Localization of anti-mitochondrial antibody in experimental canine myocardial infarcts.

Alterations in cell and subcellular membrane integrity occur during evolving ischemic myocardial injury. We tested the hypothesis that an antibody against human liver mitochondria [anti-mitochondrial antibody developing in a patient with primary biliary cirrhosis] could identify altered cell membrane integrity in experimental canine myocardial infarcts. The proximal left anterior descending coronary arteries of 12 dogs were ligated and 1 hr later 131I-labeled F(ab')2 fragments from either a control human IgG (6 dogs) or anti-mitochondrial IgG (6 dogs) were injected. The 131I-labeled F(ab')2 anti-mitochondrial fragments concentrated maximally in the central infarct subendocardium [infarct-to-normal ratio of 9.2 +/- 3.5 (mean +/- SD) vs. 4.6 +/- 3.3 for control F(ab')2 IgG, P < 0.05]. There was also 1 1/2- to 2-fold greater anti-mitochondrial antibody F(ab')2 accumulation in the central infarct epicardium and the peripheral infarct subendocardium and subepicardium. Thus, an anti-mitochondrial antibody obtained from a patient with primary biliary cirrhosis concentrates in irreversibly damaged myocardium after experimental canine myocardial infarction. Presumably this occurs because of altered cell membrane integrity, which allows exposure of mitochondria to the anti-mitochondrial antibody. The F(ab')2 fragments of anti-mitochondrial antibodies labeled with suitable radionuclides should allow noninvasive scintigraphic detection of experimental acute myocardial infarcts.