Antihypertensive therapy reduces left ventricular hypertrophy and associated arrhythmias, but it remains unproven if this independently decreases sudden cardiac death beyond blood pressure lowering.
Left ventricular hypertrophy (LVH) has been identified as one of the strongest blood pressure-independent risk factors for sudden death, acute myocardial infarction, congestive heart failure, and other cardiovascular morbidity and mortality. Hypertensive patients with LVH have a significantly greater prevalence of premature ventricular contractions and complex ventricular arrhythmias than do patients without LVH or normotensive patients. Antihypertensive therapy reduces LVH, although not all antihypertensive drugs are equipotent in this regard. Angiotensin-converting enzyme inhibitors are probably the most effective in reducing LVH, followed by calcium antagonists, diuretics, and beta-blockers. The effect of angiotensin receptor blockers on left ventricular mass is unclear at the present, some studies showing a reduction, some studies showing no effect. A reduction in LVH has been shown to diminish LVH-associated arrhythmias. However, it remains to be shown that patients with LVH and ventricular ectopy are at a higher risk for sudden death than those without ventricular ectopy and that the reduction of LVH-associated ventricular ectopy indeed confers a clinical benefit that exceeds the one from the reduction of arterial pressure alone.
Franz H. Messerli (Thu,) conducted a review in Hypertension and Left Ventricular Hypertrophy. Antihypertensive therapy was evaluated. Antihypertensive therapy reduces left ventricular hypertrophy and associated arrhythmias, but it remains unproven if this independently decreases sudden cardiac death beyond blood pressure lowering.
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