title: Secretory type II phospholipase A2 in culprit coronary lesions is associated with myocardial infarction.
abstract: BACKGROUND
  Secretory type-II phospholipase A(2) (sPLA(2)-II) is a cardiovascular risk marker since higher levels of this acute phase protein imply an increased risk for coronary artery disease. Moreover, it is hypothesized that local activity of sPLA(2)-II in the atherosclerotic plaque facilitates an inflammatory response to induce plaque instability or rupture. We have studied the presence of sPLA(2)-II in culprit lesions in the coronary arteries of patients with acute myocardial infarction (AMI) or angina pectoris.
  
  
  METHODS
  We performed a histological examination of culprit lesions in 41 patients with stable (SAP) or unstable angina pectoris (UAP), or AMI using directed coronary atherectomy (DCA). Frozen slides were analysed immuno-histochemically for the presence of sPLA(2)-II, macrophages and smooth muscle cells. Immunopositive areas were calculated as a percentage of the total tissue area using image analysis software.
  
  
  RESULTS
  Intracellular sPLA(2)-II was found in atherosclerotic lesions in the macrophages of the intima as well as in vascular smooth muscle cells. Next to this, extracellular sPLA(2)-II depositions were also found. These depositions were significantly more extensive in patients with AMI, i.e. 26%(median)[6%(25th(percentile))-44%(75th(percentile))] of the intima area, than in patients with SAP 0%(median) (0%(25th)-10%(75th); P = 0.013) or UAP 0%(median) (0%(25th)-0%(75th); P = 0.04).
  
  
  CONCLUSIONS
  Extracellular sPLA(2)-II is more abundantly present in atherosclerotic culprit lesions that have led to myocardial infarction. This suggests a role for extracellular sPLA(2)-II in the development of complications of atherosclerotic lesions in coronary arteries.
authors.affiliation: Vrije Universiteit Medical Center, Amsterdam, The Netherlands.
authors.forename: R
authors.initials: R
authors.lastname: Nijmeijer
authors.forename: M
authors.initials: M
authors.lastname: Meuwissen
authors.forename: P A J
authors.initials: PA
authors.lastname: Krijnen
authors.forename: A
authors.initials: A
authors.lastname: van der Wal
authors.forename: J J
authors.initials: JJ
authors.lastname: Piek
authors.forename: C A
authors.initials: CA
authors.lastname: Visser
authors.forename: C E
authors.initials: CE
authors.lastname: Hack
authors.forename: H W M
authors.initials: HW
authors.lastname: Niessen
mesh_terms: D000199:Actins / Q000378:metabolism; D000328:Adult; D000368:Aged; D000787:Angina Pectoris / Q000175:diagnosis*; D015415:Biomarkers / Q000032:analysis; D003324:Coronary Artery Disease / Q000175:diagnosis*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008264:Macrophages / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis*; D032389:Myocytes, Smooth Muscle / Q000473:pathology; D054467:Phospholipases A2 / Q000032:analysis*
chemical_list: D000199:Actins; D015415:Biomarkers; D054467:Phospholipases A2