Erectile disfunction. Cavernous erectile dysfunction

Erectile dysfunction is a fairly common condition, affecting up to 2/3 of men with confirmed CAD, and endothelial dysfunction is now considered a common factor explaining the association between organic erectile dysfunction and CAD in men over 40 years of age.

The appearance of erectile dysfunction may precede the development of CHD symptoms in endothelial dysfunction of the same severity due to the small size of the penis arteries (1-2 mm) compared to the coronary arteries (3-4 mm).

It has now been proven that erectile dysfunction can be a marker and possibly an independent risk factor for asymptomatic CHD, with a time window of about 2-5 years from the onset of erectile dysfunction to the first manifestations of CHD. This opens up additional opportunities to reduce the risk of CVD in men with erectile dysfunction in the absence of cardiac symptoms. Thus, erectile dysfunction can be considered as equivalent to vascular or cardiac pathology. Erectile dysfunction may precede both the chronic course of coronary artery disease and acute. The performance of stress tests does not allow to determine the subclinical condition - the presence of lipid-rich and prone to rupture atherosclerotic plaques that stenose the lumen of the coronary arteries by less than 50%. However, the latest research methods using 64-layer MSCT make it possible to detect atherosclerotic changes in a normal ECG at the maximum load of the treadmill test in patients with erectile dysfunction in the absence of cardiac symptoms.

Both men and women with cardiac pathology should be properly informed about the nature of possible sexual activity as part of a comprehensive approach to rehabilitation. Some therapies are showing promising results in the treatment of erectile dysfunction. Currently, there is no evidence that erectile dysfunction therapy increases the risk of developing heart and vascular disease, provided that men (and their partners) have been properly examined. Sexual life is part of normal life for all age groups, and there is no reason why patients with cardiac pathology cannot satisfy desires in sexual relationships.

Currently, erectile dysfunction is a fairly common condition affecting more than 150 million men worldwide. According to the results of the Massachusetts Study of the Process of Aging in Men, the incidence of erectile dysfunction was 52% in American men aged 40-70 years, progressing in proportion to age. Thus, men over 70 years of age are subject to erectile dysfunction three times more often than men aged 40 years. Given the general aging of the human population, age is no longer an obstacle to sexual activity, thereby increasing the importance of the task of identifying and treating patients with erectile dysfunction. According to the forecast, by 2025 more than 300 million people will be affected by erectile dysfunction.

Currently, a fairly large number of studies confirm the theory that erectile dysfunction is predominantly a vascular pathology with common risk factors with coronary artery disease and often occurs 2-5 years before the onset of cardiac symptoms. The presence of a common pathophysiological factor in the form of endothelial dysfunction, as well as the possibility of using erectile dysfunction as a marker or independent risk factor for asymptomatic CAD, is of great interest due to the possibility of reducing risk factors for CAD in men with erectile dysfunction in order to prevent further cardiac events.

Despite the fact that the most common cause of erectile dysfunction in men over 40 years of age is of an organic (vascular) nature, an integrated approach is very important in this situation, since the organic genesis of the disease invariably has psychological consequences in the form of depression, a decrease in self-esteem and the emergence of feelings of inferiority. Erectile dysfunction is a fairly common cause of the destruction of sexual relations, and therefore it is also desirable to involve a sexual partner in solving this problem. Thus, in addition to maintaining erectile function, the patient also needs to provide adequate psychosocial support. In turn, patients with a predominantly psychosomatic nature of erectile dysfunction may also have risk factors for CVD that require special attention.

When consulting cardiac patients about the amount of possible sexual activity, an individual approach is very important, despite the existence of statistically standardized recommendations. So, for example, taking into account the functional state of the heart (including after a myocardial infarction), it is necessary to limit physical activity depending on the volume of the infarct zone. In addition, each patient has individual questions regarding the safety of sex, the treatment of erectile dysfunction, as well as the possibility of returning to their usual daily activities, including sexual activity. When making recommendations on sexual activity, it must be remembered that many problems in this area can precede the development of cardiovascular events and have serious consequences for relationships with partners.

Cardiovascular reactions during intercourse

The cardiovascular response during intercourse is similar to moderate or moderate daily physical activity. Several studies have been performed using ambulatory ECG and BP monitoring, the purpose of which was to compare heart rate, ECG and BP during daily exercise, as well as during intercourse. Nemec and colleagues studied ten healthy married men. They found only modest differences regardless of position during intercourse. Thus, in the "man on top" position, a peak heart rate of up to 114±14 per minute was recorded, which decreased to 69±12 per minute 120 s after orgasm. In the "man from below" position, the peak heart rate was 117±4 per minute. The peak of the rise in blood pressure, the same in both positions, was 160 mm Hg. at the moment of orgasm. Bohlen and colleagues, also in a survey of ten healthy men, evaluated the performance during intercourse in various positions, during masturbation, and also when stimulating partners and found no significant difference in heart rate and blood pressure. Although there are significantly fewer studies of women who have undergone, the cardiovascular response in men and women has similar rates with a peak heart rate of 111 per minute in men and 104 per minute in women, with a recovery period of 3.1 and 2.6 minutes, respectively. On 24-hour ECG monitoring in patients with stable angina, the average heart rate was 122 per minute with a range of 102-137 per minute (30 men and 5 women) during intercourse compared to a maximum heart rate of 124 per minute during the day.

Expressed in Metabolic Equivalent Units, sexual activity in couples in long-term sexual relationships at the peak of the load during orgasm is 3-4 METs (Metabolic Equivalent Load, 1 unit corresponds to energy expenditure at rest, namely 3.5 ml of oxygen per kilogram body weight per minute). Young couples, due to their greater activity, spend up to 5-6 METs during coitus. The duration of sexual intercourse is on average about 5-15 minutes, so sex is not a prolonged or excessive load on the cardiovascular system. However, casual sex can be associated with a high cardiovascular burden due to lack of close communication or mismatch in the age of partners, most often in older men with younger women.

Thus, with the help of MET units, we can advise our patients on the amount of possible sexual activity, using simple and understandable comparisons, such as walking at a moderate pace for 1.6 km (1 mile) in 20 minutes.

Metabolic Units (METs) as an opportunity to compare daily activities and sexual activity

Risk of cardiovascular complications during sex

There is a fairly low risk of myocardial infarction associated with sexual activity. The relative risk of developing myocardial infarction within 2 hours after intercourse is presented in the table.

Relative risk of myocardial infarction within two hours of intercourse: physical health reflects the ability to be sexually active

A patient who fails to reach 3-4 METs should be further examined using angiographic diagnostic methods.

Advice to patients about sexuality, based on the principles of determining MET in the clinical setting, should include advice on avoiding stress, limiting large meals or excessive consumption of alcoholic beverages before intercourse.

Although ECG monitoring during the exercise test is a method for assessing the risk of coronary events in patients with erectile dysfunction, it does not reveal the presence of lipid-rich and prone to rupture atherosclerotic plaques in coronary arteries that occlude the lumen by less than 50%.

Erectile dysfunction in cardiac patients

Erectile dysfunction and coronary artery disease are two pathologies with common risk factors, usually found in combination with endothelial dysfunction acting as a unifying link.

The clinical consequence of endothelial dysfunction is the development of atherosclerosis, acute coronary syndrome, CHF, and erectile dysfunction. It is now known that a defect in the NO-cyclic guanosine-3′5′-monophosphate system of smooth muscle cells serves as an early marker of systemic vascular damage that appears before the development of clinically overt cardiovascular disease in men with erectile dysfunction.

Endothelial function has been found to improve with drugs that reduce cardiovascular morbidity and mortality (ACE inhibitors for CHF; statins and ACE inhibitors for CAD), as well as drugs used to treat erectile dysfunction, CHF and diabetes mellitus (phosphodiesterase inhibitors fifth type). Over the past ten years, after a direct link between erectile and endothelial dysfunction has been identified, it has become apparent that erectile dysfunction can be treated with phosphodiesterase-5 inhibitors, acting on smooth muscle cells and thereby improving endothelial function.

Risk factors for cardiovascular disease

Common risk factors for cardiovascular disease and erectile dysfunction include smoking, hyperlipidemia, diabetes mellitus, hypertension, obesity, and a sedentary lifestyle.

