Alcoholic cardiomyopathy

Abstract

Although an association between excessive alcohol intake and heart disease has been recognized for a long time, it has been appreciated only recently that excessive alcoholic intake may result in heart disease in the absence of thiamine deficiency (beriberi heart disease). The form of alcoholic heart disease discussed in this paper is associated with a low cardiac output and high peripheral vascular resistance. It is unresponsive to administration of thiamine and may occur in well nourished patients. Although the cause is unknown, it is most likely due to the direct toxic effects of alcohol on the myocardium. Viral infection, poor nutrition and various nonalcoholic constituents of wine and beer may function as conditioning factors for the toxic effects of alcohol. Although the incidence of alcoholic heart muscle disease is unknown, it appears to be more common in adults than either thyrotoxic or congenital heart disease, which have received greater emphasis. Further studies are needed to determine the magnitude of the problem of alcoholic cardiomyopathy. Indeed, there are a number of heart muscle diseases associated with cardiac dilatation and hypertrophy and progressive congestive heart failure which require further study, particularly at the molecular level. It is particularly important that practicing physicians be made aware of the problem of alcoholic cardiomyopathy and that they learn to recognize the earliest manifestations of this disease before extensive structural alterations within the myocardium result in irreversible cardiac damage. All clinical evidence indicates that the disease is completely reversible if recognized and treated early and if alcohol intake is completely eliminated. After chronic congestive heart failure has intervened, therapy is disappointing. In fact, conventional medical therapy has been so inadequate that we have instituted a program of total bed rest for periods of six months to more than a year for patients with alcoholic as well as other types of cardiomyopathy. The results of this program have been encouraging since heart size returned to normal in 50 per cent of patients. One problem in the pathologic diagnosis of alcoholic heart disease is the nonspecificity of the structural and histochemical changes. It is hoped that with continued developments in the fields of electron microscopy and histochemistry, as well as in protein chemistry, discriminatory tests will be developed permitting the various types of cardiomyopathies to be distinguished. Eventually, it is to be hoped that an exact metabolic lesion will be identified so that therapy can be directed toward correcting such a lesion. At present, however, it is most important to emphasize that alcoholic cardiomyopathy, at least in the early stages, may occur in well developed and well nourished productive persons and that the disease may be completely reversible if recognized and treated early.