HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Shah, P. K. Search for Related Content PubMed Articles by Shah, P. K.

Mechanisms of plaque vulnerability and rupture

^* 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

View larger version (97K): [in a new window]   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.

View larger version (150K): [in a new window]   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.

View larger version (18K): [in a new window]   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.