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(Stroke. 1996;27:1744-1749.)
© 1996 American Heart Association, Inc.
Articles |
Ethnic Differences in Carotid Wall Thickness
The Insulin Resistance Atherosclerosis Study
the Department of Public Health Sciences, Bowman Gray School of Medicine, Winston-Salem, NC (R.B.D'A., G.B., G.H., L.W.); Department of Radiology, New England Medical Center, Boston, Mass (D. O'L.); Department of Preventive Medicine/Biometrics, University of Colorado School of Medicine, Denver (M.R.); Division of Research, Kaiser Permanente, Oakland, Calif (J.S.); Division of Epidemiology and Clinical Applications, National Institutes of Health, National Heart, Lung, and Blood Institute, Bethesda, Md (P.J.S.); Departments of Medicine (M.F.S.) and Physiology and Biophysics (R.N.B.), University of Southern California School of Medicine, Los Angeles; and Department of Medicine, University of Texas Health Science Center at San Antonio (S.M.H.).
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Abstract |
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Background and Purpose Ethnic differences in cardiovascular disease (CVD) morbidity and mortality have been observed in US adults. However, little data exist on differences in indices of preclinical atherosclerosis such as carotid wall intima-media thickness (IMT) for US non-Hispanic whites, Hispanics, and blacks. This study was undertaken to determine whether there were ethnic differences in carotid wall IMT.
Methods Internal carotid artery (ICA) IMT and common carotid artery (CCA) IMT, indices of atherosclerosis, were assessed with the use of B-mode ultrasound in 1020 nondiabetic participants in the Insulin Resistance Atherosclerosis Study, a multicenter study designed to examine the association between insulin resistance and carotid atherosclerosis. The study included 281 blacks, 329 Hispanics, and 410 non-Hispanic whites aged 40 to 69 years.
Results Blacks had significantly greater CCA IMT than non-Hispanic whites (865 versus 808 µm); this remained significant after adjustment for major CVD risk factors and insulin sensitivity (864 versus 823 µm). There were no significant differences in ICA IMT between blacks and non-Hispanic whites. Hispanics had significantly lesser CCA IMT than non-Hispanic whites (749 versus 776 µm), and these differences remained significant after adjustment for traditional cardiovascular risk factors and insulin sensitivity (750 versus 778 µm). There were no significant differences in ICA IMT between non-Hispanic whites and Hispanics.
Conclusions We conclude that ethnic differences exist in CCA but not in ICA IMT in nondiabetic subjects. These differences in IMT, which are indicators of atherosclerosis, are a noninvasive measure that is consistent with some of the data on clinical end points. These differences may be associated with the observed differences in CVD morbidity and mortality among major ethnic groups in the United States.
Key Words: atherosclerosis • blacks • ethnic groups • Hispanic Americans • insulin
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Major ethnic differences in CVD morbidity have been reported. Blacks, particularly women, have an increased rate of CVD relative to non-Hispanic whites,1 2 3 while CVD mortality is similar or lower in Hispanics than in non-Hispanic whites.4 5 6 7 8 9
Major differences in CVD risk factors have also been noted.10 11 12 13 14 15 16 17 Blacks have an increased prevalence of both hypertension13 and NIDDM16 17 relative to non-Hispanic whites, which might increase the risk of CVD in the former group. In contrast, the higher levels of HDL cholesterol in blacks (particularly males) than in non-Hispanic whites would result in a lower risk of CVD.10 When Hispanic and non-Hispanic whites are compared, Hispanics have increased obesity,18 higher triglyceride and lower HDL cholesterol levels,19 20 and increased incidence of NIDDM.21 22 23 In addition, Hispanics have a lower24 or similar25 prevalence of hypertension than non-Hispanic whites. However, the estimated risk of CVD according to the Framingham multivariate model is considerably higher in Hispanics than in non-Hispanic whites,26 raising the question of whether protective mechanisms against atherosclerosis exist in Hispanics.
