The world population in both industrialized and developing countries is aging. In the United States, 35 million people are older than the age of 65 years, and the number of older Americans is expected to double by the year 2030. The clinical and economic implications of this demographic shift are staggering because age is the most powerful risk factor for cardiovascular diseases.
The incidence and prevalence of hypertension, coronary artery disease, congestive heart failure, and stroke, the quintessential diseases of Western society, increase steeply with advancing age (Fig. 102–1). Although epidemiologic studies have discovered that some aspects of lifestyle and genetics are risk factors for these diseases, age, per se, confers the major risk. There is a continuum of age-related alterations of cardiovascular structure and function in healthy humans.1-4 These changes appear to influence the steep increases in hypertension, atherosclerosis, stroke, left ventricular hypertrophy, chronic heart failure, and atrial fibrillation with increasing age. Specific pathophysiologic mechanisms that underlie these diseases become superimposed on cardiac and vascular substrates that have been modified by an "aging process," and the latter modulates disease occurrence and severity. In other words, age-associated changes in cardiovascular structure and function become "partners" with pathophysiologic disease mechanisms, lifestyle, and genetics in determining the threshold, severity, prognosis, and therapeutic response of cardiovascular disease in older persons.
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