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Alcoholic heart disease symptoms. Alcohol heart damage

55) Complications of diabetes mellitus: angiopathy, neuropathy, coma in diabetes mellitus. Mechanisms of development and manifestation.

57) Atherosclerosis: etiology, pathogenesis, principles of prevention and treatment. Changes in the periodontium with atherosclerosis.

58) Oxygen starvation: definition of the concept, classification, causes and mechanisms of development of certain types of hypoxia. Pathophysiological basis for the prevention and treatment of hypoxic conditions.

59) Functional and metabolic disorders during oxygen starvation. Emergency and long-term adaptive reactions during hypoxia.

61. Hemoglobinopathies, membranopathy and enzymopathies: etiology, pathogenesis, clinical and hematological manifestations.

63. Etiology, pathogenesis, clinical and hematological characteristics of iron deficiency anemia. Features of dental manifestations in iron deficiency anemia.

64. Erythrocytosis: definition of the concept, types, etiology, pathogenesis, clinical and hematological characteristics.

65. Leukocytosis: definition of the concept, types, causes and mechanisms of development, hematological characteristics. Leukemoid reactions: definition of the concept, their differences from leukocytosis and leukemia.

66. Leukopenia: definition of the concept, types, causes and mechanisms of development. Agranulocytosis: types, clinical and hematological characteristics. Features of dental manifestations in agranulocytosis.

67. Leukemia: definition of the concept, etiology, pathogenesis, classification, hematological characteristics, principles of diagnosis. Features of dental manifestations in leukemia.

68.Heart failure: definition of the concept, causes, types and their characteristics.

69. Pathogenesis of chronic heart failure: mechanisms of compensation and decompensation. The concept of cardiac remodeling in chronic heart failure.

70.Alcoholic heart damage: mechanisms of development and main manifestations.

72. Acute heart failure: types, causes and mechanisms of development.

74. Cardiac arrhythmias: etiology, pathogenesis, WHO classification.

75. Cardiac arrhythmias caused by a violation of automaticity: types, mechanisms of development, ECG characteristics, hemodynamic disorders.

77. Cardiac arrhythmias caused by conduction disturbances: types, mechanisms of development, ECG characteristics, hemodynamic disorders.

81 Respiratory failure: causes, types, recognition. Violation of the mechanics of breathing and ventilation of the lungs (pathogenetic variants of pulmonary failure).

83. Hypertension of the pulmonary circulation in pulmonary failure: mechanisms of development and compensation.

84 Violations of the structure of the respiratory act: types, their characteristics, causes and mechanisms of development.

85 Digestive insufficiency: concept, causes. Disorders of appetite, food processing in the mouth and its passage through the esophagus

86 Digestive disorders in the stomach: causes, mechanisms, consequences. Peptic ulcer of the stomach and duodenum: etiology and pathogenesis.

87 Digestive disorders in the intestines: causes, mechanisms, consequences for the body. The effect of alcohol on digestion.

88 Liver failure: definition of the concept, etiology, pathogenesis of the main manifestations. Changes in the periodontium in liver diseases. Alcoholic liver damage.

89.Hepatic encephalopathy

90. Jaundice (icterus).

91.Acute renal failure (ARF). Sudden occurrence

93. General etiology and pathogenesis of endocrinopathies.

94. Thyroid dysfunction

95.Disorders of the hypothalamic-pituitary system

96. Pathophysiology of the adrenal glands

97. General adaptation syndrome

98. General etiology and pathogenesis of damage to the nervous system.

99. Movement disorders

100 Sensory impairment

101. Pathophysiology of pain

70.Alcoholic heart damage: mechanisms of development and main manifestations.

Alcohol damage hearts develops due to the direct action of alcohol, acetaldehyde (a product of alcohol processing), deep structural changes and physicochemical disorders. With systematic alcohol intake, the contractility and performance of the myocardium (heart muscle) decreases. Heart cells swell, collapse, the number of cell nuclei decreases, the structure of muscle fibers is disrupted, cell membranes are loosened and destroyed, protein synthesis in heart cells is disrupted. Then cell degeneration, micro- and macronecrosis is detected.

In patients with alcoholism, the entire spectrum of conduction and excitability disorders is recorded. Most common atrioventricular block, premature ventricular excitation syndrome and heart blockade.

Alcoholic heart damage is complicated hypertension and vascular atherosclerosis.

The value of blood pressure in people who abuse alcohol is initially higher (10-15%) than in those who abstain from taking it. This is an additional burden on the heart.

There is a concept "alcoholic heart" It denotes the typical appearance of an alcoholic's heart observed at autopsy. The size of the heart is increased due to the enlargement of cavities and the proliferation of connective (not functional, muscle, but connective) tissue. Stopping alcohol consumption in a state of compensation stops toxic damage to the myocardium. If the impact of the damaging factor remains, decompensation develops. The strength and speed of heart contractions decrease, heart failure develops: swelling of all organs. Recovery at this stage of alcoholic heart damage is impossible.

71.Pathogenesis of the main clinical manifestations heart failure: tachycardia, shortness of breath, cyanosis, edema. Changes in basic hemodynamic parameters in heart failure.

Tachycardia - occurs reflexively and compensates for the lack of stroke volume by increasing the number of heart contractions. In the initial stages of CHF, an increase in heart rate is observed only during physical activity; later it is expressed at rest. Tachycardia occurs due to myocardial ischemia, decreased cardiac output and (or) stagnation of blood in the vessels of the lungs; due to the Bainbridge reflex from the stretching mouths of the vena cava and helps maintain cardiac output at a sufficient level.

