Intramyocardial small-vessel disease in chronic alcoholism

A morphologic study of the small (50 to 200 micron) intramyocardial coronary arteries was performed. The cases chosen for study were selected from a relatively young group of patients without clinical evidence of alcoholic cardiomyopathy or pathologic evidence of large coronary artery disease, in order to evaluate alterations in the small vessels which could possibly be attributed to the chronic alcoholic state. Five basic vascular abnormalities were described. The most common alteration found in all nine cases was vascular wall edema (48 per cent), followed by perivascular fibrosis (42 per cent), vascular sclerosis (36 per cent), subendothelial humps (13 per cent), and vascular wall inflammation (11 per cent). The significance and pathogenesis of these changes were discussed. Primary endothelial cell damage was proposed as a common pathogenic mechanism for all five types of vascular abnormality. It was suggested that following endothelial damage, fluid and macromolecules penetrate into the vessel wall or into the perivascular space where, by incompletely understood processes, they induce vascular wall myocytes to produce collagen, elastin, and basement membrane-like substances. Evidence supporting this mechanism was derived from the common observation of vascular wall edema, from the occasional presence of erythrocytes and leukocytes within the vessel wall, and from experimental data in the literature. Several possible etiologic agents were implicated in the pathogenesis of endothelial and vessel wall injury. These included alcohol itself, acetaldehyde, biogenic amines, and magnesium deficiency. It is probable, however, that there are multiple etiologic factors which affect the small cardiac vessels of the chronic alcoholic. Finally, the proposal was advanced that the nonspecific pathology of the myocardium in chronic alcoholism may be a result of ischemia secondary to disease of the small intramyocardial coronary ateries.