Race-Ethnic Disparities in the Impact of
Stroke Risk Factors
The Northern Manhattan Stroke Study
Ralph L. Sacco, MS, MD; Bernadette Boden-Albala, MPH; Gregory Abel, MD; I-Feng Lin, DrPH;
Mitchell Elkind, MD; W. Allen Hauser, MD; Myunghee C. Paik, PhD; Steven Shea, MS, MD
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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. (Stroke. 2001;32:
1725-1731.)
Key Words: data interpretation, statistical 䡲 epidemiology 䡲 risk factors 䡲 stroke
R
ecent projections estimate that the annual incidence of
stroke in the United States among all races is closer to
700 000 than the previously reported incidence of 550 000.1
Stroke continues to have a disproportionate impact on mortality rates for blacks and Hispanics compared with whites.2–5
Mortality differences have remained significant even after
accounting for differences in socioeconomic status.6 Incidence data from the Northern Manhattan Stroke Study (NOMASS) have demonstrated race-ethnic differences in stroke
incidence: blacks had a 2.4-fold increased annual stroke
incidence and Caribbean Hispanics had a 2-fold increased
annual stroke incidence compared with whites living in the
same community.7 The aging and rapid growth of the black
and Hispanic populations in the United States have the
potential to lead to increases in these disparities.
The reasons for the race-ethnic disparities in stroke incidence and mortality are not clear. Potential explanations
include variations in risk factor potency, prevalence, and
treatment arising from environmental and genetic factors.
Although no study has systematically examined differences
in the effect of risk factors in different race-ethnic groups, the
literature has consistently shown race-ethnic variations in the
prevalence of cardiovascular risk factors.8,9 For example,
blacks have the highest prevalence of hypertension regardless
of geographic location,10 although Caribbean-born blacks
have a lower prevalence of hypertension than those living in
the southern or northeastern United States.11 Other studies
have reported that diabetes is more common in blacks,
whereas coronary artery disease and atrial fibrillation are
more common in whites.12,13
Received January 3, 2001; final revision received March 8, 2001; accepted May 3, 2001.
From the Columbia University College of Physicians and Surgeons and School of Public Health, New York, NY; Department of Neurology (R.L.S.,
B.B.-A., I-F.L., M.E., W.A.H.), Sergievsky Center (R.L.S., M.E., W.A.H.), Division of Epidemiology (R.L.S., G.A., W.A.H., S.S.), Division of
Socio-Medical Science (B.B.-A.), Department of Medicine (Division of General Medicine) (G.A., S.S.), and Division of Biostatistics (I-F.L., M.C.P.).
Presented in part in abstract form at the American Heart Association 23nd International Joint Conference on Stroke and Cerebral Circulation, Orlando,
Fla, February 1998.
Correspondence to Ralph L. Sacco, MD, MS, Neurological Institute, 710 W 168th St, New York, NY 10032.
© 2001 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org
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August 2001
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The data on stroke among Hispanic Americans are scarce
and inconclusive. Moreover, studies are hampered by the
heterogeneity among Hispanics who originate from Mexico,
South America, and the Caribbean basin. Hispanics are the
most rapidly growing minority in this country. Between 1980
and 1990, the Hispanic population increased by 39% compared with 7% for the overall US population.14 The Hispanic
population accounted for 11% of the total US population in
1998 and is estimated to be 19% in 2030. Caribbean Hispanics are 1 of the 2 major groups of Hispanics in the United
States and are relatively recent immigrants from the Caribbean Islands, including the Dominican Republic and Puerto
Rico.15 They are the fastest growing ethnic group in the
northeastern United States. The northern Manhattan community provides a unique opportunity for the study of Caribbean
Hispanics. According to the 1990 census, 63% of the 260 000
persons living in this area identified themselves as Hispanic.16,17 The Hispanic population enrolled in NOMASS is
representative of the underlying Caribbean Hispanic community in New York City. This population is primarily Dominican (62%), with an additional 14% being Puerto Rican, 12%
being Cuban, and 12% reporting origins from various Caribbean islands and South America.
