title: Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction.
abstract: BACKGROUND
  Erosion and rupture of coronary atheromas are the events preceding the vast majority of acute coronary syndromes. The shoulder regions of atheromas, the sites at which erosion or rupture is most likely to occur, are the sites at which mast cells accumulate. These cells are filled with neutral proteases capable of triggering extracellular matrix degradation via activation of matrix metalloproteinases. To obtain more direct evidence for the participation of mast cells in the acute coronary syndromes, we quantified the numbers of mast cells at eroded or ruptured sites of coronary atheromas in patients who died of myocardial infarction.
  
  
  RESULTS
  In specimens of coronary arteries from 20 patients who had died of acute myocardial infarction, the site of atheromatous erosion or rupture was identified. The specimens were stained with monoclonal antibodies against the two major proteases of mast cells, tryptase and chymase, and against macrophages, T lymphocytes, and smooth muscle cells. At the immediate site of erosion or rupture, mast cells amounted to 6% of all nucleated cells, in the adjacent atheromatous area to 1%, and in the unaffected intimal area to 0.1%. The proportions of these mast cells that were activated, ie, had been stimulated to degranulate and release some of their tryptase and chymase contents, were 86% at the site of erosion or rupture, 63% in the adjacent atheromatous area, and 27% in the unaffected intima. At the site of erosion or rupture, the numbers of macrophages and T lymphocytes were also increased, but the number of smooth muscle cells was decreased.
  
  
  CONCLUSIONS
  The accumulation of activated mast cells (200-fold more than in the unaffected coronary intima) at the site of atheromatous erosion or rupture suggests that in thrombotic coronary occlusion the role played by mast cells is significant.
authors.affiliation: Wihuri Research Institute, Helsinki, Finland.
authors.forename: P T
authors.initials: PT
authors.lastname: Kovanen
authors.forename: M
authors.initials: M
authors.lastname: Kaartinen
authors.forename: T
authors.initials: T
authors.lastname: Paavonen
mesh_terms: D002452:Cell Count; D015550:Cell Degranulation; D053818:Chymases; D003324:Coronary Artery Disease / Q000473:pathology*; D003328:Coronary Thrombosis / Q000473:pathology; D003331:Coronary Vessels / Q000473:pathology*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D008264:Macrophages / Q000166:cytology; D008297:Male; D008407:Mast Cells / Q000166:cytology / Q000201:enzymology / Q000502:physiology*; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D009203:Myocardial Infarction / Q000473:pathology*; D009206:Myocardium / Q000473:pathology*; D012422:Rupture, Spontaneous; D012697:Serine Endopeptidases / Q000378:metabolism; D013601:T-Lymphocytes / Q000166:cytology; D053802:Tryptases; D017539:Tunica Intima / Q000473:pathology
chemical_list: D018836:Inflammation Mediators; D012697:Serine Endopeptidases; C083294:chymase 2; D053818:Chymases; D053802:Tryptases