• Robin P F Dullaart, L Joost van Pelt, Arjan J Kwakernaak, Bert D Dikkeschei, Iwan C C van der Horst, and René A Tio.
• Department of Endocrinology, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands. Electronic address: r.p.f.dullaart@umcg.nl.
• Clin. Chim. Acta. 2013 Sep 23; 424: 136-40.

BackgroundPlasma lipoprotein-associated phospholipase A2 (Lp-PLA2) mass predicts future cardiovascular events in the non-acute setting. We tested the extent to which Lp-PLA2 is elevated in patients with acute coronary syndrome.MethodsA total of 231 consecutive patients referred for acute chest pain participated. Of this number, 144 were diagnosed with myocardial infarction (MI; 100 were classified as MI with ST-elevation (STEMI) and 44 as MI without ST-elevation (non-STEMI)). Eighty-seven patients had non-cardiac chest pain. Plasma Lp-PLA2 mass was measured using turbidimetric immunoassay.ResultsLp-PLA2 mass was not different between MI patients and patients with non-cardiac chest pain (231±72 μg/l vs.243±88 μg/l, p=0.29), and did not relate to MI in age- and sex-adjusted logistic regression analysis (odds ratio per SD increment, 0.92 (95% CI, 0.69-1.23), p=0.58). However, Lp-PLA2 mass was elevated in STEMI compared to non-STEMI patients (246±73 vs. 198±58 ng/ml, p<0.001), and independently predicted STEMI (odds ratio, 2.35 (95% CI, 1.46-3.79), p<0.001). Among MI patients maximal creatine kinase was correlated positively with Lp-PLA2 (r=0.183, p=0.034).ConclusionsIn the acute setting, plasma Lp-PLA2 mass is not elevated in MI patients, although Lp-PLA2 mass appears to relate to the severity of myocardial damage.Copyright © 2013 Elsevier B.V. All rights reserved.

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