Erectile Dysfunction, Metabolic Syndrome, and Cardiovascular Risks

Facts and Controversies

Edward Sanchez; Alexander W. Pastuszak; Mohit Khera


Transl Androl Urol. 2017;6(1):28-36. 

In This Article

The Artery Size Hypothesis

Montorsi et al. introduced the artery size hypothesis as a pathophysiologic mechanism to address the association between ED and CVD. The study proposed that, in cases of systemic atherosclerosis, all major vascular beds should be affected to the same extent. Symptoms, however, do not manifest equally at different points in the system, likely due to larger vessels being able to tolerate the same amount of obstruction better than smaller vessels. Given the smaller size of the penile vasculature (1–2 mm) compared to coronary vasculature (3–4 mm), ED is more likely to manifest earlier than CAD. This study was one of the first to propose that ED and CAD are different manifestations of the same systemic condition. It was also one of the first studies to introduce ED as a harbinger of CAD.[24] A subsequent study supported this finding, suggesting that ED occurs prior to cardiac symptoms in virtually all patients with chronic coronary syndrome with a time interval of approximately 3 years. Those with acute coronary syndrome had a much lower prevalence of sexual dysfunction, although as the extent of CAD increased in these patients, so did the rate of ED.[25] A study by Rogers et al. provided further support for the relationship between vessel size and symptoms, reporting that the degree of stenosis within the internal pudendal arteries (52–65%) was similar to stenosis found in coronary arteries of patients with ED unresponsive to PDE5 inhibitors.[26]

Chang et al. characterized the phenotypes of coronary vasculature in CAD patients with and without ED. Thirty males with ED (average duration of 2.7 years) and asymptomatic CAD were compared to age-matched controls with angina pectoris and no ED. Subjects with ED and asymptomatic CAD had more coronary vessels involved than the angina group and were found to have a greater number of type C lesions (American Heart Association/American College of Cardiology grading system), which represent lesions with a chance of successful dilation of <60% and/or a high risk of abrupt complete vessel stenosis.[27]

One limitation of the artery size hypothesis is the fact that not all cases of vasculogenic ED are caused solely by penile atherosclerosis. In fact, while evaluating a small cohort of 31 men over 45 years old undergoing autopsy, Ponholzer et al. found that clinically significant penile atherosclerosis was relatively rare (12.9%) compared to coronary (87%) or internal iliac vessel disease (77%).[28] Though this study was relatively small, it supports the conclusion that atherosclerotic lesions do not form uniformly in all vascular areas. It is likely that other factors such as microscopic endothelial damage and alterations of the NO-cGMP pathway may play a role as well.