• 1 January 1979
    • journal article
    • research article
    • Vol. 96  (2) , 477-492
Abstract
The pathogenesis of the degenerative vascular disease and myocardial infarction that develop in mice with lupus-like disease was studied by immunofluorescence, light microscopy and EM. Medium and small coronary arteries and arterioles of infarcted and non-infarcted hearts had focal degenerative lesions consisting of deposits of periodic-acid-Schiff (PAS)-positive or eosinophilic material in the intima and to a lesser extent in the media, degenerative changes in the media without accompanying cellular inflammation and occasional proliferation or swelling of intimal cells. These lesions often narrowed and, together with platelet aggregation, occasionally occluded the vascular lumens. Granular deposits of mouse immunoglobulin, C3 [complement component 3], and occasionally gp70 were present in the walls of medium and small arteries, arterioles and venules of infarcted and non-infarcted myocardium. Dense deposits of foreign material were found by EM in areas corresponding to the immune deposits. These non-inflammatory vascular lesions are apparently caused by local deposition of antigen-antibody complexes. The immune complex-mediated injury may lead to thrombotic and/or obliterative vascular changes that contribute to decrease of the coronary blood flow and to the development of myocardial infarction.