Exercise Capacity in Hypertrophic Cardiomyopathy

Background We previously showed that exercise capacity in patients with hypertrophic cardiomyopathy (HCM) is related to peak exercise cardiac output. Cardiac output augmentation during exercise is normally dependent on heart rate (HR) response and stroke volume (SV) augmentation by increased left ventricular end-diastolic volume and/or increased contractility. We hypothesized that in contrast to normal subjects, peak exercise capacity in patients with HCM is determined by the diastolic filling characteristics of the left ventricle during exercise, which would in turn determine the degree to which SV is augmented, and that HR is a relatively unimportant determinant of peak exercise capacity. Methods and Results Twenty-three patients with HCM underwent invasive hemodynamic evaluation and measurement of maximal oxygen consumption (V̇ o 2max ) during erect treadmill exercise to assess the relative importance of changes in HR and SV in determining exercise capacity. Hemodynamic responses to erect and supine exercise were compared in 10 of these patients. In a separate group of 46 patients with HCM, the relation between V̇ o 2max and exercise diastolic filling indexes was assessed. Peak HR during erect exercise was 92±8% of predicted maximum. V̇ o 2max was 29.0±6.4 mL · kg −1 · min −1 and was related significantly to peak exercise cardiac index and SV index ( r =.71, P <.0001 and r =.66, P =.001, respectively) but not to peak HR, HR deficit, or resting or peak pulmonary capillary wedge pressure. Peak cardiac output during erect exercise was not related to peak HR ( r =.13, P =NS). When erect and supine exercise were compared, peak HR was lower in the supine position (153.3±19.9 beats per minute supine versus 172.0±17.6 beats per minute erect, P =.003), but peak exercise cardiac index was similar (7.9±2.6 L · min −1 · m −2 supine versus 7.5±2.8 L · min −1 · m −2 erect). Pulmonary capillary wedge pressure was higher at rest in the supine versus erect position (15.3±5.2 versus 8.1±6.1 mm Hg) but was not significantly higher at peak exercise in the supine versus erect position (28.5±8 versus 22.4±11.6 mm Hg erect, P =NS). In the separate group of 46 patients with HCM, V̇ o 2max was significantly inversely related to time to peak filling at peak exercise ( r =−.60, P <.0001) but did not correlate with time to peak filling at rest, resting ejection fraction, peak filling rate, or peak exercise peak filling rate. Conclusions SV is the major determinant of peak exercise capacity in the erect position in patients with hypertrophic cardiomyopathy. This in turn is determined by the exercise left ventricular diastolic filling characteristics. HR augmentation does not appear to be a major determinant of peak cardiac output in the erect position.