Abstract des Autors

Exercise after heart transplantation results in an acceleration of left ventricular relaxation, which was 2.5 times smaller than in a normal control group exercised to the same heart rate. This blunted response of left ventricular relaxation kinetics to exercise contributes to the exercise-induced elevation of left ventricular filling pressures and the reduced exercise tolerance observed in the cardiac allograft. Those allograft recipients, who had the largest elevation of left ventricular filling pressures during exercise, showed least acceleration of the left ventricular isovolumic relaxation rate during exercise. The individual response of left ventricular relaxation rate to exercise was variable, ranging from normal acceleration to paradoxical slowing. Despite similar heart rates, exercise and dobutamine infusion had unequal effects on left ventricular relaxation rate in so far that exercise resulted in a significantly slower relaxation rate and a significant elevation of left ventricular filling pressures. Compensation of reduced sympathetic stimulation by administration to a group of transplant recipients of a beta-agonist prior to exercise failed to prevent the exercise-induced elevation of left ventricular filling pressures and failed to correct the deficient acceleration of left ventricular relaxation rate during exercise. Abnormal exercise hemodynamics following cardiac transplantation are therefore not related to deficient sympathetic stimulation but probably to loss of synchronicity between changes in heart rate and venous return, which results in myocardial use of preload reserve. This counteracts lusitropic myocardial effects of beta-adrenergic stimulation, resulting in deficient acceleration of left ventricular relaxation rate, and causes elevation of left ventricular filling pressures, because of a steeper than normal diastolic left ventricular pressure-volume relation. Verf.-Referat