Chronic alcoholism for heart disease. Alcoholic cardiomyopathy: symptoms, treatment

We all know that alcohol abuse is not good for health. But, besides this, this habit can also lead to very unpleasant consequences in the form of various diseases, and in some cases even death. This happens due to the specific effect on the human body of ethyl alcohol and its decay products.

One of the consequences of excessive consumption of alcoholic beverages is heart failure, which, if not taken seriously and proper measures are not taken, eventually develops into a serious disease - cardiomyopathy.

Alcoholic cardiomyopathy (AK) is a pathology of the cardiovascular system that occurs in people who abuse alcohol, that is, those who suffer from alcoholism. With this disease, the structure of the myocardium is disturbed, the heart has characteristic lesions, and heart failure progresses.

AK is also called dilated, because due to exposure to toxic substances, the heart chambers expand, that is, dilation is observed. This disease also has other names - alcoholic damage to the heart muscle, beer heart, alcoholic myocardial dystrophy.

This pathology is observed more often in males, the average age of patients is 30-55 years. Women are less common in this category, but their course of the disease is often more severe. This phenomenon is associated with greater sensitivity and susceptibility of the female body.

In any case, a sick heart is subjected to an unbearable load for it, its dimensions become unnaturally large, over time it completely loses the ability to perform its tasks.

If proper measures are not taken in time, severe complications will necessarily begin to develop that affect the work of other organs, and eventually a fatal outcome is possible.

Causes and mechanism of development

The main cause of this disease lies in the long-term and systematic use of ultra-high doses of alcoholic beverages. Also, auxiliary reasons can be factors such as heredity, a weak immune system, frequent stress, eating junk food. Ethyl alcohol directly affects the cells of the heart muscle, in fact, destroying it and adversely affecting its functions.

Due to the effect of a toxic substance on the heart, myocardial damage occurs in several ways:


Other diseases of the cardiovascular system can also join cardiomyopathy - arterial hypertension, stroke, malfunctions of the cardiac mechanism, and in especially advanced cases, unexpected death can occur.

It should be noted that alcoholic cardiomyopathy is a wave-like disease. If the patient stops drinking alcohol, then gradually the symptoms of the disease go away, the condition improves and over time a full recovery can occur. But with the return to the use of the usual doses of alcoholic beverages, the pathological condition resumes again, even in a more aggressive form.

The main symptoms of the disease

At the very beginning of the development of the disease, there are no signs of it as such. But in the future, clear symptoms of pathology become apparent:


However, it is possible to talk about alcoholic damage to the heart only if most of the listed signs are present. The combination of various symptoms, together with alcohol dependence, just points to this pathology. While the presence of any single signs indicates possible problems in another area.

Therapeutic measures

Treatment of cardiomyopathy of alcoholic origin should be started first of all with a change in the patient's lifestyle - that is, a complete rejection of the use of alcoholic beverages. If this is not done, the disease will progress, and none of the therapeutic measures will bring the desired result. Moreover, in the early stages of the disease, this may well be enough for recovery without the use of drug therapy.

Also, an additional effect will be produced by such actions as:

  • quitting the habit of smoking;
  • moderate physical activity;
  • the fight against excess weight and maintaining it at a normal level;
  • dietary adjustments.

If the disease has already passed into the second, more serious phase, then in this case, together with the above measures, the specialist usually prescribes drug therapy.

Groups of drugs used to treat alcoholic cardiomyopathy:


This treatment is not a guarantee of absolute relief from the disease. It can only improve the general condition of the patient. Surgical intervention can be called the most cardinal method of treatment, but it does not eliminate possible complications.

During surgery, the patient may be implanted devices to facilitate the work of the heart muscle:

  • a two-chamber pacemaker (with the help of electrical impulses it coordinates the work of the ventricles);
  • cardiodefibrillator (in the event of a life-threatening arrhythmia, it sends an electrical impulse, stimulating the heart muscle);
  • in especially severe cases, a heart transplant is performed.

Possible consequences

The most serious consequence of this disease can be the death of the patient. Moreover, it does not come from the disease itself, the cause of death is complications that develop against the background of the disease. Such complications include angina pectoris, myocardial infarction, various forms of arrhythmias. Thromboembolic disease can also occur, leading to hypertension and strokes.

If no measures are taken, the disease will progress, and a person diagnosed with AK will live no more than 4-5, maximum 10 years, after which an inevitable death will occur.

It is important to remember that this disease is acquired, and only medical measures are not enough for a complete recovery. Much of the success depends on the patient himself and his desire to be cured.

Subject to all the recommendations of the doctor, among which the obligatory item is the refusal of alcohol, the patient has every chance to recover. But one should not expect this to happen within a short period of time. The body recovers gradually. As the toxins are removed, the heart will also return to its normal size, and its functioning will return to normal.

The task of the patient will be to help him in this - to lead a healthy lifestyle, follow the recommendations for proper nutrition, fight overweight, get rid of bad habits, give the body moderate physical activity and regularly undergo a cardiological examination.

Recently, the issues of diagnosis and treatment of alcoholic heart disease have become more relevant due to the high incidence of this pathology in clinical practice and certain difficulties in establishing and formulating a diagnosis. Differential diagnosis of alcoholic cardiomyopathy (ACMP) and dilated cardiomyopathy, which are similar in their clinic, is also somewhat difficult. The article details the pathogenesis and features of heart muscle damage, the clinic and course of ACMP, their differences from similar forms of heart damage. The criteria for making a diagnosis are given. Possible complications of ACM and methods for their diagnosis are listed, the predominance of sinus rhythm in this pathology and the nuances of prescribing drug therapy are emphasized. Particular emphasis is placed on the role of abstinence in the treatment of this disease, its significance repeatedly confirmed by studies in a positive prognosis and possible regression of pathological changes in the myocardium up to the complete restoration of the normal size of the heart cavities. The drug therapy of congestive heart failure, which has certain features, is described in detail. Pathogenetically justified long-term therapy with metabolic drugs with pronounced antioxidant activity and cardioprotective action is recommended.

Keywords: alcoholic cardiomyopathy, myocardial dystrophy, diagnostic criteria, complications, abstinence, antihypoxants.

For citation: Gurevich M.A., Kuzmenko N.A. Alcoholic damage to the heart // BC. 2016. No. 19. S. 1281-1284

Alcoholic heart disease
Gurevich M.A., Kuzmenko N.A.