Dyspnea more frequent and early sign CHF. characterized by a feeling of lack of air, a sharp increase in it - like suffocation. shortness of breath is accompanied by a cough, caused reflexively from congestive bronchi, or associated with expansion of the left atrium. As a result of stagnation in the vessels of the pulmonary circulation, the function of external respiration is disrupted, leading to the accumulation of lactic acid in the blood and carbon dioxide. This leads to the development of acidosis. The respiratory center responds to hypercapnia and acidosis by increasing and deepening breathing, and to hypoxia by only increasing it. In severe CHF, attacks of suffocation occur at night - cardiac asthma. An increase in circulating blood volume, a decrease in gas exchange, an increase in the tone of the vagus nerve and moderate bronchospasm play a role in its occurrence. Prolonged attacks of cardiac asthma can develop into pulmonary edema, which is manifested by suffocation, bubbling breathing, and the separation of pink, serous, foamy sputum (due to sweating of blood cells into the alveoli). On auscultation, fine and large bubble rales are heard over the entire surface of the lungs. With pulmonary edema, cyanosis increases, the pulse quickens, and its filling decreases.

Edema with CHF- arise due to an increase in hydrostatic pressure in the vessels, and subsequently due to electrolyte imbalance. The body tries to reduce hydrostatic pressure by “dumping” the liquid part of the blood from the vessels into the tissues and cavities. appear on the legs, arms, lumbar region and increase in the evening. In the early stages, hidden swelling may be observed, since retention of up to 5 liters of fluid in the body occurs outwardly unnoticed. Edematous fluid (transudate) can accumulate in serous cavities - pleural (hydrothorax), pericardial cavity (hydropericardium), in the abdominal cavity (ascites), as well as in the genital area.

Cyanosis. expressed on fingers and toes, tip of nose, lips. Its occurrence depends on an increase in the content of reduced hemoglobin in the blood as a result of insufficient arterialization of blood in the pulmonary capillaries. Cyanosis is also caused by excessive absorption of oxygen by tissues, caused by slowing blood flow and depletion of venous blood in oxyhemoglobin.

IN Lately issues of diagnosis and treatment of alcoholic heart disease are becoming increasingly relevant due to the high frequency of occurrence of this pathology in clinical practice and certain difficulties in establishing and formulating a diagnosis. Some difficulty is presented by the differential diagnosis of alcoholic cardiomyopathy (ACMP) and dilated cardiomyopathy, which are similar in their clinical picture. The article covers in detail the pathogenesis and features of damage to the heart muscle, the clinic and course of ACM, their differences from similar forms of heart damage. 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 repeatedly confirmed by research significance in a positive prognosis and possible regression pathological changes myocardium until complete restoration of the normal dimensions of the heart cavities. Drug therapy for 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 effects is recommended.

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

For quotation: Gurevich M.A., Kuzmenko N.A. Alcoholic heart disease // Breast cancer. 2016. No. 19. pp. 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 citation: 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 heart damage

Currently, alcoholic cardiomyopathy (ACMP) is divided into independent form cardiomyopathies of alcoholic etiology. ACM is observed in approximately 30% of people who regularly drink large amounts of alcohol for more than 10 years and is caused by the toxic effects of alcohol on the myocardium.
M.J. Davies (1975) observed ACM in 15 of 82 cases of primary (idiopathic) cardiomyopathies that were fatal. A study in which V.Ya. Gerwald et al. analyzed the causes of death of persons with chronic alcohol intoxication in the period from 2008 to 2015, showed that the number of diagnosed cases of ACM is growing every year. Alcohol injuries occupy 3rd place in the structure cardiovascular diseases after various forms 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 with the assistance of 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 internal organs is directly related to systematic alcohol consumption; with increasing dose, the risk of damage increases:
– 40 g per day – low risk;
– 80 g per day – average risk;
– 160 g per day – high risk.
For women, the corresponding doses are 2 times less.
The long-term effects of alcohol are not related to the type of alcoholic drink (vodka, wine, beer, etc.). The hangover syndrome depends on the amount of low-quality alcohols - fusel oils (congeners). They are found in low-grade 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 the 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 deposits (organized parietal thrombi). There are areas of fatty degeneration of muscle fibers; on the section there is focal sclerosis of the LV and papillary muscles. Atherosclerosis of the coronary arteries is moderate, arterial stenosis is rare. Microscopically in muscle fibers: uneven hypertrophy along with foci of atrophy, vacuolar degeneration, foci of necrosis of varying duration with organizational phenomena, sometimes lymphocytic infiltrates, a typical picture of accumulation of neutral lipids in cardiomyocytes. There are especially many of them in the area of the conduction system, which apparently explains the frequency of rhythm disturbances. Changes in ultrastructure include coarsening of the sarcoplasmic reticulum, swelling of mitochondria, damage to cristae, and lipid deposits.

