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Abstract Background Inflammation and inflammatory biomarkers play an important role in atherosclerosis and cardiovascular disease. Little information is available, however, on time course of serum markers of inflammation after stroke. Methods First ischemic stroke patients ≥40 years old had levels of high-sensitivity C-reactive protein (hsCRP), serum amyloid A (SAA), and fibrinogen measured in plasma samples drawn at 1, 2, 3, 7, 14, 21 and 28 days after stroke. Levels were log-transformed as needed, and parametric and non-parametric statistical tests were used to test for evidence of a trend in levels over time. Levels of hsCRP and SAA were also compared with levels in a comparable population of stroke-free participants. Results Mean age of participants with repeated measures (n = 21) was 65.6 ± 11.6 years, and 13 (61.9%) were men, and 15 (71.4%) were Hispanic. Approximately 75% of patients (n = 15) had mild strokes (NIH Stroke Scale score 0–5). There was no evidence of a time trend in levels of hsCRP, SAA, or fibrinogen for any of the markers during the 28 days of follow-up. Mean log(hsCRP) was 1.67 ± 1.07 mg/L (median hsCRP 6.48 mg/L) among stroke participants and 1.00 ± 1.18 mg/L (median 2.82 mg/L) in a group of 1176 randomly selected stroke-free participants from the same community (p = 0.0252). Conclusion Levels of hsCRP are higher in stroke patients than in stroke-free subjects. Levels of inflammatory biomarkers associated with atherosclerosis, including hsCRP, appear to be stable for at least 28 days after first ischemic stroke.

Background: Lipoprotein-associated phospholipase A2 (LpPLA2) levels are associated with stroke, though whether this extends to all populations and stroke subtypes is unknown. Methods: Serum samples from stroke-free community participants in the Northern Manhattan Study were assayed for LpPLA2 mass and activity. Participants were followed annually for stroke. Cox-proportional-hazard models were fitted to estimate hazard-ratios and 95% confidence intervals (HR, 95% CI) for the association of LpPLA2 levels with ischemic stroke (IS), after adjusting for demographic and medical risk factors. Results: Serum samples were available in 1946 participants, of whom 151 (7.8%) experienced a first IS during median follow-up 11 years. Mean age was 69 (SD 10), 35.6% were men, 20% non-Hispanic Whites, 22% non-Hispanic Blacks, and 55% Hispanics. LpPLA2 mass and activity levels were not associated with overall IS risk. LpPLA2 mass but not activity levels were associated with strokes due to large artery atherosclerosis (LAA; adjusted HR per SD 1.55, 95% CI 1.17–2.04). There was a dose-response relationship with LAA (compared to first quartile, 2nd quartile HR = 1.43, 95% CI 0.23–8.64; 3rd quartile HR = 4.47, 95% CI 0.93–21.54; 4th quartile HR = 5.07, 95% CI 1.07–24.06). The associations between LpPLA2-mass and LAA-stroke risk differed by race-ethnicity (p = 0.01); LpPLA2-mass was associated with increased risk of LAA among non-Hispanic Whites (adjusted HR per SD 1.44, 95% CI 0.98–2.11), but not other race-ethnic groups. Conclusion: LpPLA2-mass levels were associated with risk of atherosclerotic stroke among non-Hispanic White participants, but not in other race-ethnic groups in the cohort. Further study is needed to confirm these race-ethnic differences and the reasons for them. [ABSTRACT FROM AUTHOR]

