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(Stroke. 1997;28:929-935.)
© 1997 American Heart Association, Inc.
Articles |
Race-Ethnicity and Determinants of Carotid Atherosclerosis in a Multiethnic Population
The Northern Manhattan Stroke Study
From the Department of Neurology (R.L.S., J.K.R., B.B.-A., Q.G., I.-F.L., D.E.K., W.A.H.); Sergievsky Center (R.L.S., J.K.R., W.A.H.); School of Public Health, Divisions of Epidemiology (R.L.S., W.A.H., S.S.) and Biostatistics (M.C.P.); and Department of Medicine (L.B., S.S.), Columbia-Presbyterian Medical Center, New York, NY.
Correspondence to Ralph L. Sacco, MD, MS, Neurological Institute, Room 547, Columbia-Presbyterian Medical Center, 710 W 168 St, New York, NY 10032. E-mail rls1{at}columbia.edu
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Abstract |
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 Top Abstract IntroductionSubjects and MethodsResultsDiscussionReferences |
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Background and Purpose Risk factors for carotid atherosclerosis have been studied in white populations but infrequently in multiethnic cohorts. The aim of this study was to determine the importance of race-ethnicity and other factors associated with carotid atherosclerosis in a mixed population of Hispanics, blacks, and whites.
Methods As part of the Northern Manhattan Stroke Study, 526
stroke-free community residents (aged 
40 years; 41% men, 59% women;
46% Hispanic, 31% black, 23% white) were recruited through
random-digit dialing and had vascular risk factor evaluations. Maximum
internal carotid artery plaque thickness (MICPT) was measured with
B-mode ultrasound. The frequency distribution of MICPT was examined in
the three race-ethnic groups, and multivariate
regression was performed to identify factors that were independently
associated with MICPT.
Results Mean MICPT in the entire sample was 1.5±1.4 mm, increased directly with age, and was greater in whites and blacks than Hispanics. Other independent determinants of MICPT included smoking, glucose, LDL cholesterol, and hypertension. After we controlled for these covariates, Hispanic (versus non-Hispanic) race-ethnicity was still an independent determinant of less carotid plaque. There was a significant interaction between race-ethnicity and LDL cholesterol, with a greater effect of increasing LDL cholesterol among Hispanics.
Conclusions Atherosclerotic risk factors were predictive of MICPT in this mixed-ethnic cohort. Hispanics had significantly less carotid plaque after adjustment for other known risk factors, but they also had a greater impact of increasing LDL cholesterol.
Key Words: atherosclerosis • carotid arteries • epidemiology • racial differences • risk factors
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The burden of atherosclerotic-related disease varies among race-ethnic groups. In northern Manhattan, we have found that both blacks and Hispanics have a greater stroke incidence and a greater preponderance for intracranial atherosclerotic stroke than whites, yet a similar proportion of extracranial atherosclerotic stroke.1 2 Others have reported that cardiovascular mortality is greater in blacks than whites,3 4 5 yet rates are lower or similar in Hispanics compared with whites.6 7 8 These differences in the incidence, severity, and distribution of atherosclerotic disease may be partially explained by disparities in the race-ethnic distribution of vascular risk factors.9 10 11 12 13 14 15 16 Whether differences remain after controlling for risk factors, socioeconomic status, and access to medical care remains controversial.17 18
Carotid duplex Doppler sonography has emerged as an easily performed and noninvasive method of evaluating presymptomatic atherosclerosis19 and is thus useful in observational studies and clinical trials. These studies, however, have investigated predominantly white subjects with relatively little information on blacks and Hispanics.
The aim of this analysis was to investigate the determinants of carotid atherosclerosis in a multiethnic, population-based sample of stroke-free adults and, in particular, to evaluate the interrelationship among carotid atherosclerosis, race-ethnicity, and conventional vascular risk factors.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The Northern Manhattan Stroke Study (NOMASS) is a prospective community-based study designed to determine and compare incidence rates of stroke, especially among race-ethnic groups, investigate risk factors for first stroke, and identify predictors of stroke severity and outcome after stroke. The study is approved by the Institutional Review Board of Columbia University. Stroke subjects and control subjects are recruited from northern Manhattan, a heterogeneous community of approximately 260 000 residents, composed of approximately 63% Hispanics, 20% blacks, and 15% whites.
