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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 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]

Objectives: This study sought to improve global vascular risk prediction with behavioral and anthropometric factors.Background: Few cardiovascular risk models are designed to predict the global vascular risk of myocardial infarction, stroke, or vascular death in multiethnic individuals, and existing schemes do not fully include behavioral risk factors.Methods: A randomly derived, population-based, prospective cohort of 2,737 community participants free of stroke and coronary artery disease was followed up annually for a median of 9.0 years in the NOMAS (Northern Manhattan Study) (mean age 69 years, 63.2% women, 52.7% Hispanic, 24.9% African American, and 19.9% white). A global vascular risk score (GVRS) predictive of stroke, myocardial infarction, or vascular death was developed by adding variables to the traditional Framingham cardiovascular variables based on the likelihood ratio criteria. Model utility was assessed through receiver-operating characteristics, calibration, and effect on reclassification of subjects.Results: Variables that significantly added to the traditional Framingham profile included waist circumference, alcohol consumption, and physical activity. Continuous measures for blood pressure and fasting blood sugar were used instead of hypertension and diabetes. Ten-year event-free probabilities were 0.95 for the first quartile of GVRS, 0.89 for the second quartile, 0.79 for the third quartile, and 0.56 for the fourth quartile. The addition of behavioral factors in our model improved prediction of 10-year event rates compared with a model restricted to the traditional variables.Conclusions: A GVRS that combines traditional, behavioral, and anthropometric risk factors; uses continuous variables for physiological parameters; and is applicable to nonwhite subjects could improve primary prevention strategies. [ABSTRACT FROM AUTHOR]

Objectives: This study sought to improve global vascular risk prediction with behavioral and anthropometric factors. Background: Few cardiovascular risk models are designed to predict the global vascular risk of myocardial infarction, stroke, or vascular death in multiethnic individuals, and existing schemes do not fully include behavioral risk factors. Methods: A randomly derived, population-based, prospective cohort of 2,737 community participants free of stroke and coronary artery disease was followed up annually for a median of 9.0 years in the NOMAS (Northern Manhattan Study) (mean age 69 years, 63.2% women, 52.7% Hispanic, 24.9% African American, and 19.9% white). A global vascular risk score (GVRS) predictive of stroke, myocardial infarction, or vascular death was developed by adding variables to the traditional Framingham cardiovascular variables based on the likelihood ratio criteria. Model utility was assessed through receiver-operating characteristics, calibration, and effect on reclassification of subjects. Results: Variables that significantly added to the traditional Framingham profile included waist circumference, alcohol consumption, and physical activity. Continuous measures for blood pressure and fasting blood sugar were used instead of hypertension and diabetes. Ten-year event-free probabilities were 0.95 for the first quartile of GVRS, 0.89 for the second quartile, 0.79 for the third quartile, and 0.56 for the fourth quartile. The addition of behavioral factors in our model improved prediction of 10-year event rates compared with a model restricted to the traditional variables. Conclusions: A GVRS that combines traditional, behavioral, and anthropometric risk factors; uses continuous variables for physiological parameters; and is applicable to nonwhite subjects could improve primary prevention strategies. [Copyright &y& Elsevier]

Objective: There is insufficient randomized trial data to support evidence-based recommendations for tight control of fasting blood glucose (FBG) among diabetic subjects in primary stroke prevention. We explored the relationship between FBG among diabetic subjects and risk of ischemic stroke in a multiethnic prospective cohort.Research Design and Methods: Medical and social data and FBG values were collected for 3,298 stroke-free community residents: mean age +/- SD was 69 +/-10 years; 63% were women, 21% were white, 24% were black, and 53% were Hispanic; and follow-up was 6.5 years. Baseline FBG levels were categorized: 1) elevated FBG: history of diabetes and FBG >or=126 mg/dl (7.0 mmol/l); 2) target FBG: history of diabetes and FBG <126 mg/dl (7.0 mmol/l); or 3) no diabetes/reference group. Cox models were used to calculate hazard ratios (HRs) and 95% CI for ischemic stroke and vascular events.Results: In the Northern Manhattan Study, 572 participants reported a history of diabetes and 59% (n = 338) had elevated FBG. Elevated FBG among diabetic subjects was associated with female sex (P < 0.04), Medicaid (P = 0.01), or no insurance (P = 0.03). We detected 190 ischemic strokes and 585 vascular events. Diabetic subjects with elevated FBG (HR 2.7 [95% CI 2.0-3.8]) were at increased risk of stroke, but those with target FBG levels (1.2 [0.7-2.1]) were not, even after adjustment. A similar relationship existed for vascular events: elevated FBG (2.0 [1.6-2.5]) and target FBG (1.3 [0.9-1.8].Conclusions: This prospective cohort study provides evidence for the benefits of tighter glucose control for primary stroke prevention. [ABSTRACT FROM AUTHOR]

OBJECTIVE -- There is insufficient randomized trial data to support evidence-based recommendations for tight control of fasting blood glucose (FBG) among diabetic subjects in primary stroke prevention. We explored the relationship between FBG among diabetic subjects and risk of ischemic stroke in a multiethnic prospective cohort. RESEARCH DESIGN AND METHODS -- Medical and social data and FBG values were collected for 3,298 stroke-free community residents: mean age ± SD was 69 ± 10 years; 63% were women, 21% were white, 24% were black, and 53% were Hispanic; and follow-up was 6.5 years. Baseline FBG levels were categorized: 1) elevated FBG: history of diabetes and FBG ≥ 126 mg/dl (7.0 mmol/l); 2) target FBG: history of diabetes and FBG < 126 mg/dl (7.0 mmol/l); or 3) no diabetes/reference group. Cox models were used to calculate hazard ratios (HRs) and 95% CI for ischemic stroke and vascular events. RESULTS -- In the Northern Manhattan Study, 572 participants reported a history of diabetes and 59% (n = 338) had elevated FBG. Elevated FBG among diabetic subjects was associated with female sex (P < 0.04), Medicaid (P = 0.01), or no insurance (P = 0.03). We detected 190 ischemic strokes and 585 vascular events. Diabetic subjects with elevated FBG (HR 2.7 [95% CI 2.0-3.8]) were at increased risk of stroke, but those with target FBG levels (1.2 [0.7-2.11) were not, even after adjustment. A similar relationship existed for vascular events: elevated FBG (2.0 [1.6-2.5]) and target FBG (1.3 [0.9-1.8]. CONCLUSIONS-- This prospective cohort study provides evidence for the benefits of tighter glucose control for primary stroke prevention. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]