Size dependence of the end-systolic stress/volume ratio in humans: Implications for the evaluation of myocardial contractile performance in pressure and volume overload

Abstract

The end-systolic stress/volume ratio is currently recognized as a relatively load-independent index of myocardial contractile performance, but its dependence on ventricular size may limit its value for interpatient comparisons. In this study, the relation between the end-systolic stress/volume ratio and left ventricular end-diastolic volume was anglegraphically analyzed in 104 patients with normal coronary angiograms. Eighteen patients had a normal ventricle, 24 had aortic stenosis, 18 had aortic regurgitation, 9 had mitral regurgitation and 35 had cardiomyopathy.An inverse relation between the end-systolic stress/ volume ratio and left ventricular end-diastolic volume was demonstrated in the normal group (r = 0.72, p < 0.001); subjects with a larger left ventricle had a reduced index but, presumably, the same degree of contractility as that of subjects with a smaller ventricle. Attempts to normalize values by using end-diastolic volume or body surface area were unsuccessful. A similar inverse relation was demonstrated in the aortic stenosis group (r = 0.48, p < 0.05), probably because hypertrophy helps to keep wall stress normal or low despite progressive ventricular enlargement in these patients. The end-systolic stress/volume ratio was also inversely related to left ventricular chamber size in patients with volume overload due to aortic regurgitation (r = 0.80, p < 0.001) and in those with cardiomyopathy (r = 0.84, p < 0.001). However, at a given left ventricular end-diastolic volume, the end-systolic stress/volume ratio was higher in patients with aortic regurgitation than in those with cardiomyopathy, suggesting better contractile performance for a comparable degree of ventricular dilation. Finally, patients with aortic stenosis and cardiomyopathy with comparable end-diastolic volumes had similar end-systolic ratios.These data provide evidence that the end-systolic stress/ volume ratio is highly dependent on the size of the left ventricular chamber in humans and that this dependence differs according to the nature of the underlying myocardial disease.