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. CONCLUSION: 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.
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 strokepatients, 234 acute myocardial infarctionpatients, and 336 controls. APOE exon 4 and LPLS447X 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. CONCLUSION: This is the first report of an association of vascular disease with an interaction of APOE exon 4 and LPLS447X genotypes. Therefore, APOE genotypes and LPLS447X interactions with apoE, sex, and smoking may affect the risk of myocardial infarction and ischemic stroke.
Authors: Maša Umiċeviċ Mirkov; Jing Cui; Sita H Vermeulen; Eli A Stahl; Erik J M Toonen; Remco R Makkinje; Annette T Lee; Tom W J Huizinga; Renee Allaart; Anne Barton; Xavier Mariette; Corinne Richard Miceli; Lindsey A Criswell; Paul P Tak; Niek de Vries; Saedis Saevarsdottir; Leonid Padyukov; S Louis Bridges; Dirk-Jan van Schaardenburg; Tim L Jansen; Ellen A J Dutmer; Mart A F J van de Laar; Pilar Barrera; Timothy R D J Radstake; Piet L C M van Riel; Hans Scheffer; Barbara Franke; Han G Brunner; Robert M Plenge; Peter K Gregersen; Henk-Jan Guchelaar; Marieke J H Coenen Journal: Ann Rheum Dis Date: 2012-12-11 Impact factor: 19.103
Authors: Yumei Yang; Danhua Du; Peng Gao; Xuan Zhang; Ning Wu; Feng Wang; Zhenqi Wang; Lin Ye; Jiang Wu; Ian L Megson; Jun Wei Journal: Transl Stroke Res Date: 2010-12-16 Impact factor: 6.829
Authors: Jaime Madrigano; Andrea Baccarelli; Robert O Wright; Helen Suh; David Sparrow; Pantel S Vokonas; Joel Schwartz Journal: Occup Environ Med Date: 2009-11-02 Impact factor: 4.402