The safety of intravenous thrombolysis (IVT) in patients with acute ischemic stroke over age 80 is unclear. We hypothesized that patients over age 80 can be safely treated with IVT.
Admission and discharge data were collected on all patients at a single tertiary care center presenting within 12 hours of onset. Collected data included treatment with IVT, demographics, pre-treatment National Institutes of Health Stroke Scale (NIHSS) score, length of stay (LOS), mortality and discharge disposition. Analyses were restricted to patients over age 80, and the primary outcome was in-hospital mortality. Logistic regression was used to examine whether IVT was associated with mortality.
Between 1/1/05 and 6/30/10, 112 patients over age 80 presented within 3 hours of ischemic stroke onset, and 31 received IVT. There were 15 deaths. In multi-variable models adjusted for age, sex, race-ethnicity and NIHSS, treatment with IVT compared to no treatment, was not associated with in-hospital death (adjusted OR 1.2, 95% confidence interval 0.3 – 4.3).
Treating ischemic stroke patients over 80 with IVT was not associated with an increase in mortality in an urban tertiary care center.
To examine the association between a Mediterranean-style diet (MeDi) and brain MRI white matter hyperintensities (WMH). The MeDi has previously been associated with a reduced risk of cardiovascular morbidity, possibly including stroke. A greater understanding of modifiable risk factors for small vessel damage may facilitate the prevention of stroke and cognitive decline.
A cross-sectional analysis within a longitudinal population-based cohort study. A semi-quantitative food frequency questionnaire was administered and a score (range 0-9) was calculated to reflect increasing similarity to the MeDi pattern.
The Northern Manhattan Study.
1,091 participants, of which 966 had dietary information (mean age 72, 59% women, 65% Hispanic, 16% White, 17% Black).
Main outcome measures
WMH volume was measured by quantitative brain MRI. Linear regression models were constructed to examine the relation between the MeDi score and the log-transformed WMH volume as a proportion of total cranial volume, controlling for sociodemographic and vascular risk factors.
On the MeDi scale, 12% scored 0-2, 16 scored 3, 23% scored 4, 23% scored 5, 26% scored 6-9. Each 1-point increase in MeDi score was associated with a lower log WMH volume (β=-0.04, p=0.02). The only MeDi score component that was an independent predictor of WMH volume was the ratio of monounsaturated to saturated fat (β=-0.20, p=0.001).
A Mediterranean-style diet was associated with a lower WMH burden, a marker of small vessel damage in the brain. However, white matter hyperintensities are etiologically heterogenous and can include neurodegeneration. Replication by other population-based studies is needed.
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.
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.
MetS was inversely associated with MMSE score (unadjusted β = −0.67; 95% CI −0.92, −0.41). Adjusting for potential confounders, MetS was associated with lower MMSE score (adjusted β = −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.
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.
Cognitive performance; Cognitive impairment; Vascular dementia; Vascular cognitive impairment; Cerebrovascular disorders; Metabolic syndrome
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.
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.
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.
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.
Copyright © 2011 S. Karger AG, Basel
Risk perception; Stroke knowledge; Health beliefs
Chronic infections, including periodontal infections, may predispose to cardiovascular disease. We investigated the relationship between periodontal microbiota and hypertension. Methods and Results: 653 dentate men and women with no history of stroke or myocardial infarction were enrolled in INVEST. We collected 4533 subgingival plaque samples (average of 7 samples/subject). These were quantitatively assessed for 11 periodontal bacteria using DNA-DNA checkerboard hybridization. Cardiovascular risk factor measurements were obtained. Blood pressure and hypertension (systolic blood pressure≥140 mmHg, diastolic blood pressure≥90 mmHg or taking antihypertensive medication, or self-reported history) were each regressed on the level of bacteria: (1) considered causative of periodontal disease (etiologic bacterial burden); (2) associated with periodontal disease (putative bacterial burden); (3) associated with periodontal health (health associated bacterial burden). All analyses were adjusted for age, race/ethnicity, gender, education, body mass index, smoking, diabetes, LDL and HDL cholesterol. Etiologic bacterial burden was positively associated with both blood pressure and prevalent hypertension. Comparing the highest vs. lowest tertiles of etiologic bacterial burden, SBP was 9 mmHg higher, DBP was 5 mmHg higher (p for linear trend <0.001 in each case), and the odds ratio for prevalent hypertension was 3.05 (95%CI:1.60,5.82) after multivariable adjustment.
