LEFT-VENTRICULAR HYPERTROPHY AND ITS REGRESSION - PATHOPHYSIOLOGY ANDTHERAPEUTIC APPROACH - FOCUS ON TREATMENT BY ANTIHYPERTENSIVE AGENTS

Citation
Mp. Schlaich et Re. Schmieder, LEFT-VENTRICULAR HYPERTROPHY AND ITS REGRESSION - PATHOPHYSIOLOGY ANDTHERAPEUTIC APPROACH - FOCUS ON TREATMENT BY ANTIHYPERTENSIVE AGENTS, American journal of hypertension, 11(11), 1998, pp. 1394-1404
Citations number
90
Categorie Soggetti
Peripheal Vascular Diseas
ISSN journal
08957061
Volume
11
Issue
11
Year of publication
1998
Part
1
Pages
1394 - 1404
Database
ISI
SICI code
0895-7061(1998)11:11<1394:LHAIR->2.0.ZU;2-5
Abstract
in numerous studies, left ventricular hypertrophy (LVH) has been clear ly established to be a strong blood pressure (BF) independent risk fac tor for cardiovascular morbidity and mortality. in fact, increased ech ocardiographic left ventricular mass (LVM) has been shown to predict c ardiovascular complications not only in patients with arterial hyperte nsion, but also in the general population. Preliminary data revealed t hat regression of LVH reduced cardiovascular complications. As a conse quence, regression of LVH emerged as a desirable goal in patients with echocardiographically determined LVH, These findings raised the quest ion of whether certain antihypertensive drugs differ in their ability to reduce LVM. To resolve this issue, several comparative studies and some metaanalyses have been carried out. Regarding the available data until the end of 1996 including only double-blind, randomized, control led clinical studies with parallel group design, we found that angiote nsin converting enzyme (ACE) inhibitors reduced LVM by 12% (95% CI, 9. 0-141.5%), calcium channel blockers by 11% (95% CI, 7.8-13.7%), beta-b lockers by 5% (95% CI, 1.2-7.3%), and diuretics by 8% (95% CI, 3.9-11. 1%) (overall: P <.01). A similar reduction was found for posterior and septal wall thickness. Thus, ACE inhibitors and calcium channel block ers seemed to be more potent than P-blockers in their ability to reduc e LVM, with diuretics in the intermediate range. The role of new antih ypertensive agents such as AT-receptor antagonists cannot be conclusiv ely answered, because the available data source is too small at this t ime. In addition to the drug class, reduction of LVH seems to be deter mined by pretreatment LVM, decline in BP, and duration of drug treatme nt. Further prospective controlled trials will be required to finally evaluate whether the excellent reduction of LVH with ACE inhibitors an d calcium channel blockers can be transferred into improved cardiovasc ular prognosis. (C) 1998 American Journal of Hypertension, Ltd.