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Physical inactivity is an important and modifiable cardiovascular disease risk factor. Little is known about the social determinants of physical inactivity in older, urban-dwelling populations. We collected socio-demographic and medical risk factor information and physical activity questionnaires in the Northern Manhattan Study. Logistic regression models were constructed to examine whether measures of social isolation, race-ethnicity, and sex were associated with physical inactivity. Physical inactivity was present in 40.5% of the cohort. In multivariable models adjusted for medical comorbidities, Hispanic race-ethnicity (compared to non-Hispanic white) was associated with higher odds of physical inactivity (OR 2.18, 95% CI 1.78, 2.67), while women were more likely to be inactive than men (OR 1.33, 95% CI 1.15, 1.54). Having Medicaid/being uninsured (OR 1.20, 95% CI 1.02, 1.42), and having fewer than 3 friends (1.41, 95% CI 1.15, 1.72) were also associated with physical inactivity. Physical inactivity is common, particularly in Hispanics, women, and those who are socially isolated. Public health interventions aimed at increasing physical activity in these more sedentary groups are required. [ABSTRACT FROM AUTHOR]

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]

Objectives To examine the association between successful aging without subsequent cognitive decline ( SA- ND) and the Northern Manhattan Study ( NOMAS) global vascular risk score ( GVRS), which is predictive of stroke, myocardial infarction, and vascular death. Design Prospective cohort study. Setting A stroke-free sample of Hispanic, black, and white participants living in the same community enrolled in a magnetic resonance imaging ( MRI) substudy of NOMAS, a population-based prospective cohort study. Participants One thousand two hundred ninety individuals in whom a cognitive screen was administered at baseline and at enrollment in the MRI substudy. Measurements SA- ND was based on disease, disability, and cognitive function. The GVRS includes age, sex, race and ethnicity, waist circumference, alcohol intake, smoking, physical activity, blood pressure, antihypertensive medication use, fasting blood sugar, lipid levels, and peripheral vascular disease. Results Data at baseline and follow-up were available for 1,162 participants (mean age 70 ± 9; 61% women; 13% white, 16% black, 69% Hispanic; mean GVRS 8.6 ± 0.9). Logistic regression, adjusted for education, socioeconomic status, and follow-up time, showed that the odds of SA- ND were 38% greater for each additional 1-point decrease on the GVRS (odds ratio = 1.38, 95% confidence interval = 1.17-1.61; P < .001). An inverse dose-response was observed between quartiles of GVRS and SA- ND. Greater diastolic blood pressure in participants taking antihypertensive medication and a history of claudication ( P = .003) or peripheral arterial disease ( P < .001) were inversely associated with SA- ND in the fully adjusted model. Conclusion Potentially modifiable vascular risk factors were independently associated with SA- ND in a multiethnic community-based sample. Improvements in GVRSs could help promote healthy longevity in the aging population. [ABSTRACT FROM AUTHOR]

Abstract: Purpose: There are limited data on vascular predictors of long-term disability in Hispanics. We hypothesized that (1) functional status declines over time and (2) vascular risk factors predict functional decline. Methods: The Northern Manhattan Study contains a population-based study of 3298 stroke-free individuals aged 40 years or older, followed for median 11 years. The Barthel Index (BI) was assessed annually. Generalized estimating equations and Cox models were adjusted for demographic, medical, and social risk factors. Stroke and myocardial infarction occurring during follow-up were censored in sensitivity analysis. Secondarily, motor and nonmotor domains of the BI were analyzed. Results: Mean age (standard deviation) of the cohort (n = 3298) was 69.2 (10) years, 37% were male, 52% Hispanic, 22% diabetic, and 74% hypertensive. There was a mean annual decline of 1.02 BI points (P < .0001). Predictors of decline in BI included age, female sex, diabetes, depression, and normocholesterolemia. Results did not change with censoring. We found similar predictors of BI for motor and nonmotor domains. Conclusion: In this large, population-based, multiethnic study with long-term follow-up, we found a 1% mean decline in function per year that did not change when vascular events were censored. Diabetes predicted functional decline in the absence of clinical vascular events. [Copyright &y& Elsevier]

