To evaluate the relation between skeletal muscle disease (myopathy) and degenerative changes in cardiac muscle (cardiomyopathy) in patients with chronic alcoholism.
A cross-sectional study.
University medical center.
Group A included 24 patients with chronic alcoholism who had dilated cardiomyopathy; group B, 24 patients with chronic alcoholism who had normal cardiac function; group C, 12 patients with dilated cardiomyopathy because of coronary heart disease; group D, 12 patients with idiopathic dilated cardiomyopathy; group E, 24 normal participants; and group F, 5 young men who died suddenly in traffic accidents.
Clinical assessment of muscle strength, echocardiography, radionuclide cardiac angiography (groups A to E), muscle biopsy (groups A, B, E), endomyocardial biopsy of the left ventricle (group A), and examination of postmortem specimens of the left ventricle (group F).
Alcoholic patients with cardiomyopathy had less muscle strength than did alcoholic patients with normal cardiac function, patients with idiopathic dilated cardiomyopathy, and patients with coronary heart disease (all P < 0.01). Among alcoholic patients with cardiomyopathy, 20 of 24 (83%) had histologic findings of skeletal myopathy compared with 1 of 24 (4%) alcoholic patients with normal cardiac function (P < 0.001). Interstitial fibrosis occurred in all cardiac biopsy specimens, hypertrophy of the myocytes occurred in 95%, and myocytolysis occurred in 83%. Those patients with more severe cellular hypertrophy and interstitial fibrosis of the myocardium had a greater decrease in deltoid muscle strength and had worse histologic myopathy.
Diseases of skeletal and cardiac muscle in patients with chronic alcoholism are clinically and histologically related. The presence of muscle weakness in an alcoholic person suggests the likelihood of an accompanying cardiomyopathic abnormality.
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Author, Article, and Disclosure Information
From the Hospital Clinic i Provincial, University of Barcelona, Spain; Jefferson Medical College, Philadelphia, Pennsylvania.
Corresponding Author: Emanuel Rubin, MD, Department of Pathology and Cell Biology, Jefferson Medical College, 1020 Locust Street, Suite 279, Philadelphia, PA 19107-6799.
Acknowledgment: The authors thank E. Tobas for technical assistance with muscle and endomyocardial biopsies.
Grant Support: In part by research grants from Fondo de Investigaciones Sanitarias de la Seguridad Social (89/0632, 90/0749 and 92/0699), Spain.
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