Full Text Available Abstract Background Left ventricular hypertrophy (LVH) is a powerful independent risk factor for cardiovascular morbidity and mortality among hypertensive patients. Data regarding relationships between diabetes and LVH are controversial and inconclusive, whereas possible gender differences were not specifically investigated. The goal of this work was to investigate whether gender differences in left heart structure and mass are present in hypertensive patients with type 2 diabetes. Methods Five hundred fifty hypertensive patients with at least one additional cardiovascular risk factor (314 men and 246 women, age 52 to 81, mean 66 ± 6 years), were enrolled in the present analysis. In 200 (36%) of them – 108 men and 92 women – type 2 diabetes mellitus was found upon enrollment. End-diastolic measurements of interventricular septal thickness (IVS), LV internal diameter, and posterior wall thickness were performed employing two-dimensionally guided M-mode echocardiograms. LVH was diagnosed when LV mass index (LVMI) was >134 g/m2 in men and >110 g/m2 in women. Results Mean LVMI was significantly higher among diabetic vs. nondiabetic women (112.5 ± 29 vs. 105.6 ± 24, p = 0.03). In addition, diabetic women presented a significantly higher prevalence of increased IVS thickness, LVMI and left atrial diameter on intra-gender comparisons. The age adjusted relative risk for increased LVMI in diabetics vs. nondiabetics was 1.47 (95% CI: 1.0–2.2) in females and only 0.8 (0.5–1.3) in males. Conclusion Type 2 diabetes mellitus was associated with a significantly higher prevalence of LVH and left atrial enlargement in hypertensive women.

Tenenbaum Alexander; Fisman Enrique Z; Schwammenthal Ehud; Adler Yehuda; Benderly Michal; Motro Michael; Shemesh Joseph

2003-01-01

239

Low Grade Inflammation and ECG Left Ventricular Hypertrophy in Urban African Males: The SABPA Study.  

UK PubMed Central (United Kingdom)

BACKGROUND: Hypertension and vascular hyperresponsiveness have been associated with structural wall abnormalities in black Africans. Whether low grade inflammation would have an additive effect is uncertain. Therefore, a novel investigation aimed to assess whether inflammation and pressure overload would have an additive association with ECG left ventricular hypertrophy (LVH). METHODS: We included 75 African and 87 Caucasian males. Ambulatory blood pressure monitoring was done in the working week. A resting 12-lead ECG recording was used for the determination of LVH with the Cornell product formula. Fasting blood samples were obtained for high sensitivity C-reactive protein (hs-CRP) analyses after a controlled overnight stay. Men were stratified into low (?3mg/L) and high (>3mg/L) hs-CRP groups. RESULTS: African men revealed higher ambulatory blood pressure levels compared to Caucasian men independent of hs-CRP levels after adjustment for age, physical activity, cotinine, log?-GT and body surface area. In forward stepwise linear regression analyses, SBP was positively associated with ECG LVH in all Africans. Considering low grade inflammatory status (>3mg/L hs-CRP), SBP [Adj R(2)=0.49 (?=0.99, 0.45, 1.44), p?0.01] and pulse pressure [Adj R(2)=0.61 (?=0.0.34, 0.88), p?0.01] respectively, predicted ECG LVH in African but not in Caucasian men. CONCLUSIONS: Hyperdynamic blood pressure and inflammation acted in tandem as possible promoting factors to structural wall abnormalities in African men.

van der Walt C; Malan L; Uys AS; Malan NT

2013-05-01

240

Intercoronary connection with bidirectional blood flow and concentric left ventricular hypertrophy  

Scientific Electronic Library Online (English)

Full Text Available Abstract in portuguese Homem de cor branca, 54 anos, com histórias de dor esternal atípica para insuficiência coronária, iniciada há 6 meses. Antecedentes: HAS e tabagismo. O exame do aparelho cardiovascular era normal. PA = 140/100mmHg (ambos os braços). O E.C.G. de repouso revelou onda T negativa em D2, D3 e AVF. O ecocardiograma bidimensional demonstrou hipertrofia concêntrica do VE de grau moderado. No TE, protocolo de Ellestad, a frequência cardíaca não atingiu os níveis preconi (more) zados e ocorreu aumento acentuado da PA (230/140 mm Hg). Não apresentou alterações expressivas do segmento ST em relação ao repouso. No cateterismo cardíaco, a pressão do VE foi de 170/20 mm HG. O VE apresentava aspecto hipertrófico. Cinecoronariografia esquerda e direita não revelaram lesões obstrutivas. Injeção seletiva de contraste na ACD demonstrou enchimento retrógrado da porção distal da ACX até sua porção média através de conexões intercoronárias. Da mesma forma injeção seletiva na ACE demonstrou enchimento retrógrado da porção distal da ACD por conexões intercoronárias da ACX para a ACD. Revisão da literatura e possíveis mecanismos foram apresentados. Abstract in english Cardiac catheterization in a 55-year-old man, with a 6-month history of atypical chest pain and Q-waves in D1, Dili and AVF, showed concentric left ventricular (LV) hypertrophy and a large intercoronary connection between right coronary artery (RCA) and circumflex artery (CX), with bidirectional blood flow. Although the RCA and CX were normal, selective injection of CX filled RCA retrogradely and in the same way selective injection of RCA filled CX. Possible mechanisms and literature are reviewed.

Meireles, George César Ximenes; Abreu Filho, Luciano Mauricio

1994-12-01

 
 
 
 
241

The metabolic syndrome and left ventricular hypertrophy--the influence of gender and physical activity.  

UK PubMed Central (United Kingdom)

AIMS: To investigate associations between the metabolic syndrome (MetS) and left ventricular hypertrophy (LVH) as well as the influence of gender and physical activity (PA) in a population-based cross-sectional study of 60-year-old men (n = 1822) and women (n = 2049). MAJOR FINDINGS: In total, 908 (23.5%) study participants fulfilled the criteria for MetS (54.2% men). Among those, 104 (11.5%) exhibited signs of LVH (60.6% men), compared with 182 (6.1%) among those without MetS (60.4% men). Of the individual factors contained in MetS, hypertension was independently associated with LVH in both men and women (OR = 3.4; 95% CI 2.0-5.8 and 4.4; 2.5-7.8 respectively), whereas waist circumference (OR = 1.6; 95% CI 1.0-2.6), high glucose levels (OR = 1.8; 95% CI 1.1-2.8) and hyperinsulinaemia (OR = 1.7; 95% CI 1.1-2.6) were independently related to risks for LVH exclusively in women. PA did not significantly affect the association. PRINCIPAL CONCLUSION: Participants with MetS were at an increased risk of LVH, independently of PA level. Of the various components in MetS, hypertension was most strongly and independently related to LVH in both men and women. In women, abdominal obesity, high glucose levels and hyperinsulinaemia were independently related to LVH, suggesting a gender differences in the mechanisms behind development of LVH.

Halldin M; Fahlstadius P; de Faire U; Vikström M; Hellénius ML

2012-06-01

242

The prognostic value of electrocardiographic estimation of left ventricular hypertrophy in dialysis patients.  

UK PubMed Central (United Kingdom)

BACKGROUND: Left ventricular hypertrophy (LVH) is associated with poor cardiovascular outcome in CKD. Electrocardiogram (ECG) is low-cost but infrequently used to assess presence of LVH in dialysis patients. The aim of this study was to establish which ECG-determined LVH method is most sensitive in dialysis patients, and also most predictive of death. METHODS: This was a longitudinal observational study in dialysis patients from a single center, undergoing interval ECGs. Fourteen methods of ECG LVH assessment were compared. Survival was also compared between four LVH evolutionary categories: persistent LVH; new LVH; LVH regression; and no LVH. RESULTS: The study included 418 dialysis patients (46.3% women, mean age 51 years, mean follow up 67 months, 76 deaths, 37 cardiovascular deaths). LVH prevalence varied according to method (range 13.4-41.9%). No measurement predicted all-cause mortality. After Cox regression, there was an independent association between LVH and cardiovascular mortality using Novacode (HR = 3.04; 95% [CI] = 1.11-8.28, P < 0.05), but not with other methods. Patients with persistent ECG changes of LVH had increased risk of cardiovascular mortality compared to other LVH evolutionary categories (P < 0.044). CONCLUSIONS: ECG scoring of LVH can be predictive of cardiovascular mortality. The Novacode method, based on repolarization abnormalities, is a better predictor than standard ECG techniques that are based on voltage criteria. Novacode LVH estimation at dialysis initiation may prove to be a noninvasive and cost-effective bedside tool for cardiovascular risk stratification in patients receiving dialysis.

Covic AC; Buimistriuc LD; Green D; Stefan A; Badarau S; Kalra PA

2013-03-01

243

Electrocardiographic left ventricular hypertrophy in GUSTO IV ACS: an important risk marker of mortality in women.  

DEFF Research Database (Denmark)

AIM: To examine the association of left ventricular hypertrophy (LVH) on admission electrocardiography with adverse outcomes in acute coronary syndrome (ACS) patients. METHODS AND RESULTS: A total of 7443 non-ST-elevation ACS patients in Global Utilization of STrategies to Open occluded arteries (GUSTO) IV ACS trial had admission electrocardiograms analysed at a core laboratory. LVH [>or=20 mm Cornell voltage (LV voltage) (women) or >or=28 mm (men) plus strain patterns] was observed in 586 (7.9%) patients, and women accounted for 74%. LVH patients were also older and had more co-morbidities, ST-depression >or= 0.5 mm, elevated C-reactive protein and N-terminal pro-brain naturetic peptide (NT-proBNP), and lower troponin T. Invasive procedures occurred less often in LVH patients (cardiac catheterization: 31 vs. 38%, P = 0.001; percutaneous coronary intervention: 12 vs. 20%, P < 0.001). Mortality was significantly higher in patients with LVH (30 day: 5 vs. 3%, P = 0.046; 1 year: 14 vs. 7%, P < 0.001), whereas 30day myocardial infarction (MI) and death/MI did not differ. After baseline adjustment including NT-proBNP, LVH remained associated with increased hazard of 1 year mortality in women, but not in men [P-interaction = 0.033; women: adjusted hazard ratio (LVH vs. no LVH): 1.42 (1.04-1.94), P = 0.029]. CONCLUSION: Electrocardiographic-LVH identifies an important subset of ACS patients with a higher risk of long-term mortality, particularly among women. These novel findings highlight opportunities to improve treatment and outcome among similar ACS patients. Udgivelsesdato: 2007-Sep

Westerhout, Cynthia M; Lauer, Michael S

2007-01-01

244

[Interobserver agreement on electrocardiographic diagnosis of left ventricular hypertrophy in hypertensive patients in Andalusia. PREHVIA study].  

UK PubMed Central (United Kingdom)

OBJECTIVE: To assess the agreement between Primary Care (PC) doctors and a cardiology specialist in diagnosing left ventricular hypertrophy in the electrocardiograph (LVH-ECG) in hypertensive patients. DESIGN: Cross-sectional, multicentre study. SETTING: Andalusian Primary Care Centres. PARTICIPANTS: A total of 120 PC doctors who using a random sample selected patients of 35 years or more with AHT of at least 6 months of progression. PRIMARY VARIABLES: Demographic data, risk factors and cardiovascular diseases were recorded. The LVH-ECG was evaluated by applying Cornell voltage criteria, Cornell and Sokolow-Lyon product. The PC researchers read the ECG first and the cardiologist made a second reading blind. RESULTS: A total of 570 patients (mean +/- SD of age, 65 +/- 11 years; 54.5% females); the LVH-ECG prevalence was 13.7% (95% CI, 10.8-16.6; 12.6% by Cornell and 1.6% by Sokolow-Lyon). The agreement in the diagnosis between the PC doctors and the cardiologist was 0.378 (95% CI, 0.272-0.486; disagreements in 15.5% of cases). The PC doctors slightly underestimated the LVH-ECG prevalence by Cornell and slightly overestimated it by the Sokolow-Lyon criteria. The agreement was also low for all of them (kappa = 0.367; 95% CI, 0.252-0.482, for Cornell, and kappa = 0.274; 95% CI: 0.093-0.454 for Sokolow-Lyon). CONCLUSIONS: The agreement between the diagnosis by the PC doctors and the cardiologist was low. The implications of this study suggest the need to improve the reading of ECG among PC doctors. The use of computerised systems could be a good option.

Martín-Rioboó E; López Granados A; Cea Calvo L; Pérula De Torres LA; García Criado E; Anguita Sánchez MP; García Matarín L; Molina Díaz R; Ureña Fernández T

2009-05-01

245

Prevalence and covariates of electrocardiographic left ventricular hypertrophy in the Hypertension in the Very Elderly Trial.  

UK PubMed Central (United Kingdom)

OBJECTIVE: To estimate the prevalence and covariates of electrocardiographic left ventricular hypertrophy (LVH) in the Hypertension in the Very Elderly Trial. METHODS: A total of 2993 hypertensive people aged at least 80 years with technically codable ECGs without pacing, bundle branch block, or ECG myocardial infarction were studied. LVH was assessed using Sokolow-Lyon (SL-LVH), Cornell voltage (CV-LVH), and Cornell product criterion (CP-LVH). RESULTS: The prevalence of LVH varied from 2.4 to 17.5% depending on sex, race, and ECG criterion. The highest prevalence of SL-LVH (12.0%) was in Chinese men and in white women for both CV-LVH (17.5%) and CP-LVH (12.9%). Increasing SBP was an independent covariate of the presence of LVH in Chinese women independently of the criterion used (??=?0.052-0.069, P?

Antikainen RL; Beckett N; Peters R; Fagard R; Rajkumar C; Wang J; Stoyanovsky V; Barrowdale D; Bulpitt CJ

2013-06-01

246

Left ventricular hypertrophy influences cardiac prognosis in patients undergoing dobutamine cardiac stress testing.  

UK PubMed Central (United Kingdom)

BACKGROUND: This study was performed to determine the utility of dobutamine stress test results for predicting myocardial infarction (MI) and cardiac death in patients with chest pain and left ventricular hypertrophy (LVH). METHODS AND RESULTS: Three hundred fifty-three participants with a mean+/-SD age of 64+/-12 years (54%men) underwent dobutamine cardiovascular magnetic resonance stress testing and then were followed up for 6+/-2 years (mean+/-SD; range, 0.5-11.5) to assess the post-dobutamine cardiovascular magnetic resonance stress test occurrence of MI or cardiac death. LV mass and the presence or absence of ischemia were determined; LVH was defined as an LV mass index >96 g/m(2) in men and >77 g/m(2) in women. LVH was present in 62 participants (18% of the men and 17% of the women, P=0.90). Seventy-one (20%) participants experienced an MI or cardiac death during follow-up. The MI and cardiac death rate was more frequent in those with versus without LVH (32% vs 17%, P=0.009). In multivariable analysis that accounted for the presence of preexisting coronary artery disease, hypertension, diabetes, stress-induced ischemia, and reduced LV ejection fraction, LVH was an independent predictor of MI and cardiac death (hazard ratio=1.99; 95% CI, 1.13-3.50; P=0.02). CONCLUSIONS: LVH is predictive of future MI and cardiac death in patients with or without inducible ischemia during dobutamine cardiac stress testing. As a result, LVH should be reported in those referred for dobutamine cardiac stress tests, particularly in those without inducible ischemia, in whom one would otherwise assume a favorable cardiac prognosis.

Charoenpanichkit C; Morgan TM; Hamilton CA; Wallace EL; Robinson K; Ntim WO; Hundley WG

2010-07-01

247

A study of prevention and regression of cardiac hypertrophy with a prolactin inhibitor in a biological model of ventricular hypertrophy caused by aorto caval fistulae in rat.  

UK PubMed Central (United Kingdom)

BACKGROUND: The possibility of decreasing or reverting left ventricular hypertrophy and, therefore, cardiac hypertrophy (CH) is an important medical issue. The aim of the present study was to evaluate these two possibilities with a 3-week daily dose of captopril, losartan, or bromocriptine in a preventive or corrective model. METHODS: After aorto caval fistulae (ACF) surgery on adult male Wistar rats to induce CH, animals were assigned to the preventive protocol (drug treatment began immediately after surgery) or corrective protocol (hypertrophy was allowed to develop before drug treatment). After treatments, isoproterenol was administered to half of the animals to further induce CH. The groups included the passive control, the sham-operated animals, those with ACF surgery but without drug treatment, and the 3-week treatments with captopril, losartan, or the low or high dose of bromocriptine. RESULTS: Three treatments, with captopril, losartan, or the high dose of bromocriptine, significantly impeded/reverted an increase in CH-related parameters in the preventive/corrective model compared to the surgically treated group without drug treatment. The same effect was found after isoproterenol administration. The present results show an avoidance/reversion of CH with these three treatments. Better results were found with the angiotensin converting enzyme inhibitor (captopril) than with the prolactin inhibitor (bromocriptine). CONCLUSIONS: Treatments with captopril, losartan, and the high dose of bromocriptine were effective in preventing/reversing the manifestation of CH in the preventive/corrective rat models. Further studies are needed to identify the initial mediator, the key component, and the molecular events involved in the pathogenesis of CH.

Vélez JM; Chamorro GA; Calzada CC; Zuñiga CA; Vélez JJ; Ocharán E

2013-09-01

248

The left atrium, atrial fibrillation, and the risk of stroke in hypertensive patients with left ventricular hypertrophy  

DEFF Research Database (Denmark)

The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study provided extensive data on predisposing factors, consequences, and prevention of atrial fibrillation (AF) in patients with hypertension and left ventricular (LV) hypertrophy. Randomized losartan-based treatment was superior to atenolol-based treatment for reducing new-onset AF and complications, especially stroke, associated with new-onset or pre-existing AF. Potential mechanisms of AF prevention by angiotensin receptor blockade supported by LIFE results include greater reduction in left atrial size and LV hypertrophy. Differential effects of antihypertensive treatment on the left atrium and left ventricle may help prevent AF and reduce risk of stroke associated with hypertensive heart disease Udgivelsesdato: 2008/12

Wachtell, K.; Devereux, R.B.

2008-01-01

249

Regresión de la hipertrofia ventricular izquierda con el uso del captopril/ Regression of left ventricular hypertrophy with the use of captopril  

Scientific Electronic Library Online (English)

Full Text Available Abstract in spanish Fundamento: la hipertensión arterial está asociada a cambios estructurales del aparato cardiovascular que le sirve para adaptarse al funcionamiento de un entorno de tensión alta. Objetivo: determinar la efectividad del captropil en la regresión de la hipertrofia ventricular izquierda en pacientes hipertensos, atendidos en consulta especializada en hipertensión arterial del Hospital universitario Manuel Ascunce Domenech desde Enero hasta Diciembre de 2008. Método: se (more) realizó un estudio cuasi-experimental en ciento cuarenta y nueve pacientes. La muestra quedó constituida por cien pacientes. Resultados: se encontró un predominio de la hipertrofia ventricular izquierda en pacientes hipertensos entre treinta y seis y cuarenta y cinco años, después del uso del Captopril se produjo una disminución del 12,0% de pacientes con patrón geométrico anormal del ventrículo izquierdo con cuatro años de evolución de hipertensión arterial, y los pacientes con patrón geométrico anormal del ventrículo izquierdo con hipertensión arterial en estadio uno fueron veintiséis. Luego del uso de dicho fármaco veintiséis pacientes presentaron patrón geométrico normal del ventrículo izquierdo. Conclusiones: el captropil es efectivo en el tratamiento de la hipertrofia ventricular izquierda principalmente en pacientes con hipertensión en estadio uno, con menos de cuatros años de evolución. Abstract in english Background: arterial hypertension is associate to structural changes of the cardiovascular apparatus that are used for adapting to the function in a high tension environment. Objective: to determine the effectiveness of captopril in the regression of left ventricular hypertrophy in hypertensive patients, attended in a specialized consultation of arterial hypertension at the Manuel Ascunce Domenech University Hospital from January to December 2008. Method: a quasi-experime (more) ntal study in one hundred forty-nine patients was carried out. The sample was constituted by a hundred patients. Results: a prevalence of left ventricular hypertrophy in hypertensive patients between thirty-six and forty-five years was found, after the use of captopril brought about a decrease of 12,0% of patients with abnormal geometric pattern of left ventricle with four years of evolution of arterial hypertension, and patients with abnormal geometric pattern of left ventricle with arterial hypertension in stage one was twenty-six. After the use of this drug, twenty-six patients presented normal geometric pattern of left ventricle. Conclusions: captopril is effective in the treatment of left ventricular hypertrophy mainly in patients with hypertension in stage one, with less than four years of evolution.

