Related Experiment Videos
Therapeutic options in minimizing left ventricular hypertrophy
1Division of Cardiology, New York Presbyterian Hospital/Cornell Medical Center. rbdevere@mail.med.cornell.edu
Insights
Left ventricular hypertrophy (LVH) increases mortality risk in hypertensive patients. Angiotensin receptor blockers (ARBs) show promise for LVH regression, potentially offering superior benefits compared to other antihypertensives.
Area of Science:
- Cardiology
- Hypertension Research
- Pharmacology
Background:
- Left ventricular hypertrophy (LVH) is a significant risk factor for mortality in hypertensive patients.
- LVH is linked to increased risks of cardiovascular events including heart failure, stroke, and sudden death.
- The renin-angiotensin system is implicated in the development of LVH.
Purpose of the Study:
- To review the role of antihypertensive agents in LVH regression.
- To explore the potential of angiotensin receptor blockers (ARBs) in managing LVH.
- To highlight the specific mechanisms of ARBs in reducing left ventricular mass.
Main Methods:
- Review of existing literature on antihypertensive therapies and LVH.
- Analysis of studies investigating the effects of various drug classes on left ventricular mass.
- Examination of preclinical and clinical data on ARBs for LVH regression.
Main Results:
- All major antihypertensive classes can induce LVH regression, but efficacy varies.
- Angiotensin-converting enzyme inhibitors (ACE inhibitors) demonstrate significant blood pressure-independent effects on LVH.
- Angiotensin receptor blockers (ARBs) show promise, with studies indicating significant LVH regression, potentially via AT(2) receptor activation.
Conclusions:
- ARBs represent a promising therapeutic option for LVH regression in hypertensive patients.
- Targeting the renin-angiotensin system, particularly with ARBs, may offer superior benefits for reducing left ventricular mass.
- Further research is warranted to fully elucidate the long-term benefits and optimal use of ARBs in managing LVH.
Abstract:
Left ventricular hypertrophy (LVH), a target-organ response to chronic pressure or volume overload, is associated with its own independent risks of death in patients with hypertension. Numerous studies have shown that LVH increases the risk of coronary heart disease, congestive heart failure, stroke or transient ischemic attack, all-cause deaths, and sudden death. Although the mechanisms by which LVH develops are incompletely understood, the renin-angiotensin system may play an important role. All major classes of antihypertensive agents (calcium channel blockers, diuretics, beta-blockers, angiotensin-converting enzyme inhibitors) can cause LVH regression but not all to the same degree. Angiotensin-converting enzyme inhibitors may provide the most pronounced reduction in left ventricular mass per millimeter of mercury of blood pressure reduction. In addition, animal studies and human trials show promise for the regression of LVH with the use of angiotensin receptor blockers (ARBs). Because ARBs act specifically on the AT(1) receptor, angiotensin II can exert its favorable effects on cell growth inhibition through the AT(2) receptor. One small study that compared the ARB valsartan with atenolol found significant regression of LVH with the ARB by 8 months of treatment.