Despite the mounting evidence that stroke risk factors may
differ among race-ethnic groups, public health programs and
national guidelines for stroke prevention continue to focus on
the identification of risk factors in the general population
without addressing the specific needs of race-ethnic groups.18
The ability to provide targeted information to different
race-ethnic groups is dependent on epidemiological studies
capable of comparing risk differences in these groups; definitive differences among race-ethnic groups are best measured
through a comparison of individuals from the same population or community. This population-based methodology helps
to minimize biases that may arise from comparisons of
groups living in different physical, social, and healthcare
environments. The aim of the present study was to use a
population-based case-control design to determine whether
the OR, prevalence, and etiological fraction (EF) for stroke
risk factors vary among whites, blacks and Caribbean Hispanics living in the same geographically defined community.
Subjects and Methods
NOMASS is an ongoing, prospective, population-based epidemiological study designed to determine stroke incidence, risk factors,
and prognosis in a multiethnic, urban population. Northern Manhattan consists of the area north of 145th Street, south of 218th Street,
bordered on the west by the Hudson River, and bordered on the east
by the Harlem River. In 1990, ⬇260 000 persons lived in the region,
of whom 40% were aged ⬎39 years.
Selection of Patients
Patients eligible for the population-based case-control portion of
NOMASS were prospectively enrolled if they met the following
criteria: (1) diagnosed with first cerebral infarction between July 1,
1993, and June 30, 1997; (2) were aged ⬎39 years at onset of the
stroke; and (3) resided in the northern Manhattan community in a
household with a telephone. Patients with TIA (ie, neurological
deficits lasting ⬍24 hours and no ischemic infarct found on brain
imaging) were excluded. Prospective case surveillance consisted of
daily screening of all admissions, discharges, and head CT scan logs
at the Presbyterian Hospital in New York City, the only hospital in
the community. Statewide Planning and Research Cooperative System (SPARCS) data indicate that ⬇80% of all patients in northern
Manhattan with stroke are hospitalized at Presbyterian Hospital. To
ensure complete incident stroke enumeration in the region, cases
were also identified through discharge lists from 14 hospitals in
nearby areas. Ongoing community-based surveillance for nonhospitalized patients with stroke was performed through random household telephone surveys and frequent interval contacts with community physicians, senior citizen centers, visiting nurse services, and
other social and cultural community agencies. Details are enumerated elsewhere.19
Patients diagnosed with stroke, as well as a variety of other
neurological syndromes (eg, aphasia, hemiparesis, weakness, coma,
syncope), were screened by a study research assistant, and the case
was discussed with a study neurologist to confirm eligibility. With
permission from the attending physician, written informed consent
was obtained from the patient or the family. The study was approved
by the institutional review boards at Columbia-Presbyterian Medical
Center and the other 14 hospitals.
Selection of Control Subjects
Community control subjects were enrolled if they (1) had never been
diagnosed with a stroke, (2) were aged ⬎39 years, and (3) resided for
ⱖ3 months in a household with a telephone in northern Manhattan.
Stroke-free subjects were identified by random digit dialing using
dual frame sampling to identify both published and unpublished
telephone numbers.20,21 When a household was contacted, the
research objectives were explained, and a resident older than 39
years was interviewed briefly to record age, sex, race-ethnicity, and
risk factors. These telephone interviews were conducted by Audits
and Surveys, Inc, using trained bilingual interviewers. The telephone
response rate was 93%.
Interview data from control-eligible subjects was downloaded to
the NOMASS computer system and assigned to cells defined by age,
sex, and race-ethnicity. Subjects were randomly selected from cells
matched to the accumulating case group by age, sex, and raceethnicity and were recontacted by the NOMASS staff and invited to
participate in the study. Appointments were made for in-person
evaluations at the hospital or home for those who could not come in
person (7% were conducted at home). Two concurrent control
subjects were selected and matched to each stroke case by age within
5 years, sex, and race-ethnicity. The overall response rate for
selected and matched control subjects was 75%. At the time of the
in-person visit, written informed consent was obtained.
Definition of Race-Ethnicity
Race-ethnicity was based on self-identification through a series of
interview questions modeled after the US census and conforming to
the standard definitions outlined in Directive 15.22 These government directives have been mandated for all epidemiological research
funded by National Institutes of Health. Two questions were asked:
(1) Are you of Hispanic/Spanish origin? (no/yes), and (2) Which of
the following best describes your race? (white; black or AfricanAmerican; Eskimo or Aleutian (Alaskan native); Asian or Pacific
Islander; other [specify]). All participants who identified themselves
as Hispanic were classified as such regardless of the answer to
question 2. All participants who classified themselves as white
without any Hispanic origin or as black without any Hispanic origin
were classified as white, non-Hispanic, or black, non-Hispanic,
respectively. For this study, Caribbean Hispanics were classified as
those from the Dominican Republic, Puerto Rico, Cuba, and other
Caribbean basin countries.
