© 1997 American Heart Association, Inc.
Articles |
Socioeconomic Status and Progression of Carotid Atherosclerosis
Prospective Evidence From the Kuopio Ischemic Heart Disease Risk Factor Study
From the Human Population Laboratory, Public Health Institute, Berkeley, Calif (J.L., G.A.K.), and the Department of Community Health and General Practice, Research Institute of Public Health, University of Kuopio, Finland (R.S., J.T.S.).
Correspondence to John Lynch, PhD, The Human Population Laboratory, Public Health Institute, 2151 Berkeley Way, Annex 2, Suite 300, Berkeley, CA 94704. E-mail jwlynch{at}emf.net.
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Abstract |
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Abstract Socioeconomic status (SES) is importantly associated with cardiovascular morbidity and mortality, but no information exists on the relationship between SES and progression of atherosclerotic vascular disease. We investigated the association between education and income and the 4-year progression of carotid atherosclerosis in a population-based sample of Finnish men. Data from the Kuopio Ischemic Heart Disease Risk Factor Study were used to estimate changes in maximum and mean intima-media thickness (IMT) and maximum plaque height across levels of SES in 1022 men. Associations between SES and atherosclerotic progression were examined in relation to risk factors and stratified by baseline levels of atherosclerosis and prevalent ischemic heart disease (IHD). There were significant, inverse, graded relationships between levels of education and income for all three progression measures, which were largely unaffected by risk factor adjustment. For education, the age- and baseline IMT–adjusted maximum progression for those with primary schooling or less was 0.28 mm and for those who graduated from high school, 0.24 mm (P=.05). Compared with the lowest SES group, men with the highest SES had 14% to 29% less atherosclerotic progression, depending on the measure used. Associations of the same magnitude were evident in subgroups without advanced baseline IMT and in men who were free of IHD. These results show that men with poor education and low income have significantly greater progression of carotid atherosclerosis than men with more advantages. The findings strengthen the contention that SES plays a significant role early in the atherosclerotic disease process and that reducing the burden of atherosclerotic vascular disease associated with lower SES will require approaches that focus on all stages of the life course.
Key Words: socioeconomic status • atherosclerotic progression • B-mode ultrasound
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Introduction |
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The inverse association between SES and CVD morbidity and mortality has been well established. Regardless of which measures of SES were used, many studies have shown an inversely graded relationship, with increased SES associated with lower rates of disease or death.1 2 3 4 5 However, it remains unclear whether this association is limited to the clinical presentations of CVD, such as myocardial infarction, that occur late in the natural history of the disease and are a combination of underlying atherosclerotic disease and various triggering or precipitating factors, such as plaque instability or left ventricular electrical disturbances.6 Greater understanding of how SES is related to CVD might be gained by examining earlier stages of the disease process, when the clinical presentations of disease can be separated from the process of atherosclerosis itself.7
Recent advances in ultrasonographic assessment of the carotid arteries have provided opportunities to study noninvasively the prevalence and development of atherosclerosis within unselected human populations.8 9 10 B-mode imaging–based measurement of IMT in the carotid arteries has been shown to be reliable, to relate to the extent of disease in the coronary arteries, and to have predictive validity with regard to risk of coronary events.9 11 12 13 14 15 In an earlier study, we reported the inverse associations of education, income, and occupation with ultrasonographically assessed IMT.7 One limitation of this cross-sectional investigation was its inability to examine whether SES was related to the progression as well as the prevalence of atherosclerosis. The present study, to the best of our knowledge, is the first to examine prospectively the association between education and income and the 4-year progression of carotid atherosclerosis using three indicators of the atherosclerotic process: maximum IMT, plaque height, and mean IMT. Extensive information on baseline levels of atherosclerotic risk factors and prevalent disease enabled us to examine the association between SES and atherosclerotic progression with adjustment for known risk factors and stratified by both prevalent disease and the extent of atherosclerosis at baseline.