B-mode ultrasound of the carotid artery permits a noninvasive assessment of atherosclerosis27 and thus is useful in population-based studies. Carotid IMT is closely correlated with the prevalence of myocardial infarction28 and is related to risk factors for CVD.29 However, there are few data on carotid IMT among blacks and Hispanics.
The aim of this report is to evaluate IMT in the ICA and CCA in nondiabetic blacks, Hispanics, and non-Hispanic whites in the IRAS.
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Subjects and Methods |
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The IRAS is a multicenter epidemiological study whose purpose is to explore cross-sectional relationships among insulin resistance, CVD risk factors, and CVD in blacks, Hispanics, and non-Hispanic whites across a broad range of glucose tolerance. A full description of the methods and recruitment of the cross-sectional phase of the IRAS has been published.30 This study was conducted at four clinical centers. Centers in Oakland and Los Angeles, Calif, studied blacks and non-Hispanic whites recruited from Kaiser Permanente, a nonprofit health maintenance organization. The clinical centers in San Antonio, Tex, and San Luis Valley, Colo, studied Hispanics and non-Hispanic whites recruited from two ongoing population-based studies (the San Antonio Heart Study23 and the San Luis Valley Diabetes Study22 ).
The IRAS examination required two visits conducted approximately 1 week apart (range, 2 to 28 days), each lasting approximately 4 hours. Participants were asked to fast for 12 hours before each visit, to abstain from heavy exercise and alcohol for 24 hours, and to refrain from smoking the morning of the examination. Glucose tolerance status was determined during the first visit of the clinical examination with the use of a 2-hour OGTT with a 75-g glucose load (Orangedex, Custom Laboratories) and World Health Organization classification criteria.31 Individuals taking oral hypoglycemic medication were classified as having NIDDM regardless of OGTT results. Diabetics who were taking insulin at the time of the examination were excluded from the study. At the second visit, the FSIGT was performed. Blood was collected fasting and 2 hours after the glucose load.
Plasma glucose was measured on an automated autoanalyzer (Yellow Springs Equipment Co). Insulin was measured with the dextran-coated radioimmunoassay.32 On the first day, fasting blood was drawn for a complete ß-quantification procedure as described by the Lipid Research Clinics.
Resting blood pressure was measured in the right arm after 5 minutes in the seated position. A standard mercury sphygmomanometer was used, and three readings were taken according to a standard protocol. The second and third readings were averaged to obtain the blood pressure used in the analyses. Patients were classified with hypertension if their mean systolic blood pressure was greater than 140 mm/mg or mean diastolic blood pressure was greater than 90 mm/mg or if they were currently taking medication for high blood pressure.
Insulin resistance was assessed by the FSIGT33 34 with minimal model analyses.35 Two modifications of the original protocol were used. An injection of insulin rather than tolbutamide was used to ensure adequate plasma insulin levels for the computation of insulin resistance across a broad range of glucose tolerance.36 This was necessary because of the blunted or absent insulin response in diabetic subjects. Also, a reduced sampling protocol, which requires 12 rather than 30 plasma samples and shows similar results to the full protocol,37 was used because of the large number of subjects. Glucose in the form of a 50% solution was injected intravenously (0.3 g/kg) at time zero and regular human insulin (0.03 U/kg) at 20 minutes. Blood was collected at -5, 2, 4, 8, 19, 22, 30, 40, 50, 70, 100, and 180 minutes in relation to the glucose injection for determination of plasma glucose and insulin concentrations. Insulin sensitivity was calculated by mathematical modeling methods (MINMOD, version 3.0 [1994]). This modified version of the FSIGT protocol used in the IRAS has recently been compared with the hyperinsulinemic euglycemic clamp.38
Race and ethnicity were assessed by self-report. Hispanic ethnicity was defined by the US census question: "Are you of Spanish or Hispanic origin or descent?" In San Antonio, all Hispanics also met the criteria for classification as Mexican Americans.39 In the San Luis Valley, where immigration to the area from Mexico ceased more than two generations ago,22 the majority of Hispanics identify with the census categories of Spanish, Spanish American, or other Hispanic origin.
