[Cardiomyopathy in the Syrian hamster. Physiological and therapeutic aspects]

The primary hereditary cardiomyopathy of the Syrian hamster is a particularly interesting model of experimental cardiomyopathy 1) because of its slow progression to cardiac failure unlike acute experimental volume and pressure overloading; 2) because of the reproducibility and predictable nature of the mechanical, biochemical and electrophysiological abnormalities observed at each stage of the disease; 3) because of involvement of other muscle groups, and particularly, skeletal muscle. The physiopathology is not fully understood but a disturbance of intracellular calcium homeostasis appears to play a major role. From the therapeutic point of view, a number of calcium antagonists have been shown to be effective in restoring myocardial function, but they have no effect on skeletal muscular lesions. Recently, early prophylactic intervention with therapeutic doses of perindopril has been shown to prevent the decrease of certain parameters of myocardial contractility in vitro in the dilated group, before the appearance of any signs of cardiac failure. This study also showed that angiotensin converting enzyme inhibitors had no intrinsic negative inotropic effects.