Moscow Regional Research Clinical Institute named after M.F. Vladimirskiy

Recently diagnosis and treatment of alcoholic heart disease (AHD) has become more urgent due to high prevalence and difficulties in establishing and formulating the diagnosis. Differential diagnosis with alcoholic cardiomyopathy (ACMP) and dilated cardiomyopathy with similar clinical picture also brings some complexity. The paper addresses the pathogenesis and characteristics of heart muscle damage, ACMP clinical picture and flow, their distinction from similar forms of heart diseases. Criteria of diagnosis are listed as well as possible ACMP complications, methods of their diagnosis and medical therapy. Special attention is paid to abstinence in the treatment of this disease, its important role, showed in the large number of trials, in positive prognosis and possible regression of pathological myocardium changes up to the full restoration of normal-sized cardiac cavities. Medical therapy for congestive heart failure is described in detail, which has specific features. Pathogenetic long-term therapy with metabolic drugs with pronounced antioxidant and cardioprotective effect is recommended.

key words: alcoholic cardiomyopathy, myocardial dystrophy, diagnostic criteria, complications, abstinence, antihypoxants.

For quote: Gurevich M.A., Kuzmenko N.A. Alcoholic heart disease // RMJ. 2016. No. 19. P. 1281–1284.

The article is devoted to the problem of alcoholic damage to the heart

Currently, alcoholic cardiomyopathy (ACMP) is isolated as an independent form of cardiomyopathies of alcoholic etiology. ACM occurs in approximately 30% of people who have been taking systematically large amounts of alcohol for more than 10 years, and is due to the toxic effect of alcohol on the myocardium.
M.J. Davies (1975) observed ACM in 15 of 82 cases of primary (idiopathic) cardiomyopathies that ended in death. The study, in which V.Ya. Gerwald et al. analyzed the causes of death of people with chronic alcohol intoxication in the period from 2008 to 2015, showed that the number of diagnosed cases of ACM is growing every year. Alcoholic lesions take the 3rd place in the structure of cardiovascular diseases after various forms of acute and chronic coronary heart disease. This pathology is more common in men.

Pathogenesis

Most of the alcohol in the body is oxidized to acetaldehyde by alcohol dehydrogenase. Acetaldehyde is a toxic substance that has a damaging effect on the cell up to the formation of necrosis. A dangerous dose of alcohol starts with 80 g of pure ethanol. Damage to the internal organs is directly related to the systematic use of alcohol, with an increase in the dose, the risk of damage increases:
- 40 g per day - low risk;
- 80 g per day - the risk is medium;
- 160 g per day - the risk is high.
For women, the corresponding doses are 2 times less.
The long-term effects of alcohol are not related to the type of alcoholic beverage (vodka, wine, beer, etc.). The hangover syndrome depends on the amount of low-quality alcohols - fusel oils (congeners). They are found in low-grade types of vodkas, cognacs and whiskeys.
In the experiment, alcohol causes a decrease in the contractility of the left ventricular (LV) myocardium, a decrease in the volume of coronary blood flow and susceptibility of the myocardium to viral infection. Macroscopically, the heart is enlarged. Its mass reaches 550-600 g, all its cavities are expanded. The LV wall is thickened, the muscle is flabby, pale, dull, in the parietal endocardium there are foci of fibrosis and fresh thrombotic overlays (organized parietal thrombi). There are areas of fatty degeneration of muscle fibers, focal sclerosis of the left ventricle, papillary muscles in the section. Atherosclerosis of the coronary arteries is moderate, arterial stenosis is rare. Microscopically in muscle fibers: uneven hypertrophy along with foci of atrophy, vacuolar dystrophy, foci of necrosis of various prescriptions with organization phenomena, sometimes lymphocytic infiltrates, a typical pattern of accumulation of neutral lipids in cardiomyocytes. There are especially many of them in the region of the conducting system, which, apparently, explains the frequency of rhythm disturbances. Ultrastructural changes include coarsening of the sarcoplasmic reticulum, swelling of mitochondria, damage to cristae, and lipid deposits.

Clinic

ACM has all the clinical manifestations of dilated cardiomyopathy (DCM). The clinical symptoms are often dominated by frequent paroxysmal arrhythmias, especially atrial fibrillation. Chronic alcoholic myocardial damage during periods of exacerbation is manifested by acute alcoholic myocardial dystrophy, with newly appeared and increasing in dynamics changes in the final part of the ventricular ECG complex - ST segment, T wave, paroxysmal arrhythmias - atrial fibrillation, ventricular arrhythmias up to ventricular tachycardia and even fibrillation ventricles. The latter can cause sudden death and progressive heart failure (HF).
ACM predominantly affects men aged 30–55 years. The disease often begins gradually, imperceptibly, often ACM is diagnosed by chance when referring to a doctor about other diseases. Early clinical signs are a moderate increase in heart size, a gallop rhythm. As myocardial dysfunction progresses, the symptoms of congestive heart failure increase: increased dyspnea on exertion, nocturnal attacks of cardiac asthma, persistent dyspnea at rest. A decrease in cardiac output is accompanied by an increase in general weakness, increased fatigue.
Relatively late symptoms of ACMP are peripheral edema, hepatomegaly, and ascites. Dynamic ECG, chest x-ray, echocardiography, coronary arteriography, cardiac catheterization are necessary to differentiate between ACM and idiopathic DCM. The course of alcoholic cardiomyopathy often has an undulating character with alternating periods of remission and deterioration, often due to the resumption of alcohol intake. Life-threatening ventricular arrhythmias and sudden death are quite common in the advanced stage of alcoholic myocardial dystrophy. These signs are partially associated with prolongation of the QT interval, which is detected in 30-50% of these patients (S. Burch, 1981; T. Koide et al., 1982). According to T. Koide et al., atrial fibrillation in ACMP was detected in 45% of cases, thromboembolism - in 55%.

