Coronary atherosclerosis in the pig. Induced plaque injury and platelet response

R. L. Reddick, M. S. Read, K. M. Brinkhous, D. Bellinger, T. Nichols, T. R. Griggs

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

The thrombogenic potential of atherosclerotic diet-induced coronary atherosclerotic plaques was investigated in normal swine and in bleeder swine with homozygous von Willebrand disease. Fourteen paired normal and bleeder swine were placed on a 1% cholesterol diet for 1 to 16 weeks. Serum cholesterol was elevated in all animals at sacrifice. Foam cell deposits developed in all major epicardial coronary arteries, and lesions progressed over time from small subendothelial foam cell deposits to fibrous cap lesions that contained foam cells, elastic fibers, collagen, degenerative material, and smooth muscle cells. Balloon catheter injury resulted in platelet deposition, largely in a monolayer or as small platelet clumps devoid of fibrin. Lipid debris was present in injured areas of the subendothelium but did not induce thrombus formation. When the injury involved the media, platelet-fibrin thrombi were formed. Lipid was not present in these thrombi. Morphometric analysis of platelet deposition on ballooned atherosclerotic vessels showed similar numbers of platelets in both phenotypes. However, the attached platelets in bleeder pigs showed significantly less spreading than did those in the normal animals. The results show that injury to intimal foam cell and mixed cellular lesions in coronary arteries of cholesterol-fed swine does not promote the development of platelet-fibrin thrombus formation. In contrast, when the injury extended to the media, mixed thrombi were formed.

Original languageEnglish (US)
Pages (from-to)541-550
Number of pages10
JournalArteriosclerosis
Volume10
Issue number4
DOIs
StatePublished - 1990
Externally publishedYes

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Fingerprint

Dive into the research topics of 'Coronary atherosclerosis in the pig. Induced plaque injury and platelet response'. Together they form a unique fingerprint.

Cite this