Medical Policy: 02.02.14 

Original Effective Date: June 2012 

Reviewed: January 2021 

Revised: January 2015 



This policy contains information which is clinical in nature. The policy is not medical advice. The information in this policy is used by Wellmark to make determinations whether medical treatment is covered under the terms of a Wellmark member's health benefit plan. Physicians and other health care providers are responsible for medical advice and treatment. If you have specific health care needs, you should consult an appropriate health care professional. If you would like to request an accessible version of this document, please contact customer service at 800-524-9242.


Benefit Application:

Benefit determinations are based on the applicable contract language in effect at the time the services were rendered. Exclusions, limitations or exceptions may apply. Benefits may vary based on contract, and individual member benefits must be verified. Wellmark determines medical necessity only if the benefit exists and no contract exclusions are applicable. This medical policy may not apply to FEP. Benefits are determined by the Federal Employee Program.


This Medical Policy document describes the status of medical technology at the time the document was developed. Since that time, new technology may have emerged or new medical literature may have been published. This Medical Policy will be reviewed regularly and be updated as scientific and medical literature becomes available.



Coronary heart disease (CHD) accounts for 30.8% of all deaths in the United States. Established major risk factors for CHD have been identified by the National Cholesterol Education Program (NCEP) Expert Panel. These risk factors include elevated serum levels of low-density lipoprotein cholesterol (LDL-C), total cholesterol, and reduced levels of high-density lipoprotein cholesterol. Other risk factors include a history of cigarette smoking, hypertension, family history of premature CHD, and age.


The third report of the National Cholesterol Education Program Adult Treatment Panel established various treatment strategies to modify the risk of CHD, with emphasis on target goals of low-density lipoprotein cholesterol. Pathology studies have demonstrated that levels of traditional risk factors are associated with the extent and severity of atherosclerosis. The third report of the National Cholesterol Education Program Adult Treatment Panel recommended use of the Framingham criteria to further stratify those patients with two or more risk factors for more intensive lipid management. However, at every level of risk factor exposure, there is substantial variation in the amount of atherosclerosis, presumably related to genetic susceptibility and the influence of other risk factors. Thus, there has been interest in identifying a technique that can improve the ability to diagnose those at risk of developing CHD, as well as to measure disease progression, particularly for those at intermediate risk.


The carotid arteries can be well-visualized by ultrasonography, and ultrasonographic measurement of the carotid intima-media thickness (CIMT) has been investigated as a technique to identify and monitor subclinical artherosclerosis. B-mode ultrasound is most commonly used to measure CIMT. The intima-media thickness (IMT) is measured and averaged over several sites in each carotid artery. Imaging of the far wall of each common carotid artery yields more accurate and reproducible IMT measurements than imaging of the near wall. Two echogenic lines are produced, representing the lumen- intima interface and the media-adventitia interface. The distance between these two lines constitutes the IMT.


Measurement of carotid intima-media (or intimal-medial) thickness (CIMT) is primarily meant to assess risk for future disease, and therefore can be evaluated as a prognostic measure. Assessment of a prognostic measure typically focuses on 3 categories of evidence: 1) technical reliable; 2) clinically valid (i.e. a test must detect the presence or absence of a condition, the risk of developing a condition in the future, or treatment response [beneficial or adverse]); and 3) clinically useful (i.e. demonstration that use of the prognostic information clinically can alter clinical management and/or improve net health outcomes compared with patient management without use of the prognostic tool). In some cases, it is important to evaluate whether the test provides incremental information above the standard workup to determine whether the test has utility in clinical practice.


Ultrasonographic Measurement of CIMT

Clinical Context and Test Purpose

The purpose of CIMT testing in patients who are undergoing cardiac risk assessment is to inform decision whether to monitor and/or intervene to treat those at increased cardiac risk.



The relevant patient population of interest is individuals undergoing cardiac risk assessment.



Individual risk for cardiac events may be determined from multivariate risk models, such as the Framingham Risk Score.



The general outcomes of interest in CIMT measurement are to characterize the disease activity accurately and predict major adverse cardiac events, including stroke, myocardial infarction, and heart failure.



Five to ten year studies are of particular interest due to prolonged natural history of cardiovascular disease.



The primary setting for CIMT measurement is an outpatient clinic.


