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Coronary Artery Calcification Compared With Carotid Intima-Media Thickness in the Prediction of Cardiovascular Disease IncidenceThe Multi-Ethnic Study of Atherosclerosis (MESA)
Aaron R. Folsom, MD;
Richard A. Kronmal, PhD;
Robert C. Detrano, MD, PhD;
Daniel H. O’Leary, MD;
Diane E. Bild, MD;
David A. Bluemke, MD, PhD;
Matthew J. Budoff, MD;
Kiang Liu, PhD;
Steven Shea, MD;
Moyses Szklo, MD, DrPH;
Russell P. Tracy, PhD;
Karol E. Watson, MD, PhD;
Gregory L. Burke, MD
Arch Intern Med. 2008;168(12):1333-1339.
ABSTRACT
Background Coronary artery calcium (CAC) and carotid intima-media thickness (IMT) are noninvasive measures of atherosclerosis that consensus panels have recommended as possible additions to risk factor assessment for predicting the probability of cardiovascular disease (CVD) occurrence. Our objective was to assess whether maximum carotid IMT or CAC (Agatston score) is the better predictor of incident CVD.
Methods A prospective cohort study of subjects aged 45 to 84 years in 4 ethnic groups, who were initially free of CVD (n = 6698) was performed, with standardized carotid IMT and CAC measures at baseline, in 6 field centers of the Multi-Ethnic Study of Atherosclerosis (MESA). The main outcome measure was the risk of incident CVD events (coronary heart disease, stroke, and fatal CVD) over a maximum of 5.3 years of follow-up.
Results There were 222 CVD events during follow-up. Coronary artery calcium was associated more strongly than carotid IMT with the risk of incident CVD. After adjustment for each other (CAC score and IMT) and traditional CVD risk factors, the hazard ratio of CVD increased 2.1-fold (95% confidence interval [CI], 1.8-2.5) for each 1–standard deviation (SD) increment of log-transformed CAC score, vs 1.3-fold (95% CI, 1.1-1.4) for each 1-SD increment of the maximum IMT. For coronary heart disease, the hazard ratios per 1-SD increment increased 2.5-fold (95% CI, 2.1-3.1) for CAC score and 1.2-fold (95% CI, 1.0-1.4) for IMT. A receiver operating characteristic curve analysis also suggested that CAC score was a better predictor of incident CVD than was IMT, with areas under the curve of 0.81 vs 0.78, respectively.
Conclusion Although whether and how to clinically use bioimaging tests of subclinical atherosclerosis remains a topic of debate, this study found that CAC score is a better predictor of subsequent CVD events than carotid IMT.
INTRODUCTION
Prospective epidemiologic studies have consistently documented that noninvasive measures of atherosclerosis, such as coronary artery calcium (CAC) and carotid intima-media thickness (IMT), are associated positively and strongly with future incidence of cardiovascular disease (CVD). For example, a meta-analysis recently identified relative risks of coronary heart disease (CHD) of 1.0, 1.9, 4.3, 7.2, and 10.8 for CAC values of 0, 1 to 112, 100 to 400, 400 to 999, and 1000 or greater, respectively.1 Another meta-analysis reported significant relative risks of CHD of 1.26 for myocardial infarction (MI) and 1.32 for stroke for each 1–standard deviation (SD) increment of common carotid artery IMT.2
Whether and how to use these screening tests in clinical practice remains a matter of debate. Some task forces have recommended that bioimaging tests for atherosclerosis be considered for patients at intermediate risk of CHD (10%-20% risk in 10 years), for whom preventive interventions are often uncertain.1, 3 Another group recommended measuring CAC or IMT in all asymptomatic men aged 45 to 75 years and women aged 55 to 75 years as a guide to clinical decision making.4
Coronary artery calcium and IMT are only moderately correlated within individuals,5-9 so each test has some potential to be useful clinically to predict future CVD. Terry et al10 reported that CAC was associated more strongly than IMT with prevalent coronary artery stenosis. Brook et al11 confirmed this but found that an estimate of carotid plaque area predicted coronary stenosis somewhat more strongly than even CAC. Neither of these cross-sectional studies assessed CVD incidence. The prospective Rotterdam Study found that carotid plaques, increased IMT, aortic calcium, and low ankle-brachial blood pressure index predicted incident myocardial infarction (MI) fairly comparably, and the more subclinical measures present, the greater the risk.12 Their study did not examine CAC. Very recently, the first prospective study assessed the potential utility of measuring CAC vs IMT for global CVD risk prediction. Newman et al13 found that CAC and common carotid IMT similarly predicted CVD and CHD in adults 70 years or older, but IMT was the better predictor of stroke. Herein, we also address this question, prospectively, in the Multi-Ethnic Study of Atherosclerosis (MESA).