Clinic

ACMP has all the clinical manifestations inherent in dilated cardiomyopathy (DCM). Clinical symptoms are often dominated by frequent paroxysmal rhythm disturbances, especially atrial fibrillation. Chronic alcoholic damage to the myocardium during periods of exacerbation is manifested by acute alcoholic dystrophy of the myocardium, with newly appearing and increasing dynamics changes in the final part of the ventricular ECG complex– ST segment, T wave, paroxysmal rhythm disturbances – atrial fibrillation, ventricular rhythm disorders up to ventricular tachycardia and even ventricular fibrillation. The latter can cause sudden death and progressive heart failure (HF).
ACM predominantly affects men aged 30–55 years. The disease often begins gradually, unnoticeably, and ACM is often diagnosed accidentally when visiting a doctor for other diseases. Early clinical signs are a moderate increase in heart size and a gallop rhythm. As myocardial dysfunction progresses, the symptoms of congestive heart failure increase: increased shortness of breath on exertion, nocturnal attacks of cardiac asthma, persistent shortness of breath at rest. A decrease in cardiac output is accompanied by an increase in general weakness and increased fatigue.
Relatively late symptoms of ACM are peripheral edema, hepatomegaly and ascites. Requires dynamic ECG, radiography chest, EchoCG, coronary arteriography, catheterization of the heart cavities for the purpose of differentiating ACM and idiopathic DCM. The course of alcoholic cardiomyopathy often has a wave-like character with alternating periods of remission and deterioration, often caused by the resumption of drinking alcohol. Life-threatening ventricular arrhythmias and sudden death are quite common in the advanced stage of alcoholic myocardial dystrophy. The listed signs are partially associated with prolongation of the QT interval, which is detected in 30–50% of such patients (S. Burch, 1981; T. Koide et al., 1982). According to T. Koide et al., atrial fibrillation in ACM was detected in 45% of cases, thromboembolism – in 55%.

Diagnostics

According to WHO diagnostic criteria, patients with ACM have the following: long-term, 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 abstinence after 6 months. remission of ACM is possible. Small doses of alcohol - 10 and 30 g of ethanol, respectively, for women and men - do not have a damaging effect on the myocardium; there are even claims that such doses have a cardioprophylactic and antiatherogenic effect. At the same time, there is no doubt that continued drinking of alcohol against the background of existing coronary heart disease worsens the prognosis of the disease and, in combination with physical activity, in some cases leads to silent myocardial infarction. When diagnosing ACM, one should take into account the younger age of patients compared to patients with ischemic cardiopathy, signs of multiple organ damage inherent in alcoholism: liver cirrhosis, polyneuropathy, nephritis, gastroenterocolitis, etc. Hyperemia of the face and conjunctiva, mumps, Dupuytren’s contracture is often (but not necessarily ) are also found in alcoholism. Liver enzyme studies confirm liver damage, but it should be borne in mind that similar changes can occur in 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 ACM are diagnosed with coronary heart disease.
In a patient with chronic alcoholism, diastolic dysfunction and slight LV hypertrophy, a tendency to rhythm disturbances, especially atrial fibrillation, are almost always detected. The degree of impairment of LV diastolic function is directly proportional to the consumption of alcoholic beverages. IN developed countries There are tens of millions of patients with chronic alcoholism around the world, while ACM is much less common. The main diagnostic criterion for ACM is cardiomyopathy, which develops against the background of long-term (at least 10 years) systematic consumption of alcoholic beverages in quantities equivalent to 80 ml of ethyl alcohol per day.

Forecast

It has been shown that the prognosis for ACMP is more positive than for DCM. Abstinence in the early stages of the disease helps prevent its progression and even completely cure it. The results of long-term follow-up of 23 patients with ACMP and 52 with DCM have been published. The age of the patients and the severity of the disease in the two study groups were the same. Over a five-year period, 81% of patients with ACMP and 48% of patients with DCM remained alive, 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 increased 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 people 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 HF and normalization of heart size in 10 out of 15 patients; in the remaining 5, despite the presence of cardiomegaly, the severity of HF decreased significantly. In general, of the 39 patients who remained committed to alcohol, improvement occurred in only 10%, compared to 61% in the group of patients who gave up 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, established NYHA functional class IV CHF, but after 15–25 months. After stopping alcohol intake, complete normalization of the LV cavity and ejection fraction was recorded.
A significant positive effect of abstinence is observed in patients with initially severe congestive HF of NYHA functional class IV with a LV ejection fraction of less than 30%; it usually manifested itself after 6 months. from the beginning of abstinence from alcohol. Clinical improvement after abstinence more often occurs 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 DCM.

Treatment

With an early, timely diagnosis of ACM, abstinence from alcohol is crucial for recovery. With late diagnosis, organ changes may be irreversible.
Treatment of congestive HF in ACM is carried out according to the principles of therapy for circulatory decompensation in DCM. It is worth pointing out some features of the treatment of heart failure in this pathology, which are based on our own and literature data. Cardiac glycosides are extremely 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 side toxic effects when using cardiac glycosides - life-threatening ventricular arrhythmias, exacerbations of hepatic and gastrointestinal pathologies. Among cardiotropic drugs, angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor antagonists (ARA II) have been used with some success.
Treatment with ACE inhibitors was started after discontinuation of potassium supplements and potassium-sparing diuretics by prescribing captopril 6.25 mg, enalapril 2.5 mg. Subsequently, with good tolerability and 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 indicated with a dose increase to 20-40 mg/day once, quinapril - with a dose increase from 5 to 20 mg/day in 2 divided doses and ramipril - with a dose increase 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 as a single dose) provides a greater reduction in overall mortality by preventing sudden death.
In addition, isosorbide dinitrate 10 mg 3 times a day in combination with hydralazine 10–25 mg 3–4 times a day is effective for congestive heart failure. If well tolerated and there is no arterial hypotension, the dose is increased to an average of 40 mg 3 times a day and 75 mg 3-4 times a day, respectively.
For the pathology discussed, long-term therapy with antioxidants should be recommended.
Under the influence of alcohol and acetaldehyde, 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 via 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, enhance the effect of ACE inhibitors, reduce the degree of damage and apoptosis of cardiomyocytes.
Thus, taking into account the good tolerability of the drug by patients, data from published studies and the results of 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 ACM 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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The term “alcoholic cardiomyopathy” is not entirely correct. In modern cardiology, cardiomyopathy is understood as a myocardial disease of unknown cause, characterized by an enlarged heart and progression of heart failure. Therefore, it is correct to talk about alcoholic myocardial dystrophy. This heart damage occurs in people who abuse alcohol and is characterized by metabolic disorders in the cells of the heart muscle.

