Alcoholic myocardium

Introduction Long-term heavy drinking can lead to myocardial lesions, showing a similar appearance of dilated cardiomyopathy, called alcoholic cardiomyopathy (ACM). In the report of the Committee of Experts of the World Health Organization and the International Federation of Cardiology (WHO/ISFC) Working Group on the definition and classification of cardiomyopathy in 1995, alcoholic cardiomyopathy was classified as an allergic and toxic reaction in specific cardiomyopathy. Caused by cardiomyopathy. After the alcohol withdrawal, the condition can be relieved or healed by itself. The disease is mostly caused by adult males. The incidence rate in China has increased in recent years.

Cause

Alcoholic cardiomyopathy is the result of direct toxicity of ethanol and its metabolite acetaldehyde to the heart muscle. The direct toxic effects of alcohol on cardiomyocytes are mainly reflected in the following aspects:

1 damage the integrity of myocardial cell membrane, through the biological properties of alcohol-soluble fat, invading the cell membrane to cause liquefaction and change the cell membrane fat composition and molecular configuration, so that the membrane surface ion distribution and membrane potential are out of control, affecting cell-to-cell information transmission and ions exchange.

2 affecting organelle function, including mitochondrial, sarcoplasmic reticulum and other organelle dysfunction, resulting in reduced myocardial energy supply.

3 affecting the permeability of myocardial cell ions, so that potassium, phosphate or magnesium is lost from the myocardium, and calcium overload in myocardial cells can lead to decreased myocardial contractility, which is an important cause of cardiac dysfunction in alcoholic cardiomyopathy. ;

4 alcohol metabolism causes intermediate metabolism changes, such as the tricarboxylic acid cycle of certain enzymes such as aspartate aminotransferase (aspartate aminotransferase), malate dehydrogenase, isodecanoate dehydrogenase, lactate dehydrogenase And the escape of aldolase from cardiomyocytes, will affect the function of cardiomyocytes, so that it can not effectively use fatty acids to generate energy, and make triacylglycerol accumulate in the myocardium, abnormal fat operation and adenosine triphosphatase activity of myofibrils, It has a direct inhibitory effect on the heart muscle itself.

5 long-term drinking can change the structure of regulatory proteins (pro-protein and promyosin), affecting myocardial relaxation and contraction.

6 long-term heavy drinking can still cause a balanced nutritional imbalance in the human body, easily lead to vitamin deficiency, especially vitamin B deficiency, can also increase heart failure. In addition, some additives in alcohol contain toxic substances such as cobalt and lead, which may cause poisoning or myocardial damage after long-term drinking. Due to the interaction and influence of the above reasons, alcoholic cardiomyopathy can eventually occur.

an examination

Related inspection

Cardiovascular electrocardiogram

Myocardial endocardial biopsy is difficult to find specific changes associated with alcoholic cardiomyopathy, but the incidence of edema in the mitochondria and coronary lining is high, which is helpful for diagnosis.

1, X-ray examination: heart shadow is generally increased, cardiothoracic ratio of 0.55, combined with heart failure can have pulmonary congestion, pulmonary edema and even pleural effusion. With treatment and abstinence, the increased heart shadow can be significantly reduced in the short term.

2, ECG: There may be a variety of ECG abnormalities, the most common is left ventricular hypertrophy with ST-T abnormalities. Electrocardiographic changes such as low voltage, atrial fibrillation, ventricular premature contraction, atrial premature contraction, atrioventricular block, and indoor conduction block were also observed. Some patients showed pathological Q waves.

3, echocardiography: mainly for left ventricular weight increase, early interventricular septum and left ventricular posterior wall mildly thickened, without concomitant dysfunction, left ventricular diastolic diameter is normal. In the presence of congestive heart failure, both atrioventricular contraction and diastolic diameter increased, wall motion decreased, and left ventricular ejection fraction decreased. Echocardiography is of great value for early diagnosis and prognosis.

4, cardiac catheterization and cardiovascular angiography: alcoholic cardiomyopathy can have hemodynamic changes in the subclinical state, often manifested as decreased ejection fraction, increased ventricular end-diastolic pressure, increased end-diastolic volume and tension. Ventricular angiography showed a dilated left ventricle, attenuated diffuse wall motion, and decreased ventricular ejection fraction.

5. Radionuclide examination: The detection of monoclonal anti-cardiac antibodies labeled with 111 indium revealed that patients with dilated cardiomyopathy and alcoholic cardiomyopathy had increased radionuclide intake when heart function deteriorated, and decreased intake when clinical symptoms improved. Although this is not specific for the diagnosis of alcoholic cardiomyopathy, its intake is closely related to the amount of alcohol consumed, and the prognosis can be judged based on the intake.

6, laboratory tests: blood routine, urine routine, fecal routine. liver function. Enzymatic testing.

Differential diagnosis

It is differentiated from dilated cardiomyopathy, beriberi heart disease, and alcoholic liver disease.

1. Dilated cardiomyopathy: Alcoholic cardiomyopathy is similar to dilated cardiomyopathy. Some scholars compared the histology and clinical comparison. The results showed that some patients with dilated cardiomyopathy evolved from myocarditis, so the changes of cardiomyocyte hypertrophy, fibrosis and nucleus were more obvious than alcoholic cardiomyopathy. In addition, the latter's clinically measured cardiothoracic ratio, cardiac index, and systolic pressure/end-systolic volume were significantly improved after stopping the intake of alcoholic beverages, while the former were not.

2. Beriberi heart disease: Alcoholic myocarditis manifests in heart cavity dilatation, tachycardia, increased venous pressure, and lower extremity edema, which are easily confused with beriberi heart disease. However, the former is mostly caused by a decrease in ventricular contractility and a low cardiac output state, while the latter is a state of high cardiac displacement, which can be clinically identified.

3. Alcoholic cirrhosis: The occurrence of alcoholic cirrhosis is related to the drinking mode, gender, genetic factors, nutritional status of the drinker and whether it is associated with hepatitis virus infection. A large amount of drinking is more harmful than a small amount of drinking. Daily drinking is more harmful than intermittent drinking. Women who drink alcohol are more likely to develop alcoholic liver disease than men. Malnutrition, protein deficiency, combined with chronic hepatitis B or hepatitis C virus infection can increase the risk of cirrhosis.

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