Cardiac Contractility and Oxygen Consumption Under Altered Coronary Perfusion

Abstract

Left ventricular contractility and the energetic cost of contraction were assessed in various conditions of altered coronary perfusion in isolated, cross-circulated dog and rabbit hearts utilizing frameworks of Emax (left ventricular contractility index) and pressure—volume area (PVA, a measure of total left ventricular mechanical energy expenditure). PVA has been shown to correlate linearly with myocardial oxygen consumption per beat (Vo2) in a load-independent manner, and the reciprocal of the slope of theVo2-PVA relation is considered to indicate “contractile efficiency” (the energy transduction efficiency from oxygen to total mechanical energy), while the Vo2intercept (PVA-independent Vo2reflects Vo2for nonmechanical activities such as excitation-contraction coupling and basal metabolism. Contractile efficiency was not affected by depressed contractility with mildly decreased coronary perfusion pressure or stunned myocardium, or by enhanced contractility during increased coronary blood flow with adenosine. However, contractile efficiency seemingly increased during severely decreased coronary perfusion pressure, because the Vo2-PVA relation tilted down, probably due to load-dependent depression of Emax. On the other hand, the “oxygen cost of contractility,” the ratio of an increase in PVA-independent Vo2 to an increase in Emax, was higher in stunned myocardium than in normal hearts, suggesting that the energy cost of calcium handling is elevated in stunned myocardium. The oxygen cost of contractility was similar with propranolol treatment, decreased coronary perfusion pressure, or increased coronary blood flow. Furthermore, the “wall tension-regional area” area (TAA), a measure of total mechanical energy of a ventricular region obtained by analogy with PVA, was found to have a highly linear correlation with regional Vo2 in a load-independent manner. Thus, using the frameworks of Emax, PVA, and TAA, we can interconnect ventricular mechanics and energetics and better understand the pathophysiology and pathogenesis of various conditions of altered coronary perfusion.