Tuesday, February 26, 2013

Atherosclerosis

Inflammation in Atherosclerosis: From Pathophysiology to Practice
Peter Libby, capital of Minnesota M. Ridker, Göran K. Hansson, for the Leducq Transatlantic
Network on Atherothrombosis
J. Am. Coll. Cardiol. 2009;54;2129-2138
doi:10.1016/j.jacc.2009.09.009

This information is flow rate as of February 22, 2011

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http:// cognitive content.onlinejacc.org/cgi/content/full/54/23/2129

Downloaded from content.onlinejacc.org by on February 22, 2011

ledger of the American College of Cardiology
© 2009 by the American College of Cardiology Foundation
Published by Elsevier Inc.

Vol. 54, none 23, 2009
ISSN 0735-1097/09/$36.00
doi:10.1016/j.jacc.2009.09.009

STATE-OF-THE-ART PAPER

In?ammation in Atherosclerosis
From Pathophysiology to Practice
Peter Libby, MD,* Paul M Ridker, MD, MPH,*† Göran K. Hansson, MD, PHD,‡
for the Leducq Transatlantic Network on Atherothrombosis
Boston, mammy; and Stockholm, Sweden
Until recently, most envisaged atherosclerosis as a bland arterial collection of cholesterol, complicated by smooth
muscle cell accumulation.

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harmonize to that concept, endothelial denuding injury led to platelet aggregation and retire of platelet factors which would trigger the proliferation of smooth muscle cells in the arterial intima. These cells
would then elaborate an extracellular matrix that would entrap lipoproteins, forming the centering of the atherosclerotic
plaque. Beyond the vascular smooth muscle cells long accept in atherosclerotic lesions, subsequent investigations identi?ed immune cells and mediators at work in atheromata, implicating in?ammation in this disease. Multiple
independent pathways of separate now pinpoint in?ammation as a profound regulatory process that links multiple risk
factors for atherosclerosis and its complications with neutered arterial biology. Knowledge has burgeoned regarding the
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