Selection of Subjects
The cohort for this analysis was derived from the
stroke-free control subjects enrolled in NOMASS. These subjects were
identified by random-digit dialing with the use of dual-frame sampling
to identify both published and unpublished telephone numbers in their
appropriate proportions.20 21 When a household was
contacted, the research objectives were explained, and a resident older
than 39 years was interviewed for approximately 10 minutes. If there
was more than one person living in the household, one family member was
randomly selected by the telephone interviewer by a computer-generated
algorithm. To be considered eligible as a study control, the subject
must have completed the telephone interview, had no prior history of
stroke, been older than 39 years, resided in one of the five zip codes
of northern Manhattan for at least 3 months, and lived in a household
with a telephone. These interviews were conducted by Audits and Surveys
with trained bilingual interviewers, and the data were directly
downloaded to the computer system at the Stroke Service. The telephone
response rate was 94%.
The interview data from control-eligible subjects were sorted in the NOMASS data set by sex and race-ethnicity and served as a data bank from which to draw control subjects for the case-control portion of the study. Control subjects were selected on the basis of individual matching to incident stroke cases with age, sex, and race-ethnicity as matching variables. The stroke-free subjects were recontacted by the NOMASS staff and invited to participate in the study. Appointments were made for in-person evaluations at the Columbia Presbyterian Medical Center or for a home visit for those who could not come in person (7% of visits were done at home).
After informed consent was obtained, subjects were interviewed regarding sociodemographic characteristics, stroke risk factors, other medical conditions, and functional status; fasting blood specimens for lipid and glucose measurements were obtained; an electrocardiogram was performed; and a neurological examination was completed. Approximately two thirds were randomly selected to have carotid duplex Doppler sonography. This latter sample of stroke-free subjects constituted the cohort for this analysis.
Definition of Baseline Variables
All assessments were conducted in English or Spanish depending
on the primary language of the participant. Race-ethnicity was based on
self-identification through a series of interview questions modeled
after the US census. All participants responding affirmatively to being
of Hispanic/Spanish origin or identifying themselves as Hispanic were
classified as Hispanic. All participants classifying themselves as
white without any Hispanic origin or black without any Hispanic origin
were classified as white (non-Hispanic) or black (non-Hispanic),
respectively.
Trained research assistants interviewed the subjects, performed in-person measurements, and collected fasting blood samples for lipid and glucose measurements. Study physicians performed physical and neurological examinations. Standardized questions regarding sociodemographic characteristics and stroke risk factors such as hypertension, diabetes mellitus, cardiac disease, peripheral vascular disease, and other medical conditions were adapted from the Behavioral Risk Factor Surveillance System by the Centers for Disease Control and Prevention.22 Cigarette smoking and ethanol use were characterized as current or not, and the amounts were collected as packs per day, number of years smoked, and the usual number of drinks per day, week, or month, respectively.
Blood pressure measurements were determined at the clinical examination with the use of an adult-size calibrated standard aneroid sphygmomanometer (Omron). In each subject, after 5 minutes of relative immobility in a sitting position, two blood pressure measurements separated by 10 minutes were recorded. In subjects with blood pressure recordings differing by >10 mm Hg, a third measurement was obtained by the study physician. Height and weight were determined with the use of calibrated scales. Fasting glucose was measured with a Hitachi 747 automated spectrometer (Boehringer). Fasting lipid panels including total cholesterol, HDL cholesterol, triglycerides, and LDL cholesterol (calculated) were measured with a Hitachi 705 automated spectrometer (Boehringer) at the Specialized Center of Research in Atherosclerosis.
Hypertension was defined as a systolic blood pressure
recording 160 mm Hg or a diastolic blood
pressure recording 95 mm Hg based on the mean of the
two readings of the blood pressure measurements, a patient's
self-report of a history of hypertension, or antihypertensive use. A
history of diabetes mellitus was defined by patient's self-report of
such a history, insulin use, or oral hypoglycemic use. A history of
hypercholesterolemia was defined by a
patient's self-report of hypercholesterolemia
or of cholesterol-lowering drug use. Body mass index was
calculated as weight (kilograms) divided by height (meters) squared,
and obesity was defined as body mass index 27.8 for men and 27.3
for women.