Diagnostics

According to the WHO diagnostic criteria, patients with ACMP have: prolonged, more than 5 years, excessive alcohol consumption (more than 40 g of ethanol per day in women and more than 80 g in men), with withdrawal after 6 months. the onset of remission of AKMP is possible. Small doses of alcohol - 10 and 30 g of ethanol for women and men, respectively - do not have a damaging effect on the myocardium, there are even statements that such doses have a cardioprophylactic and antiatherogenic effect. At the same time, there is no doubt that continued alcohol intake against the background of already existing coronary heart disease worsens the prognosis of the disease and, in combination with physical activity, in some cases leads to painless myocardial infarction. When making a diagnosis of ACMP, one should take into account the younger age of patients compared to patients with ischemic cardiopathy, signs of multiple organ damage inherent in alcoholism: cirrhosis of the liver, polyneuropathy, nephritis, gastroenterocolitis, etc. Hyperemia of the face and conjunctiva, parotitis, Dupuytren's contracture often (but not necessarily ) are also found in alcoholism. Studies of liver enzymes confirm liver damage, but it should be borne in mind that such changes can be with chronic heart failure (CHF) of any other etiology. The diagnosis of alcoholic heart disease is often complicated by the fact that many patients hide the very fact of alcohol abuse, as a result, a number of patients with ACMP are diagnosed with coronary heart disease.
A patient with chronic alcoholism almost always reveals diastolic dysfunction and slight LV hypertrophy, a tendency to rhythm disturbances, especially to atrial fibrillation. The degree of LV diastolic dysfunction is directly proportional to the consumption of alcoholic beverages. In the developed countries of the world, there are tens of millions of patients with chronic alcoholism, while ACM is much less common. The main diagnostic criterion for ACMP is cardiomyopathy, which develops against the background of a long-term (at least 10 years) systematic use of alcoholic beverages in amounts equivalent to 80 ml of ethanol per day.

Forecast

It has been shown that the prognosis for ACMP is more positive than for DCM. Withdrawal in the early stages of the disease helps to prevent its progression and even complete cure. The results of long-term follow-up of 23 patients with ACMP and 52 with DCMP have been published. The age of patients and the severity of the disease in the studied two groups were the same. Over a five-year period, 81% of patients with ACMP and 48% of patients with DCMP survived, after 10 years - 81 and 30%, respectively. It is reported that complete abstinence from alcohol leads to a fairly rapid and significant clinical improvement and an increase in myocardial contractility in patients with ACM complicated by severe CHF. The possibility of increased individual sensitivity to ethyl alcohol should also be taken into account. Even among individuals who systematically consume large amounts of alcohol, myocardial damage with CHF is less common than liver damage.
In cases of early diagnosis and persistent abstinence, the prognosis is quite favorable, with the hope of stabilizing the patient's condition. D. McCall notes the complete absence of clinical manifestations of heart failure and normalization of heart size in 10 out of 15 patients, in the remaining 5, despite the presence of cardiomegaly, the severity of heart failure significantly decreased. In general, out of 39 patients who maintained alcohol adherence, only 10% improved compared to 61% in the group of patients who refused alcohol.
D. Pavan et al. (1987) during a repeated echocardiographic examination of 3 patients who consumed more than 2.5 liters of wine daily for 5 years, CHF IV of the NYHA functional class was established, but after 15–25 months. after the cessation of alcohol intake, complete normalization of the LV cavity and ejection fraction was registered.
A significant positive effect of abstinence is observed in patients with initially pronounced congestive heart failure of the NYHA functional class IV with an LV ejection fraction of less than 30%, usually it manifested itself after 6 months. from the beginning of abstinence from alcohol. Clinical improvement after withdrawal occurs more often in patients with lower pulmonary artery pressure and is not associated with the severity of myocardial hypertrophy and the prevalence of interstitial fibrosis (L. La Vecchia et al., 1996). It should be emphasized once again that the prognosis for ACMP is more favorable than for idiopathic DCMP.

Treatment

With an early, timely diagnosis of ACM, abstinence from alcohol is critical to recovery. With late diagnosis, organ changes can be irreversible.
Treatment of congestive heart failure in ACMP is carried out according to the principles of therapy for circulatory decompensation in DCM. Some features of the treatment of heart failure in this pathology should be pointed out, which are based on our own and literature data. Cardiac glycosides are rarely used in the treatment of HF in ACM. The rationale for this limitation is the predominance of sinus rhythm (about 79%) and the incidence of toxic side effects when using cardiac glycosides - life-threatening ventricular arrhythmias, exacerbations of hepatic and gastrointestinal pathology. Among cardiotropic drugs, angiotensin converting enzyme inhibitors (ACE inhibitors) and angiotensin II receptor antagonists (ARA II) have been used with some success.
Treatment with ACE inhibitors was started after the abolition of potassium preparations and potassium-sparing diuretics with the appointment of captopril 6.25 mg, enalapril 2.5 mg. Subsequently, with good tolerance and the absence of hypotension, the dose was adjusted: captopril 6.25-12.5 mg 3 times a day, enalapril 2.5 mg 2 times a day with a gradual increase to the target or maximum tolerated doses (for captopril - 50 mg 3 times a day, enalapril - 10 mg 2 times a day). In addition to them, lisinopril 2.5 mg is shown with an increase in dose to 20-40 mg / day once, quinapril - with an increase in dose from 5 to 20 mg / day in 2 doses and ramipril - with an increase in dose from 2.5 to 5 mg 2 times in a day.
The advantage of ARA II over ACE inhibitors is better tolerability: they do not cause hacking cough and angioedema. Losartan (12.5-50.0 mg/day once) provides a greater reduction in overall mortality by preventing sudden death.
In addition, isosorbide dinitrate 10 mg 3 times daily in combination with hydralazine 10–25 mg 3–4 times daily is effective in congestive HF. With good tolerance and the absence of arterial hypotension, the doses are increased to an average of 40 mg 3 times a day and 75 mg 3-4 times a day, respectively.
With the pathology under discussion, long-term antioxidant therapy should be recommended.
Under the influence of alcohol and acetaldehyde, the beta-oxidation of free fatty acids is inhibited and the process of their peroxidation is sharply activated with the formation of peroxides and free radicals. Products of fatty acid peroxidation have a pronounced detergent effect on the membranes of cardiomyocytes and contribute to the development of myocardial dysfunction. Increased oxidation of free fatty acids along the free radical pathway also leads to suppression of mitochondrial enzymes and a decrease in energy production processes. Antioxidants, protecting cardiomyocytes from damage by reactive oxygen species and free radicals, according to the literature and our own data, help improve central hemodynamics, regression of LV size, increase the action of ACE inhibitors, reduce the degree of damage and apoptosis of cardiomyocytes.
Thus, taking into account the good tolerability of the drug by patients, the data of published studies and the results of its use in clinical practice, thiotriazoline can be recommended as a means of complex therapy.
Despite the undoubted commonality of the treatment of congestive HF in ACMP and DCM, aimed at reducing circulatory decompensation, there are, in our opinion, certain features of the treatment of HF in alcoholic heart disease.

