Procalcitonin and Midregional Proatrial Natriuretic Peptide as Markers of Ischemic Stroke: The Northern Manhattan Study.

BACKGROUND AND PURPOSE: Chronic infections and neuroendocrine dysfunction may be risk factors for ischemic stroke (IS). We hypothesized that selected blood biomarkers of infection (procalcitonin [PCT]), hypothalamic-pituitary-axis function (copeptin), and hemodynamic dysfunction (midregional proatrial natriuretic peptide [MRproANP]) are associated with incident IS risk in the multiethnic, urban Northern Manhattan Study (NOMAS) cohort. METHODS: A nested case-control study was performed among initially stroke-free participants. Cases were defined as first IS (n=172). We randomly selected controls among those who did not develop an event (n=344). We calculated Cox proportional hazards models with inverse probability weighting to estimate the association of blood biomarkers with risk of stroke after adjusting for demographic, behavioral, and medical risk factors. RESULTS: Those with PCT and MRproANP, but not copeptin, in the top quartile, compared with the lowest quartile, were associated with IS (for PCT adjusted hazard ratio [HR], 1.9; 95% confidence interval [CI], 1.0-3.8 and for MRproANP adjusted HR, 3.5; 95% CI, 1.6-7.5). The associations of PCT and MRproANP differed by stroke etiology; PCT levels in the top quartile were particularly associated with small vessel stroke (adjusted HR, 5.1; 95% CI, 1.4-18.7) and MRproANP levels with cardioembolic stroke (adjusted HR, 16.3; 95% CI, 3.7-70.9). CONCLUSIONS: Higher levels of PCT, a marker of infection, and MRproANP, a marker for hemodynamic stress, were independently associated with IS risk. PCT was specifically associated with small vessel and MRproANP with cardioembolic stroke risk. Further study is needed to validate these biomarkers and determine their significance in stroke risk prediction and prevention.

High-sensitivity C-reactive protein and interleukin-6-dominant inflammation and ischemic stroke risk: the northern Manhattan study.

BACKGROUND AND PURPOSE: Interleukin-6 (IL-6) is a proinflammatory cytokine with known autoregulatory feedback mechanisms. We hypothesized that elevated high-sensitivity C-reactive protein (hsCRP) relative to IL-6 confers an increased risk of ischemic stroke (IS), and low hsCRP relative to IL-6 a decreased risk, for individuals in the prospective, multiethnic, population-based Northern Manhattan Study (NOMAS). METHODS: Serum hsCRP and IL-6 were measured in NOMAS participants at baseline. We created a trichotomized predictor based on the dominant biomarker in terms of quartiles: hsCRP-dominant, IL-6-dominant, and codominant groups. Cox proportional hazards models were used to calculate hazard ratios and 95% confidence intervals for the association between inflammatory biomarker group status and risk of incident IS. RESULTS: Of 3298 participants, both hsCRP and IL-6 were available in 1656 participants (mean follow-up, 7.8 years; 113 incident IS). The hsCRP-dominant group had increased risk of IS (adjusted hazard ratio, 2.62; 95% confidence interval, 1.56-4.41) and the IL-6-dominant group had decreased risk (adjusted hazard ratio, 0.38; 95% confidence interval, 0.18-0.82) when compared with the referent group, after adjusting for potential confounders. Model fit was improved using the inflammation-dominant construct, over either biomarker alone. CONCLUSIONS: In this multiethnic cohort, when hsCRP-quartile was higher than IL-6 quartile, IS risk was increased, and conversely when IL-6 quartiles were elevated relative to hsCRP, IS risk was decreased. Construct validity requires confirmation in other cohorts.

Diabetes predicts long-term disability in an elderly urban cohort: the Northern Manhattan Study.

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.

Lipoprotein-associated phospholipase A2 is associated with atherosclerotic stroke risk: the Northern Manhattan Study.

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.

Association between northern Manhattan study global vascular risk score and successful aging.

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.

Interleukin 6 plasma concentration associates with cognitive decline: the northern Manhattan study.

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 (ß = -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.

Daytime sleepiness and risk of stroke and vascular disease: findings from the Northern Manhattan Study (NOMAS).

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.

Trajectory of functional decline before and after ischemic stroke: the Northern Manhattan Study.

