Perceptions of barriers and facilitators to engaging in implementation science: a qualitative study.

OBJECTIVE: Understanding barriers and facilitators to engaging with implementation science (IS) research can provide insight into how to improve efforts to encourage more researchers to participate in IS research. STUDY DESIGN: The study design used is a grounded theory qualitative study. METHODS: We conducted semistructured telephone interviews with 20 health researchers familiar with IS that both report engaging in IS research and those that do not. We explored perceptions of barriers and facilitators to engaging in IS research. Themes surrounding difficulties defining IS, lack of training availability, and obstacles to forming research partnerships were discussed as barriers to engaging IS research. Interview topics were informed by the result of an online survey of health researchers in the US. RESULTS: Themes surrounding difficulties defining IS, lack of training availability, and obstacles to forming research partnerships were discussed as barriers to engaging IS research. While accessible mentorship, exposure to formative experiences that develop interest in IS research and an increasing IS visibility were described as motivators for engaging in IS research. CONCLUSIONS: These results highlight the importance of mentorship and exposure to IS ideas in motivating engagement in IS research and the presence of training and methodological barriers to engagement. Future research should expand this line of inquiry to include the perspectives of more junior researchers and students to better reflect the current IS environment.

Quality of life declines after first ischemic stroke. The Northern Manhattan Study.

OBJECTIVES: Quality of life (QOL) after stroke is poorly characterized. We sought to determine long-term natural history and predictors of QOL among first ischemic stroke survivors without stroke recurrence or myocardial infarction (MI). METHODS: In the population-based, multiethnic Northern Manhattan Study, QOL was prospectively assessed at 6 months and annually for 5 years using the Spitzer QOL index (QLI), a 10-point scale. Functional status was assessed using the Barthel Index (BI) at regular intervals, and cognition using the Mini-Mental State Examination at 1 year. Generalized estimating equations estimated the association between patient characteristics and repeated QOL measures over 5 years. Follow-up was censored at death, recurrent stroke, or MI. RESULTS: There were 525 incident ischemic stroke patients >/=40 years (mean age 68.6 +/- 12.4 years). QLI declined after stroke (annual change -0.10, 95% confidence interval -0.17 to -0.04), after adjusting for age, sex, race-ethnicity, education, insurance, depressed mood, stroke severity, bladder continence, and stroke laterality. This decline remained when BI >/=95 was added to the model as a time-dependent covariate, and functional status also predicted QLI. Changes in QLI over time differed by insurance status (p for interaction = 0.0017), with a decline for those with Medicaid/no insurance (p < 0.0001) but not Medicare/private insurance (p = 0.98). CONCLUSIONS: In this population-based study, QOL declined annually up to 5 years after stroke among survivors free of recurrence or MI and independently of other risk factors. QLI declined more among Medicaid patients and was associated with age, mood, stroke severity, urinary incontinence, functional status, cognition, and stroke laterality.

Metabolic syndrome and cerebral vasomotor reactivity.

BACKGROUND AND PURPOSE: Metabolic syndrome has been proposed as a risk factor for stroke and transient ischaemic attack. One pathophysiological mechanism could be impairment of endothelial function. Thus, we hypothesized that cerebral vasomotor reactivity would be decreased in patients with metabolic syndrome, compared to patients without metabolic syndrome. METHODS: In this retrospective analysis, 83 consecutive patients (aged 59.19 ± 15.98; 33 women) underwent Doppler examination for carotid artery disease including bi-hemispherical vasomotor reactivity assessment using transcranial Doppler monitoring. Vasomotor reactivity data were analyzed from the hemisphere with no or low-grade carotid stenosis (<40%). Cerebral vasomotor reactivity was calculated as percent increase in mean flow velocity per mmHg pCO(2) during 2 min of 5% CO(2) inhalation delivered by anesthesia mask (normal if ≥ 2%/mmHg). Univariate and multivariable linear regression models were used to determine factors, including metabolic syndrome, that were independently associated with pathologic vasomotor reactivity. RESULTS: After adjusting for the presence of contralateral carotid stenosis and ipsilateral stroke in the multivariable model, metabolic syndrome was independently associated with lower vasomotor reactivity values (2.27 ± 1.24% vs. 2.68 ± 1.37; ß = -0.258, P = 0.033). In this model, there was no association of cerebral vasomotor reactivity with age, gender, race, cardiac disease, current statin therapy, or small vessel disease. CONCLUSIONS: Our findings suggest that impaired cerebral vasomotor reactivity may be a mediator of stroke in patients with metabolic syndrome, a syndrome affecting a significant and growing proportion of the population. A prospective longitudinal study is warranted to study the cerebral haemodynamic effect of metabolic syndrome.