In the Massachusetts Study of Male Aging, in a large population randomized sample of 1290 healthy men aged 40-70 years, the age-standardized probability of complete erectile dysfunction was 15% in patients receiving antihypertensive therapy and 9.6% in the entire population. In another study, the presence of erectile dysfunction was noted in 17% of men with untreated arterial hypertension compared with 25% of men receiving antihypertensive therapy.

However, more recent studies of hypertensive patients show that the prevalence of erectile dysfunction in hypertension is higher. Burchardt et al. sent out a questionnaire on the international index of erectile function to 476 male patients with arterial hypertension. One hundred and four patients (mean age 62.2 years) completed the questionnaire. Of these, 68.3% had isolated manifestations of erectile dysfunction, in 7.7% of cases, erectile dysfunction was mild, in 15.4% moderate and severe in 45.2% of cases. Compared with the general population, patients with hypertension had more severe erectile dysfunction (45.2% in patients with hypertension versus about 10% of the general population, as reported by the Massachusetts Male Aging Study). The authors concluded that erectile dysfunction is a more common pathology in patients with arterial hypertension, even after adjusting for age, and the degree of erectile dysfunction is more severe than in the male population as a whole. Another study also confirmed a very high rate of erectile dysfunction among hypertensive patients. In a survey of 7689 patients (mean age 59 years) using the Sexual Health Inventory in Men (SHIM questionnaire) in 3906 people with only arterial hypertension (without diabetes mellitus), erectile dysfunction was present in 67%, which is comparable to the above data - 68%. In 2377 men with diabetes, erectile dysfunction was present in 71%, and in 1186 men with hypertension and diabetes, erectile dysfunction was present in 77%. In 65% of cases, erectile dysfunction remained without therapy, although the majority of men agreed with the need for treatment. It becomes obvious that a significant number of patients with arterial hypertension may have a clinic of erectile dysfunction.

According to the Massachusetts Male Aging Study, smoking doubled the likelihood of developing erectile dysfunction over an 8-year follow-up period and increased the incidence in men with hypertension. Smoking is also known to be a risk factor for endothelial damage and vascular disease. And while smoking cessation later in life may benefit the 3-4 mm coronary arteries, it may be too late to reverse the damage done to the small (1-2 mm) penile arteries.

Organic nitrates (nitroglycerin, isosorbide mononitrate, isosorbide dinitrate) and other nitrate-containing drugs used to treat angina pectoris, as well as amyl nitrite, are completely incompatible with phosphodiesterase-5 inhibitors. Their joint appointment leads to an increase in the level of cGMP in the cells, an unpredictable drop in blood pressure and symptoms of arterial hypotension. The duration of interaction of organic nitrates with phosphodiesterase-5 inhibitors for specific phosphodiesterase-5 inhibitors and nitrates is being studied.

If a patient taking phosphodiesterase-5 inhibitors develops chest pain, nitroglycerin should be administered no earlier than 12 hours in the case of sildenafil (or vardenafil, which has a half-life of 4 hours) and no earlier than 48 hours in the case of the use of tadalafil (half-life 17.5 hours). If a patient develops angina pectoris while taking phosphodiesterase-5 inhibitors, he should be informed about the need to stop sexual activity and assume a vertical position, then the formation of a pool in the venous bed will mimic the venodilating effect of nitrates. If the pain persists, it is necessary to prescribe other drugs under medical supervision in a hospital setting or to carry out intravenous administration of nitrates under strict medical supervision.

Co-administration of phosphodiesterase-5 inhibitors with antihypertensive agents (ACE inhibitors, ARBs, slow calcium channel blockers, β-blockers, diuretics) can lead to a slight increase in the hypotensive effect, which is usually not very pronounced. In general, the side effects of phosphodiesterase-5 inhibitors do not increase with antihypertensive therapy, even when the patient receives combination antihypertensive therapy.

parenteral therapy

Direct intracavernous injections of vasodilators began to be used in 1980. Prostaglandin-E 1 is a substance produced in the body that leads to relaxation of muscle cells and dilation of arterioles, increasing blood flow in the penis. Alprostadil is the commercial name for the dosage form of prostaglandin-E 1, the action of which develops within 5-15 minutes, and the resulting erection usually lasts longer than 30 minutes, and sometimes several hours. The initial dose of alprostadil is 1.25 mcg, it can be increased to 40 mcg depending on the effect. It is important to inform the patient about the correct injection technique, patients with impaired motor activity in the hands (due to arthritis of the joints of the hand, tremor) need the help of a partner when performing the injection. It is known that injection can be part of sexual activity. After the introduction of the drug and removal of the needle, the injection site must be firmly pressed and gently massaged for better distribution of the drug in the penis for about 30 seconds. In the case of taking anticoagulants, the injection site must be pressed for 5-10 minutes.

Erections as a result of the action of alprostadil occur without stimulation, but stimulation can increase its severity. Sometimes an erection can be painful, but the sensations are usually the same as those experienced with a natural erection. The drug should not be used more often than once every 4 days.

Alprostadil is effective in more than 80% of cases, and its use is accompanied by the resumption of spontaneous erections in 35% of patients. It is effective and safe in diabetic patients receiving insulin therapy. Despite the high efficiency, the frequency of refusal of treatment with alprostadil is quite high, which is most often associated with local pain and loss of spontaneous erections.

intraurethral therapy

Intraurethral therapy with alprostadil is an alternative to injection therapy. The intraurethral drug delivery system is intended for single use and involves the administration of a 1.4 mm diameter pill using a hand-held device after urination and approximately 15 minutes before sexual intercourse. As with the use of injection therapy, the patient must be informed about the correct technique for administering the drug. Patients should receive an initial dose of 250 micrograms of the drug with gradual titration in the range of 125-1000 micrograms under medical supervision until the effect is sufficient. Doses of the drug for intraurethral therapy are much higher than for injection therapy, since the drug is distributed in the total volume of circulating blood. During the day it is allowed to use no more than 2 doses. It is necessary to choose a dose suitable for the patient, at which an improvement would be achieved in 60%, although in the study with parenteral administration this figure decreased to 43% (70% received parenteral treatment).

Non-drug therapy

Psychotherapy

In the case of the development of psychogenic erectile dysfunction, patients need to provide specialized psychotherapeutic assistance. Even if the cause of rectile dysfunction is an organic pathology, very often there may be a secondary psychological component, which requires the joint work of the attending physician and psychotherapist.

Vacuum pumps

The vacuum pump has long been used as a means of conservative treatment of erectile dysfunction. This is a non-invasive method that provides an erection by creating a negative pressure of up to 250 mm Hg, thereby causing blood flow to the corpora cavernosa. Further, the erection is maintained by rubber rings placed on the base of the penis. However, the time of use of the constriction ring should not exceed 30 minutes due to the risk of ischemic damage.

It should be noted that while taking anticoagulant therapy, patients may develop hematomas (in 10% of cases, minor hemorrhages), which is a relative contraindication to the use of the pump. Thus, before using vacuum devices, a doctor's consultation and special training are required. The use of pumps is also not recommended for men with curvature of the penis.

Surgery

When conservative methods of treatment do not give positive results, and also if there was a history of trauma to the penis, surgery remains another treatment option. Cardiac patients should not be deprived of this type of treatment. Obviously, consultation with a doctor is necessary, and the attending physician should consult with a urologist and, together with a cardiologist, assess the risk of cardiac problems.

Testosterone

There is now increasing evidence that low testosterone levels in men are associated with all-cause mortality, and especially cardiovascular death. Thus, the question arises: will substitution therapy in old age have a beneficial effect, especially given the age-related decline in androgen levels?
Low testosterone is associated with many risk factors for CVD, including visceral obesity. Considering that testosterone replacement therapy in patients with hypogonadism reduces obesity, and obesity, in turn, is an independent risk factor for CVD, the concept of replacement therapy to reduce cardiac risk factors is of considerable interest. In addition, low testosterone levels are associated with reduced glucose tolerance, type 2 diabetes (regardless of obesity), and metabolic syndrome. Thus, the likelihood that replacement therapy in men with low testosterone levels will help prevent the development of type 2 diabetes mellitus, the progression of the metabolic syndrome and reduce the risk of developing CVD associated with these diseases increases.

With regard to the blood coagulation system, there is evidence that testosterone replacement therapy reduces fibrinogen levels and increases the activity of the fibrinolytic system, as well as reduces platelet aggregation. Low testosterone levels are associated with increased levels of inflammatory markers (interleukin-6 and C-reactive protein), which are risk factors for CVD. Data on hyperlipidemia during replacement therapy are rather contradictory (a 10% decrease in LDL levels is compensated by a 10% decrease in HDL).