Our data provide evidence of a direct relationship between the levels of subgingival periodontal bacteria and both systolic and diastolic blood pressure as well as hypertension prevalence.
infection; inflammation; hypertension; blood pressure; epidemiology; periodontitis
To explore race-ethnic differences in the relationship between plasma lipid components and risk of incident myocardial infarction (MI).
As part of the Northern Manhattan Study, 2738 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 hazard models were used to calculate hazard ratios (HR) and 95% confidence intervals (CI) for incident MI after adjusting for demographic and cardiovascular risk factors.
The mean age was 68.8±10.4 years; 36.7% men, 19.9% non-Hispanic white, 24.9% non-Hispanic black, and 52.8% Hispanic (over 80% from the Caribbean). Hispanics had lower mean HDL-C, and higher 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. TG/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).
In Hispanics, low HDL-C and TG/HDL-C>2 were not associated with MI risk. Our data suggests that a different TG/HDL ratio cutoff may be needed among Hispanics to predict MI risk.
Social isolation is associated with progression of cardiovascular disease with the most socially isolated patients being at increased risk. Increased left ventricular mass is a predictor of cardiovascular morbidity and mortality. It is not yet clear whether social isolation is a determinant of increased left ventricular mass.
We performed a cross-sectional study of Northern Manhattan Study participants who were free of clinical cardiovascular disease, had obtained transthoracic echocardiograms (n=2021) and a baseline questionnaire on social habits. Social isolation was defined as the lack of friendship networks (knowing fewer than 3 people well enough to visit within their homes). Echocardiographic left ventricular mass was indexed to height2.7, analyzed as a continuous variable and compared between exposure groups.
The prevalence of social isolation was 13.5%. The average left ventricular mass was significantly higher (50.2 gm/m2.7) in those who were, as compared to those who were not (47.6 gm/m2.7), socially isolated (p<0.05). Higher prevalence of social isolation was found among those less educated, uninsured or unemployed.There were no significant race-ethnic differences in the prevalence of social isolation. In multivariate analysis, there was a trend toward an association between social isolation and increased left ventricular mass in the total cohort (p=0.09). Among Hispanics, social isolation was significantly associated with greater left ventricular mass. Hispanics who were socially isolated averaged 3.9 gm/ht2.7 higher left ventricular mass compared to those not socially isolated (p=0.002). This relationship was not present among non-Hispanic blacks or whites.
In this urban tri-ethnic cohort, social isolation was prevalent and associated with indices of low socioeconomic status. Hispanics who were socially isolated had a greater risk for increased left ventricular mass.
social isolation; left ventricular mass; Hispanics; psychosocial factors
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.
Aim and Hypothesis
The goal of this study was to determine if individuals with coronary artery disease (CAD) and type 2 diabetes mellitus (T2DM) had greater endothelial dysfunction (ED) than individuals with only CAD.
Flow mediated dilation (FMD), calculated as percentage increase in brachial artery diameter in response to post-ischemic blood flow, was measured after an overnight fast in two cohorts. The first cohort included 76 participants in the Northern Manhattan Study (NOMAS) with CAD; 25 also had T2DM. The second cohort was composed of 27 individuals with both T2DM and CAD who were participants in a study of postprandial lipemia. Combined, we analyzed 103 patients with CAD; 52 with T2DM (T2DM+) and 51 without T2DM (T2DM−).
The 52 CAD T2DM+ subjects had a mean FMD of 3.9 ± 3.2%, while the 51 CAD T2DM− subjects had a greater mean FMD of 5.5 ± 4.0% (P<0.03). An investigating of various confounders known to affect FMD identified age and BMI as the only significant covariates in a multiple regression model. Adjusting for age and BMI, we found that FMD remained lower in T2DM+ subjects compared to T2DM− subjects (difference −1.99%, P<0.03).
In patients with CAD, the concomitant presence of T2DM is independently associated with greater ED, as measured by FMD. This finding may be relevant to the greater early and late morbidity and mortality observed in patients with both CAD and T2DM.