Physical activity and risk of ischemic stroke in the Northern Manhattan Study.

BACKGROUND: It is controversial whether physical activity is protective against first stroke among older persons. We sought to examine whether physical activity, as measured by intensity of exercise and energy expended, is protective against ischemic stroke. METHODS: The Northern Manhattan Study is a prospective cohort study in older, urban-dwelling, multiethnic, stroke-free individuals. Baseline measures of leisure-time physical activity were collected via in-person questionnaires. Cox proportional hazards models were constructed to examine whether energy expended and intensity of physical activity were associated with the risk of incident ischemic stroke. RESULTS: Physical inactivity was present in 40.5% of the cohort. Over a median follow-up of 9.1 years, there were 238 incident ischemic strokes. Moderate- to heavy-intensity physical activity was associated with a lower risk of ischemic stroke (adjusted hazard ratio [HR] 0.65, 95% confidence interval [0.44-0.98]). Engaging in any physical activity vs none (adjusted HR 1.16, 95% CI 0.88-1.51) and energy expended in kcal/wk (adjusted HR per 500-unit increase 1.01, 95% CI 0.99-1.03) were not associated with ischemic stroke risk. There was an interaction of sex with intensity of physical activity (p = 0.04), such that moderate to heavy activity was protective against ischemic stroke in men (adjusted HR 0.37, 95% CI 0.18-0.78), but not in women (adjusted HR 0.92, 95% CI 0.57-1.50). CONCLUSIONS: Moderate- to heavy-intensity physical activity, but not energy expended, is protective against risk of ischemic stroke independent of other stroke risk factors in men in our cohort. Engaging in moderate to heavy physical activities may be an important component of primary prevention strategies aimed at reducing stroke risk.

Carotid plaque, a subclinical precursor of vascular events: the Northern Manhattan Study.

BACKGROUND: Carotid atherosclerosis is a known biomarker associated with future vascular disease. The risk associated with small, nonstenotic carotid plaques is less clear. The objective of this study was to examine the association between maximum carotid plaque thickness and risk of vascular events in an urban multiethnic cohort. METHODS: As part of the population-based Northern Manhattan Study, carotid plaque was analyzed among 2,189 subjects. Maximum carotid plaque thickness was evaluated at the cutoff level of 1.9 mm, a prespecified value of the 75th percentile of the plaque thickness distribution. The primary outcome measure was combined vascular events (ischemic stroke, myocardial infarction, or vascular death). RESULTS: Carotid plaque was present in 1,263 (58%) subjects. After a mean follow-up of 6.9 years, vascular events occurred among 319 subjects; 121 had fatal or nonfatal ischemic stroke, 118 had fatal or nonfatal myocardial infarction, and 166 died of vascular causes. Subjects with maximum carotid plaque thickness greater than 1.9 mm had a 2.8-fold increased risk of combined vascular events in comparison to the subjects without carotid plaque (hazard ratio, 2.80; 95% CI, 2.04-3.84). In fully adjusted models, this association was significant only among Hispanics. Approximately 44% of the low-risk individuals by Framingham risk score had a 10-year vascular risk of 18.3% if having carotid plaque. CONCLUSIONS: Maximum carotid plaque thickness is a simple and noninvasive marker of subclinical atherosclerosis associated with increased risk of vascular outcomes in a multiethnic cohort. Maximum carotid plaque thickness may be a simple and nonexpensive tool to assist with vascular risk stratification in preventive strategies and a surrogate endpoint in clinical trials.

Gender differences in self-report of recovery after stroke: the Northern Manhattan Study.

We compared subjective responses to simple questions after stroke with interviewer-assessed stroke outcome measures. Among those in the highest functional category, women were more likely to report incomplete recovery and greater need for help than men. Among these women, depressed mood was associated with a response of a need for help despite a good functional recovery. Self-reported responses in stroke outcome assessments require further validation by gender and may need to consider the confounding effects of depression.

Projected costs of ischemic stroke in the United States.

