***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background —Smoking is a potent risk factor for coronary artery disease ( CAD ) and acute ischemic stroke ( AIS ) , but there are numerous reports of lower in-hospital mortality among smokers versus nonsmokers hospitalized for these events . Methods and Results —We analyzed all consecutive patients hospitalized with a first index CAD ( n=158 054 ) or AIS ( n=899 295 ) event in Get With The Guidelines from 2002 to 2012 ; 20.4 % of AIS and 30.4 % of patients with CAD were past-year smokers . Multivariable models and age-stratified analyses were used to estimate the adjusted odds ratio of in-hospital mortality in smokers versus nonsmokers . Smokers were younger , more often male , with fewer vascular risk factors , and were more likely to be admitted to hospitals that were large , academic , or in the South . In-hospital mortality was significantly lower among smokers in both CAD ( 2.7 % versus 5.2 % ; P<0.0001 ) and AIS ( 3.5 % versus 5.8 % ; P<0.0001 ) . The difference between unadjusted and adjusted odds ratios for smoking ( 0.57 versus 0.86 in CAD ; 0.56 versus 0.86 in AIS ) indicates the presence of substantial confounding by age and other covariates , but a significant association of past-year smoking remained . Conclusions —Among patients hospitalized with CAD and AIS , smoking is a risk factor for early age of onset , even among those with few vascular risk factors . The persistent association with lower in-hospital mortality after adjusted and stratified analyses probably represents residual unmeasured confounding , although a biological effect of smoking can not be excluded . Further clinical and prospect i ve population -based studies are needed to explore variables that contribute to outcomes in these patients OBJECTIVES This study was design ed to compare the effects of inhaled carbon monoxide ( CO ) , administered to achieve concentrations similar to those found in cigarette smoking , with the effects of cigarette smoking and air inhalation on heart rate and blood pressure , catecholamine release , platelet activation and C-reactive protein ( CRP ) , a marker of inflammation . BACKGROUND Carbon monoxide may contribute to smoking-induced cardiovascular disease . Exposure to environmental CO has been associated with increased cardiovascular morbidity and mortality . Animal and in vitro studies suggest that CO may contribute to atherosclerosis and endothelial injury . There is conflicting evidence about the hemodynamic consequences of exposure to CO and its role in platelet activation . METHODS In a single-blind , crossover design , 12 healthy smokers inhaled CO at 1,200 ppm to 1,500 ppm to simulate CO intake from cigarette smoking , inhaled air on a similar schedule and smoked 20 cigarettes per day , each for seven days . Mean carboxyhemoglobin was 5 + /- 1 % on CO treatment , 6 + /- 1 % while smoking and 0.4 + /- 0.2 % on air inhalations . RESULTS There was no difference in blood pressure between the treatments . Mean heart rate was higher during cigarette smoking compared with CO and air inhalations ( 75 beats/min vs. 66 beats/min ; p < 0.05 ) . Plasma levels of platelet factor 4 and CRP and urine epinephrine and norepinephrine were higher while smoking , with no effect of CO compared with air . CONCLUSIONS Carbon monoxide administered under conditions similar to those of cigarette smoking had no significant effect on blood pressure , heart rate , plasma catecholamines , platelet aggregation or CRP . The short-term chronotropic effect , adrenergic-activating , platelet-activating and CRP-increasing effects of smoking in healthy smokers are probably due to components of cigarette smoke other than CO BACKGROUND The effects of smoking on clinical outcomes following acute stroke remain controversial . METHODS We evaluated the influence of smoking on 90-day outcomes after acute atherothrombotic stroke in 292 Japanese men extracted from the data base of the Edaravone and Argatroban Stroke Therapy for Acute Ischemic Stroke r and omized parallel-group