title: Elevated C1rC1sC1inh levels independently predict atherosclerotic coronary heart disease.
abstract: Clinical studies as well as animal models emphasized the importance of the complement system in the pathogenesis of coronary atherosclerosis and cardiovascular diseases. Our aim was to examine the extent and clinical implication of complement system activation in patients with stable atherosclerotic coronary heart disease (ACHD). Seventy-six patients with stable angina pectoris (SAP) scheduled for elective coronary angiography were enrolled into the study. Percutaneous coronary intervention (PCI) was performed in 24 patients, in 27 patients (NOPCI group) the coronary angiography showed significant stenosis and bypass surgery (CABG) or optimal medical therapy (OMT) were advised, whereas in 25 patients the coronary angiography was negative (NC group). 115 volunteers served as healthy controls (HC). In all individuals, the plasma level of several complement activation products - C1rC1sC1inh, C3bBbP and SC5b-9 - were determined on admission, strictly before the coronary angiography. In patients with angiographically proven ACHD (PCI and NOPCI groups), the baseline C1rC1sC1inh levels were significantly higher compared to NC group and HC (p<0.0001, for both comparisons). According to the multiple logistic regression analysis, high C1rC1sC1inh level proved to be an independent biomarker of coronary heart disease (p<0.026, OR: 65.3, CI: 1.628-2616.284).
  
  
  CONCLUSIONS
  Activation of the classical complement pathway can be observed in angiographically proven coronary atherosclerosis. Elevated C1rC1sC1inh levels might represent an useful biomarker for coronary artery disease.
authors.affiliation: Research Group for Inflammation Biology and Immunogenomics of Hungarian Academy of Sciences and Semmelweis University, Róbert Károly krt. 44, 1134 Budapest, Hungary. horvzsofi@hotmail.com
authors.forename: Zsófia
authors.initials: Z
authors.lastname: Horváth
authors.forename: Dorottya
authors.initials: D
authors.lastname: Csuka
authors.forename: Katarina
authors.initials: K
authors.lastname: Vargova
authors.forename: Andrea
authors.initials: A
authors.lastname: Kovács
authors.forename: Andrea Ágnes
authors.initials: AÁ
authors.lastname: Molnár
authors.forename: Petra
authors.initials: P
authors.lastname: Gulácsi-Bárdos
authors.forename: Sarolta
authors.initials: S
authors.lastname: Leé
authors.forename: Lilian
authors.initials: L
authors.lastname: Varga
authors.forename: Róbert Gábor
authors.initials: RG
authors.lastname: Kiss
authors.forename: István
authors.initials: I
authors.lastname: Préda
authors.forename: George
authors.initials: G
authors.lastname: Füst
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000097:blood / Q000175:diagnosis*; D016022:Case-Control Studies; D015331:Cohort Studies; D003167:Complement Activation / Q000502:physiology; D003172:Complement C1 / Q000032:analysis* / Q000378:metabolism; D003174:Complement C1 Inactivator Proteins / Q000032:analysis* / Q000378:metabolism; D015923:Complement C1r / Q000032:analysis / Q000378:metabolism; D003173:Complement C1s / Q000032:analysis / Q000378:metabolism; D003324:Coronary Artery Disease / Q000097:blood / Q000175:diagnosis*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011379:Prognosis
chemical_list: D003172:Complement C1; D003174:Complement C1 Inactivator Proteins; D015923:Complement C1r; D003173:Complement C1s