BACKGROUND: There are barriers to acute stroke care in minority groups as well as a higher incidence of ischemic stroke when compared with non-Hispanic whites. OBJECTIVE: To estimate the future economic burden of stroke in non-Hispanic whites, Hispanics, and African Americans in the United States from 2005 to 2050. METHODS: We used U.S. Census estimates of the race-ethnic group populations age 45 years and older. We obtained stroke epidemiology and service utilization data from the Northern Manhattan Stroke Study and the Brain Attack Surveillance in Corpus Christi project and other published data. We estimated costs directly from Medicare reimbursement or from studies that used Medicare reimbursement. Direct and indirect costs considered included ambulance services, initial hospitalization, rehabilitation, nursing home costs, outpatient clinic visits, drugs, informal caregiving, and potential lost earnings. RESULTS: The total cost of stroke from 2005 to 2050, in 2005 dollars, is projected to be 1.52 trillion dollars for non-Hispanic whites, 313 billion dollars for Hispanics, and 379 billion dollars for African Americans. The per capita cost of stroke estimates are highest in African Americans (25,782 dollars), followed by Hispanics (17,201 dollars), and non-Hispanic whites (15,597 dollars). Loss of earnings is expected to be the highest cost contributor in each race-ethnic group. CONCLUSIONS: The economic burden of stroke in African Americans and Hispanics will be enormous over the next several decades. Further efforts to improve stroke prevention and treatment in these high stroke risk groups are necessary.

Subarachnoid hemorrhage incidence among Whites, Blacks and Caribbean Hispanics: the Northern Manhattan Study.

American blacks and Hispanics may have a greater incidence of subarachnoid hemorrhage (SAH) than whites, but incidence data are scant. We used an active hospital and community surveillance program and autopsy reports to identify incident SAH cases among white, black and Hispanic adults living in Northern Manhattan between July 1993 and June 1997. The annual incidence adjusted for age and sex to the 1990 US Census was 9.7 per 100,000 (95% CI 7.5-12.0). Compared with whites (9 cases, age- and sex-adjusted annual incidence 8.2 per 100,000), the rate ratio of SAH was 1.3 (95% CI 0.7-2.4) for Hispanics (34 cases, incidence 10.9), and 1.6 (95% CI 0.8-2.8) for blacks (9 cases, incidence 12.8). The 30-day case fatality rate was 26%. Risk of death increased significantly with age and severity at onset but was not influenced by gender or race-ethnicity.

The incidence of deep and lobar intracerebral hemorrhage in whites, blacks, and Hispanics.

BACKGROUND: Black and Hispanic Americans have a greater risk of primary intracerebral hemorrhage (ICH) than whites. Deep ICH is most often associated with hypertension, while lobar ICH is associated with cerebral amyloid angiopathy. The authors conducted a population-based incidence study to directly compare the incidence of deep vs lobar ICH in all three race-ethnic groups. METHODS: The authors used an active hospital and community surveillance program and autopsy reports to identify incident ICH cases among white, black, and Caribbean Hispanic adults in Northern Manhattan between July 1993 and June 1997. Incidence rates were adjusted for age and sex to the 1990 US Census. CIs for risk ratios (RR) were calculated with Byar's chi2 approximation of the Poisson distribution. RESULTS: The authors identified 155 cases of ICH for an annual incidence of 30.9/100,000 (26.7 to 35.0). Men had a higher risk of ICH than women (RR 1.5, 95% CI 1.2 to 1.8), driven entirely by the incidence of deep ICH (RR 1.8) rather than lobar ICH (RR 1.0). Compared with whites, RR for blacks was all ICH 3.8 (2.2 to 8.9), deep 4.8 (2.3 to 21.1), lobar 2.8 (1.2 to 14.4); RR for Hispanics was all 2.6 (1.4 to 6.1), deep 3.7 (1.7 to 16.5), lobar 1.4 (0.4 to 7.4). CONCLUSIONS: ICH is a heterogeneous disease with deep and lobar subtypes distinguishable on an epidemiologic basis. The different patterns of these two subtypes in our race-ethnically diverse population lend credence to the notion that ICH should no longer be treated as a single entity.

Heritabilities of the metabolic syndrome and its components in the Northern Manhattan Family Study.

AIMS/HYPOTHESIS: Growing evidence suggests that the traits comprising the metabolic syndrome have a genetic basis. However, studies of genetic contributions to the syndrome are sparse. Against this background, we sought to estimate the heritability of the metabolic syndrome and its component traits. MATERIALS AND METHODS: We investigated 803 subjects from 89 Caribbean-Hispanic families who have enrolled to date in the current Northern Manhattan Family Study and for whom metabolic syndrome information was available. Metabolic syndrome was defined in accordance with the National Cholesterol Education Program Adult Treatment Panel III (NCEP/ATPIII) criteria. Variance component methods were used to estimate age and sex-adjusted heritability of the metabolic syndrome and its components. To obtain the structures underlying the metabolic syndrome, we performed principal component factor analyses using six quantitative phenotypes included in the ATPIII definition. RESULTS: The heritability for the metabolic syndrome was 24% (p=0.009), and ranged from 16 to 60% for its five components. Factor analysis yielded two independent factors (factor 1: lipids/glucose/obesity; factor 2: blood pressure). Heritability analysis revealed significant genetic effects on both factors (44% for lipids/glucose/obesity, and 20% for blood pressure). CONCLUSIONS/INTERPRETATION: In the Caribbean-Hispanic families investigated, we demonstrated moderate and significant heritabilities for the metabolic syndrome itself, as well as for individual components and independent factors of the syndrome. These results provide evidence that could support future tasks of mapping susceptibility loci for this syndrome.

Social isolation and outcomes post stroke.

OBJECTIVE: To assess the relationship between social isolation and stroke outcomes in a multiethnic cohort. METHODS: As part of the Northern Manhattan Stroke Study, the authors prospectively followed a cohort of patients with stroke for 5 years. Baseline data including social isolation were collected. At follow-up, the authors documented outcome events as defined by the first occurrence of myocardial infarction (MI), stroke recurrence, or death. Cox hazard models were used to calculate the hazard ratio (HR, 95% CI) for prestroke predictors of post stroke outcomes. RESULTS: The authors followed 655 ischemic stroke cases for a mean of 5 years. The cohort was 55% women; 17% white, 27% African American, 54% Hispanic; mean age 69 +/- 12 years. There were 265 first outcome events. In univariate analysis, coronary artery disease (OR 1.3, 1.0 to 1.7), age > 70 years (OR 1.9, 1.5 to 2.5), atrial fibrillation (AF) (OR 1.8, 1.3 to 2.5), race-ethnicity (white vs Hispanic) (OR 1.7, 1.1 to 2.9), physical inactivity (OR 1.3, 1.1 to 2.6), help at home (OR 1.8, 1.4 to 2.4), and social isolation (OR 1.4, 1.2 to 1.6) were associated with increased risk of an outcome event. No association was seen for hypertension, diabetes, education, sex, insurance, occupation, marital status, or primary care physician. In the multivariable model controlling for age, AF (OR 1.9, 1.5 to 2.5), help at home (OR 1.5, 1.1 to 2.0), and social isolation (OR 1.4, 1.1 to 1.8) predicted outcome events. CONCLUSION: Prestroke social isolation is a predictor of outcome events post stroke. Lack of social support may contribute to poorer outcomes due to poor compliance, depression, and stress.

Relative elevation in baseline leukocyte count predicts first cerebral infarction.

BACKGROUND: Atherosclerosis is an inflammatory disease, and leukocyte levels are associated with future risk of ischemic cardiac disease. OBJECTIVE: To investigate the hypothesis that relative elevations in leukocyte count in a stroke-free population predict future ischemic stroke (IS). METHODS: A population-based prospective cohort study was performed in a multiethnic urban population. Stroke-free community participants were identified by random-digit dialing. Leukocyte levels were measured at enrollment, and participants were followed annually for IS, myocardial infarction (MI), and cause-specific mortality. Cox proportional hazards regression models were used to calculate hazard ratios (HRs) and 95% CIs for IS, MI, and vascular death after adjustment for medical, behavioral, and socioeconomic factors. RESULTS: Among 3,103 stroke-free community participants (mean age 69.2 +/- 10.3 years) with baseline leukocyte levels measured, median follow-up was 5.2 years. After adjusting for stroke risk factors, each SD in leukocyte count (1.8 x 10(9) cells/L) was associated with an increased risk of IS (HR 1.22, 95% CI 1.05 to 1.42), and IS, MI, or vascular death (HR 1.13, 95% CI 1.02 to 1.26). Compared with those in the lowest quartile of leukocyte count, those in the highest had an increased risk of IS (adjusted HR 1.75, 95% CI 1.08 to 2.82). The effect on atherosclerotic and cardioembolic stroke was greater than in other stroke subtypes. CONCLUSION: Relative elevations in leukocyte count are independently associated with an increased risk of future ischemic stroke and other cardiovascular events.