Clinically Valid

A test must detect the presence or absence of a condition, the risk of developing a condition in the future, or treatment response (beneficial or adverse).


Systematic Reviews and Meta-Analyses

Mookadam et. al. (2010) conducted a systemic review of the role of CIMT (carotid intima-media thickness) in predicting individual cardiovascular even risk, and as a tool for assessing therapeutic interventions. Reviewers concluded that CIMT is an independent risk factor for cardiovascular events and may be useful in determining treatment when there is uncertainty regarding the approach or patient reluctance. However, they recommended further study to identify the best approaches to screening and interventions to prevent progression of atherosclerosis.


In 2012, Den Ruijter et. al. completed a meta-analysis to determine whether common CIMT (carotid intima-media thickness) has added value in 10-year risk prediction of first time myocardial infarctions or strokes, above that of the Framingham Risk Score. Studies were included if participants were drawn from the general population, common CIMT was measured at baseline, and individuals were followed up for first-time myocardial infarction or stroke. Included was 14 population-based cohorts contributing data for 45,828 individuals. During a median follow-up of 11 years, 4007 first-time myocardial infarctions or strokes occurred. They refitted the risk factors of the Framingham Risk Score and then extended the model with common CIMT measurements to estimate the absolute 10-year risks to develop a first-time myocardial infarction or stroke in both models. The C statistic of both models was similar (0.757; 95% CI, 0.749-0.764; and 0.759; 95% CI, 0.752-0.766). The net reclassification improvement with the addition of common CIMT was small (0.8%; 95% CI, 0.1%-1.6%). In those at intermediate risk, the net reclassification improvement was 3.6% in all individuals (95% CI, 2.7%-4.6%) and no differences between men and women. The authors concluded, the added value of common CIMT in 10 year risk prediction of cardiovascular events, in addition to the Framingham Risk Score, was small and unlikely to be of clinical importance.


Lorenz et. al. (2012) completed a meta-analysis on carotid intima-media thickness (CIMT) to predict cardiovascular events in the general population, the PROG-IMT collaborative project. They identified general population studies that assessed CIMT at least twice and followed up participants for myocardial infarction, stroke, or death. The study teams collaborated in an individual participant data meta-analysis. Excluding individuals with previous myocardial infarction or stroke, we assessed the association between CIMT progression and the risk of cardiovascular events (myocardial infarction, stroke, vascular death, or a combination of these) for each study with Cox regression. The log hazard ratios (HRs) per SD difference were pooled by random effects meta-analysis. Of the 21 eligible studies, 16 with 36,984 participants were included. During a mean follow-up of 7 years, 1519 myocardial infarctions, 1339 strokes, and 2028 combined endpoints (myocardial infarction, stroke, vascular death) occurred. Yearly CIMT progression was derived from two ultrasound visits 2-7 years (median 4 years) apart. For mean common carotid artery intima-media thickness progression, the overall HR of the combined endpoint was 0.97 (95% CI 0·94-1·00) when adjusted for age, sex, and mean common carotid artery intima-media thickness, and 0.98 (0·95-1·01) when also adjusted for vascular risk factors. Although they detected no associations with CIMT progression in sensitivity analyses, the mean CIMT of the two ultrasound scans was positively and robustly associated with cardiovascular risk (HR for the combined endpoint 1·16, 95% CI 1.10-1.22, adjusted for age, sex, mean common carotid artery intima-media thickness progression, and vascular risk factors). In three studies including 3439 participants who had four ultrasound scans, CIMT progression did not correlate between occasions (reproducibility correlations between r= -0.06 and r= -0.02). The authors concluded, the association between CIMT progression assessed from two ultrasound scans and cardiovascular risk in the general population remains unproven.


In a systematic review and meta-analysis by van den Oord et. al. (2013) provided a review of the evidence on the association of CIMT with future cardiovascular events and the additional value of CIMT (carotid intima-medial thickness) to traditional cardiovascular risk prediction models. The association of CIMT with future cardiovascular events and the additional value of CIMT were calculated using random effects analysis. The literature search yielded 1196 articles of which 15 articles provided sufficient data for the meta-analysis. A 1 SD increase in CIMT was predictive for myocardial infarction (HR 1.26, 95% CI 1.20-1.31) and for stroke (HR 1.31, 95% CI 1.26-1.36). A 0.1 mm increase in CIMT was predictive for myocardial infarction (HR 1.15, 95% CI 1.12-1.18) and for stroke (HR 1.17, 95% CI 1.15-1.21). The overall performance of risk prediction models did not significantly increase after addition of CIMT data. The areas under the curve increased from 0.726 to 0.729 (p = 0.8). The authors concluded, the addition of CIMT did not statistically improve risk prediction over traditional cardiovascular risk factors.