BACKGROUND AND PURPOSE: Previous research in our cohort showed a delayed decline in functional status after first ischemic stroke. We compared the long-term trajectory of functional status before and after ischemic stroke. METHODS: The Northern Manhattan Study contains a prospective, population-based study of stroke-free individuals age ≥40 years, followed for a median of 11 years. The Barthel index (BI), a commonly used measure of activities of daily living, was assessed annually. Generalized estimating equations were used to assess functional decline over time before stroke and beginning 6 months after stroke. Follow-up was censored at the time of recurrent stroke. RESULTS: Among 3298 participants, 210 participants had an ischemic stroke during follow-up and had poststroke BI assessed. Mean age (±SD) was 77±9 years, 38% were men, 52% were Hispanic, 37% had diabetes, and 31% had coronary artery disease. There was no difference in rate of functional decline over time before and after stroke (P=0.51), with a decline of 0.96 BI points per year before stroke (P<0.0001) and 1.24 BI points after stroke (P=0.001). However, when stratified by insurance status, among those with Medicaid or no insurance, in a fully adjusted model, there was a difference in slope before and after stroke (P=0.04), with a decline of 0.58 BI points per year before stroke (P=0.02) and 1.94 BI points after stroke (P=0.001). CONCLUSIONS: In this large, prospective, population-based study with long-term follow-up, there was a significantly steeper decline in functional status after ischemic stroke compared with before stroke among those with Medicaid or no insurance, after adjusting for confounders.

Coronary death and myocardial infarction among Hispanics in the Northern Manhattan Study: exploring the Hispanic paradox.

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.

Duration of diabetes and risk of ischemic stroke: the Northern Manhattan Study.

BACKGROUND AND PURPOSE: Diabetes increases stroke risk, but whether diabetes status immediately before stroke improves prediction and whether duration is important are less clear. We hypothesized that diabetes duration independently predicts ischemic stroke. METHODS: Among 3298 stroke-free participants in the Northern Manhattan Study, baseline diabetes and age at diagnosis were determined. Incident diabetes was assessed annually (median, 9 years). Cox proportional hazard models were used to estimate hazard ratios (HR) and 95% CI for incident ischemic stroke using baseline diabetes, diabetes as a time-dependent covariate, and duration of diabetes as a time-varying covariate; models were adjusted for demographic and cardiovascular risk factors. RESULTS: Mean age was 69 ± 10 years (52% Hispanic, 21% white, and 24% black); 22% had diabetes at baseline and 10% had development of diabetes. There were 244 ischemic strokes, and both baseline diabetes (HR, 2.5; 95% CI, 1.9-3.3) and diabetes considered as a time-dependent covariate (HR, 2.4; 95% CI, 1.8-3.2) were similarly associated with stroke risk. Duration of diabetes was associated with ischemic stroke (adjusted HR, 1.03 per year with diabetes; 95% CI, 1.02-1.04). Compared to nondiabetic participants, those with diabetes for 0 to 5 years (adjusted HR, 1.7; 95% CI, 1.1-2.7), 5 to 10 years (adjusted HR, 1.8; 95% CI, 1.1-3.0), and ≥ 10 years (adjusted HR, 3.2; 95% CI, 2.4-4.5) were at increased risk. CONCLUSIONS: Duration of diabetes is independently associated with ischemic stroke risk adjusting for risk factors. The risk increases 3% each year, and triples with diabetes ≥ 10 years.

The metabolic syndrome and cognitive performance: the Northern Manhattan Study.

BACKGROUND: The metabolic syndrome (MetS) is a risk factor for diabetes, stroke, myocardial infarction, and increased mortality, and has been associated with cognition in some populations. We hypothesized that MetS would be associated with lower Mini-Mental State Examination (MMSE) scores in a multi-ethnic population, and that MetS is a better predictor of cognition than its individual components or diabetes. METHODS: We conducted a cross-sectional analysis among 3,150 stroke-free participants. MetS was defined by the modified National Cholesterol Education Program guidelines-Adult Treatment Panel III (NCEP-ATPIII) criteria. Linear regression and polytomous logistic regression estimated the association between MMSE score and MetS, its individual components, diabetes, and inflammatory biomarkers. RESULTS: MetS was inversely associated with MMSE score (unadjusted ß = -0.67; 95% CI -0.92, -0.41). Adjusting for potential confounders, MetS was associated with lower MMSE score (adjusted ß = -0.24; 95% CI -0.47, -0.01), but its individual components and diabetes were not. Those with MetS were more likely to have an MMSE score of <18 than a score of ≥ 24 (adjusted OR = 1.94; 95% CI 1.26, 3.01). There was an interaction between MetS and race-ethnicity, such that MetS was associated with lower MMSE score among non-Hispanic whites and Hispanics but not non-Hispanic blacks. CONCLUSIONS: MetS was associated with lower cognition in a multi-ethnic population. Further studies of the effect of MetS on cognition are warranted, and should account for demographic differences.

Perception of recurrent stroke risk among black, white and Hispanic ischemic stroke and transient ischemic attack survivors: the SWIFT study.

