LPL polymorphism predicts stroke risk in men.
LPL polymorphism predicts stroke risk in men.
复制标题
LPL 多态性可预测男性中风风险。
DOI:
10.1002/gepi.0191
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发表时间:
2002
影响因子:
2.1
通讯作者:
Boerwinkle,Eric
中科院分区:
文献类型:
--
作者:
Morrison,AlannaC;Ballantyne,ChristieM;Bray,Molly;Chambless,LloydE;Sharrett,ARichey;Boerwinkle,Eric
Variation in lipid levels has been associated with atherosclerotic vascular disease, including stroke. Genes contributing to interindividual variation in lipid levels may play a role in the etiology of stroke, either through their effects on lipid synthesis and metabolism or through separate pathways. For this reason, we sought to examine the association between polymorphisms in the lipoprotein lipase (LPL) and apolipoprotein E (APOE) genes and subclinical and clinical stroke in the Atherosclerosis Risk in Communities (ARIC) Study. Subclinical stroke was determined by cerebral magnetic resonance imaging (MRI). Subclinical cerebral infarct cases (n = 197) were compared to a stratified random sample identified from individuals participating in the MRI examination (n = 200). Incidence of clinical ischemic stroke was determined by following the ARIC cohort for an average of 7.5 years for potential cerebrovascular events; 218 validated clinical ischemic strokes were identified. A stratified random sample of the ARIC cohort (CRS, n = 964) was used as the comparison group for clinical cases. TheLPLS291‐carrying genotypes andAPOEϵ2‐ and ϵ4‐carrying genotypes were not significantly associated with subclinical or clinical stroke. TheLPLX447‐containing genotypes were significantly associated with subclinical (odds ratio [OR], 4.32; 95% confidence interval [CI], 1.23–15.15;P= 0.020) and clinical stroke (hazard rate ratio [HRR], 2.57; 95% CI, 1.24–5.34;P= 0.01) in men, both by themselves and after adjustment for multiple stroke risk factors. TheLPLS447X polymorphism is significantly associated with subclinical cerebral infarction and incident clinical ischemic stroke in men from a middle‐aged American population. This association does not appear to be mediated by triglyceride, high‐density lipoprotein (HDL)‐ and low‐density lipoprotein (LDL)‐cholesterol levels, or additional stroke risk factors. Genet. Epidemiol. 22:233–242, 2002. © 2002 Wiley‐Liss, Inc.