Chronic cardiac reactions. II. Mechanical and energetic consequences of myocardial transformation versus ventricular dilatation in the chronically pressure-loaded heart.

Mechanical and energetic consequences of myocardial transformation and of ventricular configuration on the other were separately analysed. The considerations were realized on representative samples of normotensive rats and spontaneously hypertensive rats (SHR) in compensated stages, as well as in SHR in a state of congestive cardiac failure. Cardiac dynamic measurements were performed under Urethane anaesthesia and open chest conditions. Myosin isoenzyme pattern was determined by pyrophosphate gel electrophoresis. Energetic calculations were based on oxygen consumption data, measured in a specified heart-lung model. In the compensated stage of SHR the concentric type of left ventricular hypertrophy with renormalized systolic auxotonic wall stress predominated. The process of cardiac hypertrophy was associated with a shift in the myosin isoenzyme pattern towards the "slow" VM-3. Myocardial transformation did not significantly reduce myocardial performance and pumping ability, but caused a decrease in oxygen consumption as related to developed stress and LV weight. Thus, the efficiency of the hypertrophied ventricle of SHR was improved. However, due to the moderate effect of isoenzyme pattern redistribution for total energy turnover and the limited adaptive reserve of normotensive controls, the extent of improvement was small. In SHR with congestive heart failure, myocardial contractility was severely impaired, when structural dilatation of the left ventricle had set in. Reduced myocardial contractility could not be explained solely on the basis of a shift in the myosin isoenzyme pattern. Both impaired myocardial contractility and structural dilatation contributed to reduced ventricular performance. Myocardial transformation, along with its energy economizing effect, failed to compensate for unfavorable energetic consequences of structural dilatation and therefore the reduced ventricular efficiency is assumed to be another deleterious factor in the dilated failing heart.