European Heart Journal Advance Access published online on November 29, 2004
European Heart Journal, doi:10.1093/eurheartj/ehi010
Copyright © 2004 by the European Society of Cardiology.
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1 Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA; University of Texas Southwestern Medical School, 5323 Harry Hines Blvd, Dallas, TX 75216, USA
* To whom correspondence should be addressed. Aims We aimed to evaluate the association of lipoprotein-associated phospholipase A2 (Lp-PLA2) with coronary artery disease (CAD) risk factors, with the severity of angiographic CAD, and with the incidence of major adverse events. Methods and results We measured Lp-PLA2 levels in 504 consecutive patients undergoing clinically indicated coronary angiography. Mean age was 60 ± 11 years and 38% were women. The mean (±SD) Lp-PLA2 level (ng/mL) was 245 ± 91. Lp-PLA2 levels correlated with male gender, LDL, HDL, and total cholesterol, fibrinogen, and creatinine. Lp-PLA2 levels correlated with the extent of angiographic CAD on univariate but not on multivariable analysis. During a median follow-up of 4.0 years, 72 major adverse events occurred in 61 of 466 (13%) contacted patients (20 deaths, 14 myocardial infarctions, 28 coronary revascularizations, and 10 strokes). Higher Lp-PLA2 levels were associated with a greater risk of events: the hazard ratio per SD was 1.28 (95% CI 1.06-1.54, P = 0.009), and remained significant after adjusting for clinical and lipid variables and C-reactive protein. Conclusion Higher Lp-PLA2 levels were associated with a higher incidence of major adverse events at follow-up, independently of traditional CAD risk factors and C-reactive protein.
Clinical research
Association of lipoprotein-associated phospholipase A2 levels with coronary artery disease risk factors, angiographic coronary artery disease, and major adverse events at follow-up
2 Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA
3 Division of Biostatistics, Mayo Clinic, Rochester, MN, USA
4 Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA
5 Division of Cardiovascular Diseases, Duke Clinical Research Institute, Durham, NC 27715, USA
Peter B. Berger, E-mail: berger.peter{at}duke.edu
Abstract 
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