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An analysis of data of contrast ventriculography before and after volume load tests in 19 males suffering of chronic alcoholism with disorders of intraventricular conduction revealed signs of alcohol involvement of the heart with signs of "latent" insufficiency of the right and left ventricles manifested in an increased rate of circular shortening of myocardial fibers, terminal diastolic and terminal systolic volumes, terminal diastolic pressure.

A combined study of patients with second- or third-stage chronic alcoholism, prone to drinking bouts or regular alcohol consumption, was carried out to evaluate the clinical course of an early stage of alcoholic heart damage (AHD). The AHD patients with second- or third-stage chronic alcoholism and periodic alcohol consumption typically exhibited recurrent chest pains, heart rhythm disorders, signs of heart failure after an alcoholic bout, and those given to regular drinking had somato-vegetative complaints.

Coronaroventriculographic data are presented for 32 patients with alcoholic heart damage (AHD). Volumetric load (400-450 ml polyglucin administration) was used to detect preclinical heart failure. Coronarography demonstrated atherosclerotic coronary arterial lesions in 7 of 32 patients. A comparative assessment of central hemodynamic and right-ventricular myocardial contractility parameters in the patients and control subjects showed that the ejection fraction was reduced in AHD patients because of a significant increment of end diastolic and end systolic volumes as well as significantly reduced right-ventricular stroke index. Repeated ventriculography after volumetric stress showed significantly increased volumes and reduced ejection fraction that were indicative of latent right-ventricular heart failure.

The authors presented the results of right contrast ventriculography with a volumetric exercise test in patients with alcoholic heart affection. An increase in right ventricular end-systolic and diastolic volumes (most of the former), a decrease in the ejection fraction in response to an increase in the right ventricular end-diastolic pressure were noted during the test. A diffuse decrease in right ventricular regional (segmental) contractility in the absence of zones of akinesia or local contractility disorder was also revealed.

Distribution of I, III, IV and V-type collagen, fibronectin, vimentin, filamin, and desmin in myocardial biopsy specimens of 8 patients with alcoholic cardiomyopathy was studied by indirect immunofluorescence. It is found that all types of collagen and fibronectin participate in formation of diffuse cardiosclerosis while small cardiosclerosis is formed by interstitial types of collagen and to a lower extent of fibronectin. Filamin and desmin distribution in cardiomyocytes proves deformation and destruction of Z-lines and intercalated discs.

Sixty chronic alcoholic patients, aged 35.6 +/- 0.7 years and an average alcoholic history of 9.3 +/- 0.5 years were examined. Atrial fibrillation was detected at 24 h ECG monitoring in 2 (3.45%) patients, and paroxysms of atrial fibrillation or flutter were detected by intracardiac electrophysiologic investigation in 6 (22.2%). Fourteen (44.8%) patients with alcoholic heart damage demonstrated atrial vulnerability, indicative of a predisposition to atrial fibrillation even at earlier stages of alcoholic heart damage.

Forty patients aged 33 to 66 years suffering from chronic alcoholism, stages II-III, were examined. All the patients were subjected to contrast ventriculography before and after exercise test to identify the latent forms of heart failure. According to the coronarography findings, 9 out of the 40 patients demonstrated the signs of atherosclerotic injury to the coronary arteries. The data of endomyocardial biopsy of the left ventricle have shown morphologic changes characteristic of alcohol-induced heart injury, namely atrophy of cardiomyocytes, fat deposition in the interstitium, lysis of myofibrils, appearance of large vacuoles in cardiomyocytes, and mitochondriosis.

33 patients with alcoholic heart damage (AHD) were studied. The diagnosis was based on clinical symptoms of chronic alcoholism, roentgenocontrast coronaroangiography and ventriculography (in some cases with endomyocardial biopsy), echocardiography, bicycle exercise test and on exclusion of other cardiovascular diseases. In all the patients intracardiac electrophysiological study was performed. Younger persons systematically abusing alcohol and having no pronounced clinical picture of cardiovascular damage exhibited symptoms of functional conduction disturbances located mainly in ventricular conduction pathways and AV-node and more rarely in the sinus node and His-Purkinje's system. AHD in younger persons could have 2 different clinical courses. 1) with prevailing damage in conductive structures; 2) with prevailing damage of contractile myocardium.