The heart in the hypertensive elderly.

Abstract

Left ventricular (LV) mass progressively increases throughout life, reaching its greatest magnitude in senescence. In the normotensive elderly, left ventricular hypertrophy (LVH) is mostly a consequence of a degenerative process in connective tissue. In hypertensive patients, LVH results from an increase in muscle mass and fibrotic tissue. LVH by echocardiographic criteria can be found in up to 50% of elderly patients 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 coronary reserve, increased number of arrhythmias and progressive deterioration in LV function. Conceivably, an increase in interstitial fibrosis and cross-linking collagen in the senescent heart is responsible for an increase in myocardial stiffness and diastolic abnormalities. Regression of LVH has been demonstrated not only to improve left ventricular filling and coronary reserve but also to diminish cardiac arrhythmias. Although few studies have demonstrated that the reduction of LV mass is associated with better cardiovascular prognosis, it seems reasonable 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.