title: Lipoprotein-associated phospholipase A2 is an independent marker for coronary endothelial dysfunction in humans.
abstract: OBJECTIVE
  The purpose of the current study was to determine whether lipoprotein-associated phospholipase A2 (Lp-PLA2) is associated with coronary endothelial dysfunction and is a predictor of endothelial dysfunction in humans.
  
  
  RESULTS
  Patients (172) with no significant coronary artery disease (<30% stenosis) undergoing assessment of coronary endothelial function were studied. Endothelial function was assessed by the change in coronary blood flow and coronary artery diameter in response to intracoronary acetylcholine. Plasma concentrations of Lp-PLA2 were measured, and patients were divided into tertiles. Patients in tertiles 2 and 3 had a significantly lower change in coronary blood flow (63.8+/-73.2 and 32.0+/-71.7 versus 78.4+/-73.2%; P<0.001) and greater epicardial coronary artery vasoconstriction (-14.1+/-14.7 and -23.3+/-25.1 versus -9.5+/-15.2% mean diameter change; P<0.001) in response to acetylcholine. Patients with coronary endothelial dysfunction had significantly higher serum concentrations of Lp-PLA2 than those with normal endothelial function (246.2+/-71.6 versus 209+/-56.7 ng/mL; P=0.001). The odds ratio for coronary endothelial dysfunction in patients with Lp-PLA2 in the highest tertile was 3.3 (95% CI, 1.6 to 6.6).
  
  
  CONCLUSIONS
  Lp-PLA2 is independently associated with coronary artery endothelial dysfunction and is a strong predictor of endothelial dysfunction in humans.
authors.affiliation: Division of Cardiovascular Diseases, Mayo College of Medicine, Rochester, MN 55905, USA.
authors.forename: Eric H
authors.initials: EH
authors.lastname: Yang
authors.forename: Joseph P
authors.initials: JP
authors.lastname: McConnell
authors.forename: Ryan J
authors.initials: RJ
authors.lastname: Lennon
authors.forename: Gregory W
authors.initials: GW
authors.lastname: Barsness
authors.forename: Geralyn
authors.initials: G
authors.lastname: Pumper
authors.forename: Stacy J
authors.initials: SJ
authors.lastname: Hartman
authors.forename: Charanjit S
authors.initials: CS
authors.lastname: Rihal
authors.forename: Lilach O
authors.initials: LO
authors.lastname: Lerman
authors.forename: Amir
authors.initials: A
authors.lastname: Lerman
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D000328:Adult; D015415:Biomarkers / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood* / Q000188:drug therapy / Q000453:epidemiology / Q000503:physiopathology*; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000378:metabolism / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D006801:Humans; D000960:Hypolipidemic Agents / Q000008:administration & dosage; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D010741:Phospholipases A / Q000097:blood*; D054467:Phospholipases A2; D011237:Predictive Value of Tests; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D000960:Hypolipidemic Agents; D010741:Phospholipases A; D054467:Phospholipases A2; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase