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London, United Kingdom 2013 30 Meta-analysis and reviews Passive smoking as a risk factor for stroke in women compared with men: a systematic review and meta-analysis D.Y. Cheng1, R.L. Chen2 King’s College London, London, UNITED KINGDOM1, King’s College London, London, UNITED KINGDOM2 BACKGROUND - Stroke has become a leading cause of mortality and disability in the 21st century, and research has established active smoking as an independent risk factor for stroke. However, the same association has not been accorded to passive smoking. This meta-analysis seeks to summarise existing evidence on the association between passive smoking and stroke incidence, and to investi-gate E-Poster Session Blue Cerebrovasc Dis 2013; 35 (suppl 3)1-854 581 the presence of gender disparity. METHODS – A systematic review was conducted on NCIB PUBMED, OVID Medline, Cochrane Library, Google Scholar and OpenSIGLE and further augmented with a manual search of bibliogra-phies of relevant articles. Data from an unpublished Chinese study investigating 4282 non-smoking participants (1114 men, 3168 women) was also included in the meta-analysis, where odds ratios were computed using binary logistic regression. Using a random effects model, a pooled estimate of risk was obtained for the meta-analysis, with heterogeneity quantified using I2 statistic. Systematic bias was assessed using funnel plots and Egger’s test. RESULTS – The unpublished study derived a multivariate-adjusted odds ratio of 1.44 (95%CI 0.81–2.58) for females and 0.59 (95%CI 0.21–1.65) for males. Amalgamating the above results with 13 eligible studies identified in the systematic review, the meta-analysis included data from 1071095 participants (251357 men, 818806 women) with a minimum of 9243 stroke incidents. The pooled risk ratio obtained was 1.28 (95%CI 1.16–1.41) for females and 1.20 (95%CI 0.92–1.56) for males. Heterogeneity was low with no evidence of systematic bias. CONCLUSION – Pooled risk estimates display a strong association between passive smoking and stroke incidence in non-smoking individuals, suggestive of a causal relationship. In addition to cre-ating tobacco prevention programmes aimed at protecting non-smokers from the harmful effects of passive smoking, policy makers should consider the presence of potential gender effects to encour-age programme efficacy. 29 Meta-analysis and reviews Genetic risk variants associated with carotid stenosis: A systematic review and meta-analysis M.L. Sagmeister1, S. Yadav2, N. Hasan3, P. Sharma4 Imperial College Cerebrovascular Research Unit (ICCRU), London, UNITED KINGDOM1, Imperial College Cerebrovascular Research Unit (ICCRU), London, UNITED KINGDOM2, Imperi-al College Cerebrovascular Research Unit (ICCRU), London, UNITED KINGDOM3, Imperial Col-lege Cerebrovascular Research Unit (ICCRU), London, UNITED KINGDOM4 Background: Carotid stenosis is a major risk factor for ischaemic stroke. Although family studies have shown heritability of 47% for carotid stenosis, specific genetic risk variants have yet to be conclusively defined. We sought to quantify the strengths of association (if any) between genetic variants and clinically relevant carotid stenosis (≥50% and ≥70%). Methods: Electronic databases were searched for case-control studies evaluating associations between gene variants and carotid stenosis ≥50% of the common and/or internal carotid artery. Pooled odds ratios (OR) and 95% Con-fidence Intervals (CI) were determined using a random-effects model. Results: Thirty-four studies investigating seventeen polymorphisms in 3,666 cases and 18,391 controls were included for me-ta- analysis. Significant associations were identified for stenosis ≥50% with the following genes; methylenetetrahydrofolate reductase (MTHFR) C677T (OR 1.28, 1.02-1.61, p=0.04), Angioten-sin- Converting Enzyme (ACE) I/D (OR 1.33, 1.01-1.75, p=0.05), ApolipoproteinE (ApoE) ε2/ε3/ε4 (OR 1.51, 1.11-2.04, p=0.008), Matrix Metalloproteinase-3 (MMP-3) 5A/6A (OR 1.91, 1.24-2.94, p=0.003) and CX3CR1 T280M (OR 0.50, 0.34-0.72, p=0.0002). Analyses for severe stenosis of ≥70% lead to higher ORs for MTHFR C677T and ACE I/D, but these results were not significantly different from those for ≥50%. Conclusion: Our study provides evidence for a genetic aetiology in carotid stenosis. Associations with five genetic variants in ≥50% carotid stenosis are reliably demon-strated. E-Poster Terminal 4


Karger_ESC London_2013
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