Alcoholic cardiomyopathy

Alcoholic dilated cardiomyopathy (alcoholic heart disease, alcoholic myocardial disease, toxic dilated cardiomyopathy) is a secondary dilated cardiomyopathy that occurs against the background of alcohol abuse - chronic alcohol intoxication - and is manifested by damage primarily to the myocardium of the left ventricle with subsequent involvement of other chambers of the heart and their expansion.

ICD-10 code

I42.6 Alcoholic cardiomyopathy.

Symptoms of Alcoholic Cardiomyopathy

Alcoholic cardiomyopathy is a disease characterized by circulatory failure in the systemic and pulmonary circulations, which occurs as a result of decreased myocardial contractility and dilation of the heart chambers. The formation of these changes is associated with the toxic effect of ethanol and acetaldehyde on myocardial contractility. The initial stage of the disease is characterized by: increased fatigue, weakness, sweating, palpitations, pain in the heart, and interruptions in the work of the heart. Pain in the heart is usually stabbing or aching, long-lasting (can last for hours), does not radiate and is not relieved by nitroglycerin. Less often, there is a burning sensation behind the breastbone and/or in the heart. Heart rhythm disturbances may occur, most often paroxysms of atrial fibrillation. Often, the listed symptoms appear or intensify the next day after an alcoholic excess. As the disease progresses, they can be provoked not only by alcohol intake, but also by physical or psycho-emotional stress. They persist for a long time, and complete regression does not occur even against the background of abstinence. Such manifestations of left ventricular failure as dyspnea and palpitations increase, which appear not only under load, but also at rest. General weakness progresses. Atrial fibrillation from paroxysmal can become permanent. Heart pain is not typical at this stage, and the disease manifests itself mainly by the rapid development of circulatory failure against the background of alcohol excess or some time after it. Against the background of pronounced dilation of the heart cavities and decreased contractility of the myocardium, especially in the presence of atrial fibrillation, thrombi form in the chambers of the heart, due to which embolism to various organs is possible.

Diagnosis of alcoholic cardiomyopathy

On examination, stigmas of chronic alcohol intoxication are revealed, as well as facial hyperemia, moist skin, acrocyanosis, large-scale hand tremor, lower limb edema, and ascites. Vesicular or harsh breathing is heard in the lungs, and congestive moist rales are heard in the lower sections. At the initial stage of the disease, moderate expansion of the heart borders, tachycardia with little exertion, weakening of the first heart sound at the apex, and increased systolic and diastolic pressure are noted. As the disease progresses, significant expansion of the heart borders in both directions, tachycardia at rest, marked weakening of the first heart sound, and a gallop rhythm are revealed. Heart sounds may be arrhythmic due to atrial fibrillation, and a systolic murmur may be heard at the apex. When palpating the abdomen, an enlarged liver can be detected, which is usually painless, soft or somewhat dense in consistency, with a rounded edge.

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Laboratory diagnostics

Increased activity of GGT, AST and ALT in blood serum.

Instrumental methods

The ECG reveals sinus tachycardia, atrial and ventricular extrasystole, paroxysms of atrial fibrillation. Also characteristic are changes in the terminal part of the ventricular complex in the form of a peaked T wave, which can subsequently decrease and become smoothed. Subsequently, atrial fibrillation becomes constant, signs of left ventricular myocardial hypertrophy may appear. Bundle branch block, mainly the left one, develops. Other more serious and complex rhythm and conduction disorders may develop. Also, in patients with alcoholic heart disease, pathological Q waves may appear on the ECG, they are deep, but do not exceed 3-4 mm in width.

Echocardiography (EchoCG) reveals an increase in the end-systolic and end-diastolic dimensions first of the left ventricle and then of other chambers of the heart, the end-diastolic pressure in the left ventricle increases, and the ejection fraction decreases. In advanced cases, significant expansion of all chambers of the heart and a decrease in the thickness of the left ventricular myocardium walls are observed. In patients who abuse beer, on the contrary, there is pronounced myocardial hypertrophy ("bull's heart"), diffuse hypokinesia, and a significant decrease in the ejection fraction.

Differential diagnostics

Differential diagnosis is carried out with myocarditis, post-infarction cardiosclerosis, and heart defects.

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Example of diagnosis formulation

Chronic alcohol intoxication. Alcoholic dilated cardiomyopathy. NK II A.

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Indications for consultation with other specialists

To select the optimal treatment regimen, a consultation with a therapist or cardiologist is required. A consultation with a therapist or cardiologist is indicated to assess the severity of clinical manifestations of heart failure and its connection with alcohol consumption, to prescribe adequate treatment. The development of focal neurological symptoms requires a consultation with a neurologist to exclude transient cerebrovascular accident.

Treatment of alcoholic cardiomyopathy

Treatment goals

• Reduction of heart failure symptoms.
• Restoration of working capacity.

Non-drug treatment

First of all, it is necessary to stop drinking alcoholic beverages at any stage of the disease. Abstinence can lead to a complete regression of symptoms and an improvement in the patient's well-being. It is advisable to limit the consumption of liquids and salt.

Drug treatment

At the initial stage of the disease, metabolic and antioxidant drugs are indicated:

• trimethylhydrazinium propionate dihydrate (mildronate) orally 0.5 g 4 times a day, intravenously 0.5 g 2 times a day;
• oxymethylethylpyridine succinate (mexidol) intramuscularly 200-300 mg 2 times a day or 1-2 times intravenously by drip;
• trimetazidine (preductal MV) 35 mg 2 times a day.

B vitamins:

• thiamine bromide (B1) 3% solution 1 ml intramuscularly;
• pyridoxine hydrochloride (B6) 1% solution 2 ml intramuscularly;
• Vitamin E tocopherol acetate 100 mg per day orally.

The course of treatment with these drugs continues for 10-15 days, with vitamin E - up to 30 days.

When symptoms of heart failure develop, the drugs of choice are:

• angiotensin-converting enzyme inhibitors;
• captopril (capoten) 12.5-25 mg 2-3 times a day;
• enalapril (renitec) 5-10 mg 2 times a day;
• beta blockers;
• atenolol 12.5-25 mg 1-2 times a day.

It is also advisable to prescribe magnesium and potassium preparations Panangin 1 tablet 3 times a day. For the purpose of preventing thromboembolic complications, acetylsalicylic acid (aspirin, thrombo-ASS) is used orally at 100 mg per day.

Further management

Determined individually in each case. Persistent heart failure symptoms require continued therapy with angiotensin converting enzyme inhibitors, beta-blockers, and acetylsalicylic acid in individually selected doses.

What is the prognosis for alcoholic cardiomyopathy?

In the early stages of the disease, when alcohol consumption is stopped, the prognosis is favorable. With continued alcohol abuse and an advanced stage of the disease, it is unfavorable. Death can occur from severe heart failure, fatal arrhythmia, thromboembolic complications.