METHODS
MESA COHORT AND RISK FACTOR ASSESSMENTS
MESA recruited 6814 adults aged 45 to 84 years from the populations near 6 field centers (Baltimore, Maryland; Chicago, Illinois; Forsyth County, North Carolina; Los Angeles, California; New York, New York; and St Paul, Minnesota) to a baseline examination between July 2000 and September 2002.14 The study participants were white (38%), African American (28%), Hispanic (22%), and Chinese American (12%) and free of clinically recognized CVD and were drawn from households in geographically defined areas (5 centers) or in an occupational union (New York). MESA conducted 3 subsequent examinations of the cohort between 2002 and 2007. Institutional review boards at each site approved the study, and all participants gave written informed consent.
Centrally trained clinical teams collected information on cardiovascular risk factors during the baseline examination. They measured resting blood pressure 3 times in seated participants with a Dinamap model Pro 1000 automated oscillometric sphygmomanometer (Critikon, Tampa, Florida). A central laboratory measured total and high-density lipoprotein cholesterol and glucose levels from blood samples obtained after a 12-hour fast. We defined diabetes as a fasting glucose level of 126 mg/dL or greater (to convert to millimoles per liter, multiply by 0.0555) or use of hypoglycemic medication.
CAC ASSESSMENT
Scanning centers assessed CAC by chest computed tomography using either a cardiac-gated electron-beam computed tomography scanner (Chicago, Los Angeles, and New York field centers) or a multidetector computed tomography system (Baltimore, Forsyth County, and St Paul field centers). Certified technologists scanned all participants twice. A phantom of known physical calcium concentration was included in the field of view. A radiologist or cardiologist read all computed tomographic scans at a central reading center (Los Angeles Biomedical Research Institute at Harbor–UCLA Medical Center in Torrance, California) using an interactive scoring system similar to that used by Yaghoubi et al.15 The reader–work station interface identified and quantified CAC from images calibrated according to the readings of the calcium phantom. The Agatston score,16 which is a pseudo–continuous variable derived from plaque densities and their areas in all coronary arteries, was computed. We used the mean phantom-adjusted Agatston score for the 2 scans in all analyses. Carr et al17 have reported the details of the MESA computed tomographic scanning and interpretation methods. Each participant and his or her physicians were notified whether the CAC scores were below average, average, or above average for the participant's age. No recommendation was made about treatment.
CAROTID IMT ASSESSMENT
Trained technicians in each field center performed B-mode ultrasonography of the right and left near and far walls of the internal carotid and common carotid arteries.18 They used the Logiq 700 ultrasound device (General Electric Medical Systems, Waukesha, Wisconsin) to record images. An ultrasound reading center (Department of Radiology, Tufts–New England Medical Center, Boston, Massachusetts) measured maximal IMT of the internal and common carotid sites as the mean of the maximum IMT of the near and far walls of the right and left sides. In addition, for this article, we created a composite z score for overall maximal IMT by summing the values of the 2 carotid IMT sites (if both were measured) after standardization (subtraction of the mean and division by the SD of each measure) and then dividing by the SD of the sum. If only 1 of the 2 measures was available, it was used. The resulting variable, hereafter referred to as z score maximum IMT, has a mean of 0 and an SD of 1. Each participant and his or her physicians were notified whether an accompanying Doppler assessment suggested significant carotid stenosis ( 50%), but no recommendation was made about treatment.
CVD FOLLOW-UP
We followed the cohort for incident CVD events for a median of 3.9 years (maximum, 5.3 years). At intervals of 9 to 12 months, a telephone interviewer contacted each participant to inquire about interim hospital admissions, cardiovascular outpatient diagnoses, and deaths. To verify self-reported diagnoses, we requested copies of all death certificates and medical records for hospitalizations and outpatient cardiovascular diagnoses. We also conducted next-of-kin interviews for out-of-hospital cardiovascular deaths. We obtained records on an estimated 98% of reported hospitalized cardiovascular events and some information on 95% of reported outpatient diagnostic encounters.
