doi: 10.1161/CIRCULATIONAHA.105.554733
(Circulation. 2005;112:620-623.)
© 2005 American Heart Association, Inc.
Editorial |
Cytokines, Interleukin-18, and the Genetic Determinants of Vascular Inflammation
From the Cardiovascular Department, LDS Hospital, University of Utah School of Medicine, Salt Lake City, Utah.
Correspondence to Jeffrey L. Anderson, Cardiovascular Department, LDS Hospital, University of Utah School of Medicine, Salt Lake City, UT 84143. E-mail jeffrey.anderson@ihc.com
Key Words: Editorials • genetics • interleukins • inflammation
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Inflammation and Vascular Disease |
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In the past decade, atherogenesis has become recognized as an active, inflammatory vascular process rather than simply the result of passive endothelial injury with subsequent lipid infiltration.1 Evidence of inflammation is found locally in the vascular wall and systemically in the circulation. Participants in the inflammatory process within atherosclerotic plaque include macrophages, T-lymphocytes, cytokines, chemokines, matrix metalloproteinases, and adhesion molecules. Systemic (circulating) markers suggesting an augmented state of vascular inflammation have been found in acute myocardial infarction, unstable angina, and chronic coronary artery disease (CAD) and in asymptomatic patients at high risk for vascular disease. These markers include the white blood cell count,2 acute-phase reactants such as high-sensitivity C-reactive protein (hs-CRP),3 serum amyloid A and fibrinogen, cytokines (eg, interleukin [IL]-6), soluble adhesion molecules, and atherosclerosis-related enzymes (eg, lipoprotein-associated phospholipase A2).3
See p 643
Despite these advances, our understanding of vascular atherothrombotic processes is incomplete, and our ability to predict cardiovascular events, especially in individual patients, continues to be limited.4,5 Atherosclerosis is a multifactorial disease with environmental and polygenetic interactions each estimated to contribute equally to disease etiology. Hence, investigation of genetic variants interacting or reflecting environmentally triggered disease processes is of interest.
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Genetics and Atherothrombotic Disease |
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Unexpected atherothrombotic events are frequently observed by the clinician in individuals with few or no traditional risk factors, implicating unrecognized inherited factors.5,6 With the completion of the Human Genome Project, optimism was high that the secrets of genetic risk would soon be unveiled. The discovery that most of the 0.1% of genetic diversity existing between 2 unrelated individuals
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