Mortality and causes of death after first ischemic stroke: the Northern Manhattan Stroke Study.

OBJECTIVE: To analyze the early and long-term causes of death after first ischemic stroke in the multiethnic northern Manhattan community. METHODS: In the prospective, population-based Northern Manhattan Stroke Study, 980 patients with first ischemic stroke (mean age 70 years; 56% women; 49% Caribbean Hispanic, 31% black, 20% white) were followed for a mean of 3 years. Causes of death were classified as vascular (incident stroke, recurrent stroke, cardiac) or nonvascular. Life table analyses were used to assess mortality risks among different race-ethnic groups. Early (< or =1 month) vs long-term (> 1 month to 5 years) causes of death were compared. RESULTS: Among the 980 patients followed, 278 (28%) died; 47 (5%) died during the first month. Cumulative mortality risk was 5% at 1 month, 16% after 1 year, 29% after 3 years, and 41% after 5 years. The proportion of vascular deaths among all deaths was 75% at 1 month and 43% thereafter (p = 0.001). Stroke, either incident (53%) or recurrent (4%), caused early deaths in 57% and long-term deaths in 14% (p = 0.001). Overall mortality risks did not differ significantly among race-ethnic groups. However, the proportion of incident stroke-related early deaths was 85% in Caribbean Hispanic patients, 33% in white patients, and 25% in black patients (p = 0.002). CONCLUSIONS: Among patients with first ischemic stroke, incident stroke is the leading cause of early deaths. A large proportion of long-term deaths are nonvascular in origin. Despite similar overall mortality rates in race-ethnic groups, our data suggest a higher incident stroke-related early mortality among Caribbean Hispanics.

Race-ethnic disparities in the impact of stroke risk factors: the northern Manhattan stroke study.

BACKGROUND AND PURPOSE: Stroke risk factors have been determined in large part through epidemiological studies in white cohorts; as a result, race-ethnic disparities in stroke incidence and mortality rates remained unexplained. The aim in the present study was to compare the prevalence, OR, and etiological fraction (EF) of stroke risk factors among white, blacks, and Caribbean Hispanics living in the same urban community of northern Manhattan. METHODS: In this population-based incident case-control study, cases (n=688) of first ischemic stroke were prospectively matched 1:2 by age, sex, and race-ethnicity with community controls (n=1156). Risk factors were determined through in-person assessment. Conditional logistic regression was used to calculate adjusted ORs in each race-ethnic group. Prevalence and multivariate EFs were determined in each race-ethnic group. RESULTS: Hypertension was an independent risk factor for whites (OR 1.8, EF 25%), blacks (OR 2.0, EF 37%), and Caribbean Hispanics (OR 2.1, EF 32%), but greater prevalence led to elevated EFs among blacks and Caribbean Hispanics. Greater prevalence rates of diabetes increased stroke risk in blacks (OR 1.8, EF 14%) and Caribbean Hispanics (OR 2.1 P<0.05, EF 10%) compared with whites (OR 1.0, EF 0%), whereas atrial fibrillation had a greater prevalence and EF for whites (OR 4.4, EF 20%) compared with blacks (OR 1.7, EF 3%) and Caribbean Hispanics (OR 3.0, EF 2%). Coronary artery disease was most important for whites (OR 1.3, EF 16%), followed by Caribbean Hispanics (OR 1.5, EF 6%) and then blacks (OR 1.1, EF 2%). Prevalence of physical inactivity was greater in Caribbean Hispanics, but an elevated EF was found in all groups. CONCLUSIONS: The prevalence, OR, and EF for stroke risk factors vary by race-ethnicity. These differences are crucial to the etiology of stroke, as well as to the design and implementation of stroke prevention programs.

High-density lipoprotein cholesterol and ischemic stroke in the elderly: the Northern Manhattan Stroke Study.