Two physicians, blinded to the CAC and IMT data, independently reviewed and classified CVD events and assigned incidence dates. If, after review and adjudication, disagreements persisted, a full mortality and morbidity review committee made the final classification. MESA criteria for events were adopted from the Atherosclerosis Risk in Communities Study, the Cardiovascular Health Study, and the Women's Health Initiative. Reviewers classified MI as definite, probable, or absent, based primarily on combinations of symptoms, electrocardiographic findings, and levels of cardiac biomarkers (generally, troponins or creatine kinase myocardial band). Reviewers graded angina based on their clinical judgment as definite, probable, or absent. Probable angina required symptoms of ischemia, as well as documentation that a physician had diagnosed and treated angina. Definite angina also required objective diagnostic evidence of CHD. In this article, we only included definite angina (n = 76) plus probable angina when accompanied by coronary revascularization (n = 5). The reviewers classified CHD or CVD death as present or absent based on hospital records and interviews with families. Definite fatal CHD required an MI within 28 days of death, chest pain within the 72 hours before death, or a history of CHD and the absence of a known nonatherosclerotic or noncardiac cause of death. Neurologists reviewed and classified stroke as present if there was a focal neurologic deficit lasting 24 hours or until death, with a clinically relevant lesion on brain imaging and no nonvascular cause.
For this report, we defined incident CVD as CHD (definite and probable MI, definite CHD death, resuscitated cardiac arrest, definite angina, and probable angina associated with coronary revascularization), stroke (fatal or nonfatal), or other atherosclerotic CVD death. Follow-up went from the baseline examination until the first CVD event, loss to follow-up, death, or January 12, 2005, whichever came first.
STATISTICAL ANALYSIS
From the 6814 MESA participants, we excluded 77 who were missing both of the carotid IMT measures, 5 who were discovered to have had CVD events before baseline, and 34 with no follow-up data, leaving 6698 participants for analysis. For most analyses, we either (1) categorized carotid IMT and CAC into 3 groups (the bottom 50% and the 2 upper quartiles) to accommodate the fact that 50% of participants had a CAC score of 0 or (2) treated IMT and the natural logarithm (ln) of (CAC score + 1) as continuous variables. The ln(CAC score + 1) transformation better normalized the CAC distribution. We used Cox proportional hazard regression to estimate hazard ratios (HRs). We performed tests for nonproportional hazards using Shoenfeld residuals; all results were nonsignificant. Covariates for multivariable models included age (continuous), sex, race/ethnicity (4 groups), smoking (current, former, or never), diabetes (yes or no), blood pressure (6 categories according to the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, including medications),19 high-density lipoprotein and total cholesterol level (continuous), and use of lipid-lowering medication (yes or no). We compared the strength of the association for IMT vs CAC score based on the relative size of their HRs and the corresponding  2 test or z score of the HRs. We also compared IMT and CAC associations with receiver operating characteristic curves modeling carotid IMT and ln(CAC score + 1) as continuous variables in Cox models. In the Figure, rates were calculated for "low, medium, and high" values of z score maximum IMT and CAC score using intervals as previously described. All analyses were performed using STATA 9.2 (StataCorp, College Station, Texas) statistical software.
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Figure. Unadjusted rate of cardiovascular disease in relation to percentiles of maximal carotid intima-media thickness (IMT) or coronary artery calcium (CAC) score (The Multi-Ethnic Study of Atherosclerosis, 2000-2004). CI indicates confidence interval.
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RESULTS
The MESA sample for this analysis comprised 6698 adults aged 45 to 84 years at baseline (3161 men and 3537 women). During 23 735 person-years of follow-up, we identified 222 incident CVD events (159 CHD events [61 MI, 81 angina, 3 resuscitated cardiac arrest, 13 CHD deaths]; 59 stroke events [3 of which included a CHD event]; and 7 other atherosclerotic CVD deaths). Of the MESA sample, 50% had detectable CAC. The mean (SD) value was 2.2 (2.5) for ln(CAC score + 1), 1.07 (0.60) mm for maximum internal carotid IMT, 0.87 (0.19) mm for maximum common carotid IMT, and 0.00 (1.00) for z score maximum IMT.
