Kaplan J D, Foster E, Redberg R F, Schiller N B
John Henry Mills Memorial Adult Echocardiography Laboratory, H. C. Moffitt-Long Hospital, University of California, San Francisco 94143-0214.
Am Heart J. 1994 Jun;127(6):1572-80. doi: 10.1016/0002-8703(94)90388-3.
The hemodynamic factors contributing to reduced exercise capacity in adults with congenital heart disease are not fully defined. We hypothesized that they would demonstrate reduced exercise capacity compared with age-matched control subjects because of abnormal exercise hemodynamics and ventricular performance demonstrable by echocardiography. We retrospectively analyzed the results of all studies in all patients with congenital heart disease (from 1988 to 1993) and found that the peak work load and double product achieved were decreased in comparison with normal values (79 +/- 47 W vs 149 +/- 52 W [p < 0.0001] and 19,210 +/- 6805 vs 25,701 +/- 6440 [p = 0.005], respectively). Seven patients achieved work loads < 40 W associated with an exaggerated exercise pulmonary artery pressure response, decreases in right and/or left ventricular function with exercise, or both. Normal or near-normal exercise tolerance was observed in the following patient groups: (1) repaired tetralogy of Fallot, (2) uncomplicated I-transposition of the great arteries, and (3) Ebstein's anomaly with atrial septal defect. We conclude that exercise echocardiography provides new hemodynamic information for evaluating functional limitations in congenital heart disease.
