(Stroke. 1996;27:480-485.)
© 1996 American Heart Association, Inc.
Articles |
Reliability of Longitudinal Ultrasonographic Measurements of Carotid Intimal-Medial Thicknesses
From the Departments of Public Health Sciences (M.A.E., T.E.C., W.A.R., C.D.F.) and Neurology (W.A.R.), Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC; and the Section of Vascular Surgery (J.C.) and the Division of Cerebrovascular Diseases (A.R.), University of Iowa College of Medicine (Iowa City).
Correspondence to Mark A. Espeland, PhD, Department of Public Health Sciences, Bowman Gray School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157-1063.
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Abstract |
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 Top Abstract IntroductionSubjects and Methods Results Discussion References |
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Background and Purpose Serial ultrasonic B-mode measurements of intimal-medial thickness (IMT) of the carotid artery are commonly used as surrogates for describing atherosclerosis progression. This report describes the longitudinal reliability of IMT measurement during a multicenter clinical trial, quantifies the error attributable to differences among readers, and discusses how studies can be efficiently designed.
Methods Serial B-mode measurements of carotid IMT from the 3-year Asymptomatic Carotid Artery Progression Study (ACAPS; formerly Asymptomatic Carotid Artery Plaque Study) were used to estimate the contributions to longitudinal measurement error of systematic reader effects, nonvisualization, and nonsystematic error and to describe the distribution of "true" progression rates that underlie the observed data. Variance components were estimated from random-effects models fitted to outcome measures formed by averaging IMTs from different sets of carotid artery walls. These were used to contrast the relative efficiency of study designs.
Results Of the total variance of measured IMT, 11% was attributable to systematic differences among readers. Nonvisualization contributed less than 7%. Thus, the predominant source of error was unaccounted for (ie, random error or "noise," which in our analyses included any drift, nonlinearity, and sonographer differences). For studies with measurement protocols similar to ACAPS, follow-up times of 2 years or more are desirable for describing the mean progression rates of cohorts, and of 6 years or more for categorizing progression within individuals. In 3-year studies, sample sizes as low as 237 provide 90% statistical power for detecting risk factors that have correlations with IMT progression of .50 or greater.
Conclusions The ACAPS measurement protocol provided highly reliable serial IMT data. Moderate-sized multicenter studies using B-mode outcomes are feasible.
Key Words: carotid artery diseases • clinical trials • prospective studies • ultrasonics
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Introduction |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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Serial ultrasonographic measurements of the IMT in the carotid artery are serving important roles in an increasing number of clinical trials and epidemiological studies.1 2 3 4 5 6 7 8 Reports that these measures have acceptable cross-sectional repeatability,9 10 11 12 13 14 15 16 17 18 significant cross-sectional correlation with other markers of atherosclerotic and vascular disease,15 19 20 21 22 and both cross-sectional and longitudinal relationships with known risk factors for atherosclerosis support their use.
To evaluate the statistical power of study designs that incorporate longitudinal measures of IMT, important assumptions about the contribution of readers to measurement error must be made. To date, however, only cross-sectional reliability data from highly controlled studies have been published, and these data do not express the potential contribution to error of changes across time. Also critical to study design are assumptions concerning the distribution of IMT progression among subjects. Observed rates of change, because they are influenced by measurement errors, have a larger variance than the "true" rates of change. No analyses have been published in which the distribution of IMT progression has been described after the influences of measurement error have been statistically removed.
This report addresses these gaps in the literature. We estimate the contributions of systematic differences among readers, nonvisualization, and nonsystematic (random) error to the measurement of IMT progression in the context of ACAPS. Data are presented showing that readers performed consistently well across the 3-year trial. The distribution of progression rates among participants is portrayed. We discuss how this information can be used to assess the statistical power of different study designs.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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Baseline and semiannual ultrasonographic IMT measurements are described from the 919 randomized ACAPS participants. These individuals were 40 to 79 years of age, had either serum LDL cholesterol concentrations of 160 to 189 mg/dL with at most one other coronary risk factor or LDL cholesterol concentrations of 130 to 159 mg/dL with two or more other risk factors, had serum triglyceride concentrations
400 mg/dL, and had
at least one "qualifying" IMT among 12 predefined wall segments
of the carotid artery on the basis of B-mode ultrasonography.