trial that tested the safety and efficacy of edaravone and argatroban therapy in 814 patients in 2004 - 2008 . Smokers were matched with non-smokers of the same age for identical age distribution in the smoker and non-smoker groups . Poor 90-day outcomes ( defined as death , Barthel index<60 , or modified Rankin score>3 ) were evaluated using a logistic regression model . Significant variables ( P<0.05 ) in univariate analysis were further evaluated by multivariate logistic regression analysis using a forward- selection method . RESULTS Body temperature , age , National Institute of Health Stroke Scale score at admission , systolic blood pressure , and smoking status were selected in the final model . Smokers had significantly increased odds of poor 90-day functional outcomes independent of other statistically significant predictor variables ( adjusted odds ratio , 2.28 ; 95 % confidence interval , 1.15 - 4.55 ; P=0.019 ) . CONCLUSIONS In Japanese men , smoking leads to poor functional outcomes at 3 months after acute atherothrombotic stroke An association between passive smoking and stroke is unclear in China , particularly the association with hemorrhagic stroke . This study included 16205 deaths due to stroke aged ≥30 years and 16205 non-stroke controls r and omly selected and frequency-matched to cases on gender and age . Smoking of spouses , defined as ≥1 cigarette per day for up to 1 year , was taken as a measure of exposure to passive smoking of subjects that was retrospectively ascertained by interviewing surviving spouses . After adjustment for variables , passive smoking increased the risk of death by 10 % ( odds ratio ( OR ) , 1.10 ; 95 % confidence interval ( CI ) , 1.05–1.16 ) for all strokes , by 10 % ( OR , 1.10 ; 95 % CI , 1.04–1.16 ) for hemorrhagic stroke , and by 12 % ( OR , 1.12 ; 95 % CI , 1.03–1.23 ) for ischemic stroke , compared with non-exposure . This finding was highly consistent in men or women and in smokers or non-smokers , and was generally consistent among zones of China despite geographic diversity . The risk significantly increased with exposure-years and quantity of cigarettes smoked daily by spouses . This study indicated that passive smoking is associated with deaths from all-type strokes . It is highly advisable for the government to promote strong tobacco prevention and cessation programs and smoke-free environments We aim ed to investigate the impact of smoking status on clinical severity in patients with ischemic stroke event ( IS ) . Patients were prospect ively identified among residents of the city of Dijon , France ( ca . 151,000 inhabitants ) , using a population -based registry , between 2006 and 2011 . Demographic and clinical data were recorded . The initial clinical severity was quantified by the means of the National Institutes of Health Stroke Scale ( NIHSS ) . Multivariable ordinal logistic regression was used to assess the effect of smoking status on severity . Among the 1,056 recorded patients with IS , data about smoking status were available for 973 ( 92.1 % ) , of whom 658 ( 67.3 % ) were non-smokers , 187 ( 19.2 % ) were current smokers , and 128 ( 13.2 % ) were former smokers . Compared with non-smoking , former smoking was associated with less severe IS ( OR 0.55 ; 95 % CI 0.38 - 0.82 , p = 0.003 ) , whereas this association was not found for current smokers ( OR 0.97 ; 95 % CI 0.69 - 1.36 , p = 0.856 ) . Further work is needed to underst and the underlying mechanisms of this finding BACKGROUND Few prospect i ve studies have investigated the relationship between spousal cigarette smoking and the risk of incident stroke . METHODS Stroke-free participants in the U.S.