OBJECTIVES: Risk modification through behavior change is critical for primary and secondary stroke prevention. Theories of health behavior identify perceived risk as an important component to facilitate behavior change; however, little is known about perceived risk of vascular events among stroke survivors. METHODS: The SWIFT (Stroke Warning Information and Faster Treatment) study includes a prospective population-based ethnically diverse cohort of ischemic stroke and transient ischemic attack survivors. We investigate the baseline relationship between demographics, health beliefs, and knowledge on risk perception. Regression models examined predictors of inaccurate perception. RESULTS: Only 20% accurately estimated risk, 10% of the participants underestimated risk, and 70% of the 817 study participants significantly overestimated their risk for a recurrent stroke. The mean perceived likelihood of recurrent ischemic stroke in the next 10 years was 51 ± 7%. We found no significant differences by race-ethnicity with regard to accurate estimation of risk. Inaccurate estimation of risk was associated with attitudes and beliefs [worry (p < 0.04), fatalism (p < 0.07)] and memory problems (p < 0.01), but not history or knowledge of vascular risk factors. CONCLUSION: This paper provides a unique perspective on how factors such as belief systems influence risk perception in a diverse population at high stroke risk. There is a need for future research on how risk perception can inform primary and secondary stroke prevention.

The inclusion of stroke in risk stratification for primary prevention of vascular events: the Northern Manhattan Study.

BACKGROUND AND PURPOSE: The Framingham coronary heart disease (CHD) risk score estimates 10-year risk of myocardial infarction (MI) and CHD death. Because preventive approaches to CHD and stroke are similar, a composite outcome may be more appropriate. We compared 10-year risk of (1) MI or CHD death; and (2) stroke, MI, or CHD death among individuals free of vascular disease. METHODS: The Northern Manhattan Study contains a prospective, population-based study of stroke- and CHD-free individuals≥40 years of age followed for a median of 10 years for vascular events. Framingham coronary heart disease risk score was calculated for each individual and for each category of predicted risk, Kaplan-Meier observed 10-year cumulative probabilities were calculated for (1) MI or CHD death; and (2) stroke, MI, or CHD death. The cumulative probability of (1) was subtracted from (2), and 95% CIs for the difference were obtained with 1000 bootstrap samples. Using stratified analyses by race-ethnicity, we compared risk differences among race-ethnic groups. RESULTS: Among 2613 participants (53% Hispanic, 25% non-Hispanic black, and 20% non-Hispanic white), observed 10-year risk of MI or CHD death was 14.20%. With stroke in the outcome, observed risk was 21.98% (absolute risk difference, 7.78%; 95% CI, 5.86% to 9.75%). The absolute risk difference among blacks was significantly larger than among whites (P=0.01). CONCLUSIONS: In this multiethnic urban population, adding stroke to the risk stratification outcome cluster resulted in a 55% relative increase in estimated risk and crossing of the absolute risk threshold (>20% over 10 years) considered for preventive treatments such as statins.

Race-ethnic differences in the association between lipid profile components and risk of myocardial infarction: The Northern Manhattan Study.

OBJECTIVE: The aim of this study was to explore race-ethnic differences in the association between plasma lipid components and risk of incident myocardial infarction (MI). DESIGN/METHODS: As part of the Northern Manhattan Study, 2,738 community residents without cardiovascular disease were prospectively evaluated. Baseline fasting blood samples were collected, and lipid panel components were analyzed as continuous and categorical variables. Cox proportional hazards models were used to calculate HRs and 95% CIs for incident MI after adjusting for demographic and cardiovascular risk factors. RESULTS: The mean age was 68.8 ± 10.4 years; 36.7% were men. Of the participants, 19.9% were non-Hispanic white; 24.9%, non-Hispanic black; and 52.8%, Hispanic (>80% from the Caribbean). Hispanics had lower mean high-density lipoprotein cholesterol (HDL-C) and higher triglycerides (TG)/HDL-C. During a mean 8.9 years of follow-up, there were 163 incident MIs. In the whole cohort, all lipid profile components were associated with risk of MI in the expected directions. However, HDL-C (adjusted HR per 10 mg/dL increase 0.93, 95% CI 0.76-1.12) and TG/HDL-C >2 (adjusted HR 0.89, 95% CI 0.51-1.55) were not predictive of MI among Hispanics but were predictive among non-Hispanic blacks and whites. Triglycerides/HDL-C per unit increase was associated with an 8% higher risk of MI among Hispanics (adjusted HR 1.08, 95% CI 1.04-1.12). CONCLUSIONS: In Hispanics, low HDL-C and TG/HDL-C >2 were not associated with MI risk. Our data suggest that a different TG/HDL ratio cutoff may be needed among Hispanics to predict MI risk.

Association of serum soluble receptor for advanced glycation end-products with subclinical cerebrovascular disease: the Northern Manhattan Study (NOMAS).

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 (891.9 pg/ml; n = 708) and non-Hispanic blacks (757.4 pg/ml; n = 197) than in non-Hispanic whites (1120.5 pg/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.

Social network types and acute stroke preparedness behavior.