Height, weight, and girths (minimum waist, waist at the umbilicus, and hip) were measured following a standardized protocol.40 BMI (weight [kilograms] divided by height [meters] squared) was used as a measure of overall adiposity. The ratio of waist-to-hip circumferences was used as a measure of body fat distribution.
Recruitment
A total of 1625 individuals participated in the IRAS (56% women).30 Participants were chosen to provide representation across glucose tolerance categories, ethnicity, and sex. The final study sample included 613 non-Hispanic whites, 548 Hispanics, and 464 blacks. Individuals with normal glucose tolerance composed the largest segment of the study sample (44%, n=719). The next largest group of subjects was the diabetics (33%), followed by persons with impaired glucose tolerance (23%). This report comprises those with normal and impaired glucose tolerance. This was done because the IRAS excluded any diabetics who were currently taking insulin and therefore the overall diabetic population may not be represented. Carotid ultrasound tests were performed on 1409 (87%) of the 1625 subjects. Among the nondiabetic subjects, 1020 of 1086 subjects (94%) had an ultrasound. Most missing data were the result of a lack of equipment at the end of the study.
Carotid Ultrasound Methods
B-mode real-time ultrasound was used to assess the IMT of the carotid artery bed with a protocol identical to that used in the Cardiovascular Health Study.41 Briefly, a bilateral assessment was made of thickness in the ICA and CCA. For the ICA, the sonographer sought the site of maximum IMT in the region of the artery between the dilation of the carotid bulb and the region of the ICA above the carotid bifurcation. Three images were obtained at this site at different interrogation angles (proximal, lateral, and anterior). For the CCA, bilateral images were obtained proximal to the dilation of the carotid bulb at a single (lateral) angle.
The images recorded on videotape were transferred to a central reading facility for measurement of IMT. The same procedure was performed at each center for recording images, and the individuals who performed the scans were all centrally trained. For each of the eight available images, the maximum IMT (taken over a 1-cm arterial segment) for the arterial wall distant from the skin surface ("far wall") was measured. Two summary measures were calculated as the mean of the six ICA sites and the mean of the two CCA sites. To allow equal weighting of the left and right arteries in the presence of missing data, the mean values of the available measures on the left ICA and the mean value of the available measures on the right ICA were calculated, and then the mean of these two means was used in the analyses. This approach is identical or similar to that used to provide an index of atherosclerosis in a wide range of epidemiological studies42 43 44 45 and clinical trials.46 47 48
Statistical Analysis
Ethnic differences in IMT were determined with ANCOVA techniques (PROC GLM in SAS statistical software, version 6.09). Since Hispanics and blacks were sampled in different centers, direct comparisons of these two ethnic groups were not made. This approach was used to ensure that ethnic differences would not be caused by geographic variations. The centers may be different in other respects in addition to geographic location. For instance, the subjects in Oakland and Los Angeles were drawn from a health maintenance organization, Kaiser Permanente, whereas the subjects in San Antonio and San Luis Valley were drawn from ongoing population-based studies. Thus, analyses were performed separately (1) for the two centers that enrolled Hispanics and non-Hispanic whites (San Antonio and San Luis) and (2) for the two centers that enrolled blacks and non-Hispanic whites (Oakland and Los Angeles). Descriptive statistics (mean and SE) were first calculated for the subjects. Next, a series of models was fit, first with CCA as the outcome, then with ICA as the outcome. Interactions of ethnicity with sex, center, and glucose status (impaired/normal glucose tolerance) were examined. No significant interactions were found for the CCA, and therefore all analyses were pooled across these variables (eg, men and women were pooled together). Some significant interactions were found for the ICA, and these were further examined with stratified analyses. Models were then fit in the following order: (1) adjusted for age, center, and sex (demographic model); (2) adjusted for factors in the demographic model plus HDL, LDL, smoking status, and hypertension (cardiovascular risk factor model); (3) adjusted for factors in the cardiovascular risk factor model plus insulin sensitivity (insulin sensitivity model); and (4) adjusted for factors in the insulin sensitivity model plus fasting glucose (full model). Adjusted means and SEs are presented for these models. In addition to the above models, we examined a series of other models. We replaced hypertension with systolic and diastolic blood pressure since it has been shown that systolic and diastolic blood pressure may have independent effects on wall thickness.49 We also examined models that included BMI, triglycerides, and smoking duration (pack-years) as covariates.