Qualifying lesions had to be from 1.6 to 3.5 mm if they were in the
bifurcation segment of the carotid artery or 1.5 to 3.5 mm if they were
in the common or internal segments.1 All participants gave
informed consent; separate institutional review boards at each site
approved and monitored the study.
IMT measurements were obtained using the high-resolution B-mode
ultrasound Biosound Phase 2 system, a high-resolution S-VHS
videocassette recorder, a study flow panel, and a personal
computer.10 The center frequency of the broadband
ultrasonic pulse was approximately 8 MHz, and the axial resolution was
approximately 0.10 mm. All readers and sonographers were centrally
trained, certified, carefully monitored, and blinded. Maximum IMT
measures were obtained from walls of three arterial
segments of both carotid arteries: the near and far wall of the
proximal 8 mm of the internal carotid artery, the near and far wall of
the carotid bifurcation beginning at the tip of the flow divider and
extending 8 mm proximally, and the near and far wall of the
arterial segment extending 8 to 16 mm proximally to the tip
of the flow divider into the common carotid artery (see Fig 1
).
At each examination, sonographers chose the angle of
interrogation that allowed measurement of the maximum IMT. Progression
of IMT in this report thus pertains to changes in the maximum IMT
across a predefined two-dimensional area of wall rather than to
changes in IMT at a fixed point. In baseline reproducibility
analyses, the mean absolute differences between blinded
replicate measures of the primary outcome measure of the ACAPS trial,
the average of these maxima from the 12 walls, was less than 0.11
mm.10
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Random-effects models23 were fitted to estimate the contributions of systematic differences (ie, biases) among readers, nonsystematic variation, and differences in progression rates to the variance of observed progression rates. Nonsystematic variation included random measurement error, nonsystematic differences among readers (eg, temporal drift), nonlinearity, and differences among sonographers (these were impossible to distinguish accurately from other nonsystematic variations because of personnel changes across time and because sonographers were "nested" within clinics). Variation attributable to readers and to nonsystematic sources constituted within-subject variance; differences in progression rates among participants constituted between-subject variance. In our random-effects models, errors were assumed to be normally distributed, which appeared reasonable on the basis of residual plots. All readers who saw 50 or more scans were included, for a total of seven readers who examined from 269 to 2022 scans.
Linear models, as warranted by the data,24 were used to express progression across time and were fitted via maximum likelihood.25 26 Separate models were fitted for the average IMT maxima across all 12 wall segments and averages of subsets of the segments. Baseline IMT was used as a covariate in all models.
At the end of ACAPS, the evidence for temporal drift among readers was examined. Participants who completed the trial were stratified by baseline IMT; 100 were randomly selected. Their paired baseline and 36-month examinations were randomly sequenced and distributed among four ACAPS readers, who were blinded to the participant's identity and the presentation sequence. The mean IMT, the difference between the original and reread IMT for baseline and 36-month examinations, and the 3-year changes (36-month minus baseline) were calculated. Ninety-five percent CIs for these mean differences and correlation coefficients between original and reread IMT were computed.
To address the contribution of nonvisualization of segments to variability, we adopted a conditional maximum-likelihood approach to impute values for missing data from IMT of other walls measured at the same examination.24 27 Random-effects models were refitted to these augmented data to estimate random error after "controlling for" the inflation or variance attributable to nonvisualization.
The estimated variance of a measured progression rate from a randomly
selected individual (
2slope) depends
on the estimated variance component for differences in progression
rates among participants (2between)
and the estimated variance component for cross-sectional
measurement error (2within). This
latter component includes reader differences and nonsystematic error
and can be reduced by adding additional examinations and/or increasing
follow-up time. Statistical powers for different values of
2slope were calculated on the
assumption that slopes were normally distributed, using expressions
provided by Lindstrom and Bates.28 The ratio of the
inverse of variances, expressed as a percentage, described the relative
efficiency of estimates: the ratio of sample sizes needed to achieve
comparable statistical power.29
If 
0 represents the "true" correlation
between a risk factor and IMT progression (ie, if IMT progression is
measured without error), the observed correlation
r0 is diminished by the measurement error:
r0=0 US,
where US is the expected correlation between the
"true" and measured IMT progression. By using the expression
US=
and standard formula for the power to detect
correlations,30 we estimated the necessary sample size for
detecting risk factor relationships of varying intensities with 90%
statistical power with two-sided tests and significance levels of
.05.
