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Background and Purpose— Although believed to be transient and self-limiting, new-onset perioperative/postoperative atrial fibrillation (POAF) might be a risk factor for stroke and mortality. We conducted a systematic review and meta-analysis to qualitatively and quantitatively evaluate the relationship of POAF with early and late risks of mortality and stroke. Methods— We searched Pubmed, EMBASE, and Cochrane Library (1966 through March 2018) to identify cohort studies that reported stroke and mortality associated with POAF. We computed a random-effects estimate based on the Mantel-Haenszel method. Odds ratios with 95% CI were used as a measure of the association between POAF and early (in-hospital or within 30 days of surgery) stroke and mortality, while hazard ratios (HR) were used for long-term outcomes. Results— Our analysis included 35 studies with 2 458 010 patients. Pooling the results from the random-effects model showed that POAF was associated with increased risks of early stroke (odds ratio, 1.62; 95% CI, 1.47–1.80), early mortality (odds ratios, 1.44; 95% CI, 1.11–1.88), long-term stroke (HR, 1.37; 95% CI, 1.07–1.77), and long-term mortality (HR, 1.37; 95% CI, 1.27–1.49). Analyses focusing on high-quality studies obtained similar results. In subgroup analyses, POAF was more strongly associated with stroke in patients undergoing noncardiac surgery (HR, 2.00; 95% CI, 1.70–2.35) than in patients undergoing cardiac surgery (HR, 1.20; 95% CI, 1.07–1.34). Conclusions— New-onset POAF is associated with an increased risk of stroke and mortality, both in the short-term and long-term. The best strategy to reduce stroke risk among these patients needs to be determined.

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IMPORTANCE Use of low-dose aspirin for the primary prevention of cardiovascular events remains controversial because increased risk of bleeding may offset the overall benefit. Among major bleeding events, intracranial hemorrhage is associated with high mortality rates and functional dependency. OBJECTIVE To assess the risk of intracranial hemorrhage associated with low-dose aspirin among individuals without symptomatic cardiovascular disease. DATA SOURCES PubMed, Embase, the Cochrane Central Register of Controlled Trials, and ClinicalTrials.gov were searched from January 1966 to October 30, 2018. STUDY SELECTION Randomized clinical trials that compared low-dose aspirin (daily dose Յ100 mg) vs control and recorded the end points of intracranial hemorrhage separately for active treatment and control groups were included. DATA EXTRACTION AND SYNTHESIS A random-effect estimate was computed based on the Mantel-Haenszel method. Relative risk with 95% CI was used as a measure of aspirin vs control on risk of intracranial hemorrhage. MAIN OUTCOMES AND MEASURES The main outcomes were any intracranial hemorrhage, intracerebral hemorrhage, subdural or extradural hemorrhage, and subarachnoid hemorrhage, for aspirin vs control. RESULTS The search identified 13 randomized clinical trials of low-dose aspirin use for primary prevention, enrolling 134 446 patients. Pooling the results from the random-effects model showed that low-dose aspirin, compared with control, was associated with an increased risk of any intracranial bleeding (8 trials; relative risk, 1.37; 95% CI, 1.13-1.66; 2 additional intracranial hemorrhages in 1000 people), with potentially the greatest relative risk increase for subdural or extradural hemorrhage (4 trials; relative risk, 1.53; 95% CI, 1.08-2.18) and less for intracerebral hemorrhage and subarachnoid hemorrhage. Patient baseline features associated with heightened risk of intracerebral hemorrhage with low-dose aspirin, compared with control, were Asian race/ethnicity and low body mass index. CONCLUSIONS AND RELEVANCE Among people without symptomatic cardiovascular disease, use of low-dose aspirin was associated with an overall increased risk of intracranial hemorrhage, and heightened risk of intracerebral hemorrhage for those of Asian race/ethnicity or people with a low body mass index.

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Background and PurposeAdditional folic acid (FA) treatment appears to have a neutral effect on reducing vascular risk in countries that mandate FA fortification of food (e.g., USA and Canada). However, it is uncertain whether FA therapy reduces stroke risk in countries without FA food fortification. The purpose of this study was to comprehensively evaluate the efficacy of FA therapy on stroke prevention in countries without FA food fortification. MethodsPubMed, EMBASE, and clinicaltrials.gov from January 1966 to August 2016 were searched to identify relevant studies. Relative risk (RR) with 95% confidence interval (CI) was used as a measure of the association between FA supplementation and risk of stroke, after pooling data across trials in a random-effects model. ResultsThe search identified 13 randomized controlled trials (RCTs) involving treatment with FA that had enrolled 65,812 participants, all of which stroke was reported as an outcome measure. After all 13 RCTs were pooled, FA therapy versus control was associated with a lower risk of any future stroke (RR, 0.85; 95% CI, 0.77 to 0.95). FA alone or combination of FA and minimal cyanocobalamin (≤0.05 mg/day) was associated with a lower risk of future stroke (RR, 0.75; 95% CI, 0.66 to 0.86) whereas combination of FA and cyanocobalamin (≥0.4 mg/day) was not associated with a lower risk of future stroke (RR, 0.95; 95% CI, 0.86 to 1.05). ConclusionsFA supplement reduced stroke in countries without mandatory FA food fortification. The benefit was found mostly in patients receiving FA alone or combination of FA and minimal cyanocobalamin.

C ognitive impairment is a major contributor to disability and dependence worldwide. Globally, stroke is the leading cause of long-term disability among adults and the second leading cause of death.1 The high cumulative risk of dementia or stroke or both conditions has been shown by the Framingham study, 2 and the urgent need to improve knowledge regarding cognition and vascular conditions has been emphasized in a specific meeting providing harmonized standards. 3Beyond their personal tolls, both of these conditions carry substantial social and economic burdens. These conditions also correlate strongly with increasing age. Given the projected substantial rise in the number of older people around the world, prevalence rates of cognitive impairment and stroke are expected to soar over the next several decades, especially in high-income countries. 4,5 Shared pathophysiologic mechanisms seem to exist between cognitive impairment and cerebrovascular disease.6 Indeed, risk factors for stroke (hypertension, hyperlipidemia, diabetes, obesity and physical inactivity) have been shown to play a role in the onset and progression of cognitive impairment, 7 and it is well established that stroke itself increases the risk of future cognitive impairment. 8 However, whether cognitive impairment increases the risk of future stroke remains unclear. Early identification and regular surveillance for cognitive impairment could potentially enable prompt initiation of treatment aimed at not only potentially limiting further deterioration of cognitive function (if mild), but also possibly reducing the risk of future stroke through timely and optimal control of risk factors.Several published studies have assessed the association between cognitive impairment and subsequent risk of stroke, but the results have not been consistent. We performed a systematic review and meta-analysis to determine the qualitative and quantitative association between baseline cognitive impairment and risk of future stroke. Methods Search strategyOur search strategy was based on the recommendations of the Meta-analysis of Observational Studies in Epidemiology group. 9 We searched MEDLINE via PubMed (1966 to November Background: Several studies have assessed the link between cognitive impairment and risk of future stroke, but results have been inconsistent. We conducted a systematic review and meta-analysis of cohort studies to determine the association between cognitive impairment and risk of future stroke.