Penile erection is largely a vascular process, and the penile endothelium and smooth muscle tissue are very sensitive to functional and structural changes. Vasculogenic ED results from an impairment of endothelial dependent or independent smooth muscle relaxation (functional vascular ED, initial stages), occlusion of the cavernosal arteries by atherosclerosis (structural vascular ED, late stages), or a combination of these.3 Current data support a complex interplay between endothelial dysfunction, subclinical inflammation, and androgen deficiency (Figure 1). The relationship between ED and CAD at the clinical level is supported by this common pathophysiological basis. The ‘artery size’ hypothesis explains why patients with CAD frequently report ED before CAD detection.10 According to this hypothesis, for a given atherosclerotic burden, the smaller penile arteries suffer obstruction earlier than the larger coronary arteries (Figure 2). The same concept holds also true in the case of non-obstructing atherosclerosis: since the smaller penile artery have a greater endothelial surface and erection requires a large degree of vasodilation to occur when compared with arteries in other organs, the same degree of endothelial dysfunction will be symptomatic in these smaller vessels but subclinical in the larger ones (i.e. coronaries). In the same context, accelerated arterial ageing (as indicated by increased arterial stiffening that also affects large arteries of ED patients) may be a common background.11,12 Erectile dysfunction is associated with an incremental inflammatory and endothelial-pro-thrombotic activation.13 Interestingly, this activation is equal to that found in CAD patients with no ED, while when these two conditions are combined the burden is additive. Androgen deficiency may be also implicated in the common pathogenetic pathways of ED and CVD; however, this warrants further substantiation.2

While all three forms of male sexual dysfunction can be found among diabetic men, this review will focus on the most common form, ED, because the literature is most mature in this area. Defined as the inability to achieve or maintain an erection sufficient for satisfactory sexual performance, ED is highly prevalent in diabetic men1 and is almost always organic in its etiology. Given that many patients feel that their ED is “in their heads” and that “their provider will dismiss any sexual problems they might bring up,”2 it may be a relief for patients to learn that their ED is physical, related to their diabetes, and treatable. To this end, the goal of this article is to review the epidemiology, pathophysiology, quality of life effect, and treatment of ED in men with type 2 diabetes.


Whereas lifestyle modification is a reasonable initial step when approaching a hypertensive patient with sexual dysfunction, finding the appropriate antihypertensive treatment is usually the next “complicated” move to care for. Several observational and clinical studieshave consistently associated antihypertensive medication with sexual dysfunction[20]. Whether one class of antihypertensive agents is associated exclusively or more with erectile dysfunction compared to another, however, is a difficult puzzle to solve as there are many other factors (comorbid conditions, concomitant medications, personal characteristics) to be taken into account at the same time. In addition, erectile dysfunction has never been studied as the primary end-point before and as a result a definite causative relationship between antihypertensive medication and sexual dysfunction has never been proven.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (25) | Google ScholarSee all References Hemodynamic stress also may cause rupture of a vulnerable atherosclerotic plaque resulting in angina, myocardial infarction, or sudden cardiac death.80x80Muller, JE. Triggering of cardiac events by sexual activity: findings from a case-crossover analysis. Am J Cardiol. 2000; 86: 14F–18F
Erectile dysfunction is an accurate predictor of heart attacks and strokes in the future. Psychogenic components play a role in erectile dysfunction, but the most common and primary cause in most men is organic vascular insufficiency, meaning not enough blood gets to the penis. Erectile dysfunction usually occurs one to five years before a male manifests overt signs of cardiovascular disease. The first sign may be death.

Conversely, and of significant clinical importance, is how often patients with ED as their first and sole clinical manifestation suffer from subclinical CAD.17 Previous studies reported a rate of inducible ischaemia by exercise stress testing (EST) in 22% (with a wide range of 5–56%) of ED patients reflecting differences in patient population, risk factors and criteria used for ED and CAD diagnosis. Interestingly, those patients further assessed with coronary angiography had obstructive atherosclerosis in >90% of cases.4,18 In a prospective angiographic study, we documented that 19% of ED patients suffer from clinically silent obstructive CAD.18