Santana Téllez, Tomás Noel; Monteagudo Canto, Alina; Segura Pujal, Leandro; del Águila Grandez, Angie Yohana

2010-12-01

250

Characterization of diastolic dysfunction in twin-twin transfusion syndrome: association between Doppler findings and ventricular hypertrophy.  

UK PubMed Central (United Kingdom)

BACKGROUND: Twin-twin transfusion syndrome (TTTS) complicates 10% to 15% of monochorionic twin pregnancies. Cardiovascular changes of variable severity, such as ventricular hypertrophy, atrioventricular valve regurgitation, and systolic dysfunction, occur predominantly in recipient twins (RTs). It was the purpose of this study to perform a detailed assessment of ventricular geometry and diastolic function between controls, donor twins (DTs), and RTs. METHODS: In this prospective, case-control study, two-dimensional, pulsed-wave, and Doppler tissue imaging were used to evaluate biventricular geometry and diastolic function in controls, DTs, and RTs. RTs were divided into two groups, severe and mild, on the basis of evidence of high central venous pressure. Specific variables evaluated included relative wall thickness, mitral valve and tricuspid valve E/A velocities, diastolic filling time corrected for heart rate, isovolumic relaxation time, and early (E') and late (A') diastolic myocardial velocities. RESULTS: A total of 120 fetuses (39 TTTS twin pairs and 42 controls) were compared. Increases in relative wall thickness and isovolumic relaxation time were seen in the mild group. In the severe group, further increases in relative wall thickness and isovolumic relaxation time as well as decreased diastolic filling time corrected for heart rate were accompanied by the appearance of a monophasic Doppler inflow profile and elevations in the E/E' ratio, consistent with elevated ventricular filling pressures. CONCLUSIONS: Concentric hypertrophy is observed in RTs affected by TTTS and is associated with impaired ventricular relaxation and shortened filling time. In severe cases, further decreases in diastolic filling time and Doppler signs of elevated ventricular filling pressures are present.

Divanovi? A; Cnota J; Ittenbach R; Tan X; Border W; Crombleholme T; Michelfelder E

2011-08-01

251

Spiral-wave dynamics in a mathematical model of human ventricular tissue with myocytes and fibroblasts.  

UK PubMed Central (United Kingdom)

Cardiac fibroblasts, when coupled functionally with myocytes, can modulate the electrophysiological properties of cardiac tissue. We present systematic numerical studies of such modulation of electrophysiological properties in mathematical models for (a) single myocyte-fibroblast (MF) units and (b) two-dimensional (2D) arrays of such units; our models build on earlier ones and allow for zero-, one-, and two-sided MF couplings. Our studies of MF units elucidate the dependence of the action-potential (AP) morphology on parameters such as [Formula: see text], the fibroblast resting-membrane potential, the fibroblast conductance [Formula: see text], and the MF gap-junctional coupling [Formula: see text]. Furthermore, we find that our MF composite can show autorhythmic and oscillatory behaviors in addition to an excitable response. Our 2D studies use (a) both homogeneous and inhomogeneous distributions of fibroblasts, (b) various ranges for parameters such as [Formula: see text], and [Formula: see text], and (c) intercellular couplings that can be zero-sided, one-sided, and two-sided connections of fibroblasts with myocytes. We show, in particular, that the plane-wave conduction velocity [Formula: see text] decreases as a function of [Formula: see text], for zero-sided and one-sided couplings; however, for two-sided coupling, [Formula: see text] decreases initially and then increases as a function of [Formula: see text], and, eventually, we observe that conduction failure occurs for low values of [Formula: see text]. In our homogeneous studies, we find that the rotation speed and stability of a spiral wave can be controlled either by controlling [Formula: see text] or [Formula: see text]. Our studies with fibroblast inhomogeneities show that a spiral wave can get anchored to a local fibroblast inhomogeneity. We also study the efficacy of a low-amplitude control scheme, which has been suggested for the control of spiral-wave turbulence in mathematical models for cardiac tissue, in our MF model both with and without heterogeneities.

Nayak AR; Shajahan TK; Panfilov AV; Pandit R

2013-01-01

252

Spiral-wave dynamics in a mathematical model of human ventricular tissue with myocytes and fibroblasts.  

Science.gov (United States)

Cardiac fibroblasts, when coupled functionally with myocytes, can modulate the electrophysiological properties of cardiac tissue. We present systematic numerical studies of such modulation of electrophysiological properties in mathematical models for (a) single myocyte-fibroblast (MF) units and (b) two-dimensional (2D) arrays of such units; our models build on earlier ones and allow for zero-, one-, and two-sided MF couplings. Our studies of MF units elucidate the dependence of the action-potential (AP) morphology on parameters such as [Formula: see text], the fibroblast resting-membrane potential, the fibroblast conductance [Formula: see text], and the MF gap-junctional coupling [Formula: see text]. Furthermore, we find that our MF composite can show autorhythmic and oscillatory behaviors in addition to an excitable response. Our 2D studies use (a) both homogeneous and inhomogeneous distributions of fibroblasts, (b) various ranges for parameters such as [Formula: see text], and [Formula: see text], and (c) intercellular couplings that can be zero-sided, one-sided, and two-sided connections of fibroblasts with myocytes. We show, in particular, that the plane-wave conduction velocity [Formula: see text] decreases as a function of [Formula: see text], for zero-sided and one-sided couplings; however, for two-sided coupling, [Formula: see text] decreases initially and then increases as a function of [Formula: see text], and, eventually, we observe that conduction failure occurs for low values of [Formula: see text]. In our homogeneous studies, we find that the rotation speed and stability of a spiral wave can be controlled either by controlling [Formula: see text] or [Formula: see text]. Our studies with fibroblast inhomogeneities show that a spiral wave can get anchored to a local fibroblast inhomogeneity. We also study the efficacy of a low-amplitude control scheme, which has been suggested for the control of spiral-wave turbulence in mathematical models for cardiac tissue, in our MF model both with and without heterogeneities. PMID:24023798

Nayak, Alok Ranjan; Shajahan, T K; Panfilov, A V; Pandit, Rahul

2013-09-04

253

Improvement of diastolic function after regression of left ventricular hypertrophy/ Mejora de la función diastólica tras regresión de la hipertrofia ventricular izquierda  

Scientific Electronic Library Online (English)

Full Text Available Abstract in spanish Objetivo: Evaluar la función diastólica después de revertir la hipertrofia ventricular izquierda, en hipertensión leve a moderada tratada con inhibidores de la enzima convertidora angiotensina (ECA) y, si era necesario, con un diurético. Métodos: Noventa y ocho pacientes hipertensos con hipertrofia ventricular izquierda e índices de función diastólica anormal del ventrículo izquierdo recibieron captopril 50 a 200 mg/día (Capotena®) más clortalidona durante 12 (more) meses para lograr el control de la presión arterial, definido como presión diastólica < 90 mm Hg y presión sistólica < 140 mm Hg. El índice de masa ventricular izquierdo fue calculado por ecocardiografía modo M y bidimensional y la función diastólica ventricular izquierda fue determinada por Doppler pulsado transmitral cada 3 meses. Resultados: Sesenta y tres pacientes eran del género femenino y 35 del género masculino, con edad de 53.4 ± 8.4 años (rango 34-70). Treinta y seis pacientes (36.7%) tenían hipertensión leve y 62 (63.3%) hipertensión moderada. El tratamiento redujo significativamente tanto la presión sistólica de 165 ± 13 a 137 ± 12.9 mm Hg (p Abstract in english Objective: To evaluate the diastolic function after regression of left ventricular hypertrophy, in mild to moderate hypertension treated with angiotensin converting enzyme(ACE) inhibitor and, if necessary, with a diuretic. Methods: Ninety-eight hypertensive patients with left ventricular hypertrophy (LVH) and abnormal left ventricle diastolic function indexes received captopril (Capotena® ) 50 to 200 mg/day plus chlortalidone during 12 months to reach blood pressure cont (more) rol, defined as a diastolic blood pressure < 90 and systolic blood pressure < 140 mm Hg. Left ventricular (LV) mass index was calculated by M mode and two-dimensional echocardiography, and left ventricular diastolic function was assessed by transmitral pulsed Doppler ultrasound every 3 months. Results: Sixty-three patients were women and 35 were men, mean age was 53.4 ± 8.4 years (range 34-70). Thirty-six patients had mild (36.7%) and 62 (63.3%) moderate hypertension. Treatment reduced significantly both systolic pressure from 165 ± 13 to 137 ± 12.9 mm Hg (p

Teniente-Valente, Raúl; Solorio, Sergio; Vargas-Salado, Enrique; Aguirre-Vázquez, Carlos; Hernández-González, Martha A; Olvera-Lopez, José Antonio; Rodríguez-Mariscal, Leticia; Luna-Ruiz, Miguel Angel; Guillén Contreras, José Manuel; Murillo Ortiz, Blanca Olivia

2008-12-01

254

Cardiotrofina-1 circulante puede diferenciar la hipertrofia ventricular fisiológica del atleta de la hipertrofia patológica del paciente hipertenso Circulating cardiotrophyn-1 may help differenciate left ventricular hypertrophy seen in athletes from pathologic left ventricular hypertrophy associated to hypertension  

Directory of Open Access Journals (Sweden)

Full Text Available Introducción: Cardiotrofina-1 (CT-1), una citoquina perteneciente a la superfamilia de la interleukina-6, se encuentra elevada en pacientes con hipertensión arterial (HTA) e hipertrofia ventricular izquierda (HVI). Sus niveles se correlacionan con el tamaño auricular izquierdo y con las presiones de llenado del ventrículo izquierdo. Los niveles de CT-1 en atletas con HVI fisiológica no han sido investigados. Métodos: Estudio transversal. Se incluyeron pacientes con HTA esencial con y sin evidencia ecográfica de cardiopatía hipertensiva (CH)(HVI y relación E/E'>10), recientemente diagnosticada y sin tratamiento. Un grupo de atletas normotensos con diagnóstico ecográfico de HVI y un grupo control de sujetos normotensos pareados por edad y sexo. En todos los sujetos se midieron los niveles plasmáticos de CT-1 (ELISA). Se definió HVI mediante diagnóstico ecocargiográfico, utilizando el índice de masa ventricular izquierda usando la fórmula de Devereux (hombres ³115 gramos/m², mujer ³95 gramos/m²). Las presiones de llenado del VI se estimaron con la relación E/E' (doppler tisular en el anillo mitral medial). Resultados: Se incluyeron 10 pacientes por grupo. Los atletas con HVI presentaron una relación E/E' Background: Cardiotrophyn-1 (CT-1), is a cytokine which is increased in patients with hypertension (HT) and left ventricular hypertrophy (LVH). This increase occurs in proportion to left atrial size and left ventricular filling pressures. CT-1 levels in athletes with LVH have not been investigated Methods: Crossectional study. We evaluated: a) hypertensive patients with LVH and E/E' > 10 by echocardiography, recently diagnosed and receiving no medications; b) normotensive athletes with LVH as shown by echocardiography, and c) normotensive subjects, paired by age and sex. Plasma levels of CT-1 (ELISA) were measured in all. LVH was defined as left ventricular mass index > 115 G/m² (males) or > 95 G/m² (females). Results: E/E' was lower in athletes than hypertensive patients with LVH (6.5 ± 1 vs 12.9 ± 1.1, p<0.01). E/E' in both control subjects and patients with HTA but no LVH did not differ from E/E' in athletes. CT-1 was lower in athletes than patients with HTA and LVH (6.6 ± 0.4 vs 18.2 ± 5.6 fmol/ml, respectively, p<0.001). CT-1 levels in control subjects and hypertensive patients without LVH did not differ from that found in athletes. Conclusion: CT-1 levels are similar in athletes compared to normal subjects and patients with HTA and no LVH. Hypertensive patients with similar grades of LVH and left ventricular diastolic dysfunction had significantly greater leves of CT-1. Thus, CT-1 levels could help differentiate pathological HVI from physiologic LVH in athletes.

Luigi Gabrielli; Fernando Yañez; María Paz Ocaranza; Iván Godoy; Pablo Castro; Douglas Greig; Claudia Hernández; Silvana Llevaneras; Jorge Jalil

2009-01-01

255

The impact of different echocardiographic diagnostic criteria on the prevalence of left ventricular hypertrophy in essential hypertension: the VITAE study. Ventriculo Izquierdo Tension Arterial Espana.  

UK PubMed Central (United Kingdom)

BACKGROUND: The prevalence of echocardiographic left ventricular hypertrophy in essential hypertension ranges from 12 to 96% depending on the threshold values used to define it, and on the selection bias. OBJECTIVE: To estimate the prevalence of echocardiographic left ventricular hypertrophy by different criteria in essential hypertensives seen in primary care centres. METHODS: Cross-sectional study in a population-based sample of 946 essential hypertensives randomly selected in 39 primary care centres across Spain. Echocardiographic studies were performed in reference hospitals by trained observers (concordance Cohen kappa index > 0.7) and analysed by a single observer. RESULTS: Prevalence of left ventricular hypertrophy ranged from 59.2% [95% confidence interval (CI) 56.1 -62.3] by Framingham criteria to 72.7% (95% CI 69.9-75.6) using the criteria of De Simone et al. (J Am Coll Cardiol 1995; 25: 1056-1062). Prevalence was higher in males by the Cornell-Penn criteria, but higher in females when using Framingham or De Simone et al. criteria. Eccentric hypertrophy was more frequent (51.3-54.1%) independently of the criteria used, particularly when adjusting wall-thickness-ratio for age (56.2-58.9%). Concentric remodelling was present in 6.5-11.4% and only 20.8-29.7% of patients had no evidence of left ventricular structural alterations. Factors independently associated with left ventricular hypertrophy in the logistic regression analysis were age, gender, systolic blood pressure, pulse pressure and body mass index. CONCLUSION: Prevalence of echo left ventricular structural alterations among essential hypertensives seen in primary care centres in Spain ranged from 70.3 to 79.2% depending on the threshold values used. Left ventricular hypertrophy ranged from 59.2 to 72.7% and age-adjusted concentric remodelling ranged from 6.5 to 11.4% depending on the criteria used. Only one-quarter of hypertensive patients were free from morphological alterations.

Coca A; Gabriel R; de la Figuera M; López-Sendón JL; Fernández R; Sagastagoitia JD; García JJ; Barajas R

1999-10-01

256

A computational model integrating electrophysiology, contraction, and mitochondrial bioenergetics in the ventricular myocyte.  

Science.gov (United States)

An intricate network of reactions is involved in matching energy supply with demand in the heart. This complexity arises because energy production both modulates and is modulated by the electrophysiological and contractile activity of the cardiac myocyte. Here, we present an integrated mathematical model of the cardiac cell that links excitation-contraction coupling with mitochondrial energy generation. The dynamics of the model are described by a system of 50 ordinary differential equations. The formulation explicitly incorporates cytoplasmic ATP-consuming processes associated with force generation and ion transport, as well as the creatine kinase reaction. Changes in the electrical and contractile activity of the myocyte are coupled to mitochondrial energetics through the ATP, Ca2+, and Na+ concentrations in the myoplasmic and mitochondrial matrix compartments. The pseudo steady-state relationship between force and oxygen consumption at various stimulus frequencies and external Ca2+ concentrations is reproduced in both model simulations and direct experiments in cardiac trabeculae under normoxic conditions, recapitulating the linearity between cardiac work and respiration in the heart. Importantly, the model can also reproduce the rapid time-dependent changes in mitochondrial NADH and Ca2+ in response to abrupt changes in workload. The steady-state and dynamic responses of the model were conferred by ADP-dependent stimulation of mitochondrial oxidative phosphorylation and Ca2+ -dependent regulation of Krebs cycle dehydrogenases, illustrating how the model can be used as a tool for investigating mechanisms underlying metabolic control in the heart. PMID:16679365

Cortassa, Sonia; Aon, Miguel A; O'Rourke, Brian; Jacques, Robert; Tseng, Hsiang-Jer; Marbán, Eduardo; Winslow, Raimond L

2006-05-05

257

Tribulosin suppresses apoptosis via PKC epsilon and ERK1/2 signaling pathway during hypoxia/reoxygenation in neonatal rat ventricular cardiac myocytes.  

UK PubMed Central (United Kingdom)

Tribulosin (tigogenin 3-O-?-D-xylopyranosyl(1-2)-[?-D-xylopyranosyl (1-3)]-?-D-glucopyranosyl (1-4)-[a-L-rhamnopyranosyl(1-2)]-?-D-galactopyranoside), a component of gross saponins of Tribulus terrestris, has been shown to produce cytoprotective effects in heart. Yet, the precise mechanisms are not fully understood. We examined the mechanisms of tribulosin on myocardial protection. Ventricular myocytes were isolated from the heart of neonatal rats and were exposed to 3 h of hypoxia followed by 2 h reoxygenation. Apoptosis was induced by hypoxia/reoxygenation (H/R), and the expression of protein kinase C epsilon (PKC?) and extracellular signal-regulated kinase 1 and 2 (ERK1/2) in cultured neonatal rat cardiac myocytes was detected. The results indicated that treatment with tribulosin in the culture medium protected cardiac myocytes against apoptosis induced by H/R. PKC? and ERK1/2 expression increased after pretreated with tribulosin. In the presence of PKC? inhibitor co-treated with tribulosin, the expression of ERK1/2 was decreased in H/R cardiac myocytes. While preconditioned with PD98059, ERK1/2 inhibitor, no effects on the expression of PKC? were detected. Tribulosin has protective effects on cardiac myocytes against apoptosis induced by H/R injury via PKC? and ERK1/2 signaling pathway.

Zhang S; Li H; Yang SJ

2011-12-01

258

Sophocarpine attenuates the Na(+)-dependent Ca2(+) overload induced by Anemonia sulcata toxin-increased late sodium current in rabbit ventricular myocytes.  

UK PubMed Central (United Kingdom)

Many studies indicate that an increase in late sodium current (I(Na.L)) of cardiomyocytes causes intracellular Na overload and subsequently raises the reverse Na/Ca exchanger current (INCX), ultimately resulting in intracellular Ca overload. Therefore, using drugs to inhibit the increased INa.L under various pathological conditions can lower intracellular Ca overload. This study was intended to explore the effect of sophocarpine (SOP) on the increase in INa.L, INCX, calcium transient and contraction in rabbit ventricular myocytes induced by Anemonia sulcata toxin II (ATX II), an opener of sodium channel, with the application of whole-cell patch-clamp techniques, the video-based motion edge detection system, and the intracellular calcium concentration determination system. The results indicate that tetrodotoxin (TTX, 4 ?M ) obviously decreased INa.L and INCX enlarged by ATX II (30 nM), and SOP (20, 40, and 80 ?M) also inhibited both the parameters concentration dependently in rabbit ventricular myocytes. However, transient sodium current remained unaffected by the above-mentioned concentrations of ATX II, TTX, and SOP. In addition, SOP also reversed diastolic calcium concentration, calcium transient amplitude, and ventricular muscle contractility augmented by ATX II. Its effects were similar to those of TTX, a specific inhibitor of the sodium channel. In conclusion, SOP inhibits INa.L, INCX, diastolic Ca concentration, and contractility in rabbit ventricular myocytes, which suggests that relief of intracellular Ca overload through inhibiting INa.L is likely to become a new therapeutic mechanism of SOP against arrhythmia and myocyte damage associated with intracellular Ca overload.

Zhang S; Ma JH; Zhang PH; Luo AT; Ren ZQ; Kong LH

2012-10-01

259

Sophocarpine attenuates the Na(+)-dependent Ca2(+) overload induced by Anemonia sulcata toxin-increased late sodium current in rabbit ventricular myocytes.  

Science.gov (United States)

Many studies indicate that an increase in late sodium current (I(Na.L)) of cardiomyocytes causes intracellular Na overload and subsequently raises the reverse Na/Ca exchanger current (INCX), ultimately resulting in intracellular Ca overload. Therefore, using drugs to inhibit the increased INa.L under various pathological conditions can lower intracellular Ca overload. This study was intended to explore the effect of sophocarpine (SOP) on the increase in INa.L, INCX, calcium transient and contraction in rabbit ventricular myocytes induced by Anemonia sulcata toxin II (ATX II), an opener of sodium channel, with the application of whole-cell patch-clamp techniques, the video-based motion edge detection system, and the intracellular calcium concentration determination system. The results indicate that tetrodotoxin (TTX, 4 ?M ) obviously decreased INa.L and INCX enlarged by ATX II (30 nM), and SOP (20, 40, and 80 ?M) also inhibited both the parameters concentration dependently in rabbit ventricular myocytes. However, transient sodium current remained unaffected by the above-mentioned concentrations of ATX II, TTX, and SOP. In addition, SOP also reversed diastolic calcium concentration, calcium transient amplitude, and ventricular muscle contractility augmented by ATX II. Its effects were similar to those of TTX, a specific inhibitor of the sodium channel. In conclusion, SOP inhibits INa.L, INCX, diastolic Ca concentration, and contractility in rabbit ventricular myocytes, which suggests that relief of intracellular Ca overload through inhibiting INa.L is likely to become a new therapeutic mechanism of SOP against arrhythmia and myocyte damage associated with intracellular Ca overload. PMID:23064241

Zhang, Shuo; Ma, Ji-Hua; Zhang, Pei-Hua; Luo, An-Tao; Ren, Zhi-Qiang; Kong, Ling-Hao

2012-10-01

260

Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis.  