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Methods |
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Subjects
Subjects were participants in the Kuopio Ischemic Heart Disease Risk Factor Study, which was designed to investigate previously unestablished risk factors for IHD and carotid atherosclerosis in a population-based sample of eastern Finnish men.16 Of the 3235 eligible men 42, 48, 54, or 60 years old who resided in the town of Kuopio or its surrounding rural communities, 198 were excluded because of death, serious disease, or migration away from the area, and of the remainder, 2682 (82.9%) agreed to participate in the study. Baseline examinations were conducted between March 1984 and December 1989. No marked sociodemographic differences have been found between participants and nonparticipants.17
At baseline, subjects were recruited in two waves. The first group comprised 1166 men 54 years old, and the second comprised an age-stratified sample of 1516 men 42, 48, 54, or 60 years old. Ultrasonographic assessment of carotid atherosclerosis at baseline was conducted between February 1987 and December 1989 on the second wave of participants only. There were no systematic differences between the two waves of recruitment for the study other than the differences in age distribution. A 4-year follow-up examination was conducted between March 1991 and December 1993 on those men who had undergone ultrasonographic examination of the carotid arteries at baseline.
Follow-up examinations were conducted at the same time of day and principally during the same month as the baseline examination. Mean follow-up time was 4.2 years (range, 3.9 to 5.2 years). Of the 1229 participants who were eligible for the follow-up examinations, 52 either had died, were suffering severe illness, or had migrated away from the area. Of the remainder, 139 could not be contacted or refused to participate. Information on progression of carotid atherosclerosis, covariates, and education was available for 1012 men and on income for 994 men. There were 233, 237, 281, and 261 men in the 42-, 48-, 54-, and 60-year-old age groups, respectively. In this sample, 73 men acted as control subjects and 73 men were participants in the treatment group of an unrelated clinical trial of pravastatin.18
Evaluation of Carotid Atherosclerotic Progression
Atherosclerotic progression was assessed with high-resolution
B-mode ultrasonographic examination of a 1.0- to 1.5-cm section of the
left and right CCAs below the carotid bulb. Images were focused on the
posterior (far) wall with the subject supine. At baseline,
ultrasonographic scanning was conducted with the ATL UM4 duplex
ultrasound system with a 10-MHz sector transducer (Advanced Technology
Laboratories). The Biosound Phase 2 equipped with a 10-MHz annular
array probe was used at the 4-year follow-up examinations. Wedge
phantom studies of this system, calibrated against an RMI 414B tissue
phantom, have demonstrated measurement precision of ±0.03
mm.19 A total of five technicians, each trained for at
least 6 months, conducted both the baseline and 4-year follow-up
scannings, which were also recorded by VCR.
Video frames of the B-mode scanning were digitized with the Data Translation DT2861 video frame grabber installed on an 80486 PC and a Panasonic AG7355 VCR. IMT was assessed with Prosound software, which incorporates an edge-detection algorithm specifically designed for use with ultrasound scanning and enables automatic detection, tracking, and recording of the lumen/intima and media/adventitia interfaces (University of Southern California).20 On average, 100 estimates of the distance between these interfaces were recorded over the 1.0- to 1.5-cm section of each CCA. The IMT of the posterior wall was measured as the distance from the leading edge of the first echogenic line to the leading edge of the second echogenic line, as explained earlier in detail.9 Measurements of the near wall were not made because of greater measurement variability.21
The present study uses three measures of IMT: (1) maximum IMT (defined
as the average of the maximum IMT in the right and left CCAs), (2)
plaque height (defined as the difference between the maximum and
minimum IMT recordings averaged over the right and left CCAs), and (3)
mean IMT (defined as the mean of the 
100 IMT readings from each
CCA). These measures were conceptualized to represent potentially
different aspects of atherosclerotic progression. Maximum IMT was
thought to provide an assessment of how deeply intima-media thickening
intruded into the lumen in this segment of the CCA. The measurement of
plaque height was conceptualized to be sensitive to the roughness of
the arterial wall by representing the range of IMT and thus assessing
how steeply atherosclerotic lesions protruded into the lumen. Mean IMT
was seen as an overall measure of the process of atherosclerosis.