CONTEXT: Elevated high-density lipoprotein cholesterol (HDL-C) levels have been shown to be protective against cardiovascular disease. However, the association of specific lipoprotein classes and ischemic stroke has not been well defined, particularly in higher-risk minority populations. OBJECTIVE: To evaluate the association between HDL-C and ischemic stroke in an elderly, racially or ethnically diverse population. DESIGN: Population-based, incident case-control study conducted July 1993 through June 1997. SETTING: A multiethnic community in northern Manhattan, New York, NY. PARTICIPANTS: Cases (n = 539) of first ischemic stroke (67% aged >/=65 years; 55% women; 53% Hispanic, 28% black, and 19% white) were enrolled and matched by age, sex, and race or ethnicity to stroke-free community residents (controls; n = 905). MAIN OUTCOME MEASURE: Independent association of fasting HDL-C levels, determined at enrollment, with ischemic stroke, including atherosclerotic and nonatherosclerotic ischemic stroke subtypes. RESULTS: After risk factor adjustment, a protective effect was observed for HDL-C levels of at least 35 mg/dL (0.91 mmol/L) (odds ratio [OR], 0.53; 95% confidence interval [CI], 0.39-0.72). A dose-response relationship was observed (OR, 0.65; 95% CI, 0.47-0.90 and OR, 0.31; 95% CI, 0.21-0.46) for HDL-C levels of 35 to 49 mg/dL (0.91-1.28 mmol/L) and at least 50 mg/dL (1.29 mmol/L), respectively. The protective effect of a higher HDL-C level was significant among participants aged 75 years or older (OR, 0.51; 95% CI, 0.27-0.94), was more potent for the atherosclerotic stroke subtype (OR, 0.20; 95% CI, 0.08-0.50), and was present in all 3 racial or ethnic groups studied. CONCLUSIONS: Increased HDL-C levels are associated with reduced risk of ischemic stroke in the elderly and among different racial or ethnic groups. These data add to the evidence relating lipids to stroke and support HDL-C as an important modifiable stroke risk factor.

Elevated white blood cell count and carotid plaque thickness : the northern manhattan stroke study.

BACKGROUND AND PURPOSE: Elevated leukocyte count has been associated with cardiovascular and cerebrovascular disease in several epidemiological studies. We sought to determine whether white blood cell count (WBC) is associated with carotid plaque thickness in a stroke-free, multiethnic cohort. METHODS: For this cross-sectional analysis, WBC was measured in stroke-free community subjects undergoing carotid duplex Doppler ultrasound. Maximal internal carotid plaque thickness (MICPT) was measured for each subject. Demographic and potential medical confounding factors were analyzed with linear and logistic regression to calculate the effect of quartile of WBC on MICPT. Odds ratios (ORs) and 95% confidence intervals (CIs) for the effect of quartile of WBC on MICPT >/=75th percentile were calculated. All analyses were stratified by race-ethnicity. RESULTS: The mean age of the 1422 subjects was 68.6+/-10.2 years; 40.0% were men; 24.4% were white, 46.9% Hispanic, and 26.7% black. Among Hispanics, compared with the lowest quartile of WBC, those in the highest quartile had significantly increased MICPT (mean difference=0.30 mm, P:=0.0086) after adjustment for age, sex, and other atherosclerotic risk factors. There was no significant increase for blacks or whites. The OR for MICPT >/=75th percentile (1.9 mm) was significantly increased for Hispanics (OR, 2.8; 95% CI, 1.4 to 5.6), marginally elevated for black non-Hispanics (OR, 1.6; 95% CI, 0.8 to 3.2), and not increased for white non-Hispanics (OR, 0.5; 95% CI, 0.2 to 1.1). CONCLUSIONS: Relative elevation in WBC is associated with carotid atherosclerosis, but this relationship differs by race-ethnicity. The association is strongest in Hispanics, intermediate in black non-Hispanics, and not present in white non-Hispanics in this population. Chronic subclinical infection or inflammation may account for this association.

Lifestyle factors and stroke risk: exercise, alcohol, diet, obesity, smoking, drug use, and stress.