Development mechanism

Alcohol has a toxic effect on the heart muscle.

Alcohol (ethanol) and its breakdown product, acetaldehyde, have a toxic effect on heart muscle cells. Energy metabolism is disrupted in them, and the formation of “fuel” for biological reactions – adenosine triphosphate (ATP) – is reduced. In addition, potassium and potassium suffer, which disrupts myocardial contractility.
Ethanol and acetaldehyde cause an increase in the concentration of catecholamines (for example, norepinephrine) in the blood, which increases the myocardial oxygen demand. Catecholamines directly damage cell membranes, activate lipid peroxidation and thereby contribute to the destruction of heart cells.

Clinical forms

A description of the clinical forms of alcoholic myocardial dystrophy was given in 1977 by E. M. Tareev and A. S. Mukhin.

Classic shape. The patient has typical chronic alcoholism. He is bothered by heart pain, especially at night, shortness of breath, and rapid heartbeat. There are interruptions in the functioning of the heart. These symptoms sharply intensify 2-3 days after taking large quantity alcoholic drinks.
Pseudo-ischemic form. The patient complains of pain in the heart area. They can be of varying duration and strength, and may or may not be associated with physical activity. Heart pain must be differentiated from manifestations of ischemic heart disease. Alcoholic myocardial dystrophy is characterized by a slight increase in body temperature, an enlarged heart, and the development of circulatory failure (shortness of breath, edema). Pain is often accompanied by rhythm disturbances.
Arrhythmic form. Rhythm disturbances come to the fore - atrial fibrillation, extrasystole, paroxysmal tachycardia, which is manifested by rapid heartbeat, interruptions in heart function, and sometimes dizziness, even episodes of loss of consciousness. In this case, the patient experiences an enlarged heart and shortness of breath.

Clinical stages

The stages during alcoholic myocardial dystrophy were described in detail by V. Kh. Vasilenko in 1989.

Stage 1 lasts up to 10 years and is characterized by episodic heart pain and sometimes rhythm disturbances.
Stage 2 develops in patients with chronic alcoholism with “experience” of more than 10 years. Heart failure appears - swelling in the legs, cough. Patients begin to develop blueness of the face, lips, and hands and feet (acrocyanosis). Dyspnea in such patients may worsen when lying down, which indicates stagnation of blood in the pulmonary circulation. Stagnation of blood in the systemic circulation is manifested, among other things, by an enlarged liver. Atrial fibrillation () and other serious rhythm disturbances develop.
Stage 3 – severe circulatory failure. There is a violation of the function of internal organs, an irreversible change in their structure.

Symptoms

Symptoms of alcoholic myocardial dystrophy are most pronounced during the abstinence period (within 8 days after an episode of excessive alcohol consumption).

Pain. Pain in the heart area is not associated with physical activity. They appear in the morning, mostly stabbing, aching, and long-lasting. Pain is felt in the area of the apex of the heart (approximately at the intersection of the 5th rib and a conventional vertical line passing 1–2 cm to the left of the middle of the left clavicle). Usually the pain is not intense. It does not go away after taking nitroglycerin. An increase in pain is observed after an episode of alcohol abuse.
Dyspnea. The patient is bothered by frequent shallow breathing and a feeling of lack of air, which intensifies even with light exertion. On fresh air health improves.
Interruptions in the functioning of the heart. The patient may be disturbed by the feeling of interruptions, “fading” of the heart, irregular pulse, and episodes of dizziness. The electrocardiogram may record supraventricular or ventricular extrasystole, atrial fibrillation and flutter, paroxysmal supraventricular tachycardia. Rhythm disturbances are especially pronounced in persons with severe heart damage.
Edema, enlarged liver. These are signs of progressive heart failure. It is also characterized by shortness of breath with little physical exertion and at rest. Shortness of breath worsens when lying down, so the patient takes a semi-sitting position. This forced position is called orthopnea.

Swelling in the legs occurs, especially in the evening, and in severe cases, widespread swelling of the entire body and an enlarged abdomen (ascites). The liver enlarges.

Diagnostics

Methods for diagnosing alcoholic cardiomyopathy are standard: ECG, echo-CG, functional tests.

To diagnose alcoholic myocardial dystrophy, electrocardiography, echocardiography (ultrasound examination of the heart), 24-hour electrocardiogram monitoring, and a stress test (for example, bicycle ergometry or treadmill test) are performed. A consultation with a narcologist is required to confirm the diagnosis of chronic alcoholism.

