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Lipoprotein‐associated phospholipase A 2 activity and mass in relation to vascular disease and nonvascular mortality
Author(s) -
AUTHOR_ID
Publication year - 2010
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.2010.02258.x
Subject(s) - lipoprotein associated phospholipase a2 , medicine , hazard ratio , simvastatin , apolipoprotein b , endocrinology , lipoprotein(a) , lipoprotein , vascular disease , body mass index , risk factor , cardiology , cholesterol , confidence interval
. Heart Protection Study Collaborative Group (Clinical Trial Service Unit, University of Oxford, Oxford, UK) Lipoprotein‐associated phospholipase A 2 activity and mass in relation to vascular disease and nonvascular mortality. J Intern Med 2010; 268 :348–358. Objectives. To assess whether associations of circulating lipoprotein‐associated phospholipase A 2 (Lp‐PLA 2 ) with vascular disease are independent of other risk factors. Methods. Lp‐PLA 2 activity and mass, lipids and other characteristics were measured at baseline in 19 037 individuals at high risk of vascular disease in a randomized trial of simvastatin with 5‐year average follow‐up. Results. Lp‐PLA 2 activity and mass were correlated with each other ( r = 0.56), lipids and other vascular risk factors. The moderate association of Lp‐PLA 2 activity with occlusive coronary events ( n = 2531) in analyses adjusted for nonlipid factors (hazard ratio per 1 SD [HR] 1.11, 95% CI 1.06–1.15) became nonsignificant after further adjustment for apolipoproteins (HR 1.02, 0.97–1.06). Such adjustment also attenuated HRs with Lp‐PLA 2 mass from 1.08 (1.03–1.12) to 1.05 (1.01–1.09). By contrast, the HR with apolipoprotein‐B100 of 1.15 (1.10–1.19) was only slightly attenuated to 1.14 (1.09–1.19) after further adjustment for apolipoprotein A 1 and Lp‐PLA 2 . Age‐ and sex‐adjusted HRs for other cardiac events ( n = 1007) with either Lp‐PLA 2 activity or mass were about 1.20, but HRs reduced after adjustment for nonlipid factors (activity: 1.11, 1.04–1.18; mass: 1.08, 1.02–1.15). Adjusted HRs for ischaemic stroke ( n = 900) were weak and nonsignificant and for nonvascular mortality ( n = 1040) were 1.01 (0.94–1.09) with activity and 1.12 (1.05–1.19) with mass. Simvastatin reduced Lp‐PLA 2 levels by about one‐quarter, but simvastatin’s vascular protection did not vary with baseline Lp‐PLA 2 concentration. Conclusions. Associations of Lp‐PLA 2 with occlusive coronary events depend considerably on lipid levels, whereas those with other cardiac events appear to reflect confounding from cardiovascular medication and prior vascular disease.