As given in Table 1, the 3 measures of carotid IMT were all positively associated with incident CVD, with age-, race/ethnicity-, and sex-adjusted HRs for the highest vs lowest quartile of 3.3 (95% confidence interval [CI], 2.1-5.2) for the maximum internal carotid IMT, 2.3 (95% CI, 1.4-3.8) for the maximum common carotid IMT, and 3.8 (95% CI, 2.2-6.4) for the z score maximum IMT (all P < .001). The remaining IMT analyses therefore focused on z score maximum IMT. For CAC score (Table 1), the HRs of CVD increased across categories, with the age-, race/ethnicity-, and sex-adjusted HR being 6.0 (95% CI, 3.9-9.1) for the highest CAC score quartile vs a CAC score of 0 (P < .001). The results for CHD risk (data not shown) were similar. For reference to recommended clinical cut points for CAC score,1, 3 the age-, race/ethnicity-, and sex-adjusted HRs for CAC scores of 0, 1 to 99, 100 to 399, and 400 or greater were 1 [Reference], 4.7 (95% CI, 2.5-8.7), 11.5 (95% CI, 6.2-21.5), and 16.1 (95% CI, 8.5-30.8), respectively (data not shown in tables).
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Table 1. Hazard Ratios (HRs) for an Incident Cardiovascular Disease Event in Relation to Quartiles of Maximal Carotid IMT or CAC Score (MESA, 2000-2004)
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When put in the same model, CAC score was more strongly associated with both CVD and CHD compared with IMT (Table 2). The multivariable-adjusted HRs of CVD and CHD per 1-SD increment were 1.9 (95% CI, 1.6-2.2) and 2.3 (95% CI, 1.9-3.8), respectively, for ln(CAC score + 1), compared with 1.2 (95% CI, 1.0-1.3) and 1.1 (95% CI, 1.0-1.3) for z score maximum IMT. Furthermore, the z scores were larger and P values were smaller for the CAC association. In contrast, for stroke, only z score maximum IMT was statistically significant (P = .01) with multivariable-adjusted HR of 1.3 (95% CI, 1.1-1.7), while the HR for ln(CAC + 1) was 1.1 (95% CI, 0.8-1.4).
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Table 2. Hazard Ratios (HRs) for an Incident CVD, CHD, or Stroke Event in Relation to a 1-SD Increment of Maximal Carotid IMT or CAC Score (MESA, 2000-2004)
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A categorical analysis (Table 3) also suggested that CAC score was a better predictor of incident CVD and CHD than was IMT. For example, the multivariable-adjusted HRs of CHD for the highest quartile vs lowest 50th percentile were 8.2 (95% CI, 4.5-15.1; P < .001) for CAC and 1.7 (95% CI, 1.1-2.7; P = .07) for z score maximum IMT.
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Table 3. Hazard Ratios (HRs) for an Incident CVD, CHD, or Stroke Event in Relation to Quartiles of Maximal Carotid IMT or CAC Score (MESA, 2000-2004)
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In supplemental research, we restricted our analyses to subjects at intermediate CHD risk, based on a Framingham risk score of 1% to 2% per year (n = 1841, with 54 CHD events). Among them, the multivariable-adjusted HRs of CHD per 1-SD increment were 2.4 (95% CI, 1.7-3.3; P < .001) for ln(CAC score + 1) and 1.3 (95% CI, 1.0-1.6; P < .05) for z score maximum IMT when both were included in the model. In the same subgroup at intermediate Framingham risk, for CVD (81 events), the multivariable-adjusted HRs were 1.8 (95% CI, 1.4-2.2; P < .001) for ln(CAC score + 1) and 1.4 (95% CI, 1.1-1.6; P = .001) for z score maximum IMT.
The Figure shows crude rates of incident CVD by 9 joint categories of z score maximum IMT and CAC score. Rates of CVD were between 1% and 2% per year for those with (1) a moderate level of CAC and high IMT or (2) a high level of CAC and low IMT. Rates of CVD were greater than 2% per year for those with a high level of CAC and either a moderate or high level of IMT. Those with a CAC score of 0 and either low or moderate IMT had almost no events during this follow-up period. Findings for CHD were similar (data not shown).
Findings from receiver operating characteristic curve analysis suggested that CAC score was a better predictor of CVD incidence than was carotid IMT. With the multiple risk factors in the model for CVD, the area under the curve (AUC) was 0.772 (95% CI, 0.74-0.80). After adding z score maximum IMT, the AUC was 0.782 (95% CI, 0.75-0.81); after substituting CAC score for IMT, the AUC was 0.808 (95% CI, 0.78-0.83); and after including both IMT and CAC score, the AUC was 0.811 (95% CI, 0.78-0.84). A similar receiver operating characteristic curve analysis for CHD produced AUCs of 0.771 (95% CI, 0.74-0.80) for risk factors alone, 0.782 (95% CI, 0.75-0.82) for risk factors plus IMT, 0.823 (95% CI, 0.79-0.85) for risk factors plus CAC score, and 0.824 (95% CI, 0.79-0.85) for risk factors plus CAC score and IMT.