Literature

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2. Ren J. Acetaldehyde and alcoholic cardiomyopathy: lessons from the ADH and ALDH2 transgenic models // Novartis Found Symp. 2007 Vol. 285. P. 69–76.
3. Velisheva L.S., Vikhert A.M., Shvalev V.N. et al. Morphobiochemical features of the myocardium and its innervation in alcoholic cardiomyopathy // Sudden death. M.: Medicine, 1982. S. 199–210.
4. Kaktursky L.V. Clinical morphology of alcoholic cardiomyopathy. Arch. Patol. 2009. No. 5. R. 21–22.
5. McKinney B. Pathology of the Cardiomyopathies. Butterworth & Co (Publishers) Ltd. 1974.
6. Piano M.R. Alcoholic cardiomyopathy. Incidence, Clinical Characteristics, and Pathophysiology, Chest. 2002 Vol. 121. No. 5. R. 1638–1650.
7. Alderman E.L., Coltart D.J. Alcohol and the heart // Br. med. Bull. 1982 Vol. 38. P. 77–80.
8. Klatsky A.L., Friedman G.D., Armstrong M.A., Kipp H. Wine, liquor, beer, and mortality. Am J Epidemiol. 2003 Vol. 158(6). R. 585–595.
9. Ronksley E.P., Brien E.S., Turner J.B. et al. Association of Alcohol Consumption With Selected Cardiovascular Disease Outcomes: A Systematic Review and Meta-Analysis. Br Med J. 2011. 342.
10. Artemchuk A.F. The prevalence of cardiovascular pathology in patients with alcoholism. M.: Medicine, 1999. S. 289–295 [Artemchuk A.F. Rasprostranennost "serdechno-sosudistoj patologii u bol" nykh alkogolizmom. M.: Meditsina, 1999. S. 289–295 (in Russian)].
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12. Moiseev S.V. Damage to internal organs in alcoholic disease // Vrach. 2004. pp. 15–18.
13. Kupari M., Koskinen P., Suokas A. et al. Left ventricular filling impairment in asymptomatic chronic alcoholics // Am J Cardiol. 1990 Vol. 66. R. 1473-1477.
14. Lazarevic A.M., Nakatani S., Neskovic A.N. et al. Early changes in left ventricular function in chronic asymptomatic alcoholics: relation to the duration of heavy drinking // J Am Coll Cardiol. 2000 Vol. 35. R. 1599-1606.
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18. Prazak P., Pfisterer M., Osswald S. et al. Differences of disease progression in congestive heart failure due to alcoholics as compare to idiopathic dilated cardiomyopathy // Eur. Heart J. 1996. Vol. 17. R. 251.
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Version: Directory of Diseases MedElement

Alcoholic cardiomyopathy (I42.6)

general information

Short description

Alcoholic cardiomyopathy is a heart disease that develops with alcohol abuse and is caused by the direct toxic effect of alcohol on the myocardium.

Classification

Allocate three clinical forms of alcoholic cardiomyopathy. This division is conditional, because the manifestations of each form are most often found in the same patient.

"Classic" form: The main clinical manifestation of the "classic" form of alcoholic cardiomyopathy is heart failure. The initial degree of HF should be assumed already in those cases when, after 7-10 days of abstinence from alcohol, the patient has tachycardia with a pulse rate of over 90-100. A characteristic feature of heart failure in alcoholic cardiomyopathy is the positive dynamics of clinical, echocardiographic manifestations when alcohol abuse is stopped. The longer the withdrawal period, the more pronounced improvement is noted in patients. Even with severe HF (NYHA FC IV, left ventricular ejection fraction less than 30%), cessation of alcohol intake leads to a significant improvement in myocardial contractility and a positive clinical effect, but this requires a long withdrawal period (about 6 months). On the contrary, the resumption of alcohol intake quickly exacerbates the manifestations of heart failure.

"Pseudo-ischemic" form: This form of alcoholic cardiomyopathy is characterized by pain in the region of the heart and changes in the electrocardiogram, similar to coronary artery disease. Cardialgia appear already at an early stage of alcoholic cardiomyopathy and become more pronounced as the disease progresses. Pain in the region of the heart in alcoholic cardiomyopathy is localized mainly in the region of the apex of the heart and is permanent. Most often, the pain is aching, pulling, sometimes stabbing, does not have a paroxysmal character, is not associated with physical activity and is not stopped by nitroglycerin, they usually appear the next day after an alcoholic excess or after several days of severe alcohol abuse.

Arrhythmic form: In the clinical picture, various arrhythmias come to the fore. Almost every fourth patient with chronic alcoholism has disturbances in the function of excitability (extrasystole, paroxysmal tachycardia, paroxysms of atrial fibrillation and flutter, a constant form of atrial fibrillation). Atrial fibrillation is present in 20% of patients with alcoholic cardiomyopathy, combined with heart failure of varying severity. The arrhythmic form of alcoholic cardiomyopathy has features: heart rhythm disturbances can be the very first and often the only manifestation of alcoholic cardiomyopathy; paroxysms of atrial fibrillation or paroxysmal tachycardia often occur after an alcoholic excess (syndrome of "holiday" or "Sunday" heart), sometimes already in the first 6 hours after taking large amounts of alcohol; paroxysmal cardiac arrhythmias can lead to the development of acute heart failure and a pronounced decrease in blood pressure (sometimes up to collapse); paroxysms of atrial fibrillation and tachycardia are usually accompanied by pronounced vegetative symptoms, there is a direct relationship between the dose of alcohol taken and the severity of arrhythmia: large doses of alcohol taken and, consequently, its high concentration in the blood cause more severe cardiac arrhythmias; and with continued alcohol abuse, paroxysmal atrial fibrillation becomes permanent; cessation of alcohol consumption reduces the severity of arrhythmias and may even lead to their disappearance. 30-50% of patients with alcoholic cardiomyopathy have a prolongation of the QT interval, which predisposes to the development of severe ventricular arrhythmias and even sudden cardiac death. Finishing the description of the arrhythmic form of alcoholic cardiomyopathy, it should be emphasized that the presence of a permanent form of atrial fibrillation in the absence of other reasons for its occurrence, especially in young men, suggests the alcoholic nature of the disease.

FROM mixed form alcoholic cardiomyopathy combines various manifestations of the above forms.