Carotid Plaque Determination
Carotid atherosclerosis was assessed with a
Siemens Quantum 2000 duplex ultrasound system with a 5-MHz probe. All
measurements were performed by technicians previously trained in
identifying and measuring carotid atherosclerosis for
the ACAPS and the ACAS. With the subject in the supine position, the
carotid arteries were imaged in the longitudinal (anterior, lateral,
and posterior views) and transverse planes. Both ICAs were examined for
the presence of atherosclerotic plaque, defined as an area of focal
hyperechoic wall thickening. If no atherosclerosis was
identified, MICPT was recorded as zero. If plaque was imaged, the
view showing the thickest plaque was frozen, and with an electronic
cursor and according to the methods of Pignoli et al,19
the intimal-medial wall thickness (which includes the thickness of the
atherosclerotic plaque) was calculated and recorded as the MICPT
for that artery. For the analysis, the greater of the right and
left MICPT was used.
Statistical Methods
The mean, SD, and range for MICPT were calculated for the entire
sample and separately by race-ethnic group. ANOVA was used to compare
mean MICPT between subgroups defined by sociodemographic variables,
atherosclerotic risk factors, and comorbid, clinically evident
atherosclerotic disease. The associations between MICPT and continuous
measurements such as fasting glucose, systolic blood pressure,
diastolic blood pressure, and lipid levels (total
cholesterol, HDL cholesterol, LDL
cholesterol, and triglycerides) were assessed
by means of Pearson correlation coefficients.
Multivariate analyses consisted of fitting nonlinear regression models to restrict the range of predicted MICPT to positive numbers. Our model assumes that the natural logarithm of mean MICPT is a linear function of covariates. We also accounted for differences in variances by assuming that the variance of MICPT is proportional to the mean. Variables were selected for multivariate analyses a priori or based on Pearson correlation or ANOVA. Interactions between variables were assessed.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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The cohort for this analysis consisted of 526 stroke-free subjects enrolled in the NOMASS. The mean age was 69.9±11.5 years (median, 71 years; range, 40 to 99 years); 41% were men and 59% were women. The majority were Hispanics (46%), followed by blacks (non-Hispanics) (31%) and whites (non-Hispanics) (23%). Socioeconomic status was assessed by education and type of medical insurance: 34% had no high school education, 16% had some high school, 19% completed high school, 15% had some college, and 15% were college graduates; 69% had Medicare, 45% had some private insurance, and 30% had Medicaid (insurance groups are not mutually exclusive).
The mean MICPT for the entire cohort was 1.5±1.4 mm. The
distribution is shown in Fig 1
. Mean MICPT values by
sociodemographic variables, atherosclerotic risk factors, and
history of comorbid atherosclerotic disease are shown in Table 1. MICPT significantly increased with age. No difference
was found between men and women or by education or Medicaid status.
Mean MICPT was significantly greater among those with a history of
hypertension, hypercholesterolemia, and
cigarette smoking, as well as fasting glucose 7.70 mmol/L (140
mg/dL). A history of diabetes, obesity, and drinking more than two
alcoholic drinks per day were not associated with MICPT. Dose-response
relationships were found for MICPT and cigarette smoking as assessed by
current or former smoking, number of cigarettes smoked per day, and
duration (in years) of smoking. Appropriate dose-response relationships
were also found for LDL cholesterol and total
cholesterol, although they did not reach statistical
significance. However, Pearson correlation coefficients showed that LDL
cholesterol and total cholesterol were
significantly associated with MICPT (0.12 [P=.006] and
0.12 [P=.007], respectively). HDL cholesterol
and triglycerides were not significantly associated with
MICPT. Subjects with a clinical history of coronary artery
disease and peripheral vascular disease had greater mean
MICPT.
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Race-ethnic differences in MICPT are shown in Table 2.
Mean MICPT was less in Hispanics (1.2±1.5 mm) than in blacks
(1.7±1.3 mm) or whites (1.7±1.3 mm). Within each
race-ethnic group, MICPT increased with age except for the white
subgroup aged 40 to 59 years, among whom the number of subjects was
quite small. In each of the age strata, Hispanics had less carotid
plaque than blacks and whites.
