Cardiac Hypertrophy

Myocardial ischemia is a condition in which the blood flow to the heart is diminished and thus the supply of oxygen and nutrients to the heart is reduced. The reperfusion to an ischemic myocardium often results in induction of infarction and cardiac dysfunction. The brief episodes of ischemia and reperfusion given before prolonged ischemia and reperfusion denotes ischemic preconditioning, which protects the heart from lethal ischemia–reperfusion injury. However, it is intriguing to note that the cardioprotective effect of preconditioning is suppressed in some pathological conditions such as hypercholesterolemia, hyperglycemia, hypertension, cardiac hypertrophy, aging, obesity and hyperhomocysteinemia. In this review, we have critically discussed the possible mechanisms involved in the modulation of cardioprotective potential of ischemic preconditioning in various pathological conditions.

bc ,g g , * ¨ Abstract Objective: Left ventricular assist devices (LVAD) are used to 'bridge' patients with end-stage heart failure to transplantation. After long-term LVAD support, ventricular function may partially recover, a process called 'reverse remodeling'. As several kinase-mediated signal transduction pathways have been implicated in the development of cardiac hypertrophy and failure, we examined the activities of the Erks, MEKs, Akt, GSK-3b, p70S6K, JNKs and p38 under LVAD support as well as during single myocyte strain and whole heart stretch. Methods: Western blotting and immunohistochemistry were performed using phospho-specific antibodies in matched samples from ten patients with end-stage heart failure before and after LVAD. Cyclic strain was performed in rat neonatal cardiac myocytes, and tensile stretch applied to Langendorff-perfused mouse hearts via a left ventricular balloon. Results: The activity of Erks and Akt in failing hearts dramatically...

Angiotensin (Ang)-(1-7) attenuates the development of heart failure. In addition to its local effects on cardiovascular tissue, Ang-(1-7) also stimulates bone marrow, which harbors cells that might complement the therapeutic effect of Ang-(1-7). We studied the effects of Ang-(1-7) either produced locally in the heart or subcutaneously injected during the development of heart failure induced by myocardial infarction (MI) and explored the role of cardiovascular progenitor cells in promoting the effects of this heptapeptide. Effects of Ang-(1-7) on bone marrow-derived mononuclear cells in rodents, particularly endothelial progenitor cells, were investigated in vitro and in vivo in rats, in mice deficient for the putative Ang-(1-7) receptor Mas, and in mice overexpressing Ang-(1-7) exclusively in the heart. Three weeks after MI induction through permanent coronary artery occlusion, effects of Ang-(1-7) either produced locally in the heart or injected into the subcutaneous space were inv...

Background: Hypertrophic cardiomyopathy (HCM) is a genetic disorder with the prevalence
of 1 in 500 globally. HCM is clinically characterized by thickening of the wall of the heart,
predominantly left ventricle (LV), and interventricular septum (IVS). Our study aims to report
the demographical, clinical and genetic profile of Indian HCM patients. Methods: HCM
patients were recruited on the basis of WHO criteria. The clinical phenotypes were analyzed
using electrocardiography, two-dimensional electrocardiography, and hotspot region of ...

End-stage renal disease patients are at a heightened risk of developing cardiovascular disease, with contributions from both “traditional” and “nontraditional” cardiovascular risk factors. Some of the nontraditional risk factors, such as extracellular volume overload, inflammation, and hyperphosphatemia, have also been shown to be important predictors of mortality in the dialysis population. This article provides an in-depth review of the evidence that supports the substantial contributions of nontraditional risk factors to adverse cardiovascular outcomes in chronic peritoneal dialysis patients. In addition, it provides evidence to demonstrate how loss of residual renal function may be central to the development of cardiovascular disease in the peritoneal dialysis population.

Heart rate varies with respiration, blood pressure, emotion, etc., and heart rate variability (HRV) is presently one of the best indices to predict fatal issues in cardiac failure and after myocardial infarction. HRV depends on various reflexes. In addition, parallel studies of HRV and the myocardial adrenergic and muscarinic transduction system in experimental models of cardiac hypertrophy (CH) have suggested that the myocardial phenotype at the sinus-node level may also play a role. A transgenic strain of mice with atrial overexpression of the 677-1 receptors was generated with attenuated HRV, which demonstrates that the phenotype itself is a determinant of HRV. HRV is explored by noninvasive techniques, including simple determination of the standard error of the mean, time-domain analysis, and Fourier transformation. We recently developed a time and frequency domain method of analysis, the smoothed pseudo-Wigner-Ville transformation, which allows better exploration of nonstationarity. Nonlinear methods have also been applied due to the extreme complexity of the biological determinants, and have provided evidence of a chaotic attractor in certain conditions. It is proposed that in steady state a very simple process, which is not completely deterministic, could better explain intermit interval regulations than chaotic behavior. In contrast, under extreme circumstances the regulation proceeds using chaotic behavior. Arrhythmias and HRV can be quantitated in 16-month-old unanesthetized spontaneously hypertensive rats (SHR). Ventricular premature beats are more frequent in SHR than in age-matched controls; they disappear after converting enzyme inhibition (CEI) relative to the reduction of both cardiac hypertrophy and ventricular fibrosis. HRV is attenuated in SHR, as it is in compensatory CH in humans. When CH is prevented, HRV returns to normal. CEI is therefore antiarrhythmic. Another pharmacological application of this concept concerns the bradycardic agents that may improve HRV.

Emerging evidence shows that ErbB2 signaling has a critical role in cardiomyocyte physiology, based mainly on findings that blocking ErbB2 for cancer therapy is toxic to cardiac cells. However, consequences of high levels of ErbB2 activity in the heart have not been previously explored. We investigated consequences of cardiac-restricted over-expression of ErbB2 in two novel lines of transgenic mice. Both lines develop striking concentric cardiac hypertrophy, without heart failure or decreased life span. ErbB2 transgenic mice display electrocardiographic characteristics similar to those found in patients with Hypertrophic Cardiomyopathy, with susceptibility to adrenergic-induced arrhythmias. The hypertrophic hearts, which are 2-3 times larger than those of control littermates, express increased atrial natriuretic peptide and β-myosin heavy chain mRNA, consistent with a hypertrophic phenotype. Cardiomyocytes in these hearts are significantly larger than wild type cardiomyocytes, with ...