Abnormal exercise hemodynamics in cardiac allograft recipients 1 year after cardiac transplantation. Relation to preload reserve.

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Abstract
The well established elevation in left ventricular filling pressures during exercise in patients afte transplantation may contribute to decreased exercise tolerance. A proposed mechanism for this increase in filling pressures is an abnormal pressure-volume homeostasis of the transplanted heart. Twenty-three patients undergoing routine 1-year evaluations performed supine bicycle exercise during right heart catheterization. Within 24 hours, these patients underwent supine bicycle exercise to the identical work load during radionuclide ventriculography. For the group, resting hemodynamics and resting left and right ventricular ejection fractions were normal. With exercise, right atrial and pulmonary wedge pressures rose markedly (from 6 .+-. 2 to 14 .+-. 7 mm Hg, p < 0.0001, and from 10 .+-. 3 to 20 .+-. 6 mm Hg, p < 0.0001, respectively). Left ventricular ejection fraction increased appropriately with exercise (from 0.58 .+-. 0.08 to 0.63 .+-. 0.07, p = 0.004). End-diastolic volume also increased mildly (from 100 .+-. 31 to 117 .+-. 39 ml, p = 0.001), but change in end-diastolic volume was highly variable. Patients with little or no change in end-diastolic volume with exercise had the greatest resting and exercise left ventricular filling pressures resulting in significant negative correlations between filling pressures and change in end-diastolic volume (r = -0.64, p = 0.002 and r = -0.50, p = 0.025, respectively). Negative linear relations between exercise life ventricular filling pressures or resting heart rates and donor to recipient body weight ratio (r = -0.35, p = 0.10, and r = -0.37, p = 0.06, respectively) suggested that initial donor heart size influenced subsequent cardiac function. However, unlike hemodynamics 3 months after transplantation, the effect of donor to recipient body weight ratio was not significant at 12 months. These data suggest that elevated exercise filling pressures in cardiac allograft recipients may result from multiple factors including volume status (resting pulmonary wedge pressure) and preload reserve (change in left ventricular end-diastolic volume), although an abnormal diastolic pressure-volume relation in some patients cannot be excluded.