By E.E Payne
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Additional resources for An Atlas of Pathology of the Brain
Willerson JT, Campbell WB, Winniford MD, et al. Conversion from chronic to acute coronary artery disease: speculation regarding mechanisms. Am J Cardiol 1984;54:1349 –54. 143. Casscells W, Hathorn B, David M, et al. Thermal detection of cellular inﬁltrates in living atherosclerotic plaques: possible implications for plaque rupture and thrombosis. Lancet 1996;347:1447–51. 144. Stefanadis C, Diamantopoulos L, Vlachopoulos C, et al. Thermal heterogeneity within human atherosclerotic coronary arteries detected in vivo: a new method of detection by application of a special thermography catheter.
Abbreviations: VCAM-1 = vascular cell adhesion molecule 1; ICAM-1 = intercellular adhesion molecule 1; MCP-1 = macrophage chemoattractant protein 1; oxLDL = oxidized low density lipoprotein. 7 on page 44. 6 Cartoon illustration of the ﬁbroatheroma. Fibroatheromas have areas of “true” necrosis surrounded by a ﬁbrous cap predominantly consisting of smooth muscle cells and proteoglycan/collagen matrix; inﬂammatory inﬁltrate is variable. Both “early” and “late” stages of necrosis are recognized. Areas of “early” necrosis typically show some free cholesterol with mostly intact macrophages and extracellular matrix made up of proteoglycans but not collagen type 1.
A postmortem angiogram showed total occlusion of the left circumﬂex (LCx) artery (arrow in A and B) and the sections showed the site of ﬁbrous cap rupture (arrow in C) and an underlying hemorrhagic necrosis (NC), just distal to the site of rupture the coronary artery showed underlying atherosclerosis with a 70% diameter stenosis and an overlying occlusive thrombus (Th) (D). Sections taken from the ﬁrst diagonal and left anterior descending (LAD) (E) and another from the third diagonal and LAD (F) show areas of thin cap ﬁbroatheroma (vulnerable plaque) with mild insigniﬁcant luminal narrowing of the LAD with positive remodeling.