Diabetes; CAD; Endothelial Function; Flow-Mediated Dilation
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.
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 7–10 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 (BI). We fitted polytomous logistic regression models using canonical link to examine the association between depressed mood after stroke and disability, comparing moderate (BI 60–95) and severe (BI < 60) disability to no disability (BI ≥ 95). Cox-proportional hazards models were created to examine the association between depressed mood and mortality.
A question about depressed mood within 7–10 days after stroke was asked in 340 of 655 ischemic stroke patients enrolled, and 139 reported that they felt depressed. In multivariate analyses controlling for socio-demographic factors, stroke severity, and medical conditions, depressed mood was associated with a greater odds of severe disability compared to no disability at one (OR 2.91, 95% CI 1.07–7.91) and two years (OR 3.72, 95% CI 1.29–10.71) after stroke. Depressed mood was not associated with all cause mortality or vascular death.
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.
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.
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.
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.
The marital/partnership dyad is the most influential type of social network for stroke preparedness behavior.
Acute stroke; Emergency department admission; Ischemic attack; Social networks; Stroke symptoms
Background and Aims
Sleep disordered breathing (SDB) is a risk factor for stroke, but its association with subclinical atherosclerosis remains controversial. Snoring and insomnia are frequently co-morbid with SDB and may contribute to stroke. Data on the relationship between snoring and insomnia with atherosclerotic disease is sparse. We investigated the relationship between insomnia, snoring and carotid intima-media thickness (IMT), a marker of subclinical atherosclerosis, in the Northern Manhattan Study (NOMAS).
A group of 1,605 participants (mean age 65 ± 8 years; 40% men; 61% Hispanic, 19% black, 20% white) who had carotid IMT measurements performed was assessed for self-reported sleep habits. Habitual snoring was defined as self-reported snoring > 4 times per week. Presence of insomnia was based on three items extracted from the Hamilton Rating Scale for Depression. Carotid IMT was expressed as a mean composite measure of IMT in the carotid bifurcation, common and internal carotid artery. Multivariate linear regression models were used to identify associations between snoring, insomnia and carotid IMT.
Habitual snoring was present in 29% of the subjects and insomnia in 26%. There was a higher prevalence of self reported snoring (84%) and insomnia (66%) among Hispanics than non-Hispanics. The mean total carotid IMT was 0.95 ± 0.09 mm; among those with self reported snoring was 0.94 ± 0.09 mm; and among those with insomnia was 0.95 ± 0.08 mm. After controlling for age, sex, race-ethnicity, BMI and cardiovascular risk factors, snoring (p= 0.986) and insomnia (p= 0.829) were not significantly associated with increased carotid IMT.
Snoring and insomnia were not significantly associated with subclinical atherosclerosis in this population based community cohort.
sleep; snoring; insomnia; African American; Hispanic; Intima-Media Thickness; Risk factors; Sonography; Ultrasound
Elevated lipoprotein(a) [Lp(a)] is associated with ischemic stroke (IS) among Whites, but data is sparse for non-White populations.
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.
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).
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.
Lipoprotein(a); Northern Manhattan Stroke Study; Ischemic stroke
Increased left ventricular (LV) mass and endothelial dysfunction are important risk factors for cardiovascular mortality and morbidity. However, it is not clear whether endothelial dysfunction is associated with increased LV mass. We tested the hypothesis that impaired flow-mediated vasodilatation (FMD) is associated with increased LV mass in a population-based multi-ethnic cohort.
As a part of the Northern Manhattan Study, we performed two-dimensional echocardiography and FMD assessment during reactive hyperemia by high-resolution ultrasonography in 867 stroke-free community participants. LV mass was calculated according to an established method. LV hypertrophy was defined as the 90th percentile of sex-specific LV mass indexed for body surface area among normal subjects. Multivariable models were used to test the association of FMD with LV mass.
