Left Ventricular Hypertrophy.

  • Liebson
  • Published 1999 in
    Current treatment options in cardiovascular…

Abstract

The presence of left ventricular hypertrophy (LVH) as a treatable entity is of particular importance in patients with primary hypertension. Because LVH is associated with a strong risk of adverse clinical events (eg, heart failure, ischemic events, and cardiovascular death) and because evidence from retrospective studies suggests that regression of LVH, along with a decrease in blood pressure, may help modify these outcomes, the use of antihypertensive agents that have been shown to promote regression of LVH has been recommended. These include diuretics, beta-blockers (except those with intrinsic sympathomimetic activity ), angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers, peripheral alpha(1)-blockers, and central alpha(2)-stimulators. Agents to be avoided include direct arterial vasodilators (eg, hydralazine and minoxidil), which have strong sympathetic stimulating properties and tend to maintain LVH despite lowering blood pressure. The use of ACE inhibitors is increasing. Unfortunately, the cost of these agents is higher than that of some other classes of agents, such as diuretics, which show excellent evidence of regression of hypertrophy. African-American and elderly persons, in particular, may benefit from diuretics for treatment of hypertension as well as reduction of left ventricular (LV) mass. Beta-blockers should be considered in the elderly, especially those with greatly thickened LV walls and small chamber sizes, factors associated with hyperdynamic systolic performance, systolic midcavity obliteration, and diastolic relaxation abnormalities on echocardiography. Calcium channel blockers may also be useful in patients with LVH who have normal systolic performance and diastolic compliance abnormalities. The purpose of serial echocardiographic studies in patients already being treated for hypertension is to ensure that LV geometry has not worsened and that function is unchanged or improved (especially with respect to previously noted diastolic Doppler inflow abnormalities). Considerable changes in estimated LV mass (>60 g on serial intrapatient evaluation) are needed before the clinician can conclude with confidence that LV mass has decreased. More specific definitive recommendations based on the outcomes of current large-scale clinical trials are awaited.

Cite this paper

@article{Liebson1999LeftVH, title={Left Ventricular Hypertrophy.}, author={Liebson}, journal={Current treatment options in cardiovascular medicine}, year={1999}, volume={1 3}, pages={219-230} }