Journal
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Volume 70, Issue 18, Pages 2278-2289Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacc.2017.09.028
Keywords
acute coronary syndromes; high-sensitivity C-reactive protein; interleukin-1; myocardial infarction
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Funding
- U.S. National Heart, Lung, and Blood Institute [HL080472]
- RRM Charitable Fund
- Novartis
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Inflammatory pathways drive atherogenesis and link conventional risk factors to atherosclerosis and its complications. One inflammatory mediator has come to the fore as a therapeutic target in cardiovascular disease. The experimental and clinical evidence reviewed here support interleukin-1 beta (IL-1 beta) as both a local vascular and systemic contributor in this regard. Intrinsic vascular wall cells and lesional leukocytes alike can produce this cytokine. Local stimuli in the plaque favor the generation of active IL-1 beta through the action of a molecular assembly known as the inflammasome. Clinically applicable interventions that interfere with IL-1 action can improve cardiovascular outcomes, ushering in a new era of anti-inflammatory therapies for atherosclerosis. The translational path described here illustrates how advances in basic vascular biology may transform therapy. Biomarker-directed application of anti-inflammatory interventions promises to help us achieve a more precise and personalized allocation of therapy for our cardiovascular patients. (C) 2017 by the American College of Cardiology Foundation.
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