Infiltrates of Activated Mast Cells at the Site of Coronary Atheromatous Erosion or Rupture in Myocardial Infarction
1995; Lippincott Williams & Wilkins; Volume: 92; Issue: 5 Linguagem: Inglês
10.1161/01.cir.92.5.1083
ISSN1524-4539
Autores Tópico(s)Mast cells and histamine
ResumoHomeCirculationVol. 92, No. 5Infiltrates of Activated Mast Cells at the Site of Coronary Atheromatous Erosion or Rupture in Myocardial Infarction Free AccessResearch ArticleDownload EPUBAboutView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticleDownload EPUBInfiltrates of Activated Mast Cells at the Site of Coronary Atheromatous Erosion or Rupture in Myocardial Infarction P. Constantinides P. ConstantinidesP. Constantinides Originally published1 Sep 1995https://doi.org/10.1161/01.CIR.92.5.1083Circulation. 1995;92:1083In the early 1960s, complete serial section studies through the whole thrombosed segment of occluded coronary arteries of myocardial infarction patients autopsied in St Louis, Mo, showed that all of the occluding thrombi had been caused by fissures of the surface of the underlying atherosclerotic plaques, fissures through which blood sometimes entered the plaque interior before they were sealed by the thrombi.1 Because essentially similar findings have since been made in Germany,2 Great Britain,3 Denmark,4 and Russia (A. Vichert, personal communication, 1985) and the same scenario was found to be responsible for cerebral artery thrombosis,5 it now seems certain that thrombosis in human atherosclerotic arteries is always triggered by a disruption of their plaque surfaces, even though the size the thrombi achieve and how long they persist probably depends on systemic factors that prevailed at the time of the disruption. In other words, plaque disruptions may occur all the time, but in some persons with high blood coagulability and/or low plasma fibrinolysin activity, they may cause large occlusive thrombi and myocardial infarction, whereas in others they may produce only small nonocclusive thrombi without myocardial necrosis. Unfortunately, the processes that induce plaque disruption are still unknown. They could be physical stresses or chemical insults emanating from the blood or the plaque interior, insults that disrupt the plaque directly or increase its vulnerability to other factors. Among the disrupting agents generally considered possible so far are (1) endothelium-injuring processes, (2) factors that damage or kill the myocytes that produce and maintain the collagenic cap of atheromata, (3) oxidases or peroxides released by subendothelial macrophages that could cross-link the polypeptide chains of the cap collagen and make the latter stiffer and more brittle than normal, (4) degradation products from the atheroma lipid pool itself, (5) circulating immune complexes that could penetrate into plaques and activate complement, and (6) autoimmune attacks against some plaque components because they may appear antigenically different from normal arterial wall constituents and therefore "foreign" to the immune system. The elegant article by Kovanen et al6 that appears in the current issue of Circulation is the first to point to a completely novel possible plaque-disrupting factor, ie, the release of collagen-degrading proteases from mast cells in the plaque.Circulating mast cell precursors could well penetrate selectively into the atheromata, because it has been shown ultrastructurally that the junctions between endothelial cells that line human plaques are often open, in contrast to junctions over the normal arterial wall, which are usually closed.8Since some antibodies attached to mast cells can trigger the release of mast cell contents whenever they encounter and bind the antigens that elicited their generation, this article also raises the theoretical possibility that even ordinary allergic reactions could promote plaque disruption. Evidently, additional morphometric studies of subthrombic plaque histology in autopsies of persons who die of myocardial infarction, such as the study by Kovanen et al, will be needed to uncover the entire spectrum of local parameter changes that can promote plaque disruption. It may well turn out that different scenarios can cause plaque disruption in different persons. After consensus is reached on the spectrum of possible plaque-disrupting processes visible at the autopsy level, the time will come to try to identify living persons at risk for plaque disruption. Fortunately, procedures for plaque protection and prevention of disruption could be developed in currently available atherosclerotic animal models in which disruption and arterial thrombosis can be triggered at will.7FootnotesCorrespondence to Paris Constantinides, MD, PhD, 430 Chester Rd, Qualicum Beach, BC, V9K 1B9, Canada. References 1 Constantinides P. Coronary thrombosis linked to fissures in atherosclerotic vessel wall. JAMA.1964; 188:35-36. CrossrefGoogle Scholar2 Sinapins D. Über Wandveränderungen bei Coronar-Thrombose. Klin Wochenschr.1965; 43:875-880. CrossrefMedlineGoogle Scholar3 Davies MJ, Thomas A. The pathological basis and microanatomy of occlusive thrombus formation in human coronary arteries. Philos Trans R Soc Lond Biol.1981; 294:225-229. CrossrefMedlineGoogle Scholar4 Falk E. Plaque rupture with severe pre-existing stenosis precipitating coronary thrombosis. Br Heart J.1983; 50:127-134.CrossrefMedlineGoogle Scholar5 Constantinides P. Pathogenesis of cerebral artery thrombosis in man. Arch Pathol.1967; 83:422-428. MedlineGoogle Scholar6 Kovanen PT, Kaartinen M, Paavonen T. Infiltrates of activated mast cells at the site of coronary atheromatous erosion or rupture in myocardial infarction. Circulation.1995; 92:1084-1088. CrossrefMedlineGoogle Scholar7 Abela GS, Picon PD, Friedl SE, Gebara OC, Miyamoto A, Federman M, Tofler GH, Muller JE. Triggering of plaque disruption and arterial thrombosis in an atherosclerotic rabbit model. Circulation.1995; 91:776-784. CrossrefMedlineGoogle Scholar8 Constantinides P, Harkey M. Electron microscopic exploration of human endothelium in early and advanced atherosclerotic lesions. Ann N Y Acad Sci.1990; 598:113-124. CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Engheta M, Urbanczyk J, Fidone E, Escobedo Y and Mixon T (2021) Kounis syndrome presenting as ST elevation acute myocardial infarction, Baylor University Medical Center Proceedings, 10.1080/08998280.2021.1907095, 34:4, (500-502), Online publication date: 4-Jul-2021. 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