Progression of carotid atherosclerosis was calculated as the arithmetic
difference between the baseline and 4-year follow-up values for each of
the three measures: maximum IMT, plaque height, and mean IMT.
Baseline IMT recordings were also classified by one physician into four categories: (1) no atherosclerotic lesion; (2) intima-media thickening; (3) nonstenotic plaque; and (4) large, stenotic plaque. Intima-media thickening (category 2) was defined as >1.0 mm between the lumen/intima interface and the media/adventitia interface in the CCAs below the carotid bulb. Nonstenotic plaque (category 3) was defined as a distinct area of mineralization or focal protrusion into the lumen. A plaque was defined as stenotic (category 4) if it obstructed >20% of the lumen diameter.9
Evaluation of Education and Income
Various measures of socioeconomic status were available from
questionnaires completed as part of the baseline examination, including
education, occupation, income, housing tenure, and ownership of
material goods.22 The present study reports results by
highest educational attainment and current income. The highest level of
education was classified into three categories: "primary school or
less" (included those who had only part of or who had completed
primary school, n=321), "some high school" (included those who
had some high school or other vocational training beyond primary,
n=490), and "completed high school or better" (included those who
finished high school or who had tertiary education, n=201). The
distribution of the respondents' current income was divided into
approximate quartiles.
Evaluation of Covariates
Lipoproteins were separated from unfrozen plasma within 3 days
of sampling. HDL and LDL fractions were separated from fresh plasma by
both ultracentrifugation and precipitation. The cholesterol content of
all lipoprotein fractions was measured enzymatically (CHOD-PAP
cholesterol method, Boehringer Mannheim) on the day after the last
spin.23 Blood pressure was measured with a random-zero
sphygmomanometer with the subject both supine and sitting, after
5-minute rests in each position. Three systolic and diastolic pressures
were taken and averaged. Average systolic pressure was used in this
analysis. Body mass index was calculated by dividing the subject's
weight by the square of his height (kg/m2). Alcohol
consumption was assessed by instructed dietary recording for a 4-day
period, and also for the previous 12 months, by self-administered
questionnaire.24 Smoking was measured by questionnaire and
classified for this analysis as "never smoked," "former
smoker," and "current smoker" (measured in pack-years).
Treatment for hypertension or hyperlipidemia was assessed by a review
of medications.
Evaluation of Prevalent IHD
Subjects were considered to have prevalent IHD at baseline if
they (1) had any history of prior myocardial infarction or angina
pectoris, (2) currently used antiangina medication, or (3) had positive
findings of angina from the London School of Hygiene Cardiovascular
Questionnaire.25
Statistical Methods
The association between SES and the progression of IMT was
assessed by estimating the mean change in each measure of IMT (maximum
thickness, mean thickness, and plaque height) for each level of
education and income. The analyses were conducted with the GLM
procedure in SAS version 6.09 on a Sun Sparc Station II.26
This procedure allows for age-adjusted least-squares mean values of IMT
to be estimated and contrasted for each level of SES while baseline IMT
and other covariates are simultaneously controlled for.
We were interested in comparing differences in mean IMT progression between the highest income or education group (reference category) and each lower category. The pairwise contrasts between the reference group (highest education or income) were adjusted for multiple comparisons to maintain an overall type 1 error of P<.05 by use of Holm's procedure as described by Aickin and Gensler.27 In addition to age, baseline levels of IMT, and covariates, all estimates were adjusted for participation in the clinical trial of pravastatin, the zooming depth of the ultrasound scan, and separate indicator variables for the individual technicians who conducted the scans.9
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Results |
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Table 1
provides means (SD) and prevalence (%) for
baseline levels of IMT and other covariates distributed across
categories of education and income. Tables 2, 3, and 4 present the estimated mean
changes in maximum thickness, plaque height, and mean thickness of the
intima-media complex by SES with adjustment for age and baseline levels
of IMT (model 1) and with additional adjustment for covariates (HDL,
LDL, systolic blood pressure, smoking, body mass index, alcohol
consumption, and treatment for hyperlipidemia and hypertension) in
model 2.
