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J Am Coll Cardiol, 2006; 48:33-46, doi:10.1016/j.jacc.2006.08.011 (Published online 16 October 2006).
© 2006 by the American College of Cardiology Foundation
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STATE-OF-THE-ART PAPER

Inflammation and Atherothrombosis

From Population Biology and Bench Research to Clinical Practice

Peter Libby, MD*,{ddagger},* and Paul M. Ridker, MD, MPH*,{dagger},{ddagger}

* Division of Cardiovascular Medicine, Center for Cardiovascular Disease Prevention
{dagger} Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital
{ddagger} Harvard Medical School, Boston, Massachusetts

Manuscript received November 29, 2005; revised manuscript received June 6, 2006, accepted June 13, 2006.

* Reprint requests and correspondence: Dr. Peter Libby, Brigham and Women's Hospital, 77 Avenue Louis Pasteur, NRB 741, Boston, Massachusetts 02115. (Email: plibby{at}rics.bwh.harvard.edu).

The concept that inflammation governs atherosclerosis and its complications has provided a new unifying hypothesis of the links between risk factors and the cellular and molecular alterations that underlie this disease. This new mechanistic insight has already begun to translate into changes in clinical practice. The preponderance of available data supports the predictive power of biomarkers of inflammation such as high-sensitivity C-reactive protein (hsCRP) in broad categories of individuals, both those who are apparently well and those with already-manifest atherosclerotic cardiovascular disease. The demonstrated clinical utility of hsCRP and potentially of other inflammatory biomarkers has engendered intense interest in evaluating their cost-effectiveness as predictive tools beyond conventional risk markers and as goals for therapy. The rapid translation of inflammation biology in cardiovascular disease from the laboratory to the clinic serves as a gratifying example of bench-to-bedside research. Ultimately, the insight that inflammation plays a fundamental role in atherosclerosis may lead to novel therapies that target aspects of the inflammatory process smoldering within the atheroma.

Abbreviations and Acronyms
  EC = endothelial cell
  ECM = extracellular matrix
  HDL = high-density lipoprotein
  hsCRP = high-sensitivity C-reactive protein
  IL = interleukin
  LDL-C = low-density lipoprotein cholesterol
  ·NO = nitric oxide
  SMC = smooth muscle cell




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