Index Evaluation of Patients and Control Subjects
Data were collected through interview of the patients and control
subjects by trained bilingual research assistants using standardized
data collection instruments, review of the medical records, physical
and neurological examination by study physicians, and fasting blood
specimens for lipid and glucose measurements. When the subject
was unable to answer questions due to aphasia, coma, dementia, or
Sacco et al
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other conditions, a proxy who was knowledgeable about the patient’s
history was interviewed. Proxy respondents were used for 26% of
patients and 1% of control subjects. Stroke-free control subjects were
interviewed in person and evaluated in the same manner as patients.
Subjects were interviewed regarding sociodemographic characteristics, stroke risk factors, and other medical conditions. Standardized
questions were adapted from the Centers for Disease Control and
Prevention Behavioral Risk Factor Surveillance System regarding
the following conditions: hypertension, diabetes, hypercholesterolemia, peripheral vascular disease, TIA, cigarette smoking, alcohol
use, and cardiac conditions such as myocardial infarction, coronary
artery disease, angina, congestive heart failure, atrial fibrillation,
other arrhythmias, and valvular heart disease.23 Standard techniques
were used to measure blood pressure, height, weight, and fasting
glucose levels. Definite hypertension was defined as a systolic blood
pressure recording of ⱖ160 mm Hg or a diastolic blood pressure
recording of ⱖ95 mm Hg based on the average of the 2 blood
pressure measurements or as a patient’s self-report of a history of
hypertension or antihypertensive drug use. Diabetes mellitus was
defined as a fasting glucose level of ⬎140 mg/dL (7.7 mmol/L), the
patient’s self-report of such a history, or insulin or hypoglycemic
drug use.24 Coronary artery disease was defined as a history of either
myocardial infarction, angina, CABG, or angioplasty or the current
use of cardiac medications. To be included in the definition of atrial
fibrillation, subjects reported they had been told they had chronic or
paroxysmal atrial fibrillation by a health professional such as a
physician. For this analysis, smoking was defined as currently
smoking cigarettes, heavy smoking was defined as ⱖ40 years of
smoking or smoking ⱖ1 pack/d for ⬎20 years, and heavy alcohol
use was defined as current drinking of ⱖ5 drinks/d. Physical activity
was assessed through a questionnaire adapted from the National
Health Interview Survey that recorded the frequency and duration of
14 activities during the 2 prior weeks.19 Body mass index was
calculated as weight (kg) divided by height (meters) squared, and
obesity was defined as body mass index of ⱖ27.8 for men and ⱖ27.3
for women.25
Statistical Analysis
The OR, prevalence, and EF were calculated for the complete sample
and for each race-ethnic group. Specifically, the risk factors evaluated among whites, blacks and Caribbean Hispanics were hypertension, diabetes, atrial fibrillation, coronary artery disease, current
smoking, heavy alcohol use, and physical inactivity. Multivariate
adjusted OR and 95% CIs were calculated using conditional logistic
regression. Prevalence rates were estimated from the proportion of
individuals identified with the risk factor among population-based
control subjects. The univariate EF, or population attributable risk,
provided an estimate of the proportion of the strokes in the
population group attributed to a particular risk factor and was
calculated with the equation EF⫽P(OR⫺1)/[1⫹P(OR⫺1)], where P
is prevalence.
In addition, multivariate EFs were estimated using multivariate
ORs and conditional prevalences (ie, prevalence of a risk factor
given the presence of the other risk factors). Prevalence rates were
TABLE 1.
