Diuretic-based therapy is less effective in reducing the @entity299 of @entity101 than the risk of @entity64 and may be less effective in reducing left ventricular (LV) mass than is therapy with @entity1289 ( @entity1289 ) inhibition. In view of the strong association of @entity4346 with cardiovascular risk, this study was designed to compare the impact of therapy with a diuretic and @entity1289 inhibition on cardiac and vascular structure. Fifty essential @entity101 (74% male, 88% nonwhite) participated in a double-blind study for 6 months and were randomized to either @entity3372 or @entity918 ( @entity918 ). Echocardiography, carotid ultrasonography, and ambulatory blood pressure (BP) monitoring were performed at baseline and 3 and 6 months after initiation of therapy. The 22 @entity3372 @entity1 were comparable to the 28 @entity918 @entity1 at baseline in age, race, and 24-h BP. Although @entity918 resulted in a greater reduction in 24-h BP, only treatment with @entity3372 resulted in a decrease in LV mass (193 to 179 g, P < .005, v 184 to 182 g, P = NS), attributable to a reduction in wall thicknesses but not in chamber diameter. In multivariate analysis, both change in BP and treatment group were independent predictors of change in LV mass. Importantly, although neither drug reduced carotid artery cross-sectional area, relative wall thickness increased due to a tendency for vessel diameter to decrease and wall thickness to increase, particularly in the diuretic group. @entity3372 caused a sustained fall in plasma @entity2178 , whereas @entity918 increased @entity2178 levels. Although diuretic therapy was more effective in lowering ambulatory BP in this predominantly nonwhite population, only therapy with @entity1289 inhibition was associated with regression of LV mass. Vascular geometry was altered consistent with the reduction in distending pressure resulting in @entity6980 .

Differential effects of XXXX inhibition and diuretic therapy on reductions in ambulatory blood pressure, left ventricular mass, and vascular hypertrophy.

@entity1 :: ('9606', 'Species') :: ['patients'] @entity3372 :: ('MESH:D017257', 'Chemical') :: ['ramipril', 'Ramipril'] @entity64 :: ('MESH:D020521', 'Disease') :: ['stroke'] @entity1289 :: ('1636', 'Gene') :: ['angiotensin converting enzyme', 'ACE'] @entity101 :: ('MESH:D006973', 'Disease') :: ['hypertensives', 'hypertension'] @entity918 :: ('MESH:D006852', 'Chemical') :: ['HCTZ', 'hydrochlorothiazide'] @entity2178 :: ('183', 'Gene') :: ['angiotensin II'] @entity6980 :: ('MESH:D066253', 'Disease') :: ['vascular remodelling'] @entity4346 :: ('MESH:D017379', 'Disease') :: ['LV hypertrophy'] @entity299 :: ('MESH:D006331', 'Disease') :: ['cardiac complications']
@entity1289 :: (1636,Gene) :: ['angiotensin converting enzyme']
