Author + information
- Received February 27, 2009
- Revision received September 4, 2009
- Accepted September 6, 2009
- Published online December 1, 2009.
- Peter Libby, MD⁎,⁎ (, )
- Paul M. Ridker, MD, MPH⁎,†,
- Göran K. Hansson, MD, PhD‡,
- Leducq Transatlantic Network on Atherothrombosis
- ↵⁎Reprint requests and correspondence:
Dr. Peter Libby, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115
Until recently, most envisaged atherosclerosis as a bland arterial collection of cholesterol, complicated by smooth muscle cell accumulation. According to that concept, endothelial denuding injury led to platelet aggregation and release 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 nidus of the atherosclerotic plaque. Beyond the vascular smooth muscle cells long recognized in atherosclerotic lesions, subsequent investigations identified immune cells and mediators at work in atheromata, implicating inflammation in this disease. Multiple independent pathways of evidence now pinpoint inflammation as a key regulatory process that links multiple risk factors for atherosclerosis and its complications with altered arterial biology. Knowledge has burgeoned regarding the operation of both innate and adaptive arms of immunity in atherogenesis, their interplay, and the balance of stimulatory and inhibitory pathways that regulate their participation in atheroma formation and complication. This revolution in our thinking about the pathophysiology of atherosclerosis has now begun to provide clinical insight and practical tools that may aid patient management. This review provides an update of the role of inflammation in atherogenesis and highlights how translation of these advances in basic science promises to change clinical practice.
This work was supported by grants from the Fondation Leducq(to Drs. Libby, Ridker, and Hansson), the Swedish Research Council(to Dr. Hansson), the Swedish Heart-Lung Foundation(to Dr. Hansson), and the Donald W. Reynolds Foundation(to Drs. Libby and Ridker). Dr. Libby is an unpaid consultant to AstraZeneca. Dr. Ridker has received research funding support from multiple not-for-profit entities including the National Heart, Lung, and Blood Institute, the National Cancer Institute, the American Heart Association, the Doris Duke Charitable Foundation, the Leducq Foundation, the Donald W. Reynolds Foundation, and the James and Polly Annenberg La Vea Charitable Trusts; he has also received investigator-initiated research support from multiple for-profit entities including AstraZeneca, Novartis, Pharmacia, Roche, Sanofi-Aventis, and Abbott, as well as nonfinancial research support from Amgen. In addition, he is listed as a coinventor on patents held by the Brigham and Women's Hospital that relate to the use of inflammatory biomarkers in cardiovascular disease that have been licensed to Siemens and AstraZeneca, and has served as a research consultant to Schering-Plough, Sanofi-Aventis, AstraZeneca, Isis, Dade, Merck, Novartis, and Vascular Biogenics.
- Received February 27, 2009.
- Revision received September 4, 2009.
- Accepted September 6, 2009.
- American College of Cardiology Foundation