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Cardiovascular Research 2002 53(1):138-146; doi:10.1016/S0008-6363(01)00480-1
© 2002 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Secretory type II phospholipase A2 binds to ischemic myocardium during myocardial infarction in humans

Remco Nijmeijera,b,d,*, Wim K Lagrandb,d, Alexi Baidoshvilia, Yvonne T.P Lubbersf, Wim Th Hermense, Chris J.L.M Meijera, Cees A Visserb,d, C.Erik Hackc,d,f and Hans W.M Niessena,d

aDepartment of Pathology, VU Medical Center Amsterdam, Room No. PA002, De Boelelaan 1117, P.O. Box 7057, 1007 MB Amsterdam, The Netherlands
bDepartment of Cardiology, VU Medical Center Amsterdam, Amsterdam, The Netherlands
cDepartment of Clinical Chemistry, VU Medical Center Amsterdam, Amsterdam, The Netherlands
dDepartment of ICAR-VU, VU Medical Center Amsterdam, Amsterdam, The Netherlands
eCardiovascular Research Institut Maastricht, University of Maastricht, Maastricht, The Netherlands
fC.L.B., Sanquin Blood Supply Foundation, Department of Immunopathology of Plasma Proteins, Amsterdam, The Netherlands

R.Nijmeijer{at}VUMC.NL

* Corresponding author. Tel.: +31-20-444-4003; fax: +31-20-444-2964

Objective: An increase of circulating secretory Phospholipase A2 (sPLA2) is a risk factor for coronary artery disease. We hypothesized that this reflects participation of sPLA2 in local inflammatory reactions ensuing in ischemic myocardium. Therefore, we studied the course of circulating sPLA2, in patients with acute myocardial infarction (AMI) or unstable angina pectoris (UAP), and investigated the presence of sPLA2 in infarcted myocardial tissue. Methods: Plasma samples of 107 patients with AMI or UAP, collected on admission and at varying intervals thereafter, were tested for the presence of sPLA2 and C-reactive protein (CRP). Cumulative release values of these parameters were calculated, which allowed for comparison of the results rearranged in time according to the onset of symptoms. By immunohistochemistry we studied the presence of sPLA2 and CRP in myocardial tissue of 30 patients who died subsequent to AMI. Results: Levels of sPLA2 became elevated during the disease course in 66 of the 87 patients with AMI, and were higher than those of the patients with UAP of whom 8 of the 20 had elevated levels. By immunohistochemistry sPLA2 was found to be localized in the infarcted myocardium, particularly in its borderzone, from 12 h after the onset of AMI. Positive staining for sPLA2 was more extensive than that for CRP. Conclusions: The localization pattern of sPLA2 in infarcted myocardium as well as its plasma course, in relation to those of CRP, are in line with a supposed pro-inflammatory role during AMI for sPLA2 as a generator of lysophospholipids serving as ligands for CRP.

KEYWORDS Enzyme (kinetics); Histo(patho)logy; Infarction; Infection/inflammation; Immunology


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