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This Month's Question:

Contrary to the traditional belief that erectile dysfunction (ED) is a late manifestation of arterial disease, a growing body of evidence indicates that ED may predict cardiovascular disease (CVD). What is the latest evidence that substantiates this paradigm shift, further supporting the link between ED and CVD, and what are the clinical implications?

Response by Robert A. Kloner, MD, PhD, Posted 06/15/07:

Today, ED is increasingly regarded as an early manifestation of atherosclerosis. If untreated, ED may predict CVD. The risk factors for ED and CVD are similar and include dyslipidemia, hypertension, smoking, diabetes, and lack of physical exertion. When a patient presents with ED, he should be assessed for these risk factors and treated by a primary care physician or a specialist. Treating these risk factors has been shown to reduce cardiovascular and cerebrovascular events, and some studies suggest that treating them also improves erectile function.1 The results of 2 landmark studies provide additional support for this theory.

Thompson et al. published a study in which 9,457 men ≥55 years of age (mean age, 62) were enrolled.2 Of the 8,063 without CVD at baseline, 81% either had ED at study entry (n=3,816, 47%) or developed ED within the 7-year study period (n=2,760, 34%). Proportional hazard regression analysis showed that these men had a significantly greater chance of experiencing any CVD than the men without ED (hazard ratio 1.45, P<.001), with the effect for transient ischemic attack highest at 1.92 (P=.02). The association of ED and CVD was similar to the risk associated with current smoking or a family history of myocardial infarction. (For a more detailed discussion of findings by Thompson et al., please click here.)

The COBRA study investigated the prevalence of ED in patients with coronary artery disease (CAD) and its relationship to the burden of coronary atherosclerosis by evaluating clinical presentation (acute vs chronic coronary syndrome) and extent of vessel involvement (1 vessel vs 2 or 3 vessels).3 Compared with patients with single-vessel disease, patients with multi-vessel disease had a significantly higher overall prevalence of ED (P<.0001) and a higher prevalence of severe ED (12.5% vs 31%, P<.01). The presence of ED was associated with a 4-fold higher risk of having multi-vessel versus single-vessel disease, and the association was time-dependent: The longer the period since diagnosis of ED, the greater the likelihood of multi-vessel disease (P=.016). In 93% of the cohort of patients with established CAD (eg, chronic coronary syndrome), the onset of sexual dysfunction preceded the onset of CAD by an average of 2 years (range, 1 to 3 years).

Because the presence of ED may constitute an early sign of CVD, screening for ED is an important step in identifying men at risk and initiating preventive intervention strategies, such as lifestyle modification, lipid and blood pressure management, diabetes control, and medical treatment of ED.1,2 PDE5 inhibitors are the most commonly prescribed treatment for ED today, and recent evidence suggests that chronic therapy with PDE5 inhibitors may improve endothelial function,4 which is believed to be the common link between CVD and ED.1

 

References

  1. Tikkanen MJ, Jackson G, Tammela T, et al. Erectile dysfunction as a risk factor for coronary heart disease: implications for prevention [review]. Int J Clin Pract. 2007;61:265-268.

  2. Thompson IM, Tangen CM, Goodman PJ, Probstfield JL, Moinpour CM, Coltman CA. Erectile dysfunction and subsequent cardiovascular disease. JAMA. 2005;294:2996-3002.

  3. Montorsi P, Ravagnani PM, Galli S, et al. Association between erectile dysfunction and coronary artery disease—role of coronary clinical presentation and extent of coronary vessels involvement: the COBRA trial. Eur Heart J. 2006;27:2632-2639.

  4. Rosano GMC, Aversa A, Vitale C, Fabbri A, Fini M, Spera G. Chronic treatment with tadalafil improves endothelial function in men with increased cardiovascular risk. Eur Urol. 2005;47:214-222.


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