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Results |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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Section A of the Table
lists estimated variance
components for average IMT measurements from the common segments, from
the common and bifurcation segments, and from all segments. Systematic
differences among readers were estimated to account for 11% of the
total within-subject variability for each outcome measure.
Nonsystematic error accounted for the remaining 89%. The total
within-subject variance was greatest when common and bifurcation
IMTs were averaged and was least when IMTs from all segments were
averaged.
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The "true" IMT progression rates of ACAPS participants had
similar variances whether all walls or only walls from the common and
bifurcation segments were averaged (Table
section B). When
averages
were computed only from the common segments, differences in IMT
progression were less pronounced: subjects appeared to have more
homogeneous rates of IMT progression.
Fig 2 shows the relative contributions of readers and
nonsystematic error to the variance of a randomly selected progression
rate for several design options: annual participant follow-up of 2,
3, 6, or 8 years and single versus replicate examinations. Variances
decreased with longer follow-up and with replication; however, the
benefits of additional follow-up and replication diminished for
longer studies. Designs involving a single (fixed) reader would have
variances reduced by the amount indicated by the black portions of the
bar graph, which were almost negligible for longer studies.
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For the 100 pairs of baseline and 36-month examinations that were reread, mean differences (original minus rereading) and 95% CIs for the average IMT across 12 walls were -0.005 mm (95% CI, -0.033 to 0.023 mm) at baseline, -0.009 mm (95% CI, -0.031 to 0.013 mm) at 36 months, and -0.004 mm (95% CI, -0.036 to 0.028 mm) for the 3-year difference. Correlations between original and rereadings were .74 at baseline, .82 at 36 months, and .63 for 3-year change.
Section C of the Table contrasts the results in section A
with those
obtained when nonvisualized IMTs were imputed. In ACAPS, near/far walls
from the common segments were visualized 99% of the time; bifurcation
and internal segments were visualized less frequently (88% and 67% of
the time). As might be expected, imputing nonvisualized data in common
segments improved the efficiency of cross-sectional measures
minimally, by only 0.9%. When nonvisualized bifurcation and internal
walls were imputed in summary measures, statistical efficiency was
increased by 1.7% to 6.1%.
Fig 3 portrays the distribution of ACAPS progression
rates for average (12 walls) IMT after variation due to measurement
error has been statistically removed. By assumption, this distribution
was gaussian, which was supported by analyses of residuals.
Also portrayed are the expected 95% CIs for the progression rate of an
individual examined annually for 3, 4, 6, and 8 years. A single reader
was assumed, and nonvisualized walls were ignored. For 4 or fewer years
of follow-up, the CI for an individual's rate spanned nearly the
entire range of the estimated ACAPS distribution. Thus, these lengths
of follow-up did not provide sufficient information to identify
accurately whether an individual progressed relatively slow or fast.
Only for 6 or 8 years of follow-up was measurement sufficiently
reliable to rule out markedly slow or rapid progression in
individuals.
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Using variance components from Table sections A and B, we
estimated the
correlation between the observed and the "true" IMT progression
rates from 3 years of annual examinations to be
US=.27 (common segments only),
US=.40 (common and bifurcation segments), and
US=.42 (all segments). The estimated correlation
was greatest when all segments were averaged: when the total
within-subject variance was least and the between-subject
variance was greatest. The correlation of observed progression with
risk factors is thus expected to be less than one half of what it
really is; a true correlation of 1.00 would be observed as .27, .40, or
.42.
Table section D lists the sample sizes necessary to achieve
90%
statistical power (two-sided tests with significance levels of .05)
for true correlations of .25, .50, and .75 after 3 years of annual
follow-up. If the true correlation is .50, 573 participants would
be required to achieve 90% statistical power if only the common
segments were measured; this required sample size would drop to 237
subjects if all 12 walls were averaged.