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Multiple regression analysis was used to assess the effect of
race-ethnicity on mean MICPT with adjustment for other risk factors
(Table 3). Because the regression model was transformed
(to restrict predicted MICPT to positive values), the regression
coefficient for race, for example, represents the natural
logarithm of the ratio of MICPT for Hispanics versus non-Hispanics.
Race-ethnicity remained an independent predictor of MICPT (less for
Hispanics versus non-Hispanics) after adjustment for age, Medicaid
status, smoking duration, hypertension, fasting glucose, and LDL
cholesterol. A significant interaction was detected between
LDL cholesterol and Hispanic race-ethnicity. MICPT
increased as LDL cholesterol increased only among
Hispanics, but not among blacks and whites (Fig 2). For
example, an increase in LDL cholesterol of 1.55 mmol/L
(60 mg/dL) would lead to a 1.26-fold increase in MICPT in a Hispanic
and no increase in MICPT in a non-Hispanic.
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Our model included sex as a basic demographic characteristic. Medicaid
status was chosen as the measure of socioeconomic status. Education,
another measure of socioeconomic status, and Medicaid status were
inversely correlated in our population (concordance rate, 67%), and
when education was used instead of Medicaid in the final
multivariate model, the results were similar except
that Medicaid was a better determinant of MICPT than education.
Duration of smoking was chosen as the best measure of smoking based on
our univariate results and a prior report in the
literature.23 Moreover, the number of cigarettes smoked
per day was not an important predictor after adjustment for duration of
smoking. When stratified by sex, our final model was similar in both
men and women with the exception of smoking. A dose-response
relationship between smoking and MICPT was seen in both sexes; however,
in men the effect was seen primarily in those who smoked 40 years,
while in women the effect was seen in both those who smoked for 20 to
39 years and those who smoked 40 years. The effect of race-ethnicity
remained in both men and women. Fasting LDL cholesterol was
chosen to be included in the final model over total
cholesterol because it is a more specific
physiological parameter and
demonstrated a better dose-response relationship in the
univariate analysis. Comorbid conditions
(coronary artery disease and peripheral vascular
disease) were not included in the multivariate
analysis because, a priori, we considered them to be associated
with or markers of MICPT rather than potentially causal.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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This is the first study, to our knowledge, to investigate the determinants of carotid atherosclerosis in a population-based, multiethnic cohort. Age-adjusted MICPT was less in Hispanics than blacks or whites, and this relationship remained significant after adjustment for other sociodemographic variables and atherosclerotic risk factors. The reason for this protective association is not entirely clear. Our model attempts to control for potential environmental risk factor differences, but there could be other acquired factors that have not been measured in our study such as dietary factors and other lipid parameters. The persistence of race-ethnic differences in carotid wall thickness after we controlled for sociodemographics and atherosclerotic risk factors may also suggest a genetic explanation. Recent work has suggested that genes account for 74.9% of phenotypic variation in ICA wall thickness.24 Cholesterol metabolism and atherosclerotic plaque formation may vary by race-ethnic group because of unmeasured acquired factors or genetic differences. We found an interesting interaction between Hispanic (versus non-Hispanic) race-ethnicity and LDL cholesterol. With an increase in LDL cholesterol, MICPT increased more rapidly in Hispanics than in non-Hispanics. The reason for this is uncertain.