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SES and IMT Progression in the Whole Sample
Progression of maximum IMT, mean IMT, and plaque height all
demonstrated similarly graded relationships with education and income.
In Table 2
, the age- and baseline IMT–adjusted 4-year average maximum
progression within categories of education was 0.28 mm for those
who had only primary education, 0.26 mm for those with some high
school, and 0.24 mm for those who had completed high school or
continued with tertiary studies (F=2.55, P=.08). Men who had
completed high school had 14% less maximum atherosclerotic progression
in 4 years than those with only primary education (P=.05).
Adjustment for covariates did not alter the magnitude of the
differences between the education categories. When income was used as
the measure of SES, men in the highest income quartile had 17% less
maximum progression than the highest income earners (P=.05).
This difference was not substantially altered by adjustment for
covariates.
The pattern of results for progression of plaque height was very
similar to that for maximum IMT progression. In Table 3, the age- and
baseline IMT–adjusted 4-year mean progression of plaque height within
categories of education was 0.29 mm for those who had only primary
education, 0.27 mm for those with some high school, and 0.24
mm for those who had completed high school or continued with tertiary
studies (F=3.74, P=.02). Men who had completed high school
had 17% lower 4-year progression in plaque height than those with only
primary education (P=.01). Adjustment for covariates did not
alter the magnitude of the differences between the education
categories. Similarly, graded, significant associations were seen for
quartiles of income in model 1, with the lowest income group having
14% less progression of plaque height than the highest income
group.
Overall, a consistent pattern of results emerged when progression of
mean IMT was used as the outcome, although somewhat stronger gradients
were found for income as opposed to education (Table 4.) The age- and
baseline IMT–adjusted 4-year progression of mean IMT within income
quartiles was 0.14, 0.11, 0.12, and 0.10 mm for the lowest to
highest income quartiles, respectively (F=3.1, P=.03). Men
in the highest income quartile experienced 29% less progression in
mean IMT than men in the lowest income group (P=.02). The
magnitude of this difference was not affected by adjustment for
atherosclerosis risk factors.
SES and IMT Progression in Men Without Stenosis or Nonstenotic
Plaque at Baseline
Table 5 shows the relationship between education
and progression of maximum IMT, plaque height, and mean IMT in a
subgroup that excluded 315 men with ultrasonographic evidence of 
20%
carotid stenosis or nonstenotic atherosclerotic plaque (categories 3
and 4). Each measure of IMT progression showed strong, significant,
inverse gradients with higher levels of education. Men without carotid
stenosis or nonstenotic plaque at baseline who had completed a high
school education had 17% (P=.02), 14% (P=.04),
and 23% (P=.12) less progression of maximum IMT, plaque
height, and mean IMT, respectively, than men with primary schooling or
less. The magnitude of these differences was not greatly affected by
adjustment for atherosclerosis risk factors.
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SES and IMT Progression in Men With No Prevalent IHD at
Baseline
Table 6 shows the relationship between education
and progression of maximum IMT, plaque height, and mean IMT in a
subgroup that included only those men who were free of IHD at baseline
(n=783). Both progression of maximum IMT and plaque height showed
strong, significant, inverse gradients with higher levels of education.
Although the magnitude of the differences for mean IMT progression
between educational groups conformed to the overall pattern of results,
the differences were not statistically significant. Men with no
prevalent IHD at baseline who had completed a high school education had
14% (P=.08), 14% (P=.04), and 17%
(P=.28) less progression of maximum IMT, plaque height, and
mean IMT, respectively, than men with primary schooling or less.
