Mechanisms of plaque vulnerability and rupture
Prediman K. Shah, MD, FACC*,*
* Division of Cardiology and Atherosclerosis Research Center, Burns and Allen Research Institute and Department of Medicine, Cedars Sinai Medical Center and UCLA School of Medicine, Los Angeles, California, USA
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Figure 1 Panel A shows a cross-section of the epicardial coronary artery, demonstrating a thin fibrous cap (arrowheads) overlying a crescentic, lipid-rich core (x30). Panel B, with a higher magnification of the margin of the cap, demonstrates dense infiltration by foamy macrophages (x300) (Hematoxylin and eosin). Copyright 2002, Massachusetts Medical Society. All rights reserved. N Engl J Med 1997;336:1276–82.
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Figure 2 Panel A shows a cross-section of the epicardial coronary artery, demonstrating a rupture of the shoulder region of the plaque with a luminal thrombus (x30). Panel B, at a higher magnification than Panel A, shows a ruptured thin cap densely infiltrated by macrophages and an adjacent fibrin-platelet thrombus (black reflects the post-mortem injection of contrast material) (x120). In Panel C, showing an eroded plaque, a subocclusive luminal thrombus is visible in cross-section of the epicardial coronary artery (x20). Panel D, at a higher magnification, demonstrated a luminal thrombus (left) overlying SMC fibrin-rich plaque (x100). (Movat pentachrome) Copyright 2002, Massachusetts Medical Society. All rights reserved. N Engl J Med 1997;336:1276–82.
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Figure 3 Conceptual model depicting the potential pathophysiologic mechanisms of plaque vulnerability, rupture, and thrombosis. Ox-LDL = oxidized low-density lipoprotein; MMP = matrix degrading metalloproteinases; SMC = smooth muscle cells; TF = tissue factor.
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