Left ventricular (LV) mass progressively increases throughout life, re
aching its greatest magnitude in senescence. In the normotensive elder
ly, left ventricular hypertrophy (LVH) is mostly a consequence of a de
generative process in connective tissue, In hypertensive patients, LVH
results from an increase in muscle mass and fibrotic tissue. LVH by e
chocardiographic criteria can be found in up to 50% of elderly patient
s with hypertension. Although associated with aging, LVH is associated
with a higher rate of non-fatal and fatal cardiovascular events, Even
in the absence of coronary stenosis, LVH is associated with reduced c
oronary reserve, increased number of arrhythmias and progressive deter
ioration in LV function. Conceivably, an increase in interstitial fibr
osis and cross-linking collagen in the senescent heart is responsible
for an increase in myocardial stiffness and diastolic abnormalities. R
egression of LVH has been demonstrated not only to improve left ventri
cular filling and coronary reserve but also to diminish cardiac arrhyt
hmias, Although few studies have demonstrated that the reduction of LV
mass is associated with better cardiovascular prognosis, it seems rea
sonable to consider it a goal of antihypertensive therapy. Of all anti
hypertensive agents, angiotensin-converting-enzyme inhibitors seem to
be the most powerful in reducing LV mass.