Previous work has described carotid atherosclerosis in blacks and whites, but there are few reports concerning Hispanics. The Insulin Resistance Atherosclerosis Study recently reported that Hispanics have significantly smaller CCA wall thickness and slightly, although not statistically significant, smaller ICA wall thickness than whites after adjustment for demographics, cardiovascular risk factors, and insulin resistance.25 In their study, in a separate cohort, blacks had a significantly greater CCA wall thickness and nonsignificantly smaller ICA wall thickness than whites. Hispanics could not be directly compared with blacks in their study. The ARIC study enrolled blacks in two of the four participating communities; at one location both blacks and whites were enrolled in proportion to their total numbers, while at the other location only blacks were enrolled.26 This was done to increase the overall representation of blacks in the study. In their report on cardiovascular risk factors and carotid wall thickness, however, race-ethnicity was not examined because the study design controlled for race-ethnicity through matching.27 Moreover, it may not be possible to compare race-ethnicity among subjects from different communities. In the Multicenter Isradipine Diuretic Atherosclerosis Study, the prevalence of carotid plaque was different between hypertensive blacks from Michigan and Georgia after adjustment for demographics and atherosclerosis risk factors.28 In another large nonreferral study of carotid atherosclerosis, the CHS, blacks accounted for only 4.7% of 5201 persons.29 Other nonreferral studies included few, if any, blacks.30 31 32 33 34
Some studies that have compared carotid atherosclerosis among whites and blacks have been subject to referral and selection biases because they were not population based, relied on angiographic techniques that were performed in selected subsamples, depended on patients referred to a carotid ultrasound laboratory, or combined symptomatic and asymptomatic patients. Among patients studied by arteriography for symptomatic carotid disease, there were more asymptomatic atherosclerotic lesions of the intracranial arteries in blacks, while whites had greater extracranial atherosclerotic involvement.35 Race was found to be an independent risk factor for predicting carotid stenosis among 99 black and 106 white patients evaluated by duplex Doppler in symptomatic patients,36 while others failed to confirm these observations.37 Among 1578 persons referred for carotid ultrasound including 153 blacks, whites showed significantly more plaque than blacks in the ICA, bifurcation, and external carotid artery after adjustment for age, sex, diabetes, hypertension, and cigarette smoking, while blacks had slightly more plaque than whites in the CCA.38
It is important to emphasize that there were other independent determinants of carotid atherosclerosis beside race-ethnicity in our multiethnic cohort, which included age, Medicaid status, hypertension, smoking duration, fasting glucose, and LDL cholesterol. Most of these findings are in agreement with those atherosclerotic risk factors identified in previously investigated, predominantly white, cohorts. In most studies age was strongly associated with carotid wall thickness, as in our study.27 29 30 31 32 39 We did not find sex to be a predictor of carotid plaque in our cohort, but our study population consisted of older subjects. The sex difference in plaque prevalence has been reported to be more marked at younger ages and decreases in the elderly.30 We used Medicaid status as a marker of socioeconomic status in our final model and found that it was independently associated with increased MICPT. The Kuopio Ischemic Heart Disease Risk Factor Study also found that low income was significantly associated with carotid atherosclerosis.40 These findings regarding socioeconomic status may reflect a variety of factors including decreased access to medical care, particularly those involving preventive health measures.
Modifiable risk factors for carotid atherosclerotic plaque, found in
our cohort as well as prior studies, were
hypertension,27 29 30 39 41
diabetes,29 32 39 42 and smoking.27 29 30 39
We found that duration of smoking was the best measure of cigarette
smoking exposure as a predictor of carotid plaque in our multiple
regression model. MICPT increased with pack-years smoked, but adding
the amount smoked did not significantly improve the model after
duration was included. It has been suggested previously that duration
of smoking was the most important smoking risk factor.23
Although a shorter duration of smoking had more of an effect among
women than among men, a dose-response relationship between smoking and
MICPT was observed for both sexes. When examined as continuous
variables, total cholesterol and LDL
cholesterol were significantly correlated with MICPT, while
HDL cholesterol and triglycerides were not. In
our final model, LDL cholesterol was a predictor of carotid
plaque among Hispanics. In a nested case-control study within the ARIC
study comparing those with the greatest with those with the least wall
thickness, LDL cholesterol was a significant determinant,
but only when those with LDL cholesterol 160 mg/dL and
those with LDL cholesterol 
100 mg/dL were
compared.27 Total triglycerides level
(categorized as 170 mg/dL or <170 mg/dL) was also independently
significant, but HDL cholesterol was not. The CHS, on the