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Discussion |
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TopAbstractIntroductionSubjects and Methods Results Discussion References |
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The ACAPS protocol yielded markedly more reliable measures of IMT progression than expected. The original study design, based on very limited longitudinal data, was projected to provide 90% power to detect differences of 0.08 to 0.09 mm/y in IMT progression. Post hoc calculations indicated that the study had 90% power to detect differences in IMT progression rates less than 0.02 mm/y. This improved reliability was attributed to careful training and quality control, a detailed protocol, and less than expected variability in progression rates among subjects.
The contribution of systematic differences among readers to measurement error in ACAPS was acceptably low, and little if any temporal drift was evident. This has important implications for the design of longitudinal studies. The good agreement among readers indicates that with careful and centralized training it is feasible to employ more than one reader per site and that it is not necessary to ensure that longitudinal scans for subjects are read by the same person. At least one other study, however, has encountered problems with differences among readers and drifts across time,31 indicating the need for careful and continual training and monitoring.
We were unable to estimate the contributions of any differences among sonographers to overall variability. As reported elsewhere,10 however, duplicate examinations collected at baseline and at 3 years during ACAPS indicate that sonographers were at least as interchangeable as readers. This supports the feasibility of multicenter studies.
Random error was least when all walls were averaged to compute the outcome measure. This suggests that greater stability of IMT outcome measures is obtained by including measurements from the bifurcation and internal walls, even though individually these walls may have more variability than walls from the common segments. Reader differences were not affected by the choice of outcome measure.
Progression rates among individual subjects appeared to vary most when the bifurcation segment was included in outcome measures. This was also the segment for which the greatest treatment effect was observed in ACAPS,24 32 so some of this variability may be attributed to intervention. Outcome measures that differ more among subjects may offer greater potential for detecting treatment effects than outcome measures that differ little.
Statistical methods that address missing data should be adopted in studies that measure the internal carotid artery. The estimated gains in statistical efficiency in cross-sectional measurement (eg, 6.1%) can correspond to significant financial savings in trials such as ACAPS. Statistical techniques that compensate for missing data continue to be developed, so that even greater gains in efficiency may be available.
ACAPS data indicate that the B-mode ultrasonography used in ACAPS,
although well able to detect cross-sectional differences in IMT
among individual patients, is at present insufficiently precise to
identify slow or fast IMT progression rates (relative to those observed
in the ACAPS cohort) unless follow-up is long term. The ratio of
random error to the variability among progression rates is large, and
only by repeated measures or longer follow-up times can the
contributions of random error be sufficiently decreased to allow
individual diagnoses. Fig 3 demonstrates the impact of
extending the
length of follow-up. More modest gains in efficiency can be
attained by increasing the frequency of examinations: progression rates
based on weekly examinations across a single year would be less precise
than those from annual examinations across 3 years.
In 3-year studies similar to ACAPS, observed correlations between IMT progression and its risk factors are expected to be about one third of the true correlations. Despite this, however, it would appear that good statistical power is available from many of the recent studies. One would expect a trial such as ACAPS (n=919) to detect most major correlates among the measured potential risk factors.
B-mode ultrasonography is a demonstrably useful and reliable research tool for population studies of IMT progression. Benchmarks from first-generation clinical trials such as ACAPS have provided important empirical information for statistical decisions on design and analysis of future trials. Since the design of ACAPS, substantial technical progress has been made in alternative strategies for the measurement of IMT progression that appear to have good cross-sectional repeatability.33 34 35 36 As these newer approaches become more widely used, evaluations of their reliability across the course of longitudinal field studies will be important for understanding the advantages they offer.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported by National Institutes of Health grants R01-HL-38194 and R03-HL-54533, Merck, Sharpe & Dohme Research Laboratories, and E.I. DuPont De Nemours & Co, Inc.
Received August 31, 1995; revision received December 21, 1995; accepted December 21, 1995.