Etiology and pathogenesis

The risk of developing alcoholic cardiomyopathy is directly proportional to the amount of alcohol consumed and the duration of its use.
ABOUT The main factor in the pathogenesis of alcoholic cardiomyopathy is the direct toxic effect of ethanol on the myocardium in combination with changes in the nervous regulation and microcirculation characteristic of alcoholism. The resulting metabolic disorders lead to focal or diffuse myocardial dystrophy, which can be manifested by corresponding changes in the electrocardiogram, various cardiac arrhythmias, and symptoms of heart failure. It should be emphasized that alcoholic heart disease has a fairly clear staging of the development of clinical manifestations of the disease. Pathological anatomical examination of an alcoholic heart reveals an increase in its size with uneven hypertrophy of the walls of the ventricles, thickening of individual sections of the endocardium according to the type of fibroapastosis, interstitial and perivascular fibrosis, mild cell infiltration characteristic of chronic inflammation, dystrophic and atrophic changes in muscle fibers with vacuolization, the disappearance of transverse striation and pycnosis nuclei. At histochemical researches accumulation of neutral lipids in muscle fibers is noted; the content of dehydrogenases and oxidases is reduced. Electron microscopy reveals degenerative changes in the mitochondria of muscle fibers.

Epidemiology

Alcoholic cardiomyopathy most often develops in men aged 30-55 who abuse strong alcoholic beverages (whiskey, cognac, vodka), beer or wine for more than 10 years. Women suffer from alcoholic cardiomyopathy much less frequently, and the period of alcohol abuse necessary for the manifestation of its cardiotoxic effect and the development of the disease is usually shorter than in men. The total cumulative dose of alcohol (lifetime dose of alcohol), which causes the development of alcoholic cardiomyopathy in women, is much lower and amounts to 60% of this dose in men. This is due to the significantly greater sensitivity of women to the cardiotoxic effects of alcohol.


WHO assesses the situation as dangerous when drinking alcohol in an amount of more than 8 liters per 1 person per year.

Alcoholic cardiomyopathy is more common among the lower socioeconomic strata of the population, especially among the homeless, malnourished people who abuse alcohol, often patients are well-to-do people.

Clinical picture

Symptoms, course

Subjective manifestations of alcoholic cardiomyopathy are non-specific and manifest as rapid fatigue, general weakness, excessive sweating, shortness of breath and a feeling of pronounced palpitations during physical exertion, pain in the heart area of ​​a permanent nature. Initially, these complaints are usually presented by patients the next day after drinking large amounts of alcohol (alcoholic excess). Then, with abstinence from alcohol intake, the above-mentioned subjective manifestations of alcoholic cardiomyopathy are significantly reduced, but with prolonged alcohol abuse they do not disappear completely. In the future, as the disease progresses, palpitations and shortness of breath become constant, many patients develop asthma attacks at night, swelling in the legs. These symptoms indicate the development of severe heart failure.

On examination, characteristic external signs are found that indicate prolonged alcohol abuse: puffiness, cyanosis, “bruising” of the face; pronounced expansion of capillaries, especially in the nose, which gives it a purple-cyanotic color; hand tremor; sweating; Dupuytren's contracture; gynecomastia; significant underweight or, on the contrary, obesity, the development of which is largely due to the high calorie content of alcohol; scleral vascular injection and scleral subicteria; cold extremities.

Cardiomegaly is an early clinical sign of alcoholic cardiomyopathy, the percussion borders of the heart are expanded to the left. On auscultation, heart sounds are muffled or muffled, tachycardia, often heart rhythm disturbances. Arrhythmias, especially paroxysmal atrial fibrillation, may be the first clinical manifestation of the disease. With a significant increase in the cavities of the heart, a systolic murmur is heard in the region of the apex of the heart (manifestation of mitral regurgitation) or in the region of the xiphoid process (due to relative tricuspid insufficiency).

Severe heart failure and cardiomegaly are accompanied by the appearance of a gallop rhythm (protodiastolic with the appearance of a pathological III tone or presystolic with the appearance of an IV tone), as well as an accent of the II tone over the pulmonary artery. Physical examination of patients with alcoholic cardiomyopathy reveals symptoms that are extremely similar to dilated cardiomyopathy, which forces a thorough differential diagnosis of these two diseases.

Diagnostics

Electrocardiography
ECG changes are found in patients in the absence of clinical manifestations of the disease. The most frequently recorded changes in the terminal part of the ventricular complex are: shift of the ST interval downward from the isoline (sometimes even a horizontal type of shift, which requires differential diagnosis with coronary artery disease), a decrease in the amplitude of a significant or negative T wave, can be smoothed out. A biphasic or high T wave is recorded in the chest leads. There may be signs of overload of the left or right atria, which is manifested by a change in the P wave on the ECG.

Sometimes, in severe alcoholic cardiomyopathy, a pathological Q wave is detected in some ECG leads. Two circumstances characteristic of alcoholic cardiomyopathy are of great differential diagnostic significance: the appearance for the first time or an increase in existing ECG changes after alcoholic excess; positive dynamics of ECG changes after stopping alcohol intake. It should also be taken into account that alcoholic cardiomyopathy can be combined with coronary artery disease, especially in the elderly. Myocardial infarction and exertional angina in young people who abuse alcohol are much more common than in people of the same age who do not drink alcohol.

The most common types of cardiac arrhythmias are sinus tachycardia, ventricular extrasystole, paroxysmal atrial fibrillation, atrial flutter. As the disease progresses, a permanent form of atrial fibrillation and varying degrees of atrioventricular conduction disturbance, blockade of the right or left bundle branch often develop. In many patients, there is a prolongation of the QT interval, which is accompanied by paroxysmal ventricular tachycardia.

echocardiography
The main echocardiographic changes in alcoholic cardiomyopathy are: dilatation of all four cavities of the heart; global decline in ventricular function; mitral and tricuspid regurgitation; pulmonary hypertension; diastolic dysfunction; the presence of intracardiac (intraatrial or intraventricular) thrombi; left ventricular hypertrophy. The severity of manifestations of alcoholic cardiomyopathy depends on the stage of the disease.

Myocardial scintigraphy
Myocardial scintigraphy with radioactive thallium 201T1 may reveal multiple defects in isotope accumulation. This is usually observed in severe alcoholic cardiomyopathy and may be due to the formation of multiple foci of fibrosis in the myocardium.

X-ray examination
With fluoroscopy or x-ray of the chest organs, an increase in the size of the heart is determined, and with the development of heart failure, signs of venous congestion in the lungs may appear in the pleural cavities.

