Role of actin and myosin in the mechanism of the decrease of myocardial contractility and efficiency of energy transformation by myocardial myofibrils in chronic heart failure in humans.

Experiments with hybrid myocardial fibers showed that abnormalities of actin (basic protein of fine sarcomer threads) are responsible for reduced contraction rate, decreased developed force, and low efficiency of cardiomyocyte contraction in chronic heart failure caused by dilatation and ischemic cardiomyopathies and infective allergic myocarditis. Wastefulness of the contractile process in cardiomyocyte under conditions of pronounced energy deficit play a key role in progression of chronic heart failure. Hence, actin hypothesis of reduced contractile activity of myocardial contractile protein system in acute heart failure transforms into the actomyosin concept in chronic heart failure.