title: The common Y402H variant in complement factor H gene is not associated with susceptibility to myocardial infarction and its related risk factors.
abstract: Recently, the genetic variant Y402H in the CFH (complement factor H) gene was associated with an increased risk for MI (myocardial infarction) in a prospective Caucasian cohort. In another nested case-control study, however, the CFH-Y402H variant did not carry susceptibility to MI. The aim of the present study was to test for an association between the CFH-Y402H variant and MI in a large case-control sample with a familial background for CAD (coronary artery disease). A total of 2161 individuals from the German MI family study were studied by questionnaire, physical examination and biochemical analyses. MI patients (n=1188; 51.4+/-8.6 years at first MI) were recruited from families with at least two members affected by MI and/or severe CAD. Spouses, sisters-in-law and brothers-in-law respectively, without MI/CAD were included as unaffected controls (n=973; 56.9+/-9.8 years). Genotyping was performed using a TaqMan assay. The common Y402H variant in the CFH gene was not associated with classical cardiovascular risk factors (diabetes, hypercholesterolaemia, hypertension, obesity, smoking and C-reactive protein serum levels). No association was found between the CFH-Y402H variant and susceptibility to MI. Separate analyses in both men and women revealed no gender-specific influence of the gene variant on cardiovascular risk factors or MI. This investigation was unable to replicate the association between the common CFH-Y402H variant and susceptibility to MI in our large Caucasian population which is enriched for genetic factors. We conclude that the CFH-Y402H variant has no relevant risk-modifying effect in our population.
authors.affiliation: Klinik und Poliklinik für Innere Medizin II, Klinikum der Universität Regensburg, Regensburg, Germany.
authors.forename: Klaus
authors.initials: K
authors.lastname: Stark
authors.forename: Katharina
authors.initials: K
authors.lastname: Neureuther
authors.forename: Kamil
authors.initials: K
authors.lastname: Sedlacek
authors.forename: Wibke
authors.initials: W
authors.lastname: Hengstenberg
authors.forename: Marcus
authors.initials: M
authors.lastname: Fischer
authors.forename: Andrea
authors.initials: A
authors.lastname: Baessler
authors.forename: Silke
authors.initials: S
authors.lastname: Wiedmann
authors.forename: Andreas
authors.initials: A
authors.lastname: Jeron
authors.forename: Stephan
authors.initials: S
authors.lastname: Holmer
authors.forename: Jeanette
authors.initials: J
authors.lastname: Erdmann
authors.forename: Heribert
authors.initials: H
authors.lastname: Schunkert
authors.forename: Christian
authors.initials: C
authors.lastname: Hengstenberg
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D017242:Complement Factor H / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology / Q000235:genetics*; D011446:Prospective Studies; D012307:Risk Factors
chemical_list: D017242:Complement Factor H