Purpose: Prior studies have reported that Hispanics have lower cardiovascular disease (CVD) mortality despite a higher burden of risk factors. We examined whether Hispanic ethnicity was associated with a lower risk of nonfatal myocardial infarction (MI) coronary death (CD) and vascular death. Methods: A total of 2671 participants in the Northern Manhattan Study without clinical CVD were prospectively evaluated. Cox models were used to calculate hazard ratios (HR) and 95% confidence intervals (CI) for the association of race–ethnicity with nonfatal MI, CD, and vascular death after adjusting for demographic and CVD risk factors. Results: Mean age was 68.8 (10.4) years; 52.8% were Hispanic (88% Caribbean-Hispanic). Hispanics were more likely to have hypertension (73.1% vs. 62.2%, p < .001) and diabetes (22.0% vs. 13.3%, p < .001), and less likely to perform any physical activity (50.1% vs. 69.2%, p < .001) compared to non-Hispanic whites (NHW). During a mean 10 years of follow-up there were 154 nonfatal MIs, 186 CD, and 386 vascular deaths. In fully adjusted models, Hispanics had a lower risk of CD (adjusted HR = 0.36, 95% CI: 0.21–0.60), and vascular death (adjusted HR = 0.62, 95% CI: 0.43–0.89), but not nonfatal MI (adjusted HR = 0.95, 95% CI: 0.56–1.60) when compared to NHW. Conclusions: We found a “Hispanic paradox” for coronary and vascular deaths, but not nonfatal MI. [Copyright &y& Elsevier]

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]

Abstract: Objective: Serum levels of the soluble Receptor for Advanced Glycation End-products (sRAGE) have been associated with risk of cardiovascular disease. We hypothesized that sRAGE levels are associated with subclinical cerebrovascular disease in an ethnically diverse population. Methods: Clinically stroke-free participants in the multi-ethnic Northern Manhattan Study (NOMAS) underwent brain MRI to quantify subclinical brain infarcts (SBI) and white matter hyperintensity volume (WMHV) (n =1102). Serum levels of sRAGE were measured by ELISA. Logistic and multiple linear regression were employed to estimate associations of sRAGE with SBI and WMHV, after adjusting for demographics and vascular risk factors. Results: Median sRAGE levels were significantly lower in Hispanics (891.9pg/ml; n =708) and non-Hispanic blacks (757.4pg/ml; n =197) than in non-Hispanic whites (1120.5pg/ml; n =170), and these differences remained after adjusting for other risk factors. Interactions were observed by race-ethnicity between sRAGE levels and MRI measurements, including for SBI in Hispanics (p =0.04) and WMHV among blacks (p =0.03). In Hispanics, increasing sRAGE levels were associated with a lower odds of SBI, with those in the upper sRAGE quartile displaying a 50% lower odds of SBI after adjusting for sociodemographic and vascular risk factors (p =0.05). Among blacks, those in the upper quartile of sRAGE had a similarly reduced increased risk of SBI (p =0.06) and greater WMHV (p =0.04). Conclusion: Compared to whites, Hispanics and blacks have significantly lower sRAGE levels, and these levels were associated with more subclinical brain disease. Taken together, these findings suggest sRAGE levels may be significantly influence by ethnicity. Further studies of sRAGE and stroke risk, particularly in minorities, are warranted. [Copyright &y& Elsevier]

Context: Elevated lipoprotein(a) [Lp(a)] is associated with ischemic stroke (IS) among Whites, but data is sparse for non-White populations. Objective: Using a population-based case-control study design with subjects from the Northern Manhattan Stroke Study, we assessed whether Lp(a) levels were independently associated with IS risk among Whites, Blacks and Hispanics. Design and Setting: Lp(a) levels were measured in 317 IS cases (mean age 69 ± 13 years; 56% women; 16% Whites, 31% Blacks and 52% Hispanics) and 413 community-based controls, matched by age, race/ethnicity and gender. In-person assessments included demographics, socioeconomic status, presence of vascular risk factors and fasting lipid levels. Logistic regression was used to determine the independent association of Lp(a) and IS. Stratified analyses investigated gender and race/ethnic differences. Results: Mean Lp(a) levels were greater among cases than controls (46.3 ± 41.0 vs. 38.9 ± 38.2 mg/dl; p < 0.01). After adjusting for stroke risk factors (hypertension, diabetes mellitus, coronary artery disease, cigarette smoking), lipid levels, and socioeconomic status, Lp(a) levels ≥30 mg/dl were independently associated with an increased stroke risk in the overall cohort (adjusted odds ratio, OR, 1.8, 95% confidence interval, CI, 1.20–2.6; p = 0.004). There was a significant linear dose-response relationship between Lp(a) levels and IS risk. The association between IS risk and Lp(a) ≥30 mg/dl was more pronounced among men (adjusted OR 2.0, 95% CI 1.1–3.5; p = 0.02) and among Blacks (adjusted OR 2.7, 95% CI 1.2–6.2; p = 0.02). Conclusion: Elevated Lp(a) levels were significantly and independently associated with increased stroke risk, suggesting that Lp(a) is a risk factor for IS across White, Black and Hispanic race/ethnic groups. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background Arterial stiffness, an intermediate pre-clinical marker of atherosclerosis, has been associated with an increased risk of stroke and cardiovascular disease. The metabolic syndrome and its components are established cardiovascular disease risk factors and may also increase arterial stiffness; however, data regarding this are limited. Aim The goal of this study was to determine the association between the metabolic syndrome and carotid artery stiffness in an elderly multi-ethnic cohort. Methods Carotid artery stiffness was assessed by carotid ultrasound as part of the Northern Manhattan Study, a prospective population-based cohort of stroke-free individuals. Carotid artery stiffness was calculated as [ln(systolic BP/diastolic BP)/strain], where strain was [(systolic diameter−diastolic diameter)/diastolic diameter]. Metabolic syndrome was defined by the National Cholesterol Education Program: Adult Treatment Panel III criteria. LogSTIFF was analysed as the dependent variable in linear regression models, adjusting for demographics, education, current smoking, presence of carotid plaque and intima–media thickness. Results Carotid artery stiffness was analysed in 1133 Northern Manhattan Study subjects (mean age 65 ± 9 years; 61% women; 58% Hispanic, 22% Black and 20% Caucasian). The prevalence of the metabolic syndrome was 49%. The mean LogSTIFF was 2·01 ± 0·61 among those with the metabolic syndrome and 1·90 ± 0·59 among those without the metabolic syndrome ( P=0·003). The metabolic syndrome was significantly associated with increased logSTIFF in the final adjusted model (parameter estimate β=0·100, P=0·01). Among individual metabolic syndrome components, waist circumference and elevated blood pressure were most significantly associated with a mean increase in logSTIFF ( P<0·01). Conclusion The metabolic syndrome is significantly associated with increased carotid artery stiffness in a multiethnic population. Increased carotid artery stiffness may, in part, explain a high risk of stroke among individuals with the metabolic syndrome. [ABSTRACT FROM AUTHOR]

Abstract: Background: Tissue plasminogen activator (tPA), the only approved treatment for acute ischemic stroke (IS), is significantly underutilized likely due to poor lay information about stroke as an emergency. In order to improve outcomes in acute IS, it is critical to raise awareness and recognition of stroke symptoms particularly among minority populations. This manuscript describes the application of a stroke preparedness behavioral intervention and includes baseline information in a multi-ethnic population of stroke and transient ischemic attack (TIA) survivors. Methods: In the Stroke Warning Information and Faster Treatment Study (SWIFT), we prospectively identified, and randomized IS and TIA patients to determine efficacy of a culturally tailored interactive stroke preparedness strategy. Data collected at baseline included acute stroke parameters, stroke knowledge, severity, social resources and vascular risk assessment. Results: Of the 736 enrolled to date, 76% were IS and 24% TIA events. The cohort was 51% female: 45% Hispanic, 26% White and 25% Black. Over 75% reported hypertension, 36% diabetes, and 16% cardiac disease. Mean time from onset to emergency department (ED) arrival was 46h (median 13h) differing significantly between Whites (mean 52h, median 11h) and Blacks (mean 52h, median 17h) versus Hispanics (mean 39h, median 11h). Knowledge that a stroke occurs in the brain differed significantly by between Whites (85%), Blacks (64%), Hispanics (66%, p <0.000). Conclusions: Disparities remain in both action and knowledge surrounding acute stroke. Use of written information has not proven an effective means of changing health behaviors. We propose an interactive culturally tailored intervention to address behavioral change in acute stroke. [Copyright &y& Elsevier]

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]