other hand, found that LDL cholesterol and HDL
cholesterol, in an age- and sex-adjusted model, were
significantly correlated with maximum ICA wall
thickness.29
Differences in the demographics and risk factors of the study population may contribute to varying wall thickness in multiple studies. Our subjects were derived from northern Manhattan and may not be representative of race-ethnic groups in other parts of the United States. For example, our Hispanic residents are predominantly from the Dominican Republic and other Caribbean islands and may be different from Mexican Americans. Our urban population may differ from a more rural population, be older than other population samples that have more adults younger than 40 years, and have a lower socioeconomic status than other samples. Overall, mean MICPT in our study was 1.5±1.4 mm. In both the white and black subjects, mean MICPT was 1.7±1.3 mm, and this corresponds to the 90th percentile for wall thickness in this carotid segment in the ARIC study, which consisted of whites and blacks.27 Thus, our population had greater ICA wall thickening than those evaluated in the ARIC study. However, the mean age of our cohort was 69.9±11.5 years, while the ARIC study enrolled a generally younger population of subjects aged 45 to 64 years and would be expected to have less atherosclerosis. The CHS, which enrolled older subjects, found a mean maximal ICA wall thickness (by averaging the maximum values obtained for both the near and far walls of both carotids) similar to our values (women with CHD, 1.56±0.70 mm; women without CHD, 1.35±0.64 mm; men with CHD, 1.87±0.73 mm; men without CHD, 1.57±0.67 mm).43
In addition to study populations differing by age and race-ethnicity, it is sometimes difficult to compare results regarding carotid plaque among various studies because of differences in measurement methodologies. Our measurements were performed by ultrasound technicians who had been trained in the techniques used in two large studies of carotid atherosclerosis (ACAS and ACAPS). Studies were done systematically in all patients in each of the race-ethnic groups. In our study we recorded the maximal thickness of plaque, a focal echogenic wall thickening with encroachment on the vessel lumen, in both ICAs and used the larger of the two values in our analysis. In vessels without evidence of plaque, no measure of wall thickness was attempted, and the value was recorded as zero. Increased intimal-medial wall thickness without obvious plaque is thought to represent early atherosclerosis. Thus, our method may be less sensitive for early changes of atherosclerosis, but this would be true for all race-ethnic groups.
Other studies have measured wall thickness in multiple areas of the carotid and not just the ICAs, as was performed in our study. CCA wall thickness measurements have often been used because the CCA is more easily visualized than more distal arterial segments and because less variability has been reported.44 45 In the ARIC cohort, atherosclerosis at one site in the carotid artery (CCA or ICA) is correlated with atherosclerosis at other sites; however, this association diminishes with increasing wall thickness since atherosclerotic plaque can be quite focal and does not always imply the existence of thick plaque elsewhere.44 Moreover, despite the potential difficulties of measuring ICA wall thickness, the CHS found that a measurement of maximum ICA wall thickness is more related to clinical atherosclerotic disease than maximum CCA wall thickness,43 supporting our choice to use a single maximal measurement in the ICA.
In summary, in the northern Manhattan community, Hispanics had significantly less carotid atherosclerosis than blacks and whites after we controlled for sociodemographic variables and atherosclerotic risk factors. The differentiation between genetic and environmental reasons for some of these race-ethnic disparities in atherosclerotic vascular disease is the subject of ongoing investigations. The increased atherogenicity of LDL cholesterol in Hispanics compared with blacks and whites has not previously been reported. Our findings suggest that control of dyslipidemia should be particularly targeted in the Hispanic population to control atherosclerosis and atherosclerotic-related disease. Clearly, certain preventative health recommendations that are aimed at reducing the burden of vascular disease can be made now and modified in the future as the reasons for these race-ethnic differences are clarified.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study 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 RR00645). Dr Berglund is a Florence Irving Associate Professor of Medicine and an Established Scientist of the American Heart Association, New York City Affiliate. We acknowledge the support of Dr J.P. Mohr, Director of Cerebrovascular Research, and Dr Henry Ginsberg, Director of the Irving Clinical Research Center, and the assistance provided by Drs Robert Gan and Mitchell S. Elkind, fellows in stroke and neuroepidemiology.
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Footnotes |
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Presented in part in abstract form at the 20th International Joint Conference on Stroke and Cerebral Circulation, Charleston, SC, February 9-11, 1995.
Received December 26, 1996; revision received February 27, 1997; accepted February 27, 1997.
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