Development of Complement-Fixing 19S, Anti-Heart Mitochondria Autoantibody, Following Myocardial Infarction in Dogs
The development of anti-heart autoantibody following experimental myocardial infarction in dogs was studied with respect to (1) the subcellular localization of the heart autoantigen(s), (2) the incidence of autoantibody following myocardial infarction, and (3) the temporal development of the autoantibody and its relation to serum enzyme elevations and electrocardiographic changes. Complement-fixing anti-heart autoantibody developed following myocardial infarction induced by either two-stage coronary artery ligation or by the injection of microspheres directly into the coronary circulation. The autoantibody was directed toward an autoantigen residing in the mitochondrial fraction of myocardial tissue and was found to be associated with the 19S class of immunoglobulin. Eighteen of 20 dogs with infarction produced anti-heart mitochondria autoantibody 10 days following induction of myocardial damage; the autoantibody persisted 4 to 6 weeks thereafter. In these dogs the presence of anti-heart mitochondria autoantibody was diagnostic of myocardial infarction at times when the serum enzymes and electrocardiograms were within normal limits. Our studies indicate that a serologic test, based on the detection of complement-fixing anti-heart mitochondria autoantibody, may be a valuable adjunct to tests currently available for diagnosing recent myocardial infarction.
- coronary artery disease
- myocardial ischemia
- coronary artery ligation
- myocardial autoimmunity
- coronary microsphere embolism
- creatine phosphokinase
- Received April 16, 1971.
- Accepted July 19, 1971.
- © 1971 American Heart Association, Inc.