The aging heart.

Abstract

Pathologic studies of the myocardium and valvular structures have failed to provide convincing evidence of gross or microscopic changes that can be ascribed to aging alone. Lipofuscin accumulation and basophilic degeneration in cardiac muscle cells appear to be the most consistent findings associated with aging, but they are found in other conditions. Without doubt, pathologic changes in the myocardium, valves, and coronary arteries are found more frequently in the hearts of elderly persons, but those changes are caused by disease processes associated with an aging population rather than the aging process itself. Both the sinus and atrioventricular nodes decrease in size with age owing to a loss of cellularity. These structures become infiltrated with collagen, elastic tissue, and reticular fibers. Some have found infiltration also with fat. Amyloid deposition, basophilic degeneration of cells, and lipofuscin accumulation occur but probably do not cause functional abnormalities. Similar but less dramatic changes occur in the bundle of His and individual bundle branches. Most of the data suggests that these aging changes are not due to vascular insufficiency. Age-related changes in intrinsic mechanical function have been identified as a prolongation of contraction duration, decreased inotropic responses to catecholamines and cardiac glycosides, and an increase in mechanical refractoriness. Other possible age-related changes include alterations in relaxation, which may or may not be independent of the prolongation of contraction, and changes in the viscoelastic properties of cardiac muscle. When examined in the context of the components of a model of excitation-contraction coupling, changes in action potential duration and the function of the sarcoplasmic reticulum emerge as the most likely bases for the changes. The electrical characteristics of sinus, atrioventricular, and His-Purkinje cells as well as atrial and ventricular muscle cells change with age. The sinus rate decreases, as do the escape rates of other automatic cells. The sensitivity and electrical changes produced by cardiac drugs also is affected by aging. Transmembrane electrical aging changes have been attributed to changes in the slow inward current caused by calcium and alterations in potassium conductance as well as other ionic currents. An age-related change in the function of the sarcoplasmic reticulum may be contributory. There appear to be age-related changes in both the anatomy and physiology of major arteries.(ABSTRACT TRUNCATED AT 400 WORDS)