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Association between 9p21 genomic markers and ischemic stroke risk: evidence based on 21 studies.

ABSTRACT: Epidemiological studies indicate a genetic contribution to ischemic stroke risk, but specific genetic variants remain unknown. Recently independent studies reported an association between coronary heart disease and single-nucleotide polymorphisms (SNPs) located at chromosome 9p21 (rs10757278 and proxy SNPs). Given that stroke is a common complication after myocardial infarction, several validation studies have been conducted among various ethnic populations to investigate if the same loci was associated with ischemic stroke (IS), but the results have been inconsistent. To investigate this inconsistency and derive a more precise estimation of the relationship, a meta-analysis of 34,128 cases and 153,428 controls from 21 studies was performed. Potential sources of heterogeneity including ethnicity, sample size, control source and ischemic stroke subtypes were also assessed. Overall, the summary odds ratio of IS was 1.11 (95% CI: 1.07-1.15, P<10(-5)) for rs10757278. In the subgroup analysis by ethnicity, significantly increased risks were found in East Asians (3188 cases and 4503 controls; OR?=?1.14, 95% CI: 1.07-1.21, P<10(-5)) and Caucasians (30505 cases and 145153controls; OR?=?1.08, 95% CI: 1.04-1.12, P<10(-5)) for the polymorphism; while no significant associations were found among African Americans (435 cases and 3772 controls; OR?=?0.97, 95% CI: 0.63-1.51, P?=?0.90) in all genetic models. In the subgroup analyses by IS subtypes, significant association was detected only in large vessel stroke group, while no significant associations among small vessel or cardioembolic stroke. When stratified by sample size, and control source, significantly increased risks were found for the polymorphism in all genetic models. This meta-analysis provides accurate and comprehensive estimates of the association of genetic variant at chromosome 9p21 and IS, but these associations vary in different ethnic populations.

SUBMITTER: Ni X

PROVIDER: S-EPMC3953076 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Association between 9p21 genomic markers and ischemic stroke risk: evidence based on 21 studies.

Ni Xiaoqing X Zhang Jiawei J

PloS one 20140313 3

Epidemiological studies indicate a genetic contribution to ischemic stroke risk, but specific genetic variants remain unknown. Recently independent studies reported an association between coronary heart disease and single-nucleotide polymorphisms (SNPs) located at chromosome 9p21 (rs10757278 and proxy SNPs). Given that stroke is a common complication after myocardial infarction, several validation studies have been conducted among various ethnic populations to investigate if the same loci was as ...[more]

PMID: 24625579

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Project description:ObjectiveTo explore the relationship between sleep habits (sleep duration, sleep efficiency, sleep onset timing) and ischemic stroke, and whether there is an interaction between sleep habits and ischemic stroke susceptibility gene loci.MethodsA questionnaire survey, physical examination, blood biochemical testing and genotyping were conducted among rural residents in Beijing, and the gene loci of ischemic stroke suggested by previous genome-wide association studies (GWAS) were screened. Multivariable generalized linear model was used to analyze the correlation between sleep habits, sleep-gene interaction and ischemic stroke.ResultsA total of 4 648 subjects with an average age of (58.5±8.7) years were enrolled, including 1 316 patients with ischemic stroke. Compared with non-stroke patients, stroke patients with sleep duration ≥9 hours, sleep efficiency < 80%, and sleep onset timing earlier than 22:00 accounted for a higher proportion (P < 0.05). There was no significant association between sleep duration and risk of ischemic stroke (OR=1.04, 95%CI: 0.99-1.10, P=0.085). Sleep efficiency was inversely associated with the risk of ischemic stroke (OR=0.18, 95%CI: 0.06-0.53, P=0.002). The risk of ischemic stroke in the subjects with sleep efficiency < 80% was 1.47-fold (95%CI: 1.03-2.10, P=0.033) of that in the subjects with sleep efficiency ≥80%. Falling asleep earlier than 22:00 was associated with 1.26 times greater risk of stroke than falling asleep between 22:00 and 22:59 (95%CI: 1.04-1.52, P=0.017). Multifactorial adjustment model showed that rs579459 on ABO gene had an interaction with sleep time (P for interaction =0.040). When there were two T alleles for rs579459 on the ABO gene, those who fell asleep before 22:00 had 1.56 times (95%CI: 1.20-2.04, P=0.001) the risk of stroke compared with those who fell asleep between 22:00 and 22:59, and there was no significant difference when the number of pathogenic alleles was 0 or 1. In the model adjusted only for gender, age and family structure, sleep duration and the number of T allele rs2634074 on PITX2 gene had an interaction with ischemic stroke (P for interaction=0.033).ConclusionDecreased sleep efficiency is associated with increased risk of ischemic stroke, and falling asleep earlier than 22:00 is associated with higher risk of ischemic stroke. Sleep onset timing interacted with rs579459 in ABO gene and the risk of ischemic stroke. Sleep duration and PITX2 rs2634074 may have a potential interaction with ischemic stroke risk.

Project description:Although stroke centers are widely accepted and supported, little is known about their effect on patient outcomes.To examine the association between admission to stroke centers for acute ischemic stroke and mortality.Observational study using data from the New York Statewide Planning and Research Cooperative System. We compared mortality for patients admitted with acute ischemic stroke (n = 30,947) between 2005 and 2006 at designated stroke centers and nondesignated hospitals using differential distance to hospitals as an instrumental variable to adjust for potential prehospital selection bias. Patients were followed up for mortality for 1 year after the index hospitalization through 2007. To assess whether our findings were specific to stroke, we also compared mortality for patients admitted with gastrointestinal hemorrhage (n = 39,409) or acute myocardial infarction (n = 40,024) at designated stroke centers and nondesignated hospitals.Thirty-day all-cause mortality.Among 30,947 patients with acute ischemic stroke, 15,297 (49.4%) were admitted to designated stroke centers. Using the instrumental variable analysis, admission to designated stroke centers was associated with lower 30-day all-cause mortality (10.1% vs 12.5%; adjusted mortality difference, -2.5%; 95% confidence interval [CI], -3.6% to -1.4%; P < .001) and greater use of thrombolytic therapy (4.8% vs 1.7%; adjusted difference, 2.2%; 95% CI, 1.6% to 2.8%; P < .001). Differences in mortality also were observed at 1-day, 7-day, and 1-year follow-up. The outcome differences were specific for stroke, as stroke centers and nondesignated hospitals had similar 30-day all-cause mortality rates among those with gastrointestinal hemorrhage (5.0% vs 5.8%; adjusted mortality difference, +0.3%; 95% CI, -0.5% to 1.0%; P = .50) or acute myocardial infarction (10.5% vs 12.7%; adjusted mortality difference, +0.1%; 95% CI, -0.9% to 1.1%; P = .83).Among patients with acute ischemic stroke, admission to a designated stroke center was associated with modestly lower mortality and more frequent use of thrombolytic therapy.

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Association between 9p21 genomic markers and ischemic stroke risk: evidence based on 21 studies.

Publications

Association between 9p21 genomic markers and ischemic stroke risk: evidence based on 21 studies.

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