Erectile dysfunction in the practice of a cardiologist

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The development of modern medicine along the path of narrow specialization has led to the emergence of specialists in coronary heart disease, arterial hypertension, etc. At the same time, it is obvious that it is impossible to consider these diseases in isolation from the whole body: they lead to damage to all organs and systems, including the development of erectile dysfunction.

Erectile dysfunction (ED) is defined as “the inability to achieve and / or maintain an erection sufficient to satisfy sexual activity” (Impotence. NIH Consensus Development Panel on Impotence. 1993) in the event that these disorders have been observed for at least 3 months.

In fact, for most men, the main cause of erectile dysfunction is vascular disease. Almost all epidemiological studies on ED have revealed a link between its occurrence with arterial hypertension (AH) and atherosclerosis. Moreover, according to some authors, the detection of ED may indicate the presence of one of these diseases in a latent form in a patient (Nusbaum M. R. et al., 2002).

With atherosclerosis, the walls of blood vessels lose elasticity and narrow due to the atherosclerotic plaques covering them, which leads to the development of heart attacks and strokes. Due to the atherosclerotic lesion of the vessels of the penis, not only a mechanical violation of blood flow occurs, but the production of neurotransmitters is also disrupted, the elasticity of the vessels decreases. Often, various manifestations of atherosclerosis (for example, coronary heart disease and ED) develop in parallel, since the risk factors for endothelial dysfunction and atherosclerosis affecting penile blood vessels are the same as the risk factors for coronary heart disease – smoking, dyslipidemia, diabetes mellitus (Kloner R. A., Speakman M., 2002). The risk of developing coronary disease in patients over the age of 50 years is significantly increased in the presence of ED (Speel T. G. W. et al., 2003). It is assumed that ED can serve as a marker of cardiovascular diseases, and its severity can be used to judge the progression of coronary heart disease (Greenstein A. et al., 1997, Kirby M. et al., 2001, Solomon H. et al., 2003). With a significant decrease in penile blood flow according to ultrasound Dopplerography, some authors even recommend performing stress ECG tests before starting ED treatment (Kawanishi Y. et al., 2001).

Arterial hypertension also contributes to the occurrence of ED, even in the absence of atherosclerosis. According to Roth A. and co-author. (2003), the frequency of ED among patients with hypertension is 46%. International experimental studies on arterial hypertension and ED were summarized at the European Conference on Hypertension in 2003 in Milan. According to the presented data, arterial hypertension promotes the proliferation of muscle tissue in the cavernous bodies and blood vessels, causes fibrosis of the cavernous tissue and increases the amount of collagen III in it. At the same time, the severity of these changes is directly proportional to the degree of increase in systolic blood pressure.

In addition, the development of ED is often associated with inadequate hypotensive therapy. It is believed that 25% of cases of ED are somehow associated with taking medications (Slag M. F. et al., 1983, O’Keefe M. et al., 1995). The clinical signs of drug-induced ED are considered to be a relatively rapid onset, a temporary connection with taking a drug that negatively affects various parts of sexual intercourse, and a decrease in the severity of the disorder or its complete disappearance after discontinuation of the drug. Very often, the occurrence of ED is associated with the use of antihypertensive drugs, especially thiazide diuretics and b – blockers (Fogari R, Zoppi A., 2002, Mickley H., 2002, Ralph D., McNicholas T., 2000). Several studies, which together took more than 30 years, showed that from 2.4% to 58% of men with arterial hypertension experience one or more symptoms of sexual dysfunction of varying severity during treatment with antihypertensive drugs. The occurrence of erectile disorders certainly reduces the patients ‘ adherence to treatment and, ultimately, worsens the prognosis of these patients. Thus, in a five-year study by the Medical Research Council, which included 17,354 patients with arterial hypertension, it was shown that violations of sexual function are a common cause of patients ‘ non-compliance with the treatment regimen or complete refusal of patients from taking antihypertensive drugs. Premature discontinuation of treatment due to ED was observed significantly more often in patients taking a thiazide diuretic or a b-blocker, compared with patients receiving a placebo (12.6%, 6.3% and 1.3% per 1000 person–years, respectively).

