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Lipoprotein-associated phospholipase A₂ activity is associated with coronary artery disease and markers of oxidative stress: a case-control study^1,2,3

¹ From the Yonsei University Research Institute of Science for Aging (JYK, YJH, YJ, JSC, and JHL), the National Research Laboratory of Clinical Nutrigenetic/Nutrigenomics (JYK, YJH, JSC, and JHL), the Department of the Graduate Program in Science for Aging (SEK and HYY), and the Cardiovascular Genome Center, Yonsei Medical Institute (YJ), Yonsei University, Seoul, Korea; the Cardiology Division, Yonsei Cardiovascular Center, Yonsei University College of Medicine, Seoul, Korea (YJ); the Division of Cardiology, Sanggyepaik Hospital, Inje University College of Medicine, Seoul, Korea (BKL); the National Research Laboratory of Lipid Metabolism and Atherosclerosis, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea (T-SJ); and the Division of Cardiology, Department of Internal Medicine, Cardiovascular Center, National Health Insurance Corporation Ilsan Hospital, Goyang-si, Korea (DWJ). JYK and YJH contributed equally to the study and the manuscript

Background:Lipoprotein-associated phospholipase A₂ (Lp-PLA₂) is a lipoprotein-bound enzyme that can release atherogenic isoprostanes from esterified phospholipids and that may be involved in inflammation and atherosclerosis.

Objective:This study investigates the association between Lp-PLA₂ activity and coronary artery disease (CAD) in relation to oxidative stress markers, in particular urinary 8-epi-prostaglandin F₂ (8-epi-PGF₂).

Design:We conducted a case-control study in which the cross-sectional relation between Lp-PLA₂ activity, lipoproteins, and oxidative stress markers was determined in 799 patients with angiographically confirmed CAD and 925 healthy controls.

Results:Lp-PLA₂ activity was significantly (P < 0.001) higher in CAD cases than in controls (32.9 ± 0.46 and 29.7 ± 0.42 nmol · mL^–1 · min^–1, respectively). Both elevated Lp-PLA₂ activity and urinary excretion concentrations of 8-epi-PGF₂ were associated with greater CAD risk (P for trend < 0.001). Odds ratios for the upper quartiles of Lp-PLA₂ activity and 8-epi-PGF₂.excretion were 2.47 (95% CI: 1.79, 3.40) and 2.19 (1.52, 3.15), respectively, after adjustment for sex, age, BMI, blood pressure, smoking and alcohol consumption status, and LDL and HDL cholesterol. When we examined the additive effect of both markers for CAD risk, the relation between 8-epi-PGF₂ and CAD was weakened above the second quartile of Lp-PLA₂ activity. Moreover, Lp-PLA₂ activity was positively correlated with urinary excretion concentrations of 8-epi-PGF₂ in controls (r = 0.277, P < 0.001) and cases (r = 0.202, P < 0.001) and with the tail moment of lymphocyte DNA (r = 0.213, P < 0.001) in controls.

Conclusion:This study shows an association of elevated Lp-PLA₂ activity with CAD risk in relation to oxidant stress and thus supports a proatherogenic role of Lp-PLA₂.