THE INFLUENCE OF ACE-INHIBITION ON MYOCARDIAL MASS AND DIASTOLIC FUNCTION IN CHRONIC-HEMODIALYSIS PATIENTS WITH ADEQUATE CONTROL OF BLOOD-PRESSURE

The objectives of this study were to evaluate the specific effect of t he ACE-inhibitor lisinopril on myocardial mass and diastolic function in uremic patients using a protocol designed to leave blood pressure u nchanged. Nineteen hemodialysis patients (7 males; mean age: 55 +/- 13 years; mean time on dialysis: 44 +/- 35 months) received lisinopril f or 6 months in addition to their preexistent antihypertensive treatmen t regimens (mean: 1.4 +/- 0.8 drugs). Doses of antihypertensive drugs were adjusted to keep both systolic and diastolic blood pressure stabl e. Nine patients were withdrawn from lisinopril treatment after 43 +/- 33 days because of hypotension (n = 4), withdrawn consent (n = 3), st roke (n = 1) and cough (n = 1). Seven of them were further studied as controls. Ten patients received 6.4 +/- 4 mg lisinopril as a mean for 6 months. Mean myocardial mass, calculated by M-mode echocardiography, was 324 +/- 103 g before, and 313 +/- 79 g after 6 months of lisinopr il treatment. In the control patients, myocardial mass was 318 +/- 110 g initially, and after 6 months, it was 334 +/- 159 g. Early and late transmitral diastolic flow velocities were not significantly influenc ed by lisinopril. Throughout the study, both the systolic and diastoli c 24-h mean blood pressure levels remained stable (systolic: before: 1 45 +/- 19 mmHg, at 6 months: 147 +/- 17 mmHg; diastolic: before: 87 +/ - 12 mmHg, at 6 months 87 +/- 10 mmHg). Thus, no specific effect of li sinopril on regression of myocardial hypertrophy or improvement of dia stolic function could be observed within a 6-month period in this smal l group of hemodialysis patients. We conclude that the ineffectiveness is due to the lack of lowering blood pressure. Our findings further s trengthen the crucial role of hypertension even in the distinct entity of ''uremic cardiomyopathy''.