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Alteration in lipoprotein-associated phospholipase A2 levels during acute coronary syndrome and its relationship to standard biomarkers

Petr Ostadal1*, Dagmar Vondrakova1, Andreas Kruger1, Marek Janotka1, Hana Psotova1 and Miroslav Prucha2

Author Affiliations

1 Department of Cardiology, Heart Center, Na Homolce Hospital, Roentgenova 2, 150 30, Prague, Czech Republic

2 Department of Clinical Biochemistry, Hematology, and Immunology, Na Homolce Hospital, Prague, Czech Republic

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Lipids in Health and Disease 2012, 11:153  doi:10.1186/1476-511X-11-153

Published: 10 November 2012



Lipoprotein-associated phospholipase A2 (Lp-PLA2) probably plays an important role in the development of acute coronary syndrome (ACS); elevated levels of Lp-PLA2 are associated with a poorer prognosis in patients with ischemic heart disease. Alterations of Lp-PLA2 levels during ACS and its relationship to standard biomarkers are, however, unclear.


Fifty-one consecutive ACS patients were enrolled in the study. All were managed with early invasive strategy and according to the current guidelines for pharmacotherapy; intensive statin therapy was started in all patients at admission. Serum levels of Lp-PLA2, LDL-cholesterol (LDL), troponin l (Tnl), and C-reactive protein (CRP) were assessed at admission (D0), on the first morning (D1), and on the second morning of hospitalization (D2). Mean serum levels of Lp-PLA2 (ng/mL) decreased from 264.6±19.1 at D0, to 193.2±14.4 at D1 (P < 0.001 vs. D0) and 189.8±22.6 at D2 (P = 0.002 vs. D0; P = not significant vs. D1). Alterations in Lp-PLA2 levels significantly correlated with changes in LDL (r = 0.43; P = 0.008). On the other hand, no relationship between Lp-PLA2 and Tnl or CRP was found.


Initially, serum levels of Lp-PLA2 were significantly elevated in ACS patients, but decreased within the first 24 hours after admission and subsequently remained stable. Lp-PLA2 levels correlated with LDL levels but not with Tnl or CRP levels. Our results demonstrated dynamic alterations in Lp-PLA2 levels during the early stages of ACS and, therefore, indirectly support the hypothesis of an active role for Lp-PLA2 in the pathogenesis of ACS.

Acute coronary syndrome; C-reactive protein; Lipoprotein-associated phospholipase A2; Low-density lipoprotein; Troponin I