Background The link between daily changes in ambient fine particulate matter air pollution (PM2.5) and cardiovascular morbidity and mortality is well established. Whether PM2.5 at levels below current US National Ambient Air Quality Standards also increases the risk of ischemic stroke remains uncertain. Methods We reviewed the medical records of 1705 Boston-area patients hospitalized with neurologist-confirmed ischemic stroke and abstracted data on the time of symptom onset and clinical characteristics. PM2.5 concentrations were measured at a central monitoring station. We used the time-stratified case-crossover study design to assess the association between the risk of ischemic stroke onset and PM2.5 levels in the hours and days preceding each event. We examined whether the association with PM2.5 differed by ischemic stroke etiology and patient characteristics. Results The estimated odds ratio of ischemic stroke onset was 1.34 (95% confidence interval (CI): 1.13, 1.58; p<0.001) following a 24-hour period classified as “moderate” (PM2.5 15–40 μg/m3) by the US Environmental Protection Agency’s (EPA) Air Quality Index compared to a 24-hour period classified as “good” (≤15 μg/m3). Considering PM2.5 as a continuous variable, the estimated odds ratio of ischemic stroke onset was 1.11 (95% CI: 1.03, 1.20; p=0.006) per interquartile range increase in PM2.5 (6.4 μg/m3). The increase in risk was greatest within 12–14 hours of exposure to PM2.5 and was most strongly associated with markers of traffic-related pollution. Conclusion These results suggest that exposure to PM2.5 levels considered generally safe by the US EPA increase the risk of ischemic stroke onset within hours of exposure.

Irrespective of the side of the ischemia, post-acute stroke patients showed a parasympathetic cardiac deficit. Additionally, sympathetic cardiovascular modulation was increased in patients after right-sided stroke. Post-acute stroke patients might be at an increased risk for cardiac arrhythmia after unopposed sympathetic stimulation.

Background: Among patients with acute ischemic stroke, impaired kidney function has been shown to increase the mortality risk, but the shape of this relationship has not been evaluated in detail. Methods: We estimated the glomerular filtration rate (eGFR) at the time of hospitalization in 1,175 consecutive patients hospitalized with acute ischemic stroke at the Beth Israel Deaconess Medical Center and examined the shape of the association between eGFR and all-cause mortality. Results: There were 508 deaths during a median follow-up of 40.3 months, resulting in a ‘U’-shaped relationship between eGFR and all-cause mortality. The curve was relatively flat between 75 and 110 ml/min/1.73 m² but increased sharply at lower and higher levels of eGFR (test for nonlinearity: p < 0.0001). Conclusions: Among patients with acute ischemic stroke, a reduced or highly elevated eGFR at hospital admission is associated with a higher mortality rate compared to patients with moderate levels of eGFR.

Background and Purpose-Previous research suggests that regular heavy alcohol consumption increases the risk for ischemic stroke, whereas frequent light to moderate alcohol intake may decrease the risk. However, the risk of ischemic stroke associated with transient exposure to alcohol remains unclear. In this study, we used a case-crossover approach to test the hypothesis that alcohol consumption affects the acute risk of ischemic stroke, to determine the length of time between alcohol intake and the onset of symptoms (induction time), and to examine whether the risk varies by the type of alcohol. Methods-In this multicenter study, we interviewed 390 patients (209 men, 181 women) between January 2001 and November 2006 (median 3 days after stroke). Alcohol consumption in the hour before stroke symptoms was compared with its expected frequency based on the usual frequency of alcohol consumption over the prior year. Results-Of the 390 patients, 248 (64%) reported alcohol consumption in the prior year, 104 within 24 hours and 14 within 1 hour of stroke onset. The relative risk of stroke in the hour after consuming alcohol was 2.3 (95% CI, 1.4 to 4.0; Pϭ0.002). The relative risks were similar for different types of alcoholic beverages and when the sample was restricted to those who were not simultaneously exposed to other potential triggers. Conclusions-The risk of stroke onset is transiently elevated in the hour after alcohol ingestion. (Stroke. 2010;41:1845-1849.) Key Words: alcohol Ⅲ case-crossover Ⅲ cerebrovascular disorders Ⅲ epidemiology Ⅲ stroke M oderate 1 and high 2-4 intakes of alcohol have been documented to have acute potentially deleterious physiological effects within hours after consumption, including impaired fibrinolysis 2,3 and increased platelet activation, 4 blood pressure, and heart rate. 1 On the other hand, moderate consumption of alcohol has been associated with protective effects within hours, 5-7 weeks, 8 -12 or years, 13-15 including enhanced fibrinolytic activity 7,8 and improvements in lipid profile, 12 inflammatory markers, 8,11 flow-mediated vasodilatation, 5,6 soluble vascular adhesion molecules, 11,14 insulin sensitivity, 9,15 and adipokines. 9,14 However, only a few studies 16 -18 have examined the risk of ischemic stroke associated with transient exposure to alcohol.In this study, we used a case-crossover approach to test the hypothesis that alcohol consumption affects the acute risk of ischemic stroke, to determine the length of time between alcohol intake and the onset of symptoms (induction time), and to examine whether the risk varies by the type of alcohol. Methods Study PopulationThe were interviewed a median of 3 days (range, 0 to 14 days) after sustaining an acute ischemic stroke. Research staff identified eligible patients by reviewing admission logs and charts of patients admitted to each hospital's stroke service. Additionally, patients with new onset of an acute neurological syndrome compatible with stroke were screened on admission to emergency departments. Presumed ...