In multiple linear regression analyses adjusting for age, sex, body mass index, systolic blood pressure, antihypertensive medications, low-density lipoprotein cholesterol, diabetes, smoking, hematocrit, and race-ethnicity, FMD was inversely associated with LV mass (β = −1.21 ± 0.56, P = 0.03). The association persisted after further adjustment for any component of blood pressure (systolic, mean, and pulse pressure). In univariate logistic regression analysis, each 1% decrease in FMD was associated with a 8% higher risk of LV hypertrophy [odds ratio (OR) 1.08, 95% confidence interval (CI) 1.03–1.13 per each FMD point P< 0.01].
Impaired FMD is associated with LV mass, independent of other factors associated with increased LV mass. Endothelial dysfunction might be a potential risk factor for LV hypertrophy.
Prior studies suggest that the causes of calcific aortic valve (AV) disease involve chronic inflammation, lipoprotein levels, and calcium metabolism, all of which may differ among race-ethnic groups. We sought to determine whether AV thickness differs by race-ethnicity in a large multi-ethnic population-based cohort.
The Northern Manhattan Study (NOMAS) includes stroke-free community-based Hispanic (57%), non-Hispanic black (22%), and non-Hispanic white (21%) participants. The relation between AV thickness on transthoracic echocardiography and clinical risk factors for atherosclerosis was evaluated among 2085 participants using polytomous logistic regression models. AV thickness was graded in three categories (normal, mild, and moderate/severe) based on leaflet thickening and calcification.
Mild AV thickness was present in 44.4% and moderate/severe thickness in 5.7% of the cohort, with the lowest frequency of moderate/severe thickness seen particularly among Hispanic females. In multivariate models adjusting for age, sex, race-ethnicity, body mass index, hypertension, coronary artery disease, blood glucose, and high-density lipoprotein cholesterol, Hispanics had significantly less moderate/severe AV thickness (odds ratio (OR) 0.43, 95% confidence interval (95% CI) 0.25 to 0.73) than non-Hispanic whites. Men were almost 2-fold as likely to have moderate/severe AV thickness compared to women (OR 1.96, 95% CI 1.24 to 3.10).
In this large multi-ethnic population-based cohort, there were ethnic differences in the degree of AV thickness. Hispanic ethnicity was strongly protective against AV thickness. This effect was not related to traditional risk factors, suggesting that unmeasured factors related to Hispanic ethnicity and AV thickness may be responsible.
Background and Purpose
The objective of this study was to determine the relationship between chronic kidney disease (CKD), race–ethnicity, and vascular outcomes.
A prospective, multiracial cohort of 3298 stroke-free subjects with 6.5 years of mean follow-up time for vascular outcomes (stroke, myocardial infarction, vascular death) was used. Kidney function was estimated using serum creatinine and Cockcroft-Gault formula. Cox proportional hazards models were fitted to evaluate the relationship between kidney function and vascular outcomes.
In multivariate analysis, Cockcroft-Gault formula between 15 and 59 mL/min was associated with a significant 43% increased stroke risk in the overall cohort. Blacks with Cockcroft-Gault formula between 15 and 59 mL/min had significantly increased risk of both stroke (hazard ratio, 2.65; 95% CI, 1.47 to 4.77) and combined vascular outcomes (hazard ratio, 1.59; 95% CI, 1.10–2.92).
Chronic kidney disease is a significant risk factor for stroke and combined vascular events, especially in blacks.
cardiac; chronic kidney disease; epidemiology; outcome; risk factors; stroke
Common infections may be associated with stroke risk, though no single infection is likely a major independent predictor.
To determine the association between a composite measure of serologies to common infections (Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, Herpes Simplex Virus 1 and 2) and stroke risk in a prospective cohort study.
Prospective cohort followed longitudinally for median 8 years.
Randomly selected stroke-free participants from a multiethnic urban community.
Northern Manhattan Study (NOMAS).
Main Outcome measure
Incident stroke and other vascular events.
All five infectious serologies were available from baseline samples in 1625 participants (mean age 68.5 ± 10.1 years; 64.9% women). Cox proportional hazards models were used to estimate associations of each positive serology with stroke. Individual parameter estimates were then combined into a weighted index of infectious burden (IB) and used to calculate hazard ratios and confidence intervals (HR, 95% CI) for association with risk of stroke and other outcomes, adjusted for risk factors. Each individual infection was positively though not significantly associated with stroke risk after adjusting for other risk factors. The IB index was associated with an increased risk of all strokes (adjusted HR per standard deviation 1.39, 95% CI 1.02–1.90) after adjusting for demographics and risk factors. Results were similar after excluding those with coronary disease (adjusted HR 1.50, 95% CI 1.05–2.13) and adjusting for inflammatory biomarkers.