Treatment

The main therapeutic factor is cessation of alcohol consumption.
To improve metabolic processes in the myocardium, drugs are prescribed that stimulate protein synthesis in heart cells (Mildronate), as well as improve energy metabolism (Cytochrome C, Neoton, etc.). Multivitamins are used for the same purpose.
To suppress lipid peroxidation in cell membranes and stop their damage, antioxidant agents, such as vitamin E, are prescribed.
With the development of certain types of arrhythmias, calcium antagonists (for example, Verapamil) are prescribed. It affects calcium metabolism in cells, providing an antiarrhythmic effect. In addition, these drugs improve tissue respiration, normalize the relaxation of myocardial cells, and stabilize cell membranes.
To stabilize lysosomal membranes, Essentiale or Parmidine are prescribed. As a result, the release of aggressive lysosomal enzymes into the cells and the death of myocardiocytes are prevented.
To eliminate oxygen starvation and “acidification” of the internal environment of the body, patients with alcoholic myocardial dystrophy are recommended to stay in the fresh air, take oxygen cocktails, inhale humidified oxygen, and hyperbaric oxygenation sessions. In addition, antihypoxants are prescribed (for example, Mexidol).
To normalize the electrolyte balance, the body is saturated with potassium salts. A potassium diet is prescribed. It may be recommended to take potassium chloride orally along with orange or tomato juice. Often, when health deteriorates, potassium preparations are administered intravenously. This is especially important in the presence of rhythm disturbances.
To eliminate the effect of excess catecholamines on the myocardium, beta-blockers (for example, Anaprilin) are prescribed. With the development of heart failure and arrhythmias, treatment of these syndromes is carried out according to appropriate regimens.

Which doctor should I contact?

If symptoms of alcoholic heart damage appear, you should consult a cardiologist. However, treatment will be unsuccessful without treating addiction to alcohol, so the patient needs treatment from a narcologist.

Alcoholic cardiomyopathy is a diffuse lesion of the heart that develops when long-term use large amounts of alcohol as a result of the direct toxic effect of ethyl alcohol on myocardial cells. Manifestations of the disease include progressive heart failure, and possible ischemia (decreased blood circulation) of the myocardium.

ICD-10	I42.6
ICD-9	425.5
eMedicine	med/286
MeSH	D002310
MedlinePlus	000174

General information

For the first time, the clinic of alcoholic myocardial damage was described in detail in 1893 by G. Steel.

The main symptoms of the disease (shortness of breath during physical effort and rapid heartbeat) and the connection of these symptoms with alcohol consumption were also considered by J. Mackenzie in 1902.

Mackenzie noted that decompensation occurring in a latent form can be detected due to attacks of paroxysmal tachycardia, during which a relatively normal-sized heart enlarges for several hours, the patient’s lips swell, the veins in the neck pulsate, and the face becomes bluish.

Subacute alcoholic myocarditis, which due to its slow development can remain unrecognized for a long period, was first described by N. Vaquez in 1921.

The term “alcoholic cardiomyopathy” itself is currently considered not entirely correct, since V. Brigden, the author of this term, classified as cardiomyopathies a group of myocardial diseases of non-coronary origin that arose for an unknown reason. Since the cause of the disease in this case is clear (toxic effects of alcohol), the disease is often called alcoholic myocardial dystrophy.

Since R.B. Hudson in 1970 proposed a more detailed and extensive definition for the concept of “cardiomyopathy” (he proposed to include all diseases of the myocardium, pericardium and endocardium as cardiomyopathies, regardless of their functional characteristics and origin); the disease also continues to be called alcoholic cardiomyopathy.

There are no exact statistics on the prevalence of the disease, since alcohol abusers try to hide this fact. In Europe, alcoholic cardiomyopathy accounts for about 30% of all identified cases. The disease is detected in half of people suffering from alcoholism.

The mortality rate from alcoholic cardiomyopathy is about 12-22% of all cases of the disease. Alcoholic heart disease is detected in 35% of cases of sudden coronary death.

The disease is more often observed in men 30-55 years old, but in women the period of development of alcoholic cardiomyopathy is shorter.

Forms

Clinical forms of alcoholic myocardial dystrophy were described in 1977 by E. M. Tareev and A. S. Mukhin, who identified:

The classic form of the disease, characteristic of patients suffering from typical chronic alcoholism. This form is characterized by shortness of breath, rapid heartbeat and heart pain, which especially bothers the patient at night. There are interruptions in the functioning of the heart. Symptoms sharply increase 2-3 days after drinking a significant amount of alcohol.
Pseudo-ischemic form, in which pain in the heart area varies in strength and duration, can be associated with physical activity or manifest itself at rest, resembling coronary heart disease. This form of alcoholic myocardial dystrophy is accompanied by a slight increase in temperature, an enlarged heart and the appearance of edema and shortness of breath due to the development of circulatory failure. Painful sensations may be accompanied by violations heart rate.
An arrhythmic form, the main symptoms of which include atrial fibrillation, extrasystole, paroxysmal tachycardia, accompanied by disturbances in the functioning of the heart and rapid heartbeat. In some cases, dizziness and episodes of loss of consciousness are observed. The heart is enlarged and there is shortness of breath.

Reasons for development

Alcoholic cardiomyopathy develops with excessive and long-term consumption of alcoholic beverages as a result of the damaging effects of ethanol and its metabolites on the structure of myocardial cells. With prolonged alcohol consumption, degenerative changes occur in the walls of the coronary arteries and nerve fibers of the heart, metabolism in the myocardium is disrupted, and myocardial hypoxia develops.