UK PubMed Central (United Kingdom)

Long-term exercise training is associated with characteristic structural and functional changes of the myocardium, termed athlete's heart. Several research groups investigated exercise training-induced left ventricular (LV) hypertrophy in animal models; however, only sporadic data exist about detailed hemodynamics. We aimed to provide functional characterization of exercise-induced cardiac hypertrophy in a rat model using the in vivo method of LV pressure-volume (P-V) analysis. After inducing LV hypertrophy by swim training, we assessed LV morphometry by echocardiography and performed LV P-V analysis using a pressure-conductance microcatheter to investigate in vivo cardiac function. Echocardiography showed LV hypertrophy (LV mass index: 2.41 ± 0.09 vs. 2.03 ± 0.08 g/kg, P < 0.01), which was confirmed by heart weight data and histomorphometry. Invasive hemodynamic measurements showed unaltered heart rate, arterial pressure, and LV end-diastolic volume along with decreased LV end-systolic volume, thus increased stroke volume and ejection fraction (73.7 ± 0.8 vs. 64.1 ± 1.5%, P < 0.01) in trained versus untrained control rats. The P-V loop-derived sensitive, load-independent contractility indexes, such as slope of end-systolic P-V relationship or preload recruitable stroke work (77.0 ± 6.8 vs. 54.3 ± 4.8 mmHg, P = 0.01) were found to be significantly increased. The observed improvement of ventriculoarterial coupling (0.37 ± 0.02 vs. 0.65 ± 0.08, P < 0.01), along with increased LV stroke work and mechanical efficiency, reflects improved mechanoenergetics of exercise-induced cardiac hypertrophy. Despite the significant hypertrophy, we observed unaltered LV stiffness (slope of end-diastolic P-V relationship: 0.043 ± 0.007 vs. 0.040 ± 0.006 mmHg/?l) and improved LV active relaxation (?: 10.1 ± 0.6 vs. 11.9 ± 0.2 ms, P < 0.01). According to our knowledge, this is the first study that provides characterization of functional changes and hemodynamic relations in exercise-induced cardiac hypertrophy.

Radovits T; Oláh A; Lux Á; Németh BT; Hidi L; Birtalan E; Kellermayer D; Mátyás C; Szabó G; Merkely B

2013-07-01

 
 
 
 
261

Hipertrofia cardíaca esquerda e direita em necropsias de hipertensos Left and right ventricular hypertrophy at autopsy of hypertensive individuals  

Directory of Open Access Journals (Sweden)

Full Text Available OBJETIVO: Medir a espessura ventricular direita e esquerda em falecidos com história de hipertensão arterial, submetidos a necropsias clínicas. MÉTODOS: Foram selecionados 90 casos do Serviço de Verificação de Óbitos de Recife -PE, de ambos os sexos, com história de hipertensão arterial essencial, com relação à espessura das paredes cardíacas, além da correlação com outros achados de necropsia e informes clínicos. RESULTADOS: Observouse associação significativa entre a presença de hipertrofia ventricular esquerda (HVE) e direita (HVD), e de cardiopatia hipertensiva grave e HVD. Houve predomínio da HVD e HVE em homens, na faixa etária dos 60-79 anos, com maior prevalência nas etnias parda e negra, e naqueles com estado nutricional adequado ou com sobrepeso e em obesos. CONCLUSÃO: Observou-se que a presença de HVD relaciona-se com HVE, sugerindo que há fatores patogênicos semelhantes envolvidos no desenvolvimento da hipertrofia bilateral. A HVD parece associar-se à doença cardíaca mais grave, podendo, a partir de outros estudos, ser considerada novo fator prognóstico na avaliação dos pacientes hipertensos.OBJECTIVE: To measure the right and left ventricular thickness in deceased individuals with a history of hypertension submitted to clinical autopsies. METHODS: We selected 90 cases from the Death Verification Service of the city of Recife, state of Pernambuco, Brazil, of both sexes, with a history of essential arterial hypertension related to heart wall thickness, in addition to correlation with autopsy findings and other clinical reports. RESULTS: There was a significant association between the presence of left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH) and between severe hypertensive cardiomyopathy and RVH. There was a predominance of RVH and LVH in men aged 60-79 years and a higher prevalence in the Brazilian mulatto and Black ethnic groups and in those with adequate nutritional status or overweight and obese individuals. CONCLUSION: It was observed that the presence of RVH was related to LVH, suggesting that there are similar pathogenic factors involved in the development of bilateral hypertrophy. The RVH seems to be associated with more severe heart disease and may, based on other studies, be considered as a new prognostic factor in the evaluation of hypertensive patients.

Mirella Pessoa Sant'Anna; Roberto José Vieira de Mello; Luciano Tavares Montenegro; Mônica Modesto Araújo

2012-01-01

262

Self-reported weight and height: implications for left ventricular hypertrophy detection. An Italian multi-center study.  

UK PubMed Central (United Kingdom)

We examined the difference between self-reported and measured body size values and their impact on detection of left ventricular hypertrophy (LVH) by echocardiographic LV mass indexation. A total of 1963 subjects referred by their practitioners for routine echocardiographic examination to nine outpatient echocardiographic laboratories across Italy were included in the study. Left ventricular hypertrophy was defined according to two gender- specific criteria as: A) Left ventricular mass (LVM) index ?49 g/h(2.7) in men and ?45 g/h(2.7) in women; B) LVM index ?125 g/m(2) in men and ?110 g/m(2) in women. Prevalence of LVH was calculated by indexing LVM to both self-reported and measured anthropometric values. In the whole population, LVH tended to be underestimated by self-reported values by 5.4% according to criterion A (48.5% vs. 53.9%, p < 0.001) and by 1.2% according to criterion B (29.6% vs. 30.8%, p < 0.01); similar findings were observed in the hypertensive subgroup encompassing one-half of the sample. Underestimation of LVH was more pronounced in older patients than in younger patients: 8.6% vs. 3.2% (p < 0.001) by criterion A, 3.1% vs. 0.1% (p < 0.001) by criterion B, in women than in men (8.6% vs. 3.3% (p < 0.001) by criterion A and 1.8% vs. 0.5% (p < 0.01) by criterion B. In a sample of outpatients attending echocardiographic laboratories, LVH is misclassified when left ventricular mass is normalized to self-reported weight and height. The error is related to the clinical characteristics of patients and is more pronounced when LVM is normalized to height(2.7).

Cuspidi C; Negri F; Giudici V; Muiesan ML; Grandi AM; Ganau A; Lonati L; Degli Esposti D; Capra A; Milan A; Sala C; Longo M; Morganti A

2011-01-01

263

Evaluation of left ventricular hypertrophy using thallium-201 myocardial scintigraphy, echocardiography and vectorcardiography. Comparison between pressure and volume overloading  

Energy Technology Data Exchange (ETDEWEB)

Thallium-201 (/sup 201/Tl) myocardial scintigraphy was performed in 40 patients with left ventricular hypertrophy(LVH). Twelve out of 40 patients had pressure overloading (aortic stenosis: 5, hypertension: 7), 14 patients had volume overloading (aortic regurgitation: 9, mitral regurgitation: 5) and 14 had idiopathic cardiomyopathy (hypertrophic type (HCM): 8, congestive type (CCM): 6), respectively. LV area, LV uptake index and wall uptake ratio were calculated from left anterior oblique view of /sup 201/Tl myocardial images. These three indices of both pressure overloading and volume overloading were significantly higher than those of controls. The degree of LVH was indicated by both LV area and LV uptake index. LV area was significantly larger in volume overloading than in pressure overloading. In idiopathic cardiomyopathy, these three indices of HCM and LV area and LV uptake index of CCM were significantly increased compared with those of controls. LV area of CCM was significantly larger than that of HCM, while wall uptake ratio of HCM was significantly higher than that of CCM. LV uptake index and wall uptake ratio of HCM became higher according as left ventricular cavity became smaller. LV area of CCM became larger in proportion as left ventricular cavity became larger and as left ventricular wall thickness became thinner. (author).

Tsukahara, Yasunori; Owada, Kenji; Suzuki, Shigebumi

1983-09-01

264

Influence of hypertensive left ventricular hypertrophy on detection of ischemic area with exercise thallium-201 myocardial scintigraphy  

Energy Technology Data Exchange (ETDEWEB)

Sixty-four patients with single left anterior descending artery disease having effort angina (group A: 40 patients with hypertrophic hypertension, group B: 10 patients with hypertrophic hypertension, group C: 14 patients with non-hypertrophic hypertension) were assessed to determine the influence of hypertensive left ventricular (LV) hypertrophy on detection of ischemic area. The criterion of hypertrophy by two-dimensional echocardiography was >12 mm in the wall thickness of interventricular septal or posterior wall. Population in Group B might show low detectability in ischemic area by [sup 201]Tl myocardial scintigraphy (positive thallium rate 60%, defect score 2.7[+-]3.6), and high lung thallium uptake and high frequence of ECG positive among three groups. In semiquantitative analysis, the washout rate of the posterolateral wall and %RD (delayed %uptake-initial %uptake) of the septal wall in patients with Group B were lowest among three groups. However, the washout rate in the septal wall against the posterior wall, and the initial %uptake and the delayed %uptake of the septal wall were not significantly different among three groups. We could conclude that the decreased washout rate in nonischemic area with hypertensive LV hypertrophy might make the ischemic area masked. (author).

Toyama, Takuji; Nishimura, Tsunehiko; Uehara, Toshiisa (National Cardiovascular Center, Suita, Osaka (Japan)) (and others)

1992-11-01

265

Coronary artery calcification and ECG pattern of left ventricular hypertrophy or strain identify different healthy individuals at risk  

DEFF Research Database (Denmark)

PURPOSE:: To improve risk stratification for development of ischaemic heart disease, several markers have been proposed. Both the presence of coronary artery calcification (CAC) and ECG pattern of left ventricular hypertrophy/strain have been shown to provide independent prognostic information. In this study, we investigated the association between established risk factors, ECG measurements and the presence of coronary artery calcification. METHOD:: A random sample of healthy men and women aged 50 or 60 years were invited to the screening study. Established risk factors were measured. A noncontrast computed tomographic (CT) scan was performed to assess the CAC score. ECG analysis included left ventricular hypertrophy (LVH) using the Sokolow-Lyon criteria and the Cornell voltage?×?QRS duration product, and strain pattern based on ST segment depression and T-wave abnormalities. The association between the presence of CAC, clinical variables and ECG findings was evaluated by means of multivariate logistic regression. RESULTS:: Of 1825 invited individuals, 1226 accepted the screening. The prevalence of hypertension was 50%. Hypertensive patients frequently had LVH and/or strain when compared with nonhypertensive individuals (21 vs. 14%, P?

Diederichsen, SØren Zöga; Gerke, Oke

2013-01-01

266

Nebivolol treatment improves resistant arterial function and reduces ventricular hypertrophy and angiotensin II in spontaneously hypertension rats.  

UK PubMed Central (United Kingdom)

OBJECTIVE: The objective of this article is to assess the effects of nebivolol on resistant vascular reactivity, ventricular hypertrophy and the renin-angiotensin system in spontaneously hypertension rats (SHR). METHODS: Rats were divided into: SHR treated with nebivolol (8 mg/kg, i.g.)/atenolol(80 mg/kg, i.g.); SHR control group; normotensive Wistar-Kyoto (WKY) control group. Vascular responses to KCl, noradrenaline (NA), endothelin-1 (ET-1), angiotensin II (Ang II), acetylcholine (ACh) and sodium nitroprusside (SNP) were tested on the femoral and renal artery. Left ventricle weight/body weight ratio (LVW/BW) was measured. Ang II and angiotensin-converting enzyme (ACE) activity in plasma and the left ventricle were determined. Plasma renin activity (PRA) was quantified. RESULTS: Systolic blood pressure was decreased after nebivolol treatment in SHR. Compared with WKY, the contractions to KCl, NA, Ang II and ET-1 were increased in SHR while the relaxation to ACh was impaired. LVW/BW was higher in SHR. Levels of Ang II and ACE activity in plasma and the left ventricle were increased in SHR, but PRA was similar in these groups. Compared with atenolol, nebivolol markedly improved resistant vascular reactivity and decreased LVW/BW and Ang II. But nebivolol had no influence on ACE activity and PRA in SHR. CONCLUSION: Nebivolol treatment improved resistant arterial reactivity and reduced left ventricular hypertrophy and Ang II in SHR.

Wang Y; Zhang MS; Liu Y

2013-06-01

267

Coculture of embryonic ventricular myocytes and mouse embryonic stem cell enhance intercellular signaling by upregulation of connexin43.  

Science.gov (United States)

Background: Stem cell therapy has been proposed as a potential treatment strategy for ischemic cardiomyopathy in recent years. A variety of stem cells or stem cell-derived cells can potentially be used for transplantation. Despite improved cardiac function after treatment, one of the major problems is the poor integration between host and donor cells which can lead to post-transplantation arrhythmia and poor long-term outcome. Methods: In the present study, we cocultured murine embryonic stem cells (mES) with murine embryonic ventricular myocytes (mEVs) in hanging drops to assess the cellular interaction and function of mES-derived cardiomyocytes under these conditions. Results: We found that when mEVs are added to a culture system of embryonic stem cells, the number of spontaneously beating areas in embryoid bodies (EBs) increases, intercellular gap junction communication is enhanced by upregulation of Cx43 expression at the mid-developmental stage and Cx43 is distributed more orderly between cardiomyocytes. Conclusions: Our findings suggest mES-derived cardiomyocytes are able to form effective signaling pathways through coculture with mEVs which is important for providing more functional grafts for cardiac cell therapy by improving the integration between transplanted and host cells. PMID:23867886

Li, Hui; Tang, Ming; Liang, Huamin; Li, Yuting; Wang, Jian; Song, Yuanlong; Zheng, Yunjie; Xi, Jiaoya; Zhang, Jinxia; Hescheler, Jürgen; Zhu, Minjie

2013-07-04

268

Development of morphology and function of neonatal mouse ventricular myocytes cultured on a hyaluronan-based polymer scaffold.  

UK PubMed Central (United Kingdom)

In recent years cardiac tissue engineering has emerged as a promising field aimed at developing suitable techniques to repair the infarcted myocardium with a combination of cells, biomaterials, and regulative factors. In particular it could stand for an alternative strategy to simple in situ cellular implantation. In the present study our purpose was to analyze the interaction between a hyaluronan-based mesh (HYALONECT®) and neonatal murine ventricular myocytes (NMVMs). Specifically, we investigated morphological and functional characteristics of cardiomyocytes cultured on HYALONECT® in view of its employment in heart repair. Both living and fixed cells analysis was performed on in toto scaffolds with confocal microscopy. NMVMs adhesion on HYALONECT® was studied by tracking sarcomeric ?-actinin immunofluorescence staining. The structural features of NMVMs adherent onto HYALONECT® were investigated at 24, 48, 72 h, and 7 days of culture by immunofluorescence for sarcomeric ?-actinin and connexin-43. We observed a progressive morphological organization of the cells inside the biopolymer, with both clear sarcomeric arrangement along the scaffold fibers and gap junctions development between adjacent cells. Finally, in vivo intracellular calcium measurements performed using calcium fluorimetric confocal imaging revealed the presence of spontaneous calcium transients and contractile activity of NMVMs adherent onto HYALONECT® up to 48 h from seeding, indicating a progressive differentiation of the cells toward the adult phenotype. In conclusion, our results demonstrate that HYALONECT® allowed NMVMs to adhere to the fibers and to develop functional properties, displaying suitable features as a scaffold to perform heart tissue engineering.

Gallina C; Dolgetta S; Alloatti G; Levi R; Gallo MP

2012-03-01

269

Inhibition of the calcium-activated chloride current in cardiac ventricular myocytes by N-(p-amylcinnamoyl)anthranilic acid (ACA).  

Science.gov (United States)

N-(p-amylcinnamoyl)anthranilic acid (ACA), a phospholipase A(2) (PLA(2)) inhibitor, is structurally-related to non-steroidal anti-inflammatory drugs (NSAIDs) of the fenamate group and may also modulate various ion channels. We used the whole-cell, patch-clamp technique at room temperature to investigate the effects of ACA on the Ca(2+)-activated chloride current (I(Cl(Ca))) and other chloride currents in isolated pig cardiac ventricular myocytes. ACA reversibly inhibited I(Cl(Ca)) in a concentration-dependent manner (IC(50)=4.2 ?M, n(Hill)=1.1), without affecting the L-type Ca(2+) current. Unlike ACA, the non-selective PLA(2) inhibitor bromophenacyl bromide (BPB; 50 ?M) had no effect on I(Cl(Ca)). In addition, the analgesic NSAID structurally-related to ACA, diclofenac (50 ?M) also had no effect on I(Cl(Ca)), whereas the current in the same cells could be suppressed by chloride channel blockers flufenamic acid (FFA; 100 ?M) or 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS;100 ?M). Besides I(Cl(Ca)), ACA (50 ?M) also suppressed the cAMP-activated chloride current, but to a lesser extent. It is proposed that the inhibitory effects of ACA on I(Cl(Ca)) are PLA(2)-independent and that the drug may serve as a useful tool in understanding the nature and function of cardiac anion channels. PMID:20971070

Gwanyanya, Asfree; Macianskiene, Regina; Bito, Virginie; Sipido, Karin R; Vereecke, Johan; Mubagwa, Kanigula

2010-10-28

270

Inhibition of the calcium-activated chloride current in cardiac ventricular myocytes by N-(p-amylcinnamoyl)anthranilic acid (ACA).  

UK PubMed Central (United Kingdom)

N-(p-amylcinnamoyl)anthranilic acid (ACA), a phospholipase A(2) (PLA(2)) inhibitor, is structurally-related to non-steroidal anti-inflammatory drugs (NSAIDs) of the fenamate group and may also modulate various ion channels. We used the whole-cell, patch-clamp technique at room temperature to investigate the effects of ACA on the Ca(2+)-activated chloride current (I(Cl(Ca))) and other chloride currents in isolated pig cardiac ventricular myocytes. ACA reversibly inhibited I(Cl(Ca)) in a concentration-dependent manner (IC(50)=4.2 ?M, n(Hill)=1.1), without affecting the L-type Ca(2+) current. Unlike ACA, the non-selective PLA(2) inhibitor bromophenacyl bromide (BPB; 50 ?M) had no effect on I(Cl(Ca)). In addition, the analgesic NSAID structurally-related to ACA, diclofenac (50 ?M) also had no effect on I(Cl(Ca)), whereas the current in the same cells could be suppressed by chloride channel blockers flufenamic acid (FFA; 100 ?M) or 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS;100 ?M). Besides I(Cl(Ca)), ACA (50 ?M) also suppressed the cAMP-activated chloride current, but to a lesser extent. It is proposed that the inhibitory effects of ACA on I(Cl(Ca)) are PLA(2)-independent and that the drug may serve as a useful tool in understanding the nature and function of cardiac anion channels.

Gwanyanya A; Macianskiene R; Bito V; Sipido KR; Vereecke J; Mubagwa K

2010-11-01

271

Inhibitory Effects of Glycyrrhetinic Acid on the Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes and HERG Channel  

Science.gov (United States)

Background. Licorice has long been used to treat many ailments including cardiovascular disorders in China. Recent studies have shown that the cardiac actions of licorice can be attributed to its active component, glycyrrhetinic acid (GA). However, the mechanism of action remains poorly understood. Aim. The effects of GA on the delayed rectifier potassium current (IK), the rapidly activating (IKr) and slowly activating (IKs) components of IK, and the HERG K+ channel expressed in HEK-293 cells were investigated. Materials and Methods. Single ventricular myocytes were isolated from guinea pig myocardium using enzymolysis. The wild type HERG gene was stably expressed in HEK293 cells. Whole-cell patch clamping was used to record IK (IKr, IKs) and the HERG K+ current. Results. GA (1, 5, and 10??M) inhibited IK (IKr, IKs) and the HERG K+ current in a concentration-dependent manner. Conclusion. GA significantly inhibited the potassium currents in a dose- and voltage-dependent manner, suggesting that it exerts its antiarrhythmic action through the prolongation of APD and ERP owing to the inhibition of IK (IKr, IKs) and HERG K+ channel.