Laboratory diagnostics

Blood test

There are no pathognomonic changes for alcoholic cardiomyopathy. In many patients, the general blood test is normal, however, after a pronounced alcoholic kurtosis, a moderate increase in ESR and the number of leukocytes is possible. Often a picture is found that is characteristic of iron deficiency anemia: hypochromia of erythrocytes, a decrease in color index, microcytosis, anisocytosis, poikilocytosis of erythrocytes. 40% of patients with chronic alcoholism have megaloblastic anemia associated with a decrease in the intake of folic acid from food and with the antifolic effect of alcohol.

Analysis of urine

As a rule, in the absence of extracardiac alcoholic lesions, the general analysis of urine is not changed.

Blood chemistry

No pathognomonic changes are found. In severe alcoholic cardiomyopathy and severe heart failure, a mildly pronounced increase in blood levels of creatine phosphokinase (CPK) and aspartic aminotransferase (AST) is possible. With concomitant alcoholic liver damage, a high blood level of ALT, LDH, GGTP is determined.

Differential Diagnosis

It is necessary to differentiate alcoholic cardiomyopathy with a number of diseases, but primarily with ischemic cardiomyopathy and dilated cardiomyopathy. Sometimes this is very difficult, since patients, as a rule, deny alcohol abuse.

The main differential diagnostic differences between alcoholic and ischemic cardiomyopathies are presented in the table. When making a differential diagnosis of alcoholic and ischemic cardiomyopathy, it should be remembered that people suffering from ischemic cardiomyopathy and other forms of coronary heart disease may abuse alcohol. In this situation, it can be very difficult to correctly interpret clinical and laboratory data. With this combination of chronic alcohol intoxication and coronary artery disease, it should be taken into account that pain in the heart area meets the criteria for angina pectoris, and cicatricial changes are more often found on the ECG after myocardial infarction.

Differential diagnosis of alcoholic and ischemic cardiomyopathy

signs Alcoholic

cardiomyopathy

 Ischemic

cardiomyopathy
Other visceral lesions

Presence of alcoholic stigmas on external examination (puffy purple-cyanotic face, expansion of the network of skin capillaries of the face, enlargement of the parotid glands, gynecomastia, hand tremor, testicular atrophy)

Laboratory signs of chronic alcohol intoxication:

Increased blood levels of gamma-glutamyl transpeptidase and non-carbohydrate (desialized) transferrin;

Increase in mean volume of erythrocytes

 Characterized by the development of alcoholic hepatitis,

liver cirrhosis,

calculous

pancreatitis

Characteristically

Present

 Non-alcoholic liver enlargement

in the development

insufficiency

blood circulation

Missing

Missing

Differential diagnosis of idiopathic dilated cardiomyopathy and alcoholic cardiomyopathy is relatively simple, taking into account the diagnostic criteria for dilated cardiomyopathy, the absence of anamnestic data on alcohol abuse and clinical and laboratory manifestations of signs of alcohol intoxication in individuals with dilated cardiomyopathy.

Differential diagnosis of alcoholic cardiomyopathy should also be carried out with other types of cardiomyopathy. In addition, alcoholic cardiomyopathy should be differentiated from all diseases that lead to cardiomegaly and HF (congenital and acquired heart defects, amyloidosis, myocardial hemochromatosis, exudative and constrictive pericarditis, and other diseases). This takes into account the symptoms of these diseases and the absence of prolonged alcohol abuse.

Complications

Complications of cardiomyopathy are usually expressed by chronic cardiovascular insufficiency or thromboembolic syndrome due to the presence of blood clots in the heart cavities.

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Treatment

In treatment, it is important complete and persistent abstinence, which can significantly improve the condition of some patients and achieve its stabilization.

From non-drug methods treatment should be noted limitation of physical activity, salt intake, especially in the presence of edematous syndrome.

Medical therapy
ACE inhibitors are the first choice. The appointment of these drugs (in the absence of contraindications) is advisable at all stages of the development of the disease, even in the absence of severe clinical manifestations of CHF. ACE inhibitors are able to prevent necrosis of cardiomyocytes, the development of cardiofibrosis; contribute to the reverse development of hypertrophy, reduce the amount of afterload (intramyocardial tension), reduce the degree of mitral regurgitation. the use of ACE inhibitors significantly increases the life expectancy of patients.

Initial dose of the drug: enalapril 2.5 mg 2 times a day; ramipril 1.25 mg once a day; perindopril 2 mg once a day. With good tolerance, the dose should be increased (20-40 mg / day for enalapril, 10 mg for ramipril, 4 mg for perindopril).

B-blockers it is advisable to combine with ACE inhibitors. β-blockers are especially indicated in patients with persistent sinus tachycardia, as well as in patients with atrial fibrillation. Use any b-blockers (metoprolol, bisoprolol, atenolol, carvedilol). Treatment begins with small doses of drugs, gradually increasing them to the maximum tolerated. In some patients, in the first 2-3 weeks of treatment with b-blockers, a decrease in EF, SV and some deterioration in the condition may be observed, which is mainly due to the negative inotropic effect of these drugs. However, in most of these patients, the positive effects of b-blockers begin to prevail over time, due to the stabilization of the neurohormonal regulation of blood circulation, the restoration of the density of b-adrenoreceptors on the cell membranes of cardiomyocytes, and a decrease in the cardiotoxic effect of catecholamines. EF gradually increases and the clinical manifestations of CHF decrease.

Diuretics used in the presence of stagnation of blood in the small and/or in the systemic circulation. Apply thiazide, thiazide-like and loop diuretics according to the usual scheme. In the presence of a pronounced edematous syndrome, it is advisable to combine the listed diuretics with the appointment of aldosterone antagonists (aldactone, veroshpiron).
For the treatment of patients with chronic left ventricular failure, as an additional drug, you can use nitrates- isosorbide-dinatrates or isosorbide-5-mononitrates. The latter are distinguished by high bioavailability and predictability of action (olicard, imdur). These drugs contribute to the deposition of blood in the venous bed, reduce the amount of preload and stagnation of blood in the lungs.

cardiac glycosides shown to patients with a permanent form of atrial fibrillation.

The use of cardiac glycosides in severe patients with severe LV systolic dysfunction and sinus rhythm is possible only in combination with ACE inhibitors, diuretics under the control of electrolytes and ECG monitoring. Long-term use of non-glycoside inotropic agents is not recommended, as it significantly increases the mortality of these patients. Short-term use of non-glycoside inotropic drugs (levodopa, dobutamine, milrinone, amrinone) is justified in preparing patients for heart transplantation.

