Cardiac manifestations in alcoholic liver disease.

Alcoholic liver disease is the most prevalent cause of progressive liver disease in Europe. Alcoholic cirrhosis occurs in 8%-20% of cases of alcoholic liver disease. It has significant influence on cardiovascular system and haemodynamics through increased heart rate, cardiac output, decreased systemic vascular resistance, arterial pressure and plasma volume expansion. Cirrhotic cardiomyopathy is characterised by systolic and diastolic dysfunction and electrophysiological abnormalities, if no other underlying cardiac disease is present. It is often unmasked only during pharmacological or physiological stress, when compensatory mechanisms of the heart become insufficient to maintain adequate cardiac output. Low-to-moderate intake of alcohol can be cardioprotective. However, heavy drinking is associated with an increased risk of cardiovascular diseases, such as alcoholic cardiomyopathy, arterial hypertension, atrial arrhythmias as well as haemorrhagic and ischaemic stroke. Alcoholic cardiomyopathy is characterised by dilated left ventricle (LV), increased LV mass, normal or reduced LV wall thickness and systolic dysfunction.

[Forensic medical expertise of sudden cardiac death from alcoholic cardiomyopathy in the subjects having a low ethanol concentration in the blood and urine].

The objective of the present study was to evaluate the cases of sudden cardiac death from alcoholic cardiomyopathy of the subjects having a low ethanol concentration in the blood and urine; the second objective was the statistical analysis of the data thus obtained. It was shown that sudden cardiac death from alcoholic cardiomyopathy occurs in the men more frequently than in the women despite rather low ethanol levels in the blood and urine of both genders or even in the cases of complete absence of ethanol in these fluids. It is concluded that ethanol concentration in the blood and urine of the subjects who died from the alcohol-induced heart injury depends on their age and sex.

Study of oxidative stress and trace element levels in patients with alcoholic and non-alcoholic coronary artery disease.

Alcohol consumption induces oxidative stress, and leads to lipid peroxidation. These effects have been linked to alcohol-related toxicity and diseases are considered relevant to alcohol-atherosclerosis interrelationship. Deficiency of many antioxidants and trace elements may impair the antioxidant defense leading to ethanol induced oxidative stress. In the present study, our aim was to investigate the lipid peroxidation, lipid profile, antioxidant enzymes and trace elements in patients with and without alcoholic coronary artery disease (CAD). Our study included 61 patients suffering from CAD, 124 patients suffering from alcoholic CAD with high to moderate alcohol intake, 75 controls were randomly selected for our study. Increased serum lipid peroxidation, total cholesterol, triglycerides, LDL cholesterol and copper levels were high while levels of HDL cholesterol, glutathione peroxdiase, superoxide dismutase, trace elements like Selenium and Zinc were low in high alcoholic CAD patients compared with moderate and non alcoholic CAD patients. The results obtained from present study indicate that high alcohol intake predicts low antioxidant enzyme and that trace element may contribute to the increased susceptibility for the development of CAD.

Biochemical indicators and cardiac function tests in chronic alcohol abusers.

AIM: To determine the effect of chronic alcohol abuse on cardiac function, antioxidant system, trace elements, and liver function tests. METHODS: Mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyl transferase (GGT), superoxide dismutase (SOD), malondialdehyde (MDA), as well as zinc, magnesium, and copper were assayed in 25 chronic alcoholic patients and their 25 healthy relatives matched in age and gender. Echocardiographic parameters were evaluated for subjects. RESULTS: Mean corpuscular volume (96.7 fL vs 92.4 fL) and mean corpuscular hemoglobin levels (31.4 pg vs 30.5 pg) were found to be significantly increased in the patient group (P=0.002 and P=0.048, respectively). The results of the SOD and MDA assays showed no significant differences between the two groups. AST (38.7 U/L vs 22.1 U/L) and GGT (104.2 U/L vs 34.2 U/L) levels were found to be significantly increased in the patient group compared with controls (P=0.005 and P<0.001, respectively). Magnesium (1.6 mmol/L vs 1.8 mmol/L) and zinc levels (14.9 micromol/L vs 19.2 micromol/L) were significantly decreased, whereas copper levels (19.3 micromol/L vs 17.9 micromol/L) were increased in alcoholics (P=0.042, P<0.001 and P=0.003, respectively). Echocardiographic examination showed a significant decrease in mitral and tricuspid ratio of peak early and atrial flow velocity (E/A ratio) in alcoholics. CONCLUSION: Decrease in mitral and tricuspid E/A ratios accompanied with low levels of magnesium and zinc, and increased levels of copper indicate that alcoholics already have heart muscle disease even chronic alcohol exposure.

