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Erectile dysfunction and quality of life

An article from the e-journal of the ESC Council for Cardiology Practice

Erectile dysfunction (ED) is not only an indicator of unsatisfactory sexual intercourse, it is also closely interrelated with cardiovascular disease. ED is much more common in subjects with atherosclerotic disease and with risk factors for atherosclerosis. On the other hand, ED may be an early sign of atherosclerotic disease or an independent risk factor for cardiovascular disease.

Drugs used in the treatment of ED can have, in coronary patients treated with nitrates, detrimental consequences and should therefore be -in this population- prescribed very carefully.

Risk Factors and Prevention

Erectile dysfunction, representing the inability to develop and maintain an erection or satisfactory sexual intercourse, is not just an important determinant of quality of life, but it needs to be considered as a significant public health concern related also to cardiovascular diseases. The data show that nearly half of all men between the ages of 45 and 65 may have erectile dysfunction. It is increasingly prevalent in men at the age of 70 in whom a rate of erectile dysfunction  increases to close to 70 % (1).

The development of an erection is a complex event involving the integration of psychological, neurological, endocrine, vascular and local anatomic systems. Among them, atherosclerotic vascular disease represents one of the most important and frequent causes of erectile dysfunction and it is much more common in people who have cardiovascular risk factors.

In one epidemiological study, the prevalence of complete ED among patients with hypertension, ishaemic heart disease and peripheral vascular disease was 26 %, 38% and 57 %, respectively, compared with 18.6 % for the full study population (2). Reported ED in patients hospitalised for myocardial infarction or coronary artery surgery is in the 57 to 64% range (3). Solomon and coworkers found that ED shares the same risk factors as coronary artery disease and that 30% of patients with ED had an intermediate or high cardiovascular risk (4).

On the other hand, erectile dysfunction may be an early sign of atherosclerotic disease or a risk factor for coronary heart disease, stroke or peripheral arterial occlusive disease. It was shown that in patients with ED, there is a 16% risk of severe ishaemic heart disease (5) and a statistically significant correlation was shown between ED and a number of occluded coronary vessels (6).

The relationship between ED and atherosclerotic cardiovascular disease is present not only in vasogenic impotence, where the patients have similar lesions in penile as well as in coronary and other parts of arterial system, but is expected in subjects with functional circulatory disturbances represented by endothelial dysfunction as well. The endothelium namely plays a very important role in cardiovascular homeostasis through the release of vasoactive substances including nitric oxide (NO). Decreased bioavailability of nitric oxide as a cause for endothelial dysfunction is not only the earliest indicator of vascular damage in atherosclerotic disease, but is also involved in erectile function. Nitric oxide is thought to be released from non-adrenergic, non-holinergic nerves and endothelial cells. Nitric oxide stimulates the guanylate cyclase enzyme system in penile smooth muscles. This results in an increased level of cyclic guanosine monophosphate and ultimately in smooth muscle relaxation and in the enhancement of blood flow. The presence of atherosclerotic disease and risk factors that increase oxidative stress cause increased consumption of NO and endothelial dysfunction in different parts of the circulatory system (7). As the endothelial dysfunction is usually a systemic disorder, it is expected that all factors that influence the endothelial function of peripheral or coronary arteries could be involved in the development of ED (8).

The identification of patients with ED is very important not only for the quality of life of an individual patient, but as a risk indicator for cardiovascular events. Therefore, in patients with ED, risk factors for atherosclerosis should be identified and aggressively treated. With the treatment of risk factors for atherosclerosis, the improvement of endothelial dysfunction and ED is expected. Thus, proper identification of risk factors for atherosclerosis is of utmost importance for both the prevention of cardiovascular events and ED.

The most popular drugs used for treatment of ED are phosphodiesterase type-5 (PDE-5) inhibitors, which include sildenafil (Viagra), vardenafil (Levitra) and tadalafil (Cialis). These drugs have shown to be safe in most patients with heart disease. However PDE-5 drugs can be dangerous for some patients with coronary heart disease, since they can interact with other medications especially nitrates and cause critical decrease of blood pressure (9). Therefore all three drugs are contraindicated in patients who use nitroglycerin or nitrate-containing compounds – medications commonly used to treat coronary heart disease.

Further, vardenafil is contraindicated in patients using doxazosin, terazosin, or tamsulosin. Tadalafil is contraindicated in patients using doxazosin and terazosin. In patients who take 50 mg of sildenafil or higher and use alpha-blockers, sildenafil dosing should be avoided for at least 4 hours after the administration of the alpha-blocker dose. In patients who take 25 mg of sildenafil, the use of any of the alpha-blockers is considered safe (10).

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.

Conclusion:

Therefore ED and cardiovascular disease are, because of their similar  ethiopathogenetic mechanisms, closely interrelated. However the drugs used in treatment of ED may have detrimental effects in patients with coronary heart disease.

References


1. Laumann EO, Paik A, Rosen RC. Sexual dysfunction in the United States; prevalence and predictors. JAMA 1999; 281: 537-44.
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2. Chew KK, Earle CM, Stuckey BGA, et al. Erectile dysfunction in general medical  practice: prevalence and clinical correlates. Int J Impot Res 2000; 12: 1-5.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10982311&query_hl=6&itool=pubmed_docsum

3. Gundle MJ, Reeves BR, Tate S, et al. Psychosocial outcome after aortocoronary artery surgery. Am J Psychiatry 1980; 137: 1591-4.
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4. Solomon H, Man J, Werzbicki AS, OBrien T, Jackson G. Erectile dysfunction:cardiovascular risk and the role of the cardiologist.  Int J Clin Pract 2003; 57: 96-9.
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5. Anderson M, Nicholson B, Louie E, Mulhall JP. An analysis of vasculogenic erectile dysfunction as a potential predictor of occult cardiac disease. J Urol 1998; 159 (5): 30: 118.
6. Greenstein A, Chen J, Miller H, et al. Does severity of ischaemic coronary disease correlate with erectile funciton? Int J Impot Res 1997; 9: 123-6.
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7. Poredoš P. Endothelial dysfunction and cardiovascular disease. Clin Appl Thromb 2002; 32: 274-7.
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8.  Feldman HA, Mc Kinlay JB, Goldstein I, Longcope C. Erectile dysfunction, cardiovascular disease and cardiovascular risk factors: prospective results in a large random sample of Massachusestts men. J Urol 1998; 159: 91: 347.

9.  DeBusk 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: 175-81.
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10. DeBusk RF, Pepine CJ, Glasser DB, Shpilsky A, DeRiesthal H, Sweeney M. Efficacy and safety of sildenafil citrate in men with erectile dysfunction and stable coronary artery disease. Am J Cardiol. 2004; 93: 147-53.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14715338&query_hl=45&itool=pubmed_docsum

VolumeNumber:

Vol4 N°16

Notes to editor


Pavel Poredoš
Department of Vascular Diseases, University Medical Centre, Ljubljana, SloveniaChairperson of the ESC Working Group on Peripheral Circulation

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.