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Results |
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Table 1
shows the descriptive data by ethnic group for blacks, Hispanics, and non-Hispanic whites. There was a higher percentage of women in the black group than in the non-Hispanic white group. In addition, blacks had increased prevalence of hypertension, lower insulin sensitivity values, and greater CCA IMT (unadjusted) than non-Hispanic whites. Hispanics were similar to non-Hispanic whites except that they were younger, had a higher rate of current smokers, and had lesser CCA IMT (unadjusted).
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CCA IMT
Table 2 shows the results for carotid IMT in four successive models in which additional adjustments for covariates are made to determine whether the differences in IMT measures could be attributable to demographic, CVD risk factor, or glycemic differences observed across the ethnic groups.
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Blacks had significantly greater CCA IMT (57.1 µm difference) than non-Hispanic whites after adjustment for age, sex, and center (model 1). After further adjustment for cardiovascular risk factors (HDL, LDL, hypertension, and smoking), blacks still had significantly greater CCA IMT (43.5 µm). When insulin sensitivity was added to the model, the difference between blacks and non-Hispanic whites was now less but still statistically significant (40.8 µm). In the final model (model 4), with fasting glucose added, the difference between blacks and non-Hispanic whites was nearly unchanged (40.1 µm).
Hispanics had lesser CCA IMT than non-Hispanic whites. This difference was significant for the demographic model (model 1) (26.8 µm). It became larger as covariates were added to the model: The difference was 30.4 µm for the cardiovascular risk factor model, 27.9 µm for the insulin sensitivity model, and 28.2 µm for the full model. These differences persisted when systolic and diastolic blood pressure measurements were used instead of hypertension. In addition, for both the black/non-Hispanic white and Hispanic/non-Hispanic white models, the inclusion of BMI, triglycerides, and smoking duration (pack-years) did not change the above findings. Among these additional covariates, pack-years did have an impact on the Hispanic and non-Hispanic white comparison, with the ethnic difference in CCA IMT now 26.4 µm (P=.05). This reduction in the ethnic difference may be due to the fact that Hispanics had a higher rate of current smoking that non-Hispanic whites.
ICA IMT
There were no statistically significant ethnic differences for ICA IMT when we compared either blacks and non-Hispanic whites or Hispanics and non-Hispanic whites in any of the four models considered. These results are shown in Table 2
. Blacks had slightly lesser ICA IMT than non-Hispanic whites after adjustment for insulin sensitivity, although this difference was not significant. Differences in ICA IMT between Hispanics and non-Hispanic whites were very small (
10 µm) for all models.
Stratified analyses were performed when significant interactions with ethnicity were observed for the ICA. The results from these analyses were inconsistent and further confirmed the lack of significant ethnic differences in ICA IMT.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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We have shown that blacks have significantly greater CCA IMT than non-Hispanics. This difference persisted after adjustment for several sets of confounding variables, including insulin resistance. The additional adjustment for insulin resistance is potentially important since blacks were more insulin resistant50 than non-Hispanic whites. This additional adjustment reduced the difference between blacks and non-Hispanic whites slightly, but it did not fully explain the observed ethnic difference. Our data are consistent with previous data from the ARIC Study,51 which observed a significantly greater CCA IMT in blacks than in non-Hispanic whites in both men and women. The ARIC report did not assess insulin sensitivity, and thus our finding goes beyond the previous findings. In addition, since in the ARIC Study blacks were assessed in two centers in the southeastern United States, our observations of similar ethnic differences for CCA IMT in both Los Angeles and Oakland make it less likely that this difference is due to geographic factors.