Stroke Risk Factor Differences
1727
TABLE 2. Overall Multivariate ORs for NOMASS Matched for
Age, Sex, and Race-Ethnicity and Adjusted for the Listed
Risk Factors
OR (95% CI)
P
Hypertension
2.0 (1.5–2.5)
0.0001
Diabetes
1.7 (1.3–2.2)
0.0001
Atrial fibrillation
2.5 (1.6–3.9)
0.0001
Coronary artery disease
1.4 (1.1–1.9)
0.01
Physical Inactivity
2.7 (2.1–3.4)
0.0001
Heavy alcohol (ⱖ5 drinks/d)
2.3 (1.0–5.0)
0.04
Current smoking
1.1 (0.8–1.4)
0.7
Education
0.5 (0.3–0.6)
0.0001
compared among whites, blacks, and Caribbean Hispanics. CIs
excluding 1.0 were considered to demonstrate significantly different
prevalence rates. We used the bootstrap method to calculate CIs and
demonstrate significance for each of the multivariate EFs.26
Results
From July 1, 1993, to June 30, 1997, 688 patients with first
ischemic stroke and 1156 stroke-free control subjects were
enrolled (Table 1). The mean age of the subjects was 70
years, and 56% of patients and 60% of control subjects were
women. The overall race-ethnic distribution of cases was
50% Caribbean Hispanic, 28% black, and 20% white; 2%
were classified as “others.” Control subjects were more
educated than stroke patients, with 48% of control subjects
and 35% of patients having completed high school.
The multivariate model for stroke risk factors in the overall
study sample demonstrated that hypertension, atrial fibrillation, diabetes, coronary artery disease, physical inactivity,
and heavy alcohol use (ⱖ5 drinks/d) were independent risk
factors for ischemic stroke (Table 2). These ORs were
calculated after matching by age, sex, and race-ethnicity and
are adjusted for socioeconomic confounding by adding education to the multivariate model. Neither current cigarette
smoking nor heavy smoking was an independent risk factor
for ischemic stroke in this older cohort and was not controlled
Demographics for NOMASS Participants
Patients
(n⫽688)
Control Subjects
(n⫽1156)
Mean age, y
70⫾13
70⫾12
Women, %
56
60
Race-ethnicity, %
White
20
22
Black
28
32
Hispanic
50
45
35
48
Education completed
High school, %
Figure 1. Hypertension: OR and prevalence in NOMASS.
Matched for age and sex and adjusted for diabetes mellitus,
atrial fibrillation, coronary artery disease, physical inactivity, and
education. *Significant difference in prevalence compared with
whites (P⬍0.05).
1728
Stroke
August 2001
Figure 2. Diabetes mellitus: OR and prevalence in NOMASS.
Matched for age and sex and adjusted for hypertension, atrial
fibrillation, coronary artery disease, physical inactivity, and education. #Significant difference in OR compared with whites
(P⬍0.05); *significant difference in prevalence compared with
whites (P⬍0.02).
Figure 4. Coronary artery disease: OR and prevalence in
NOMASS. Matched for age and sex and adjusted for hypertension, diabetes mellitus, atrial fibrillation, physical inactivity, and
education. *Significant difference in prevalence compared with
whites (P⬍0.05).
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among whites (P⬍0.05). The EF for diabetics was small for
the elderly white subgroup. Finally, physical inactivity was a
strong stroke risk factor for all 3 race-ethnic groups, although
the prevalence was significantly greater among Caribbean
Hispanics, and the EF was twice as great among Caribbean
Hispanics (EF 38%) as among whites (EF 18%).
for or included in further analysis. The prevalence of any
smoking was 40%, whereas that of current smoking was only
18%. Also, we excluded heavy alcohol use from the stratified
models because the number of heavy drinkers by race-ethnic
group was too small.
Figures 1 through 5 show a comparison of the OR and
prevalence for each risk factor by race-ethnic subgroup. Table
3 demonstrates the EF and 95% CI for each risk factor
stratified by race-ethnicity. Among whites, the OR, EF, and
prevalence were greatest for atrial fibrillation (OR 4.4, EF
20%) and coronary artery disease (OR 1.3, EF 16%). For
atrial fibrillation, we found a significantly greater OR
(P⬍0.003) and EF among whites than among Caribbean
Hispanics.