The vascular effect of testosterone is also considered to be potentially beneficial, influencing smooth muscle cells directly through potassium and calcium channels. The experiment revealed the development of dilatation of the coronary arteries after a single injection of testosterone. In men with stable angina, after 3 months of transdermal testosterone administration, there was a decrease in ischemia during exercise, as well as an increase in the threshold for angina pectoris.

The results of the European Prospective Investigation into Cancer in Norfolk (EPIC-Norfolk) study have recently been published. During the 6-10-year study of the causes of death from cancer and CVD, testosterone levels were also assessed. Baseline endogenous testosterone levels were inversely related to all causes of death. Although the authors concluded that low testosterone levels may be a marker of high CV risk, they noted the need for a randomized, placebo-controlled trial. The Rancho-Bernardo study found similar results over a 20-year follow-up period, including that men with testosterone levels in the lower quartile had a 40% higher risk of dying mainly from diseases of the cardiovascular and respiratory systems. Interestingly, this indicator did not depend on age, lifestyle, hyperlipidemia and obesity.

Currently, there is not enough evidence that testosterone replacement therapy reduces the risk of developing CVD, which raises the question of the need for an extensive placebo-controlled study. Reassuringly, replacement therapy does not increase the risk of CVD and can also be used safely in patients with hypogonadism.

Advice for cardiac patients on sexual issues

Arterial hypertension

• Not a contraindication if recommendations for blood pressure control are followed

• If the patient is receiving medical therapy: antihypertensive drugs (mono- or combination therapy) are not a contraindication, but care must be taken when prescribing doxazosin (and other non-selective α-adrenergic blockers) and phosphodiesterase-5 inhibitors

• You can use any means for the treatment of erectile dysfunction

• The antihypertensive agents least likely to cause erectile dysfunction include angiotensin receptor blockers and doxazosin.

angina pectoris

• Patients with stable angina have a minimal chance of complications from sexual activity or treatment of erectile dysfunction.

• Taking nitrates or nicorandil is a contraindication for phosphodiesterase-5 inhibitors. Removing them is safe in most cases.

• Drugs that reduce heart rate are the most effective antianginal agents: β-blockers, verapamil, diltiazem.

• If necessary, use exercise ECG for risk stratification.

Past myocardial infarction (postinfarction cardiosclerosis)

• To determine the possibility of resuming sexual activity, you can conduct a stress test with ECG registration before and after discharge; in case of satisfactory results, the resumption of sexual activity should not be delayed

• Given the decline in confidence of both the patient and his partner, a gradual return to previous sexual activities should be recommended.

• Rehabilitation programs have a positive effect.

• Sexual relations should be avoided in the first two weeks (during the period of maximum risk).

Condition after major and percutaneous interventional surgery

• If the intervention is successful, the risk of complications is low.

• The sternal suture may be painful; recommended position on the side and the position when the patient is on top. You can use a soft pillow, placing it in the area of ​​the sternal suture.

• If in doubt, use an exercise test with ECG recording.

Heart failure

• The risk of complications is low if exercise tolerance is good.

• If symptoms are present, select appropriate drugs; the patient should take a more passive side in sexual relations.

• In the case of severe symptoms, sexual activity may be unacceptable due to the limitation of physical activity, and may also contribute to decompensation of CHF.

• A physical rehabilitation program may facilitate a return to sexual activity; physical condition reflects opportunities for sexual activity.

Valvular defects

• In mild cases, the risk is low.

• Severe aortic stenosis can lead to sudden death and is aggravated by the use of phosphodiesterase-5 inhibitors due to their vasodilating effect.

Arrhythmias

• Controlled atrial fibrillation does not increase the risk of complications, which depends on the cause and exercise capacity.

• Warfarin is not a contraindication to vacuum devices, but care must be taken when using them and when injecting.

• Complicated arrhythmias: Perform 24-48 hour ECG monitoring and exercise testing, and follow up after treatment.

• The presence of artificial pacemakers is not a contraindication.

• In ICD, a stress test should be done first to determine the possibility of sexual activity. In most cases, this is not a hindrance.

Other states

• In the case of pericarditis, it is necessary to wait for a complete recovery, after which there is no increase in the risk of complications.

• In the case of obliterating diseases of the vessels of the lower extremities, stroke or transient cerebrovascular accident, the risk of developing myocardial infarction is increased, therefore, additional examinations are necessary before making recommendations.

• In hypertrophic obstructive cardiomyopathy, there is an increased risk of syncope and sudden death on exertion. It is recommended to perform a stress test with ECG recording. Phosphodiesterase-5 inhibitors and alprostadil can lead to an increase in the degree of obstruction due to a vasodilatory effect. It is recommended to start treatment with a trial dose in a hospital under the supervision of medical personnel.

Conclusion

Patients with heart disease may have concerns about sexual activity due to their unfounded beliefs about a possible increased risk of complications. Erectile dysfunction is a frequent occurrence in patients with CVD, as there are common risk factors that have a negative impact on endothelial function. Symptoms of erectile dysfunction often precede overt symptoms of heart disease, so clinical evaluation for CVD is warranted in these patients even in the absence of a history of cardiovascular disease. Currently, there is an increasing amount of information about the treatment of erectile dysfunction, but many patients are reluctant to accept advice. In routine clinical practice, physicians should discuss with patients with cardiovascular disease the problems of the possibility of sexual activity and advise them on the treatment of erectile dysfunction. Treatment is currently available. With support, encouragement and detailed explanation, patients with CVD who have received appropriate advice can continue sexual relationships.

Future prospects

Knowing that erectile dysfunction is an early warning sign of the presence of asymptomatic lesions of the coronary and other vessels, it is always necessary to conduct a screening examination of men with erectile dysfunction and without symptoms of cardiovascular pathology. According to the Princeton Consensus Guidelines, all men with erectile dysfunction who do not have symptoms of heart disease should be treated as having a heart (or vascular) disease until proven otherwise. Such patients should be given a complete medical evaluation to determine whether their cardiovascular risk is high, moderate, or low. Patients at low risk should be advised to make lifestyle changes, including increased physical activity and weight loss, as well as regular monitoring and evaluation by their physician. Patients at increased risk for adverse cardiovascular events should undergo exercise testing and risk-reducing treatment.

Although an exercise stress test with ECG recording is encouraged to identify patients at increased cardiovascular risk, this method will only help detect stenosing, blood-limiting coronary artery disease. Whenever possible, patients of intermediate and high risk should be referred for selective CT, coronary angiography to identify atherosclerotic plaques containing lipids that do not restrict blood flow, but are prone to rupture. Prior to these studies, taking advantage of the 2-5 year "time window" between the development of symptoms of erectile dysfunction and coronary artery disease, early aggressive therapy should be initiated, if possible, aimed at reducing the risk of developing CVD in patients at high risk. However, to fully realize this potential, a comprehensive education program is needed to encourage men with erectile dysfunction to seek medical attention as early as possible when symptoms appear. In addition, an interdisciplinary approach is required, including the joint work of the family doctor, nurses, pharmacist, urologist, diabetologist and cardiologist.

Diseases of the heart and blood vessels. Ed. A.J. Camm, T.F. Luscher, P.V. Serrius. Translation from English. / Ed. E.V. Shlyakhto

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Impotence (Erectile Dysfunction)

Impotence (Erectile Dysfunction) is the inability to achieve and/or maintain an erection sufficient for satisfactory sexual activity.
Erectile dysfunction can occur at any age, but is most common in older men. The prevalence of the disease in people aged 40 to 70 years is 52%, increasing with age. If up to 40% of men experience potency disorders of varying severity by the age of 40, then by the age of 70 their number reaches 67%.

Etiology and pathogenesis of erectile dysfunction.

Erectile dysfunction (impotence) is a multifactorial state. Any factors leading to a decrease in blood flow to the cavernous bodies (arterial insufficiency of the penis) or to an increase in outflow from them (veno-occlusive dysfunction) can be the cause of erectile disorders. Erectile dysfunction is usually associated with chronic diseases, primarily with atherosclerosis, arterial hypertension, diabetes mellitus, depression and neurosis-like diseases. Erectile disorders often occur when exposed to adverse environmental factors - radiation, electromagnetic radiation. Cause of impotence there may be chronic diseases of the vascular, endocrine, nervous systems, pelvic, or spinal injury. Loss of erectile function may be the result of radical operations on the pelvic organs.