To date, there are a lot of reports about the occurrence of ED against the background of therapy with b-blockers. D. T. Ko et al. (2002) conducted a meta-analysis and evaluated the safety of the use of b-blockers in arterial hypertension and coronary heart disease. It was shown that the use of drugs of this group is associated with a small, but statistically significant risk of sexual dysfunction (1 additional case for every 199 patients treated with b-blockers during the year). first-generation b-blockers are more likely to cause ED than modern drugs, and their ability to cause ED does not depend on the degree of lipophilicity.

According to L. M. Prisant (2002), the combined use of bisoprolol at a dose of 2.5-10 mg per day and hydrochlorothiazide at a dose of 6.25 mg per day does not provoke the development of ED. We conducted a study on the comparative assessment of the effect of monotherapy with atenolol and bisoprolol on erectile function in men with arterial hypertension. The study included 144 male patients with arterial hypertension aged 25 to 50 years (average age 39.2 years). Bisoprolol, to a much lesser extent than atenolol, affected the erectile component of the MCF scale, increased the linear velocity of blood flow (according to Dopplerography) and blood filling of the penis (according to radioisotope phallography).

It is assumed that ED may occur due to a decrease in blood flow to the penis, but it is unclear whether this decrease is a consequence of a decrease in systemic blood pressure with effective antihypertensive therapy, a result of vascular disease or a manifestation of any other unknown effects of the drug (Bansal S., 1988). If a decrease in blood pressure itself contributed to the development of ED, then it would develop against the background of any hypotensive therapy. It has been proven, however, that many antihypertensive drugs do not cause ED. Thus, in a randomized double-blind cross-design study by R. Fogari et al. (1999), against the background of taking the angiotensin receptor inhibitor valsartan, there was even a tendency to increase male sexual activity. Similar data on losartan were obtained by J. L. Llisterri et al. (2001), who evaluated its effectiveness and safety in 82 men with sexual dysfunction. Against the background of therapy with this drug at a dose of 50 mg per day for 12 weeks, a noticeable and statistically significant increase in sexual satisfaction was noted – from 7.3% of patients initially to 58.5% after treatment (p<0.001). In addition, the use of this drug increased the proportion of patients with a high frequency of sexual intercourse (40.5% compared to 62.3%), improved the quality of life in 73% of patients and reduced the proportion of patients who reported ED (75.3% compared to 11.8%).

The multicenter controlled study “LIFE”, which included about 10,000 patients aged 50-80 years, also did not reveal a negative effect of losartan on the sexual function of men. As it was noted at the European Conference on Arterial Hypertension in 2003 in Milan, the use of angiotensin receptor blockers significantly reduces changes in the cavernous tissue that develop with arterial hypertension.

It is believed that calcium antagonists also do not worsen male sexual function. In any case, in the study of J. E. Marley (1989), who studied the tolerability of long-acting nifedipine (20 mg 2 times a day), 4 weeks after the start of therapy, the frequency of ED decreased both in the group of patients who had previously received treatment with b-blockers and diuretics, and in the group of patients who had not previously received treatment.

In many cases, changing the medication regimen can help the patient overcome the negative changes in the sexual sphere observed with some types of treatment. In addition, it is advisable to choose such a hypotensive treatment that would not only be highly effective in terms of reducing blood pressure, but also would preserve the quality of life of the patient. For example, with the development of ED in patients with arterial hypertension, thiazide diuretics and non-selective b-blockers are canceled. In this situation, preference is given to calcium antagonists, angiotensin-converting enzyme inhibitors and a-blockers, which have a lesser effect on the sexual sphere (Khan M. A. et al., 2002, Ferrario C. M., Levy P., 2002) or angiotensin receptor inhibitors, which can even slightly increase the sexual activity of men (Fogari R, Zoppi A., 2002). If it is necessary to prescribe b-blockers (in patients with arterial hypertension, ischemic disease, with heart rhythm disorders), modern highly selective drugs, such as bisoprolol, become the drugs of choice in patients with ED.

So, a practical doctor should remember about the possibility of the influence of antihypertensive therapy on the sexual sphere of men and discuss this problem with his patients (Ferrario C. M., Levy R., 2001). It is believed that it takes only 4-6 minutes on average for a practitioner to collect a medical, sexual history and analyze the psychological state of a patient (Kuritzky L., 2002). But how much is it necessary for the patient? In a study by Bedell S. T. et al. (2002) 188 men (average age 75 years) who suffered from arterial hypertension in 54%, with a history of myocardial infarction in 41% and diabetes mellitus in 11% of cases answered the questions of the cardiologist questionnaire.

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