Wu, Delin; Jiang, Linqing; Wu, Hongjin; Wang, Shengqi; Zheng, Sidao; Yang, Jiyuan; Liu, Yuna; Ren, Jianxun; Chen, Xianbing

2013-01-01

272

Effect of antipsychotic drug perphenazine on fast sodium current and transient outward potassium current in rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

Antipsychotic drug perphenazine belongs to the phenothiazine group commonly reported to induce ECG changes and tachyarrhythmias. Data about its effect on ionic membrane currents in cardiomyocytes are missing. We analyzed the effect of perphenazine (0.1-100 microM) on fast sodium current I (Na) and transient outward potassium current I (to) in enzymatically isolated rat right ventricular myocytes by the whole-cell patch-clamp technique at room temperature. Perphenazine reversibly blocked I (Na) (reducing its amplitude; IC(50) = 1.24 +/- 0.10 microM) and I (to) (accelerating its apparent inactivation with a slight decrease of its amplitude; IC(50) = 38.2 +/- 3.5 microM, evaluated from changes of the time integral). The fast time constant of I (to) inactivation was significantly decreased in a concentration-dependent manner (IC(50) = 30.0 +/- 6.6 microM). Both blocks were use and frequency dependent at 3.3 Hz. We conclude that perphenazine causes concentration-, use-, and frequency-dependent block of I (Na) and I (to) . Computer simulations suggest that perphenazine interacts preferentially with I (Na) channels in inactivated states and with I (to) channels in both open and open-inactivated states.

Bébarová M; Matejovic P; Pásek M; Jansová D; Simurdová M; Nováková M; Simurda J

2009-08-01

273

Coculture of embryonic ventricular myocytes and mouse embryonic stem cell enhance intercellular signaling by upregulation of connexin43.  

UK PubMed Central (United Kingdom)

Background: Stem cell therapy has been proposed as a potential treatment strategy for ischemic cardiomyopathy in recent years. A variety of stem cells or stem cell-derived cells can potentially be used for transplantation. Despite improved cardiac function after treatment, one of the major problems is the poor integration between host and donor cells which can lead to post-transplantation arrhythmia and poor long-term outcome. Methods: In the present study, we cocultured murine embryonic stem cells (mES) with murine embryonic ventricular myocytes (mEVs) in hanging drops to assess the cellular interaction and function of mES-derived cardiomyocytes under these conditions. Results: We found that when mEVs are added to a culture system of embryonic stem cells, the number of spontaneously beating areas in embryoid bodies (EBs) increases, intercellular gap junction communication is enhanced by upregulation of Cx43 expression at the mid-developmental stage and Cx43 is distributed more orderly between cardiomyocytes. Conclusions: Our findings suggest mES-derived cardiomyocytes are able to form effective signaling pathways through coculture with mEVs which is important for providing more functional grafts for cardiac cell therapy by improving the integration between transplanted and host cells.

Li H; Tang M; Liang H; Li Y; Wang J; Song Y; Zheng Y; Xi J; Zhang J; Hescheler J; Zhu M

2013-01-01

274

Ventricular rate determines early bradycardic electrical remodeling.  

UK PubMed Central (United Kingdom)

OBJECTIVES: The purpose of this study was to isolate chronic ventricular rate as the primary determinant of early bradycardic ventricular electrical remodeling. BACKGROUND: Ventricular repolarization delay predisposing to potentially lethal tachydysrhythmias occurs during chronic bradycardia. Prolonged QT intervals and torsades de pointes are associated with down-regulated ventricular myocyte delayed rectifier potassium (K(+)) currents. METHODS: Transcatheter AV node ablation in rabbits was followed by chronic right ventricular pacing at either 140 bpm (n = 16) or the near-physiologic rate of 280 bpm (n = 9). ECG QT intervals were assessed in vivo at days 0 and 8 of paced AV block. Repolarizing currents in isolated left and right ventricular myocytes were assessed using whole-cell patch clamp technique. RESULTS: Bradycardic rabbits had increased steady-state QT intervals (230 +/- 6 ms vs 206 +/- 7 ms [mean +/- SE], day 8 vs day 0; P < .001). Biventricular myocyte expression of the delayed rectifier K(+) currents I(Kr) and I(Ks) was down-regulated in bradycardic rabbits, with no change in the transient outward current I(to) or inwardly rectifying current I(K1). None of these changes were observed in rabbits paced at 280 bpm. Pause-dependent torsades de pointes was documented in one bradycardic animal on day 8. No heart failure or ventricular hypertrophy was apparent. CONCLUSIONS: Bradycardic ventricular electrical remodeling proceeds independently of structural remodeling, heart failure, or AV synchrony and is prevented by maintenance of near-physiologic ventricular rate.

Suto F; Zhu W; Cahill SA; Greenwald I; Navarro AL; Gross GJ

2005-03-01

275

Effects of propofol on contractile response and electrophysiological properties in single guinea-pig ventricular myocyte.  

Science.gov (United States)

Effects of propofol on contractile response, action potential, resting membrane potential and L-type voltage-dependent calcium channel current were examined in guinea-pig single cardiac myocyte. Propofol (10(-4) M) inhibited contractile response induced by electrical stimulation (83.6% of control, n = 5), but did not change the resting membrane potential. On the other hand, propofol reduced the overshoot of action potential (10(-4) M), and shortened the duration of action potential (10(-5) and 10(-4) M). Whole-cell voltage clamp experiment showed inhibition of L-type calcium channel current (ICa, 10(-5) M: 90.8+/-1.39, 10(-4) M: 83.4+/-1.53% of control, n = 5). In addition, propofol showed use-dependent block of ICa. It is concluded that negative inotropic effect of propofol is caused by suppression of action potential, and that inhibition of ICa plays a role in shortening of the duration of action potential. PMID:10522749

Shigemura, T; Hatakeyama, N; Shibuya, N; Yamazaki, M; Masuda, A; Chen, F S; Momose, Y; Ito, Y

1999-09-01

276

Effects of propofol on contractile response and electrophysiological properties in single guinea-pig ventricular myocyte.  

UK PubMed Central (United Kingdom)

Effects of propofol on contractile response, action potential, resting membrane potential and L-type voltage-dependent calcium channel current were examined in guinea-pig single cardiac myocyte. Propofol (10(-4) M) inhibited contractile response induced by electrical stimulation (83.6% of control, n = 5), but did not change the resting membrane potential. On the other hand, propofol reduced the overshoot of action potential (10(-4) M), and shortened the duration of action potential (10(-5) and 10(-4) M). Whole-cell voltage clamp experiment showed inhibition of L-type calcium channel current (ICa, 10(-5) M: 90.8+/-1.39, 10(-4) M: 83.4+/-1.53% of control, n = 5). In addition, propofol showed use-dependent block of ICa. It is concluded that negative inotropic effect of propofol is caused by suppression of action potential, and that inhibition of ICa plays a role in shortening of the duration of action potential.

Shigemura T; Hatakeyama N; Shibuya N; Yamazaki M; Masuda A; Chen FS; Momose Y; Ito Y

1999-09-01

277

Obesidad central y regresión de hipertrofia ventricular izquierda/ Central obesity and left ventricular hypertrophy regression/ Obesidade central e regressão da hipertrofia esquerda  

Scientific Electronic Library Online (English)

Full Text Available Abstract in portuguese Em sujeitos hipertensos, os níveis de pressão arterial per se seriam a principal determinante do desenvolvimento de hiperetrofia ventricular esquerda. Por outra parte, o índice de massa corporal e o perímetro de cintura se associaram em forma lineal, contínua e positiva com o índice de massa ventricular esquerdo ainda em não hipertensos. Um tratamento insuficiente seria a principal causa da falta de regressão do dano no órgão branco. O objetivo do presente traba (more) lho é determinar o impacto da obesidade central sobre a regressão do índice de massa ventricular esquerdo. Material e métodos: incluíram-se 102 pacientes (p) HTA que concorreram por primeira vez a um consultório especializado em forma consecutiva, mediulhes o índice de massa ventricular esquerdo (IMVE) pelo método de Devereux ao início e logo de pelo menos 1 ano de tratamento. Foram divididos em dois grupos: GA: perímetro cintura (PC) Abstract in spanish En sujetos hipertensos, los niveles de presión arterial per se serían el principal determinante del desarrollo de hipertrofia ventricular izquierda. Por otra parte, el índice de masa corporal y el perímetro de cintura se han asociado en forma lineal, continua y positiva con elíndice de masa ventricular izquierdo aún en no hipertensos. Un tratamiento insuficiente sería la principal causa de falta de regresión del daño en órgano blanco. El objetivo del presente tr (more) abajo es determinar el impacto de la obesidad central sobre la regresión del índice de masa ventricular izquierdo. Material y métodos: se incluyeron 102 pacientes (p) HTA que concurrieron por primera vez a un consultorio especializado en forma consecutiva, se les midió el índice de masa ventricular izquierdo (IMVI) por método de Devereux al inicio y luego de al menos 1 año de tratamiento. Fueron divididos en dos grupos: GA: perímetro cintura (PC) Abstract in english Blood pressure per se may be the main determinant of left ventricle hypertrophy development in hypertensive subjects. On the other side, body mass index and waist circumference are related to left ventricle mass index (LVMI) positively, continuously and linearly even in non hypertensive patients. An insufficient treatment may be the main reason of not achieving regression of target organ damage. The objective of this trial is to establish the impact of central obesity on (more) LVMI regression. Material and methods: 102 consecutive hypertensive patients (p) wich attended for the first time to a specialized consultory room were included. LVMI was measured with the Devereux method at the begining and after at least one year of treatment. The patients were divided into two groups: GA: waist circumference (WC)

Piskorz, Daniel; Citta, Luciano; Citta, Norberto; Lanzotti, Marcelo; Lanzotti, Roberto; Locatelli, Horacio; Tommasi, Alicia

2007-12-01

278

Left ventricular hypertrophy increases cardiovascular risk independently of in-office and out-of-office blood pressure values.  

UK PubMed Central (United Kingdom)

OBJECTIVES: Previous studies have shown that left ventricular hypertrophy (LVH) represents a cardiovascular risk factor independently of clinic blood pressure (BP). The present study was aimed at determining the impact of LVH on the incidence of cardiovascular morbid and fatal events taking into account not only classical risk factors but also home and ambulatory BP values, which have been shown to have an important independent prognostic impact. METHODS: In 1716 patients belonging to the 'Pressioni Arteriose Monitorate E Loro Associazioni' population of Monza, we quantified left ventricular mass index and identified LVH by standard cutoff values. We also measured clinic, home and 24-h ambulatory BPs together with serum glucose and lipids. RESULTS: During a follow-up of 148 months, the rate of fatal and nonfatal (hospitalizations) cardiovascular events as well as of all-cause death was markedly greater (four-fold to five-fold) in patients as compared with those without LVH. In LVH individuals, the increased risk remained significant even when data were adjusted for a large number of other confounding factors including home BP, 24-h mean BP and ambulatory BP. Results were similar when left ventricular mass was indexed by height and body surface area. A 10% increase in left ventricular mass index was associated with a significant increase in cardiovascular risk or all-cause deaths. In multivariate analysis, left ventricular mass index was always an independent predictor of cardiovascular events and death for any cause. CONCLUSION: Our data provide evidence that LVH is an important risk factor even when the contribution of different BPs to risk is fully taken into account.

Bombelli M; Facchetti R; Carugo S; Madotto F; Arenare F; Quarti-Trevano F; Capra A; Giannattasio C; Dell'Oro R; Grassi G; Sega R; Mancia G

2009-12-01

279

Clinical impact of ' in-treatment' wall motion abnormalities in hypertensive patients with left ventricular hypertrophy: the LIFE study  

DEFF Research Database (Denmark)

Objectives Left ventricular systolic wall motion abnormalities have prognostic value. Whether wall motion detected by serial echocardiographic examinations predicts prognosis in hypertensive patients with left ventricular hypertrophy ( LVH) without clinically recognized atherosclerotic disease has, however, never been investigated. We examined whether 'in- treatment' wall motion abnormalities predicted outcome in the Losartan Intervention For Endpoint ( LIFE) reduction in hypertension echocardiographic substudy. Methods We studied 749 patients without coronary artery disease, myocardial infarction ( MI), or stroke history. Echocardiographic segmental wall motion abnormalities at baseline and annual re-evaluations (' as time- varying covariate') were examined in relation to endpoints ( cardiovascular mortality, MI, stroke, and hospitalized heart failure). Adjusted Cox regression was used to analyze the primary composite endpoint of cardiovascular death, MI, or stroke and, separately, for fatal and nonfatal MI and hospitalized heart failure. Results During a mean follow-up of 4.8 years, an event was recorded in 67 ( 9%) patients. In Cox models after adjusting for age, gender, treatment, blood pressure lowering, and serial change of left ventricular mass index, ' in-treatment' segmental wall motion abnormalities were associated with subsequent composite endpoint [ hazard ratio =2.1, 95% confidence interval ( CI) 1.1-3.8; P=0.019] and MI [ hazard ratio =3.7 ( 1.5 - 8.9); P=0.004]. Conclusion In hypertensive patients with LVH and no history of cardiovascular disease, ' in- treatment' left ventricular wall motion abnormalities are associated with increased likelihood of subsequent cardiovascular events independent of age, gender, blood pressure lowering, treatment modality, and in- treatment left ventricular mass index Udgivelsesdato: 2008/4

Cicala, S.; Simone, G. de

2008-01-01

280

Synergistic prognostic values of cardiac sympathetic innervation with left ventricular hypertrophy and left atrial size in heart failure patients without reduced left ventricular ejection fraction: a cohort study.  

UK PubMed Central (United Kingdom)

OBJECTIVES: This study tested whether cardiac sympathetic innervation assessed by metaiodobenzylguanidine (MIBG) activity has long-term prognostic value in combination with left ventricular hypertrophy (LVH) and left atrial size in heart failure (HF) patients without reduced left ventricular ejection fraction (LVEF). DESIGN: A single-centre prospective cohort study. SETTING/PARTICIPANTS: With primary endpoints of cardiac death and rehospitalisation due to HF progression, 178 consecutive symptomatic HF patients with 74% men, mean age of 56 years and mean LVEF of 64.5% were followed up for 80 months. The entry criteria consisted of LVEF more than 50%, completion of predischarge clinical evaluations including cardiac MIBG and echocardiographic studies and at least more than 1-year follow-up when survived. RESULTS: Thirty-four patients with cardiac evens had larger left atrial dimension (LAD), increased LV mass index, reduced MIBG activity quantified as heart-to-mediastinum ratio (HMR) than did the others. Multivariable Cox analysis showed that LAD and HMR were significant predictors (HR of 1.080 (95% CI 1.00 to 1.16, p=0.044) and 0.107 (95% CI 0.01 to 0.61, p=0.012, respectively). Thresholds of HMR (1.65) and LAD (37 mm) were closely related to identification of high-risk patients. In particular, HMR was a significant determinant of cardiac events in both patients with and without LV hypertrophy. Reduced HMR with enlarged LAD or LV hypertrophy identified patients at most increased risk; overall log-rank value, 11.5, p=0.0032 for LAD and 17.5, p=0.0002, respectively. CONCLUSIONS: In HF patients without reduced LV ejection fraction, impairment of cardiac sympathetic innervation is related to cardiac outcomes independently and synergistically with LA size and LV hypertrophy. Cardiac sympathetic innervation assessment can contribute to better risk-stratification in combination with evaluation of LA size and LV mass but is needed to be evaluated for establishing aetiology-based risk assessment in HF patients at increased risk.

Doi T; Nakata T; Hashimoto A; Yuda S; Wakabayashi T; Kouzu H; Kaneko N; Hase M; Tsuchihashi K; Miura T

2012-01-01

 
 
 
 
281

Carbonic anhydrase II promotes cardiomyocyte hypertrophy.  

Science.gov (United States)

Pathological cardiac hypertrophy, the maladaptive remodelling of the myocardium, often progresses to heart failure. The sodium-proton exchanger (NHE1) and chloride-bicarbonate exchanger (AE3) have been implicated as important in the hypertrophic cascade. Carbonic anhydrase II (CAII) provides substrates for these transporters (protons and bicarbonate, respectively). CAII physically interacts with NHE1 and AE3, enhancing their respective ion transport activities by increasing the concentration of substrate at their transport sites. Earlier studies found that a broad-spectrum carbonic anhydrase inhibitor prevented cardiomyocyte hypertrophy (CH), suggesting that carbonic anhydrase is important in the development of hypertrophy. Here we investigated whether cytosolic CAII was the CA isoform involved in hypertrophy. Neonatal rat ventricular myocytes (NRVMs) were transduced with recombinant adenoviral constructs to over-express wild-type or catalytically inactive CAII (CAII-V143Y). Over-expression of wild-type CAII in NRVMs did not affect CH development. In contrast, CAII-V143Y over-expression suppressed the response to hypertrophic stimuli, suggesting that CAII-V143Y behaves in a dominant negative fashion over endogenous CAII to suppress hypertrophy. We also examined CAII-deficient (Car2) mice, whose hearts exhibit physiological hypertrophy without any decrease in cardiac function. Moreover, cardiomyocytes from Car2 mice do not respond to prohypertrophic stimulation. Together, these findings support a role of CAII in promoting CH. PMID:23210439

Brown, Brittany F; Quon, Anita; Dyck, Jason R B; Casey, Joseph R

2012-11-23

282

Different roles of the cardiac Na+/Ca2+-exchanger in ouabain-induced inotropy, cell signaling, and hypertrophy.  

UK PubMed Central (United Kingdom)

Previous studies have shown that digitalis drugs, acting as specific inhibitors of cardiac Na(+)/K(+)-ATPase, not only cause positive inotropic effects, but also activate cell signaling pathways that lead to cardiac myocyte hypertrophy. A major aim of this work was to assess the role of Na(+)/Ca(2+)-exchanger, NCX1, in the above two seemingly related drug effects. Using a mouse with ventricular-specific knockout (KO) of NCX1, ouabain-induced positive inotropy that was evident in isolated wild-type (Wt) hearts was clearly reduced in KO hearts. Ouabain also increased Ca(2+) transient amplitudes in Wt myocytes, but not in KO myocytes. Ouabain-induced activations of ERK 1/2 were noted in Wt myocytes, but not in KO myocytes; however, ouabain activated PI3K1A and Akt in both Wt and KO myocytes. Protein synthesis rate, as a measure of hypertrophy, was increased by ouabain in Wt and KO myocytes; these drug effects were prevented by a PI3K inhibitor but not by a MEK/ERK inhibitor. Hypertrophy caused by ET-1, but not that induced by ouabain, was accompanied by upregulation of BNP gene in Wt and KO myocytes. The findings indicate 1) the necessity of NCX1 for positive inotropic action of ouabain; 2) the irrelevance of NCX1 and ERK 1/2 activation to ouabain-induced hypertrophy; and 3) that hypertrophy caused by ouabain through the activation of PI3K1A/Akt pathway is likely to be beneficial to the heart.

Bai Y; Morgan EE; Giovannucci DR; Pierre SV; Philipson KD; Askari A; Liu L

2013-02-01

283

Cardiac MRI assessed left ventricular hypertrophy in differentiating hypertensive heart disease from hypertrophic cardiomyopathy attributable to a sarcomeric gene mutation  

International Nuclear Information System (INIS)

To evaluate the value of cardiac magnetic resonance imaging (CMRI)-assessed left ventricular hypertrophy (LVH) in differentiating between hypertensive heart disease and hypertrophic cardiomyopathy (HCM). 95 unselected subjects with mild-to-moderate hypertension, 24 patients with HCM attributable to the D175N mutation of the ?-tropomyosin gene and 17 control subjects were studied by cine CMRI. Left ventricular (LV) quantitative and qualitative characteristics were evaluated. LV maximal end-diastolic wall thickness, wall thickness-to-LV volume ratio, end-diastolic septum thickness and septum-to-lateral wall thickness ratio were useful measures for differentiating between LVH due to hypertension and HCM. The most accurate measure for identifying patients with HCM was the LV maximal wall thickness ?17 mm, with a sensitivity, specificity, negative predictive value, positive predictive value, and accuracy of 90%, 93%, 86%, 95% and 91%, respectively. LV maximal wall thickness in the anterior wall, or regional bulging in left ventricular wall was found only in patients with HCM. LV mass index was not discriminant between patients with HCM and those with LVH due to hypertension. LV maximal thickness measured by CMRI is the best anatomical parameter in differentiating between LVH due to mild-to-moderate hypertension and HCM attributable to a sarcomeric mutation. CMRI assessment of location and quality of LVH is also of value in differential diagnosis. (orig.)

