Alcoholic cardiomyopathy

Alcohol dilated cardiomyopathy (alcoholic heart disease, alcoholic myocardial damage, toxic dilated cardiomyopathy) is a secondary dilated cardiomyopathy that occurs against the background of alcohol abuse-chronic alcohol intoxication-and manifests itself mainly in myocardial left ventricular involvement, followed by involvement of other heart chambers and their expansion.

ICD-10 code

I42.6 Alcoholic cardiomyopathy.

Symptoms of alcoholic cardiomyopathy

Alcoholic cardiomyopathy is manifested by circulatory failure along a large and small circle resulting from a decrease in the contractility of the myocardium and expansion of the heart chambers. The formation of these changes is associated with the toxic effects of ethanol and acetaldehyde on the contractility of the myocardium. For the initial stage of the disease are characterized by: increased fatigue, weakness, sweating, palpitations, pain in the heart, irregularities in the heart. Pains in the heart area usually stitching or aching, prolonged (may last for hours), do not radiate and are not stopped by nitroglycerin. Less often burn the burning of the sternum and / or in the heart. There may be irregularities in the rhythm, more often paroxysms of atrial fibrillation. Often the listed symptoms appear or intensify the next day after an alcoholic kurtosis. As the disease progresses, it can be provoked not only by taking alcohol, but also by physical or psychoemotional loads. They persist for a long time, and complete regression does not occur even against the background of abstinence. The signs of left ventricular failure, such as shortness of breath and palpitations, that appear not only during exercise, but also at rest, are increasing. General weakness is progressing. Atrial fibrillation and paroxysmal can change to a permanent form. Pain in the heart at this stage is not characteristic, and the disease manifests itself primarily by the rapid development of insufficient circulation of blood on the background of alcoholic excesses or some time after it. Against the backdrop of severe dilatation of the heart cavities and a decrease in the contractility of the myocardium, especially in the presence of atrial fibrillation, thrombi form in the chambers of the heart, so embolisms to various organs are possible.

Diagnosis of alcoholic cardiomyopathy

When examined, the stigmata of chronic alcohol intoxication are revealed, as well as flushing of the face, moist skin, acrocyanosis, large-scale tremor of hands, edema of the lower extremities, ascites. In the lungs they listen to vesicular or hard breathing, in the lower parts - stagnant moist wheezing. In the initial stage of the disease, moderate expansion of the heart borders, tachycardia with a slight load, a decrease in I tone at the apex, an increase in systolic and diastolic pressure are noted. When the disease progresses, a significant expansion of the heart borders in both directions is revealed, tachycardia at rest, pronounced weakening of the I tone, rhythm of the gallop. Cardiac tones can be arrhythmic due to atrial fibrillation, systolic murmur at the tip can be heard. When palpating the abdomen, you can identify an increase in the liver, which is usually painless, soft or somewhat dense, with a rounded edge.

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Laboratory diagnostics

Increase in the serum of the activity of GGT, ACT and ALT.

Instrumental methods

On the ECG, sinus tachycardia, atrial and ventricular extrasystoles, atrial fibrillation paroxysms are detected. Also, changes in the end part of the ventricular complex in the form of a pointed T. Tooth are characteristic which can subsequently decrease and become smoothed. Later, atrial fibrillation becomes permanent, signs of myocardial hypertrophy of the left ventricle may appear. The blockages of the legs of the bundle of the Hisnus, mainly the left one, are developing. Perhaps the development of other more serious and complex rhythm and conduction disorders. Also, in patients with alcoholic heart damage, the appearance of pathological Q-waves on the ECG is possible, they are deep, but do not exceed 3-4 mm in width.

In echocardiography (EchoCG), an increase in the final systolic, terminal diastolic size at first of the left ventricle and then in the other chambers of the heart is determined, the final diastolic pressure in the left ventricle increases, and the ejection fraction decreases. When the process is far gone, there is a significant expansion of all the chambers of the heart, a decrease in the thickness of the walls of the myocardium of the left ventricle. In patients who abused beer, on the contrary, severe myocardial hypertrophy ("bovine heart"), diffuse hypokinesia, a significant decrease in the ejection fraction.

Differential diagnostics

Differential diagnosis is carried out with myocarditis, postinfarction cardiosclerosis, heart defects.

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Example of the formulation of the diagnosis

Chronic alcohol intoxication. Alcohol dilated cardiomyopathy. NC II A.

[14], [15], [16], [17], [18], [19], [20], [21], [22]

Indications for consultation of other specialists

For the selection of the optimal treatment regimen, consultation of a therapist or cardiologist is required. Consultation of a therapist or cardiologist is indicated for assessing the severity of the clinical manifestations of heart failure and its association with alcohol use, for the purpose of appropriate treatment. The development of focal neurological symptoms requires consultation of a neurologist to exclude transient impairment of cerebral circulation.

Treatment of alcoholic cardiomyopathy

Objectives of treatment

• Reduction of the phenomena of heart failure.
• Restoration of work capacity.

Non-drug treatment

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

Medication

In the initial stage of the disease, metabolic and antioxidant drugs are shown:

• trimethylhydrazinium propionate dihydrate (mildronate) inside 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 drip;
• trimetazidine (preductal MB) 35 mg 2 times a day.

Vitamins of group B:

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

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

With the development of symptoms of heart failure, the drugs of choice are:

• inhibitors of the angiotensin-converting enzyme;
• Captopril (kapoten) for 12.5-25 mg 2-3 times a day;
• enalapril (renitek) 5-10 mg 2 times a day;
• beta-blockers;
• Atenolol 12.5-25 mg 1-2 times a day.

It is also advisable to administer magnesium and potassium panangin preparations 1 tablet 3 times a day. To prevent thromboembolic complications, acetylsalicylic acid (aspirin, trombo-ACC) is administered orally, not 100 mg per day.

Further management

Determine in each case individually. The persisting phenomena of heart failure require continued therapy with angiotensin converting enzyme inhibitors, beta-adrenoblockers, acetylsalicylic acid in individually selected doses.

What is the prognosis of alcoholic cardiomyopathy?

The early stages of the development of the disease with the cessation of alcohol consumption is favorable. With continued abuse of alcohol and the far-advanced stage of the disease - unfavorable. Death can come from severe heart failure, fatal arrhythmia, thromboembolic complications.