Reduction of left ventricular hypertrophy: how beneficial?

Left ventricular hypertrophy (LVH) can no longer be considered a compensatory adaptation of the heart serving to normalize the increased wall stress in hypertension. Recent studies have indicated that LVH is a powerful pressure-independent risk factor for cardiovascular morbidity and mortality. The pathophysiologic sequelae of LVH are reduced ventricular filling and contractility, ventricular dysrhythmias, and diminished coronary reserve or myocardial ischemia. Left ventricular hypertrophy can be reduced by antihypertensive therapy, although not all drugs are equipotent in this regard. Recent studies have shown that such a reduction also improves the pathophysiologic sequelae of LVH, that is, ventricular filling, coronary reserve, and ventricular dysrhythmias, and maintains left ventricular pump function. Although the reversal of these pathophysiologic findings is encouraging, it remains unknown whether a reduction of LVH will ultimately reduce the excessive risk of sudden death, acute myocardial infarction, and congestive heart failure that has been associated with this disorder independent of arterial pressure.