Cardiac adaptation and its limitation in an experimental model of congestive heart failure

To elucidate mechanisms of adaptation and maladaptation in heart failure, abnormalities of left ventricular function and their relationships to myocardial contractile protein were studied in the Syrian hamster Bio 14.6. Left ventricular and heart weights were both increased in 20-week-old cardiomyopathic hamsters, indicating cardiac hypertrophy as a compensatory mechanism to the disease process of cardiomyopathy. However further increase in the left ventricular weight was not observed in older (40-week-old) cardiomyopathic hamsters. On the other hand left ventricular volume and volume/mass ratio were increased progressively. Correspondingly, V3 type myosin was increased and myosin sliding velocity was decreased. Left ventricular function of cardiomyopathic hamsters evaluated using an isovolumically beating perfused heart preparation was depressed, and this functional impairment was also progressive. Chronic administration of metoprolol, a beta-blocking agent, induced further increase in left ventricular volume and mass without changing left ventricular function and myosin isozyme pattern. Thus in cardiomyopathic hamsters, left ventricular function progressively deteriorates in spite of a variety of adaptive mechanisms, and remodeling occurs.