Cardiovascular aging is a universal phenomenon associated with an increased likelihood of the development of cardiovascular diseases and of adverse outcomes once disease does develop (1). In fact, most complications of cardiovascular disease, including myocardial infarction, stroke, congestive heart failure, atrial fibrillation, and cardiovascular death, occur in the increasing number and proportion of our population that is 65 years of age and older (2).

Age-associated vascular changes include endothelial dysfunction and intimal proliferation, a recognized mechanism and substrate, respectively, for the development, progression, and manifestations of atherosclerotic disease; and increased central vascular stiffness, the most important etiology for isolated systolic hypertension in older persons. Age-associated changes in cardiac muscle include impaired early diastolic filling at rest and diminished performance during exercise and other stresses, manifested by decreased cardiac output, ejection fraction, and heart rate; and higher end-systolic and end-diastolic volumes. Increased vascular load and depressed cardiovascular performance contribute to impaired ventricular/vascular “coupling” during exercise (3).

These age-associated changes increase the likelihood that the older patient will develop heart failure symptoms in the setting of a tachycardic, ischemic, or hypertensive insult that would not precipitate failure in the younger patient. Another important age-associated change is a decrease in the number and/or function of endothelial progenitor cells, which contribute to repair and/or regeneration of damaged vascular tissue (4 and 5). These cells may also transdifferentiate to form myocytes and aid in myocardial repair in the setting of ischemic or other injury (6).

Journal of the American College of Cardiology, Volume 47, Issue 2, 17 January 2006, Pages 398-402,
Timothy E. Meyer, Sándor J. Kovács, Ali A. Ehsani, Samuel Klein, John O. Holloszy, Luigi Fontana
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