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References |
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|
TopAbstractIntroductionSubjects and Methods Results Discussion References |
|---|
1. The ACAPS Group. Rationale and design for the Asymptomatic Carotid Artery Plaque Study (ACAPS). Control Clin Trials. 1992;13:293-314. [Medline] [Order article via Infotrieve]
2. Crouse JR, Byington RP, Bond MG, Espeland MA, Sprinkle JW, McGovern M, Furberg CD. Pravastatin, lipids, and atherosclerosis in the carotid arteries: design features of a clinical trial with carotid atherosclerosis outcome. Control Clin Trials. 1992;13:495-506. [Medline] [Order article via Infotrieve]
3. Fried LP, Borhani NO, Enright P, Furberg CD, Gardin JM, Kronmal RA, Kuller LH, Manolio TA, Mittelmark MB, Newman A, O'Leary DH, Psaty B, Rautaharju P, Tracy RP, Weiler PG. The Cardiovascular Health Study: design and rationale. Ann Epidemiol. 1991;1:263-276. [Medline] [Order article via Infotrieve]
4.
The ARIC Investigators. The
Atherosclerosis Risk in Communities (ARIC) Study:
design and objectives. Am J Epidemiol. 1989;129:687-702.
5. Salonen R, Salonen JT. Progression of carotid atherosclerosis and its determinants: a population-based ultrasonography study. Atherosclerosis. 1990;81:33-40. [Medline] [Order article via Infotrieve]
6.
Hennerici M, Klephas W, Gries FA. Regression of
carotid plaques during low-density-lipoprotein
cholesterol elimination. Stroke. 1991;22:989-992.
7. Furberg CD, Borhani NA, Byington RP, Gibbons ME, Sowers JR. Calcium antagonists and atherosclerosis: the Multicenter Isradipine/Diuretic Atherosclerosis Study. Am J Hypertens. 1993;6:24S-29S. [Medline] [Order article via Infotrieve]
8.
Blankenhorn DH, Selzer RH, Crawford DW, Barth JD, Liu
C-R, Liu C-H, Mack WJ, Alaupovic P. Beneficial effects of
colestipol-niacin therapy on the common carotid artery: two- and
four-year reduction of intima-media thickness measured by
ultrasound. Circulation. 1993;88:20-28.
9.
O'Leary DH, Bryan FA, Goodison MW, Rifkin MD, Gramiak
R, Ball M, Bond MG, Dunn RA, Goldberg BB, Toole JF, Wheller HG,
Gustafson N, Ekholm S, Raines J. Measurement variability of
carotid atherosclerosis: a real-time (B-mode)
ultrasonography and angiography. Stroke. 1987;18:1011-1017.
10.
Riley WA, Barnes RW, Applegate WB, Dempsey R, Hartwell
T, Davis VG, Bond MG, Furberg CD. Reproducibility of noninvasive
ultrasonic measurement of carotid atherosclerosis: the
Asymptomatic Carotid Artery Plaque Study.
Stroke. 1992;23:1062-1068.
11. Bond MG, Barnes RW, Riley WA, Wilmoth SK, Chambless LE, Howard G, Owens B, for the ARIC Study Group. High-resolution B-mode ultrasound scanning methods in the Atherosclerosis Risk in Communities (ARIC) cohort. J Neuroimaging. 1991;1:68-73. [Medline] [Order article via Infotrieve]
12.
O'Leary DH, Polak JF, Wolfson SK, Bond ME, Bommer W,
Sheth S, Psaty BMN, Sharrett AR, Manolio TA. The use of
sonography to evaluate carotid atherosclerosis in the
elderly: the Cardiovascular Health Study.
Stroke. 1991;22:1155-1163.
13. Riley WA, Barnes RW, Bond MG, Evans GW, Chambless LEW, Heiss G. High-resolution B-mode ultrasound reading methods in the Atherosclerosis Risk in Communities (ARIC) cohort. J Neuroimaging. 1991;1:168-172. [Medline] [Order article via Infotrieve]
14. Persson J, Stavenow L, Wikstrand J, Israelsson B, Formgren J, Berglund G. Noninvasive quantification of atherosclerotic lesions: reproducibility of ultrasonographic measurement of arterial wall thickness and plaque size. Arterioscler Thromb. 1992;12:61-66.
