Erectile Dysfunction and Cardiovascular Disease: A Review

Erectile dysfunction (ED) is defined as the inability to achieve or maintain a penile erection for satisfactory sexual performance and it is estimated that >300 million men will suffer from this condition in 2025. ED is recognized as a harbinger of cardiovascular disease. Endothelial dysfunction and macrovascular atherosclerotic disease together represent the probable pathophysiological link between vasculogenic ED, coronary artery disease (CAD) and peripheral vascular disease (PAD), and research in these common areas in recent years has led to the emergence of a compelling body of evidence to support erectile dysfunction as the sentinel clinical event. The bidirectional relationship between low testosterone and components of metabolic syndrome (MetS) supports the conclusion that normal sex hormone production is an integral component for both metabolic and sexual health for the development of subsequent cardiac events and an improvement in overall health. Recent findings suggest that hormonal and cardiovascular investigations in men with erectile dysfunction even without any obvious cardiovascular disease (CVD), may ultimately lead to early identification and treatment of cardiovascular risk factors and a reduction in the later development of cardiac events and an improvement in overall health. Such investigation might include assessment of serum testosterone, fasting glucose, HgbA1c, C reactive protein and lipid levels as well as selective non-invasive testing. dysfunction is central to this relationship, the artery hypothesis theory proposed by Montorsi et al. in 2005 provides a compelling macrovascular model in support of the concept that ED may be the first manifestation of a single clinical disease spectrum that will ultimately progress to include coronary artery disease (CAD) and peripheral artery disease (PAD) at a later stage [5]. Furthermore, low testosterone or hypogonadism has been associated with erectile dysfunction, metabolic syndrome (MetS), and cardiovascular morbidity, as well as arterial stiffness, a major atherogenic risk factor [6,7]. In this review, we will discuss the evidence for the EDcardiovascular disease link and the clinical implications of cardio metabolic risk reduction. The Relationship between Erectile Dysfunction and Cardiovascular Disease The Massachusetts Male Aging Study established the association between ED and CAD, demonstrating a 39% probability of complete ED in men with heart disease and subsequent studies have shown rates of ED in patients with CAD as high as 75% [2,8,9]. Atherosclerosis and Macrovascular Disease That ED and CAD are distinct manifestations of the same disease process and are tied by macrovascular atherosclerosis and endothelial dysfunction is a concept which has gained increasing acceptance amongst urologists and cardiologists and is evidenced by common independent predictors and a clear association between both disorders. Several important observations have validated this hypothesis: Not only do patients with ED have high rates of both macrovascular atherosclerosis and hyperlipidemia, but in patients with ED, the presence of CAD is correlated with obstructive atherosclerotic lesions between the aortic bifurcation and the distal internal pudendal artery (IPA) [10,11]. Support for this association comes from the demonstration that ED precedes the development of symptomatic CAD typically by 2-5 years [12-14]. In 2003, Montorsi et al. showed that of 300 consecutive patients presenting with acute coronary syndromes, 71% had symptoms of sexual dysfunction prior to the onset of CAD symptoms. ED preceded the onset of CAD by 38 months in this study. Charles N Walker1*, Stephanie M Meller2, Erik Stilp3, and Carlos Mena-Hurtado3 1Yale University School of Medicine, Department of Surgery, Section of Urology, USA 2Yale University School of Medicine, New Haven, CT, USA 3Yale University School of Medicine, Department of Internal Medicine, Section of Cardiovascular Medicine, USA Address for Correspondence Charles Walker MD, Yale University School of Medicine, Department of Urology, 789 Howard Avenue, FMP 323, New Haven, CT 06519, USA, E-mail: [email protected] Submission: 26 August 2013 Accepted: 07 October 2013 Published: 10 October 2013 Review Article Open Access