[Heart aging and its clinical implications].

Abstract

Aging-induced cardiac modifications are almost never different--at least qualitatively--from those linked to chronic pathologies that are usually found in advanced age. Due to many factors, as myocyte hypertrophy, increase in the amount of collagen and subepicardial fat accumulation, the aging heart increases its own weight. All cardiac structures undergo regressive modifications: valvular apparatus show fibrosis, collagen fragmentation, lipid accumulation and calcifications, the coronary arteries are characterized by tortuosity, minimal atherosclerotic lesions, calcium precipitates and--at least in animals--by an imbalance between the capillary bed extension and the myocyte hypertrophy. The most peculiar changes of interstitium, aside from fibrosis, are represented by lipofuscins and amyloid deposits. From a functional point of view, the aging heart does not show any substantial difference from the adult one in the basal state. Cardiac output seems to be maintained during exercise in the elderly. Nevertheless, such a result is achieved by an end-diastolic volume increase, instead of positive chronotropic and inotropic response and to the peripheral resistance decrease of the younger. This could be partly due to a damped cardiovascular response to sympathetic beta-receptor stimulation. The diastolic phase undergoes a progressive dysfunction, as its duration increases, the early filling falls and the atrial contribution plays a major role. The reduction of many mitochondrial enzymatic processes--such as fatty acid oxidation and oxidative phosphorylation--has been documented in animals, as well as transmembrane ionic fluxes alteration. The maximal oxygen consumption is progressively reduced, although this does not seem to be due to a cardiac performance impairment.(ABSTRACT TRUNCATED AT 250 WORDS)