15.
Pignoli P, Tremoli E, Oreste PL, Paoletti R.
Intima plus media thickness of the arterial wall: a direct
measurement with ultrasound imaging.
Circulation. 1986;74:1399-1406.
16.
Wikstrand J, Wiklund O. Frontiers in
cardiovascular science: qualitative measurements of
atherosclerotic manifestations in humans.
Arterioscler Thromb. 1992;12:114-119.
17. Mercuri M, Bond MG, Nichols FT, Carr AA, Flack JM, Byington R, Raines J. Baseline reproducibility of B-mode ultrasound imaging measurements of carotid intima media thickness: the Multicenter Isradipine Diuretic Atherosclerosis Study (MIDAS). J Cardiovasc Diag Proc. 1993;11:241-255.
18. Berglund GL, Riley WA, Barnes RW, Furberg CD. Quality control in ultrasound studies on atherosclerosis. J Intern Med. 1994;236:581-586. [Medline] [Order article via Infotrieve]
19. Wong M, Edelstein J, Wollman J, Bond MG. Ultrasonic pathological comparison of the human arterial wall: verification of intima-medial thickness. Arterioscler Thromb. 1993;12:482-486.
20.
Wofford JL, Kahl FR, Howard GR, McKinney WM, Toole JF,
Crouse JR. Relation of extent of extracranial carotid artery
atherosclerosis as measured by B-mode ultrasound to the
extent of coronary atherosclerosis.
Arterioscler Thromb. 1991;11:1786-1794.
21.
Craven TE, Ryu JE, Espeland MA, Kahl FR, McKinney WM,
Toole JF, McMahan MR, Thompson CJ, Heiss G, Crouse JR.
Evaluation of the associations between carotid artery
atherosclerosis and coronary artery
stenosis: a case-control study.
Circulation. 1990;82:1230-1242.
22.
Waters D, Craven TE, Lesperance J. Prognostic
significance of progression of coronary
atherosclerosis.
Circulation. 1993;87:1067-1075.
23. Laird NM, Ware JH. Random-effects models for longitudinal data. Biometrics. 1982;38:963-974. [Medline] [Order article via Infotrieve]
24.
Furberg CD, Adams HP, Applegate WB, Byington RP,
Espeland MA, Hartwell T, Hunninghake DB, Lefkowitz DS, Probstfield
J, Riley WA, Young B. Effect of lovastatin on early
carotid atherosclerosis and
cardiovascular events.
Circulation. 1994;90:1679-1687.
25. Jennrich RI, Schluchter MD. Unbalanced repeated measures models with structured covariance matrices. Biometrics. 1986;42:805-820. [Medline] [Order article via Infotrieve]
26. SAS Technical Report P-229, SAS/STAT Software: Changes and Enhancements, Release 6.06. Cary, NC: SAS Institute Inc; 1992.
27. Espeland MA, Byington RP, Hire D, Davis VG, Hartwell T, Probstfield J. Analysis strategies for serial multivariate ultrasonographic data that are incomplete. Stat Med. 1992;11:1041-1056.[Medline] [Order article via Infotrieve]
28. Lindstrom MJ, Bates DM. Newton-Raphson and EM algorithms for linear mixed-effects models for repeated measures data. J Am Stat Assoc. 1988;83:1014-1022.
29. Lehmann EL. Testing Statistical Hypotheses. New York, NY: John Wiley & Sons Inc; 1959.
30. Snedecor GW, Cochran WG. Statistical Methods. 7th ed. Ames, Iowa: The Iowa State University Press; 1980.
31. Furberg CD, Byington RP, Craven TE. Lessons learned from clinical trials with ultrasound end-points. J Intern Med. 1994;236:575-580. [Medline] [Order article via Infotrieve]
32. Adams HP, Byington RP, Hoen H, Dempsey R, Furberg CD. Effect of cholesterol-lowering medications on progression of mild atherosclerotic lesions of the carotid arteries and on the risk of stroke. Cerebrovasc Dis. 1995;5:171-177.