2011-01-01

284

Cardiac MRI assessed left ventricular hypertrophy in differentiating hypertensive heart disease from hypertrophic cardiomyopathy attributable to a sarcomeric gene mutation  

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To evaluate the value of cardiac magnetic resonance imaging (CMRI)-assessed left ventricular hypertrophy (LVH) in differentiating between hypertensive heart disease and hypertrophic cardiomyopathy (HCM). 95 unselected subjects with mild-to-moderate hypertension, 24 patients with HCM attributable to the D175N mutation of the {alpha}-tropomyosin gene and 17 control subjects were studied by cine CMRI. Left ventricular (LV) quantitative and qualitative characteristics were evaluated. LV maximal end-diastolic wall thickness, wall thickness-to-LV volume ratio, end-diastolic septum thickness and septum-to-lateral wall thickness ratio were useful measures for differentiating between LVH due to hypertension and HCM. The most accurate measure for identifying patients with HCM was the LV maximal wall thickness {>=}17 mm, with a sensitivity, specificity, negative predictive value, positive predictive value, and accuracy of 90%, 93%, 86%, 95% and 91%, respectively. LV maximal wall thickness in the anterior wall, or regional bulging in left ventricular wall was found only in patients with HCM. LV mass index was not discriminant between patients with HCM and those with LVH due to hypertension. LV maximal thickness measured by CMRI is the best anatomical parameter in differentiating between LVH due to mild-to-moderate hypertension and HCM attributable to a sarcomeric mutation. CMRI assessment of location and quality of LVH is also of value in differential diagnosis. (orig.)

Sipola, Petri [Kuopio University Hospital, Department of Clinical Radiology, Kuopio (Finland); University of Eastern Finland, Institute of Clinical Medicine, Faculty of Health Sciences, Kuopio (Finland); Magga, Jarkko; Peuhkurinen, Keijo [Kuopio University Hospital, Department of Medicine, Kuopio (Finland); Husso, Minna [Kuopio University Hospital, Department of Clinical Radiology, Kuopio (Finland); Jaeaeskelaeinen, Pertti; Kuusisto, Johanna [Kuopio University Hospital, Department of Medicine, Kuopio (Finland); Kuopio University Hospital, Heart Center, P.O. Box 1777, Kuopio (Finland)

2011-07-15

285

The ginsenoside Rg1 prevents transverse aortic constriction-induced left ventricular hypertrophy and cardiac dysfunction by inhibiting fibrosis and enhancing angiogenesis.  

UK PubMed Central (United Kingdom)

BACKGROUND: Ginsenoside Rg1, an important and active ingredient of Panax ginseng, has been shown to exert cardioprotective effects in vivo. The present study aimed to test the hypothesis that ginsenoside Rg1 attenuates cardiac dysfunction in a transverse aortic constriction (TAC)-induced left ventricular hypertrophy in vivo via proangiogenic and antifibrotic effects. METHODS: This study investigated the effects of ginsenoside Rg1 in a rat model of TAC-induced left ventricular hypertrophy. Cardiac function was assessed by echocardiography. The antifibrotic and proangiogenic effects were assessed by histopathology and mRNA expression of procollagen I, III, and vascular endothelial growth factor (VEGF) through quantitative real-time PCR. The expression of phosphorylation of Akt, p38 mitogen-activated protein kinase (MAPK), hypoxia inducible factor-1 (HIF-1), and VEGF proteins were examined by Western blotting. RESULTS: Ginsenoside Rg1 treatment significantly decreased TAC-induced myocardial fibrosis and left ventricular hypertrophy, and preserved cardiac function. Ginsenoside Rg1 administration enhanced angiogenesis by increasing the expression of HIF-1 and VEGF. These cardioprotective effects of ginsenoside Rg1 are partially related to the activation of phospho-Akt and inhibition of p38 MAPK. CONCLUSIONS: Ginsenoside Rg1 exhibited protective effect against TAC-induced left ventricular hypertrophy and cardiac dysfunction, which is potentially associated with phospho-Akt activation and p38 MAPK inhibition.

Zhang YJ; Zhang XL; Li MH; Iqbal J; Bourantas CV; Li JJ; Su XY; Muramatsu T; Tian NL; Chen SL

2013-07-01

286

Role of oxidative stress in the aortic constriction-induced ventricular hypertrophy in rat  

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Full Text Available Introduction:Severe abdominal aortic constriction above the renal arteries induces arterial hypertension above the stenotic site that is the cause of cardiac hypertrophy. Previous studies have shown that high blood pressure induces myocardial oxidative stress with conflicting results. In the present study, we assessed the effects of acute hypertension on the myocardial oxidative stress and its relation with cardiac hypertrophy. Methods:Experiments were performed on two groups of rats, sham and hypertensive (n=5 each group). Rats were made acutely hypertensive by aortic constriction above the renal arteries. After 10 days, the carotid artery pressure of rats was recorded and hearts were removed. Following tissue homogenization, superoxide dismutase (SOD) and catalase (CAT) activities, as well as glutathione (GSH) and malondialdehyde (MDA) levels were determined by biochemical methods in heart tissues. Results:Arterial pressure and cardiac hypertrophy index (heart weight/body weight, g/kg) were increased in hypertensive rats 66% and 74%, respectively. SOD and CAT activity were significantly higher in hypertensive rats (34.42±2.51 and 38.63±4.03 U/mg protein, respectively) compared to sham animals (28.58±0.28 and 23.27±2.13 U/mg protein, respectively). Aortic-banding significantly increased GSH content of myocardium by 47%, and there was not any significant difference in the myocardial MDA between the two groups. Conclusion:The findings of this study indicate that acutely elevated arterial blood pressure induces cardiac hypertrophy concomitant with oxidative stress in rat myocardium. This study also reconfirms that oxidative stress may play an important role in the development of cardiac hypertrophy during hypertension.

Zahra Jahanbakhsh; Mohammad Taghi Mohammadi; Mahvash Jafari; Ali Khoshbaten; Maryam Salehi

2012-01-01

287

Acute myocardial ischemia associated with latent left ventricular outflow tract obstruction in the absence of left ventricular hypertrophy.  

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Left ventricular outflow tract obstruction (LVOTO) is a recognized feature in hypertrophic cardiomyopathy, but can occur in other clinical scenarios such as acute myocardial ischemia. In some patients, LVOTO may only be detectable with provocation testing such as exercise stress. Accurate and timely...

Page, SP; Pantazis, A; Elliott, PM

288

Right ventricular myocardial performance index is decreased with severe pressure-overload cardiac hypertrophy in young rats.  

Science.gov (United States)

Although the right ventricular (RV) myocardial performance index (MPI) usually is increased in the presence of RV dysfunction and pressure overload, debate continues over the correlation between the RV MPI and functional derangement in patients with RV pressure-overload congenital heart disease (CHD). To address this controversy, this study took serial measurements of the RV MPI in addition to invasive RV hemodynamic measurements during the acute stage of mild to severe pressure overload. Right ventricle pressure overload was induced by partial pulmonary arterial banding (PAB) in 3-week-old rats. The rats were divided into two groups: mild pulmonary stenosis (PS) group (20-40 % stenosis; n = 20) and severe PS group (40-70 % stenosis; n = 28). Sham-treated animals (sham group; n = 30) underwent the same surgical procedure without PAB. Pressure-overload RV hypertrophy was documented by weighing the heart, by evaluating echocardiograms, and by evaluating cardiac hypertrophy-associated gene expression. The RV MPI was checked 1, 2, 3, 5, and 8 weeks after PAB. The MPI was calculated as the sum of the isovolumic contraction time and the isovolumic relaxation time (IRT) divided by the ejection time. The RV MPI of the mild PS group did not differ significantly from that of the sham group. The RV MPI of the severe PS group, however, was lower than that of the sham group (0.27 ± 0.01 vs 0.29 ± 0.01) 2 to 8 weeks after PAB: 0.19 ± 0.01 at 2 weeks (P < 0.001), 0.16 ± 0.01 at 3 weeks (P < 0.001), 0.20 ± 0.01 at 5 weeks (P = 0.021), and 0.18 ± 0.01 at 8 weeks (P < 0.001) after PAB. The decreased RV MPI was associated with decreased IRT and increased ejection time. RV hypertrophy contributes to the decrease in the RV MPI in the severe pressure-overload condition. PMID:23467728

Ko, Jeong-Hyeon; Eom, Gwang Hyeon; Cho, Hwa Jin; Nam, Kwang-Il; Ma, Jae Sook; Kook, Hyun; Cho, Young Kuk

2013-03-07

289

AT1 blockade abolishes left ventricular hypertrophy in heterozygous cMyBP-C null mice: role of FHL1.  

UK PubMed Central (United Kingdom)

This research investigated the impact of angiotensin AT1 receptor (Agtr1) blockade on left ventricular (LV) hypertrophy in a mouse model of human hypertrophic cardiomyopathy (HCM), which carries one functional allele of Mybpc3 gene coding cardiac myosin-binding protein C (cMyBP-C). Five-month-old heterozygous cMyBP-C knockout (Het-KO) and wild-type mice were treated with irbesartan (50 mg/kg/day) or vehicle for 8 weeks. Arterial blood pressure was measured by tail cuff plethysmography. LV dimension and function were accessed by echocardiography. Myocardial gene expression was evaluated using RT-qPCR. Compared with wild-type littermates, Het-KO mice had greater LV/body weight ratio (4.0 ± 0.1 vs. 3.3 ± 0.1 mg/g, P < 0.001), thicker interventricular septal wall (0.70 ± 0.02 vs. 0.65 ± 0.01 mm, P < 0.02), lower Mybpc3 mRNA level (-43%, P < 0.02), higher four-and-a-half LIM domains 1 (Fhl1, +110%, P < 0.01), and angiotensin-converting enzyme 1 (Ace1, +67%, P < 0.05), but unchanged Agtr1 mRNA levels in the septum. Treatment with irbesartan had no effect in wild-type mice but abolished septum-predominant LV hypertrophy and Fhl1 upregulation without changes in Ace1 but with an increased Agtr1 (+42%) in Het-KO mice. Thus, septum-predominant LV hypertrophy in Het-KO mice is combined with higher Fhl1 expression, which can be abolished by AT1 receptor blockade, indicating a role of the renin-angiotensin system and Fhl1 in cMyBP-C-related HCM.

Vignier N; Le Corvoisier P; Blard C; Sambin L; Azibani F; Schlossarek S; Delcayre C; Carrier L; Hittinger L; Su JB

2013-04-01

290

AT1 blockade abolishes left ventricular hypertrophy in heterozygous cMyBP-C null mice: role of FHL1.  

Science.gov (United States)

This research investigated the impact of angiotensin AT1 receptor (Agtr1) blockade on left ventricular (LV) hypertrophy in a mouse model of human hypertrophic cardiomyopathy (HCM), which carries one functional allele of Mybpc3 gene coding cardiac myosin-binding protein C (cMyBP-C). Five-month-old heterozygous cMyBP-C knockout (Het-KO) and wild-type mice were treated with irbesartan (50 mg/kg/day) or vehicle for 8 weeks. Arterial blood pressure was measured by tail cuff plethysmography. LV dimension and function were accessed by echocardiography. Myocardial gene expression was evaluated using RT-qPCR. Compared with wild-type littermates, Het-KO mice had greater LV/body weight ratio (4.0 ± 0.1 vs. 3.3 ± 0.1 mg/g, P Mybpc3 mRNA level (-43%, P < 0.02), higher four-and-a-half LIM domains 1 (Fhl1, +110%, P < 0.01), and angiotensin-converting enzyme 1 (Ace1, +67%, P < 0.05), but unchanged Agtr1 mRNA levels in the septum. Treatment with irbesartan had no effect in wild-type mice but abolished septum-predominant LV hypertrophy and Fhl1 upregulation without changes in Ace1 but with an increased Agtr1 (+42%) in Het-KO mice. Thus, septum-predominant LV hypertrophy in Het-KO mice is combined with higher Fhl1 expression, which can be abolished by AT1 receptor blockade, indicating a role of the renin-angiotensin system and Fhl1 in cMyBP-C-related HCM. PMID:23600722

Vignier, Nicolas; Le Corvoisier, Philippe; Blard, Charlotte; Sambin, Lucien; Azibani, Feriel; Schlossarek, Saskia; Delcayre, Claude; Carrier, Lucie; Hittinger, Luc; Su, Jin Bo

2013-04-11

291

Right ventricular myocardial performance index is decreased with severe pressure-overload cardiac hypertrophy in young rats.  

UK PubMed Central (United Kingdom)

Although the right ventricular (RV) myocardial performance index (MPI) usually is increased in the presence of RV dysfunction and pressure overload, debate continues over the correlation between the RV MPI and functional derangement in patients with RV pressure-overload congenital heart disease (CHD). To address this controversy, this study took serial measurements of the RV MPI in addition to invasive RV hemodynamic measurements during the acute stage of mild to severe pressure overload. Right ventricle pressure overload was induced by partial pulmonary arterial banding (PAB) in 3-week-old rats. The rats were divided into two groups: mild pulmonary stenosis (PS) group (20-40 % stenosis; n = 20) and severe PS group (40-70 % stenosis; n = 28). Sham-treated animals (sham group; n = 30) underwent the same surgical procedure without PAB. Pressure-overload RV hypertrophy was documented by weighing the heart, by evaluating echocardiograms, and by evaluating cardiac hypertrophy-associated gene expression. The RV MPI was checked 1, 2, 3, 5, and 8 weeks after PAB. The MPI was calculated as the sum of the isovolumic contraction time and the isovolumic relaxation time (IRT) divided by the ejection time. The RV MPI of the mild PS group did not differ significantly from that of the sham group. The RV MPI of the severe PS group, however, was lower than that of the sham group (0.27 ± 0.01 vs 0.29 ± 0.01) 2 to 8 weeks after PAB: 0.19 ± 0.01 at 2 weeks (P < 0.001), 0.16 ± 0.01 at 3 weeks (P < 0.001), 0.20 ± 0.01 at 5 weeks (P = 0.021), and 0.18 ± 0.01 at 8 weeks (P < 0.001) after PAB. The decreased RV MPI was associated with decreased IRT and increased ejection time. RV hypertrophy contributes to the decrease in the RV MPI in the severe pressure-overload condition.

Ko JH; Eom GH; Cho HJ; Nam KI; Ma JS; Kook H; Cho YK

2013-10-01

292

An assessment of regression of left ventricular hypertrophy following alcohol ablation of the interventricular septum in patients with hypertrophic cardiomyopathy with left ventricular outflow tract obstruction.  

UK PubMed Central (United Kingdom)

BACKGROUND: Hypertrophic obstructive cardiomyopathy (HOCM) is characterised by asymmetric myocardial hypertrophy, which is most pronounced in the interventricular septum (IVS) and is responsible for the dynamic obstruction of the left ventricular outflow tract (LVOT). Successful alcohol septal ablation (ASA) of the IVS allows to reduce the thickness of the parabasal part of the IVS myocardium and, in most cases, to permanently reduce the gradient in the LVOT. AIM: To assess, using cardiac magnetic resonance imaging (MRI) and transthoracic echocardiography (TTE), the impact of gradient reduction in the LVOT on the type and severity of left ventricular (LV) remodelling. METHODS: The study included 30 patients (aged 56.9 ± 11.9 years) with HOCM and the mean peak gradient (PG) in the LVOT of 123 ± 33 mm Hg who underwent ASA. MRI measurements were performed before and at 6 months after ASA and TTE measurements were performed before, at 3 months and at 6 months after ASA. RESULTS: PG in the LVOT decreased to an average of 52 ± 37 mm Hg (p ? 0.0001) at 3 months after ASA and to 37 ± 28 mm Hg (p ? 0.0001) at 6 months after ASA. TTE revealed a decrease in IVS thickness outside the scar following ASA from 23.6 ± 3.5 mm to 19.3 ± 4.0 mm (p ? 0.0001) and 19.4 ± 0.4 mm (p ? 0.0001) at 3 and 6 months, respectively. There was also a decrease in lateral wall (PW) thickness from 15.9 ± 3.2 mm to 14.9 ± 2.9 mm (p = 0.046) and 14.16 ± 2.00 (p = 0.0065) at 3 and 6 months, respectively. MRI revealed a decrease in IVS thickness from 23.7 ± 2.8 mm to 18.04 ± 4.00 mm (p = 0.0001) at 6 months following ASA. We observed a regression of the PW hypertrophy from 13.2 ± 3.35 mm to 12.18 ± 2.4 mm (p = 0.0225). There was a decrease in IVS mass from 108.9 ± 20 g to 91.5 ± 29 g (p = 0.0006). There was a trend towards a decreased LV mass and LV mass excluding IVS mass at 6 months. CONCLUSIONS: A significant decrease in PG in the LVOT is associated with a decrease in LV mass and with regression of LV hypertrophy outside the scar after ASA.

D?browski M; Chojnowska L; Ma?ek L; Spiewak M; Ku?mierczyk B; Koziarek J; Klisiewicz A; Mi?ko J; Witkowski A

2012-01-01

293

Effect of haloperidol on transient outward potassium current in rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

Although sigma ligand haloperidol is known to affect repolarization in heart, its effect on potassium currents in cardiomyocytes has not yet been studied. We analyzed the effect of 1 micromol/l haloperidol on transient outward K(+) current (I(to)) in enzymatically isolated rat right ventricular cardiomyocytes using the whole-cell patch-clamp technique at room temperature. Haloperidol induced a decrease of amplitude and an acceleration of apparent inactivation of I(to), both in a voltage-independent manner. The averaged inhibition of I(to), evaluated as a change of its time integral, was 23.0+/-3.2% at stimulation frequency of 0.1 Hz. As a consequence of slow recovery of I(to) from the haloperidol-induced block (time constant 1482+/-783 ms), a cumulation of the block up to about 40% appeared at 3.3 Hz. We conclude that haloperidol causes a voltage-independent block of I(to) that cumulates at higher stimulation frequencies. Based on the computer reconstruction of experimental data, a block of I(to)-channels in both open and open-inactivated states appears to be likely mechanism of haloperidol-induced inhibition of I(to).

Bébarová M; Matejovic P; Pásek M; Nováková M

2006-11-01

294

The functional role of cardiac T-tubules explored in a model of rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

The morphology of the cardiac transverse-axial tubular system (TATS) has been known for decades, but its function has received little attention. To explore the possible role of this system in the physiological modulation of electrical and contractile activity, we have developed a mathematical model of rat ventricular cardiomyocytes in which the TATS is described as a single compartment. The geometrical characteristics of the TATS, the biophysical characteristics of ion transporters and their distribution between surface and tubular membranes were based on available experimental data. Biophysically realistic values of mean access resistance to the tubular lumen and time constants for ion exchange with the bulk extracellular solution were included. The fraction of membrane in the TATS was set to 56%. The action potentials initiated in current-clamp mode are accompanied by transient K+ accumulation and transient Ca2+ depletion in the TATS lumen. The amplitude of these changes relative to external ion concentrations was studied at steady-state stimulation frequencies of 1-5 Hz. Ca2+ depletion increased from 7 to 13.1% with stimulation frequency, while K+ accumulation decreased from 4.1 to 2.7%. These ionic changes (particularly Ca2+ depletion) implicated significant decrease of intracellular Ca2+ load at frequencies natural for rat heart.

Pásek M; Simurda J; Christé G

2006-05-01

295

The functional role of cardiac T-tubules explored in a model of rat ventricular myocytes.  

