Abstract

Hypertension is a major risk factor for cardiovascular morbidity and mortality. Antihypertensive therapy consistently reduces complications from stroke and congestive heart failure, whereas benefits from the treatment of ischemic heart disease events are variable. Several plausible explanations, including hemodynamic hypotheses, have been put forth to account for the failure of treatment to more favorably influence mortality from ischemic heart disease. The effect of hypertension on coronary heart disease is probably much more complex than a simple elevation of arterial pressure. Some of these complexities include the potential separate risks of high total peripheral resistance, high cardiac output, increased myocardial power that reflects pressure times flow, and several structural and functional vascular changes. These factors may act in concert to unfavorably alter the balance between myocardial oxygen supply and demand. Several of these factors will be highlighted in an attempt to offer alternative or adjunctive pathophysiologic examinations for the high-risk subgroups of obesity and the failure of antihypertensive therapy to normalize the rate of coronary heart disease events.

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