Adjustment for atherosclerosis risk factors did not greatly affect the
magnitude of the educational differences. A similar pattern of findings
was obtained when income was used as the SES measure. The
Figure shows the age- and baseline IMT–adjusted
associations between levels of education and progression of maximum IMT
in the whole sample, in men with no prevalent IHD, and in men without
carotid stenosis or nonstenotic plaque.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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These results show that men with low education and low incomes had significantly greater 4-year progression of carotid atherosclerosis than men with more advantages. All the measures of carotid atherosclerotic progression demonstrated similarly graded, inverse relationships across levels of SES. The magnitude of these relationships was largely unaffected by adjustment for known atherosclerosis risk factors. However, SES is associated with both baseline levels of atherogenesis risk factors and changes in those risk factors over time. Because of this, the analytic strategy of examining the association of SES with changes in carotid atherosclerosis by adjusting for baseline levels of atherogenesis risk factors is somewhat problematic. Thus, the lack of confounding from these risk factors should not necessarily be interpreted as evidence that the association between SES and progression of carotid atherosclerosis is "independent" of these risk factors. In fact, we reported earlier that the cross-sectional association between SES and carotid atherosclerosis in the same population was largely mediated by a similar group of known atherosclerosis risk factors.7 It is also possible that temporal variations in risk factor levels were not captured by single measurements at baseline and so reduce their ability to act as confounders. Furthermore, there are other potential risk factors for atherosclerosis progression, such as hemostatic variables, that were not included in these analyses.
Although these results implicated SES in the progression of IMT, we
conducted a more stringent examination of the role of SES in its
relation to the early stages of atherosclerosis by excluding men who at
baseline showed any evidence of stenosis or nonstenotic plaque. The
same magnitude of associations between SES and progression was revealed
in this group of men who did not have advanced thickening at baseline
and suggests that SES is influential early in the natural history of
carotid atherosclerotic progression. This finding is even more
compelling in light of the fact that low-SES men had much higher
prevalence of advanced atherosclerosis at baseline and so were
disproportionately excluded from these analyses. Table 1 shows that
45.5% of the least educated group compared with 14.4% of the most
educated group had advanced atherosclerosis at baseline.
To examine whether the association between levels of SES and progression of IMT was a reflection of the fact that those who had less education or lower incomes were more likely to have higher prevalent IHD, we repeated the analysis in a healthy subsample. All men who had any indication of prevalent IHD at baseline were excluded from the analysis. In this healthy subsample, the same graded, inverse relationship between SES and progression of maximum IMT, plaque height, and mean IMT was observed. The magnitude of the differences between the most extreme categories of SES was similar to those obtained within the whole sample.
Our results are important for a number of reasons. This study is the first in a large, unselected sample to show strong relationships between SES and the early signs of atherosclerotic vascular disease progression. These findings strengthen the contention that SES plays a significant role early in the atherosclerotic disease process in addition to its more well-established associations with the clinically relevant and distal manifestations of CVD.28 Although this sample is limited to middle-aged men, our findings are consistent with a recent cross-sectional study by Diez-Rouz et al10 in the United States that found similar relationships between measures of SES and IMT in men and women and in blacks and whites.
Second, the results are consistent across different measures of atherosclerosis progression, with education and income showing similar associations with progression of maximum IMT, plaque height, and mean IMT. Although the differential pathological importance of changes in these measures remains to be clearly established, it seems reasonable to suggest that SES is associated with progression of the overall atherosclerotic burden as well as in the development of focal lesions that protrude into the lumen and increase the surface roughness of the CCA. The development of roughened arterial walls with steep-sided projections into the lumen is likely to subject the lesion to increased shear stress and flow turbulence, thus raising the potential for plaque fissuring and possible rupture.
Third, the differences in IMT progression between extreme categories of SES observed in these data have potentially important clinical and public health interpretations. Although there is little information on the relationship between carotid atherosclerotic progression and clinical events, Salonen and Salonen9 demonstrated cross-sectionally that a 0.1-mm difference in maximum IMT raised the risk of acute myocardial infarction significantly, by 11% (95% confidence interval, 6% to 16%; P<.001).
