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Fine cardiomyopathy (Cardiology) means a lot of morbidity and long-term alcohol intake is closely related to dilated cardiomyopathy with typical hemodynamic changes, symptoms, signs and imaging findings, the disease and relieve itself after drinking or cure of a cardiac disease.
Alcoholic cardiomyopathy high incidence of men than women. Europe, America and Russia and other countries with a high incidence in the rest of the world. Reported cases of domestic distribution.
Symptoms:
1.10 years of drinking history, alcohol intake per day more than 125ml; 2. Palpitations, chest symptoms of more common, few patients with atypical angina and syncope; 3. Cardiomegaly; 4. Heart failure; 5. Arrhythmia disorder; 6. in some cases the phenomenon of combined embolization; 7. peripheral neuropathy and ataxia; 8. enlargement of the liver cirrhosis.
Diagnosis based on:
1. A long history of alcohol abuse; 2. Cardiomegaly and congestive heart failure performance; 3. Abstinence symptoms improved after 4-8 weeks.
Treatment:
Treatment principles 1. To persuade or mandatory alcohol; 2. Bed rest; 3. Treatment of heart failure; 4. Management of arrhythmias; 5. Supplementary vitamins, nutrition support therapy.
The principle of a drug. The disease is a long-term high intake of alcohol-related cardiomyopathy, drug therapy focuses on symptomatic treatment rather than radical treatment. 2. Digitalis poisoning prone to the disease, should be small doses.
Prevention o


f common sense:
The occurrence of alcoholic cardiomyopathy and long-term high intake of alcohol is closely related to their treatment is the key to abstinence. No matter how severe the disease, most cases of alcohol is expected to get the disease after remission. Drug treatment itself is only an expedient measure, not completely stop drinking, the disease treatment will fail.
Alcoholic cardiomyopathy caused by what?Alcoholic cardiomyopathy is due to ethanol and its metabolite acetaldehyde on myocardial direct result of poisoning, alcohol on the direct toxic effects of myocardial cells mainly in the following aspects: the integrity of myocardial cell membrane damage, the Department of fat-soluble by alcohol biological characteristics, invasion and cell membrane changes caused by liquefaction of fat cell membrane composition and molecular structure, the surface of the membrane ion distribution and membrane potential loss of control of information transfer between cells and ion exchange; affect cell function, including mitochondrial, sarcoplasmic reticulum, etc. organelle dysfunction, resulting in reduction of myocardial energy supply; ion permeability of myocardial cells, allowing potassium, phosphate or magnesium is lost from the myocardium, and myocardial intracellular calcium overload, can lead to decreased myocardial contractility, is caused by alcoholic cardiomyopathy a major cause of heart failure; caused when alcohol metabolism changes in intermediary metabolism, so that some of the three carboxylic acid cycle enzymes such as aspartate aminotransferase (AST), malate dehydrogenase, different citrate dehydrogenase, lactate dehydrogenase and aldolase escape from the myocardial cells, will affect the myocardial cell function, it can not effectively use fatty acids to produce energy, and to triglyceride accumulation in the myocardium, fat operation abnormal and myofibrillar adenosine triphosphate activity changes have a direct inhibitory effect on myocardial itself; long-term drinking can be changed regulatory protein (the original and the original Ning myosin protein) structure of myocardial contraction and relaxation; drinking large quantities of wine can still cause the body balanced nutrition disorders, easily lead to vitamin deficiency, especially lack of vitamin B group, but also increase heart failure, in addition, some additives containing alcohol cobalt, lead, toxic substances, long-term drinking can cause poisoning or myocardial injury, due to the interaction and impact of the above reasons, eventually lead to the occurrence of alcoholic cardiomyopathy.1. Pathogenesis
(1) alcohol (ethanol) in the absorption, distribution and metabolism: Alcohol is a simple two-carbon compounds, after drinking the entire gastrointestinal tract, especially the spof the duodenum in a simple way to quickly absorb the higher the concentration, absorption faster, then the role of alcohol dehydrogenase in the liver under the oxidation of toxic acetaldehyde, then oxidized by the aldehyde dehydrogenase to acetate, into the citric acid cycle, oxidized to carbon dioxide and water.
(2) on myocardial injury: Long-term heavy drinking can cause heart damage, but there are also studies that the incidence of alcoholic cardiomyopathy and alcohol is not the time and dose-effect relationship, and there are individual differences, alcohol actually cause disease or only conditions of risk factors is not clear, fine wine, the mechanism of myocardial damage is not entirely clear, at present the that alcohol caused mainly by the following aspects of myocardial damage.
alcohol and its metabolites in a direct toxic effect: alcohol and its metabolite acetaldehyde cardiac toxicity with the following: A. interfere with mitochondrial respiration, influence on the ion permeability of myocardial cell membrane and inhibit the binding of calcium ion transport and its myogenic The interaction between the fibers, interference excitation - contraction coupling, thereby inhibiting myocardial contractility; B. inhibition of sodium pump activity, the potassium and magnesium loss from the cells increased, causing uneven depolarization and repolarization, conduction slowing as reentrant and self-discipline based electrophysiological abnormalities; C. to the citric acid cycle enzymes such as aspartate aminotransferase certain, malate dehydrogenase, different citrate dehydrogenase, lactate dehydrogenase and aldolase escape from the myocardial cells, heart cells to make use of barriers of fatty acids, triglycerides in myocardial cells, phosphatidyl ethanol, fatty acids, acetyl ester accumulation, resulting in irreversible myocardial injury, increased excitability of myocardial cells, prone to cause arrhythmias; D. can promote the release of catecholamines, myocardial concentrations of catecholamines by high long-term stimulation of cardiac hypertrophy and arrhythmia can; E. excited sympathetic nerve stimulation on coronary artery


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