LEFT-VENTRICULAR HYPERTROPHY - SHOULD IT BE REDUCED

Left ventricular hypertrophy (LVH) is a structural adaptation of the heart to sustained hypertension, serving to normalize increased wall stress. Recent clinical studies have indicated that LVH is a powerful pressure-independent risk factor for cardiovascular morbidity and mortality, particularly sudden death, acute myocardial infarction, and congestive failure. The pathophysiologic sequelae of LVH consist of reduced ventricular filling and contractility, ventricular dysrhythmias, and diminished coronary reserve or myocardial ischemia. LVH can be reduced by antihypertensive therapy, although not all drugs are equipotent in this regard. Angio-tensin-converting enzyme (ACE) inhibition seems to be the most powerful monotherapeutic modality for reducing LVH. Recent studies have shown that such a reduction also improves the pathophysiologic sequelae of LVH and maintains left ventricular pump function. Although the reversal of these pathophysiologic events is encouraging, it remains unknown whether reducing LVH will ultimately decrease the excessive risk of sudden death, acute myocardial infarction, and congestive heart failure that has been associated with this disorder independently of arterial pressure.