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J Am Coll Cardiol, 2006; 48:1800-1807, doi:10.1016/j.jacc.2006.03.070
(Published online 16 October 2006). © 2006 by the American College of Cardiology Foundation |
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* Kaiser Permanente Division of Research, Oakland, California
Departments of Epidemiology, Biostatistics, and Medicine, University of California, San Francisco, California
Stanford Prevention Research Center
Division of Cardiovascular Medicine
|| Department of Health Research and Policy, Stanford University School of Medicine, Stanford, California
Manuscript received December 19, 2005; revised manuscript received February 10, 2006, accepted March 16, 2006.
* Reprint requests and correspondence: Dr. Carlos Iribarren, Research Scientist, Kaiser Permanente, Division of Research, 2000 Broadway, Oakland, California 94612. (Email: cgi{at}dor.kaiser.org).
OBJECTIVES: We sought to examine the association between the metabolic syndrome (MetS) (defined both by the 2001 National Cholesterol Educational Program Adult Treatment Panel III [ATP-III] definition and the American Heart Association/National Heart, Lung and Blood Institute [AHA/NHLBI] revision incorporating the lower threshold for impaired fasting glucose [IFG]) and early-onset coronary artery disease (CAD).
BACKGROUND: The impact of MetS on premature CAD has not been studied extensively. Lowering the threshold to define the IFG component (from 110 to 100 mg/dl) and the value of the syndrome as a whole versus its individual components are subjects of intense debate.
METHODS: We performed a case-control study with 393 early-onset CAD subjects (acute myocardial infarction, angina with
50% stenosis, or coronary revascularization) in men under age 46 years or women under age 56 years and 393 control subjects individually matched for gender, age, and race/ethnicity.
RESULTS: By conditional logistic regression, presence of ATP-III MetS without diabetes (adjusted odds ratio [adj-OR] 4.9; 95% confidence interval [CI] 3.4 to 8.0) and with diabetes (adj-OR 8.0, 95% CI 4.39 to 14.6) was a strong independent determinant of early-onset CAD. Using the AHA/NHLBI revision, these ORs became slightly stronger. However, neither definition of MetS remained significantly associated with early-onset CAD in multivariate models adjusting for individual components.
CONCLUSIONS: The presence of MetS imparts a high risk of early-onset clinical CAD, but the prognostic information associated with the syndrome is not greater than the sum of its parts.
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