Left ventricular hypertrophy and its regression: pathophysiology and therapeutic approach: Focus on treatment by antihypertensive agents

In numerous studies, left ventricular hypertrophy (LVH) has been clearly established to be a strong blood pressure (BP) independent risk factor for cardiovascular morbidity and mortality. In fact, increased echocardiographic left ventricular mass (LVM) has been shown to predict cardiovascular complications not only in patients with arterial hypertension, but also in the general population. Preliminary data revealed that regression of LVH reduced cardiovascular complications. As a consequence, regression of LVH emerged as a desirable goal in patients with echocardiographically determined LVH. These findings raised the question 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, controlled clinical studies with parallel group design, we found that angiotensin converting enzyme (ACE) inhibitors reduced LVM by 12% (95% CI, 9.0–14.5%), calcium channel blockers by 11% (95% CI, 7.8–13.7%), β-blockers 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 blockers seemed to be more potent than β-blockers in their ability to reduce LVH, with diuretics in the intermediate range. The role of new antihypertensive agents such as AT-receptor antagonists cannot be conclusively answered, because the available data source is too small at this time. In addition to the drug class, reduction of LVH seems to be determined by pretreatment LVM, decline in BP, and duration of drug treatment. Further prospective controlled trials will be required to finally evaluate whether the excellent reduction of LVH with ACE inhibitors and calcium channel blockers can be transferred into improved cardiovascular prognosis.