-based Health and Retirement Study ( HRS ) aged > or=50 years and married at baseline ( n=16,225 ) were followed , on average , 9.1 years between 1992 and 2006 ) for proxy or self-report of first stroke  ( 1,130 events ) . Participants were stratified by gender and own smoking status ( never-smokers , former smokers , or current smokers ) , and the relationship assessed between the spouse 's smoking status and the risk of incident stroke . Analyses were conducted in 2007 with Cox proportional hazards models . All models were adjusted for age ; race ; Hispanic ethnicity ; Southern birthstate ; parental education ; paternal occupation class ; years of education ; baseline income ; baseline wealth ; obesity ; overweight ; alcohol use ; and diagnosed hypertension , diabetes , or heart disease . RESULTS Having a spouse who currently smoked was associated with an increased risk of first stroke among never-smokers ( hazard ratio=1.42 , 95 % CI=1.05 , 1.93 ) and former smokers ( hazard ratio=1.72 , 95 % CI=1.33 , 2.22 ) . Former smokers married to current smokers had a stroke risk similar to respondents who themselves smoked . CONCLUSIONS Spousal smoking poses important stroke risks for never-smokers and former smokers . The health benefits of quitting smoking likely extend to both the individual smoker and his or her spouse BACKGROUND AND PURPOSE Active smokers with myocardial infa rct ion were shown to have enhanced benefit with clopidogrel compared with aspirin . Whether this " paradox " exists in ischemic stroke patients is unknown . We aim ed to investigate whether smoking status has a differential impact on the efficacy of clopidogrel vs. aspirin in patients with non-cardioembolic strokes . METHODS This single-center study retrospectively assessed 1792 non-cardioembolic ischemic stroke patients discharged from January 2013 to October 2014 , and followed for 12months . Patients were categorized as current-smokers and never-smokers . Primary outcome was a composite of secondary ischemic stroke , myocardial infa rct ion and all-cause death . Secondary outcome was secondary ischemic stroke . RESULTS 1066 patients were current-smokers and 726 were never-smokers . Compared with never-smokers , current-smokers had significantly higher rates of ischemic stroke ( 4.3 % vs. 1.2 % ; adjusted OR : 3.60 , 95%CI : 1.50 - 8.64 , p=0.004 ) . Regarding the primary outcome , among smokers , rates showed a lower trend in clopidogrel vs. aspirin groups ( 3.7 % vs. 6.4 % ; adjusted OR 0.57 , 95%CI : 0.31 - 1.07 , p=0.08 ) , but no difference among never-smokers ( 2.1 % vs. 1.0 % ; adjusted OR : 1.67 , 95%CI : 0.47 - 5.89 , p=0.42 ) . Similarly , among smokers , trending lower rates for recurrent ischemic stroke were observed in clopidogrel vs. aspirin group ( 3.1 % vs. 5.0 % ; adjusted OR : 0.60 , 95%CI : 0.31 - 1.18 , p=0.14 ) ; but no difference between the two groups among never-smokers ( 1.7 % vs. 1.0 % ; adjusted OR 1.36 , 95%CI : 0.36 - 5.52 , p=0.65 ) . CONCLUSIONS Smoking is a major risk factor for recurrent stroke in our retrospective non-cardioembolic ischemic stroke cohort . Active-smokers trend toward better cardiovascular outcomes when on clopidogrel . This finding needs to be confirmed in a prospect i ve cohort Diet may influence the risk of ischemic stroke by several mechanisms . A potential and hitherto unknown mechanism may relate to an effect on the lipophilic index , which is a new and convenient indicator of membrane fluidity . This study investigated the association between the adipose tissue lipophilic index and ischemic stroke and its subtypes . A case-cohort study was conducted based on the Danish cohort study Diet , Cancer , and Health , which includes 57,053 subjects aged 50–64 years at enrolment . A subcohort ( n = 3500 ) was r and omly drawn from the whole cohort . All ischemic stroke cases were vali date d and categorized into subtypes . The lipophilic index was calculated based on fatty acid profiles in adipose tissue . Subjects were divided into quintiles and a weighted Cox proportional hazards regression model was used to calculate hazard ratios . After appropriate exclusions , a subcohort of 3194 subjects and 1752 cases of ischemic stroke were included . When comparing the fifth quintile of the lipophilic index with the first quintile , the hazard ratio for ischemic stroke was 0 
    Output:
    
This meta- analysis showed that smoking was not a protective factor for poor prognosis of IS .