REGRESSION OF LEFT-VENTRICULAR HYPERTROPHY IN HYPERTENSIVE DIALYZED UREMIC PATIENTS ON LONG-TERM ANTIHYPERTENSIVE THERAPY

There have been no studies of the possibility of reversing the left ve ntricular hypertrophy (LVH) of chronically hemodialyzed hypertensive u remics (HDH) with long-term antihypertensive therapy. We have measured left ventricular sizes of eight (6 male, 2 female, aged 29 to 61 year s) HDH with M-mode echocardiography, before and 12, 18 and 24 months a fter the start of a combined antihypertensive therapy which included A CE-inhibitors, beta-blockers and calcium-antagonists. Pre-treatment va lues for mean blood pressure (MBP), 116.6 +/- 2.9 mm Hg, end diastolic diameter (EDD), 62.6 +/- 6.6 mm, interventricular septum (IVS), 14.2 +/- 3.0 mm, and left ventricular mass index (LVMi) , 239 +/- 61 g/m2, were all significantly higher than those for nine sex- and age-matched hemodialyzed normotensive subjects (HDN) with comparable hemoglobin ( Hb) levels. During the antihypertensive treatment, both the systolic a nd diastolic BP decreased steadily (P = 0.0001; P = 0.0003; ANOVA) and significantly by the third month (P < 0.05; P < 0.01), reaching level s comparable to those of the HDN group after 12 months. At this time t he LVMi (204 +/- 67) and the IVS (13.1 +/- 2.7), although both signifi cantly lower than baseline, were still higher than in the HDN group, w hile the EDD was similar. After 24 months, however, both the IVS (12.3 +/- 3.1) and the LVMi (161 +/- 65 ) were no longer different from tho se of the HDN group. Thus, this study is the first to demonstrate that prolonged antihypertensive therapy with strict blood pressure control is able to considerably reduce the LVH of chronically hemodialyzed ur emic patients, indicating the key role of arterial hypertension in ind ucing pathological growth of the LVM in these subjects.