Normal male sexual function requires a complex interaction of vascular, neurological, hormonal, and psychological systems. The initial obligatory event is acquisition and maintenance of an erect penis, which is a vascular phenomenon. Normal erections require blood flow into the corpora cavernosae and corpus spongiosum. As the blood accelerates, the pressure within the intracavernosal space increases dramatically to choke off penile venous outflow. This combination of increased intracavernosal blood flow and reduced venous outflow allows a man to acquire and maintain a firm erection.
PubMed | Google ScholarSee all References This prolonged excretion half-life produces enhanced erections up to 36 hours after oral dosing, thereby potentially allowing for more spontaneous engagement of intercourse. The efficacy of tadalafil in the treatment of ED has been proved in randomized double-blind, placebo-controlled trials.78x78Porst, H, Padma-Nathan, H, Giuliano, F, Anglin, G, Varanese, L, and Rosen, R. Efficacy of tadalafil for the treatment of erectile dysfunction at 24 and 36 hours after dosing: a randomized controlled trial. Urology. 2003; 62: 121–125
Co-authors Stacy Mandras, M.D., Patricia Uber, Pharm. D., and Mandeep Mehra, M.D., conducted systematic independent literature searches using the MEDLINE database and examined a broad range of medical research that focused on chronic heart failure, sexual activity and sexual dysfunction. This literature included data from patient surveys and clinical trials.
This category of treatments includes external vacuum therapies: devices that go around the penis and produce erections by increasing the flow of blood in, while constricting the flow out. Such devices imitate a natural erection, and do not interfere with orgasm. External vacuum therapy mechanisms are approximately 95 percent successful in causing and sustaining an erection. All are portable, and costs range between $200-$500, covered under most insurance plans and Medicare Part B.
For many men, stopping smoking is an erectile dysfunction remedy, particularly when ED is the result of vascular disease, which occurs when blood supply to the penis becomes restricted because of blockage or narrowing of the arteries. Smoking and even smokeless tobacco can also cause the narrowing of important blood vessels and have the same negative impact. 
PubMed | Google ScholarSee all References Unlike sildenafil, vardenafil has been associated with a slight prolongation of the QT interval and thus should not be used by patients with a congenital QT prolongation or by any patient currently taking antiarrhythmic medications.67x67Vardenafil (levitra) for erectile dysfunction. Med Lett Drugs Ther. 2003; 45: 77–78
Experimental in vivo studies have implicated central and peripheral neuropathy, impaired neurotransmission, and endothelial dysfunction in the pathogenesis of diabetic ED.26,27 Copulatory behavior and penile reflexes are uniformly impaired 4–12 months after the onset of diabetes in the BB rat.26,27 McVary et al.26 found that peripheral neuropathy accounts for only part of the dysfunctional findings, and that spinal sexual reflexes were also severely impaired.

Erectile dysfunction can be a symptom of heart disease. An erection is caused by engorgement of blood into the penile tissues which later becomes rigid for penetration. Men with heart problem suffer from an inadequate blood flow to the smooth tissues of the penis to achieve erection. A major cardiovascular disease known as Atherosclerosis is a result of fat accumulation in the arterial blood vessels. This build up of multiple plaques or fatty material causes the arteries to narrow and harden thus limiting blood flow. The arteries supplying your penis are smaller than those supplying your heart. In fact, ED can be an initial symptom of heart diseases like Atherosclerosis. Cardiovascular problems can also damage penile nerves and arteries, inhibiting erectile function. Experts found a consistent link between ED and heart disease. Other recent research conducted by health professionals has shown a direct connection between erection dysfunctions and heart problems.
Crossref | PubMed | Scopus (539) | Google ScholarSee all References Aside from the economic costs, ED can have severe psychological effects, resulting in poor self-image, decreased self-esteem, depression, and mental stress, and negative effects on personal relationships.2x2NIH Consensus Development Panel on Impotence. NIH Consensus Conference: impotence. JAMA. 1993; 270: 83–90
This form of therapy has a response rate of well over 70%. The sympathetic nervous system normally maintains the penis in a flaccid or non-erect state. All of the vasoactive drugs, when injected into the corpora cavernosae, inhibit or override sympathetic inhibition to encourage relaxation of the smooth muscle trabeculae. The rush of blood engorges the penile corpora cavernosae sinusoidal spaces and creates an erection.
Abstract | Full Text | Full Text PDF | PubMed | Scopus (95) | Google ScholarSee all References During this period, 130 deaths were reported to the US FDA; 41 of these men died or had cardiac arrest within 4 to 5 hours after taking sildenafil, and 27 died or had cardiac arrest either during or immediately after sexual activity. The average age of these men was 64 years. Of the 77 men in this group who died of documented cardiovascular-related events, 41 died of definite or suspected myocardial infarction, 27 died after cardiac arrest, and 6 had symptoms of cardiac disease at the time of death. Sixteen of the men had taken nitroglycerin or organic nitrates in association with sildenafil; another 3 had nitroglycerin in their possession at the time of death. In 48 men, the cause of death was unknown, and another 3 died of cerebrovascular accidents. Overall, it was concluded that sildenafil was not associated with an excess of cardiovascular death.
• Blood Vessels: Diabetes damages blood vessels, especially the smallest blood vessels such as those in the penis. Diabetes can also cause heart disease and other circulatory problems. Proper blood flow is absolutely crucial to achieving erection. “Erection is a hydraulic phenomenon that occurs involuntarily,” says Arturo Rolla, MD, of Harvard University School of Medicine. “Nobody can will an erection!” Anything that limits or impairs blood flow can interfere with the ability to achieve an erection, no matter how strong one’s sexual desire.
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