Science.gov (United States)

The morphology of the cardiac transverse-axial tubular system (TATS) has been known for decades, but its function has received little attention. To explore the possible role of this system in the physiological modulation of electrical and contractile activity, we have developed a mathematical model of rat ventricular cardiomyocytes in which the TATS is described as a single compartment. The geometrical characteristics of the TATS, the biophysical characteristics of ion transporters and their distribution between surface and tubular membranes were based on available experimental data. Biophysically realistic values of mean access resistance to the tubular lumen and time constants for ion exchange with the bulk extracellular solution were included. The fraction of membrane in the TATS was set to 56%. The action potentials initiated in current-clamp mode are accompanied by transient K+ accumulation and transient Ca2+ depletion in the TATS lumen. The amplitude of these changes relative to external ion concentrations was studied at steady-state stimulation frequencies of 1-5 Hz. Ca2+ depletion increased from 7 to 13.1% with stimulation frequency, while K+ accumulation decreased from 4.1 to 2.7%. These ionic changes (particularly Ca2+ depletion) implicated significant decrease of intracellular Ca2+ load at frequencies natural for rat heart. PMID:16608703

Pásek, Michal; Simurda, Jiri; Christé, Georges

2006-05-15

296

Role of Na(+)-H(+) exchange in the modulation of L-type Ca(2+) current during fluid pressure in rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

Application of fluid pressure (FP) using pressurized fluid flow suppresses the L-type Ca(2+) current through both enhancement of Ca(2+) release and intracellular acidosis in ventricular myocytes. As FP-induced intracellular acidosis is more severe during the inhibition of Na(+)-H(+) exchange (NHE), we examined the possible role of NHE in the regulation of I(Ca) during FP exposure using HOE642 (cariporide), a specific NHE inhibitor. A flow of pressurized (~16 dyn/cm(2)) fluid was applied onto single rat ventricular myocytes, and the I(Ca) was monitored using a whole-cell patch-clamp under HEPES-buffered conditions. In cells pre-exposed to FP, additional treatment with HOE642 dose-dependently suppressed the I(Ca) (IC(50) = 0.97 ± 0.12 ?M) without altering current-voltage relationships and inactivation time constants. In contrast, the I(Ca) in control cells was not altered by HOE642. The HOE642 induced a left shift in the steady-state inactivation curve. The suppressive effect of HOE642 on the I(Ca) under FP was not altered by intracellular high Ca(2+) buffering. Replacement of external Cl(-) with aspartate to inhibit the Cl(-)-dependent acid loader eliminated the inhibitory effect of HOE642 on I(Ca). These results suggest that NHE may attenuate FP-induced I(Ca) suppression by preventing intracellular H(+) accumulation in rat ventricular myocytes and that NHE activity may not be involved in the Ca(2+)-dependent inhibition of the I(Ca) during FP exposure.

Kim JC; Woo SH

2013-02-01

297

Effect of trimetazidine treatment on the transient outward potassium current of the left ventricular myocytes of rats with streptozotocin-induced type 1 diabetes mellitus  

Directory of Open Access Journals (Sweden)

Full Text Available Cardiovascular complications are a leading cause of mortality in patients with diabetes mellitus (DM). The present study was designed to investigate the effects of trimetazidine (TMZ), an anti-angina drug, on transient outward potassium current (Ito) remodeling in ventricular myocytes and the plasma contents of free fatty acid (FFA) and glucose in DM. Sprague-Dawley rats, 8 weeks old and weighing 200-250 g, were randomly divided into three groups of 20 animals each. The control group was injected with vehicle (1 mM citrate buffer), the DM group was injected with 65 mg/kg streptozotocin (STZ) for induction of type 1 DM, and the DM + TMZ group was injected with the same dose of STZ followed by a 4-week treatment with TMZ (60 mg·kg-1·day-1). All animals were then euthanized and their hearts excised and subjected to electrophysiological measurements or gene expression analyses. TMZ exposure significantly reversed the increased plasma FFA level in diabetic rats, but failed to change the plasma glucose level. The amplitude of Ito was significantly decreased in left ventricular myocytes from diabetic rats relative to control animals (6.25 ± 1.45 vs 20.72 ± 2.93 pA/pF at +40 mV). The DM-associated Ito reduction was attenuated by TMZ. Moreover, TMZ treatment reversed the increased expression of the channel-forming alpha subunit Kv1.4 and the decreased expression of Kv4.2 and Kv4.3 in diabetic rat hearts. These data demonstrate that TMZ can normalize, or partially normalize, the increased plasma FFA content, the reduced Ito of ventricular myocytes, and the altered expression Kv1.4, Kv4.2, and Kv4.3 in type 1 DM.

Yu-luan Xiang; Li He; Jun Xiao; Shuang Xia; Song-bai Deng; Yun Xiu; Qiang She

2012-01-01

298

Diverse effects of renal denervation on ventricular hypertrophy and blood pressure in DOCA-salt hypertensive rats  

Scientific Electronic Library Online (English)

Full Text Available Abstract in english Cardiac hypertrophy that accompanies hypertension seems to be a phenomenon of multifactorial origin whose development does not seem to depend on an increased pressure load alone, but also on local growth factors and cardioadrenergic activity. The aim of the present study was to determine if sympathetic renal denervation and its effects on arterial pressure level can prevent cardiac hypertrophy and if it can also delay the onset and attenuate the severity of deoxycorticost (more) erone acetate (DOCA)-salt hypertension. DOCA-salt treatment was initiated in rats seven days after uninephrectomy and contralateral renal denervation or sham renal denervation. DOCA (15 mg/kg, sc) or vehicle (soybean oil, 0.25 ml per animal) was administered twice a week for two weeks. Rats treated with DOCA or vehicle (control) were provided drinking water containing 1% NaCl and 0.03% KCl. At the end of the treatment period, mean arterial pressure (MAP) and heart rate measurements were made in conscious animals. Under ether anesthesia, the heart was removed and the right and left ventricles (including the septum) were separated and weighed. DOCA-salt treatment produced a significant increase in left ventricular weight/body weight (LVW/BW) ratio (2.44 ± 0.09 mg/g) and right ventricular weight/body weight (RVW/BW) ratio (0.53 ± 0.01 mg/g) compared to control (1.92 ± 0.04 and 0.48 ± 0.01 mg/g, respectively) rats. MAP was significantly higher (39%) in DOCA-salt rats. Renal denervation prevented (P>0.05) the development of hypertension in DOCA-salt rats but did not prevent the increase in LVW/BW (2.27 ± 0.03 mg/g) and RVW/BW (0.52 ± 0.01 mg/g). We have shown that the increase in arterial pressure level is not responsible for cardiac hypertrophy, which may be more related to other events associated with DOCA-salt hypertension, such as an increase in cardiac sympathetic activity

Cabral, A.M.; Silva, I.F.; Gardioli, C.R.; Mauad, H.; Vasquez, E.C.

1998-04-01

299

Accuracy of advanced versus strictly conventional 12-lead ECG for detection and screening of coronary artery disease, left ventricular hypertrophy and left ventricular systolic dysfunction  

Directory of Open Access Journals (Sweden)

Full Text Available Abstract Background Resting conventional 12-lead ECG has low sensitivity for detection of coronary artery disease (CAD) and left ventricular hypertrophy (LVH) and low positive predictive value (PPV) for prediction of left ventricular systolic dysfunction (LVSD). We hypothesized that a ~5-min resting 12-lead advanced ECG test ("A-ECG") that combined results from both the advanced and conventional ECG could more accurately screen for these conditions than strictly conventional ECG. Methods Results from nearly every conventional and advanced resting ECG parameter known from the literature to have diagnostic or predictive value were first retrospectively evaluated in 418 healthy controls and 290 patients with imaging-proven CAD, LVH and/or LVSD. Each ECG parameter was examined for potential inclusion within multi-parameter A-ECG scores derived from multivariate regression models that were designed to optimally screen for disease in general or LVSD in particular. The performance of the best retrospectively-validated A-ECG scores was then compared against that of optimized pooled criteria from the strictly conventional ECG in a test set of 315 additional individuals. Results Compared to optimized pooled criteria from the strictly conventional ECG, a 7-parameter A-ECG score validated in the training set increased the sensitivity of resting ECG for identifying disease in the test set from 78% (72-84%) to 92% (88-96%) (P Conclusion Resting 12-lead A-ECG scoring is more accurate than strictly conventional ECG in screening for CAD, LVH and LVSD.

Schlegel Todd T; Kulecz Walter B; Feiveson Alan H; Greco E; DePalma Jude L; Starc Vito; Vrtovec Bojan; Rahman M; Bungo Michael W; Hayat Matthew J; Bauch Terry; Delgado Reynolds; Warren Stafford G; Núñez-Medina Tulio; Medina Rubén; Jugo Diego; Arheden Håkan; Pahlm Olle

2010-01-01

300

Super-resolution scanning patch clamp reveals clustering of functional ion channels in adult ventricular myocyte.  

UK PubMed Central (United Kingdom)

RATIONALE: Compartmentation of ion channels on the cardiomyocyte surface is important for electric propagation and electromechanical coupling. The specialized T-tubule and costameric structures facilitate spatial coupling of various ion channels and receptors. Existing methods such as immunofluorescence and patch clamp techniques are limited in their ability to localize functional ion channels. As such, a correlation between channel protein location and channel function remains incomplete. OBJECTIVE: To validate a method that permits routine imaging of the topography of a live cardiomyocyte and study clustering of functional ion channels from a specific microdomain. METHODS AND RESULTS: We used scanning ion conductance microscopy and conventional cell-attached patch clamp with a software modification that allows controlled increase of pipette tip diameter. The sharp nanopipette used for topography scan was modified into a larger patch pipette that could be positioned with nanoscale precision to a specific site of interest (crest, groove, or T-tubules of cardiomyocytes) and sealed to the membrane for cell-attached recording of ion channels. Using this method, we significantly increased the probability of detecting activity of L-type calcium channels in the T-tubules of ventricular cardiomyocytes. We also demonstrated that active sodium channels do not distribute homogenously on the sarcolemma instead, they segregate into clusters of various densities, most crowded in the crest region, that are surrounded by areas virtually free of functional sodium channels. CONCLUSIONS: Our new method substantially increases the throughput of recording location-specific functional ion channels on the cardiomyocyte sarcolemma, thereby allowing characterization of ion channels in relation to the microdomain where they reside.

Bhargava A; Lin X; Novak P; Mehta K; Korchev Y; Delmar M; Gorelik J

2013-04-01

 
 
 
 
301

Hipertrofia ventricular esquerda em pacientes com doença renal crônica em tratamento conservador/ Left ventricular hypertrophy in patients with chronic kidney disease under conservative treatment  

Scientific Electronic Library Online (English)

Full Text Available Abstract in portuguese A doença cardiovascular (DCV) permanece sendo uma das maiores causas de morte em pacientes com doença renal crônica (DRC). A hipertrofia ventricular esquerda (HVE) está presente em 75% dos pacientes ao iniciarem diálise, sugerindo que esta deve estar presente precocemente no curso da DRC. Poucos estudos avaliaram a prevalência de HVE na pré-diálise. Foram avaliados 309 pacientes clinicamente estáveis em acompanhamento por pelo menos três meses em cinco Centros n (more) o Brasil. Perfil bioquímico e marcadores inflamatórios foram avaliados. Dados são apresentados como media ± DP. Observamos que a HVE esteve presente em 53% dos pacientes, idade = 60 ± 13 anos, e 55 ± 14 anos para aqueles sem HVE. Diabetes mellitus como doença de base esteve presente em 35% dos pacientes em ambos os grupos. Filtração glomerular estimada foi 30 ± 11 e 32 ± 12 mL/min para pacientes com HVE e sem, respectivamente (p = 0,19). A distribuição de pacientes mostrou que 60% com HVE se encontravam no estágio 4. Análise logística multivariada mostrou que eram determinantes independentes para HVE: idade (p Abstract in english Cardiovascular disease (CVD) remains the major cause of death in patients with chronic kidney disease (CKD). Left ventricular hypertrophy (LVH) is present in 75% of patients starting dialysis, suggesting that LVH might be present from an early stage of CKD. Few studies have addressed the predialysis prevalence of LVH. This study evaluated 309 clinically stable patients under treatment for at least three months at five Brazilian centers. Biochemical profile and inflammator (more) y markers were assessed. Data were shown as mean ± SD. Left ventricular hypertrophy was present in 53% of the patients, whose mean age was 60 ± 13years. The mean age of those without LVH was 55 ± 14 years. Diabetes mellitus was the underlying disease in 35% of the patients in both groups. Estimated glomerular filtration rate was 30 ± 11 and 32 ± 12 mL/min for patients with and without LVH, respectively (p = 0.19). The distribution of patients showed that 60% of those with LVH were in stage 4. Multivariate logistic regression analysis indicated the following independent determinants for LVH: age (p

Bregman, Rachel; Lemos, Carla; Pecoits Filho, Roberto; Abensur, Hugo; Draibe, Sergio; Bastos, Marcus Gomes; Canziani, Maria Eugênia

2010-03-01

302

Quercetin Inhibits Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats and Inhibits Angiotensin II-Induced H9C2 Cells Hypertrophy by Enhancing PPAR-? Expression and Suppressing AP-1 Activity  

Science.gov (United States)

Background Quercetin is the most abundant flavonoid in fruit and vegetables and is believed to attenuate cardiovascular disease. We hypothesized that quercetin inhibits cardiac hypertrophy by blocking AP-1 (c-fos, c-jun) and activating PPAR-? signaling pathways. Methodology/Principal Findings The aim of this study was to identify the mechanism underlying quercetin-mediated attenuation of cardiac hypertrophy. Quercetin therapy reduced blood pressure and markedly reduced the ratio of left ventricular to body weight (LVW/BW) (Pquercetin also significantly attenuated Ang II-induced H9C2 cells hypertrophy, as indicated by its concentration dependent inhibitory effects on [3H]leucine incorporation into H9C2 cells (64% reduction) and by the reduced hypertrophic surface area in H9C2 cells compared with the Ang II group (Pquercetin-treated group both in vivo and in vitro when analyzed using immunofluorescent or immunohistochemical assays (Pquercetin-treated group, as was the downstream hypertrophy gene, including mRNA levels of ANP and BNP (Pquercetin-treated group (Pquercetin inhibition on mRNA expression levels of genes such as ANP and BNP in hypertrophic H9C2 cells. Conclusions Our data indicate that quercetin may inhibit cardiac hypertrophy by enhancing PPAR-? expression and by suppressing the AP-1 signaling pathway.

Yan, Lei; Zhang, Ji Dong; Wang, Bo; Lv, Yi Jing; Jiang, Hong; Liu, Gui Lin; Qiao, Yun; Ren, Ming; Guo, Xue Feng

2013-01-01

303

LONG-TERM EFFECTS OF CHLORTHALIDONE VS HYDROCHLOROTHIAZIDE ON ELECTROCARDIOGRAPHIC LEFT VENTRICULAR HYPERTROPHY IN THE MULTIPLE RISK FACTOR INTERVENTION TRIAL  

Science.gov (United States)

Chlorthalidone (CTD) reduces 24-hour blood pressure more effectively than hydrochlorothiazide (HCTZ), but whether this influences electrocardiographic left ventricular hypertrophy (LVH) is uncertain. One source of comparative data is the Multiple Risk Factor Intervention Trial (MRFIT), which randomly assigned 8,012 hypertensive men to special intervention (SI) or usual care (UC). SI participants could use CTD or HCTZ initially; previous analyses have grouped clinics by their main diuretic used (C-clinics: CTD; H-clinics: HCTZ). After 48 months, SI participants receiving HCTZ were recommended to switch to CTD, in part, because higher mortality was observed for SI compared to UC participants in H-clinics, while the opposite was found in C-clinics. In this analysis, we examined change in continuous measures of electrocardiographic LVH using both an ecologic analysis by previously-reported C- or H-clinic groupings, and an individual participant analysis where use of CTD or HCTZ by SI participants was considered and updated annually. Through 48 months, differences between SI and UC in LVH were larger for C-clinics compared to H-clinics (Sokolow-Lyon: ?93.9 vs ?54.9 ?V, P=0.049; Cornell voltage: ?68.1 vs ?35.9 ?V, P=0.019; Cornell voltage product: ?4.6 vs ?2.2 ?V/ms, P=0.071; left ventricular mass: ?4.4 vs ?2.8 gm, P=0.002). At the individual participant level, Sokolow-Lyon and left ventricular mass were significantly lower for SI men receiving CTD compared to HCTZ through 48 months and 84 months of follow-up. Our findings on LVH support the idea that greater blood pressure reduction with CTD than HCTZ may have led to differences in mortality observed in MRFIT.

Ernst, Michael E.; Neaton, James D.; Grimm, Richard H.; Collins, Gary; Thomas, William; Soliman, Elsayed Z.; Prineas, Ronald J.

2011-01-01

304

Characteristics of left ventricular hypertrophy estimated by MIBG and BMIPP cardiac scintigraphy in patients undergoing peritoneal dialysis  

International Nuclear Information System (INIS)

Left ventricular hypertrophy (LVH) has been reported as a major factor in morbidity and mortality in chronic dialysis patients. However, cardiovascular mortality in peritoneal dialysis (PD) patients with LVH is substantially similar to that in hemodialysis (HD) patients. The present study sought to study whether sympathetic nerve activity and fatty acid metabolism of the myocardium estimated by 123I metaiodobenzylguanidine (MIBG) and 123I ?-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) myocardial scintigraphy are impaired or not in PD patients with LVH. The underlying disease of 45 PD patients enrolled in this study was chronic glomerulonephritis in all cases. Serum levels of natriuretic peptides (arterial natriuretic peptide (ANP), brain natriuretic peptide (BNP)) and free carnitine and MIBG, BMIPP myocardial scintigraphy and 2-dimensional echocardiography were measured in these 45 PD patients. The following results were obtained. The prevalence of increased left ventricular mass index (LVMI) was 84.4%. LVMI correlated with age, and serum levels of ANP and BNP, and inversely correlated with a heart-to-mediastinum ratio (H/M) estimated by MIBG and BMIPP myocardial scintigraphy. Percentages of the normal image of MIBG and BMIPP measured with a single photon emission computed tomography (SPECT) were 37.8% and 62.2%, respectively. The PD patients showing the diffuse defect of MIBG or BMIPP imaging had the decrease in left ventricular ejection fraction (LVEF). Especially, the serum level of free carnitine was reduced in the PD patients with diffuse defect of BMIPP SPECT. From these results, we concluded that PD patients with LVH showed impaired sympathetic nerve activity and fatty acid metabolism of the myocardium. Metabolic and functional disturbances of the myocardium may influence mortality in PD patients. (author)

2002-01-01

305

Characteristics of left ventricular hypertrophy estimated by MIBG and BMIPP cardiac scintigraphy in patients undergoing peritoneal dialysis  

Energy Technology Data Exchange (ETDEWEB)

Left ventricular hypertrophy (LVH) has been reported as a major factor in morbidity and mortality in chronic dialysis patients. However, cardiovascular mortality in peritoneal dialysis (PD) patients with LVH is substantially similar to that in hemodialysis (HD) patients. The present study sought to study whether sympathetic nerve activity and fatty acid metabolism of the myocardium estimated by {sup 123}I metaiodobenzylguanidine (MIBG) and {sup 123}I {beta}-methyl-p-iodophenyl-pentadecanoic acid (BMIPP) myocardial scintigraphy are impaired or not in PD patients with LVH. The underlying disease of 45 PD patients enrolled in this study was chronic glomerulonephritis in all cases. Serum levels of natriuretic peptides (arterial natriuretic peptide (ANP), brain natriuretic peptide (BNP)) and free carnitine and MIBG, BMIPP myocardial scintigraphy and 2-dimensional echocardiography were measured in these 45 PD patients. The following results were obtained. The prevalence of increased left ventricular mass index (LVMI) was 84.4%. LVMI correlated with age, and serum levels of ANP and BNP, and inversely correlated with a heart-to-mediastinum ratio (H/M) estimated by MIBG and BMIPP myocardial scintigraphy. Percentages of the normal image of MIBG and BMIPP measured with a single photon emission computed tomography (SPECT) were 37.8% and 62.2%, respectively. The PD patients showing the diffuse defect of MIBG or BMIPP imaging had the decrease in left ventricular ejection fraction (LVEF). Especially, the serum level of free carnitine was reduced in the PD patients with diffuse defect of BMIPP SPECT. From these results, we concluded that PD patients with LVH showed impaired sympathetic nerve activity and fatty acid metabolism of the myocardium. Metabolic and functional disturbances of the myocardium may influence mortality in PD patients. (author)

Ohashi, Hiroshige; Oda, Hiroshi; Ohno, Michiya; Watanabe, Sachirow; Kotoo, Yasunori; Matsuno, Yukihiko [Gifu Prefectural Hospital (Japan)

2002-12-01

306

Differentiation between left bundle branch block and left ventricular hypertrophy: implications for cardiac resynchronization therapy.  

Science.gov (United States)

Recent clinical trials have demonstrated that cardiac resynchronization therapy (CRT) reduces heart failure hospitalizations and mortality in patients with complete left bundle branch block (LBBB), but potentially not those with right bundle branch block or nonspecific LV conduction delay, such as that due to LV hypertrophy (LVH). Furthermore, endocardial mapping and simulation studies have suggested that one-third of patients diagnosed with LBBB by conventional electrocardiographic criteria are misdiagnosed, and these patients likely have a combination of LVH, LV chamber dilatation and delayed initiation of LV activation (incomplete LBBB). Increase in LV size due to hypertrophy/dilatation and slowed intramyocardial conduction velocity prolong QRS duration in patients with LVH, which can frequently go above the QRS duration threshold of 120 ms conventionally used to diagnose LBBB. New strict criteria for diagnosing complete LBBB have been proposed that utilize longer QRS duration thresholds (130 ms in women and 140 ms in men) and require the presence of mid-QRS notching/slurring in at least 2 of the leads I, aVL, V1, V2, V5 or V6. The emergence of CRT has led to an increased need to differentiate complete LBBB from LVH and other types of intraventricular conduction delay, which should be further studied. PMID:23022304

Strauss, David G

2012-09-28

307

Differentiation between left bundle branch block and left ventricular hypertrophy: implications for cardiac resynchronization therapy.  

