title: Diagnostic performance of plasma high sensitive C-reactive protein in detecting three-vessel coronary artery disease: modification by apolipoprotein E genotype.
abstract: OBJECTIVE
  Plasma high sensitive C-reactive protein (hsCRP) concentration is an important clinical test of systemic inflammation and, like apoE epsilon4 allele, an important risk factor of coronary artery disease (CAD). We investigated whether the diagnostic performance of plasma hsCRP in detecting severe 3-vessel CAD may be modified by apoE epsilon4 carrier status.
  
  
  METHODS
  The study population (Angiography and Genes Study) comprised 485 Finnish subjects (336 men and 149 women, mean age 64.0+/-1.0) undergoing coronary angiography. ApoE genotypes were determined by the PCR-based method and by hsCRP using an automatic analyser.
  
  
  RESULTS
  The diagnostic performance of hsCRP concentration in distinguishing 3-vessel CAD from its less widespread forms (non-3-vessel CAD) was assessed by receiver operating characteristic curve (ROC) analysis separately in apoE epsilon4 non-carriers and epsilon4 carriers. ROC analysis showed that hsCRP predicted 3-vessel CAD in apoE epsilon4 non-carriers (AUC 0.646; SE 0.035; p = 0.0001; 95 % CI 0.578-0.714) but not in epsilon4 carriers (AUC 0.518; SE 0.049; p = 0.719; 95 % CI 0.422-0.615). Multinomial logistic regression analysis revealed a significant (p<0.05) apoE epsilon4 group versus hsCRP group (<1.0 mg/L/>or=1.0 mg/L) interaction in relation to incidence of 3-vessel CAD. In apoE epsilon4 non-carriers, high hsCRP (>or=1.0 mg/L) was significantly (OR 2.1; 95 % CI 1.233-3.562; p = 0.006) associated with high incidence of 3-vessel CAD after adjustment for major CAD risk factors.
  
  
  CONCLUSIONS
  The diagnostic performance of hsCRP in distinguishing 3-vessel CAD from less extensive forms of coronary atherosclerosis is more accurate in a group of subjects without the apoE epsilon4 allele than in patients with it.
authors.affiliation: Heart Center, Tampere University Hospital and Tampere University Medical School, Tampere, Finland. ari.mennander@pshp.fi
authors.forename: Ari
authors.initials: A
authors.lastname: Mennander
authors.forename: Pekka
authors.initials: P
authors.lastname: Kuukasjärvi
authors.forename: Jari
authors.initials: J
authors.lastname: Laurikka
authors.forename: Kjell
authors.initials: K
authors.lastname: Nikus
authors.forename: Pekka J
authors.initials: PJ
authors.lastname: Karhunen
authors.forename: Matti
authors.initials: M
authors.lastname: Tarkka
authors.forename: Terho
authors.initials: T
authors.lastname: Lehtimäki
mesh_terms: D000483:Alleles; D001057:Apolipoproteins E / Q000235:genetics*; D002097:C-Reactive Protein / Q000032:analysis*; D003324:Coronary Artery Disease / Q000097:blood* / Q000175:diagnosis*; D005260:Female; D006579:Heterozygote; D006801:Humans; D008297:Male; D008875:Middle Aged; D012372:ROC Curve; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: D001057:Apolipoproteins E; D002097:C-Reactive Protein