The determining factor in the development of the disease is the amount of alcohol consumed by the patient. Epidemiological studies have convincingly proven that mortality from coronary heart disease and the amount of alcohol consumed by the patient are in a U-shaped relationship - the highest mortality is observed in people who do not drink alcohol at all and in people who abuse alcohol. People who drink alcohol moderately are less likely to suffer from coronary artery disease, and mortality from this disease is low in this group.

There is no consensus on a safe minimum daily dose of alcohol. There is also no reliable data on how long a “dangerous dose” must be taken for the development of alcoholic cardiomyopathy.

According to studies conducted in the USA, Canada and the European Union, alcoholic cardiomyopathy develops in patients with daily ethanol consumption:

for 10 years, if the daily dose is 125 ml;
after 5 years, if the daily dose exceeds 80 g;
for 20 years, if the daily dose is 120 g.

Alcoholic cardiomyopathy develops in different individuals at different daily doses and in different terms. There are no exact data, since people differ in their individual sensitivity to alcohol-containing drinks (it depends on the genetically determined activity of enzyme systems that are involved in the metabolism of alcohol).

According to researchers, the development of the disease is affected by any alcoholic drink consumed in excessive quantities.

Pathogenesis

Ethanol (ethyl alcohol) and its toxic metabolite acetaldehyde inhibit the activity of the enzyme sodium-potassium adenosine triphosphatase (Na+K+-ATa3bi), which is located in the plasma membrane of cells and transports K+ ions into the cell, and Na+ ions into the external environment. As a result, Na+ ions accumulate in cardiomyocytes and a lack of K+ ions is observed.

Disturbances in the activity of Ca++-ATPase also occur, causing a massive entry of Ca++ ions into the cell and their accumulation.

When electrolyte-ion homeostasis is disrupted, the processes of excitation and contraction of cardiomyocytes become uncoupled. This disorder is aggravated by the resulting changes in the properties of contractile proteins of cardiomyocytes.

Ethanol and acetaldehyde also inhibit the p-oxidation of free fatty acids, which are the main source of energy production for the myocardium (the synthesis of 60-90% of all ATP is provided by free fatty acids).

Alcohol activates the formation of free radicals and peroxides due to the peroxidation of free fatty acids. Free radicals and peroxides have a sharp damaging effect on the membranes of cardiomyocytes, so the patient gradually develops myocardial dysfunction.

The effect of alcohol and its metabolite reduces the amount of mitochondrial oxidative enzymes (including Krebs cycle enzymes necessary for the synthesis of ATP from glucose) in the myocardium and their activity, which also reduces energy production in the myocardium.

As a result of exposure to acetaldehyde, the synthesis of protein and glycogen in cardiomyocytes is also disrupted.

With a decrease in energy production in the myocardium and reduced Ca++-ATPase activity, disturbances in the contractile function of the myocardium occur.

Ethyl alcohol and acetaldehyde also affect the synthesis and increased release of increased amounts of catecholamines (formed in the adrenal glands), so the myocardium is subjected to a kind of catecholamine stress, which increases the need for oxygen. Elevated levels of catecholamines have a cardiotoxic effect, provoke cardiac arrhythmias and cause overload of the myocardium with calcium ions.

Impaired microcirculation in the myocardium develops already in the early stages of the disease. The endothelium of small vessels is affected, the permeability of their walls increases, and platelet microaggregates appear in the microvasculature. These lesions provoke hypoxia and cause the development of myocardial hypertrophy and diffuse cardiosclerosis.

The direct effect of alcohol on the myocardium also contributes to the appearance of protein deficiency in the myocardium (observed in less than 10% of patients suffering from chronic alcoholism). Disorders of protein metabolism have a significant impact on the development of alcoholic cardiomyopathy, since the heart in alcoholism is affected by the type of dysproteinemic myocardosis.

In some patients, vitamin B deficiency may be added to the pathogenetic factors in the development of alcoholic cardiomyopathy.

According to the researchers, immunological disorders may be involved in the development of myocardial damage in the case of alcohol intoxication, since in half of the patients with a severe form of the disease, antibodies to acetaldehyde-modified myocardial proteins were detected in the blood. These antibodies can aggravate the damaging effects of ethanol and acetaldehyde on the myocardium.

Chronic alcohol intoxication suppresses T-cell immunity, promoting long-term survival of various viruses in the body of patients with alcoholic cardiomyopathy.

The development of alcoholic cardiomyopathy is also influenced by arterial hypertension, which occurs when the daily dose of alcohol is exceeded (more than 20 grams) in 10-20% of patients. Arterial hypertension aggravates myocardial hypertrophy and dysfunction, but when the dose is reduced below 15 g. or complete cessation of alcohol consumption, blood pressure in most cases returns to normal.

Symptoms

The first signs of alcoholic cardiomyopathy that the patient complains of are the appearance of sleep disturbances, heart rhythm and headache. Then the symptoms are joined by shortness of breath and swelling that occurs with exertion. In most cases, patients do not admit that they have a harmful addiction to alcohol and do not see a connection between the symptoms of the disease and alcoholism.

The symptoms manifest themselves most clearly during the abstinence period (within a week after consuming alcohol in excess). Symptoms of alcoholic cardiomyopathy include:

Prolonged, aching or stabbing morning pain in the apex of the heart, which occurs regardless of physical activity. In most cases, the pain is not intense, but intensifies after drinking alcohol. Does not disappear when taking nitroglycerin.
Shortness of breath, which worsens even with minimal exertion. The patient's breathing is shallow and rapid, there is a feeling of lack of air. Fresh air makes you feel better.
Interruptions in cardiac activity, which the patient perceives as a “fading” heart, attacks of dizziness and an irregular pulse. An electrocardiogram may reveal supraventricular or ventricular extrasystole, presence of fibrillation
(uncoordinated contraction) and atrial flutter, paroxysmal supraventricular tachycardia. The more severe the heart damage, the more pronounced the rhythm disturbances.
Swelling and enlargement of the liver, characteristic of progressive heart failure. With enlarged liver, shortness of breath is present even at rest, worsening in a lying position (orthopnea, in which the patient is forced to take a semi-sitting position). Swelling first appears in the evening on the legs, and as the disease progresses, it spreads to the whole body. Ascites (enlarged abdomen) is also observed.

Alcoholic cardiomyopathy may be accompanied by:

redness of the facial skin;
dilation of blood vessels in the nose and a change in its color to blue-purple;
hand tremors;
redness of the eyes and yellowness of the sclera;
weight gain or sudden weight loss;
excited behavior, verbosity, fussiness.

Clinical stages

V. Kh. Vasilenko in 1989 identified the following stages of alcoholic cardiomyopathy:

Stage 1, which lasts about 10 years. Pain in the heart occurs sporadically, and rhythm disturbances are sometimes observed.
Stage 2, which is typical for patients suffering from chronic alcoholism for more than 10 years. At this stage, a cough appears, patients complain of shortness of breath and swelling that occurs in the legs. The face and lips acquire a bluish tint (), and the hands and feet may turn blue. Shortness of breath often worsens in a supine position as a result of stagnation of blood in the pulmonary circulation. When blood stagnates in the systemic circulation, an enlarged liver is observed. Atrial fibrillation (atrial fibrillation) and other heart rhythm disturbances are present.
Stage 3, which is accompanied by severe circulatory failure and subsequent dysfunction of internal organs with irreversible changes in their structure.

Diagnostics

Diagnosis of alcoholic myocardial dystrophy is difficult due to the lack of specific signs of the disease (diagnostic signs of alcoholic cardiomyopathy may accompany other types of cardiovascular diseases). Alcoholic heart damage may be accompanied by dysfunction of the pancreas and liver, which makes diagnosis difficult in the absence of an established alcohol history.

The diagnosis is made based on:

patient complaints and medical history, if the patient does not hide his alcohol consumption;
electrocardiogram data, allowing to identify changes in the ST segment, the presence of myocardial hypertrophy, and record disturbances in conduction and heart rhythm;
X-ray data, which help to identify the presence of myocardial hypertrophy at an early stage of the disease, dilatation (expansion of the chambers of the heart) and congestion in the lungs;
echocardiogram data, allowing to identify myocardial hypertrophy and dysfunction, the presence of diastolic and systolic insufficiency.

Also carried out:

Daily monitoring of the electrocardiogram, which helps to identify disturbances in the rhythm and conduction of the heart.
Load test. Typically, a treadmill test is used, in which an electrocardiographic study is carried out during physical activity on a treadmill (treadmill), or bicycle ergometry, in which a special bicycle is used for loading.

If necessary, sounding is carried out for the purpose of morphological examination of cardiobiopathies.

Alcoholic cardiomyopathy is suspected in the presence of atrial fibrillation,
cardiomegaly (increase in heart size), congestive heart failure and the absence of an apparent cause for these disorders in young men.

The patient must undergo a consultation with a doctor who confirms the presence of chronic alcoholism.

Treatment

The main therapeutic factor is the complete exclusion of alcohol.

Treatment is aimed at improving metabolism, energy metabolism and stimulating protein synthesis in the myocardium.

Patients are prescribed:

Mildronate, which stimulates protein synthesis, eliminates the accumulation of toxins in cells and restores the balance between the supply and demand of cells for oxygen;
Cytochrome C, Neoton and multivitamins that improve energy metabolism;
vitamin E, which suppresses lipid peroxidation in cell membranes;
Verapamil and other calcium antagonists, which have an antiarrhythmic effect, stabilize cell membranes and improve tissue respiration;
Parmidine or Essentiale, stabilizing lysosomal membranes;
Mexidol or other antihypoxants to eliminate oxygen starvation;
potassium salts, normalizing electrolyte balance;
Anaprilin or other beta-blockers that neutralize the effects of excess catecholamines;
diuretics that relieve swelling;
cardiac glycosides that have antiarrhythmic and cardiotonic effects in heart failure.

Surgical treatment is indicated only in in case of emergency, since complications may develop.

Alcoholic cardiomyopathy also requires frequent exposure to fresh air and a diet that includes significant amounts of protein, potassium and vitamins.

Forecast

In the absence of alcohol and timely treatment, the size of the heart in patients often decreases, but restoration of myocardial function occurs very slowly, so relative recovery is observed after a long period of time.

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Recently, issues of diagnosis and treatment of alcoholic heart disease have become increasingly relevant due to the high incidence of this pathology in clinical practice and certain difficulties in establishing and formulating a diagnosis. Some difficulty is presented by the differential diagnosis of alcoholic cardiomyopathy (ACMP) and dilated cardiomyopathy, which are similar in their clinical picture. The article covers in detail the pathogenesis and features of damage to the heart muscle, the clinic and course of ACM, their differences from similar forms of heart damage. 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 repeatedly confirmed by research significance 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. Drug therapy for 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 effects is recommended.

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

For quotation: Gurevich M.A., Kuzmenko N.A. Alcoholic heart disease // Breast cancer. 2016. No. 19. pp. 1281-1284

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

Moscow regional research clinical institute named after M.F. Vladimirskiy

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

For citation: 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 heart damage

Currently, alcoholic cardiomyopathy (ACMP) is classified as an independent form of cardiomyopathies of alcoholic etiology. ACM is observed in approximately 30% of people who regularly drink large amounts of alcohol for more than 10 years and is caused by the toxic effects of alcohol on the myocardium.
M.J. Davies (1975) observed ACM in 15 of 82 cases of primary (idiopathic) cardiomyopathies that were fatal. A study in which V.Ya. Gerwald et al. analyzed the causes of death of persons with chronic alcohol intoxication in the period from 2008 to 2015, showed that the number of diagnosed cases of ACM is growing every year. Alcohol-related injuries occupy third 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 with the assistance of 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 internal organs is directly related to systematic alcohol consumption; with increasing dose, the risk of damage increases:
– 40 g per day – low risk;
– 80 g per day – average risk;
– 160 g per day – high risk.
For women, the corresponding doses are 2 times less.
The long-term effects of alcohol are not related to the type of alcoholic drink (vodka, wine, beer, etc.). The hangover syndrome depends on the amount of low-quality alcohols - fusel oils (congeners). They are found in low-grade 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 the 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 deposits (organized parietal thrombi). There are areas of fatty degeneration of muscle fibers; on the section there is focal sclerosis of the LV and papillary muscles. Atherosclerosis of the coronary arteries is moderate, arterial stenosis is rare. Microscopically in the muscle fibers: uneven hypertrophy along with foci of atrophy, vacuolar degeneration, foci of necrosis of varying duration with organizational phenomena, sometimes lymphocytic infiltrates, a typical picture of accumulation of neutral lipids in cardiomyocytes. There are especially many of them in the area of the conduction system, which apparently explains the frequency of rhythm disturbances. Changes in ultrastructure include coarsening of the sarcoplasmic reticulum, swelling of mitochondria, damage to cristae, and lipid deposits.

Clinic

ACMP has all the clinical manifestations inherent in dilated cardiomyopathy (DCM). Clinical symptoms are often dominated by frequent paroxysmal rhythm disturbances, especially atrial fibrillation. Chronic alcoholic damage to the myocardium during periods of exacerbation is manifested by acute alcoholic dystrophy of the myocardium, with newly emerging and increasing dynamics of changes in the final part of the ventricular complex of the ECG - ST segment, T wave, paroxysmal rhythm disturbances - atrial fibrillation, ventricular rhythm disorders 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, unnoticeably, and ACM is often diagnosed accidentally when visiting a doctor for other diseases. Early clinical signs are a moderate increase in heart size and a gallop rhythm. As myocardial dysfunction progresses, the symptoms of congestive heart failure increase: increased shortness of breath on exertion, nocturnal attacks of cardiac asthma, persistent shortness of breath at rest. A decrease in cardiac output is accompanied by an increase in general weakness and increased fatigue.
Relatively late symptoms of ACM are peripheral edema, hepatomegaly and ascites. Dynamic ECG, chest x-ray, echocardiography, coronary arteriography, and catheterization of the cardiac cavities are necessary to differentiate between ACM and idiopathic DCM. The course of alcoholic cardiomyopathy often has a wave-like character with alternating periods of remission and deterioration, often caused by the resumption of drinking alcohol. Life-threatening ventricular arrhythmias and sudden death are quite common in the advanced stage of alcoholic myocardial dystrophy. The listed signs are partially associated with prolongation of the QT interval, which is detected in 30–50% of such patients (S. Burch, 1981; T. Koide et al., 1982). According to T. Koide et al., atrial fibrillation in ACM was detected in 45% of cases, thromboembolism – in 55%.

Diagnostics

According to WHO diagnostic criteria, patients with ACM have the following: long-term, 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 abstinence after 6 months. remission of ACM is possible. Small doses of alcohol - 10 and 30 g of ethanol, respectively, for women and men - do not have a damaging effect on the myocardium; there are even claims that such doses have a cardioprophylactic and antiatherogenic effect. At the same time, there is no doubt that continued drinking of alcohol against the background of existing coronary heart disease worsens the prognosis of the disease and, in combination with physical activity, in some cases leads to silent myocardial infarction. When diagnosing ACM, one should take into account the younger age of patients compared to patients with ischemic cardiopathy, signs of multiple organ damage inherent in alcoholism: liver cirrhosis, polyneuropathy, nephritis, gastroenterocolitis, etc. Hyperemia of the face and conjunctiva, mumps, Dupuytren’s contracture is often (but not necessarily ) are also found in alcoholism. Liver enzyme studies confirm liver damage, but it should be borne in mind that similar changes can occur in 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 ACM are diagnosed with coronary heart disease.
In a patient with chronic alcoholism, diastolic dysfunction and slight LV hypertrophy, a tendency to rhythm disturbances, especially atrial fibrillation, are almost always detected. The degree of impairment of LV diastolic function 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 ACM is cardiomyopathy, which develops against the background of long-term (at least 10 years) systematic consumption of alcoholic beverages in quantities equivalent to 80 ml of ethyl alcohol per day.

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