Remodeling of Cardiac Myocytes in Chronic Heart Disease
Congestive heart failure is generally characterized by a dilated, relatively thin-walled ventricle. Isolated myocyte data obtained from failing explanted human hearts with and without ischemic disease indicate that alterations in cell shape may be largely, if not exclusively, responsible for this anatomical change. Specifically, myocyte length and length: width ratio are significantly increased. The increase in myocyte length: width ratio, the cellular analogue of chamber diameter: wall thickness, is clearly maladaptive, since this parameter is normally maintained within a very narrow range. Though cell lengthening appears to be the cause of chamber dilation, stunted or arrested growth of the myocyte transverse area may be the underlying cellular defect. Data from humans and animal experiments suggest that transverse growth may be arrested at a relatively normal level in nonhypertensives with heart failure. In hypertensives, the maladaptive increase in myocyte length may begin after transverse growth reaches an upper limit of approximately 350–400 μm2. Understanding the molecular basis of maladaptive myocyte growth may lead to newer and more effective therapies in the treatment and prevention of heart failure.
KeywordsCardiac Hypertrophy Cardiac Myocyte Aortocaval Fistula Systolic Wall Stress Myocyte Size
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