The main risk factors for erectile dysfunction are age, smoking, overweight. Among smokers, impotence occurs 15-20% more often than among non-smoking men.

More than 200 drugs are known that can inhibit sexual function. These include some antihypertensives (clonidine, beta-blockers, reserpine), gastrointestinal (cimetidine, ranitidine, metoclopramide), psychotherapeutic (amitriptyline, fluoxetine) and all antineoplastic drugs.

The pathogenesis of erectile dysfunction is variable. There are psychogenic, organic and mixed forms of erectile disorders.

Psychogenic erectile dysfunction is caused by central suppression of the erection mechanism. The main conditions leading to psychogenic erectile dysfunction are depression and phobic neuroses. In some cases, disorders occur according to the psychosomatic type.

Organic erectile dysfunction is divided into vasculogenic, neurogenic and hormonal forms.

Vasculogenic erectile dysfunction can be associated with both arterial and veno-occlusive disorders.

Among neurogenic erectile dysfunction, spinal trauma and multiple sclerosis are in the first place in terms of frequency of occurrence.

Hormonal erectile dysfunction occurs with Pasqualini's syndrome, Itsengo-Cusheng's disease, endocrinopathies leading to hyperprolactinemia and a decrease in testosterone levels. It should be noted that in most cases of organic erectile dysfunction, secondary psychogenic disorders are noted.

Symptoms and clinical course of the disease.

Terminologically, it is customary to single out adequate, spontaneous and masturbatory erections. Adequate means erections that occur during sexual contact. Spontaneous erections are reflex, occur outside of sexual activity, more often in the phase of REM sleep, disappearing upon awakening (another term is nocturnal penile tumescence). Tumescence (blood filling, swelling of the penis to the size of an erect organ) is one of the phases of erection development.

Manifestations of erectile dysfunction largely depend on the etiopathogenetic form of suffering. For psychogenic impotence, as a rule, a sudden, sharp weakening of adequate erections is characteristic, with the preservation of spontaneous and masturbatory ones. The quality of sexual function may be dependent on the sexual partner, forms of coitus and situational circumstances. In some cases, there are disorders of ejaculation, orgasm and libido.

Vasculogenic forms of erectile dysfunction lead to a gradual weakening, sometimes up to the complete disappearance, of both adequate and spontaneous erections. Libido (sexual desire), as a rule, is preserved. For vascular lesions, episodes of detumescence without ejaculation are characteristic (a sharp weakening of the tension of the penis, making it impossible to continue coitus). Generalized vascular damage (atherosclerosis, obliterating endarteritis, Leriche's syndrome) can manifest itself as a "steal syndrome": with intense friction, the erection weakens due to the redistribution of blood to working muscles. The vasculogenic nature of impotence may be indicated by an increase in erection in orthostasis and a weakening in clinostasis. A long period of tumescence can be observed in arterial insufficiency.

Manifestations of erectile dysfunction of neurogenic etiology depend on the level of damage to the nervous system. With cortical and "high" spinal disorders, spontaneous erections and erections with tactile stimulation can be preserved according to the reflex type. "Low" spinal and peripheral neuroreceptor lesions lead to suppression of both spontaneous and adequate erections while maintaining libido. Often, neurogenic impotence is accompanied by ejaculation disorders.

Impotence, developing against the background of androgen deficiency, hyperprolactinemia in most cases progresses gradually and is accompanied by a weakening of libido.

Diagnostics

Diagnosis of impotence(erectile dysfunction) - is based on sexological testing, which involves a comprehensive assessment of the state of sexual function and begins with a thorough collection of an anamnesis of the disease. In the course of a confidential conversation, attention should be paid to all aspects of the patient's sexual life (the form and conditions of coition, the development and nature of erectile dysfunction, both adequate and spontaneous, the preservation of libido, the presence of orgasm and ejaculation disorders). It is also necessary to take into account the relationship in the couple and the attitude sexual partner to the existing problem, as this information determines the relevance and motivation. When collecting anamnesis, it is necessary to try to find out the causative factors, the presence of risk factors, chronic diseases, in particular diabetes mellitus, arterial hypertension, neurological diseases, injuries, surgical interventions on the bladder, prostate gland, rectum.

The severity of erectile disorders can be determined already at the stage of analysis of anamnestic data. There are compensated (minimal), subcompensated (moderate) and decompensated (pronounced) forms of erectile dysfunction.

On examination, attention is paid to constitutional features, the development of secondary male sexual characteristics, the condition of the external genitalia, and the prostate gland.

Laboratory diagnostics includes the study of the hormonal blood profile (testosterone, estradiol, prolactin, gonadotropic hormones).
Artificial pharmacological erection (pharmacological test) is used to assess the quality and duration of erection. A vasoactive drug (prostaglandin E1, papaverine, phentolamine, or a combination thereof) is administered intracavernously to induce blood supply to the cavernous bodies. The degree of erection is assessed according to the Yunema scale (1987):
Er0 - no response to the drug administration.
Er1 - insignificant tumescence.
Er2 - incomplete tumescence.
Er3 - complete tumescence without rigidity.
Er4 - partial rigidity.
Er5 - complete rigidity (erection) of the penis.

Registration of nocturnal tumescence of the penis is carried out using a ring equipped with control threads, worn on the penis during sleep. (Figure 1). Breakage of the control threads indicates the presence of spontaneous erection (tumescence). A qualitative assessment of spontaneous blood filling is assessed using the Rigiscan device, which graphically registers changes in the tension of the penis using strain gauges installed on it. Pharmacodopplerography - ultrasound Doppler scanning of the vessels of the penis in combination with an intracavernous pharmacological test allows you to assess the state of blood flow in the penis in various phases of erection. Hemodynamic parameters obtained at baseline and 10 minutes after intracavernous administration of a vasoactive drug are compared. In addition to objective data on the state of arterial blood flow, Doppler sonography makes it possible to detect indirect signs of a violation of the veno-occlusive cavernous mechanism.

Cavernosography– method of X-ray diagnostics of cavernous veno-occlusive dysfunction and cavernous fibrosis. The radiopaque preparation is administered intracavernously. On the radiograph, the structural state of the cavernous bodies and the filling of the venous outflow tracts with a contrast agent are recorded. 10 minutes after the intracavernous injection of a vasoactive drug, the study is repeated. A sign of veno-occlusive dysfunction is contrasting of the spongy bodies of the glans penis and urethra, deep dorsal vein, internal pudendal veins and prostate-vesical plexus, which persists after the administration of a vasoactive drug. (Figure 2). Local decrease and heterogeneity of contrasting of the cavernous bodies can be regarded as a sign of focal (partial) sclerosis of the cavernous tissue. (Figure 3).

Electromyography of the penis- a method for diagnosing neurogenic erectile dysfunction. It is carried out in combination with an intracavernous pharmacological test using surface or needle electrodes. The criteria for evaluating the innervation of the penis are the amplitude, frequency, shape and synchronism of the recorded potentials. Normally, the amplitude and frequency of synchronous potentials decrease as tumescence increases, and isoelectric silence is recorded at the height of erection.

Examination of a patient with erectile dysfunction should be carried out in collaboration with specialists of related specialties - a psychoneurologist, neuropathologist, endocrinologist and, if necessary, include additional examination methods (for example, in case of degenerative diseases of the spine - radiography and magnetic resonance imaging of the spine). Anamnestic indications of trauma to the pelvis and / or perineum are an indication for magnetic resonance imaging of the pelvic floor and penis (diagnosis of structural disorders, local fibrosis).

Must be etiopathogenetic. Etiotropic therapy involves the treatment of diseases that led to the occurrence of erectile disorders, such as diabetes mellitus, degenerative diseases of the spine, hyperprolactinemia, and neuroses.

Methods for the treatment of impotence can be both conservative and operative. For long-term drug treatment of erectile dysfunction, adaptogens and biogenic stimulants (extracts and tinctures of ginseng, eleutherococcus, zamaniha, aralia, pantocrine), angioprotectors, antiplatelet agents, vasodilators, alpha-blockers, antioxidants, drugs based on plant derivatives in combination with physiotherapeutic drugs are used. methods aimed at stimulating blood circulation. Course therapy with the above drugs is aimed at stabilizing vascular tone, increasing the elasticity of the vascular wall and is effective in compensated forms of vasculogenic erectile dysfunction.

