Hypertrophy, Hyperplasia and Structural Dilatation of the Human Heart

Abstract

The human heart can exceed the critical heart weight of 500 g in the course of pathological structural adaptation. This abnormal growth is performed not only by an increase in size (hypertrophy) but also in number (hyperplasia) of cardiac muscle cells. Coronary insufficiency, dilatation and chronic heart failure are noted frequently in hearts above this critical heart weight. Chronic heart failure is not a direct consequence of local destruction and scar formation following coronary insufficiency. Unlike acute cardiac dilatation with failure, chronic dilatation is not associated with stretching or overstretching of cardiac muscle cells. Starling's law is not applicable for explaining heart failure in these chronic cases. Chronic dilatation is a structural dilatation (Gefugedilatation) produced by sliding displacements (slippage) of heart muscle cells leading to a decrease in the number of muscle layers in the ventricular wall. Chronic heart failure in man therefore is rather a physical consequence of structural dilatation which severely impairs the working conditions, the efficiency and the effectiveness of the heart muscle cells than an immediate result of coronary insufficiency of inflammation with local metabolic alterations, which, of course, additionally impair the quality of the myocardium and the conducting system.

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