[Pathomorphological manifestations of various forms of alcohol disease]. / Patomorfologicheskie proiavleniia razlichnykh form alkogol'noi bolezni.

In acute poisoning with ethanol a cardiac variant of tanatogenesis prevails. Signs for ethanol surrogates of DIC syndrome are more characteristic. Alcohol cardiomyopathy and liver cirrhosis are typical as causes of death for chronic forms of alcoholic disease. Histochemical features in the brain are found characteristic for some forms of alcoholic disease.

Comparison of alcoholic cardiomyopathy in women versus men.

To compare the prevalence and cardiac status of male and female alcoholics with alcoholic cardiomyopathy during a 5-year period, all chronic alcoholics with dilated cardiomyopathy who had clinical symptoms of heart failure were included. Alcoholic cardiomyopathy was diagnosed in 10 chronic alcoholic women and in 26 men; the prevalence of alcoholic cardiomyopathy was similar in both sexes. No significant differences were observed in age, nutritional parameters, and clinical and radiologic data of heart failure between the 2 groups. Alcoholic women reported a significantly lower daily dose of ethanol (p = 0.002), a shorter duration of alcoholism (p = 0.017), and a lower total lifetime dose of ethanol consumption (p = 0.001), and had a lower New York Heart Association functional class than men. Women also had lesser ventricular dysfunction than men. In a multivariate analysis, left ventricular systolic dysfunction was related to the total lifetime dose of ethanol consumption (p <0.04), but not to gender. Finally, when patients were matched for left ventricular ejection fraction, women had consumed a lower total lifetime dose of ethanol than men (p <0.001). The prevalence of alcoholic women with dilated cardiomyopathy was found to be similar to that of alcoholic men, although women required a lower total lifetime dose of ethanol to develop the disease.

Ethyl alcohol and dilative cardiomyopathy.

The ethanol-induced dilative cardiomyopathy has a complex clinical and paraclinical picture because of the direct action of the alcohol and the indirect action of its metabolites on human myocardium and neuroendocrine system. Ventricular arrhythmias, atrial arrhythmias, and heart failure are significant and show a great sensitivity of the conduction system. Working myocardium is also affected, which is proved by the impaired systolic and diastolic function of the heart and by the nitroglycerine-resistant isovolumetric relaxation time.

[The fibrinolytic system in patients with dilated myocardiopathy]. / Estudio del sistema fibrinolítico en pacientes con miocardiopatía dilatada.

OBJECTIVES: To study the fibrinolytic system in dilated cardiomyopathy (DCM) patients, and the relationship between the degree of severity (NYHA degree), and the presence of complications (atrial fibrillation, intracavity thrombus, and peripheral embolism). We also analyzed the influence of the antithrombotic therapy on the fibrinolysis's proteins. PATIENTS AND METHODS: We included 18 patients, stratified in two etiologic groups: 9 with idiopathic and 9 with ethyl DCM. The fibrinolytic system was investigated through the plasma levels of antigenic and functional t-PA and PAI-1. We also carried out a venous occlusion test to investigate the fibrinolytic the fibrinolytic activity in t-PA secretion. The clinical aspects were recorded. We included 30 healthy individuals matched for age and sex, as controls. RESULTS: The antigenic levels of t-PA and PAI-1, were significantly higher in the DCM group than in the control group (p < 0.01). The venous occlusion test responses were normal. No relationship between the fibrinolytic parameters and clinical data were observed. DISCUSSION: The high levels of antigenic t-PA found in DCM patients were considered as a vascular injury marker, and a atherothrombotic risk factor. Furthermore, there is a hypofibrinolytic condition shown by a PAI-1 augmentation. In conclusion, we are prone to consider long term oral anticoagulation in the management of DCM patients.