Prospective Cohort Studies

In 2010, Lorenz et. al. reported on 10-year follow-up of 4904 subjects from the Carotid Atherosclerosis Progression Study (CAPS) without pre-existing vascular disease included cardiovascular events and total mortality. Using Cox models and reclassification statistics, they investigated the usefulness of CIMT (carotid intima-medial thickness) in individual risk prediction beyond the Framingham and the SCORE models, using risk strata of 0-5, 5-10, 10-20, and ≥ 20% over 10 years. Carotid intima media thickness was significantly and independently predictive for cardiovascular events. Compared with a model using the Framingham risk factors, a second model that included the common CIMT led to the reclassification of 357 subjects (8.1%). In 107 subjects (30.0%), this reclassification was correct as confirmed with the actual outcome over 10 years. Net reclassification improvement was -1.41% (P = NS); integrated discrimination improvement was 0.04% (P = NS). More subjects were shifted to lower than to higher risk categories by the inclusion of CIMT. Analyses including other endpoint definitions, other carotid segments, and the SCORE risk model for baseline prediction did not result in consistently better risk prediction with CIMT. The authors concluded, despite CIMT being predictive for cardiovascular endpoints, it did not consistently improve the risk classification of individuals.


Raiko et. al. (2010) compared CAD risk scoring tools for identification of CHD risk with CIMT (carotid intima-medial thickness) results in 2204 healthy adults, ages 24 to 39 years from the Cardiovascular Risk in Young Finns study. The CVD risk scoring tools evaluated included the Framingham Risk Score, Reynolds Risk Score, Systematic Coronary Risk Evaluation (SCORE), PROCAM, and FINRISK. In this population based follow-up study, the authors found all CVD risk scores performed equally well in predicting subclinical atherosclerosis, as measured by high CIMT 6 years later.


In 2015, Baber et. al. reported on the BioImage Study (A Clinical Study of Burden of Atherosclerotic Disease in an At-Risk Population) sought to identify imaging biomarkers that predict near-term (3-year) atherothrombotic events. The BioImage Study enrolled 5,808 asymptomatic U.S. adults (mean age: 69 years, 56.5% female) in a prospective cohort evaluating the role of vascular imaging on cardiovascular risk prediction. All patients were evaluated by CAC (coronary artery calcium) score and novel 3-dimensional carotid ultrasound. Plaque areas from both carotid arteries were summed as the carotid plaque burden (cPB). The primary endpoint was the composite of major adverse cardiac events (MACE) (cardiovascular death, myocardial infarction, and ischemic stroke). A broader secondary MACE endpoint also included all-cause death, unstable angina, and coronary revascularization. Over a median follow-up of 2.7 years, MACE occurred in 216 patients (4.2%), of which 82 (1.5%) were primary events. After adjustment for risk factors, and compared with individuals without any cPB, hazard ratios for MACE were 0.78 (95% confidence interval [CI]: 0.31 to 1.91), 1.45 (95% CI: 0.67 to 3.14), and 2.36 (95% CI: 1.13 to 4.92) with increasing cPB tertile, with similar results for CAC. Net reclassification significantly improved with either cPB (0.23) or CAC (0.25). MACE rates increased simultaneously with higher levels of both cPB and CAC. The authors concluded, detection of subclinical carotid or coronary atherosclerosis improves risk predictions and reclassification compared with conventional risk factors, with comparable results for either modality.