UK PubMed Central (United Kingdom)

Recent clinical trials have demonstrated that cardiac resynchronization therapy (CRT) reduces heart failure hospitalizations and mortality in patients with complete left bundle branch block (LBBB), but potentially not those with right bundle branch block or nonspecific LV conduction delay, such as that due to LV hypertrophy (LVH). Furthermore, endocardial mapping and simulation studies have suggested that one-third of patients diagnosed with LBBB by conventional electrocardiographic criteria are misdiagnosed, and these patients likely have a combination of LVH, LV chamber dilatation and delayed initiation of LV activation (incomplete LBBB). Increase in LV size due to hypertrophy/dilatation and slowed intramyocardial conduction velocity prolong QRS duration in patients with LVH, which can frequently go above the QRS duration threshold of 120 ms conventionally used to diagnose LBBB. New strict criteria for diagnosing complete LBBB have been proposed that utilize longer QRS duration thresholds (130 ms in women and 140 ms in men) and require the presence of mid-QRS notching/slurring in at least 2 of the leads I, aVL, V1, V2, V5 or V6. The emergence of CRT has led to an increased need to differentiate complete LBBB from LVH and other types of intraventricular conduction delay, which should be further studied.

Strauss DG

2012-11-01

308

Mechanism of extracellular ATP-induced increase of cytosolic Ca2+ concentration in isolated rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

1. Changes in the cytosolic Ca2+ concentration ([Ca2+]i) of isolated rat ventricular myocytes in suspension were measured in response to extracellular ATP using the fluorescent Ca2+ indicators Quin-2 and Fura-2. 2. ATP produced a concentration-, time- and Mg(2+)-dependent, biphasic increase of [Ca2+]i whereas slowly hydrolysable ATP analogues produced a slow, monophasic increase of [Ca2+]i and the non-hydrolysable ATP analogues were without effect. 3. Extracellular Ca2+ was required for the ATP-induced increase of [Ca2+]i and pre-treatment of the cells with caffeine, ryanodine, verapamil or nimodipine partially inhibited the [Ca2+]i increase. 4. Whole-cell patch-clamp experiments revealed that ATP activated an ionic current that had a linear current-voltage relationship with a reversal potential near O mV. Quinidine, a putative P2 purinergic receptor blocker, abolished the ATP-activated current. The ATP-activated current was Mg2+ dependent. 5. Associated with the ATP-activated current was cellular depolarization. In a physiological solution, ATP depolarized cells to the threshold for the firing of action potentials. In the presence of the voltage-activated ion channel blockers tetrodotoxin, 4-aminopyridine, caesium and nitrendipine, ATP depolarized cells to -44 +/- 6 mV from a resting potential of -66 +/- 4 mV (n = 11). 6. Sodium dodecyl sulphate (SDS) polyacrylamide gel electrophoresis and autoradiography demonstrated that extracellular ATP stimulated the phosphorylation of several extracellular membrane-bound proteins. The phosphorylation of these proteins was concentration, time and Mg2+ dependent. Pre-treatment of cells with the slowly hydrolysable ATP analogues inhibited the ATP-induced phosphorylation. Adenosine 5'-O-3-thiotriphosphate (ATP gamma S) thiophosphorylated proteins with the same apparent molecular weight as the proteins phosphorylated by ATP. 7. These results suggest that the ATP-induced increase of [Ca2+]i is a result of the activation, possibly by protein phosphorylation, of a novel ion channel carrying inward current. The ATP-activated channel may be permeable to Na+ and Ca2+ and causes [Ca2+]i to rise. More importantly, this inward current depolarizes the cell to the threshold of inducing spontaneous firing of action potentials. The firing of action potentials results in the influx of Ca2+ through L-type Ca2+ channels which would trigger Ca2+ release from the sarcoplasmic reticulum and lead to the increase in [Ca2+]i.

Christie A; Sharma VK; Sheu SS

1992-01-01

309

Role of t-tubules in the control of trans-sarcolemmal ion flux and intracellular Ca2+ in a model of the rat cardiac ventricular myocyte.  

UK PubMed Central (United Kingdom)

The t-tubules of mammalian ventricular myocytes are invaginations of the surface membrane that form a complex network within the cell, with restricted diffusion to the bulk extracellular space. The trans-sarcolemmal flux of many ions, including Ca(2+), occurs predominantly across the t-tubule membrane and thus into and out of this restricted diffusion space. It seems possible, therefore, that ion concentration changes may occur in the t-tubule lumen, which would alter ion flux across the t-tubule membrane. We have used a computer model of the ventricular myocyte, incorporating a t-tubule compartment and experimentally determined values for diffusion between the t-tubule lumen and bulk extracellular space, and ion fluxes across the t-tubule membrane, to investigate this possibility. The results show that influx and efflux of different ion species across the t-tubule membrane are similar, but not equal. Changes of ion concentration can therefore occur close to the t-tubular membrane, thereby altering trans-sarcolemmal ion flux and thus cell function, although such changes are reduced by diffusion to the bulk extracellular space. Slowing diffusion results in larger changes in luminal ion concentrations. These results provide a deeper understanding of the role of the t-tubules in normal cell function, and are a basis for understanding the changes that occur in heart failure as a result of changes in t-tubule structure and ion fluxes.

Pásek M; Šimurda J; Orchard CH

2012-06-01

310

Three-dimensional high-resolution imaging of cardiac proteins to construct models of intracellular Ca2+ signalling in rat ventricular myocytes.  

UK PubMed Central (United Kingdom)

Quantitative understanding of the Ca(2+) handling in cardiac ventricular myocytes requires accurate knowledge of cardiac ultrastructure and protein distribution. We have therefore developed high-resolution imaging and analysis approaches to measure the three-dimensional distribution of immunolabelled proteins with confocal microscopy. Labelling of single rat cardiac myocytes with an antibody to the Z-line marker alpha-actinin revealed a complex architecture of sarcomere misalignment across single cells. Double immunolabelling was used to relate the Z-line structure to the distribution of ryanodine receptors (RyRs, the intracellular Ca(2+) release channels) and the transverse tubular system. Both RyR and transverse tubular system distributions exhibited frequent dislocations from the simple planar geometry generally assumed in existing mathematical models. To investigate potential effects of these irregularities on Ca(2+) dynamics, we determined the three-dimensional distribution of RyR clusters within an extended section of a single rat ventricular myocyte to construct a model of stochastic Ca(2+) dynamics with a measured Ca(2+) release unit (CRU) distribution. Calculations with this model were compared with a second model in which all CRUs were placed on flat planes. The model with a realistic CRU distribution supported Ca(2+) waves that spread axially along the cell at velocities of approximately 50 mum s(-1). By contrast, in the model with planar CRU distribution the axial wave spread was slowed roughly twofold and wave propagation often nearly faltered. These results demonstrate that spatial features of the CRU distribution on multiple length scales may significantly affect intracellular Ca(2+) dynamics and must be captured in detailed mechanistic models to achieve quantitative as well as qualitative insight.

Soeller C; Jayasinghe ID; Li P; Holden AV; Cannell MB

2009-05-01

311

Genetic predisposition to left ventricular hypertrophy and the potential involvement of cystatin-C in untreated hypertension.  

UK PubMed Central (United Kingdom)

BACKGROUND: The angiotensinogen M235T and aldosterone synthase C-344T gene polymorphisms have been associated with cardiac and structure function. However, these associations in untreated hypertension remain unknown. We examined whether these variants determined both echocardiography indices and the potential associated underlying mechanisms, including cystatin-C and vascular inflammation. METHODS: The study population consisted of 319 untreated patients and 191 healthy individuals. Polymorphisms were determined by polymerase chain reaction technique. Left cardiac indices of geometry and function were assessed by echocardiography. Cystatin-C, intracellular cell adhesion molecule 1, and vascular cell adhesion molecule 1 levels were measured by enzyme-linked immunosorbent assay, whereas high sensitivity C-reactive protein levels were measured by immunonephelometry. RESULTS: There was no significant interaction between the angiotensinogen genotypes on left ventricular mass index (LVMI) and diastolic function indices in all study groups. Regarding C-344T polymorphism, TT homozygous hypertensive subjects exhibited higher values of LVMI compared with C allele carriers (P = 0.02) and higher prevalence of concentric hypertrophy (P < 0.001). However, this polymorphism was not associated with variations in left atrial volume and diastolic dysfunction. Cystatin-C levels were correlated with LVMI values (r = 0.22; P = 0.002) and mean E/A ratio (r = -0.24; P < 0.001). Interestingly, a linear increase of LVMI with cyctatin-C quartiles has been revealed (F = 5.01; P < 0.001). Moreover, post hoc tests showed that increased levels of cystatin-C (above 75th percentile) were significantly different between both the first (P = 0.009) and the second quartile (P = 0.02). CONCLUSIONS: We have shown that C-344T potentially predicts higher values of LVMI and concentric hypertrophy in untreated hypertension, independently of renal function and subclinical inflammation. Increased levels of cystatin-C were correlated with higher LVMI values.

Tousoulis D; Androulakis E; Papageorgiou N; Miliou A; Chatzistamatiou E; Oikonomou E; Moustakas G; Kallikazaros I; Stefanadis C

2013-05-01

312

Long-term control of arterial hypertension and regression of left ventricular hypertrophy with treatment of primary aldosteronism.  

UK PubMed Central (United Kingdom)

Primary aldosteronism (PA), a common cause of high blood pressure (BP), induces left ventricular (LV) hypertrophy and an excess rate of cardiovascular events. Whether its treatment provides long-term cure of hypertension and regression of cardiovascular damage remains uncertain. To the aim of assessing the effect of treatment of PA on BP and LV changes, we prospectively recruited 323 patients in a long-term follow-up study entailing serial echocardiography evaluations. Of them, 180 had PA and were assigned to either adrenalectomy (n=110) or medical therapy (n=70) on the basis of the adrenal vein sampling. The remaining 143 were consecutive optimally treated primary hypertensive patients. At baseline, the PA patients had more inappropriate LV mass than PH patients (27.1% versus 16.2%; P=0.020), despite similar BP values. At a median follow-up of 36 months (range, 6-225), BP was lowered (P<0.0001 versus baseline) to similar values in adrenalectomized (135±15/83±9 mm Hg), medically treated PA (133±11/83±7 mm Hg), and PH (139±15/86±9 mm Hg) patients. To this end, the adrenalectomized patients required significantly less drugs than the other groups. In PA patients, the LV mass index and the rate of LV hypertrophy fell through LV inward remodeling to the level of optimally treated PH patients, indicating that the LV work markedly decreased. Findings were similar when long-term (?5 and ?10 years) data were examined. Thus, an early diagnosis and a specific treatment of PA warrant normalization of BP and reversal of detrimental LV changes at long term.

Rossi GP; Cesari M; Cuspidi C; Maiolino G; Cicala MV; Bisogni V; Mantero F; Pessina AC

2013-07-01

313

Plzf as a Candidate Gene Predisposing the Spontaneously Hypertensive Rat to Hypertension, Left Ventricular Hypertrophy, and Interstitial Fibrosis.  

UK PubMed Central (United Kingdom)

BACKGROUND: The spontaneously hypertensive rat (SHR) is the most widely used model of essential hypertension and is susceptible to left ventricular hypertrophy (LVH) and myocardial fibrosis. Recently, a quantitative trait locus (QTL) that influences heart interstitial fibrosis was mapped to chromosome 8. Our aim was to dissect the genetic basis of this QTL(s) predisposing SHR to hypertension, LVH, and interstitial fibrosis. METHODS: Hemodynamic and histomorphometric analyses were performed in genetically defined SHR.PD-chr.8 minimal congenic strain (PD5 subline) rats. RESULTS: The differential segment, genetically isolated within the PD5 subline, spans 788kb and contains 7 genes, including the promyelocytic leukemia zinc finger (Plzf) gene that has been implicated in hypertrophy and cardiac fibrosis. Mutant Plzf allele contains a 2,964-bp deletion in intron 2. The PD5 congenic strain, when compared with the SHR, showed significantly reduced systolic blood pressure by approximately 15mm Hg (P = 0.002), amelioration of LVH (0.23±0.02 vs. 0.39±0.02g/100g body weight; P < 0.00001), and reduced interstitial fibrosis (17,478±1,035 vs. 41,530±3,499 ?m(2); P < 0.0001). The extent of amelioration of LVH and interstitial fibrosis was disproportionate to blood pressure decrease in congenic rats, suggesting an important role for genetic factors. Cardiac expression of Plzf was significantly reduced in prehypertensive (8 and 21 days) congenic animals compared with controls. CONCLUSIONS: These results provide compelling evidence of a significant role for genetic factors in regulating blood pressure, LVH, and cardiac fibrosis and identify mutant Plzf as a prominent candidate gene.

Liska F; Mancini M; Krupková M; Chylíková B; Krenová D; Seda O; Silhavy J; Mlejnek P; Landa V; Zídek V; D Amati G; Pravenec M; Kren V

2013-08-01

314

Usefulness of thallium-201 scintigraphy in predicting the development of angina pectoris in hypertensive patients with left ventricular hypertrophy  

Energy Technology Data Exchange (ETDEWEB)

Hypertension and left ventricular (LV) hypertrophy are independent risk factors for the development of coronary artery disease. To determine whether patients at higher risk for coronary artery disease can be identified, 40 asymptomatic hypertensive men with LV hypertrophy were prospectively studied using exercise thallium-201 scintigraphy and exercise radionuclide angiography. Endpoints indicative of coronary artery disease were defined as the subsequent development of typical angina pectoris, which occurred in 8 patients during a median follow-up of 38 months, or myocardial infarction, which did not occur. The exercise electrocardiogram was interpreted by standard ST-segment criteria and by a computerized treadmill exercise score. Abnormal ST-segment responses were present in 16 of the 40 hypertensives (40%), whereas the treadmill score was positive in 8 of those same 40 patients (20%). Scintigraphic perfusion defects assessed both visually and semiquantitatively were observed in 8 of 40 (20%) patients. An abnormal ejection fraction response to exercise was present in 40% (16 of 40) of patients, and 3 of 40 (7.5%) developed new wall motion abnormalities during exercise. Six of 8 patients with either perfusion defects or abnormal treadmill score developed typical angina during follow-up. All 5 patients with concordant positive exercise scintigrams and treadmill score developed chest pain during follow-up and had coronary artery disease confirmed by coronary angiography. However, only 7 of 16 (44%) patients with positive ST changes or abnormal ejection fraction responses during exercise developed chest pain during follow-up. In contrast, of 32 patients with negative scintigrams only 2 developed atypical chest pain syndromes, and significant coronary artery disease was excluded by angiography in 1 patient.

Tubau, J.F.; Szlachcic, J.; Hollenberg, M.; Massie, B.M.

1989-07-01

315

Usefulness of thallium-201 scintigraphy in predicting the development of angina pectoris in hypertensive patients with left ventricular hypertrophy  

International Nuclear Information System (INIS)

[en] Hypertension and left ventricular (LV) hypertrophy are independent risk factors for the development of coronary artery disease. To determine whether patients at higher risk for coronary artery disease can be identified, 40 asymptomatic hypertensive men with LV hypertrophy were prospectively studied using exercise thallium-201 scintigraphy and exercise radionuclide angiography. Endpoints indicative of coronary artery disease were defined as the subsequent development of typical angina pectoris, which occurred in 8 patients during a median follow-up of 38 months, or myocardial infarction, which did not occur. The exercise electrocardiogram was interpreted by standard ST-segment criteria and by a computerized treadmill exercise score. Abnormal ST-segment responses were present in 16 of the 40 hypertensives (40%), whereas the treadmill score was positive in 8 of those same 40 patients (20%). Scintigraphic perfusion defects assessed both visually and semiquantitatively were observed in 8 of 40 (20%) patients. An abnormal ejection fraction response to exercise was present in 40% (16 of 40) of patients, and 3 of 40 (7.5%) developed new wall motion abnormalities during exercise. Six of 8 patients with either perfusion defects or abnormal treadmill score developed typical angina during follow-up. All 5 patients with concordant positive exercise scintigrams and treadmill score developed chest pain during follow-up and had coronary artery disease confirmed by coronary angiography. However, only 7 of 16 (44%) patients with positive ST changes or abnormal ejection fraction responses during exercise developed chest pain during follow-up. In contrast, of 32 patients with negative scintigrams only 2 developed atypical chest pain syndromes, and significant coronary artery disease was excluded by angiography in 1 patient

1989-07-01

316

Modulation of basal L-type Ca2+ current by adenosine in ferret isolated right ventricular myocytes.  

UK PubMed Central (United Kingdom)

1. The whole-cell configuration of the gigaohm seal voltage clamp and an internal perfusion technique were used to study the effects of adenosine on the basal L-type Ca2+ current (ICa) in enzymatically isolated right ventricular myocytes of ferrets. Basal L-type ICa was isolated by using a Na(+)- and K(+)-free saline (replacement by N-methyl-D-glucamine+, Cs+ and TEA+, respectively). All experiments were conducted at room temperature (22-24 degrees C). 2. Basal ICa was markedly reduced during exposure to adenosine in a concentration-dependent manner with a half-inhibitory concentration (IC50) of 0.3 microM and maximum inhibition of 35%. This effect was completely abolished by 50 nM 8-cyclopentyl-1,3-dipropylxanthine (CPDPX), a specific A1 adenosine receptor antagonist with an inhibition constant, Ki = 0.48 nM. Inhibition was also observed in the presence of 1 microM atropine. 3. Adenosine decreased basal ICa by decreasing the peak amplitude of ICa without significantly altering (i) the voltage dependence of the current-voltage relationship, (ii) the apparent reversal potential, (iii) the voltage dependence of steady-state activation and inactivation, (iv) the kinetics of inactivation at 0 mV, and (v) the kinetics of recovery from inactivation at -70 mV. 4. Pretreatment of cells with 0.4 microns/ml pertussis toxin (PTX) for 4 h at 37 degrees C produced greater than 90% ADP ribosylation of PTX-sensitive G proteins. PTX pretreatment significantly attenuated the adenosine-mediated decrease in ICa (35% in control; 4.6% after PTX pretreatment). 5. The peptide inhibitor (PKI) of cyclic AMP-dependent protein kinase A at a concentration of 2 microM neither inhibited basal ICa nor attenuated the effects of adenosine on basal ICa. However, PKI decreased the stimulatory effects of 100 microM cAMP on ICa. 6. Increasing intracellular cAMP to a supra-saturable level by using 10 mM cAMP and 100 microM papaverine did not prevent adenosine from inhibiting ICa. 7. Consistent with the reduction of basal ICa, adenosine produced an inhibitory effect on the action potential under basal conditions, i.e. hyperpolarization of the plateau phase and marked shortening of action potential duration. These effects were concentration dependent. 8. These results demonstrate a reduction of the basal L-type ICa by adenosine in ferret ventricular myocardium. This reduction is not mediated by modification of voltage-dependent properties of macroscopic ICa. The shortening of action potentials may be explained in part by the reduction in ICa.(ABSTRACT TRUNCATED AT 400 WORDS)

Qu Y; Campbell DL; Whorton AR; Strauss HC

1993-11-01

317

Olmesartan improves left ventricular function in pressure-overload hypertrophied rat heart by blocking angiotensin II receptor with synergic effects of upregulation of angiotensin converting enzyme 2.  

UK PubMed Central (United Kingdom)

It is not clear how the blocking effect of angiotensin II receptors by olmesartan affects the functional recovery of pressure-overload hypertrophied heart. Hypertrophied heart was created by abdominal aortic banding above the celiac artery in Wistar rats at the age of eight weeks. Hypertrophied heart was excised and studied at 10 and 16 weeks after the operation (HT groups). For the last four weeks before the experiment, olmesartan (0.2 mg/kg per day) was administered subcutaneously by osmotic minipumps (Olm groups). Left ventricular function was measured by Langendorff perfusion. The levels of mRNA for angiotensin-converting enzyme (ACE), ACE2 and extracellular signal-regulated kinases (ERKs) in myocardium were analyzed by RT-PCR. Left ventricular systolic (+dP/dt(max), left ventricular systolic pressure) and diastolic functions (-dP/dt(max), tau) were impaired in HT groups, while in Olm groups they were significantly improved. The left ventricle to body weight (LV/BW) ratio increased significantly in HT groups, but in Olm groups the LV/BW ratio decreased significantly in comparison with HT groups. The ACE2 mRNA level was significantly higher in Olm groups as compared with HT groups. Plasma angiotensin II and the ERK mRNA level in HT groups increased significantly, but decreased in Olm groups in comparison with HT groups significantly. Olmesartan improved left ventricular function and hypertrophy through the increase of the ACE2 mRNA and decrease of both angiotensin II and ERK mRNA in pressure-overload rat heart.

