Relation of "inotropic reserve" to functional capacity in heart failure secondary to ischemic or nonischemic cardiomyopathy.

Exercise capacity in patients with dilated cardiomyopathy, measured by peak oxygen consumption (VO(2)) during exercise, has virtually no relation to resting left ventricular (LV) function. We hypothesized that exercise-induced inotropic reserve may explain some of the variation between peak VO(2) and resting LV function. Treadmill stress echocardiography was performed simultaneously with peak VO(2) measurements in 35 patients with dilated cardiomyopathy. Resting and immediate postexercise echocardiographic images were scored for change in segmental contractility using the American Society of Echocardiography 16-segment system. Segment scores were summed and divided by 16 to determine the wall motion index. Right ventricular (RV) function was quantified on a 4-point scale. Patients had a mean age of 52 +/- 12 years (8 women) and a mean ejection fraction of 30 +/- 10 (25 nonischemic patients). Average peak VO(2) was 17.0 +/- 6 ml/kg/min. Patients were divided into 2 groups by peak VO(2): a high VO(2) group, >17 ml/kg/min (17 patients) and a low VO(2) group, < or =17 ml/kg/min (18 patients). LV ejection fraction was similar between the high and low VO(2) groups (31 +/- 9% vs 28 +/- 11%, p = NS) as were etiology of heart failure, medications used, and LV volume. In the high VO(2) group, wall motion index improved from 2.28 +/- 0.20 to 2.12 +/- 0.31 during exercise (p = 0.009). There was no improvement in the low VO(2) group. Resting RV function was significantly better in the high VO(2) group (1.4 +/- 0.8 vs 0.6 +/- 0.6 p = 0.004). Therefore, in patients with dilated cardiomyopathy and similar resting LV function, the presence of demonstrable LV inotropic reserve and preserved RV function partially account for variation in exercise performance.