Passive smoking, as well as active smoking, increases the risk of acute stroke. Tob Control 8:156-160

Department of Medicine, Faculty of Medicine and Health Science, University of Auckland, New Zealand.
Tobacco Control (Impact Factor: 5.93). 06/1999; 8(2):156-60. DOI: 10.1136/tc.8.2.156
Source: PubMed


To estimate the relative risk of stroke associated with exposure to environmental tobacco smoke (ETS, passive smoking) and to estimate the risk of stroke associated with current smoking (active smoking) using the traditional baseline group (never-smokers) and a baseline group that includes lifelong non-smokers and long-term (> 10 years) ex-smokers who have not been exposed to ETS.
Population-based case-control study in residents of Auckland, New Zealand.
Cases were obtained from the Auckland stroke study, a population-based register of acute stroke. Controls were obtained from a cross-sectional survery of major cardiovascular risk factors measured in the same population. A standard questionnaire was administered to patients and controls by trained nurse interviewers.
Information was available for 521 patients with first-ever acute stroke and 1851 community controls aged 35-74 years. After adjusting for potential confounders (age, sex, history of hypertension, heart disease, and diabetes) using logistic regression, exposure to ETS among non-smokers and long-term ex-smokers was associated with a significantly increased risk of stroke (odds ratio (OR) = 1.82; 95% confidence interval (95% CI) = 1.34 to 2.49). The risk was significant in men (OR = 2.10; 95% CI = 1.33 to 3.32) and women (OR = 1.66; 95% CI = 1.07 to 2.57). Active smokers had a fourfold risk of stroke compared with people who reported they had never smoked cigarettes (OR = 4.14; 95% CI = 3.04 to 5.63); the risk increased when active smokers were compared with people who had never smoked or had quit smoking more than 10 years earlier and who were not exposed to ETS (OR = 6.33; 95% CI = 4.50 to 8.91).
This study is one of the few to investigate the association between passive smoking and the risk of acute stroke. We found a significantly increased risk of stroke in men and in women. This study also confirms the higher risk of stroke in men and women who smoke cigarettes compared with non-smokers. The stroke risk increases further when those who have been exposed to ETS are excluded from the non-smoking reference group. These findings also suggest that studies investigating the adverse effects of smoking will underestimate the risk if exposure to ETS is not taken into account.

