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Hypertrophy, hyperplasia and structural dilatation of the human heart
Insights
Pathological heart growth, exceeding 500g, involves cardiac muscle cell hypertrophy and hyperplasia. Chronic heart failure results from structural dilatation, not coronary insufficiency, impairing heart muscle cell function.
Area of Science:
- Cardiology
- Pathology
- Physiology
Background:
- Pathological heart growth can exceed a critical weight of 500g.
- Abnormal cardiac growth involves both cardiac muscle cell hypertrophy (size increase) and hyperplasia (number increase).
- Hearts exceeding this weight often exhibit coronary insufficiency, dilatation, and chronic heart failure.
Purpose of the Study:
- To investigate the mechanisms underlying chronic heart failure in enlarged human hearts.
- To differentiate the causes of chronic heart failure from acute cardiac events.
- To re-evaluate the applicability of Starling's law in chronic heart failure.
Main Methods:
- Analysis of pathological structural adaptation in human hearts exceeding critical weight.
- Comparison of mechanisms in acute versus chronic cardiac dilatation and failure.
- Examination of cellular and structural changes in the ventricular wall.
Main Results:
- Chronic heart failure is not a direct result of coronary insufficiency or scar formation.
- Chronic cardiac dilatation does not involve stretching or overstretching of cardiac muscle cells.
- Structural dilatation (Gefugedilatation) due to muscle cell slippage decreases ventricular wall muscle layers, impairing heart function.
Conclusions:
- Chronic heart failure in humans is primarily a physical consequence of structural dilatation.
- The slippage of cardiac muscle cells impairs the working conditions and efficiency of the heart.
- Starling's law is not applicable to explaining heart failure in these chronic structural dilatation cases.
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.