title: Lack of association between complement factor H polymorphisms and coronary artery disease or myocardial infarction.
abstract: Complement factor H (CFH) plays a critical role in the protection of host cells and tissues from damage by complement activation and has been suggested to protect against the progression of atherosclerosis. A polymorphism in the CFH gene, Y402H, known to be strongly associated with age-related macular degeneration, has been analyzed in relation to coronary artery disease (CAD) in several studies with conflicting results. We investigated the association of polymorphisms of the CFH gene in two large-scale studies on CAD and myocardial infarction (MI). The AtheroGene Study included a cohort of cases with CAD (n = 1,303) prospectively followed for a median period of 6.2 years, among whom198 experienced a cardiovascular event, and a group of 483 control subjects. The AtheroGene Study population was genotyped for the Y402H, I62V, and E936D polymorphisms. There was no significant difference in genotypic or allelic frequencies between CAD cases and controls. Among cases, no significant association was found with prospective cardiovascular outcome. Many inflammatory proteins, including the C-reactive protein, were measured, and none of the polymorphisms showed an association with these markers. The Etude Cas-Témoin de l'Infarctus du Myocarde (ECTIM) Study compared 1,034 patients with MI and 1,039 controls from France and United Kingdom. The ECTIM Study population was genotyped for the Y402H polymorphism. Genotype and allele frequencies were similar in cases and controls. These results do not support an involvement of common nonsynonymous polymorphisms of the CFH gene in predisposition to CAD and its complications.
authors.affiliation: INSERM UMR S525, Faculté de Médecine Pitié-Salpêtrière, 91 Boulevard de l'Hôpital, Paris, 75013, France.
authors.forename: Viviane
authors.initials: V
authors.lastname: Nicaud
authors.forename: Carole
authors.initials: C
authors.lastname: Francomme
authors.forename: Jean-Bernard
authors.initials: JB
authors.lastname: Ruidavets
authors.forename: Gérald
authors.initials: G
authors.lastname: Luc
authors.forename: Dominique
authors.initials: D
authors.lastname: Arveiler
authors.forename: Frank
authors.initials: F
authors.lastname: Kee
authors.forename: Alun
authors.initials: A
authors.lastname: Evans
authors.forename: Caroline
authors.initials: C
authors.lastname: Morrison
authors.forename: Stefan
authors.initials: S
authors.lastname: Blankenberg
authors.forename: François
authors.initials: F
authors.lastname: Cambien
authors.forename: Laurence
authors.initials: L
authors.lastname: Tiret
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D017242:Complement Factor H / Q000235:genetics*; D003324:Coronary Artery Disease / Q000453:epidemiology / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease / Q000453:epidemiology*; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D020125:Mutation, Missense; D009203:Myocardial Infarction / Q000453:epidemiology / Q000235:genetics*; D011110:Polymorphism, Genetic
chemical_list: D017242:Complement Factor H