Background: Mass levels of lipoprotein-associated phospholipase A2 (Lp-PLA2), a leukocyte-derived enzyme involved in the metabolism of low-density lipoprotein to pro-inflammatory mediators, are associated with prognosis after stroke. Lp-PLA2 mass correlates only moderately with levels of Lp-PLA2 activity. The relationship of Lp-PLA2 activity to risk of stroke recurrence is unknown. We hypothesized that Lp-PLA2 activity levels would predict risk of recurrence. Methods: In the population-based Northern Manhattan Stroke Study, first ischemic stroke patients ≥40 years were followed for recurrent stroke. Levels of Lp-PLA2 activity were assessed in 467 patients, and categorized by quartile. Cox proportional hazard models were used to calculate hazard ratios (HR) and 95% confidence intervals (95% CI) for risk of recurrent stroke associated with marker quartiles after adjusting for demographics, vascular risk factors, and high-sensitivity C-reactive protein (hsCRP). Results: Mean age was 68.9 ± 12.7 years; 54.6% were women; 53.3% Hispanic, 27.2% black, and 17.8% white. Median follow-up was 4.0 years, and there were 80 recurrent strokes. Compared to the lowest quartile of Lp-PLA2 activity, those in the highest had an increased risk of recurrent stroke (adjusted HR 2.54, 95% CI 1.01–6.39). Conclusion: Stroke patients withLp-PLA2 activity levels in the highest quartile, compared to those in the lowest quartile, had an increased risk of recurrence after first ischemic stroke. Further studies are warranted to determine whether this biomarker has clinical utility in determining high-risk populations of stroke survivors, and whether anti-inflammatory strategies that reduce levels of activity of Lp-PLA2 reduce the risk of stroke recurrence. Copyright © 2008 S. Karger AG, Basel [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 >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]

The article discusses a study investigating the relationship of inflammatory markers C-reactive protein (CRP) and lipoprotein-associated phospholipase A2 (Lp-PLA2) with ischemic stroke. The results showed that high-sensitivity CRP, but not Lp-PLA2, was associated with stroke severity. After adjusting for confounding factors, CRP was found to be associated with risk of death but not risk of recurrent stroke or myocardial infarction.

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]

The association of apolipoproteins A-I and B (apo A-I and apo B) with cardiovascular disease has been studied in younger populations, but there is sparse information in the elderly. We determined whether apo A-I and apo B were associated with carotid artery atherosclerosis (CAA) in 507 stroke-free elderly community residents (mean age 70.1±11.7 years, 60% women, 41% Hispanics, 30% African American, 28% Caucasian). CAA severity was normal (no plaque or carotid stenosis) in 39%, mild (maximum plaque thickness &les;1.8 mm or carotid stenosis <40%) in 25%, and moderate/severe (maximum plaque thickness >1.8 mm or carotid stenosis &ges;40%) in 36%. CAA severity increased with age in all race/ethnic groups (P<0.01). CAA was similar among African Americans and Caucasians, but less in Hispanics (age adjusted OR: 0.5, CI: 0.4–0.8). apo A-I <1.2 g/l (OR: 2.0, CI: 1.0–3.3) and apo B &ges;1.4 g/l (OR: 2.0, CI: 1.1–3.6) were associated with moderate–severe CAA. An apo B/apo A-I ratio &ges;1 was associated with moderate–severe CAA (OR: 2.4, CI: 1.3–4.4), and the association varied by race (Hispanics OR: 4.3, CI: 1.8–10; non-Hispanics, OR: 1.4, CI: 0.6–3.2). Total cholesterol, triglycerides and low density lipoprotein cholesterol were not associated with moderate–severe CAA, while high density lipoprotein cholesterol was protective (OR: 0.4, CI: 0.2–0.8). Thus, in an elderly population, apo A-I and B were determinants of moderate–severe CAA, and the degree of association varied by race/ethnicity [Copyright &y& Elsevier]

Presents a study to evaluate the association between high-density lipoprotein cholesterol (HDL-C) and ischemic stroke in an elderly, multiethnic population. Analysis of data from the Northern Manhattan Stroke Study; Methods; Results; Evidence that high levels of HDL-C were associated with a reduced risk of ischemic stroke; Conclusion.

Presents research which studied the relationship between moderate alcohol consumption and ischemic stroke. Consumption protective for coronary heart disease; Design; Setting; Patients and participants; Main outcome measure; Consumption protective for stroke after adjustments; Protective effect according to groups; Increased risk of stroke for those consuming seven or more drinks per day; Conclusion.