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Available from: Ruth Bonita, Sep 29, 2015
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    • "Among all these included cohort studies , 11 reported all-cause mortality, 23 reported CVD, 15 reported CHD, and 11 reported stroke. The characteristics of 17 case–control studies [38] [39] [40] [41] [42] [43] [44] [45] [46] [47] [48] [49] [50] [51] [52] [53] [54] are presented in Table 2. Three studies were conducted in the US, 5 in Europe, 5 in Australia and/or New Zealand, 3 in Asia, and 1 in Argentina. The number of case subjects ranged from 34 to 4838, with a corresponding number of control subjects ranging from 68 to 763. "
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    ABSTRACT: Emerging studies have assessed the association between secondhand smoke (SHS) exposure and cardiovascular disease (CVD) as well as all-cause mortality. However, findings were not consistent due to the heterogeneity of study characteristics. PubMed and Embase were searched through May 2014 for prospective cohort and case-control studies investigating the associations of SHS exposure in never smokers with all-cause mortality and the risk of CVD. The main analysis was performed in studies using self-reported SHS exposure and secondary analysis was performed in studies using objectively measured SHS exposure. Summary estimates were calculated using random-effects models. Twenty-three prospective and 17 case-control studies were included. The pooled relative risks (RR) for never smokers exposed to SHS in comparison with those unexposed were 1.18 [95% confidence interval (CI): 1.10-1.27] for all-cause mortality (12 studies), and 1.23 (1.16-1.31) for CVD (38 studies). The association of SHS exposure with CVD was markedly stronger among studies conducted in China (RR=1.65, 95% CI 1.27-2.13) than that in the US (RR=1.09, 95% CI 1.03-1.16). Studies using objectively measured SHS exposure demonstrated a slightly higher risk for CVD compared with those using self-reported SHS exposure. Exposure to SHS significantly increased the risk for all-cause mortality and CVD. The risk associated with SHS exposure was large in China while the risk was only modest in the US. Studies using objectively measured SHS exposure may yield a higher risk of CVD than those using self-reported SHS exposure. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    International journal of cardiology 07/2015; 199:106-115. DOI:10.1016/j.ijcard.2015.07.011 · 4.04 Impact Factor
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    • "Study patients were dichotomized into subgroups according to their general characteristics and many other variables. These included the presence of defined (hypertension [13], dyslipidemia [14], carotid stenosis [15], [16], and PAF [17]) and potential (smoking [18], diabetes [19], prior ischemic heart disease [20], and mitral valve insufficiency [21], [22]) causal risk factors for ischemic stroke, cardiac echoparameters, cCT based volume measurements, and adipose tissue measurements (Figure 1). "
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    ABSTRACT: Left atrial appendage (LAA) volume has been shown to be increased in patients with acute cryptogenic stroke. Atrial fibrillation (AF) is a well-recognized risk factor but it is not the only one associated with LAA enlargement. The aim of the study was to clarify the multifactorial etiology of LAA enlargement in cardiogenic stroke/TIA patients without AF. Altogether 149 patients with suspected cardioembolic stroke/TIA (47 females; mean age 61 years) underwent cardiac CT. Diagnosed AF on admittance was an exclusion criteria but 24-hour Holter ambulatory ECG revealed paroxysmal AF (PAF) in 20 patients. Body surface area adjusted LAA volume was evaluated. Eighteen different variables were registered including general characteristics, definite and potential causal risk factors for ischemic stroke/TIA, clinical echoparameters and CT based cardiac volumetric and adipose tissue measurements. A stepwise linear regression analysis was performed to achieve a model adjusted for the number of predictors of LAA volume increase. In linear regression analysis, the best model accounted for 30% of the variability in LAA volume, including PAF (19%) and enlarged left atrial volume (6%), enlarged left ventricle end-systolic diameter (3%) and decreased pericardial adipose tissue (2%). No multi-colinearity between variables was observed. In addition to PAF, no other definitive or potential causal risk factors could account for the LAA volume in these patients. LAA volume increase seems to be poorly associated with currently known stroke/TIA risk factors, except for AF. Targeting more comprehensive ECG monitoring for stroke patients with increased LAA volume should be considered.
    PLoS ONE 03/2014; 9(3):e90903. DOI:10.1371/journal.pone.0090903 · 3.23 Impact Factor
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    • "However, this result should not be interpreted to mean that smoking has no effect on stroke. On the contrary, previous epidemiological evidences have showed a strong association between smoking and having an increased risk of stroke.17,23,24 In an earlier 28-year follow-up period of this study population by Harmsen et al.25 smoking was found to be a risk factor for stroke during the first 21 years, but for the final period of 7 years no significant association was found. "
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    ABSTRACT: AimsThe aim of this study was to examine the short-term and long-term cumulative risk of coronary heart disease (CHD) and stroke separately based on age, sex, smoking status, systolic blood pressure, and total serum cholesterol.Methods and resultsThe Primary Prevention Study comprising 7174 men aged between 47 and 55 free from a previous history of CHD, stroke, and diabetes at baseline examination (1970-73) was followed up for 35 years. To estimate the cumulative effect of CHD and stroke, all participants were stratified into one of five risk groups, defined by their number of risk factors. The estimated 10-year risk for high-risk individuals when adjusted for age and competing risk was 18.1% for CHD and 3.2% for stroke which increased to 47.8 and 19.6%, respectively, after 35 years. The estimates based on risk factors performed well throughout the period for CHD but less well for stroke.Conclusion The prediction of traditional risk factors (systolic blood pressure, total serum cholesterol, and smoking status) on short-term risk (0-10 years) and long-term risk (0-35 years) of CHD of stroke differs substantially. This indicates that the cumulative risk in middle-aged men based on these traditional risk factors can effectively be used to predict CHD but not stroke to the same extent.
    European Heart Journal 01/2013; 34(14). DOI:10.1093/eurheartj/ehs458 · 15.20 Impact Factor
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