[Genetic aspects of heart lesions in patients with chronic alcoholism]. / Geneticheskie aspekty porazheniia serdtsa u bol'nykh khronicheskim alkogolizmom.

Parents and their children from 40 families of the first generation and 38 families of the second generation were examined genetically for catalase activity in the serum. It was found that children of the first generation suffered from chronic alcoholism more frequently in the families in which either mother or both parents abused alcohol. Low activity of serum catalase occurred in those children of the second generation, whose both parents were chronic alcoholics and had low catalase activity, especially of their mother. If the son was a chronic alcoholic, the inheritance of low catalase activity from his mother caused alcoholic damage to the heart. The risk was still higher in the second generation, especially in girls because of X-chromosome effect.

[The role of ketone bodies in the development of postalcoholic-intoxication heart damage in rats]. / Issledovanie roli ketonovykh tel v razvitii postintoksikatsionnogo alkogol'nogo povrezhdeniia serdtsa u krys.

Experiments on rats subjected to forced alcoholization for 5.5 days were made to measure the content of ethanol, acetaldehyde and ketone bodies in the blood during intoxication and 2 days after ethanol withdrawal and to estimate the intensity of postintoxication disorders in heart activity on the third day after alcoholization withdrawal. A positive correlation was discovered between depression of left ventricular contractility and the blood content of acetaldehyde and ketone bodies. The magnitude of the threshold of heart fibrillation did not correlate well with the concentration of ethanol during alcoholization. However, it agreed well with ethanol concentration in the postintoxication period. Additional administration to the animals of beta-hydroxybutyrate or caprylic acid in the postintoxication period intensified heart contractility depression. The conclusion is drawn that elimination of ketosis in ethanol withdrawal as well as a progressive taking out of alcoholic patients from dipsomania can prevent the development or attenuate the intensity of postintoxication heart injury.

[Characteristics of the dynamics of rapid changes in blood phosphoinositides in patients with alcoholic heart diseases]. / Ossobennosti dinamiki bystrykh izmenenii fosfoinozitidov v krovi bol'nykh s alkogol'nym porazheniem serdtsa.

A total of 42 patients who had been abusing alcoholic beverages during different periods and 12 healthy individuals were examined. Their intracardiac hemodynamic parameters were evaluated by echocardiography and rapid changes in inositol-containing blood lipids were determined by thin-layer flow chromatography. The patients showed significantly reduced contractility of the left ventricle, its wall hypertrophy and greater cavity dimensions. These abnormalities were more pronounced in patients with an over 10-year history. Biochemical studies revealed a time course of rapid changes in inositol-containing lipids in patients, which showed more fluctuations in the content of phosphoinositides and their lower baseline and final levels and differed from that in healthy persons. It was stressed that the changes in inositol-containing lipids were also related to the duration of alcohol abuse and they reflected the mechanisms of the toxic action of ethanol on the myocardium, which might be useful in the assessment of the severity of cardiovascular events in alcoholism.

[Determination of the leading factors in the pathogenesis of an alcoholic lesion of the heart]. / Opredelenie vedushchikh faktorov v patogeneze alkogol'nogo porazheniia serdtsa.

Male rats were given per os 25% ethanol solution twice a day at 9.00 and 21.00 for 5.5 consecutive days. Every single dose was 2 to 5 g/kg 2 and 12 hours after 8th gavage ethanol, acetaldehyde and acetone concentrations were measured in blood, 2-8 hours after the last (11th) gavage isolated hearts were perfused by Krebs-Henseleit solution. Applying of Spearman rank correlation method demonstrated negative correlation between mean acetaldehyde concentration and maximal systolic pressure, tension-time index of left ventricle and velocity of contraction and relaxation. Negative correlation has been shown between maximal ethanol concentration (MEC) and rate heart whereas positive correlation has been noticed between MEC and leakage of creatine phosphokinase.

[Dynamics of blood viscosity indices in patients with alcoholic myocardiodystrophy]. / Dinamika pokazatelei viazkosti krovi u bol'nykh alkogol'noi miokardiodistrofiei.