Finally, these findings provide some of the strongest evidence to date against the "drift" or "selection" hypothesis, which has been proposed as a potential explanation for the observed inverse associations between SES and health.29 According to this notion, any association between SES and health may occur because sick individuals "drift down" the social hierarchy, so that lower socioeconomic position is a consequence of the disease process. Although this no doubt occurs to some extent, it is unlikely to explain the overwhelming burden of disease borne by those with lower SES.30 Demonstrating the same significant, graded differences in carotid atherosclerosis progression across categories of SES in the whole population as well as in a healthy subgroup who were free of prevalent IHD provides cogent evidence that lower SES is importantly involved in greater atherosclerotic vascular disease before any clinical evidence of illness occurs.
In summary, the evidence presented here indicates that the impact of SES is apparent early in the natural history of atherosclerotic vascular disease and is importantly related to disease progression. It seems entirely plausible that lower SES should be related to the early phases of atherosclerotic progression, at least in part because of its well-reported associations with higher levels of smoking, blood pressure, lipids, and other CVD risk factors.31 32 33 34 35 Moreover, recent evidence from the Kuopio Ischemic Heart Disease Risk Factor study also shows that lower SES during childhood is an important predictor of adult smoking, physical activity, diet, and a number of adult psychosocial characteristics.36 Although adjustment for some of these atherosclerotic risk factors did not greatly affect the magnitude of the associations reported here, it is likely that lower SES is important in influencing the complex accumulation of biological, behavioral, and psychosocial risk factors that influence the progression of atherosclerosis.37 If this is true, reducing the atherosclerotic vascular disease burden associated with lower SES will require approaches that focus on all stages of the life course.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported in part by grant HL-44199 from the National Heart, Lung, and Blood Institute and by grants from the Academy of Finland and the Finnish Ministry of Education.
Received February 29, 1996; accepted July 11, 1996.
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 F. Tabassum, M. Kumari, A. Rumley, G. Lowe, C. Power, and D. P. Strachan Effects of Socioeconomic Position on Inflammatory and Hemostatic Markers: A Life-Course Analysis in the 1958 British Birth Cohort Am. J. Epidemiol., June 1, 2008; 167(11): 1332 - 1341. [Abstract] [Full Text] [PDF]
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 M Rosvall, G Engstrom, L Janzon, G Berglund, and B Hedblad The role of low grade inflammation as measured by C-reactive protein levels in the explanation of socioeconomic differences in carotid atherosclerosis Eur J Public Health, August 1, 2007; 17(4): 340 - 347. [Abstract] [Full Text] [PDF]
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 L. Keltikangas-Jarvinen, L. Pulkki-Raback, S. Puttonen, J. Viikari, and O. T. Raitakari Childhood Hyperactivity as a Predictor of Carotid Artery Intima Media Thickness Over a Period of 21 Years: The Cardiovascular Risk in Young Finns Study Psychosom Med, July 1, 2006; 68(4): 509 - 516. [Abstract] [Full Text] [PDF]
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S. A. James, J. Van Hoewyk, R. F. Belli, D. S. Strogatz, D. R. Williams, and T. E. Raghunathan Life-Course Socioeconomic Position and Hypertension in African American Men: The Pitt County Study Am J Public Health, May 1, 2006; 96(5): 812 - 817. [Abstract] [Full Text] [PDF]
