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Selection of antihypertensive therapy: cardiac and extracardiac considerations
1Department of Internal Medicine, Ochsner Clinic, New Orleans, La 70121.
Insights
Left ventricular hypertrophy (LVH) impacts heart function through several mechanisms. While certain antihypertensive drugs effectively reduce LVH, it is unclear if this reduction improves cardiovascular outcomes beyond blood pressure control.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Left ventricular hypertrophy (LVH) is linked to cardiovascular morbidity and mortality through four key pathophysiological mechanisms.
- These include impaired left ventricular filling, reduced coronary reserve, increased ventricular arrhythmias, and decreased contractility over time.
Purpose of the Study:
- To review the impact of antihypertensive drugs on LVH.
- To assess the potential benefits of LVH reduction on cardiovascular outcomes.
Main Methods:
- Review of existing meta-analyses and studies on antihypertensive therapies and LVH.
- Analysis of pathophysiological mechanisms linking LVH to cardiovascular events.
Main Results:
- ACE inhibitors and calcium channel blockers are potent in reducing LVH, more so than beta-blockers or diuretics.
- Reduction of LVH with ACE inhibitors and calcium channel blockers has shown improvements in ventricular function and ectopy, and increased coronary reserve.
Conclusions:
- Antihypertensive drugs vary in their efficacy for reducing LVH.
- While reducing LVH shows promising pathophysiological benefits, its impact on reducing cardiovascular morbidity and mortality beyond blood pressure reduction alone requires further investigation.
Abstract:
There are four possible pathophysiological mechanisms which may relate left ventricular hypertrophy (LVH) with cardiovascular morbidity and mortality: LVH diminishes left ventricular filling; LVH decreases coronary reserve and hampers myocardial oxygenation; LVH is commonly associated with ventricular arrhythmias, and with long-standing LVH, left ventricular contractility decreases. LVH can be reduced by a range of antihypertensive drugs, although not all drugs are equipotent in this regard. Two recent meta-analyses have indicated that ACE inhibitors are among the most powerful monotherapeutic modalities to reduce LVH. Calcium channel blockers are almost as effective, whereas beta-blockers and diuretics seem to have a lesser effect, despite equipotent antihypertensive properties. Reducing LVH with ACE inhibitors and calcium channel blockers has been shown to improve contractility and left ventricular filling, and diminish ventricular ectopy. A preliminary study also indicates that coronary reserve increases after reduction in LVH. Despite these promising pathophysiological signs, it remains unknown whether or not a reduction in LVH will reduce morbidity and mortality over and above the reduction achieved by a reduction in arterial pressure alone.