Geisel et. al. (2017), compared coronary artery calcification, carotid intima-media thickness (CIMT) and ankle-branchial index for predicting 10 year incident cardiovascular events in the general population, 3108 subjects (mean age 59.2 ± 7.7, 47.1% male). Associations with incident major CV events (coronary event, stroke, CV death; n = 223) were assessed during a follow-up period of 10.3 ± 2.8 years with Cox proportional regressions in the total cohort and stratified by Framingham risk score (FRS) groups. Discrimination ability was evaluated with Harrell's C. All three markers were associated with CV events (hazard ratio [95% confidence interval (CI)]: CAC: 1.31 (1.23-1.39) per 1-unit increase in log (CAC + 1) vs. CIMT: 1.27 (1.13-1.43) per 1 SD vs. ABI: 1.30 (1.14-1.49) per 1 SD, in FRS adjusted models). Considering reclassification, CAC lead to highest reclassification in the total cohort, while also for CIMT and ABI significant improvement in net-reclassification was observed [NRI (95% CI): CAC: 0.55 (0.42-0.69); CIMT: 0.32 (0.19-0.45); ABI: 0.19 (0.10-0.28)]. The authors concluded, CIMT did not significantly improve the prediction of cardiac risk for patients with an intermediate Framingham Risk Score.


In 2017, Villines et. al. prospectively assessed a cohort of 3801 African American (AA) patients free of CVD at baseline. At the baseline examination (2000 to 2004) of the Jackson Heart Study, AA adults 21 to 94 years of age (mean 54) underwent bilateral far-wall CIMT measurement (mean 0.76 mm). Incident CVD events were then assessed over 7 to 11 years of follow-up (2000 to 2011) from samples of 2,463 women (107 CVD events) and 1,338 men (64 CVD events) who were free of clinical CVD at baseline. Each 0.2-mm increase in CIMT was associated with age-adjusted incident CVD hazard ratios of 1.4 (95% confidence interval 1.2, 1.5) for women and 1.3 (1.1, 1.6) for men. Classification accuracy improved only slightly when comparing multivariable models that used traditional risk factors alone with models that added CIMT: C-statistics 0.837 (0.794, 0.881) versus 0.842 (0.798, 0.886) in women and 0.754 (0.683, 0.826) versus 0.763 (0.701, 0.825) in men. Similarly, risk reclassification was only mildly improved by adding CIMT: Net Reclassification Index 0.13 (p = 0.05) and 0.05 (p = 0.50) for women and men, respectively; Integrated Discrimination Improvement 0.02 (p = 0.02) and 0.01 (p = 0.26) for women and men, respectively. Risk reclassification improved only slightly when adding CIMT to a model that included only traditional risk factors for CVD.



Evidence from prospective cohort studies has established that carotid intima-media thickness (CIMT) is an independent risk factor for CAD. However, systematic reviews and meta-analyses have shown that the use of CIMT data to reclassify patients into clinically relevant categories is modest and may not be clinically important. The uncertainty concerning the ability to reclassify patients into clinically relevant categories limits the potential for CIMT to improve health outcomes.


Clinically Useful

A test is clinically useful if the use of the results informs management decisions that improve the net health outcome of care. The net health outcome can be improved if patients receive correct therapy, or more effective therapy, or avoid unnecessary therapy, or avoid unnecessary testing.


Direct evidence of clinical utility is provided by studies that have compared health outcomes for patients managed with and without the test. Because these are intervention studies, the preferred evidence would be from randomized controlled trials (RCTs).


Indirect evidence on clinical utility rests on clinical validity. If the evidence is insufficient to demonstrate test performance, no inferences can be made about clinical utility.


In 2011, Johnson et. al. prospectively studied the effects of office based carotid ultrasound screening (CUS) on physician decision-making and patient health related behaviors (HRBs). Physicians from 5 non-academic, community practices recruited patients ≥40 years old with ≥1 CVD risk factor. Abnormal carotid ultrasound screening (AbnlCUS) was defined as carotid intima-media thickness >75th percentile or carotid plaque presence. Subjects completed questionnaires before and immediately after CUS, then 30 days later to determine self-reported behavioral changes. Odds ratios (OR) for changes in physician management and patient HRBs were determined from multivariate hierarchical logistic regression models. There were 355 subjects (mean [standard deviation] 53.6 [7.9] years old, 2.3 [0.9] risk factors, 58% women); 266 (74.9%) had AbnlCUS. Presence of AbnlCUS altered physicians’ prescription of aspirin (p<0.001) and cholesterol medications (p<0.001). Immediately after CUS, subjects reported increased ability to change HRBs (p=0.002), regardless of their test results. Subjects with AbnlCUS reported increased CVD risk perception (OR 4.14, p<0.001), intentions to exercise (OR 2.28, p=0.008), make dietary changes (OR 2.95, p<0.001), and quit smoking (OR 4.98, p=0.022). After 30 days, 34% increased exercise frequency and 37% reported weight loss; but these changes were not predicted by the CUS results. AbnlCUS modestly predicted reduced dietary sodium (OR 1.45, p=0.002) and increased fiber (OR 1.55, p=0.022) intake. Although this study performed a prospective intervention and each physician and patient served as their own control, it was not a randomized clinical trial, so a strategy of CUS was not compared to standard care or to CVD risk counseling alone. Randomized trials are needed to determine the long-term clinical effects of atherosclerosis screening on health-related behaviors and clinical outcomes; however, our observations suggest that the results of screening on patient behaviors are modest, at best. Such trials should be guided by behavioral theory to best identify patients who are most likely to respond to imaging feedback.