The EF and prevalence of hypertension were greatest
among blacks (hypertension 62%, EF 37%) and Caribbean
Hispanics (hypertension 58%, EF 32%) compared with
whites (hypertension 43%, EF 25%). In addition, both Caribbean Hispanics and blacks demonstrated a significantly
greater prevalence of diabetes, and the OR for diabetes was
significant among Caribbean Hispanics compared with that
We found variation in the prevalence, ORs, and EFs for key
stroke risk factors among whites, blacks, and Caribbean
Hispanics living in northern Manhattan. Although differences
in the OR for stroke risk have previously been reported
between whites and blacks for factors such as cardiac disease
and diabetes,8 –13 this is the first study to examine such
differences in a community-based, multiethnic population
using the EF and controlling for common stroke risk factors.
The EF estimates the proportion of strokes attributable to a
specific stroke risk factor. Specifically, the use of the EF in
this study provides information on the proportion of the
population at risk of stroke who would be eliminated with the
control of a specific risk factor. The EF is a function of both
the OR and the prevalence of a risk factor and provides
Figure 3. Atrial fibrillation: OR and prevalence in NOMASS.
Matched for age and sex and adjusted for hypertension, diabetes mellitus, coronary artery disease, physical inactivity, and
education. #Significant difference in OR compared with whites
(P⬍0.05); *significant difference in prevalence compared with
whites (P⬍0.02).
Figure 5. Physical inactivity: OR and prevalence in NOMASS.
Matched for age and sex and adjusted for hypertension, diabetes mellitus, atrial fibrillation, coronary artery disease, and education. *Significant difference in prevalence compared with
whites (P⬍0.04).
Discussion
Sacco et al
Stroke Risk Factor Differences
1729
TABLE 3. EFs and 95% CIs for Stroke Risk Factors Among Whites, Blacks, and
Hispanics for NOMASS Participants
Risk Factor
Whites
Blacks
Hispanics
Hypertension
0.25 (0.01 to 0.45)
0.37 (0.16 to 0.57)
0.32 (0.15 to 0.43)
Diabetes
0 (⫺0.08 to 0.10)
0.14 (0.04 to 0.25)
0.10 (0.04 to 0.15)
Atrial fibrillation
0.20 (0.06 to 0.39)
0.03 (⫺0.02 to 0.08)*
0.02 (0.00 to 0.04)*
Coronary artery disease
0.16 (⫺0.008 to 0.35)
0.02 (⫺0.06 to 0.13)
0.06 (0.001 to 0.14)
Physical activity
0.18 (0.07 to 0.36)
0.29 (0.19 to 0.44)
0.38 (0.24 to 0.44)
*Significantly different EF attributed to atrial fibrillation in whites compared with blacks and
Hispanics.
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important information that is useful in the planning of stroke
intervention and implementing health policy in different
subpopulations. The usefulness of the EF lies in the ability to
use this calculation to measure the impact of the risk factor in
a population and thus to estimate the benefit of risk elimination. EF is best used when risk factors are considered to be
modifiable and more proximate in the causal chain of events
leading to disease such as stroke. Although statistically
significant differences in the EF of risk factors were found
only with atrial fibrillation, the potential public health importance is no less significant. Our study demonstrates significant differences in prevalence and risk, as well as trends
toward significance in EF. We demonstrate the disproportionate burden of these modifiable risk factors among whites,
blacks, and Caribbean Hispanics and suggest that differential
prevention strategies by race-ethnicity are needed to reduce
the number of strokes.
Blacks and Caribbean Hispanics had a greater stroke EF
for hypertension than did whites in the present study. It has
been shown that both the prevalence and the effect of
hypertension are greater among blacks than among whites
using the more traditional measures of OR and prevalence.27
Results of preliminary ecological and cross-sectional studies
of hypertension in Hispanic Americans compared with nonHispanic whites have been conflicting for Hispanics, depending on the place of origin of Hispanics.28 –31 A limitation of
these studies was the inability to make direct comparisons of
whites, blacks, and Hispanics living in the same community
and to provide a summary measurement of differential risk
for public health planning.