In the treatment of neurogenic erectile disorders, prozerin, duplex, B vitamins, and methods of physiotherapy are used.

Hormone therapy is carried out strictly according to indications, depending on the nature of endocrine disorders. With androgen deficiency, testosterone derivatives are used.

Separate place in erectile dysfunction treatment occupied by the methods of sexual adaptation of patients, aimed at a one-time increase in natural or induction of an artificial (pharmacological) erection used to commit coitus within the framework of one sexual excess. These include various vacuum erectors, peripherally acting vasoactive drugs for injectable intracavernous (alprostadil, papaverine hydrochloride, phentolamine) or endourethral (alprostadil "MUSE") use, as well as tableted sildenafil citrate (Viagra). These forms of drug correction are indicated for subcompensated and decompensated stages of vasculogenic erectile dysfunction. In patients with psychogenic erectile dysfunction, the appointment of intracavernous vasoactive drugs, or Viagra, in combination with psychotherapy can help normalize the psychological status and restore sexual activity.

Surgical treatment of impotence is indicated for subcompensated and decompensated forms of organic erectile dysfunction. With arterial insufficiency of the penis and veno-occlusive dysfunction caused by excessive venous discharge, operations are performed aimed at creating additional arterial inflow to the cavernous bodies (revascularization of the penis). The most widespread revascularization operations according to the methods of Virag, Hauri, Kovalev - various types of anastomoses between the lower epigastric artery and the dorsal vein of the penis.

The essence of operations aimed at correcting veno-occlusive disorders (spongiolysis, ligation and resection of the deep dorsal vein, immersion of the deep dorsal vein into the duplication of the albuginea, plication of the pedicles of the penis) is to eliminate the predominant path of the pathological venous outflow from the cavernous bodies. Currently, venous surgery techniques are used in combination with penile revascularization in cases of veno-occlusive dysfunction.

Decompensated forms of erectile dysfunction, especially those caused by cavernous (myogenic) insufficiency, cavernous fibrosis, ineffectiveness of drug therapy and revascularization of the penis are indications for phalloendoprosthetics. Modern plastic and especially hydraulic models of prostheses make it possible to model the penis, imitating a natural erection in accordance with the functional need.

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Latest answers to questions from a urologist - andrologist on the topic of erectile dysfunction

Kirill 02.11.2015 | Moscow

Good afternoon! I am being treated for erectile dysfunction, I have poor blood flow, and testosterone is now normal. The doctor prescribed me to drink Cialis (5 mg). At first he said that you need to drink from 1 month to 3 months. And when he was at the last consultation, he said that he would drink these pills all his life, because it is a chronic disease. It turns out that erectile dysfunction is not fully restored in order to have sexual intercourse without pills, or did the doctor say it wrong? Why, then, they write everywhere that erek ...

Sergey May 29, 2013 | Moscow

Good afternoon! I'm 55 and have erectile dysfunction. The problems started about 5 years ago. Passed a paid examination at the Hospital on Turgenevskaya. I have on hand the results of all tests (general blood, urine, blood biochemistry, infections, ELISA, PSA, PSR, prostate secretion and testosterone levels). Almost all tests are good, there are no infections and diseases. Diagnosis - chronic prostatitis and low (below the lower limit) testosterone levels. I am a pensioner and have no money for paid treatment. Can I get...

Erectile dysfunction (ED)(IMPOTENCE) - is one of the most common diseases of modern andrology. According to the latest data, ED occurs in 53-55% of men over 45 years of age. In Russia, according to some data, every third man over 40 suffers from ED; in Ukraine, this figure for men reaches 52%.

According to the modern definition, ED is understood as "the inability to achieve and (or) maintain an erection of the penis sufficient for satisfactory sexual activity."

For many years it was believed that the occurrence of ED is more of a psychogenic factor. Based on numerous studies, it has been proven that ED is most often based on the factor of vascular damage.

In accordance with the currently generally recognized classification of ED, 7 types of ED are distinguished according to the etiopathogenetic principle:

I. Psychogenic erectile dysfunction
The leading pathogenetic link in psychogenic impotence is a decrease in the sensitivity of the cavernous tissue to the effects of erection neurotransmitters as a result of a direct inhibitory effect of the cerebral cortex or an indirect effect of the cortex through the spinal centers and an increase in the level of peripheral catecholamines. These phenomena are based on overwork, depression, sexual fears and deviations, religious prejudice, etc. In recent years, with the development of methods for objective diagnosis of erectile dysfunction, psychogenic impotence in its pure form is diagnosed much less frequently.

II. Vasculogenic erectile dysfunction
It is divided into 2 forms:
Arteriogenic erectile dysfunction.
The age and pathomorphological dynamics of atherosclerotic lesions of the coronary and penile arteries approximately correspond to each other, which makes it possible to consider erectile dysfunction as a disease of age. Other causes of arteriogenic impotence are trauma, congenital anomalies, smoking, diabetes mellitus, hypertension. In the presence of limited arterial inflow, the intracellular metabolism of the cavernous tissue and the endothelium of the afferent vessels suffers significantly, which forms a vicious circle and often leads to irreversible dysfunction of the cavernous tissue.

Venogenic erectile dysfunction.
For reasons of violation of venocclusive function, 3 types of venous erectile dysfunction are distinguished:
Primary venous erectile dysfunction occurs with congenital pathological drainage of the cavernous bodies through large dorsal saphenous veins or enlarged cavernous or leg veins, cavernous-spongiform shunting, etc.
Secondary venous erectile dysfunction occurs due to a decrease in the elasticity of the cavernous tissue, as a result of which there is no compression of the emissary veins of the albuginea and the implementation of a passive veno-occlusive mechanism. The reasons for this are the functional insufficiency of the cavernous erectile tissue as a result of a lack of neurotransmitters, psychogenic inhibition, smoking, sclerosis and fibrosis of the cavernous tissue.
Corporovenous insufficiency occurs due to insufficiency of the albuginea as a result of traumatic rupture, Peyronie's disease, primary or secondary thinning.

III. Hormonal erectile dysfunction
The cause of hormonal erectile dysfunction is a lack of male sex hormone, either due to congenital or acquired hypogonadism, or due to age-related decline in male sex hormone (PADAM syndrome).
With androgen deficiency, the pathogenesis of erectile dysfunction has three components:
Decreased sexual desire (emotional and motivational tension) and, as a result, a decrease in erectile function
Inhibition of the formation and release of neurotransmitters and nitric oxide (the main mediator of erection). these processes are hormone-dependent.
Reversible dystrophy of the cavernous tissue with androgen deficiency, which leads to a decrease in its elasticity and the formation of secondary venous erectile dysfunction.

IV. Neurogenic erectile dysfunction
It occurs as a result of injuries or diseases of the brain or spinal cord, as well as peripheral nerves that prevent the passage of nerve impulses to the cavernous bodies. The most common cause of non-genic erectile dysfunction is spinal cord injury (up to 75%). Other causes may be neoplasms, cerebrovascular pathology, syringomyelia, multiple sclerosis, herniated disc, etc.

V. Medical erectile dysfunction
Drug-induced erectile dysfunction occurs in individuals taking medications that adversely affect sexual function.
The drugs most commonly associated with ED include:
- cardiovascular drugs (hypotensive, β-blockers, sympatholytics, diuretics, cardiac glycosides),
- hormonal (estrogens, corticosteroids, antiandrogens, progestins),
- psychotropic drugs (antidepressants, MAO inhibitors, lithium preparations, tranquilizers)
- drugs of other groups (cytostatics, non-steroidal anti-inflammatory drugs, weight loss agents).

VI. Cavernous erectile dysfunction
The causes of cavernous insufficiency are different. These causes lead to dystrophy of the smooth muscles of the cavernous tissue, to a decrease in the percentage of elastic fibers and induction of the development of fibrous tissue. All this leads to a decrease in the elasticity of the cavernous bodies and the formation of secondary venous leakage. This is due to a violation of vascular, nervous and biochemical processes in the cavernous tissue against the background of the underlying disease.
The main causes of cavernous erectile dysfunction are diabetes mellitus, chronic intoxication (alcoholism, chronic heavy metal poisoning), smoking, etc.

