[The biochemical bases of cardiovascular aging]

The majority of reports concerning the performance of senescent heart in both human and animal models states that, at rest, most hemodynamic parameters are substantially unchanged during aging, with the exception of a prolongation of left ventricular ejection time and a decrease in the early diastolic filling rate. A biochemical rationale for the increased early diastolic filling time with age seems to be the enhanced stiffness of left ventricular wall due to either myocardial hypertrophy or collagen tissue accumulation. The prolonged time of contraction and the inadequate response to stress of cardiac muscle in elderly subjects may be the consequence of changes in different steps of the excitation-contraction coupling, namely altered intracellular calcium homeostasis, reduced availability of highly energetic compounds, and impaired response to adrenergic stimulation. These defects can cause major hemodynamic changes when the heart is subjected to volume or pressure overload. In fact, during exercise, elderly subjects can reach a maximal heart rate slower than that of younger people. The possibility that the toxicity of oxygen reactive forms may provoke some age-related myocardial lesions such as structural alteration of membranes and enzyme inactivation is very attractive but the linkage between the most functional perturbations of aged hearts and peroxidative stress remains to be clarified.