Our findings regarding the variation in the EF for hypertension emphasize the need for specific risk factor targeting
in various communities or populations with respect to blood
pressure control. Possible explanations for the greater EF of
hypertension for blacks include genetic, environmental, and
treatment factors. Researchers have found several gene mutations implicated in the pathogenesis of hypertension that
have a higher incidence in blacks.32 In addition, several
studies have found a correlation between the prevalence of
hypertension in blacks and both higher levels of lipoprotein(a) and greater thickness of the left ventricular septal and
posterior walls.33,34 It has also been shown that African
Americans respond less favorably to certain antihypertensive
drug therapies, particularly ␤-blockers and ACE inhibitors.35
Sociocultural, economic, and environmental determinants
may also influence the potency of certain risk factors such as
hypertension in blacks and Hispanics. For example, it has
been demonstrated that blacks are less aware of their hypertension status, perhaps as a result of poorer education on
health issues or differences in access to primary medical
care.36 Among Mexican Americans, data from the San Antonio Heart Study demonstrated an inverse association between
diastolic blood pressure and sociocultural status, especially
education and “structural assimilation,” described as the
“process by which minority groups enter the clubs, cliques
and institutions of a broader society.”27
For atrial fibrillation, the prevalence, OR, and EF differences found among whites, blacks, and Caribbean Hispanics
confirm earlier studies that demonstrated a greater likelihood
of atrial fibrillation as a stroke risk factor among whites
versus blacks.37 Others have suggested that although prevalence differences in atrial fibrillation between white and
blacks may be small, a differential potency of the risk factor
may contribute to it having a greater impact in whites.38
Findings from the Cardiovascular Health Study suggested the
prevalence of atrial fibrillation was similar between blacks
and whites; however, this comparison was made in a very
small group of blacks, and EF was not calculated.39 There
have been no studies that assessed atrial fibrillation in
Caribbean Hispanics compared with both whites and blacks.
Although some of the race-ethnic differences in the burden of
atrial fibrillation may be attributed to the younger age of the
present study Caribbean Hispanics (mean age 66 years) and
blacks (mean age 68 years) compared with the whites (mean
age 77 years), age would not affect the Ors, because patients
and control subjects were matched by age. The present
finding that whites have a greater EF for atrial fibrillation
(20%) than Caribbean Hispanics (2%) and blacks (3%)
suggests that more aggressive identification and control of
this risk factor are especially needed among white
communities.
One of the more important findings from this study is the
elevated EF for physical inactivity found in all 3 race-ethnic
groups. Numerous studies have shown that physical fitness is
an independent predictor of death from cardiovascular disease among healthy, middle-aged men and women.40 – 43
Recent findings continue to provide evidence of the overwhelming benefit of physical activity on stroke prevention.44 – 46 Criticisms of this literature include the idea that
subjects who report a lack of physical activity may have an
undiagnosed or subclinical condition that prevents such
activity and that physically fit subjects may adopt other
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August 2001
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health-promoting habits. The present work suggests that
decreasing the risk burden of physical inactivity could substantially alter stroke risk among all race-ethnic groups. In
addition, targeted intervention for Caribbean Hispanics is
crucial, because they have the highest EF for lack of physical
inactivity (38%), as well as the highest OR (3.3) and
prevalence (37%).
The results from the NOMASS support the idea that
effective educational and interventional stroke programs
should take into account differences in OR, prevalence, and
EF of stroke risk factors in different race-ethnic groups. This
notion is particularly important to current public health
initiatives because there continues to be a significant disparity
in both stroke incidence and mortality rates among raceethnic groups. Stroke prevention guidelines must account for
these differences in statements to healthcare professionals.
The failure to use information that describes the differences
in risk factor potency in different race-ethnic groups when
creating prevention and treatment programs may be responsible for the continued failure to achieve goals in terms of risk
factor control and regulation. Targeted public health programs, when designed in conjunction with data on race-ethnic
EF, may be the most cost-effective means to reduce the stroke
burden in multiethnic communities.
Acknowledgments
This work was supported by grants from the National Institute of
Neurological Disorders and Stroke (R01-NS-27517, R01-NS-29993,
and T32-NS-07153) and the General Clinical Research Center
(2-M01-RR-00645). We acknowledge the support of Dr J.P. Mohr,
MD, MS, Director of Cerebrovascular Research, and the help
provided by Sarah Evers, Yukmila Soriano, and Chris Kleeman.
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Race-Ethnic Disparities in the Impact of Stroke Risk Factors: The Northern Manhattan
Stroke Study
Ralph L. Sacco, Bernadette Boden-Albala, Gregory Abel, I-Feng Lin, Mitchell Elkind, W. Allen
Hauser, Myunghee C. Paik and Steven Shea
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Stroke. 2001;32:1725-1731
doi: 10.1161/01.STR.32.8.1725
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