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Original Article

Diagnostic performance of plasma high sensitive C‐reactive protein in detecting three‐vessel coronary artery disease: modification by apolipoprotein E genotype

, , , , , & show all
Pages 714-719 | Received 22 Feb 2008, Accepted 25 Apr 2008, Published online: 08 Jul 2009
 

Abstract

Objectives. Plasma high sensitive C‐reactive protein (hsCRP) concentration is an important clinical test of systemic inflammation and, like apoE ε4 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 ε4 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 ε4 non‐carriers and ε4 carriers. ROC analysis showed that hsCRP predicted 3‐vessel CAD in apoE ε4 non‐carriers (AUC 0.646; SE 0.035; p = 0.0001; 95 % CI 0.578–0.714) but not in ε4 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 ε4 group versus hsCRP group (<1.0 mg/L/⩾1.0 mg/L) interaction in relation to incidence of 3‐vessel CAD. In apoE ε4 non‐carriers, high hsCRP (⩾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. Conclusion. 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 ε4 allele than in patients with it.

Acknowledgements

This study received financial support through grants from the Medical Research Fund of Tampere University Hospital, Finnish Foundation for Cardiovascular Research, The Academy of Finland (grant number 104821), The Emil Aaltonen Foundation (T.L) and the Elli and Elvi Oksanen Fund of the Pirkanmaa Fund under the auspices of the Finnish Cultural Foundation.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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