Key result
Hypertrophied human ventricles lose the small baseline ~15% V1 myosin fraction without altering ATPase activity.
Why the study?
The regulation of cardiac contractility by changes in myosin isomyosin composition in volume overload and its relevance in human hypertrophied hearts was unclear.
Population
Rat hearts with chronic volume overload and human left ventricles from normal and valvular disease patients (N=30)
Comparison
Isomyosin composition and mechanical function in normal versus hypertrophied hearts
Design
Experimental measurement of isomyosin composition and mechanical function in rat and human hearts
Authors
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Questions functional relevance of myosin isoform shifts for ATPase in human hypertrophy; leaves open their role in disease progression.
Schwartz et al. (1984) studied Valvular disease and cardiac hypertrophy (n=30). Valvular disease / Cardiac hypertrophy vs. Normal hearts was evaluated on Isomyosin composition and myosin Ca2+-stimulated ATPase activities. Human ventricular myosin is predominantly V3, with small amounts of V1 (1-15%) in normal hearts that are absent in hypertrophied hearts, without significant changes in overall ATPase activity.
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