1016-51 From Myocardial O2 Consumption to Mean Arterial Power — Analysis of Optimal Cardiovascular Performance

Mathematical model and numerical simulation are used to analyze optimal conditions of cardiovascular performance, with an emphasis on the effect of ventricular-arterial (VA) coupling. The following research questions were posed: Does the VA-coupling affect the cardiovascular system (CVS) performance in addition to the direct effects of the left ventricle and of the vascular load? Is there an optimal coupling state? Does the CVS in human subjects, either healthy or diseased, operate with optimal VA-coupling? and finally, is it possible to improve the CVS performance by controlling the VA-coupling? To answer these questions, a clinically oriented integral model of the CVS is introduced, based on the ventricular and arterial elastances. The main advantages of the model are its simplicity and the fact that all its variables can be measured non-invasively in the clinical practice. Traditionally, the optimal state of CVS operation was evaluated by two criteria — the energetic efficiencyof the left ventricle and the efficiency of energy transfer through the vascular system. In the present study a combined criterion of the total energetic efficiency is utilized — from the input metabolic energy consumed by the ventricle to the net energy available to the peripheral tissues. It is found that optimal coupling for maximal global efficiency depends in a complex, non-linear way on all the classical determinants of CVS performance — the preload, the myocardial contractility, the afterload and the heart rate. Response surfaces of the analyzed variables as function of two independent variables were generated by numerical simulation. Based on the analysis of the global efficiency as the optimization criterion, answers to the research questions were found: The VA-coupling affects the CVS performance in addition to the direct effects of its determinants; there is an optimal state of coupling which results in maximal efficiency; the CVS in healthy subject operates in the region of optimal coupling; during stress, changes in the state of coupling result in additional contribution to CVS performance; in patients with left ventricular dysfunction the efficiency is reduced and it further decreases during exercise. The model shows that there is, however, an optimal coupling which improves performance even in cases of severe heart failure. This optimal state can theoretically be approached by titrating the vascular resistance and the end-diastolic volume (the preload) to optimal levels. These results suggest, and lay the theoretical foundation for the notion, that vasodilator drugs can be used to optimize VA-coupling and CVS performance in heart failure patients