COMMENT
This prospective analysis of the MESA cohort who were initially free of symptomatic CVD found that carotid maximum IMT and CAC score, 2 measures of subclinical atherosclerosis, predicted future CVD events. However, CAC score was the better predictor for CHD and total CVD. Intima-media thickness was a modestly better predictor of stroke than CAC score, although there were few stroke events. The associations observed were consistent with those reported by meta-analyses of prospective studies of each subclinical measure of atherosclerosis studied separately.1-2 They were somewhat inconsistent with a small prospective study in elderly people, in which common carotid IMT was similiar to CAC in predicting CVD and CHD.13 It may be that IMT becomes more predictive of CVD in old age, but the smaller sample size of that study also may have limited its ability to show differences between CAC and IMT associations with CVD.
Although previous consensus statements indicated that CAC score and IMT are global atherosclerosis measures and either might be used clinically for refinement of CVD risk assessment,4, 20 our data suggest that in asymptomatic 45- to 84-year-old US adults, CAC score may be the better choice over IMT. As judged by proportional hazards modeling and by the AUC, CAC score added more to CVD prediction, beyond traditional risk factors, than did IMT. Coronary artery calcium was also associated with CHD more strongly than IMT within the group of individuals at intermediate risk, for whom a subclinical atherosclerosis assessment may be most appropriate.1, 3, 20 When more CVD events accrue in MESA, we can more thoroughly address the issue of what novel measures (eg, CAC score, IMT, C-reactive protein level, and others) might improve CVD risk prediction in intermediate-risk patients.
The modestly better prediction of stroke by IMT and clearly better prediction of CHD by CAC score likely reflects their different vascular territories. The potential choice between measuring CAC or IMT or neither in preventive cardiology depends on other considerations as well (eg, differences in radiation exposure, cost, and availability). The CAC score may be most relevant in the United States, where CHD is common. If risk of stroke in families with histories of early stroke were a concern, then carotid IMT may be very relevant. Also, in MESA, there are substantial ethnic differences in CAC score (highest in whites),21 and to a lesser degree for IMT (highest in African Americans),22 which may have an impact on clinical use.
Strengths of this study include its multiethnic sample, standardized subclinical atherosclerosis assessments and risk factor measurements, and its reliance on symptomatic end points to avoid detection bias related to CVD events being diagnosed more readily in subjects with known subclinical atherosclerosis. Limitations include, first, the relatively short follow-up period and the relatively small number of strokes to date. Results could be different for long-term CVD prediction, especially as this population ages and the ratio of strokes to CHD events increases. Second, the shapes of distributions differ for IMT and CAC, with many 0 values for CAC score. However, our analyses using both categorical and continuous measures of IMT and CAC placed them on a more comparable footing. Third, although all end points were symptomatic, we included both "hard" CHD (MI and CHD death) and "soft" CHD (angina) to provide adequate statistical power. Fourth, for ethical reasons, we felt compelled to report high CAC and IMT values to participants and refer them to their physicians. More participants were referred for high CAC score (17%) than for high IMT (1%), which could have affected our findings if participants changed risk factors differentially. Yet, this seems unlikely, since a clinical trial suggested that telling patients their CAC score does not motivate significant health behavior change.23
In conclusion, although whether and how to use bioimaging tests for subclinical atherosclerosis remains a topic of debate, this study found that CAC score was a better predictor of subsequent CVD events than was carotid IMT.
AUTHOR INFORMATION
Corresponding Author: Aaron R. Folsom, MD, Division of Epidemiology & Community Health, School of Public Health, University of Minnesota, 1300 S Second St, Ste 300, Minneapolis, MN 55454-1015 (folso001{at}umn.edu).
Accepted for Publication: November 26, 2007.
Author Contributions: Dr Folsom had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: Folsom, Kronmal, Detrano, O’Leary, Bild, Bluemke, Shea, and Tracy. Acquisition of data: Folsom, Kronmal, Detrano, O’Leary, Budoff, Liu, Shea, Szklo, Tracy, Watson, and Burke. Analysis and interpretation of data: Folsom, Kronmal, O’Leary, Bild, Budoff, Liu, and Burke. Drafting of the manuscript: Folsom, Kronmal, and O’Leary. Critical revision of the manuscript for important intellectual content: Kronmal, O’Leary, Bild, Bluemke, Budoff, Liu, Shea, Szklo, Tracy, Watson, and Burke. Statistical analysis: Kronmal and Liu. Obtained funding: Kronmal, O’Leary, Bluemke, Shea, Tracy, and Burke. Administrative, technical, and material support: Kronmal, O’Leary, Bild, Shea, and Tracy. Study supervision: O’Leary, Budoff, Shea, and Watson.
