Mechanism of hypertrophy of the heart and experimental prevention of acute cardiac insufficiency.

It is known that hyperfunction of the heart arising from cardiac defects, systemic hypertension, pulmonary hypertension, and over activity of non-affected regions of the heart in cardiac infarction, is regularly followed by myocardial hypertrophy, which after a prolonged period not infrequently results in chronic cardiac insufficiency. Thus hyperfunction, hypertrophy, and cardiac insufficiency represent three links of a unique process having a fundamental importance in modem cardiology. The dynamics of structural, biochemical, and physiological alterations constituting this process has already been the object of extensive investigations and has been described in numerous reviews and monographs (Meerson, I960; Sonnenblick, I968; Spann et al., I965; Meerson, I969a, b; Gudbjarnason, Telerman, and Bing, I964; Buchner and Weyland, I968). This allows us to restrict our paper to analysis of the principal mechanism of development of cardiac hypertrophy and to the consequences of the current concept of this mechanism in the prevention of acute cardiac insufficiency in overload of the heart.