According to I. V. Strel'chuk's classification, 120 patients with alcoholic myocardiodystrophy induced by stage I-III chronic alcoholism were examined. The control group included 25 normal men. The rheological blood parameters (fluidity limit, apparent viscosity, red blood cell aggregation ratio, and hematocrit) were examined over time: before treatment, after its discontinuance, and one month after discharge from hospital. It was shown that blood viscosity increased with the disease gravity, whereas the results of the treatment correlated well with the initial patient's status. In stages I and II chronic alcoholism, the study parameters could return to normal, while in stage III, blood viscosity remained significantly higher than normal both towards the end of the treatment at hospital and on control examination one month after discharge. The control over blood rheology performed over time may be recommended as an additional method for assessing the disease gravity and efficacy of the treatment of alcohol-induced abnormalities.

Plasma uric acid levels in ethanol-fed turkey poults treated with allopurinol.

Plasma uric acid levels were determined in ethanol-fed poults following administration of allopurinol. In young poults, allopurinol at a dose of 50 mg/kg significantly depressed plasma uric acid levels 6 hr post-dosing. At 11 hr post-dosing, plasma uric acid levels were significantly elevated in the allopurinol-treated poults when compared with control poults. During a period of ethanol abstinence, allopurinol at a dose of 40 mg/kg significantly depressed plasma uric acid levels up to 8 hr post-dosing. At a dose of 30 mg/kg, plasma uric acid levels were similar to control values at 4 and 6 hr post-dosing. Data suggest that plasma uric acid levels can be depressed in ethanol poults when allopurinol is administered every 8 hr at a dose of 40-50 mg/kg of body weight.

[Decrease of the serum level of selenium in chronic alcoholics with or without dilated cardiomyopathy]. / Baisse du taux sérique de sélénium chez les alcooliques chroniques avec ou sans cardiomyopathie dilatée.

Serum selenium concentrations were measured by electrothermal atomic absorption spectrophotometry in 31 controls and 101 patients with the following results (mean +/- s.e.m; microgram . l-1: controls: 86.27 +/- 2.26; 24 chronic alcoholics without denutrition: 63.29 +/- 3.19; 38 patients with denutrition (64.75 +/- 3.68) divided into chronic alcoholics (n = 27); 65.24 +/- 3.49 and non-alcoholics (n = 11): 63.55 +/- 4.15; 39 patients with cardiomyopathy (68.89 +/- 3.43) divided into chronic alcoholics (n = 21): 67.61 +/- 3.10 and non-alcoholics (n = 18): 72.56 +/- 3.82. Compared with values in the control group, the fall in mean serum selenium concentrations was statistically significant (P less than 0.001) in all groups of patients. In contrast, there was no significant difference in mean serum selenium concentrations between patients with cardiomyopathy and those with denutrition, alcoholic or not. Chronic alcoholism and denutrition are accompanied by a fall in blood selenium level. The decrease of serum selenium concentrations in alcoholic and non-alcoholic patients of the third group suggests that congestive cardiomyopathy is associated with selenium deficiency. These findings indicate that patients with congestive cardiomyopathy should be evaluated not only for alcoholism, but also for their nutritional status.

Etiology of QT prolongation and T wave changes in chronic alcoholism.

Etiology of QT prolongation and T wave high voltage was studied in 90 chronic alcoholics in relation to history of alcoholism, blood chemical values, heart rate and QRS voltage with a technic of multiple regression analysis. Incidences of QT prolongation (22%), T wave high voltage in lead V2 (9%), hypopotassemia (23%), hypocalcemia (26%) and hypomagnesemia (28%) were high, despite these examinations were done after relatively long abstention period (35 days on average). Sinus tachycardia (19%) and QRS high voltage (SV1 + RV5 exceeding 4 mV, 41%) were also frequent. Unexpectedly, QT interval did not correlate to serum electrolytes, including calcium. Major factors associated with QT prolongation were sinus tachycardia, longer abstention period and larger amount of daily alcohol consumption. Although the reason of each association was not quite clear, alcoholic myocardial damage may be a cause of QT prolongation. Voltage of T wave in lead V2 was sensitive to serum potassium level, but the observed tendency of hypopotassemia acted to the direction against high voltage of T wave. The sole factor positively associated with high voltage of TV2 was high QRS voltage, which may be a manifestation of left ventricular hypertrophy.