Financial Disclosure: Dr O’Leary serves as consultant to Sankyo Pharma, Sanofi-Aventis, GlaxoSmithKline, Eli Lilly, Schering-Plough, Pfizer, AstraZeneca, and Merck and owns stock in Medpace. Dr Budoff has received honoraria for speaking on behalf of General Electric.
Funding/Support: This research was supported by grants N01-HC-95159 through N01-HC-95169 from the National Heart, Lung, and Blood Institute.
Role of the Sponsor: The National Heart, Lung, and Blood Institute staff had input in the design and conduct of this study; the collection, management, analysis, and interpretation of the data; and the preparation of the manuscript.
Additional Contributions: We thank the other investigators, the staff, and the participants of the MESA Study for their valuable contributions. A full list of participating MESA investigators and institutions can be found at http://www.mesa.nhlbi.org.
Author Affiliations: Division of Epidemiology & Community Health, School of Public Health, University of Minnesota, Minneapolis (Dr Folsom); Collaborative Health Studies Coordinating Center, University of Washington, Seattle (Dr Kronmal); Department of Radiological Sciences, University of California at Irvine (Dr Detrano); Caritas Carney Hospital, Dorchester, Massachusetts (Dr O’Leary); Division of Prevention & Population Sciences, National Heart, Lung, and Blood Institute, Bethesda, Maryland (Dr Bild); Departments of Radiology (Dr Bluemke) and Epidemiology (Dr Szklo), Johns Hopkins University School of Medicine, Baltimore, Maryland; Division of Cardiology, Los Angeles Biomedical Research Institute at Harbor–UCLA Medical Center, Torrance, California (Dr Budoff); Department of Preventive Medicine, Northwestern University Medical School, Chicago, Illinois (Dr Liu); Departments of Medicine and Epidemiology, Columbia University, New York, New York (Dr Shea); Departments of Pathology and Biochemistry, University of Vermont, Colchester (Dr Tracy); Division of Cardiology, UCLA School of Medicine, Los Angeles, California (Dr Watson); and Division of Public Health Sciences, Wake Forest University Health Sciences, Winston-Salem, North Carolina (Dr Burke).
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Improvements in risk stratification for the occurrence of cardiovascular disease by imaging subclinical atherosclerosis: a systematic review
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Heart 2012;98:177-184.
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Heart Disease and Stroke Statistics--2012 Update: A Report From the American Heart Association
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Circulation 2012;125:e2-e220.
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Imaging Assessment of Cardiovascular Risk in Asymptomatic Adults
Lin and Hwang
Am. J. Roentgenol. 2011;197:W1046-W1051.
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The Associations of Fetuin-A With Subclinical Cardiovascular Disease in Community-Dwelling Persons: The Rancho Bernardo Study
Ix et al.
J Am Coll Cardiol 2011;58:2372-2379.
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The Epidemiology of Vascular Dysfunction Relating to Chronic Obstructive Pulmonary Disease and Emphysema
Barr
Proc Am Thorac Soc 2011;8:522-527.
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Psychosocial Predictors of Coronary Artery Calcification Progression in Postmenopausal Women
Low et al.
Psychosom. Med. 2011;73:789-794.
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Common Carotid Artery Intima-Media Thickness Progression as a Predictor of Stroke in Multi-Ethnic Study of Atherosclerosis
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Stroke 2011;42:3017-3021.
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Impact of Subclinical Atherosclerosis on Cardiovascular Disease Events in Individuals With Metabolic Syndrome and Diabetes: The Multi-Ethnic Study of Atherosclerosis
Malik et al.
Diabetes Care 2011;34:2285-2290.
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Association of Small Artery Elasticity With Incident Cardiovascular Disease in Older Adults: The Multi-Ethnic Study of Atherosclerosis
Duprez et al.
Am J Epidemiol 2011;174:528-536.
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Burden of atherosclerosis improves the prediction of coronary heart disease but not cerebrovascular events: The Rotterdam Study
Elias-Smale et al.
Eur Heart J 2011;32:2050-2058.
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Association of lipoprotein-associated phospholipase A2 and endothelial function in the Multi-Ethnic Study of Atherosclerosis (MESA)
Garg et al.