Various lifestyle factors have been associated with increasing the risk of stroke. These include lack of exercise, alcohol, diet, obesity, smoking, drug use, and stress. Guidelines endorsed by the Centers for Disease Control and Prevention and the National Institutes of Health recommend that Americans should exercise for at least 30 minutes of moderately intense physical activity on most, and preferably all, days of the week. Recent epidemiologic studies have shown a U-shaped curve for alcohol consumption and coronary heart disease mortality, with low-to-moderate alcohol consumption associated with lower overall mortality. High daily dietary intake of fat is associated with obesity and may act as an independent risk factor or may affect other stroke risk factors such as hypertension, diabetes, hyperlipidemia, and cardiac disease. Homocysteine is another important dietary component associated with stroke risk, while other dietary stroke risk factors are thought to be mediated through the daily intake of several vitamins and antioxidants. Smoking, especially current smoking, is a crucial and extremely modifiable independent determinant of stroke. Despite the obstacles to the modification of lifestyle factors, health professionals should be encouraged to continue to identify such factors and help improve our ability to prevent stroke.

Predictors of resource use after acute hospitalization: the Northern Manhattan Stroke Study.

OBJECTIVE: To determine demographic and clinical predictors of discharge destinations following acute care hospitalization for stroke in the community of northern Manhattan. METHODS: A group of 893 patients (mean age, 70 +/- 12 years; 56% women; 51% Hispanic, 30% African-American, 19% white) who survived acute care hospitalization for a first ischemic stroke were followed prospectively. Stroke severity was assessed by the NIH Stroke Scale and categorized as mild (< or = 5), moderate (6 to 13), and severe (> or = 14). Polytomous logistic regression was used to determine predictors for rehabilitation and nursing home placement versus returning home. RESULTS: Among the survivors of acute stroke care hospitalization, 611 (68%) patients were discharged to their homes, 168 (19%) to rehabilitation, and 114 (13%) to nursing homes. Patients with moderate and severe neurologic deficits had more than a threefold increased risk of being sent to a nursing home and more than an eightfold increased risk of being sent to rehabilitation. Age over 65 and cognitive impairment were associated with placement to a nursing home (age over 65: OR, 2.4; 95% CI, 1.0 to 5.6; cognitive impairment: OR, 2.9; 95%, CI 1.4 to 5.7), and rehabilitation (age over 65: OR, 1.8; 95% CI, 1.1 to 2.9; cognitive impairment: OR, 2.9; 95% CI, 1.4 to 5.7). CONCLUSION: Our results demonstrated that one-third of patients with acute stroke from the community of northern Manhattan required placement in a temporary or a long-term disability care institution following acute care hospitalization. Severity of stroke is an important factor that influences discharge planning following acute care hospitalization and its reduction can improve health care resource usage.

Cost and outcome of mechanical ventilation for life-threatening stroke.

BACKGROUND AND PURPOSE: Hospital mortality rates of 50% to 90% have been reported for stroke patients treated with mechanical ventilation. These data have raised serious questions about the cost-effectiveness of this intervention. We sought to determine how often stroke patients are mechanically ventilated, identify predictors of 30-day survival among ventilated patients, and evaluate the cost-effectiveness of this intervention. METHODS: We identified mechanically ventilated patients in a population-based multiethnic cohort of 510 incidence stroke patients who were hospitalized between July 1993 and June 1996. Factors affecting 30-day survival were identified in a multiple logistic regression analysis. We calculated the cost per patient discharged alive, life-year saved, and quality-adjusted life-year saved using a zero-cost, zero-life assumption. RESULTS: Ten percent of patients (n=52) were mechanically ventilated. Thirty-day mortality was 65% overall and did not differ significantly by stroke subtype. Glasgow Coma Scale score on the day of intubation (P:<0.01) and subsequent neurological deterioration (P:=0.02) were identified as predictors of 30-day mortality. The cost (1996 US dollars) of hospitalization per patient discharged alive was $89 400; the cost per year of life saved was $37 600; and the cost per quality-adjusted life-year saved was $174 200. Functional status of most survivors was poor; at 6 months, half were severely disabled and completely dependent. In a worst-case scenario of quality of life preferences, mechanical ventilation resulted in a net deficit of meaningful survival. CONCLUSIONS: Two thirds of mechanically ventilated stroke patients die during their hospitalization, and most survivors are severely disabled. Survival is particularly unlikely if patients are deeply comatose or clinically deteriorate after intubation. In our multiethnic urban population, mechanical ventilation for stroke was relatively cost-effective for extending life but not for preserving quality of life.