Abstract

Endothelial dysfunction underlies both atherosclerosis and erectile dysfunction (ED). Therefore, the incidence of coronary artery disease (CAD) is inevitably increased in patients with ED. Patients with ED, who are typically unable to develop or maintain an erection, are able to engage in sexual activity when treated with phosphodiesterase 5 inhibitors. Acute coronary syndromes and cardiac sudden death are precipitated by either vulnerable plaque erosion or rupture, or by the development of sudden myocardial ischemia. The physical activity of sexual intercourse is associated with increased myocardial oxygen demand (MVo(2)) and increased sympathetic nervous system activation, both of which can result in myocardial ischemia in the presence of CAD. The effect of sexual activity on total body oxygen consumption (Vo(2)) and MVo(2) has been studied in the past, but not extensively. Available research shows that sexual intercourse increases Vo(2) to a modest extent. As studied, Vo(2) is increased modestly to 3 to 5 metabolic equivalents. Further, this increase in Vo(2) lasts only for a brief period. The small increase in the incidence of myocardial infarction that accompanies sexual activity within 2 hours of onset is likely related to sympathetic activation and to an increase in MVo(2). The evidence for this hypothesis is reviewed in this article.

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