Purpose antiplatelet agents shown to all patients, since in 30% of cases the course of the disease is complicated by intracardiac thrombosis and the development of thromboembolism. For this purpose, a constant intake of acetylsalicylic acid at a dose of 0.25-0.3 g per day is used, the use of other antiplatelet agents according to the schemes (trental, dipyridamole, vazobral). In patients with atrial fibrillation, the appointment of indirect anticoagulants (warfarin) under the control of coagulogram parameters is indicated. Doses of the drug are selected so that the value of the INR is 2-3 units.

Surgery

Heart transplantation is a highly effective treatment for drug-refractory cardiomyopathy.
Indications for transplantation are: rapid progression of heart failure, lack of effect from conservative therapy; the occurrence of life-threatening cardiac arrhythmias; high risk of thromboembolic complications.

Forecast

With prolonged cessation of alcohol consumption, stabilization of the patient's condition is observed, partial or complete disappearance of symptoms of heart failure and cardiomegaly is possible. . The positive effect of abstinence in patients with alcoholic cardiomyopathy and functional class IV heart failure appears after about 6 months, sometimes later.
Continued alcohol intake dramatically worsens the prognosis of patients with alcoholic cardiomyopathy. Heart failure progresses, and patients die after 3-4 years, with about 30-35% dying from ventricular fibrillation. However, many patients with alcoholic cardiomyopathy live 5 to 10 years after the onset of congestive heart failure.

Hospitalization

Indications for hospitalization:

Progression of heart failure that does not stop on an outpatient basis.
- Paroxysmal arrhythmias.
- Thromboembolism.

Information

Information

  1. CLINICAL RECOMMENDATIONS OF THE EUROPEAN SOCIETY OF CARDIOLOGY-2007 M., 2008 - 186 p.
  2. E.N. Amosova CARDIOMYOPATHY. Kyiv, "Book plus", 1999
  3. P. Kh. Dzhanashiya, V. A. Krulov, V. A. Nazarenko, S. A. Nikolenko CARDIOMYOPATHY AND MYOCARDITIS. Tutorial. M.: RGMY, 2000. 112 p., ill.
  4. Dzyak V. N., Mikunis R. I., Skupnik A. M. Alcoholic cardiomyopathy. - Kyiv: Healthy "I", 1980.-208 p.
  5. Guide to outpatient cardiology, edited by Yu. N. Belenkov, R. G. Oganov, GEOTAR-Media publishing house, - 2007.-400 p.
  6. Polyakov V.P., Nikolaevsky V.N., Pichko G.A. Non-coronary and infectious diseases of the heart (modern aspects of the clinic, diagnosis, treatment): Monograph.-Samara, 2010,-355p.
  7. Internal diseases according to Tinsley R. Harrison / Ed. E. Fauci, J. Braunwald, K. Isselbacher, J. Wilson, J. Martin, D. Kasper, S. Hauser and D. Longo: In 7 vols. - M.: Practice -Mc-Grow_Hill, 2005.
  8. Clinical guidelines. Cardiology / Ed. Yu.N. Belenkova, R.G. Oganov. - M.: GEOTAR-Media, 2007.

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So what are the heart diseases with alcoholism and how to recognize them in a timely manner every person should know. In this article, we will dwell on this issue in detail and tell you what to do in a situation where your loved one or loved one has problems with the “motor”!

There is practically no person on the planet who would not drink alcohol at least once in his life. However, alcohol abuse can lead to serious consequences and disturbances in the work of internal organs and systems. Ethyl alcohol has a devastating effect on the brain, liver, kidneys, gastrointestinal tract, psyche, central nervous system and "motor". In general, the negative impact of alcohol on the “motor” and the problems that arise because of this are commonly called heart disease in alcoholism .

Ethyl alcohol contained in any type of alcohol is a toxic substance, and it is not specifically ethanol that is poisonous, but its decay products - acetic acid, fusel oils and other toxins. Appearing after the breakdown of ethanol, these components destroy internal organs at the cellular level:

  1. When considering the response of the myocardium - the main contracting muscle of the heart - it can be seen that cardiomyocytes are transformed and stop accumulating nutrients and quickly use up what they have.
  2. Violation of the cell membrane does not allow in the required amount extract nutrients from the blood, saturate the tissues with oxygen, and transmit nerve impulses.
  3. Disorders of metabolic processes leads to changes in the structure of the myocardium , the fibers are stretched, lose their ability to contract.

Eventually developing heart disease with alcoholism, accompanied by shortness of breath, swelling and other unpleasant and dangerous symptoms.

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Remember that only a complete rejection of alcohol will stop developing disorders in the heart and the work of the whole organism as a whole.

Symptoms and signs of heart disease in alcoholism

If after taking alcohol the next day a person worried about heart pain or between the shoulder blades, then you should be seriously concerned. Such a signal is a sign of the development of a dangerous condition and a malfunction in a vital organ. Excessive alcohol consumption causes a deficiency of potassium, as well as B vitamins in the cells of the tissues of the body. Sharp, aching pain, usually lasts for a short period , no more than 2-3 hours. After that, the state is normalized (most likely).

In addition, alcohol can cause other symptoms indicating a problem with the "motor" of the whole organism:

  1. Angina is characterized by a feeling tightness in the region of the heart , with the migration of unpleasant sensations to the left side - the shoulder or arm. The attack lasts no more than 30-40 minutes.
  2. Myocardial infarction causes angina-like pain , with a gradual increase and a duration of more than a few hours.
  3. Heart failure may be accompanied by arrhythmias , shortness of breath, dizziness, pressing pains in the chest.

Most often, people who abuse alcohol for more than three years complain of similar symptoms with alcoholism. If you give up alcohol and carry out restorative therapy, you can restore your health and eliminate the risk of developing serious complications and pathological changes.

Heart failure from alcohol

One of the common problems with alcoholism is heart failure, which we will talk about in a little more detail. This diagnosis refers to a condition in which heart muscle is damaged . The myocardium weakens and is unable to perform its functions as a pump for pumping blood in the body. As a result, there is a lack of oxygen and nutrients in all tissues and organs.

The problem of such insufficiency is a consequence of coronary disease, or a previous heart attack and angina pectoris. To the factors disease provoking also include:

  • Arterial hypertension;
  • Heart disease;
  • Cardiomyopathy.

The main symptoms indicating the development of the problem are consider shortness of breath and general weakness . These signs do not appear from the very beginning of the development of the disease of the organ, but after a while (we are still talking about alcoholism). Symptoms are gradual and progressive. Heart failure, provoked by water retention in the body, causes swelling, which first forms in the ankles and then spreads throughout the limb.

