TY - JOUR
T1 - Associations of apolipoprotein E exon 4 and lipoprotein lipase S447X polymorphisms with acute ischemic stroke and myocardial infarction
AU - Baum, L.
AU - Ho, K.N.
AU - Ka, S.W.
AU - Tomlinson, B.
AU - Rainer, T.H.
AU - Chen, Xiangyan
AU - Wing, S.C.
AU - Tang, J.
AU - Tam, W.W.S.
AU - Goggins, W.
AU - Tong, C.S.W.
AU - Chan, D.K.Y.
AU - Thomas, G.N.
AU - Chook, P.
AU - Kam, S.W.
PY - 2006/3/1
Y1 - 2006/3/1
N2 - 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 ?2 and ?4 homozygotes were increased in stroke (4.5% vs. 1.0%, p = 0.008), while in myocardial infarction the ?4 allele was increased (12.6% vs. 9.5%, p = 0.006) but ?2 was decreased (3.7% vs. 12.1%, p = 0.000006). For subjects with either APOE ?2 or ?4 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. © 2006 by Walter de Gruyter.
AB - 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 ?2 and ?4 homozygotes were increased in stroke (4.5% vs. 1.0%, p = 0.008), while in myocardial infarction the ?4 allele was increased (12.6% vs. 9.5%, p = 0.006) but ?2 was decreased (3.7% vs. 12.1%, p = 0.000006). For subjects with either APOE ?2 or ?4 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. © 2006 by Walter de Gruyter.
KW - Apolipoprotein E
KW - Ischemic
KW - Lipoprotein lipase
KW - Polymorphism
KW - Smoking
UR - http://www.scopus.com/inward/record.url?scp=33644831718&partnerID=8YFLogxK
U2 - 10.1515/CCLM.2006.047
DO - 10.1515/CCLM.2006.047
M3 - Journal article
C2 - 16519597
SN - 1434-6621
VL - 44
SP - 274
EP - 281
JO - Clinical Chemistry and Laboratory Medicine
JF - Clinical Chemistry and Laboratory Medicine
IS - 3
ER -