Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References Overall, sexual intercourse does not lead to an extremely exaggerated heart rate or blood pressure level when performed in a familiar setting with one's usual partner.82x82Hellerstein, HK and Friedman, EH. Sexual activity and the postcoronary patient. Arch Intern Med. 1970; 125: 987–999


Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References Overall, sexual intercourse does not lead to an extremely exaggerated heart rate or blood pressure level when performed in a familiar setting with one's usual partner.82x82Hellerstein, HK and Friedman, EH. Sexual activity and the postcoronary patient. Arch Intern Med. 1970; 125: 987–999

Abstract | Full Text | Full Text PDF | PubMed | Scopus (66) | Google ScholarSee all References However, patients with hypertrophic obstructive cardiomyopathy and idiopathic hypertrophic subaortic stenosis are at increased risk of syncope and sudden death after exercise.51x51DeBusk, R, Drory, Y, Goldstein, I et al. Management of sexual dysfunction in patients with cardiovascular disease: recommendations of the Princeton Consensus Panel. Am J Cardiol. 2000; 86: 62F–68F
Although ED can become a permanent condition, this typically isn’t the case for men who experience occasional erectile difficulties. If you have diabetes, you may still be able to overcome ED through a lifestyle that includes sufficient sleep, no smoking, and stress reduction. ED medications are usually well-tolerated, and can be used for many years to help overcome any ED problems.
Cardiovascular disease remains our nation’s biggest killer, responsible for about one-third of deaths in the U.S.1 Erectile dysfunction (ED) is typically the first clinical manifestation of cardiovascular disease, making it a helpful early marker for men who are likely to die of heart attacks. There is a strong relationship between erectile dysfunction and high blood pressure, high cholesterol, angina, stroke, heart attack and a premature death.2, 3

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


Finally, prevalence rates will be affected by whether the study population is accrued from a single hospital/clinic setting or from a more general population of men with diabetes. For example, Siu et al.4 studied 500 Chinese diabetic men (of which 97% had type 2 disease) seen at a single medical clinic in Hong Kong during 1999 and found the overall prevalence of ED to be 63.6%. Contrast this to Fedele et al.,5 who studied 9,756 diabetic men accrued from 178 diabetes centers in Italy. Among the 8,373 men with type 2 diabetes, only 37% reported ED, considerably less than in the Chinese study.
Alprostadil is an ED drug that comes in two forms. One form (Caverject, Caverject Impulse, or Edex) is injected into the side of the penis to increase blood flow and cause an erection within 5 to 20 minutes. Its effects last 1 hour or less. The most common side effect is pain. Other side effects include bruising, redness, numbness, bleeding, and irritation.
Taking one of these tablets will not automatically produce an erection. Sexual stimulation is needed first to cause the release of nitric oxide from your penile nerves. These medications amplify that signal, allowing some men to function normally. Oral erectile dysfunction medications are not aphrodisiacs, will not cause excitement and are not needed in men who get normal erections.
Since 1998, when sildenafil (brand name Viagra) first came on the market, oral therapy has been successfully used to treat erectile dysfunction in many men with diabetes. (Sildenafil was followed in 2003 by the drugs tadalafil [Cialis], vardenafil [Levitra] and avanafil [Stendra], which work in much the same way.) Some 50% of men with Type 1 diabetes who try the drugs report improved erections, and some 60% men with Type 2 diabetes do, too. However, that leaves a large percentage of men with diabetes and erectile dysfunction who do not respond to therapy with one of these pills. This article takes a look at what can be done to treat those men who do not respond to oral therapy.
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