The difference between blacks and non-Hispanic whites in ICA IMT was not significant and in fact appears to possibly be the reverse of the CCA IMT relationship after adjustment for insulin sensitivity. This finding, while not significant, agrees with that of the ARIC Study,51 in which ICA IMT was significantly greater in non-Hispanic white men than in black men in all models. In the ARIC Study, a similar relationship was found in women after adjustment for covariates. A similar finding of greater CCA IMT and lesser ICA IMT in blacks than in non-Hispanic whites was also found by Tell et al.52
Hispanics had lesser CCA IMT than non-Hispanic whites, and these differences became more significant with adjustment for additional covariates. We found no significant differences in ICA IMT between Hispanics and non-Hispanic whites. One published abstract53 reported an examination of ethnic differences in carotid IMT between Hispanics and non-Hispanic whites. This abstract also reported thinner walls (smaller plaques) in Hispanics than in non-Hispanic whites. Other than that abstract, there have been no previous full reports published examining possible ethnic differences in carotid IMT between Hispanics and non-Hispanic whites. Previous data on cardiovascular mortality and morbidity suggested similar or slightly lower rates in Hispanics than in non-Hispanic whites.4 5 6 7 8 9 Our findings are consistent with these lower rates. The fact that our results for the CCA became more significant when we adjusted for cardiovascular risk factors may be due to the fact that the Hispanics had a lower prevalence of hypertension and lower LDL levels.
Our results for nondiabetic subjects are consistent with previous reports of greater CVD mortality in blacks than in non-Hispanic whites1 2 3 and lower CVD mortality in Hispanics than in non-Hispanic whites.4 5 6 Interestingly, these differences persist after we controlled for CVD risk factors thought to partially underlie the mortality differences. The ethnic differences in IMT could potentially be explained by inclusion of other CVD risk factors not measured in the IRAS or by a more comprehensive or accurate measurement of those included. While the ethnic differences in IMT may represent nonatherosclerotic differences, their congruence with the known ethnic differences in CVD mortality seems to suggest that they might be at least partially responsible for the ethnic differences in atherosclerosis.
One weakness of this report was that our sample size was relatively smaller than in studies such as the ARIC Study, and we may have lacked the power to detect ethnic differences in the ICA in blacks and non-Hispanic whites. On the other hand, these data make it possible to compare ethnic groups in different geographic regions of the country.
In contrast, this report has a number of unique strengths. It is the first study examining carotid IMT to compare the three major ethnic groups in the United States. Ethnic comparisons with non-Hispanic whites were available in each center. The San Luis Valley and the San Antonio centers' samples were drawn from well-characterized ongoing population studies,22 23 and the Oakland and Los Angeles centers' samples were drawn from large health maintenance organizations (Kaiser Permanente). Lastly, a direct measure of insulin resistance (insulin sensitivity) was carefully assessed and allowed us to control for a possibly important covariate. While the focus of this report is on ethnic differences in carotid IMT, the IRAS investigators are actively examining the relationship of carotid IMT and risk factors. In fact, a recent report has shown that insulin resistance (insulin sensitivity) is related to carotid IMT.54
In conclusion, we show differences in CCA IMT in blacks, Hispanics, and non-Hispanic whites. These largely remain after adjustment for a wide range of risk factors for CVD. Our results are consistent with previous reports on CVD in these ethnic groups. Prospective data on the progression of carotid atherosclerosis will be helpful in explaining these findings.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported by National Heart, Lung, and Blood Institute grants HL-47887, HL-47889, HL-47890, HL-47892, and HL-47902 and the General Clinical Research Centers Program (NCRR GCRC, MO1 RR43, MO1 RR341, and MO RR01346). The authors would like to thank Carey D'Agostino, Leora Henkin, and Terri Windham for their help in assembling this manuscript.
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Footnotes |
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Reprint requests to Ralph B. D'Agostino, Jr, PhD, Department of Public Health Sciences, Bowman Gray School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157-1063. E-mail ralphd@elvis.bgsm.wfu.edu.
Received March 8, 1996; revision received June 14, 1996; accepted July 12, 1996.
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