BACKGROUND: Anthracycline-treated patients (AP) are at risk for cardiac dysfunction years after treatment. Cardiac function has not been evaluated during exercise in AP. The purpose of this study was to assess exercise tolerance, left ventricular (LV) function, and hemodynamics during progressive exercise. PROCEDURE: We studied 47 AP (cumulative dose: 36-504 mg/m(2)) who were in complete remission and 12 healthy controls (CON). AP were further grouped by cumulative dose (LOW <or= 260 mg/m(2); HIGH >or= 260 mg/m(2)) and resting echocardiographic function. All subjects performed 3-min incremental stages on a semi-recumbent cycle ergometer until volitional fatigue. Using echocardiography and Doppler, LV dimensions, posterior wall thickness (LVPWs), peak aortic velocity (PAoV), shortening fraction (SF), rate-corrected mean velocity of fiber shortening (MVCFc), wall stress at peak systole (sigmaPS), stroke volume index (SVI), and cardiac index (CI) were determined. Measurements were performed at rest, during each stage of exercise, and in recovery. RESULTS: AP did less work than CON (P < 0.050). CON and LOW had similar resting function, while HIGH had a lower SF and MVCFc (P < 0.050) and a higher sigmaPS (P < 0.001). Resting SVI and CI were also lower in HIGH. At peak exercise, MVCFc and sigmaPS remained different in HIGH, and both AP groups had a lower SF, SVI, and CI (P < 0.001). AP had an abnormal SVI response to exercise. AP showed a smaller initial increase in SVI that was not maintained throughout exercise. CONCLUSIONS: AP have reduced exercise tolerance. There also appears to be a dose-related effect on myocardial contractility and SVI. These findings may help to guide treatment.
BACKGROUND:Anthracycline-treated patients (AP) are at risk for cardiac dysfunction years after treatment. Cardiac function has not been evaluated during exercise in AP. The purpose of this study was to assess exercise tolerance, left ventricular (LV) function, and hemodynamics during progressive exercise. PROCEDURE: We studied 47 AP (cumulative dose: 36-504 mg/m(2)) who were in complete remission and 12 healthy controls (CON). AP were further grouped by cumulative dose (LOW <or= 260 mg/m(2); HIGH >or= 260 mg/m(2)) and resting echocardiographic function. All subjects performed 3-min incremental stages on a semi-recumbent cycle ergometer until volitional fatigue. Using echocardiography and Doppler, LV dimensions, posterior wall thickness (LVPWs), peak aortic velocity (PAoV), shortening fraction (SF), rate-corrected mean velocity of fiber shortening (MVCFc), wall stress at peak systole (sigmaPS), stroke volume index (SVI), and cardiac index (CI) were determined. Measurements were performed at rest, during each stage of exercise, and in recovery. RESULTS: AP did less work than CON (P < 0.050). CON and LOW had similar resting function, while HIGH had a lower SF and MVCFc (P < 0.050) and a higher sigmaPS (P < 0.001). Resting SVI and CI were also lower in HIGH. At peak exercise, MVCFc and sigmaPS remained different in HIGH, and both AP groups had a lower SF, SVI, and CI (P < 0.001). AP had an abnormal SVI response to exercise. AP showed a smaller initial increase in SVI that was not maintained throughout exercise. CONCLUSIONS: AP have reduced exercise tolerance. There also appears to be a dose-related effect on myocardial contractility and SVI. These findings may help to guide treatment.