SUMMARY One hundred and forty-five alcoholics without known causes of heart disease, who were serially admitted to the alcohol detoxification centre, were studied to see the incidence of cardiac abnormalities and dose related effects of ethanol. All patients were divided into heavy (consumed more than the equivalent amount of 125 ml of pure ethanol daily for 10 years or more) and moderate drinkers (consumed 75 to 125 ml of ethanol daily). All of them were ambulatory and free from cardiac symptoms. There was no difference among heavy and moderate drinkers in the incidence of abnormalities detected by the electrocardiograms and chest x-ray films. In the alcoholics, the most frequent finding was a prolonged QTc interval of more than 0.44 s on the electrocardiogram (62 patients, 42-8%), unrelated to serum electrolytes imbalance. Cardiomegaly on chest x-ray film was observed in 25 patients (17-2%). M-mode echocardiogram was recorded in randomly selected patients and compared with age and sex matched controls. The interventricular septum and posterior wall were thicker in alcoholics, while left ventricular volume showed no difference. Left ventricular muscle mass was significantly increased only in heavy drinkers. Left ventricular function at rest was not depressed in these patients at an average of 31 days after the last drink of ethanol. Severe heart failure was not found even among the group of heavy drinkers, of whom more than 90% had liver dysfunction. Cardiac hypertrophy seems to occur in heavy drinkers, but is clinically well compensated in the majority of alcoholics.Chronic and heavy consumption of ethanol has been said to have deleterious effects upon the cardiovascular system, causing cardiomegaly and severe heart failure.' 2 Inability to reproduce human alcoholic cardiomyopathy in the experimental animal, however, and its rare incidence among chronic alcoholics made us wonder whether ethanol was the sole cause of the disease.' 3 Moreover, most of the clinical observations were based on selected patients with severe heart failure; the majority of asymptomatic alcoholics were not well studied. 5If ethanol is the real cause of alcoholic cardiomyopathy, one can expect latent cardiac abnormalities according to the level of ethanol consumption. To the best of our knowledge, however, the evidence of dose related effects of ethanol is still scarce.6 7The purpose of this study is to evaluate the dose related effects of ethanol according to the estimated *

The incidence of the coexistence of left ventricular false tendons and premature ventricular contractions (PVCs) was evaluated prospectively. Over 14 months, left ventricular false tendons were found in 71 (6.4%) of 1 1 17 consecutive patients examined echocardiographically. Two types of false tendons were observed: longitudinal, from the ventricular septum to the posteroapical wall (n = 62), and transverse, between the septum and the lateral wall (n = 9). Among 62 patients with PVCs and no underlying heart disease, false tendons were detected in 35 (56%); 28 had unifocal and seven had bifocal PVCs. Episodes of ventricular tachycardia were documented in one of the 28 patients with unifocal PVCs and in one of the seven patients with bifocal PVCs. These PVCs were poorly controlled by antiarrhythmic drugs but easily suppressed by exercise. Left ventricular false tendons were detected in 36 patients on routine echocardiographic examinations performed in the other 1055 subjects, and 10 of these patients were judged to have no underlying heart disease. PVCs were detected in two (20%) of these 10 patients. Although a definite conclusion that left ventricular false tendons are arrhythmogenic cannot be derived from these results, the unexpectedly high incidence of the coexistence suggests that left ventricular false tendons may be an etiologic factor in the development of PVCs, especially the ratedependent and medically uncontrollable PVCs seen in apparently healthy individuals.

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To correlate left ventricular function and histologic features in patients with dilated cardiomyopathy, precise indexes of hemodynamics and semiquantitative histologic data were combined for multivariate analysis. Right endomyocardial biopsy was performed at the time of cardiac catheterization. Five hemodynamic indexes were used for functional assessment: ejection fraction, ratio of end-systolic stress to volume index, end-diastolic stress, time constant (T) of left ventricular pressure fall, and end-systolic stress. Six histologic findings (disarray of myofibers, hypertrophy of myofibers, scarcity of myofibrils, nuclear changes of myofibers, vacuolization of myofibers and proliferation of collagen fibers) were graded from (-) to (4+). Each finding was assigned to category (-) or (+) according to the absence or presence of significant abnormality. Ordinary statistical analysis revealed that, although ejection fraction was lower in category (+) for proliferation of collagen fibers, ratio of end-systolic to volume index was reduced for category (+) of hypertrophy of myofibers. A significant correlation was present between hypertrophy of myofibers and proliferation of collagen fibers by Spearman rank correlation. When principal component analysis was applied to the hemodynamic data, two principal components could be extracted. Fisher's discriminant analysis could clearly differentiate two categories (-) and (+) in the semiquantitative histologic finding of proliferation of collagen fibers. The analysis indicated that contractility was reduced with elevated afterload in that category (+). Thus, proliferation of collagen fibers may play a pivotal role in deteriorating contractility in patients with dilated cardiomyopathy.

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