Vasc Med 2011;16:247-252.
ABSTRACT
Predictors of Coronary Heart Disease Events Among Asymptomatic Persons With Low Low-Density Lipoprotein Cholesterol: MESA (Multi-Ethnic Study of Atherosclerosis)
Blankstein et al.
J Am Coll Cardiol 2011;58:364-374.
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High-Intensity Signals in Carotid Plaques on T1-Weighted Magnetic Resonance Imaging Predict Coronary Events in Patients With Coronary Artery Disease
Noguchi et al.
J Am Coll Cardiol 2011;58:416-422.
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Sex Differences in Subclinical Atherosclerosis by Race/Ethnicity in the Multi-Ethnic Study of Atherosclerosis
Kim et al.
Am J Epidemiol 2011;174:165-172.
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Gene expression variation between African Americans and whites is associated with coronary artery calcification: the multiethnic study of atherosclerosis
Huang et al.
Physiol. Genomics 2011;43:836-843.
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High-Sensitivity C-Reactive Protein, Obesity, and Subclinical Atherosclerosis: Implications of JUPITER From the MESA Study
Targher
Arterioscler. Thromb. Vasc. Bio. 2011;31:1251-1252.
FULL TEXT
Association Between Obesity, High-Sensitivity C-Reactive Protein >=2 mg/L, and Subclinical Atherosclerosis: Implications of JUPITER from the Multi-Ethnic Study of Atherosclerosis
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Arterioscler. Thromb. Vasc. Bio. 2011;31:1430-1438.
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Associations of occupation, job control and job demands with intima-media thickness: The Multi-Ethnic Study of Atherosclerosis (MESA)
Fujishiro et al.
Occup. Environ. Med. 2011;68:319-326.
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Coronary Calcium Score and Prediction of All-Cause Mortality in Diabetes: The Diabetes Heart Study
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Diabetes Care 2011;34:1219-1224.
ABSTRACT
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Texas Atherosclerosis Imaging Bill: Quiet Origins, Broad Implications
Khera
Arch Intern Med 2011;171:281-283.
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Assessing the Role of Circulating, Genetic, and Imaging Biomarkers in Cardiovascular Risk Prediction
Wang
Circulation 2011;123:551-565.
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Heart Disease and Stroke Statistics--2011 Update: A Report From the American Heart Association
Roger et al.
Circulation 2011;123:e18-e209.
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Cardiovascular Imaging for Assessing Cardiovascular Risk in Asymptomatic Men Versus Women: The Multi-Ethnic Study of Atherosclerosis (MESA)
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Circ Cardiovasc Imaging 2011;4:8-15.
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2010 ACCF/AHA Guideline for Assessment of Cardiovascular Risk in Asymptomatic Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines
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Circulation 2010;122:e584-e636.
FULL TEXT
2010 ACCF/AHA Guideline for Assessment of Cardiovascular Risk in Asymptomatic Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the American Society of Echocardiography, American Society of Nuclear Cardiology, Society of Atherosclerosis Imaging and Prevention, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance
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J Am Coll Cardiol 2010;56:e50-e103.
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The Ankle-Brachial Index and Incident Cardiovascular Events in the MESA (Multi-Ethnic Study of Atherosclerosis)
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J Am Coll Cardiol 2010;56:1506-1512.
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Association of Combinations of Lipid Parameters With Carotid Intima-Media Thickness and Coronary Artery Calcium in the MESA (Multi-Ethnic Study of Atherosclerosis)
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J Am Coll Cardiol 2010;56:1034-1041.
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Carotid Ultrasound, Coronary Calcium, and Dyslipidemia Patterns in the MESA (Multi-Ethnic Study of Atherosclerosis) Cohort
Mancini and Frohlich
J Am Coll Cardiol 2010;56:1042-1044.
FULL TEXT
Pioglitazone Versus Glimepiride on Coronary Artery Calcium Progression in Patients With Type 2 Diabetes Mellitus: A Secondary End Point of the CHICAGO Study
Davidson et al.
Arterioscler. Thromb. Vasc. Bio. 2010;30:1873-1876.
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Screening Asymptomatic Subjects for Subclinical Atherosclerosis: Can We, Does It Matter, and Should We?
Shah
J Am Coll Cardiol 2010;56:98-105.
ABSTRACT
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Imaging of atherosclerosis: carotid intima-media thickness
O'Leary and Bots
Eur Heart J 2010;31:1682-1689.