33. Rosenfield K, Boffetti P, Kaufman J, Weinstein R, Razvi S, Isner JM. Three-dimensional reconstruction of human carotid arteries from images obtained during noninvasive B-mode ultrasound examination. Am J Cardiol. 1992;70:379-384. [Medline] [Order article via Infotrieve]
34. Pretorius DH, Nelson TR, Jaffe JS. 3-dimensional sonographic analysis based on color flow Doppler and gray scale image data: a preliminary report. J Ultrasound Med. 1992;11:225-232. [Abstract]
35. Tsushima M, Koh H, Suzuki M, Kyotani S, Waki M, Nishioeda Y, Harano Y, Omae T. Noninvasive quantitative evaluation of early atherosclerosis and the effect of monatepil, a new antihypertensive agent. Am J Hypertens. 1994;7:154S-160S. [Medline] [Order article via Infotrieve]
36. Massonneau M, Caillard P, de Chassey L, Mouren X, Thebault B, Cloarec M. Short-term evaluation of plaque area measurement reproducibility from computer-assisted sonography. Angiology. 1995;46:375-381.
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N. Hosomi, K. Mizushige, H. Ohyama, T. Takahashi, M. Kitadai, Y. Hatanaka, H. Matsuo, M. Kohno, and J. A. Koziol Angiotensin-Converting Enzyme Inhibition With Enalapril Slows Progressive Intima-Media Thickening of the Common Carotid Artery in Patients With Non-Insulin-Dependent Diabetes Mellitus Stroke, July 1, 2001; 32(7): 1539 - 1545. [Abstract] [Full Text] [PDF]
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E. M. Lonn, S. Yusuf, V. Dzavik, C. I. Doris, Q. Yi, S. Smith, A. Moore-Cox, J. Bosch, W. A. Riley, and K. K. Teo Effects of Ramipril and Vitamin E on Atherosclerosis : The Study to Evaluate Carotid Ultrasound Changes in Patients Treated With Ramipril and Vitamin E (SECURE) Circulation, February 20, 2001; 103(7): 919 - 925. [Abstract] [Full Text] [PDF]
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 S Manzi, L H Kuller, D Edmundowicz, and K Sutton-Tyrrell Vascular imaging: changing the face of cardiovascular research Lupus, March 1, 2000; 9(3): 176 - 182. [Abstract] [PDF]
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P. H. Davis, J. D. Dawson, L. T. Mahoney, and R. M. Lauer Increased Carotid Intimal-Medial Thickness and Coronary Calcification Are Related in Young and Middle-Aged Adults : The Muscatine Study Circulation, August 24, 1999; 100(8): 838 - 842. [Abstract] [Full Text] [PDF]
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M. A. Espeland, R. Tang, J. G. Terry, D. H. Davis, M. Mercuri, and J. R. Crouse III Associations of Risk Factors With Segment-Specific Intimal-Medial Thickness of the Extracranial Carotid Artery Stroke, May 1, 1999; 30(5): 1047 - 1055. [Abstract] [Full Text] [PDF]
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C. Palombo, M. Kozakova, C. Morizzo, F. Andreuccetti, A. Tondini, P. Palchetti, G. Mirra, G. Parenti, and N. G. Pandian Ultrafast Three-Dimensional Ultrasound : Application to Carotid Artery Imaging Stroke, August 1, 1998; 29(8): 1631 - 1637. [Abstract] [Full Text] [PDF]
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S. D.J.M. Kanters, A. Algra, M. S. van Leeuwen, and J.-D. Banga Reproducibility of In Vivo Carotid Intima-Media Thickness Measurements : A Review Stroke, March 1, 1997; 28(3): 665 - 671. [Abstract] [Full Text]
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J. F. Polak, R. A. Kronmal, G. S. Tell, D. H. O'Leary, P. J. Savage, J. M. Gardin, G. H. Rutan, and N. O. Borhani Compensatory Increase in Common Carotid Artery Diameter: Relation to Blood Pressure and Artery Intima-Media Thickness in Older Adults Stroke, November 1, 1996; 27(11): 2012 - 2015. [Abstract] [Full Text]
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