Kaiqiang Ji; Minakawa M; Fukui K; Suzuki Y; Fukuda I

2009-04-01

318

Olmesartan improves left ventricular function in pressure-overload hypertrophied rat heart by blocking angiotensin II receptor with synergic effects of upregulation of angiotensin converting enzyme 2.  

Science.gov (United States)

It is not clear how the blocking effect of angiotensin II receptors by olmesartan affects the functional recovery of pressure-overload hypertrophied heart. Hypertrophied heart was created by abdominal aortic banding above the celiac artery in Wistar rats at the age of eight weeks. Hypertrophied heart was excised and studied at 10 and 16 weeks after the operation (HT groups). For the last four weeks before the experiment, olmesartan (0.2 mg/kg per day) was administered subcutaneously by osmotic minipumps (Olm groups). Left ventricular function was measured by Langendorff perfusion. The levels of mRNA for angiotensin-converting enzyme (ACE), ACE2 and extracellular signal-regulated kinases (ERKs) in myocardium were analyzed by RT-PCR. Left ventricular systolic (+dP/dt(max), left ventricular systolic pressure) and diastolic functions (-dP/dt(max), tau) were impaired in HT groups, while in Olm groups they were significantly improved. The left ventricle to body weight (LV/BW) ratio increased significantly in HT groups, but in Olm groups the LV/BW ratio decreased significantly in comparison with HT groups. The ACE2 mRNA level was significantly higher in Olm groups as compared with HT groups. Plasma angiotensin II and the ERK mRNA level in HT groups increased significantly, but decreased in Olm groups in comparison with HT groups significantly. Olmesartan improved left ventricular function and hypertrophy through the increase of the ACE2 mRNA and decrease of both angiotensin II and ERK mRNA in pressure-overload rat heart. PMID:19171689

Kaiqiang Ji; Minakawa, Masahito; Fukui, Kozo; Suzuki, Yasuyuki; Fukuda, Ikuo

2009-01-26

319

Left Ventricular Mass and Hypertrophy by Echocardiography and Cardiac Magnetic Resonance: The Multi-Ethnic Study of Atherosclerosis.  

UK PubMed Central (United Kingdom)

BACKGROUND: Left ventricular mass (LVM) and hypertrophy (LVH) are important parameters, but their use is surrounded by controversies. We compare LVM by echocardiography and cardiac magnetic resonance (CMR), investigating reproducibility aspects and the effect of echocardiography image quality. We also compare indexing methods within and between imaging modalities for classification of LVH and cardiovascular risk. METHODS: Multi-Ethnic Study of Atherosclerosis enrolled 880 participants in Baltimore city, 146 had echocardiograms and CMR on the same day. LVM was then assessed using standard techniques. Echocardiography image quality was rated (good/limited) according to the parasternal view. LVH was defined after indexing LVM to body surface area, height(1.7) , height(2.7) , or by the predicted LVM from a reference group. Participants were classified for cardiovascular risk according to Framingham score. Pearson's correlation, Bland-Altman plots, percent agreement, and kappa coefficient assessed agreement within and between modalities. RESULTS: Left ventricular mass by echocardiography (140 ± 40 g) and by CMR were correlated (r = 0.8, P < 0.001) regardless of the echocardiography image quality. The reproducibility profile had strong correlations and agreement for both modalities. Image quality groups had similar characteristics; those with good images compared to CMR slightly superiorly. The prevalence of LVH tended to be higher with higher cardiovascular risk. The agreement for LVH between imaging modalities ranged from 77% to 98% and the kappa coefficient from 0.10 to 0.76. CONCLUSIONS: Echocardiography has a reliable performance for LVM assessment and classification of LVH, with limited influence of image quality. Echocardiography and CMR differ in the assessment of LVH, and additional differences rise from the indexing methods.

Armstrong AC; Gjesdal O; Almeida A; Nacif M; Wu C; Bluemke DA; Brumback L; Lima JA

2013-08-01

320

High risk blood pressure and obesity increase the risk for left ventricular hypertrophy in African-American adolescents.  

UK PubMed Central (United Kingdom)

OBJECTIVE: To examine the relative effects of high blood pressure (HBP) and obesity on left ventricular mass (LVM) among African-American adolescents; and if metabolic or inflammatory factors contribute to LVM. STUDY DESIGN: Using a 2 × 2 design, African-American adolescents were stratified by body mass index percentile (body mass index <95th percentile = non-obese; ? 95th percentile = obese) and average blood pressure (BP) (normal BP <120/80 mm Hg; HBP ? 120/80). Glucose, insulin, insulin resistance, lipids, and inflammatory cytokines were measured. From echocardiography measures of LVM, calculated LVM index (LVMI) ? 95th percentile defined left ventricular hypertrophy (LVH). RESULTS: Data included 301 adolescents (48% female), mean age 16.2 years, 51% obese, and 29% HBP. LVMI was highest among adolescents with both obesity and HBP. The multiplicative interaction of obesity and HBP on LVH was not significant (OR = 2.35, P = .20) but the independent additive associations of obesity and HBP with log-odds of LVH were significant; obesity OR = 3.26, P < .001; HBP OR = 2.92, P < .001. Metabolic and inflammatory risk factors were associated with obesity, but had no independent association with LVMI. Compared with those with average systolic BP (SBP) <75th percentile, adolescents with SBP from the 75th percentile to 90th percentile had higher LVMI (33.2 vs 38.7 g/m(2.7), P < .001) and greater LVH (18% vs 43%, P < .001), independent of obesity. CONCLUSIONS: Prevalence of LVH is highest among African-American adolescents with average BP ? 120/80 mm Hg and obesity. There also is an independent association of LVMI with BP, beginning at the 75th SBP percentile.

Falkner B; DeLoach S; Keith SW; Gidding SS

2013-01-01

 
 
 
 
321

Relation between abdominal obesity, insulin resistance and left ventricular hypertrophy diagnosed by electrocardiogram and magnetic resonance imaging in hypertensive patients.  

UK PubMed Central (United Kingdom)

Obesity is related to left ventricular hypertrophy (LVH). Whether LVH on electrocardiography (ECG-LVH) is a result of increased cardiac electrical activity or due to increased left ventricular mass (LVM) remains to be determined. The aims of the present study were to investigate the relation between obesity and ECG-LVH and LVM by magnetic resonance imaging (MRI-LVM) in patients with hypertension and to investigate the relation of insulin resistance (IR) and LVH. Patients with hypertension (n = 421) were evaluated using Sokolow-Lyon voltage, Cornell voltage, and cardiac magnetic resonance imaging. Waist circumference was used as a measure of abdominal obesity. Linear regression analysis revealed an inverse relation (adjusted ? = -0.02, 95% confidence interval -0.02 to -0.01) between waist circumference and Sokolow-Lyon voltage, indicating a decrease of 0.02 mV per 1-cm increase in waist circumference. There was a positive relation between waist circumference and MRI-LVM (? = 0.49, 95% confidence interval 0.32 to 0.67). Patients in the highest quartile of LVM had a worse metabolic profile than patients with the Sokolow-Lyon voltage criterion. The relations of IR with ECG-LVH and MRI-LVM were similar to those of waist circumference in relation to ECG-LVH and MRI-LVM. In conclusion, there is an inverse relation between waist circumference and ECG-LVH and a positive relation between waist circumference and MRI-LVM. This study indicates that obesity has a different relation to voltage criteria for LVH compared to anatomic criteria for LVH, supporting the hypothesis that IR decreases electrocardiographic voltages, despite an increase in MRI-LVM. The clinical implication is that especially in patients with IR, Sokolow-Lyon voltage is low in contrast to high MRI-LVM.

Vernooij JW; Cramer MJ; Visseren FL; Korndewal MJ; Bots ML; Meijs MF; Doevendans PA; Spiering W

2012-07-01

322

Relation between abdominal obesity, insulin resistance and left ventricular hypertrophy diagnosed by electrocardiogram and magnetic resonance imaging in hypertensive patients.  

Science.gov (United States)

Obesity is related to left ventricular hypertrophy (LVH). Whether LVH on electrocardiography (ECG-LVH) is a result of increased cardiac electrical activity or due to increased left ventricular mass (LVM) remains to be determined. The aims of the present study were to investigate the relation between obesity and ECG-LVH and LVM by magnetic resonance imaging (MRI-LVM) in patients with hypertension and to investigate the relation of insulin resistance (IR) and LVH. Patients with hypertension (n = 421) were evaluated using Sokolow-Lyon voltage, Cornell voltage, and cardiac magnetic resonance imaging. Waist circumference was used as a measure of abdominal obesity. Linear regression analysis revealed an inverse relation (adjusted ? = -0.02, 95% confidence interval -0.02 to -0.01) between waist circumference and Sokolow-Lyon voltage, indicating a decrease of 0.02 mV per 1-cm increase in waist circumference. There was a positive relation between waist circumference and MRI-LVM (? = 0.49, 95% confidence interval 0.32 to 0.67). Patients in the highest quartile of LVM had a worse metabolic profile than patients with the Sokolow-Lyon voltage criterion. The relations of IR with ECG-LVH and MRI-LVM were similar to those of waist circumference in relation to ECG-LVH and MRI-LVM. In conclusion, there is an inverse relation between waist circumference and ECG-LVH and a positive relation between waist circumference and MRI-LVM. This study indicates that obesity has a different relation to voltage criteria for LVH compared to anatomic criteria for LVH, supporting the hypothesis that IR decreases electrocardiographic voltages, despite an increase in MRI-LVM. The clinical implication is that especially in patients with IR, Sokolow-Lyon voltage is low in contrast to high MRI-LVM. PMID:22483385

Vernooij, Joris W P; Cramer, Maarten J M; Visseren, Frank L J; Korndewal, Marjolein J; Bots, Michiel L; Meijs, Matthijs F L; Doevendans, Pieter A F M; Spiering, Wilko

2012-04-05

323

Typical coronary appearance of dilated cardiomyopathy versus left ventricular concentric hypertrophy: coronary volumes measured by multislice computed tomography.  

UK PubMed Central (United Kingdom)

Several coronary angiographic studies have reported that enlarged and tortuous epicardial coronary arteries are characteristic of patients with left ventricular concentric hypertrophy (LVCH). Recently, we showed that small volumes opacified by contrast medium can be accurately measured by 64-multislice computed tomography (MSCT) and that there is a direct relationship between the coronary artery volume and left ventricular (LV) mass. However, the relationship of coronary artery volume with LV mass in patients with dilated cardiomyopathy (DCM) is unknown. The present study was designed to investigate this issue. Thirteen patients with DCM and 18 patients with LVCH who underwent MSCT angiography were included in this analysis. The coronary arteries were segmented on a workstation, and the appropriate window settings obtained from the results of the phantom experiments were applied to the volume-rendered images to calculate the total coronary artery volume (right and left coronary arteries). The absolute coronary lengths and volumes in patients with LVCH and DCM were greater than those in controls. The coronary artery volumes adjusted for LV mass in patients with DCM were found to be smaller than those in patients with LVCH or in controls, and these values did not differ between patients with LVCH and controls (DCM 4.1 ± 0.9, LVCH 5.4 ± 1.4, controls 5.5 ± 2.3 ml/100 g of LV mass, P < 0.005; DCM vs LVCH, P < 0.01; and DCM vs control, P < 0.0005). This study showed that the increase in the coronary artery volume in patients with LVCH matched the increase in LV mass, but a decreased coronary volume with regard to LV mass was characteristic of patients with DCM.

Ehara S; Matsumoto K; Shirai N; Nakanishi K; Otsuka K; Iguchi T; Hasegawa T; Nakata S; Yoshikawa J; Yoshiyama M

2013-03-01

324

Local renin-angiotensin system regulates left ventricular hypertrophy induced by swimming training independent of circulating renin: a pharmacological study.  

UK PubMed Central (United Kingdom)

INTRODUCTION: This study addressed the role of the local renin-angiotensin system (RAS) in the left ventricular hypertrophy (LVH) induced by swimming training using pharmacological blockade. MATERIALS AND METHODS: Female Wistar rats treated with enalapril maleate (60 mg.kg(-1).d( -1), n=38), losartan (20 mg.kg(-1).d(-1), n=36) or high salt diet (1% NaCl, n=38) were trained by two protocols (T1: 60-min swimming session, 5 days per week for 10 weeks and T2: the same T1 protocol until the 8(th) week, then 9(th) week they trained twice a day and 10(th) week they trained three times a day). Salt loading prevented activation of the systemic RAS. Haemodynamic parameters, soleus citrate synthase (SCS) activity and LVH (left ventricular/body weight ratio, mg/g) were evaluated. RESULTS: Resting heart rate decreased in all trained groups. SCS activity increased 41% and 106% in T1 andT2 groups, respectively. LVH was 20% and 30% in T1 andT2 groups, respectively. Enalapril prevented 39% of the LVH in T2 group (p<0.05). Losartan prevented 41% in T1 and 50% inT2 (p<0.05) of the LVH in trained groups. Plasma renin activity (PRA) was inhibited in all salt groups and it was increased in T2 group. CONCLUSIONS: These data provide evidence that the physiological LVH induced by swimming training is regulated by local RAS independent from the systemic, because the hypertrophic response was maintained even when PRA was inhibited by chronic salt loading. However, other systems can contribute to this process.

Oliveira EM; Sasaki MS; Cerêncio M; Baraúna VG; Krieger JE

2009-03-01

325

Renal insufficiency in non-diabetic subjects: relationship of MTHFR C677t gene polymorphism and left ventricular hypertrophy.  

UK PubMed Central (United Kingdom)

BACKGROUND: Association of methylenetetrahydrofolate reductase (MTHFR) 677C>T gene polymorphism with hyperhomocysteinemia, renal failure, and cardiovascular events is controversial. We investigated the relationship of MTHFR 677C>T polymorphisms with left ventricular hypertrophy (LVH) and renal insufficiency. METHODS: Glomerular filtration rate (GFR) and left myocardial ventricular mass/m2 were assessed in 138 non-diabetic subjects (age, 50.93 ± 14.85 years; body mass index, 27.95 ± 5.98 kg/m(2)), 38 no-mutation wild MTHFR C677CC, 52 heterozygous MTHFR C677CT, and 48 homozygous MTHFR C677TT, all with adequate adherence to current international healthy dietary guidelines. Serum homocysteine, insulin resistance, high-sensitivity C-reactive-protein (hsCRP), parathyroid hormone, and renal artery resistive index (RRI) were challenged by odds ratio analysis and multiple linear regression models. RESULTS: MTHFR 677C>T polymorphism showed higher GFR (73.8 ± 27.99 vs. 58.64 ± 29.95; p= 0.001) and lower renal failure odds (OR, 0.443; 95% confidence interval, 0.141-1.387) in comparison with wild MTHFR genotype. A favorable effect on GFR of MTHFR polymorphism is presented independently by the negative effects of LVH, increased intra-renal arterial resistance, and hyperparathyroidism; GFR is the significant predictive factor to LVH. CONCLUSIONS: Renal insufficiency in non-diabetic subjects is explained by interactions of MTHFR C677T polymorphism mutation with LVH, hsCRP, intact parathyroid hormone (iPTH), and RRI. Sign of these predictive effects is opposite: subjects with MTHFR 677C>T polymorphism have lower likelihood of renal insufficiency; differently, wild-type MTHFR genotype subjects have lower GFR and greater hsCRP, iPTH, RRI, and LVH.

Trovato GM; Catalano D; Ragusa A; Martines GF; Tonzuso A; Pirri C; Buccheri MA; Di Nora C; Trovato FM

2013-01-01

326

Effect of hypertrophy on left ventricular diastolic function in patients with hypertrophic cardiomyopathy  

Directory of Open Access Journals (Sweden)

Full Text Available Background. Hypertrophic cardiomyopathy (HCM) is characterized by asymmetric LV hypertrophy (LVH) and impairment in diastolic function. We assess the relationship between LVH and invasive indexes of diastolic function. Methods. 21 HCM patients underwent cardiac catheterization to assess pulmonary capillary wedge pressure, LV end-diastolic pressure (measured by microtip catheters), and LV volumes (calculated by simultaneous radionuclide angiography). We calculated from LV pressure the time constant of isovolumetric relaxation (?, variable asymptote method, ms), and from LV pressure and volume the constant of chamber stiffness (k, ml-1). LVH was assessed by different indexes: maximal wall thickness, number of hypertrophied LV segments, LVH index, and Wigle’s score. Results. Wigle’s score was directly related to pulmonary capillary Wedge pressure (r=0.436, p=0.048), peak V wave of pulmonary capillary wedge pressure (r=0.503, p=0.024), LV end-diastolic pressure (r=0.643, p=0.002) and k (r=0.564, p=0.015). HCM patients were divided into 2 groups according to Wigle’s score: 10 with mild or moderate LVH (< 8), and 11 with severe LVH (? 8). HCM patients with severe LVH showed a higher pulmonary capillary Wedge pressure (15.1±7.2 vs 9.5±2.4, p=0.033), peak V wave of pulmonary capillary wedge pressure (20.7±4.6 vs 14.6±4.9, p=0.011), LV end-diastolic pressure (23.9±10.9 vs 10.6±2.5, p=0.002), k (0.0465±0.032 vs 0.015±0.007, p=0.022) and LV outflow tract gradient (72±36 mmHg vs 29±30 mmHg, p=0.01). ? was similar in the two groups. Other indexes of LVH were not related to diastolic function. Conclusions. Wigle’s score is the only index of LVH that relates to invasive indices of diastolic function.

Quirino Ciampi; Sandro Betocchi; Maria Angela Losi; Raffaella Lombardi; Bruno Villari; Massimo Chiariello

2006-01-01

327

Effect of hypertrophy on left ventricular diastolic function in patients with hypertrophic cardiomyopathy  

Directory of Open Access Journals (Sweden)

Full Text Available Background. Hypertrophic cardiomyopathy (HCM) is characterized by asymmetric LV hypertrophy (LVH) and impairment in diastolic function. We assess the relationship between LVH and invasive indexes of diastolic function. Methods. 21 HCM patients underwent cardiac catheterization to assess pulmonary capillary wedge pressure, LV end-diastolic pressure (measured by microtip catheters), and LV volumes (calculated by simultaneous radionuclide angiography). We calculated from LV pressure the time constant of isovolumetric relaxation (?, variable asymptote method, ms), and from LV pressure and volume the constant of chamber stiffness (k, ml-1). LVH was assessed by different indexes: maximal wall thickness, number of hypertrophied LV segments, LVH index, and Wigle’s score. Results. Wigle’s score was directly related to pulmonary capillary Wedge pressure (r=0.436, p=0.048), peak V wave of pulmonary capillary wedge pressure (r=0.503, p=0.024), LV end-diastolic pressure (r=0.643, p=0.002) and k (r=0.564, p=0.015). HCM patients were divided into 2 groups according to Wigle’s score: 10 with mild or moderate LVH (< 8), and 11 with severe LVH (? 8). HCM patients with severe LVH showed a higher pulmonary capillary Wedge pressure (15.1±7.2 vs 9.5±2.4, p=0.033), peak V wave of pulmonary capillary wedge pressure (20.7±4.6 vs 14.6±4.9, p=0.011), LV end-diastolic pressure (23.9±10.9 vs 10.6±2.5, p=0.002), k (0.0465±0.032 vs 0.015±0.007, p=0.022) and LV outflow tract gradient (72±36 mmHg vs 29±30 mmHg, p=0.01). ? was similar in the two groups. Other indexes of LVH were not related to diastolic function. Conclusions. Wigle’s score is the only index of LVH that relates to invasive indices of diastolic function.

Quirino Ciampi; Sandro Betocchi; Maria Angela Losi; Raffaella Lombardi; Bruno Villari; Massimo Chiariello

2010-01-01

328

[Cardiac morphology and performance alterations and analysis of determinant factors of left ventricular hypertrophy in 40 patients with acromegaly].  

UK PubMed Central (United Kingdom)

Acromegaly has a high mortality rate due mainly to cardiovascular complications. The aim was to evaluate the determinant factors of left ventricular hypertrophy (LVH) and cardiac alterations in 40 acromegalic patients submitted to clinical-laboratorial studies and echocardiogram. The variables analyzed were age, sex, disease duration, arterial hypertension (AH),