VII. Mixed form of erectile dysfunction
With a mixed form of erectile dysfunction, various etiological factors can be the cause.

Turning to the urologist with complaints of weakening of erection, in most cases, the doctor mistakenly puts the emphasis of diagnosis on the identification of any form of prostatitis and its further treatment. Of course, prostatitis can cause weakening of erections, but more often the reason is not in it.

Erectile dysfunction (ED) due to inflammatory diseases of the genital organs. The cause of ED can be inflammatory processes in the genital organs caused by sexually transmitted infections (chlamydial, mycoplasmal, gonococcal, trichomonas). The pathogenesis of these lesions lies in the fact that, on the one hand, ED can develop as a result of lesions of the genital organs (prostate gland, seminal tubercle, seminal vesicles), and on the other hand, as psychogenic. In ED caused by these diseases, along with damage to the receptor apparatus, there is a violation of other parts of the nervous regulation of sexual function, in particular, sexual spinal centers are involved in the pathological process. Patients often present with various neurological disorders.

The chronic course of inflammatory processes in the genital organs, frequent relapses, fear of complications that can lead to violations of sexual function, excessive fixation of patients' attention on their condition cause a permanent and prolonged psycho-traumatic situation. Often, the patient's attempt to have sexual intercourse ends in failure due to the lack of an adequate erection at the necessary moment. As a result, the clinical course of ED worsens.

The clinical picture of ED caused by inflammatory lesions of the genital organs is characterized by a progressive decrease in potency with a weakening of erection while maintaining sexual desire. However, in some cases, such patients also showed a decrease in sexual desire. Characterized by weakness, sleep disturbance, decreased performance, depression, which are caused by impaired sexual function and in themselves can be the causes of functional disorders, maintain the spinal centers of erection and ejaculation in a state of pathological excitation, and thereby contribute to the development of ED.

DIAGNOSTICS.

So, we can distinguish the main diagnostic methods for erectile dysfunction:
1. Physical examination and conversation with the patient.
2. Laboratory tests (general blood count, urine, blood glucose, cholesterol).
3. Blood test for sex hormones.
4. Testing the patient according to the international index of erectile function (IIEF).
5. Tests with the use of vasoactive drugs.
6. Dopplerography of the vessels of the penis (at rest and erection).
7. Cavernosography.
8. Ultrasound of the abdominal cavity and small pelvis.
9. Urethral secretion analysis, prostate secretion analysis, prostate secretion culture tank.
10. Examination for STDs.

The scope of the examination is carried out selectively and individually for each patient and depends on many factors.

TREATMENT.
The treatment of ED today includes non-invasive (drug therapy, the use of vacuum constrictor devices) and invasive methods (intracavernous injections (ICI) of vasoactive substances and surgical treatment).

In the treatment of ED, three lines of therapy can be distinguished:
First line therapy.
The first line of therapy consists of prescribing a range of oral medications. To date, there are three selective phosphodiesterase type 5 inhibitors on the market, approved by the European Medicines Agency, with proven efficacy and safety in the treatment of ED: sildenafil (Viagra), tadalafil (Cialis), vardenafil (Levitra).
Vacuum-constrictive devices. Can be used by patients who do not want to take medications or in the complex therapy of ED. The device creates a negative pressure around the penis, which promotes the flow of venous blood into it, which is then retained in it with the help of a compression ring worn on the base of the penis. Side effects of this treatment include penile pain, numbness, and delayed ejaculation.
Psychotherapy. Psychotherapy is the leading method of treatment for all forms of sexual disorders. It can serve both as monotherapy and in combination with other therapeutic methods. Practice shows that even with organic disorders of potency, when resorting to surgical correction, psychotherapeutic effects must be applied both before surgery and after surgical treatment.

Second line therapy.
Patients not responding to oral medications, as well as in complex therapy, can be offered intracavernous injections or intraurethral drugs eg. Prostaglandin E1 (underutilized recently). Several drugs have been proposed for intracavernous administration, they can be used individually and/or in combination. An erection occurs after 5-15 minutes, its duration depends on the administered dose of the drug.

third line therapy.
The third line of therapy includes surgical treatment, namely endophalloprosthetics and vascular surgery. Surgical implantation of penile prostheses may be offered to patients for whom medical treatment has failed or who prefer a permanent solution to their problem.

Of course, today, the most effective method of treating severe forms of erectile dysfunction is endophalloprosthetics, but, in most cases, preference is given to non-surgical methods of treatment.

We use all modern non-invasive and invasive treatments for all types of erectile dysfunction, including the most modern technique - low-energy shock wave therapy (NUVT), which promotes neoaniogenesis in the cavernous bodies of the penis.

Impotence is a violation of potency, sexual impotence, manifested in the inability of a man to have sexual intercourse. It often serves as a manifestation of the underlying disease and is eliminated by its cure (endocrine, nervous, cardiovascular disorders, diseases of the urogenital area). Erectile dysfunction can cause deep psychological depression, disharmony of sexual and family relationships. Erectile dysfunction or impotence is manifested by the inability to achieve an erection sufficient for a full-fledged sexual intercourse while maintaining psychological comfort during it.

General information

- violation of potency, sexual impotence, manifested in the inability of a man to have sexual intercourse. It often serves as a manifestation of the underlying disease and is eliminated by its cure (endocrine, nervous, cardiovascular disorders, diseases of the urogenital area). Erectile dysfunction can cause deep psychogenic depression, disharmony of sexual and family relationships.

Erectile dysfunction or impotence is manifested by the inability to achieve an erection sufficient for a full-fledged sexual intercourse while maintaining psychological comfort during it. Recently, the pathogenesis and causes of erectile dysfunction have been sufficiently studied in order to restore normal sexual life, and today the problem of impotence is not difficult to solve.

Physiology of erection and detumescence

The smooth muscles of the cavernous bodies and the walls of the arteries and arterioles perform the main function in the process of erection and in the process of detumescence - a decline in erection after ejaculation or due to reasons that prevented the natural end of sexual intercourse. In a calm state, the smooth muscles of the penis are under the influence of sympathetic nerve endings. At the moment of sexual arousal or stimulation of the penis, impulses transmitted through parasympathetic nerve fibers cause the release of erection neurotransmitters, blood filling of the cavernous bodies occurs. This complex chemical process takes place with the mandatory participation of nitric oxide. First, there is relaxation and relaxation of smooth muscles, which in turn contributes to unimpeded blood filling. Increasing in size from the incoming arterial blood, the cavernous bodies partially block the outflow of venous blood. Due to the difference in the volume of inflow and outflow of blood, intracavernous pressure increases, which contributes to the development of a rigid erection.

Immediately after ejaculation, the cessation of sexual stimulation, or for other reasons, the reverse process begins - detumescence. After the activation of synaptic structures, such neurotransmitters as norepinephrine and neuropeptide are released into the blood.

Both of these processes are controlled by the middle preoptic zone of the cerebral cortex; in general, the sexual activity and sexual behavior of a man depends on the concentration of dopamine-like substances that have a stimulating effect, and seratonin-like substances that have an inhibitory effect. Violations in any link of the whole process can lead to impotence.

Symptoms of impotence

Depending on the pathogenesis of erectile dysfunction, there are several types of impotence.

Psychogenic impotence can be both permanent and temporary, this type of impotence can occur in men who are subject to frequent mental and physical overwork, having certain psychological difficulties or problems finding a partner. Temporary psychogenic impotence disappears after the normalization of lifestyle.

Psychogenic impotence, in the pathogenesis of which lies a decrease in the sensitivity of the cavernous tissue to neurotransmitters due to the inhibitory effect of the cerebral cortex or due to indirect influence through the spinal centers, can occur against the background of sexual phobias and deviations, associative psychotraumas and religious prejudices. Today, thanks to the development of diagnostics between true and psychogenic erectile dysfunction, psychogenic impotence in its purest form, as, for example, happens with serious sexual deviations (pedophilia, bestiality) is diagnosed less often.

Neurogenic impotence occurs against the background of injuries and diseases of the central nervous system and peripheral nerves. The pathogenetic link is the difficulty or complete absence of the passage of nerve impulses into the cavernous bodies. In 75% of cases, the cause of neurogenic impotence is spinal cord injury. The remaining 25% account for neoplasms, cerebrovascular pathologies, herniated discs, multiple sclerosis, syringomyelia and other neurogenic diseases.