Background: Epidemiologic studies linking ambient air pollution to the onset of acute cardiovascular events often rely on date of hospital admission for exposure assessment. Methods: We investigated the extent of exposure misclassification resulting from assigning exposure to PM2.5 based on 1) date of hospital admission, or 2) time of hospital presentation compared to PM2.5 exposure based on time of stroke symptom onset. We performed computer simulations to evaluate the impact of this source of exposure misclassification on estimates of air pollution health effects in the context of a time-stratified case-crossover study. Results: Among 1101 patients admitted for a confirmed acute ischemic stroke to a Boston area hospital, symptom onset occurred a median of 1 calendar day before hospital admission (range = 0 – 30 days). The difference between ambient PM2.5 exposure based on the calendar day of admission versus time of symptom onset ranged from −47 to 36 μg/m3 (−0.1 ± 7.1 μg/m3; mean ± standard deviation). The simulation study indicated that for nonnull associations, exposure assessment based on hospitalization date led to estimates that were biased toward the null by 60%–66%, whereas assessment based on time of hospital presentation yielded estimates that were biased toward the null by 37%–42%. Conclusions: Epidemiologic studies of air pollution-related risk of acute cardiovascular events that assess exposure based on date of hospitalization likely underestimate the strength of associations. Using data on time of hospital presentation would marginally attenuate, but not eliminate, this important source of bias.

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Heart failure is characterized by sodium and fluid retention, sympathetic overactivity, parasympathetic withdrawal, vasoconstrictor activation and cytokine elevation. Current treatment for acute heart failure consists of vasodilators, diuretics and inotropes. Nesiritide (human B-type natriuretic peptide) is a promising new class of drugs that has been given to almost 1,000 patients in numerous clinical investigations. The clinical development of nesiritide included dosing studies (utilizing repetitive boluses, continuous infusions, or a combination of bolus plus infusion), pivotal efficacy trials, and comparative safety studies, which have repeatedly demonstrated that intravenous nesiritide decreases pulmonary capillary wedge pressure, systemic vascular resistance, mean right atrial pressure and pulmonary artery pressure, while increasing cardiac index and stroke volume. Improvement in both clinical assessment and signs and symptoms of heart failure has been reported by patient and physician alike. Plasma levels of neurohormones and endothelin-1 are significantly reduced with nesiritide treatment. Compared with dobutamine, nesiritide is not proarrhythmic and does not affect heart rate. In comparison with intravenous nitroglycerin in the treatment of decompensated heart failure, nesiritide improves hemodynamics and symptomatology (dyspnea) faster and more effectively than nitroglycerin. Fewer patients receiving nesiritide reported any adverse event. Incidence of hypotension was comparable, but more intravenous nitroglycerin patients developed headache and abdominal pain. Current research supports an important role for the use of nesiritide in the treatment of decompensated heart failure.