There is no direct evidence on the clinical utility of measuring carotid intima-media thickness (CIMT) for cardiac risk stratification. The available evidence on reclassification into clinically relevant categories does not indicate that use of CIMT will improve net health outcomes.


Summary of Evidence

For individuals who are undergoing cardiac risk assessment who receive ultrasonic measurement of carotid intima-media (or intimal-medial) thickness (CIMT), the evidence includes prospective cohort studies, systematic reviews and meta-analyses. The results of these studies and reviews/meta-analyses have demonstrated the predictived value of CIMT is uncertain, and the predictive ability for any level of population risk cannot be determined with precision. Also, available studies do not define how use of CIMT in clinical practice improves outcomes. There is no scientific literature that directly tests the hypothesis that measurement of CIMT results in improved patient outcomes and no specific guidance on how measurements of CIMT should be incorporated into risk assessment and risk management. The evidence is insufficient to determine the effects of the technology on net health outcomes.


Practice Guidelines and Position Statements

U.S. Preventative Services Task Force (USPSTF)

In July 2018, the U.S. Preventative Services Task Force (USPSTF) updated their recommendation regarding cardiovascular disease risk assessment with nontraditional risk factors. This current recommendation states the following:


Summary of Recommendation

The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of adding the ankle-brachial index (ABI), high-sensitivity C-reactive protein (hsCRP) level, or coronary artery calcium (CAC) score to traditional risk assessment for cardiovascular disease (CVD) in asymptomatic adults to prevent CVD events.


This recommendation currently does not include or address the use of carotid intima-medial thickness regarding cardiovascular disease risk assessment.


American College of Cardiology Foundation (ACCF)/American Heart Association (AHA)

In 2010, the American College of Cardiology Foundation (ACCF)/American Heart Association (AHA) issued a practice guideline for the assessment of cardiovascular risk in asymptomatic adults which indicates, the measurement of carotid artery intima-media thickness is reasonable for assessment of cardiovascular risk assessment in asymptomatic adults at intermediate risk. The guidelines note an increased CIMT reading may be used as a guide in determining clinical utility, but evidence has not demonstrated improvements in outcomes when incorporating CIMT measurement into treatment decision making. Additionally, the guidelines state “clinical tools integrating carotid IMT within global risk scoring system are not available. The incremental value of carotid IMT and cost effectiveness beyond that available from standard risk assessments to improve overall patient outcomes is not established.”


American College of Cardiology (ACC) /American Heart Association (AHA)

In 2013, the American College of Cardiology (ACC)/American Heart Association (AHA) issued a guideline on the assessment of cardiovascular risk which indicates, CIMT is not recommended for routine measurement in clinical practice for risk assessment for first atherosclerotic cardiovascular disease (ASCVD) event. (Grade N (No Recommendation For or Against); Level of Evidence B (Limited populations evaluated; data derived from a single randomized trial or nonrandomized studies); ACC/AHA Class III (No benefit – procedure/test not helpful).


In 2019, the American College of Cardiology (ACC)/American Heart Association (AHA) issued updated the 2017 guideline on the primary prevention of cardiovascular disease, this guideline does not include or indicate the use of CIMT as a routine measurement in clinical practice for the prevention of cardiovascular disease.