OBJECTIVES: Presence of informal social networks has been associated with favorable health and behaviors, but whether different types of social networks impact on different health outcomes remains largely unknown. We examined the associations of different social network types (marital dyad, household, friendship, and informal community networks) with acute stroke preparedness behavior. We hypothesized that marital dyad best matched the required tasks and is the most effective network type for this behavior. METHODS: We collected in-person interview and medical record data for 1,077 adults diagnosed with stroke and transient ischemic attack. We used logistic regression analyses to examine the association of each social network with arrival at the emergency department (ED) within 3 h of stroke symptoms. RESULTS: Adjusting for age, race-ethnicity, education, gender, transportation type to ED and vascular diagnosis, being married or living with a partner was significantly associated with early arrival at the ED (odds ratio = 2.0, 95% confidence interval: 1.2-3.1), but no significant univariate or multivariate associations were observed for household, friendship, and community networks. CONCLUSIONS: The marital/partnership dyad is the most influential type of social network for stroke preparedness behavior.

Insulin resistance and risk of ischemic stroke among nondiabetic individuals from the northern Manhattan study.

BACKGROUND: Whether insulin resistance predicts ischemic stroke (IS) is still a matter of debate. OBJECTIVE: To determine the association between insulin resistance (IR) and risk of first ischemic stroke in a large, multiethnic, stroke-free cohort without diabetes. DESIGN: Prospective, population-based cohort study. SETTING: Longitudinal epidemiologic study. PARTICIPANTS: A cohort of 1509 nondiabetic participants from the Northern Manhattan Study (mean [SD] age, 11 [10] years; 64.2% women; 58.9% Hispanics). MAIN OUTCOME MEASURES: Insulin sensitivity, expressed by the homeostasis model assessment (HOMA) of insulin sensitivity (HOMA index = [fasting insulin × fasting glucose] / 22.5). Insulin resistance was defined by a HOMA-IR index in the top quartile (Q4). Cox proportional hazards models were used to determine the effect of HOMA-IR on the risk of incident IS, myocardial infarction (MI), vascular death, and combined outcomes (IS, MI, and vascular death). RESULTS: The mean (SD) HOMA-IR was 2.3 (2.1), and Q4 was at least 2.8. During mean follow-up of 8.5 years, vascular events occurred in 180 participants; 46 had fatal or nonfatal IS, 45 had fatal or nonfatal MI, and 121 died of vascular causes. The HOMA-IR Q4 vs less than Q4 significantly predicted the risk of IS only (adjusted hazard ratio, 2.83; 95% confidence interval, 1.34-5.99) but not other vascular events. This effect was independent of sex, race/ethnicity, traditional vascular risk factors, and metabolic syndrome and its components. CONCLUSIONS: Insulin resistance estimated using the HOMA is a marker of increased risk of incident stroke in nondiabetic individuals. These findings emphasize the need to better characterize individuals at increased risk for IS and the potential role of primary preventive therapies targeted at IR.

Early depressed mood after stroke predicts long-term disability: the Northern Manhattan Stroke Study (NOMASS).

BACKGROUND AND PURPOSE: Depression is highly prevalent after stroke and may influence recovery. We aimed to determine whether depressed mood acutely after stroke predicts subsequent disability and mortality. METHODS: As part of the Northern Manhattan Stroke Study, a population-based incident stroke case follow-up study performed in a multiethnic urban population, participants were asked about depressed mood within 7 to 10 days after stroke. Participants were followed every 6 months the first 2 years and yearly thereafter for 5 years for death and disability measured by the Barthel Index. We fitted polytomous logistic regression models using a canonical link to examine the association between depressed mood after stroke and disability comparing moderate (Barthel Index 60 to 95) and severe (Barthel Index <60) disability with no disability (Barthel Index >or=95). Cox proportional hazards models were created to examine the association between depressed mood and mortality. RESULTS: A question about depressed mood within 7 to 10 days after stroke was asked in 340 of 655 patients with ischemic stroke enrolled, and 139 reported that they felt depressed. In multivariate analyses controlling for sociodemographic factors, stroke severity, and medical conditions, depressed mood was associated with a greater odds of severe disability compared with no disability at 1 (OR 2.91, 95% CI 1.07 to 7.91) and 2 years (OR 3.72, 95% CI 1.29 to 10.71) after stroke. Depressed mood was not associated with all-cause mortality or vascular death. CONCLUSIONS: Depressed mood after stroke is associated with disability but not mortality after stroke. Early screening and intervention for mood disorders after stroke may improve outcomes and requires further research.

Increased stroke risk and lipoprotein(a) in a multiethnic community: the Northern Manhattan Stroke Study.

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 > or =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) > or =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.

Metabolic syndrome increases carotid artery stiffness: the Northern Manhattan Study.

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 beta=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.