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 L. L. Yan, K. Liu, M. L. Daviglus, L. A. Colangelo, C. I. Kiefe, S. Sidney, K. A. Matthews, and P. Greenland Education, 15-year risk factor progression, and coronary artery calcium in young adulthood and early middle age: the Coronary Artery Risk Development in Young Adults study. JAMA, April 19, 2006; 295(15): 1793 - 1800. [Abstract] [Full Text] [PDF]
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 N. Ranjit, A. V. Diez-Roux, L. Chambless, D. R. Jacobs Jr, F. J. Nieto, and M. Szklo Socioeconomic Differences in Progression of Carotid Intima-Media Thickness in the Atherosclerosis Risk in Communities Study Arterioscler. Thromb. Vasc. Biol., February 1, 2006; 26(2): 411 - 416. [Abstract] [Full Text] [PDF]
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 A. D. Mackinnon, P. Jerrard-Dunne, M. Sitzer, A. Buehler, S. von Kegler, and H. S. Markus Rates and Determinants of Site-Specific Progression of Carotid Artery Intima-Media Thickness: The Carotid Atherosclerosis Progression Study Stroke, September 1, 2004; 35(9): 2150 - 2154. [Abstract] [Full Text] [PDF]
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T. Truelsen, N. Nielsen, G. Boysen, and M. Gronbaek Self-Reported Stress and Risk of Stroke: The Copenhagen City Heart Study Stroke, April 1, 2003; 34(4): 856 - 862. [Abstract] [Full Text] [PDF]
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C. Espinola-Klein, H.-J. Rupprecht, S. Blankenberg, C. Bickel, H. Kopp, A. Victor, G. Hafner, W. Prellwitz, W. Schlumberger, and J. Meyer Impact of Infectious Burden on Progression of Carotid Atherosclerosis Stroke, November 1, 2002; 33(11): 2581 - 2586. [Abstract] [Full Text] [PDF]
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M. Rosvall, P.-O. Ostergren, B. Hedblad, S.-O. Isacsson, L. Janzon, and G. Berglund Life-Course Perspective on Socioeconomic Differences in Carotid Atherosclerosis Arterioscler. Thromb. Vasc. Biol., October 1, 2002; 22(10): 1704 - 1711. [Abstract] [Full Text] [PDF]
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L. E. Chambless, A. R. Folsom, V. Davis, R. Sharrett, G. Heiss, P. Sorlie, M. Szklo, G. Howard, and G. W. Evans Risk Factors for Progression of Common Carotid Atherosclerosis: The Atherosclerosis Risk in Communities Study, 1987-1998 Am. J. Epidemiol., January 1, 2002; 155(1): 38 - 47. [Abstract] [Full Text] [PDF]
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M. K. Kapral, H. Wang, M. Mamdani, J. V. Tu, B. Boden-Albala, and R. L. Sacco Effect of Socioeconomic Status on Treatment and Mortality After Stroke * Editorial Comment Stroke, January 1, 2002; 33(1): 268 - 275. [Abstract] [Full Text] [PDF]
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L. C. Gallo, K. A. Matthews, L. H. Kuller, K. Sutton-Tyrrell, and D. Edmundowicz Educational Attainment and Coronary and Aortic Calcification in Postmenopausal Women Psychosom Med, November 1, 2001; 63(6): 925 - 935. [Abstract] [Full Text] [PDF]
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R. Din-Dzietham, D. Liao, A. Diez-Roux, F. J. Nieto, C. Paton, G. Howard, A. Brown, M. Carnethon, and H. A. Tyroler Association of Educational Achievement with Pulsatile Arterial Diameter Change of the Common Crotid Artery The Atherosclerosis Risk in Communities (ARIC) Study, 1987-1992 Am. J. Epidemiol., October 1, 2000; 152(7): 617 - 627. [Abstract] [Full Text] [PDF]
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M. Rosvall, P. O. Ostergren, B. Hedblad, S-O. Isacsson, L. Janzon, and G. Berglund Occupational Status, Educational Level, and the Prevalence of Carotid Atherosclerosis in a General Population Sample of Middle-aged Swedish Men and Women: Results from the Malmo Diet and Cancer Study Am. J. Epidemiol., August 15, 2000; 152(4): 334 - 346. [Abstract] [Full Text] [PDF]
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J. Lynch, N. Krause, G. A. Kaplan, R. Salonen, and J. T. Salonen Workplace Demands, Economic Reward, and Progression of Carotid Atherosclerosis Circulation, July 1, 1997; 96(1): 302 - 307. [Abstract] [Full Text]
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