Regulatory Status

In February 2003, SonoCalc® (SonoSite) was cleared for marketing by the U.S. Food and Drug Administration (FDA) through the 510(k) process. The FDA determined that this software was substantially equivalent to existing image display products for use in the automatic measurement of the IMT of the carotid artery from images obtained from ultrasound systems. Subsequently, several other devices have been approved through the 510(k) process.


Prior Approval:

Not applicable



Ultrasonographic measurement of carotid intima-media thickness carotid intima-media thickness (CIMT) as a technique of identifying subclinical atherosclerosis is considered investigational for use in the screening, diagnosis, or management of atherosclerotic disease.


Based on peer reviewed medical literature the available studies do not define how the use of carotid intima-media thickness (CIMT) in clinical practice improves outcomes. Also, there is no scientific literature that directly tests the hypothesis that measurement of carotid intima-media thickness (CIMT) results in improved patient outcomes and no specific guidance on how measurements of carotid intima-media thickness (CIMT) should be incorporated into risk assessment and risk management. The evidence is insufficient to determine the effects of this technology on net health outcomes.


Procedure Codes and Billing Guidelines:

To report provider services, use appropriate CPT* codes, Modifiers, Alpha Numeric (HCPCS level 2) codes, Revenue codes, and/or diagnosis codes.

  • 93895 Quantitative carotid intima media thickness and carotid atheroma evaluation, bilateral


Selected References:

  • Lorenz MW, Polak JF, Kavousi M et al. Carotid intima-media thickness progression to predict cardiovascular events in the general population (the PROG-IMT collaborative project): a meta-analysis of individual participant data. Lancet. 2012 Jun 2; 379(9831):2053-62. Epub 2012 Apr27.
  • Peters SA, den Ruijter HM, Bots ML et al. Improvements in risk stratification for the occurrence of cardiovascular disease by imaging subclinical atherosclerosis: a systematic review. Heart 2012; 98(3):177-84.
  • Roger VL, Go AS, Lloyd-Jones DM et al. on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics-2012 update: a report from the American Heart Association. Circulation. 2012; 125:e2-e220.
  • Johnson HM, Turke TL, Grossklaus M et al. Effects of an office-based carotid ultrasound screening intervention. J AM Soc Echocardiogr 2011; 24(7):738-47.
  • Ikeda K, Takahashi T, Yamada H et al. Effect of intenstive statin therapy on regression of carotid intima-media thickness in patients with subclinical atherosclerosis (a prospective, randomized trial: PEACE (Pitavastatin Evaluation of Atherosclerosis Regression by Intensive Cholesterol-lowering Therapy) study. Eur J Prev Cardiol. 2012 Jun 11. [Epub ahead of print].
  • Polak JF, Pencina MJ, O’Leary DH et al. Common carotid artery intima-media thickness progression as a predictor of stroke in multi-ethnic study of atherosclerosis. Stroke. 2011 Nov; 42(11):2017-21. Epub 2011 Sep 1.
  • Bis JC, Kavousi M, Franceschini N et al. Meta-analysis of genome-wide association studies for the CHARGE consortium identifies common variants associated with carotid intima media thickness and plaque. Nat genet. 2011 Sep 11; 43(10): 940-7. doi: 10.1038/ng.920.
  • Polak JF, Pencina MJ, Pencina KM et al. Carotid-wall intima-media thickness and cardiovascular events. N Engl J Med. 2011 Jul 21; 365(3):213-21.
  • Polak JF, Funk LC, O’Leary DH. Inter-reader differences in common carotid artery intima-media thickness: implications for cardiovascular risk assessment and vascular age determination. J Ultrasound Med. 2011 Jul; 30(7):915-20.
  • Plichart M, Celermajer DS, Zureik M et al. Carotid intima-media thickness in plaque-free site, carotid plaques and coronary heart disease risk prediction in older adults. The Three-City Study. Atherosclerosis 2011; 219(2):917-24.
  • Keo HH, Baumgartner I, Hirsch AT et al. Carotid plaque and intima-media thickness and the incidence of ischemic events in patients with atherosclerotic vascular disease. Vasc Med 2011; 16(5):323-30.
  • Nambi V, Chambless L, He M et al. Common carotid artery intima-media thickness is as good as carotid intima-media thickness of all carotid artery segments in improving prediction of coronary heart disease risk in the Atherosclerosis Risk Communities (ARIC) study. Eur Heart J 2012; 33(2):183-90.
  • Xie W, Liang L, Zhao L et al. Combination of carotid intima-media thickness and plaque for better predicting risk of ischaemic cardiovascular events. Heart 2011; 97(16):1326-31.
  • Costanzo P, Perrone-Filardi P, Vassallo E et al. Does carotid intima-media thickness regression predict reduction of cardiovascular events? A meta-analysis of 41 randomized trials. J Am Coll Cardiol. 2010 Dec 7; 56(24):2006-20.
  • Mookadam F, Moustafa SE, Lester SJ et al. Subclinical atherosclerosis: evolving role of carotid intima-media thickness. Prev Cardiol. 2010 Fall; 13(4):186-97. doi: 10.1111/j/1751-7141.2010.00072.x.
  • ECRI, Carotid Intima-Media Thickness for Assessing Coronary Artery Disease Risk, June 2012
  • U.S. Preventative Service Task Force Using Nontraditional Risk Factors in Coronary Heart Disease Risk Assessment, Recommendation Statement, October 2009.
  • 2010 ACCF/AHA Guideline for Assessment of Cardiovascular Risk in Asymptomatic Adults: Executive Summary, Philip Greenland, M.D., FACC, FAHA et al. Journal of the American College of Cardiology Vol. 56, No. 25, 2010
  • Goff D, Lloyd-Jones DM, Bennet G, et. al. 2013 ACC/AHA Guideline on the Assessment of Cardiovascular Risk: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation, published online November 12, 2013. PMID 24222018
  • Lim LS, et. al. Atherosclerotic Cardiovascular Disease Screening in Adults: American College of Preventative Medicine Position Statement on Preventative Practice, AM J Prev Med. 2011 Mar; 40(3):381.el-10.
  • Hester M. Den Ruijter, PhD, Sanne A.E. Peters, MSc, et. al, Common Carotid Intima_Media Thickness Measurements in Cardiovascular Risk Prediction: A Meta-Analysis, JAMA 2012;308(8):796-803.doi:10.1001
  • Micheil L. Bots M.D., Hester M. den Ruijter, PhD, Should We Indeed Measure Carotid Intima-Media Thickness for Improving Prediction of Cardiovascular Events After IMPROVE Journal of American College of Cardiology 2012.
  • UpToDate. Carotid Intima-Media Thickness, Eric de Groot, M.D., PhD, John JP Kastelein, M.D., PhD, FESC, Raphael Duivenvoorden, M.D., PhD. Topic last updated November 13, 2018.
  • Baber U, Mehran R, Satori S, et. al. Prevalence, Impact, and Predictive Value of Detecting Subclinical Coronary and Carotid Atherosclerosis in Asymptomatic Adults: The BioImage Study. J Am Coll Cardiol. Mar 24 2015;65(11):1065-1074