A quantitative weighted index of infectious burden was associated with risk of first stroke in this cohort. Future studies are needed to confirm these findings and to further define optimal measures of IB as a stroke risk factor.
Awareness of stroke warning symptoms and risk factors (stroke literacy), as well as knowledge of available treatment options, may be poor in high-risk populations. We sought to evaluate stroke literacy among residents of Central Harlem, a predominantly African American population, in a cross-sectional study.
Ten community-based sites in Central Harlem were identified between 2005 and 2006 for administration of a stroke knowledge survey. Trained volunteers administered in-person closed-ended questionnaires focused on stroke symptoms and risk factors.
A total of 1,023 respondents completed the survey. African Americans comprised 65.7% (n = 672) of the survey cohort. The brain was correctly identified as the site where a stroke occurs by 53.7% of respondents, whereas the heart was incorrectly identified by 20.8%. Chest pain was identified as a symptom of stroke by 39.7%. In multivariable analyses, African Americans (odds ratio [OR] 2.20, 95% confidence interval [CI] 1.09–4.45) and Hispanics (OR 5.27, 95% CI 2.46–11.30) were less likely to identify the brain as the damaged organ in stroke. Hispanics were more likely to incorrectly identify chest pain as a stroke symptom, compared with whites (OR 3.40, 95% CI 1.49–7.77). No associations were found between calling 911 and race/ethnicity and stroke knowledge, although women were more likely than men to call 911 (OR 0.50, 95% CI 0.30–0.80).
Significant deficiencies in stroke literacy exist in this high-risk population, especially when compared with national means. Culturally tailored and sustainable educational campaigns should be tested in high-risk populations as part of stroke public health initiatives.
= Behavioral Risk Factor Surveillance Survey;
= confidence interval;
= Second Delay in Accessing Stroke Healthcare;
= emergency medical services;
= face, arm, speech, time;
= odds ratio.
To improve global vascular risk prediction with behavioral and anthropometric factors.
Few cardiovascular risk models are designed to predict the global vascular risk of MI, stroke, or vascular death in multi-ethnic individuals, and existing schemes do not fully include behavioral risk factors.
A randomly-derived, population-based, prospective cohort of 2737 community participants free of stroke and coronary artery disease were followed annually for a median of 9.0 years in the Northern Manhattan Study (mean age 69 years; 63.2% women; 52.7% Hispanic, 24.9% African-American, 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 criterion. Model utility was assessed through receiver operating characteristics, calibration, and effect on reclassification of subjects.
Variables which 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 to a model restricted to the traditional variables.
A global vascular risk score that combines both traditional, behavioral, and anthropometric risk factors, uses continuous variables for physiological parameters, and is applicable to non-white subjects could improve primary prevention strategies.
Cardiovascular Disease; Cerebrovascular Disease; Prevention; Risk Factors; Epidemiology
Understanding how the timing of exposure to the US Stroke Belt (SB) influences stroke risk may illuminate mechanisms underlying the SB phenomenon and factors influencing population stroke rates.
Stroke mortality rates for United States–born black and white people aged 30–80 years were calculated for 1980, 1990, and 2000 for strata defined by birth state, state of adult residence, race, sex, and birth year. Four SB exposure categories were defined: born in a SB state (North Carolina, South Carolina, Georgia, Tennessee, Arkansas, Mississippi, or Alabama) and lived in the SB at adulthood; non-SB born but SB adult residence; SB-born but adult residence outside the SB; and did not live in the SB at birth or in adulthood (reference group). We estimated age-, sex-, and race-adjusted odds ratios for stroke mortality associated with timing of SB exposure.
Elevated stroke mortality was associated with both SB birth and, independently, SB adult residence, with the highest risk among those who lived in the SB at birth and adulthood. Compared to those living outside the SB at birth and adulthood, odds ratios for SB residence at birth and adulthood for black subjects were 1.55 (95% confidence interval 1.28, 1.88) in 1980, 1.47 (1.31, 1.65) in 1990, and 1.34 (1.22, 1.48) in 2000. Comparable odds ratios for white subjects were 1.45 (95% confidence interval 1.33, 1.58), 1.29 (1.21, 1.37), and 1.34 (1.25, 1.44). Patterns were similar for every race, sex, and age subgroup examined.
