title: Lipoprotein-associated phospholipase A2 and C-reactive protein for risk-stratification of patients with TIA.
abstract: OBJECTIVE
  Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) is a marker of unstable atherosclerotic plaque, and is predictive of both primary and secondary stroke in population-based studies.
  
  
  METHODS
  We conducted a prospective study of patients with acute TIA who presented to the ED. Clinical risk scoring using the ABCD(2) score was determined and Lp-PLA(2) mass (LpPLA(2)-M) and activity (LpPLA(2)-A) and high-sensitivity C-reactive protein (CRP) were measured. The primary outcome measure was a composite end point consisting of stroke or death within 90 days or identification of a high-risk stroke mechanism requiring specific early intervention (defined as >or=50% stenosis in a vessel referable to symptoms or a cardioembolic source warranting anticoagulation).
  
  
  RESULTS
  The composite outcome end point occurred in 41/167 (25%) patients. LpPLA(2)-M levels were higher in end point-positive compared to -negative patients (mean, 192+/-48 ng/mL versus 175+/-44 ng/mL, P=0.04). LpPLA(2)-A levels showed similar results (geometric mean, 132 nmol/min/mL, 95% CI 119 to 146 versus 114 nmol/min/mL, 95% CI 108 to 121, P=0.01). There was no relationship between CRP and outcome (P=0.82). Subgroup analysis showed that both LpPLA(2)-M (P=0.04) and LpPLA(2)-A (P=0.06) but not CRP (P=0.36) were elevated in patients with >50% stenosis. In multivariate analysis using cut-off points defined by the top quartile of each marker, predictors of outcome included LpPLA(2)-A (OR 3.75, 95% CI 1.58 to 8.86, P=0.003) and ABCD(2) score (OR 1.30 per point, 95% CI 0.97 to 1.75, P=0.08).
  
  
  CONCLUSIONS
  Many patients with TIA have a high-risk mechanism (large vessel stenosis or cardioembolism) or will experience stroke/death within 90 days. In contrast to CRP, both Lp-PLA(2) mass and activity were associated with this composite end point, and LpPLA(2)-A appears to provide additional prognostic information beyond the ABCD(2) clinical risk score alone.
authors.affiliation: Department of Neurology, University of Pennsylvania Medical Center, Philadelphia, PA 19104, USA. cucchiar@mail.med.upenn.edu
authors.forename: Brett L
authors.initials: BL
authors.lastname: Cucchiara
authors.forename: Steve R
authors.initials: SR
authors.lastname: Messe
authors.forename: Lauren
authors.initials: L
authors.lastname: Sansing
authors.forename: Larami
authors.initials: L
authors.lastname: MacKenzie
authors.forename: Robert A
authors.initials: RA
authors.lastname: Taylor
authors.forename: James
authors.initials: J
authors.lastname: Pacelli
authors.forename: Qaisar
authors.initials: Q
authors.lastname: Shah
authors.forename: Scott E
authors.initials: SE
authors.lastname: Kasner
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000097:blood*; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D005260:Female; D006801:Humans; D002546:Ischemic Attack, Transient / Q000097:blood* / Q000175:diagnosis / Q000453:epidemiology*; D008297:Male; D008875:Middle Aged; D017063:Outcome Assessment, Health Care; D011237:Predictive Value of Tests; D011379:Prognosis; D011446:Prospective Studies; D012307:Risk Factors; D020521:Stroke / Q000097:blood* / Q000175:diagnosis / Q000453:epidemiology*
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase