Plasma lipoprotein-associated phospholipase A 2 mass is elevated in STEMI compared to non-STEMI patients but does not discriminate between myocardial infarction and non-cardiac chest pain Robin P.F. Dullaart a, ⁎, L. Joost van Pelt b , Arjan J. Kwakernaak c , Bert D. Dikkeschei d , Iwan C.C. van der Horst e , René A. Tio e a Department of Endocrinology, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands b Laboratory Center, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands c Department of Nephrology, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands d Department of Cardiology, University of Groningen and University Medical Center Groningen, Groningen, The Netherlands e Department of Clinical Chemistry, Isala Klinieken, Zwolle, The Netherlands abstract article info Article history: Received 27 April 2013 Received in revised form 30 May 2013 Accepted 31 May 2013 Available online 10 June 2013 Keywords: Acute coronary syndrome Atypical chest pain Lipoprotein-associated phospholipase A 2 STEMI Non-STEMI Background: Plasma lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ) mass predicts future cardiovascular events in the non-acute setting. We tested the extent to which Lp-PLA 2 is elevated in patients with acute coronary syndrome. Methods: A 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-PLA 2 mass was measured using turbidimetric immunoassay. Results: Lp-PLA 2 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 anal- ysis (odds ratio per SD increment, 0.92 (95% CI, 0.69–1.23), p = 0.58). However, Lp-PLA 2 mass was elevated in STEMI compared to non-STEMI patients (246 ± 73 vs. 198 ± 58 ng/ml, p b 0.001), and independently predicted STEMI (odds ratio, 2.35 (95% CI, 1.46–3.79), p b 0.001). Among MI patients maximal creatine kinase was correlated positively with Lp-PLA 2 (r = 0.183, p = 0.034). Conclusions: In the acute setting, plasma Lp-PLA 2 mass is not elevated in MI patients, although Lp-PLA 2 mass appears to relate to the severity of myocardial damage. © 2013 Elsevier B.V. All rights reserved. 1. Introduction Lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ), also known as platelet-activating factor (PAF) acetylhydrolase, is abundantly present within advanced atherosclerotic lesions, where it co-localizes with macrophages and foam cells [1–4]. In plasma Lp-PLA 2 is predomi- nantly bound to low density lipoproteins (LDL) [3,4]. Lp-PLA 2 is able to hydrolyze LDL-derived oxidized phospholipids, a process which results in the generation of pro-inflammatory oxidized free fatty acids and lysophosphatidylcholine [3,4]. The potential role of Lp-PLA 2 in cardio- vascular disease (CVD) has initially been regarded to be controversial [3,4], but a meta-analysis comprising 32 prospective epidemiological studies has demonstrated robust positive relationships of incident car- diovascular events with both plasma Lp-PLA 2 activity and mass, even independent of clinical risk factors and plasma lipids [5]. Likewise, plas- ma Lp-PLA 2 may predict (recurrent) events in post-infarction patients [6], in patients referred for coronary angiography [7,8], as well as in patients with stable coronary artery disease [9]. Plasma Lp-PLA 2 mass measurement has also been suggested to improve cardiovascular risk classification in subjects initially free of clinically manifest CVD [10]. Despite intensive study concerning the impact of plasma Lp-PLA 2 in predicting (recurrent) cardiovascular events, little information is available about the relevance of plasma Lp-PLA 2 measurement in the work-up of patients suspected for an acute coronary syndrome. Plasma Lp-PLA 2 has been documented to be elevated in acute coronary syndrome patients compared to healthy control subjects [11]. In the acute setting, Lp-PLA 2 determination could furthermore improve patients risk stratification for subsequent cardiac events (including admission for severe heart failure and life threatening arrhythmias) [12]. On the other hand, plasma Lp-PLA 2 mass and activity obtained shortly after hospital admission for unstable angina or myocardial infarction (MI) failed to predict subsequent death or recurrent major cardiovascular events [13]. Another study showed that plasma Lp-PLA 2 measured after 30 days but not within Clinica Chimica Acta 424 (2013) 136–140 ⁎ Corresponding author at: Department of Endocrinology, University Medical Centre Groningen, University of Groningen, P.O. Box 30.001, Groningen, 9700 RB, The Netherlands. Fax: +31 503619392. E-mail address: r.p.f.dullaart@umcg.nl (R.P.F. Dullaart). 0009-8981/$ – see front matter © 2013 Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.cca.2013.05.026 Contents lists available at SciVerse ScienceDirect Clinica Chimica Acta journal homepage: www.elsevier.com/locate/clinchim