Arteriogenic impotence is an age-related pathology, since atherosclerotic changes in the coronary and penile vessels are identical. At an early age, arteriogenic impotence can occur due to congenital vascular anomalies, smoking, hypertension, diabetes mellitus, or due to trauma. Insufficient arterial blood flow is not able to fully nourish the cavernous tissues and vascular endothelium, local metabolism is disturbed, which can lead to irreversible dysfunctional disorders of the cavernous tissue.

Pathogenesis venogenic impotence not studied enough, but its development is facilitated by disturbances in the venous bloodstream, in which the lumen of the veins increases. This happens with ectopic drainage of the cavernous bodies through the venous vessels of the penis, with traumatic ruptures of the albuginea, resulting in its insufficiency. Venogenic impotence often accompanies Peyronie's disease and functional insufficiency of the cavernous erectile tissue. Smoking and alcohol abuse exacerbate the symptoms of venogenic impotence.

Hormonal impotence most often develops against the background of diabetes mellitus, since in diabetes mellitus changes in penile vessels and cavernous tissue are quite serious. But at the same time, the cause of hormonal impotence is not so much in a decrease in testosterone levels, but in a violation of its absorption, because in individuals with hypogonadism, erection problems were not observed when stimulating. But with hypogonadism and male menopause, hormone replacement therapy is carried out as the main treatment for erectile dysfunction.

Cavernous insufficiency or dysfunction of the cavernous tissue can also lead to impotence. In the pathogenesis of this type of impotence are changes in the cavernous bodies, blood vessels and nerve endings that disrupt the erection mechanism.

Kidney diseases, in which extracorporeal dialysis is indicated for patients, in half of the cases are combined with erectile dysfunction, while after kidney transplantation, two-thirds of patients restore erectile abilities. Prostatitis can cause impotence both due to insufficient serum testosterone levels and due to circulatory psychogenic disorders: pain during ejaculation, premature ejaculation and iatrogenic conditions in which failure syndrome is formed.

In patients with bronchial asthma, in a post-infarction state, impotence is due to the fear of an exacerbation of the disease during intercourse.

Prostatitis is not the main cause of impotence, it can only aggravate its course, this should be borne in mind, since most men believe that only prostatitis can cause erectile dysfunction.

Diagnosis of impotence

All diagnostic procedures are aimed at establishing the cause of impotence, which means the possibility of restoring erectile function and eliminating emotional experiences. To do this, first of all, it is necessary to differentiate psychogenic and organic impotence. A simple and reliable method is to monitor nocturnal erections and intracavernous injection test (coverject test). If, according to these methods, the organic nature of impotence is confirmed, then a number of additional examinations are carried out to identify the underlying cause.

impotence treatment

Modern andrology has a fairly wide choice of schemes and methods for the treatment of erectile dysfunction. The choice of treatment method is based on the decision of the andrologist and on the acceptability of the use for the given patient. Drug therapy for impotence is a traditional method of treatment, usually they resort to testosterone replacement therapy and drugs from the group of adrenergic blockers. Against the background of the main treatment, courses of such drugs as trazodone, trimipramine, nitroglycerin, metachlorphenylpiperazine are periodically carried out - they are used in the form of ointment applications. The effectiveness of drug therapy does not exceed 30%, so drugs are not indicated for all patients.

Psychotherapy can be the main treatment for psychogenic and neurogenic impotence, but on condition that psychotherapeutic procedures are carried out professionally. Vacuum-erectile therapy, which was developed in 1970 by Dr. D. Osbon, if carried out correctly, gives an efficiency of up to 83%; complications in the form of petechial hemorrhages, painful intercourse occur in isolated cases.

Intracavernous drug therapy is a relatively new treatment for impotence. For the first time, papaverine was administered intracavernously to improve erectile function (1982), then phentolamine, prostaglandin E1 and other drugs began to be used. Minimal side effects, high efficiency and ease of use gives the drug prostaglandin E1; the use of this technique in 80% of cases allows you to have a quality sex life without any restrictions.

When using papaverine and phentolamine for intracavernous drug therapy of impotence, priapism and cavernous fibrosis sometimes occurred as complications, which is extremely rare when using prostaglandin E1. The only disadvantage of this method of impotence therapy is the pain of injections, therefore, after injections of prostaglandin E1, an injection of 7.5% sodium bicarbonate is made to relieve pain. Since this method of treating impotence with minimal intervention gives good results, non-injection methods of intracavernous administration of drugs are being developed.

Intracavernous phalloprosthesis was first successfully carried out in 1936 by the Soviet professor Bogoraz, rib cartilage was used as a prosthesis. And already in the mid-70s, intracavernous penile prosthesis began to be widely used for the treatment of impotence. To date, prostheses have different principles of action and give complete freedom to lead a normal sexual life. The reliability of the systems used for prosthetics and the quality of the technique made it possible to reduce the number of complications to 3.5-5%, and among patients using penile prostheses to correct impotence, more than 80% give good recommendations to this technique.

Moreover, if impotence is of an organic nature, patients should be advised to immediately undergo phaloprosthetics. Because according to statistics, most of the men who use penile prostheses first used drug therapy, vacuum therapy and intracavernous self-injections. The main reason why intracavernous penile prosthesis is preferred by most patients who are faced with the problem of impotence is the natural erection, the absence of the need for painful injections and constant medication, and the minimum number of complications.

The cavernous bodies are the central link in the erection phenomenon.
From the point of view of hydrodynamics, cavernous bodies are a hydrodynamic system. During an erection, a certain balance of blood flow is created in this system (first, the inflow exceeds the outflow, then it equalizes, and then, with detumescence, the outflow becomes less). Erectile dysfunction is an imbalance of the components of this system, due to the deviation of the values ​​of one or both components above a critical level.

An erection occurs when three structural units of the cavernous bodies interact:

Systems of smooth muscle cells of the cavernous tissue and their ability to adequate relaxation.
- The system of "supporting" elements of the cavernous tissue, when a certain ratio of elastic and connective tissue fibers, creates such an extensibility that allows blocking the infrathecal venous plexus and implementing the veno-occlusive mechanism.
- A system of structures that provide a passive veno-occlusive mechanism - infrathecal venous plexus, perforating veins, albuginea.
All this system during the development of an erection works as a whole, providing blood pressure in the cavernous bodies close to systolic, and before ejaculation 2-4 times higher than it.

I. Systemic processes affecting the functional ability and structural organization of the cavernous bodies include:

Endothelial dysfunction
. diabetic microangiopathy
. hypercholesterolemia
. hypoxia of the cavernous bodies
. androgen deficiency

II. Processes affecting individual functional structures of the cavernous bodies.

1. Violations of the smooth muscle apparatus of the cavernous bodies:
. Reversible sympathetic hypertonicity due to vegetative-vascular disorders of various origins
. Organic penile angiospasm. This is an irreversible lesion of vasomotor regulation, which occurs with chronic smoking, diabetes mellitus, vasculitis, angiotrophic syndrome, and chronic intoxication.

2. Violations of the structural organization of the cavernous bodies - the causes of cavernous fibrosis:
. priapism, especially lasting more than 72 hours
. intracavernous injections
. penile fracture and rupture of the cavernous bodies
. introduction into the cavernous bodies of various oils and gels
. consequences of the postponed cavernitis
. effects of penetrating radiation

3. Violations of the structures that ensure the implementation of the veno-occlusive mechanism of erection - pathology of the albuginea and venous vessels of the cavernous bodies:
. Congenital insufficient rigidity of the albuginea, which does not provide adequate compression of the infrathecal venous plexus during erection in the presence of sufficient elasticity of the cavernous tissue.
. Peyronie's disease
. Spongiocavernous shunting
. Dilated venous graduates of congenital and acquired genesis
. Congenital and acquired arteriovenous fistulas

There are five types of cavernous erectile dysfunction.

