The most prevalent confusion with the alcoholic heart disease caused by thiamine and nutritional deficiency is with viral or idiopathic chronic DCM. Between 20 and 35% of all cases ofDCM are thought to occur because of excessive ethanol intake , However, in both alcoholic and idiopathic chronic DCM, the clinical picture is similar. In the early stages of both categories of congestive heart failure, the patients often show some response to bedrest, salt restriction, diuretics, and digitalis. Afterwards there is slight-to-moderate cardiac dilatation. Still later the heart becomes markedly enlarged. Once cardiac failure appears, life expectancy can be measured in months or, at the most, a few years. Death is usually from heart failure, uncontrolled arrhythmias, or thromboembolism. In both, the electrocardiogram may show conduction disturbances, nonspecific ST-T abnormalities, and even anterior infarction.
The pathology of the heart in alcoholic patients with chronic DCM is somewhat different from non-alcoholics with chronic DCM. The alcoholics tend to have more myocardial hypertrophy, interstitial fibrosis, and electrical irritability [26,27], Although gross microscopic examination has not been able to distinguish chronic idiopathic DCM from the chronic DCM found in alcoholics , electron microscopy has shown that patients who have also been chronic alcoholics have swelling of the sarcoplasmic reticulum which is more severe and generalized rather than focal [29,30], However, these differences from the DCM in non-alcoholics do not mean that the severe cardiomyopathy was caused by the alcohol but may only mean that the alcohol, in addition to the other causes of idiopathic DCM, can cause characteristic pathologic changes. Likewise, even though it is true that patients with chronic DCM due to alcohol have less muscle strength and more histologic findings of skeletal myopathy than patients with idiopathic DCM, this does not prove that the DCM was caused by alcohol , The skeletal pathology may be the result of a combination of congestive heart failure from any cause plus the alcohol.
That alcohol may not be entirely responsible for the chronic DCM in alcoholics is suggested by the lack of correlation between the quantity of alcohol consumed and the development of such DCM  and also by the finding that most alcoholics who have been drinking heavily for at least 5 years show no clinical evidence of heart failure. The incidence of chronic DCM in alcoholics is relatively low, at about 12% , After 4 months of daily heavy drinking, an S3 and elevated venous pressure can develop, signs which can revert to normal on stopping the alcohol if this was the sole cause of the failure [16,32,33], However, many of those with the usual diagnosis of alcoholic cardiomyopathy will not have their congestive heart failure signs disappear merely on stopping the alcohol ,
There are studies that suggest that alcohol modifies the incidence and course of cardiomyopathies caused by other agents, the most likely being viral [34,35], It is probable that many cases of so-called idiopathic DCM are viral in origin. In one study of non-alcoholic patients with idiopathic DCM, 30% showed enteroviral RNA on endomyocardial biopsy , Hibbs et al.  found that electron microscopic examination showed evidence of virus-like particles in the heart of a patient who had an alcoholic cardiomyopathy. It is conceivable that many alcoholics with DCM may have had a mild or forgotten viral infection and their chronic DCM may represent a modified form ofburned out viral myocarditis , About one third of patients with a past history of proven Coxsackie viral myocarditis show a depression of myocardial function 2-5 years after the acute episode , In India, about 15% of patients with proven viral myocarditis had persistent heart failure when seen 3 months later ,
The absence of evidence of a viral etiology is no proof that the idiopathic chronic DCM was not viral in etiology. Considerable evidence indicates that cardiac injury in clinical and experimental cardiotropic Coxsackie B-3 virus-induced myocarditis is mediated by the immune system. In the murine infection, detectable virus is absent in the heart and body fluids even when inflammation and necrosis are maximum. In addition, inoculation of T-lymphocyte-deficient mice with the virus does not result in significant myocarditis even when the virus is isolated from the heart , This suggests that the virus initiates an immune response which produces inflammation and necrosis but the virus does not directly induce significant cardiac injury. It is possible that alcohol influences the myocardial immune response to produce more inflammation and necrosis.
Another clue to the possibility that alcoholics may have a viral pathogenesis for their chronic DCM is a little-known experiment on viral myocarditis in mice. Morin et al.  administered Coxsackie B virus to 48 mice. One half received laboratory chow and alcohol and the other half received laboratory chow and sweetened water. At the end of 5 weeks, 80% of the alcohol group showed microscopic cardiac involvement. Only 30% of the non-alcohol group had cardiac lesions (p = 0.02). The cardiac involvement in the mice that received the alcohol was not only more frequent but also more severe than in the non-alcohol group [4T|. How the damage of a viral attack on the myocardium can be augmented by alcohol is unknown, although there are many possibilities. It has been suggested, for example, that it may be due to the loss of potassium and magnesium from the myocardium or the ability of alcohol to inhibit the active transport of cations across the cell membrane [27,42], An analogy may be made with the rather similar incidence of liver cirrhosis in chronic alcoholics (about 8%) because this also points to the possibility that an infection caused by a hepatotropic virus may be made more damaging by the presence of alcohol.
However, no matter what the reason for the synergistic effect of alcohol with a viral cardiomyopathy, we are notjustified in using the term 'alcoholic cardiomyopathy' for the chronic DCM found in alcoholics that does not respond within a few weeks to good nutrition and withdrawal from alcohol. That term suggests more than we know since it may be a viral cardiomyopathy in an alcoholic. Although an alcoholic is no more likely to have a myotropic viral infection than a non-alcoholic, the virus may have much more chance of producing severe myocardial damage.
Thus, for those alcoholics with either an acute or chronic heart failure syndrome that responds to good nutrition, thiamine, and a withdrawal from alcohol, the term 'alcoholic cardiomyopathy' is appropriate. However, for the alcoholic with a chronic DCM that does not respond to good nutrition and alcohol withdrawal, the preferred terminology is 'idiopathic DCM in an alcoholic'.
Was this article helpful?