Stroke Belt birth and adult residence appear to make independent contributions to stroke mortality risk.
= confidence interval;
= Stroke Belt.
Arterial Stiffness, an intermediate pre-clinical marker of atherosclerosis, has been associated with an increased risk of stroke and cardiovascular disease (CVD). The metabolic syndrome and its components are established CVD risk factors and may also increase arterial stiffness, but data on this potential relationship is limited. The goal of this study was to determine the association between the metabolic syndrome (MetSyn) and carotid artery stiffness (STIFF) in an elderly multi-ethnic cohort.
STIFF was assessed by carotid ultrasound as part of the Northern Manhattan Study (NOMAS), a prospective population-based cohort of stroke-free individuals. STIFF was calculated as [ln(systolicBP/diastolicBP)/Strain], where Strain was [(Systolic Diameter Diastolic Diameter)/Diastolic Diameter]. MetSyn was defined by the National Cholesterol Education Program: Adult Treatment Panel III (NCEP ATP III) criteria. LogSTIFF was analyzed as the dependent variable in linear regression models, adjusting for demographics, education, current smoking, presence of carotid plaque and intima-media thickness.
STIFF was analyzed in 1133 NOMAS subjects (mean age 65±9 years; 61% women; 58% Hispanic, 22% Black, 20% White). The prevalence of MetSyn was 49%. The mean LogSTIFF was 2.01±0.61 among those with and 1.90±0.59 among those without MetSyn (p=0.003). MetSyn was significantly associated with increased logSTIFF in the final adjusted model (parameter estimate β=0.100, p=0.01). Among individual MetSyn components, waist circumference and elevated blood pressure were most significantly associated with a mean increase in logSTIFF (p<0.01).
MetSyn 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.
metabolic syndrome; arterial stiffness; atherosclerosis; elderly; race-ethnicity
To explore the relationship between lipid profile components and incident ischemic stroke in a stroke-free prospective cohort.
Population-based prospective cohort study.
Northern Manhattan, New York.
Stroke-free community residents.
As part of the Northern Manhattan Study, baseline fasting blood samples were collected on stroke-free community residents followed up for a mean of 7.5 years.
Main Outcome Measures
Cox proportional hazard models were used to calculate hazard ratios and 95% confidence intervals for lipid profile components and ischemic stroke after adjusting for demographic and risk factors. In secondary analyses, we used repeated lipid measures over 5 years from a 10% sample of the population to calculate the change per year of each of the lipid parameters and to impute time-dependent lipid parameters for the full cohort.
After excluding those with a history of myocardial infarction, 2940 participants were available for analysis. Baseline high-density lipoprotein cholesterol, triglyceride, and total cholesterol levels were not associated with risk of ischemic stroke. Low-density lipoprotein cholesterol (LDL-C) and non–high-density lipoprotein cholesterol levels were associated with a paradoxical reduction in risk of stroke. There was an interaction with use of cholesterol-lowering medication on follow-up, such that LDL-C level was only associated with a reduction in stroke risk among those taking medications. An LDL-C level greater than 130 mg/dL as a time-dependent covariate showed an increased risk of ischemic stroke (adjusted hazard ratio, 3.81; 95% confidence interval, 1.53–9.51).
Baseline lipid panel components were not associated with an increased stroke risk in this cohort. Treatment with cholesterol-lowering medications and changes in LDL-C level over time may have attenuated the risk in this population, and lipid measurements at several points may be a better marker of stroke risk.
To determine the association between insulin resistance and risk of first ischemic stroke in a large multiethnic, stroke-free cohort without diagnosis of diabetes.
