title: Associations of apolipoprotein E exon 4 and lipoprotein lipase S447X polymorphisms with acute ischemic stroke and myocardial infarction.
abstract: BACKGROUND
  Because apolipoprotein E (apoE) and lipopoprotein lipase (LPL) polymorphisms interact with each other and with other factors to affect lipid metabolism, we sought to determine their separate and combined effects in association with ischemic vascular disease.
  
  
  METHODS
  We performed a case-control study of 816 subjects: 246 acute ischemic stroke patients, 234 acute myocardial infarction patients, and 336 controls. APOE exon 4 and LPL S447X genotypes were determined.
  
  
  RESULTS
  APOE epsilon2 and epsilon4 homozygotes were increased in stroke (4.5% vs. 1.0%, p = 0.008), while in myocardial infarction the epsilon4 allele was increased (12.6% vs. 9.5%, p = 0.006) but epsilon2 was decreased (3.7% vs. 12.1%, p = 0.000006). For subjects with either APOE epsilon2 or epsilon4 alleles, LPL X alleles were increased in vascular disease (OR = 2.2, p = 0.01). LPL X alleles displayed opposite tendencies toward association with disease when subjects were divided by sex, smoking, or APOE genotype. Meta-analysis and regression analysis of previous studies supported the sex and smoking dichotomies.
  
  
  CONCLUSIONS
  This is the first report of an association of vascular disease with an interaction of APOE exon 4 and LPL S447X genotypes. Therefore, APOE genotypes and LPL S447X interactions with apoE, sex, and smoking may affect the risk of myocardial infarction and ischemic stroke.
authors.affiliation: Department of Medicine and Therapeutics, Chinese University of Hong Kong, Shatin, Hong Kong. lwbaum@cuhk.edu.hk
authors.forename: Larry
authors.initials: L
authors.lastname: Baum
authors.forename: Ho Keung
authors.initials: HK
authors.lastname: Ng
authors.forename: Ka Sing
authors.initials: KS
authors.lastname: Wong
authors.forename: Brian
authors.initials: B
authors.lastname: Tomlinson
authors.forename: Timothy Hudson
authors.initials: TH
authors.lastname: Rainer
authors.forename: Xiangyan
authors.initials: X
authors.lastname: Chen
authors.forename: Wing Sze
authors.initials: WS
authors.lastname: Cheung
authors.forename: Jinling
authors.initials: J
authors.lastname: Tang
authors.forename: Wilson Wai San
authors.initials: WW
authors.lastname: Tam
authors.forename: William
authors.initials: W
authors.lastname: Goggins
authors.forename: Cindy See Wai
authors.initials: CS
authors.lastname: Tong
authors.forename: Daniel Kam Yin
authors.initials: DK
authors.lastname: Chan
authors.forename: G Neil
authors.initials: GN
authors.lastname: Thomas
authors.forename: Ping
authors.initials: P
authors.lastname: Chook
authors.forename: Kam Sang
authors.initials: KS
authors.lastname: Woo
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D053327:Apolipoprotein E4; D001057:Apolipoproteins E / Q000235:genetics*; D005091:Exons / Q000235:genetics*; D005260:Female; D005838:Genotype; D006723:Hong Kong; D006801:Humans; D008071:Lipoprotein Lipase / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology / Q000235:genetics*; D011110:Polymorphism, Genetic; D012044:Regression Analysis; D018570:Risk Assessment; D012307:Risk Factors; D012907:Smoking; D020521:Stroke / Q000453:epidemiology / Q000235:genetics*
chemical_list: D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D008071:Lipoprotein Lipase