Clinical and prognostic implications of circulating pentraxin 3 levels in non ST-elevation acute coronary syndrome Kai M. Eggers a, ⁎, Paul W. Armstrong d , Robert M. Califf e , Nina Johnston a , Maarten L. Simoons f , Per Venge b , Stefan K. James a,c a Dept. of Medical Sciences, Cardiology, Uppsala University, 75237 Uppsala, Sweden b Dept. of Medical Sciences, Clinical Chemistry, Uppsala University, 75237 Uppsala, Sweden c Uppsala Clinical Research Center, Uppsala University, 75237 Uppsala, Sweden d Dept. of Medicine, Division of Cardiology, University of Alberta, Edmonton, AB T6G2H7, Canada e Duke Translational Medicine Institute, Duke University School of Medicine, 2301 Erwin Road, Durham, NC 27710, USA f Thoraxcenter, Dept. of Cardiology, Erasmus Medical Center, 's Grafendijkwal 230, 3000 CA Rotterdam, The Netherlands abstract article info Article history: Received 29 March 2013 Received in revised form 11 August 2013 Accepted 27 August 2013 Available online 5 September 2013 Keywords: Pentraxin 3 Inflammatory biomarkers Acute coronary syndrome Mortality Outcome prediction Objectives: Pentraxin 3 (PTX3) is the prototype of the long pentraxin family. PTX3 is involved in inflamma- tory processes affecting the cardiovascular system, and PTX3 levels have been shown to be elevated and indepen- dently prognostic in ST-elevation myocardial infarction. Data on PTX3 levels in non-ST-elevation acute coronary syndrome (NSTE-ACS), in contrast, are limited. The aim of the present analysis was to investigate the implications of PTX3 levels in a fairly large sample of NSTE-ACS patients and in comparison to levels of C-reactive protein (CRP). Design and methods: We measured levels of PTX3 and CRP in both 82 healthy controls and 401 NSTE-ACS patients from the GUSTO IV study, and studied the associations of these biomarkers to clinical data and 1-year mortality. Results: NSTE-ACS patients had significantly higher median PTX3 levels compared to healthy controls (3.8 vs. 1.9 μg/L; p b 0.001). PTX3 levels in patients with NSTE-ACS were independently related to female sex and cardiac troponin T levels, but not to age or cardiovascular risk factors. PTX3 levels were higher in patients who died with- in 1 year but did not emerge as an independent predictor of 1-year mortality (adjusted OR 1.2 [95% CI 0.6–2.3]). This was in contrast to CRP (adjusted OR 1.5 [95% CI 1.1–2.3]). Neither PTX3 nor CRP yielded significant discrim- inative value regarding mortality prediction. Conclusions: PTX3 levels are elevated in NSTE-ACS. However, the prognostic information provided by PTX3 levels is limited and inferior compared to CRP. Our data, thus, do not support the measurement of PTX3 in pa- tients with NSTE-ACS. © 2013 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved. 1. Introduction Measurement of circulating biomarkers is an integral part of the risk assessment in patients with non ST-elevation acute coronary syndrome (NSTE-ACS). Besides biomarkers of cardiomyocyte necrosis and left- ventricular performance, research has focused much on inflammatory biomarkers given the contribution of inflammatory processes to athero- sclerotic plaque rupture and myocardial injury. In particular the short pentraxin C-reactive protein (CRP) has been widely evaluated. However, its use for prognostication is still debated: CRP is not specific for cardio- vascular inflammation, it is uncertain whether it acts as a pathogenetic component or simply reflects systemic inflammation, and its prognostic value relative to other circulating biomarkers is only moderate [1]. Pentraxin 3 (PTX3), the prototype of the long pentraxin family, has been proposed as a promising alternative in this regard. Following in- flammatory stimuli, PTX3 is expressed locally in various vascular cell types and appears to exhibit protective effects [2–4]. PTX3 may also be produced in cardiomyocytes subjected to ischemia/reperfusion injury [5,6], and has been shown to modulate myocardial tissue damage in this setting. This is supported by animal studies demonstrating that PTX3-deficient mice developed larger areas of infarcted myocardium, larger no-reflow areas, and a greater degree of apoptosis [6]. PTX3 levels are raised and predictive of higher mortality risk in humans with ST-elevation myocardial infarction [5,7]. Data on the clinical impli- cations of PTX3 in NSTE-ACS, in contrast, are sparse and restricted to smaller cohorts [8,9]. In the present study, we aimed to investigate PTX3 levels in NSTE-ACS patients participating in the Global Use of Strategies To Open Occluded Coronary Arteries (GUSTO) IV study. We hypothesized that PTX3 might provide greater prognostic utility than CRP. Clinical Biochemistry 46 (2013) 1655–1659 ⁎ Corresponding author at: Department of Medical Sciences, Cardiology, Uppsala University, S-751 85 Uppsala, Sweden. Fax: +46 18 50 66 38. E-mail address: kai.eggers@ucr.uu.se (K.M. Eggers). 0009-9120/$ – see front matter © 2013 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.clinbiochem.2013.08.014 Contents lists available at ScienceDirect Clinical Biochemistry journal homepage: www.elsevier.com/locate/clinbiochem