title: Asp92Asn polymorphism in the myeloid IgA Fc receptor is associated with myocardial infarction in two disparate populations: CARE and WOSCOPS.
abstract: OBJECTIVE
  Statins reduce inflammation and risk of myocardial infarction (MI). Because the myeloid IgA Fc receptor encoded by FCAR mediates inflammation, we hypothesized that the FCAR Asp92Asn polymorphism is associated with risk of MI and that this risk would be modified by pravastatin.
  
  
  RESULTS
  In the placebo arm of the Cholesterol and Recurrent Events (CARE) study, male carriers of the 92Asn allele had an adjusted hazard ratio for incident MI of 1.68 (95% CI 1.10 to 2.57); relative risk reduction by pravastatin was 69% in carriers and 12% in noncarriers (P(interaction)=0.007). In the placebo arm of the all-male West of Scotland Coronary Prevention Study (WOSCOPS), carriers had an adjusted odds ratio for incident coronary heart disease (CHD) of 1.46 (90% CI 1.05 to 2.03); for pravastatin compared with placebo treatment, the adjusted odds ratios were 0.55 (95% CI 0.32 to 0.93) in carriers and 0.65 (95% CI 0.51 to 0.83) in noncarriers (P(interaction)=0.55).
  
  
  CONCLUSIONS
  Carriers of 92Asn had increased risk of MI in CARE and increased odds of CHD in WOSCOPS. Pravastatin significantly reduced risk in carriers in both CARE and WOSCOPS. A genotype by treatment interaction was observed in CARE but not in WOSCOPS.
authors.affiliation: Celera Inc, 1401 Harbor Bay Parkway, Alameda, CA 94502, USA. olga.iakoubova@celeradiagnostics.com
authors.forename: Olga A
authors.initials: OA
authors.lastname: Iakoubova
authors.forename: Carmen H
authors.initials: CH
authors.lastname: Tong
authors.forename: Anand P
authors.initials: AP
authors.lastname: Chokkalingam
authors.forename: Charles M
authors.initials: CM
authors.lastname: Rowland
authors.forename: Todd G
authors.initials: TG
authors.lastname: Kirchgessner
authors.forename: Judy Z
authors.initials: JZ
authors.lastname: Louie
authors.forename: Lynn M
authors.initials: LM
authors.lastname: Ploughman
authors.forename: Marc S
authors.initials: MS
authors.lastname: Sabatine
authors.forename: Hannia
authors.initials: H
authors.lastname: Campos
authors.forename: Joseph J
authors.initials: JJ
authors.lastname: Catanese
authors.forename: Diane U
authors.initials: DU
authors.lastname: Leong
authors.forename: Bradford A
authors.initials: BA
authors.lastname: Young
authors.forename: David
authors.initials: D
authors.lastname: Lew
authors.forename: Zenta
authors.initials: Z
authors.lastname: Tsuchihashi
authors.forename: May M
authors.initials: MM
authors.lastname: Luke
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Packard
authors.forename: Kim E
authors.initials: KE
authors.lastname: Zerba
authors.forename: Peter M
authors.initials: PM
authors.lastname: Shaw
authors.forename: James
authors.initials: J
authors.lastname: Shepherd
authors.forename: James J
authors.initials: JJ
authors.lastname: Devlin
authors.forename: Frank M
authors.initials: FM
authors.lastname: Sacks
mesh_terms: D000483:Alleles; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D015703:Antigens, CD / Q000235:genetics*; D001216:Asparagine / Q000235:genetics*; D001224:Aspartic Acid / Q000235:genetics*; D003327:Coronary Disease / Q000209:etiology / Q000235:genetics / Q000517:prevention & control; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006801:Humans; D008297:Male; D009203:Myocardial Infarction / Q000209:etiology / Q000235:genetics* / Q000517:prevention & control; D016017:Odds Ratio; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D017035:Pravastatin / Q000627:therapeutic use; D011961:Receptors, Fc / Q000235:genetics*; D012307:Risk Factors; D012606:Scotland
chemical_list: D000924:Anticholesteremic Agents; D015703:Antigens, CD; C036832:Fc(alpha) receptor; D011961:Receptors, Fc; D001224:Aspartic Acid; D001216:Asparagine; D017035:Pravastatin