Research Design and Methods
A cohort of 1,509 non-diabetic participants from the Northern Manhattan Study (mean age 68±10 years; 64% women; 59% Hispanics) was analyzed for insulin sensitivity, expressed by the Homeostatic Model Assessment of Insulin Sensitivity (HOMA index = [fasting insulin (µU/ml]×[fasting glucose (mmol/L)] ÷ 22.5). Insulin resistance (IR) was defined by a HOMA-IR index in the top quartile (Q4). Cox proportional hazard models were used to determine the effect of HOMA-IR on the risk of incident ischemic stroke (IS), myocardial infarction (MI), vascular death, and combined outcomes (IS, MI, or vascular death).
The mean HOMA-IR was 2.3 ± 2.1, and Q4 was ≥2.8. During a mean follow-up of 8.5 years, vascular events occurred among 180 subjects; 46 had fatal or non-fatal ischemic stroke, 45 had fatal or non-fatal MI, and 121 died of vascular causes. The top quartile of the HOMA-IR vs.
Insulin resistance estimated by the homeostatic model assessment is a marker of increased risk of incident stroke among non-diabetic individuals. Our findings emphasize the need to better characterize individuals at increased risk of stroke, and the potential role for primary preventive therapies targeted at insulin resistance.
insulin resistance; incident ischemic stroke; vascular disease; cohort; prospective; population-based
The overall burden of prior infections may contribute to atherosclerosis and stroke risk. We hypothesized that serological evidence of common infections would be associated with carotid plaque thickness in a multi-ethnic cohort.
Antibody titers to five common infectious microorganisms (i.e. Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpesvirus 1 and 2) were measured among stroke-free community participants, and a weighted index of infectious burden (IB) was calculated based on Cox models previously derived from for the association of each infection with stroke risk. High-resolution carotid duplex Doppler studies were used to assess maximum carotid plaque thickness (MCPT). Weighted least squares regression was used to measure the association between IB and MCPT after adjusting for other risk factors.
Serological results for all five infectious organisms were available in 861 participants with MCPT measurements available (mean age 67.2+/−9.6 yrs). Each individual infection was associated with stroke risk after adjusting for other risk factors. The IB index (n=861) had a mean of 1.00 ± standard deviation 0.35, median 1.08. Plaque was present in 52% of participants (mean 0.90+/−1.04 mm). IB was associated with MCPT (adjusted increase in MCPT 0.09 mm, 95% confidence interval 0.03–0.15 mm, per standard deviation increase of IB).
A quantitative weighted index of infectious burden, derived from the magnitude of association of individual infections with stroke, was associated with carotid plaque thickness in this multi-ethnic cohort. These results lend support to the notion that past or chronic exposure to common infections, perhaps by exacerbating inflammation, contributes to atherosclerosis. Future studies are needed to confirm this hypothesis and to define optimal measures of infectious burden as a vascular risk factor.
Background and Purpose
Several factors predict functional status after stroke, but most studies have included hospitalized patients with limited follow-up. We hypothesized that ischemic stroke patients experience functional decline over 5 years independent of recurrent stroke and other risk factors.
In the population-based Northern Manhattan Study, incident ischemic stroke patients ≥40 years were prospectively followed using the Barthel index (BI) at 6 months and annually to 5 years. Baseline stroke severity was categorized as mild (NIH Stroke Scale <6), moderate (6–13), and severe (≥14). Follow-up was censored at death, recurrent stroke, or myocardial infarction. Generalized Estimating Equations provided odds ratios (OR) and 95% confidence intervals (95%CI) for predictors of favorable (BI≥95) versus unfavorable (BI<95) functional status, after adjusting for demographic and medical risk factors.
Of 525 patients, mean age was 68.6±12.4 years, 45.5% were male, 54.7% Hispanic, 54.7% had Medicaid/no insurance, and 35.1% had moderate stroke. The proportion with BI≥95 declined over time (OR 0.91, 95% CI 0.84–0.99). Changes in BI by insurance status were confirmed by a significant interaction term (β for interaction=−0.167, p=0.034); those with Medicaid/no insurance declined (OR 0.84, p=0.003), whereas those with Medicare/private insurance did not (OR 0.99, p=0.92).
The proportion of patients with functional independence after stroke declines annually for up to 5 years, and these effects are greatest for those with Medicaid or no health insurance. This decline is independent of age, stroke severity, and other predictors of functional decline, and occurs even among those without recurrent stroke or myocardial infarction.
disability; stroke; recovery
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