Type 1 is caused by erectile dysfunction due to a too large diameter of the veins through which it flows from the cavernous bodies.
Type 2 is caused by overstretching of the veins due to deformation of the albuginea in Peyronie's disease.
Type 3 is caused by impaired relaxation of the smooth muscle cells of the cavernous bodies due to sclerosis or fibrosis.
Type 4 is caused by a deficiency of mediators of relaxation of smooth muscle cells against the background of systemic processes (endothelial dysfunction, diabetic microangiopathy, etc.) or against the background of neurogenic and psychogenic erectile dysfunction
Type 5 is due to abnormal communication between the cavernous and spongy bodies (spongiocavernous bypass surgery for priapism)

When planning conservative treatment of erectile dysfunction, it is necessary to clearly understand its possibilities:

First of all. With erectile dysfunction, organic damage to arterial vessels and cavernous bodies is often combined with increased smooth muscle reactivity of varying severity (angiodystonia and functional angiospasm). By eliminating the functional component of the arterial component, it is possible to reduce the deficiency of arterial inflow, and hence improve the quality of erection.

Secondly. The cause of erectile dysfunction is often a combination of arterial and venous insufficiency. In the presence of mild venous insufficiency, but in the absence of insufficiency of arterial inflow, the necessary intracavernous pressure will be achieved and maintained at a satisfactory level if the increasing arterial inflow exceeds the venous "leak". Although the "margin of safety" of the positive balance of blood flow will be low. In the event of arterial insufficiency, the positive balance of blood flow can be easily disturbed and will be insufficient to create the necessary intracavernous pressure, which will provoke the onset of erectile dysfunction. In this case, the restoration and strengthening of arterial inflow will restore the lost balance in the hydrodynamic system "Penis" and will contribute to the restoration of normal erections.

Thirdly. With systemic factors, the emerging sclerosis of the cavernous bodies reduces the elasticity of the cavernous tissue, which leads to incomplete occlusion of the infrathecal venous plexus and the formation of secondary venous insufficiency. Improving the elasticity (extensibility) of the cavernous tissue will contribute to a more complete venous occlusion during the development of an erection and the creation of a positive blood flow balance.

Fourth. Cavernous tissue, like no other muscle structure, needs adequate oxygenation, which is provided by a developed microcirculation system. Even a slight pathology of the microvasculature, leading to a decrease in oxygenation, reduces the activity of biochemical processes for the synthesis of relaxing factors, which can be the cause of erectile dysfunction. Improvement of microcirculation and oxygenation of the cavernous tissue is a necessary condition for the restoration of erectile function in most patients with vasculogenic erectile dysfunction.

The most important for the development of cavernous erectile dysfunction are systemic processes that affect the functional ability and structural organization of the cavernous bodies:
. endothelial dysfunction
. hypoxia of the cavernous bodies
. diabetic myroangiopathy
. hypercholesterolemia

Endothelial dysfunction and cavernous erectile dysfunction.

Erection is initiated by the sacral parasympathetic nerves, whose preganglionic neurotransmitter is acetylcholine. The postganglionic dilating effect of the parasympathetic nervous system is carried out by fibers, the impulse transmission in which is mediated by neurotransmitters that are characteristic only for this type of nerve endings. They are called non-adrenergic non-cholinergic neurotransmitters. They are nitric oxide and vaso-intestinal polypeptide.
The endothelial layer of the lacunae of the cavernous tissue has synapses of the cholinergic nervous system. When stimulated with acetylcholine, endothelial cells produce an endothelial relaxation factor - nitric oxide, which can have a relaxing effect on the underlying smooth muscle layer. Endothelial relaxing factors also include prostaglandins synthesized by endothelial cells. Synthesis of nitric oxide is produced by nitric oxide synthetases (NOS - NO synthase), which affect the amino acid arginine using molecular oxygen. As a result, the amino acid citrulline and nitric oxide are formed. Distinguish between endothelial NO synthetase (eNOS) and nervous tissue (nNOS). Their activity depends on the partial pressure of molecular oxygen.
Diffusion of non-adrenergic non-cholinergic neurotransmitters and endothelial relaxation factor - nitric oxide into the smooth muscle cells of the cavernous tissue activates guanylate cyclase and accumulates cGMP, triggering a cascade of biochemical reactions, the result of which is the relaxation of smooth muscle cells.
All pathological processes leading to hypoxia, hyperglycemia, hypercholesterolemia, hypertension damage the endothelium, resulting in endothelial dysfunction. At the same time, the synthesis of endothelial relaxation factors (nitric oxide and prostaglandins) is sharply inhibited, which leads to the impossibility of smooth muscle relaxation. Deficiency of prostaglandins leads to disinhibition of collagen synthesis, and increased formation of endothelin-1 supports the contraction of smooth muscle elements of the trabeculae of the cavernous tissue, prevents vasodilation and, thereby, exacerbates hypoxia. Against this background, the transformation factor B1 is activated, the synthesis of which is controlled by prostaglandins. Transformation factor B1 induces the synthesis of collagen and its accumulation in the cavernous tissue, which leads to atrophy and fibrous transformation of smooth muscle cells. Thus, impaired relaxation of smooth muscle cells, vasoconstriction and sclerotic changes in cavernous tissue are a key link in the pathogenesis of cavernous erectile dysfunction due to endothelial dysfunction.

Hypoxia and cavernous erectile dysfunction.

A very important role in the regulation of neurophysiological and biochemical processes in the cavernous tissue is played by blood oxygen saturation - the partial pressure of blood oxygen in the cavernous bodies. The value of the partial pressure of oxygen of the blood flowing through the cavernous bodies of the non-erect penis is equal to the partial pressure of oxygen of the venous blood (25-45 mm Hg). During an erection, increased blood flow through the dilated penile arteries rapidly raises the partial pressure of oxygen in the cavernous tissue to the level in the arterial blood (100 mmHg). Studies have shown that changes in intracavernous oxygen partial pressure play an active role in the regulation of penile erection. The low value of oxygen pressure in the non-erect penis leads to inhibition of the synthesis of nitric oxide, which prevents the relaxation of the smooth muscle fibers of the trabeculae of the cavernous tissue. Inhibition of the synthesis of nitric oxide is a necessary condition for finding the penis in a relaxed state. With vasodilation and an increase in the partial pressure of oxygen in the blood, the synthesis of the endothelial relaxation factor, nitric oxide and prostaglandin E, is stimulated, the effect of which causes smooth muscle relaxation.
Hypoxia of endothelial cells leads to an increase in their synthesis of endothelin-1. It is a peptide synthesized by the endothelium of the cavernous tissue and has a strong constrictor effect. It is believed that endothelin provides contraction of smooth muscle fibers to maintain a relaxed state of the penis.
A state of hypoxia with an increased content of endothelin-1 leads to the expression of transformation factor B1, which is a pleiotropic cytokinin that induces collagen synthesis and accumulation, and also stimulates the growth of fibroblasts. These changes lead to phenotypic changes in the cavernous tissue, namely, to increased synthesis and accumulation of collagen with an outcome in cavernous fibrosis.
It has been established that 48 hours after erection, the degree of hypoxia develops in the cavernous tissue, at which the transformation factor B1 is induced. In a man with normal sexual function, even if not sexually active, 4-8 episodes of spontaneous erection during nocturnal sleep provide sufficient oxygenation of the cavernous tissue to prevent changes leading to fibrosis of the cavernous tissue. Oxygenation of the cavernous tissue during nocturnal erections regulates the normal ratio of the synthesis of cytokinins, growth factors, nitric oxide and prostaglandins. It is important to note that prostaglandins synthesized by the endothelium of the cavernous tissue are directly involved in the regulation of collagen formation in the cavernous tissue. Prostaglandins inhibit transformation factor B1 and thus block collagen synthesis.
Thus, a quality erection that creates maximum oxygenation of the cavernous tissue reproduces the next erection. The penis for normal functioning just needs regular and long erections.
In this regard, two things must be emphasized.
Firstly, with age, to maintain an adequate readiness for erection of the cavernous tissue, its oxygenation is insufficient only during nocturnal erections. In humans, in the absence of a regular sexual life, poor oxygen supply to the cavernous tissue many times accelerates the "aging" of the penis.
Secondly, any pathological conditions that contribute to the weakening of erectile function, and hence the oxygenation of the cavernous tissue, trigger the pathological process of impaired relaxation of smooth muscle cells, vasoconstriction and collagen synthesis, which leads to the closure of the circle of pathogenesis.

Diabetes mellitus and cavernous erectile dysfunction.

Hypercholesterolemia and cavernous erectile dysfunction.

Hypercholesterolemia leads to structural changes in the cavernous tissue. In patients with elevated cholesterol levels, collagen synthesis is increased and the elasticity of the trabeculae of the cavernous bodies is reduced.