Left ventricular hypertrophy (LVH) can no longer be considered a compe
nsatory adaptation of the heart serving to normalize the increased wal
l 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 ventr
icular filling and contractility, ventricular dysrhythmias, and dimini
shed coronary reserve or myocardial ischemia. Left ventricular hypertr
ophy can be reduced by antihypertensive therapy, although not all drug
s 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 o
f these pathophysiologic findings is encouraging, it remains unknown w
hether a reduction of LVH will ultimately reduce the excessive risk of
sudden death, acute myocardial infarction, and congestive heart failu
re that has been associated with this disorder independent of arterial
pressure.