ANGIOTENSIN-CONVERTING ENZYME-INHIBITION BY CAPTOPRIL INFLUENCES CARDIAC WORK IN HEALTHY HEARTS

Although beneficial effects of angiotensin converting enzyme (ACE) inh ibition have been demonstrated in ill (ischemic, failing) hearts, it h as not been proved that ACE inhibition induces changes in healthy hear ts. The question is of clinical relevance, as many hypertensive patien ts do not display cardiac damage at the onset of treatment with ACE in hibitors, and possible changes in cardiac work might turn out more or less advantageous in the development of hypertensive heart disease. In a refined working heart preparation allowing measurement of cardiac w ork, including the contribution of atrial work and paracrine cardiac r egulation, effects of captopril on cardiac dynamics were assessed, Cor onary overflow of bradykinin, norepinephrine, and lactate was measured . Hearts were perfused for 20 min with vehicle or captopril at 3 x 10( -8) 3 x 10(-7), 3 x 10(-6), and 3 x 10(-5) mol/L. At the highest conce ntration, captopril increased coronary how. Extending previous studies , the present study demonstrates that, in a concentration-dependent ma nner, captopril decreased oxygen consumption and maximal left ventricu lar pressure although the bradykinin outflow was not affected. From th ese influences of the drug on cardiac work and metabolism in healthy h earts, a protective influence of captopril in acute, critical situatio ns of cardiac malnourishment or cardiac overload may be derived. (C) 1 998 American Journal of Hypertension, Ltd.