Erectile Dysfunction and Cardiovascular Disease: A Review

Despite its early description and documentation in 1948, erectile dysfunction (ED) has only been recognized as an organic failure of the normal neurovascular function of the penis within the past 2 to 3 decades [1]. Defined as the inability to achieve or maintain a penile erection for satisfactory sexual performance, ED affects >50% of men aged 40 to 70 years and 70% of men aged 70 years or older [2,3]. Moreover, the prevalence increases with age and is expected to further rise, potentially affecting over 300 million men worldwide by the year 2025 [4]. Organic, vasculogenic ED can result from aberrations in arterial and venous flow, endothelial and cavernosal smooth muscle function, and tunica albuginea compliance. The most common form of vascular ED results from penile arterial insufficiency, which will serve as the main focus for this review. Atherosclerotic occlusion or narrowing of the common iliac arteries, internal iliac arteries, and the internal pudendal arteries and their downstream branches may cause ED. Chronic arteriolar insufficiency leads to diminished neuronal and endothelial nitrous oxide (NO), and therefore causes impaired cavernosal smooth muscle relaxation resulting in ED. That ED and cardiovascular disease share many risk factors for atherosclerosis is well established and in many patients, particularly those with early onset ED, sexual dysfunction is a predictor of subsequent cardiovascular disease. While it is clear that endothelial 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.