Objectives: Pentraxin 3 (PTX3) is the prototype of the long pentraxin family. PTX3 is involved in inflammatory processes affecting the cardiovascular system, and PTX3 levels have been shown to be elevated and independently 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. <. 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 within 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 discriminative 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 patients with NSTE-ACS.

Acute coronary syndrome, Inflammatory biomarkers, Mortality, Outcome prediction, Pentraxin 3
dx.doi.org/10.1016/j.clinbiochem.2013.08.014, hdl.handle.net/1765/68619
Clinical Biochemistry
Department of Cardiology

Eggers, K.M, Armstrong, P.W, Califf, R.M, Johnston, N, Simoons, M.L, Venge, P, & James, S.K. (2013). Clinical and prognostic implications of circulating pentraxin 3 levels in non ST-elevation acute coronary syndrome. Clinical Biochemistry, 46(16-17), 1655–1659. doi:10.1016/j.clinbiochem.2013.08.014