  • Steinl D and Kaufman B, Ultrasound Imaging for Risk Assessment in Atherosclerosis. Int J Mol Sci 2015 May, 16(5):9749-9769
  • Writing Group Members, Mozaffarian D, Benjamin EJ, et al. Heart disease and stroke statistics-2016 update: a report from the American Heart Association. Circulation. Jan 26 2016;133(4):e38-360. PMID 26673558
  • Den Ruijter HM, Peters SA, Anderson TJ, et al. Common carotid intima-media thickness measurements in cardiovascular risk prediction: a meta-analysis. JAMA. Aug 22 2012;308(8):796-803. PMID 22910757
  • van den Oord SC, Sijbrands EJ, ten Kate GL, et al. Carotid intima-media thickness for cardiovascular risk assessment: systematic review and meta-analysis. Atherosclerosis. May 2013;228(1):1-11. PMID 23395523
  • Lorenz MW, Schaefer C, Steinmetz H, et al. Is carotid intima media thickness useful for individual prediction of cardiovascular risk? Ten-year results from the Carotid Atherosclerosis Progression Study (CAPS). Eur Heart J. Aug 2010;31(16):2041-2048. PMID 20530503
  • Patel J, Al Rifai M, Blaha MJ, et. al. Coronary artery calcium improves risk assessment in adults with family history of premature coronary heart disease: results from multiethnic study of atherosclerosis. Circ Cardiovasc Imaging. Jun 2015;8(6);e003186. PMID 26047825
  • Baber U, Mehran R, Sartori S, et al. Prevalence, impact, and predictive value of detecting subclinical coronary and carotid atherosclerosis in asymptomatic adults: the BioImage study. J Am Coll Cardiol. Mar 24 2015;65(11):1065-1074. PMID 25790876
  • Johnson HM, Turke TL, Grossklaus M, et al. Effects of an office-based carotid ultrasound screening intervention. J Am Soc Echocardiogr. Jul 2011;24(7):738-747. PMID 21477989
  • U.S. Preventative Services Task Force (USPSTF) Cardiovascular Disease Risk Assessment with Nontradiational Risk Factors. Updated recommendation released July 2018.
  • Paramsothy P, Knopp RH, Bertoni AG, et al. Association of combinations of lipid parameters with carotid intimamedia thickness and coronary artery calcium in the MESA (Multi-Ethnic Study of Atherosclerosis). J Am Coll Cardiol. Sep 21 2010;56(13):1034-1041. PMID 20846602
  • Blaha MJ, Rivera JJ, Budoff MJ, et al. Association between obesity, high-sensitivity C-reactive protein >2 mg/L, and subclinical atherosclerosis: implications of JUPITER from the Multi-Ethnic Study of Atherosclerosis. Arterioscler Thromb Vasc Biol. Jun 2011;31(6):1430-1438. PMID 21474823
  • Raiko JR, Magnussen CG, Kivimaki M, et al. Cardiovascular risk scores in the prediction of subclinical atherosclerosis in young adults: evidence from the cardiovascular risk in a young Finns study. Eur J Cardiovasc Prev Rehabil. Oct 2010;17(5):549-555. PMID 20354441
  • Geisel MH, Bauer M, Hennig F, et al. Comparison of coronary artery calcification, carotid intima-media thickness and ankle-brachial index for predicting 10-year incident cardiovascular events in the general population. Eur Heart J. Jun 14 2017;38(23):1815-1822. PMID 28379333
  • Villines TC, Hsu LL, Blackshear C, et al. Relation of carotid intima-media thickness to cardiovascular events in Black Americans (From the Jackson Heart Study). Am J Cardiol. Nov 1 2017;120(9):1528-1532. PMID 28844515
  • UpToDate. Diagnostic and Prognostic Implications of Coronary Artery Calcification. Thomas C. Gerber M.D., PhD, FACC, FAHA, Christopher M. Kramer M.D., FACC, FAHA. Topic last updated October 25, 2017.
  • UpToDate. Overview of Possible Risk Factors for Cardiovascular Disease. Peter WF Wilson M.D., Topic last updated August 30, 2018.
  • Benjamin E, Virani S, Callaway C, et. al. AHA Statistical Update, Heart Disease and Stroke Statistics 2018 Update. Circulation 2018 Vol. 137, No. 12 e67-e492
  • Arnett et. al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease. Circulation 2019
  • Benjamin EJ, Muntner P, Alonso A, et. al. AHA 2019 Heart Disease and Stroke Statistics. Circulation 2019; Jan 31


Policy History:

  • January 2021 - Annual Review, Policy Renewed
  • January 2020 - Annual Review, Policy Renewed
  • January 2019 - Annual Review, Policy Renewed
  • January 2018 - Annual Review, Policy Renewed
  • January 2017 - Annual Review, Policy Renewed
  • January 2016 - Annual Review, Policy Renewed
  • January 2015 - Annual Review, Policy Revised
  • February 2014 - Annual Review, Policy Revised
  • May 2013 - Annual Review, Policy Renewed
  • June 2012 - New Policy

Wellmark medical policies address the complex issue of technology assessment of new and emerging treatments, devices, drugs, etc.   They are developed to assist in administering plan benefits and constitute neither offers of coverage nor medical advice. Wellmark medical policies contain only a partial, general description of plan or program benefits and do not constitute a contract. Wellmark does not provide health care services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors in private practice and are neither employees nor agents of Wellmark or its affiliates. Treating providers are solely responsible for medical advice and treatment of members. Our medical policies may be updated and therefore are subject to change without notice.


*CPT® is a registered trademark of the American Medical Association.