… the relevance of the topic is due to the critically high prevalence of alcoholic disease and heart disease in Russia, which often accompany each other and have a clear causal relationship.

Under the term "alcoholic cardiomyopathy" understand the entire spectrum of myocardial damage associated with the toxic effects of ethanol.

Patients with alcoholic cardiomyopathy range from 23 before 40% all patients with myocardial injury. This condition in 86% of cases develops in men. At the same time, despite the decrease in alcohol consumption in Western industrialized countries, new cases of alcoholic cardiomyopathy are recorded with an unnamed frequency. Alcoholic cardiomyopathy is associated with a worse prognosis in black subjects.

Alcoholic cardiomyopathy exists in two forms: preclinical (asymptomatic) and manifest(clinic of chronic heart failure). Very important is the fact that, according to a large number of authors, the severity of alcohol abuse does not correlate with changes in the structure and function of the myocardium. Only Urbano-Marquez et al. revealed a linear relationship between mean daily alcohol intake and both an increase in left ventricular mass and a decrease in left ventricular ejection fraction.

However, several general conclusions can be drawn regarding the association between alcohol consumption patterns and alcoholic cardiomyopathy. alcohol abusers without clinical signs of chronic heart failure consume more than 90 g/day of pure alcohol for 5 years or more. Thus, if we consider a standard serving equal to 12 g of pure alcohol, then a patient with alcoholic cardiomyopathy drink 8-21 such servings per day.

Little is known about alcohol consumption in patients with manifest alcoholic cardiomyopathy.. Mathews et al. showed that in patients with alcoholic cardiomyopathy with signs of chronic heart failure, compared with asymptomatic forms, only the duration of abuse (at least 10 and 6 years, respectively) is longer, but not the dose. Similar data were obtained by Urbano-Marquez et al.: the average duration of abuse was 24.8 years in the group of chronic heart failure and 16.2 years in the group without chronic heart failure; dose differences were small, 286 g/day and 243 g/day, respectively.

Thus, it is the duration of alcohol abuse that is the main factor in the appearance of clinical symptoms of chronic heart failure, while combined risk factors, for example, arterial hypertension and arrhythmias, are of some importance. It has been convincingly shown that the frequent intake of significant amounts of alcohol contributes to an increase in the incidence of lesions of the cardiovascular system and aggravation of the severity of their course.

The following mechanisms of development of alcoholic cardiomyopathy are distinguished: direct toxic effect of alcohol on cardiomyocytes; thiamine deficiency associated with nutritional status in alcohol abuse; the effect of other substances added to alcoholic beverages (for example, cobalt, which is used as a preservative in the production of canned beer).

The toxic effect of alcohol and its metabolite acetaldehyde is manifested in the effect on calcium transport and binding, mitochondrial function, lipid metabolism, protein synthesis by cardiomyocytes, and myofibrillar ATPase activity. Alcohol causes loss of intracellular potassium, decreased cellular uptake of free fatty acids, and increased excretion of triglycerides. The connection of the damaging effect with magnesium deficiency and a number of other factors is not excluded. Long-term alcohol consumption leads to a decrease in the number of 1-adrenergic and muscarinic receptors in the heart. Alcohol and its metabolites can weaken myocardial contractility and alter the conduction of excitation in the atria and ventricles.

In the development of heart pathology with alcohol abuse, the importance of viruses cannot be excluded.. In patients with myocardial damage, markers of infection with Coxsackie viruses are often found. Inhibition of T-cell immunity in chronic alcohol intoxication may affect the persistence of various viral infections in patients of this group. At the same time, the detection of these laboratory markers of viruses does not exclude in many cases the leading role of chronic alcohol intoxication in the development of pathology.

Myocardial damage can be manifested by ECG changes, various rhythm and conduction disturbances of the heart, and symptoms of heart failure. A change in the atrial complex with the appearance of dilated PI,II waves or high PII,III waves indicates atrial overload. Especially characteristic of alcoholic cardiomyopathy is ST segment depression and a decrease in amplitude or inversion of the T wave. Changes in the atrial complex and T wave height are very variable and are usually recorded only on the first day after alcoholization. ST segment depression and T-wave inversion persist for several weeks and are sometimes persistent. Similar violations are found in ischemic heart disease therefore, the clinical picture of the disease and the dynamics of ECG changes should be taken into account.

Alcoholic heart damage can be manifested by paroxysms of atrial fibrillation or tachycardia that occur after alcohol abuse. Appearance connection cardiac arrhythmias with the use of alcoholic beverages is usually traced by the patients themselves. Continued alcohol abuse can lead to the formation of a permanent form of atrial fibrillation. Alcoholic cardiomyopathy is often accompanied by a violation of myocardial contractility and a manifestation of heart failure. Its early signs are persistent tachycardia and shortness of breath that do not correspond to the load, especially in young and middle-aged men (without signs of other cardiac or pulmonary pathology).

As well as dilated cardiomyopathy, alcoholic cardiomyopathy is characterized by an increase in the mass of the left ventricle, expansion of the cavities of the heart, thinning of the walls, and dysfunction of the ventricles in the absence of changes in the coronary arteries. The clinical characteristics of dilated cardiomyopathy and alcoholic cardiomyopathy also do not differ. In two comparative studies conducted, patients of both groups (with idiopathic dilated cardiomyopathy and alcoholic cardiomyopathy) had similar hemodynamic, echocardiographic changes, as well as the average FC of CHF according to NYHA. A number of studies report that the prognosis (survival) of patients with alcoholic cardiomyopathy is worse than with dilated cardiomyopathy. However, in these studies, the factor of abstinence from alcohol was not studied, and in one of them, patients with arterial hypertension and coronary heart disease were included in the group of alcoholic cardiomyopathy. The determinants of clinical outcome in alcoholic cardiomyopathy include pulmonary artery pressure at the time of hospital admission and pulmonary capillary wedge pressure.

Unfortunately, until now, there have been no works on the pharmacotherapy of alcoholic cardiomyopathy that fully meet the requirements of evidence-based medicine. Alcohol abuse was an exclusion criterion for almost all large multicenter studies. Therefore, in all clinical guidelines for the treatment of chronic heart failure, including Russian ones, attention is drawn to the fact that the treatment regimen, depending on the etiology of chronic heart failure, does not fundamentally differ. It should be noted that the participation of a narcologist in the therapeutic process can reduce the pathological craving for alcohol, significantly improve clinical outcomes in alcoholic cardiomyopathy and prevent the occurrence of this condition.