Hypertension: The Link Between Erectile Dysfunction and Coronary Artery Disease

Abstract

The ability to attain and then maintain an erection is the result of a dynamic balance between arterial inflow and cavernosal outflow. Any imbalance that either decreases arterial inflow and/or increases cavernosal outflow may result in symptomatic erectile dysfunction (ED). Current data suggest that vasculogenic ED is of arterial origin and primarily the result of the development of systemic endothelial dysfunction (EnD). Since systemic EnD is heralded as an early marker of cardiovascular disease, specifically coronary artery atherosclerotic heart disease (CAD), it has been suggested that the onset of ED can be used as a marker for either the presence, or future development, of CAD. However, the failure to find arterial dysfunction in some young men with largely vasculogenic ED, combined with the recognition that most men with ED, regardless of age, appear to have at least some cavernosal smooth muscle dysfunction, has prompted a reexamination of the roles of vascular endothelium and the cavernosal smooth muscle in the development of aging-related ED, as well as a reexamination of the significance of ED as a marker of subsequent cardiovascular disease. The unifying concept that explains all these events is the aging-related apoptosis that occurs within vascular smooth muscle. In the penis, this smooth muscle apoptosis will cause cavernosal veno-occlusive dysfunction (CVOD), which initially affects a man's refractory period. In the peripheral vascular system, the apoptotic process leads to an increase in peripheral vascular resistance, and patients may present with hypertension. Hypertension and CVOD, then, represent the same pathophysiologic disorder in two different organ systems.