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Imaging of coronary atherosclerosis by computed tomography
Achenbach and Raggi
Eur Heart J 2010;31:1442-1448.
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Intake of fish and marine n-3 fatty acids in relation to coronary calcification: the Rotterdam Study
Heine-Broring et al.
Am J Clin Nutr 2010;91:1317-1323.
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Coronary Artery Calcium, Brain Function and Structure: The AGES-Reykjavik Study
Vidal et al.
Stroke 2010;41:891-897.
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Carotid Intima-Media Thickness and Presence or Absence of Plaque Improves Prediction of Coronary Heart Disease Risk: The ARIC (Atherosclerosis Risk In Communities) Study
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J Am Coll Cardiol 2010;55:1600-1607.
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Carotid Intima-Media Thickness, Plaques, and Cardiovascular Disease Risk: Implications for Preventive Cardiology Guidelines
Stein and Johnson
J Am Coll Cardiol 2010;55:1608-1610.
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The USPSTF Recommendation Statement on Coronary Heart Disease Risk Assessment
Budoff
ANN INTERN MED 2010;152:403-404.
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Heart Disease and Stroke Statistics--2010 Update: A Report From the American Heart Association
WRITING GROUP MEMBERS et al.
Circulation 2010;121:e46-e215.
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The Value of Carotid Intima-Media Thickness for Predicting Cardiovascular Risk
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Arterioscler. Thromb. Vasc. Bio. 2010;30:182-185.
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A High Ankle Brachial Index Is Associated With Greater Left Ventricular Mass: MESA (Multi-Ethnic Study of Atherosclerosis)
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J Am Coll Cardiol 2010;55:342-349.
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The SHAPE Paradigm: A Commentary
Shah
Circ Cardiovasc Qual Outcomes 2010;3:106-109.
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Structural and Functional Vascular Alterations and Incident Hypertension in Normotensive Adults: The Multi-Ethnic Study of Atherosclerosis
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Am J Epidemiol 2010;171:63-71.
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Carotid intima-media thickness measurement in cardiovascular screening programmes
Plantinga et al.
European Journal of Cardiovascular Prevention & Rehabilitation 2009;16:639-644.
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HIV positivity, protease inhibitor exposure and subclinical atherosclerosis: a systematic review and meta-analysis of observational studies
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Heart 2009;95:1826-1835.
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Emerging Risk Factors for Coronary Heart Disease: A Summary of Systematic Reviews Conducted for the U.S. Preventive Services Task Force
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ANN INTERN MED 2009;151:496-507.
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18F-FDG PET/CT Identifies Patients at Risk for Future Vascular Events in an Otherwise Asymptomatic Cohort with Neoplastic Disease
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JNM 2009;50:1611-1620.
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Selective Use of Coronary Artery Calcium Screening: Worth the Cost?
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J Am Coll Cardiol 2009;54:1268-1270.
FULL TEXT
Meta-analysis: Retinal Vessel Caliber and Risk for Coronary Heart Disease
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ANN INTERN MED 2009;151:404-413.
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Coronary Artery Calcification Screening: Estimated Radiation Dose and Cancer Risk
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Arch Intern Med 2009;169:1188-1194.
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Outcomes Research in Cardiovascular Imaging: Report of a Workshop Sponsored by the National Heart, Lung, and Blood Institute
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J Am Coll Cardiol Img 2009;2:897-907.
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Outcomes Research in Cardiovascular Imaging: Report of a Workshop Sponsored by the National Heart, Lung, and Blood Institute
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Circ Cardiovasc Imaging 2009;2:339-348.
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The Year in Coronary Artery Disease
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J Am Coll Cardiol Img 2009;2:774-786.
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Vitamin K supplementation and progression of coronary artery calcium in older men and women
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Am J Clin Nutr 2009;89:1799-1807.
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The Year in Atherothrombosis
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J Am Coll Cardiol 2009;53:1326-1337.
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Atherosclerosis Imaging: Prognostically Useful or Merely More of What We Know?
Kaul and Douglas
Circ Cardiovasc Imaging 2009;2:150-160.
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Heart Disease and Stroke Statistics--2009 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee
WRITING GROUP MEMBERS et al.
Circulation 2009;119:e21-e181.
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Prevalence and Progression of Subclinical Atherosclerosis in Younger Adults With Low Short-Term but High Lifetime Estimated Risk For Cardiovascular Disease: The Coronary Artery Risk Development in Young Adults Study and Multi-Ethnic Study of Atherosclerosis
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Circulation 2009;119:382-389.
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