Background: Interleukin 6 (IL-6) is an inflammatory cytokine that has been associated with vascular disease and cognitive impairment, but few studies have examined these relationships in population-based studies that include Hispanic and Black people who often have a greater prevalence of vascular risk factors and are at an elevated risk of dementia than Whites. We examined relative elevations of plasma IL-6 concentrations in relation to cognitive decline in a stroke-free racially/ethnically diverse community-based sample from Northern Manhattan. Methods: We used mixed effects models to measure the effect of IL-6 on change in performance on the modified Telephone Interview for Cognitive Status (TICS-m) measured annually in our cohort, adjusting for sociodemographic and vascular risk factors. Results: There were 1,224 participants with IL-6 levels (median 1.5 pg/ml, interquartile range 0.83-2.57 pg/ml) and TICS-m data available (mean = 31.6 points, SD 6.5). The mean age was 71 (SD 9.3; 64% women, 59% Hispanic, 19% Black, 19% White) with 3,406 person-years and a median 3.0 years of follow-up (interquartile range 1.1-4.0 years). Participants with IL-6 levels above the median showed greater cognitive decline on the TICS-m compared to those with levels below the median, adjusting for sociodemographic and vascular factors (β = -0.17 points/year, p = 0.02). Decline on the TICS-m among participants with IL-6 above the median differed by age (p for interaction <0.001). There was no interaction by race/ethnicity, vascular risk factors, C-reactive protein, apolipoprotein ε4 allele status, or the metabolic syndrome among nondiabetics. Conclusions: IL-6 associated with cognitive decline among older participants in this racially/ethnically diverse sample independent of other vascular risk factors and C-reactive protein. Copyright © 2013 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Recent studies have suggested that poor quality and diminished quantity of sleep may be independently linked to vascular events although prospective and multiethnic studies are limited. This study aimed to explore the relationship between daytime sleepiness and the risk of ischemic stroke and vascular events in an elderly, multiethnic prospective cohort.Methods and Results: As part of the Northern Manhattan Study, the Epworth Sleepiness Scale was collected during the 2004 annual follow-up. Daytime sleepiness was trichotomized using previously reported cut points of no dozing, some dozing, and significant dozing. Subjects were followed annually for a mean of 5.1 years. Cox proportional hazards models were used to calculate hazard ratios and 95% confidence intervals for stroke, myocardial infarction, and death outcomes. We obtained the Epworth Sleepiness Scale on 2088 community residents. The mean age was 73.5 ± 9.3 years; 64% were women; 17% were white, 20% black, 60% Hispanic, and 3% were other. Over 44% of the cohort reported no daytime dozing, 47% some dozing, and 9% significant daytime dozing. Compared with those reporting no daytime dozing, individuals reporting significant dozing had an increased risk of ischemic stroke (hazard ratio, 2.74 [95% confidence interval, 1.38-5.43]), all stroke (3.00 [1.57-5.73]), the combination of ischemic stroke, myocardial infarction, and vascular death (2.38 [1.50-3.78]), and all vascular events (2.48 [1.57-3.91]), after adjusting for medical comorbidities.Conclusions: Daytime sleepiness is an independent risk factor for stroke and other vascular events. These findings suggest the importance of screening for sleep problems at the primary care level. [ABSTRACT FROM AUTHOR]

Background and Purpose. Residing in "disadvantaged" communities may increase morbidity and mortality independent of individual social resources and biological factors. This study evaluates the impact of population-level disadvantage on incident ischemic stroke likelihood in a multiethnic urban population. Methods. A population based case-control study was conducted in an ethnically diverse community of New York. First ischemic stroke cases and community controls were enrolled and a stroke risk assessment performed. Data regarding population level economic indicators for each census tract was assembled using geocoding. Census variables were also grouped together to define a broader measure of collective disadvantage. We evaluated the likelihood of stroke for population-level variables controlling for individual social (education, social isolation, and insurance) and vascular risk factors. Results. We age-, sex-, and race-ethnicity-matched 687 incident ischemic stroke cases to 1153 community controls. The mean age was 69 years: 60% women; 22% white, 28% black, and 50% Hispanic. After adjustment, the index of community level disadvantage (OR 2.0, 95% CI 1.7-2.1) was associated with increased stroke likelihood overall and among all three raceethnic groups. Conclusion. Social inequalities measured by census tract data including indices of community disadvantage confer a significant likelihood of ischemic stroke independent of conventional risk factors. [ABSTRACT FROM AUTHOR]