BlueCross and BlueShield of Montana Medical Policy/Codes
Ultrasonographic Measurement of Carotid Intimal-Medial Thickness (IMT) as an Assessment of Subclinical Atherosclerosis
Chapter: Radiology
Current Effective Date: September 24, 2013
Original Effective Date: August 20, 2012
Publish Date: September 24, 2013
Revised Dates: August 29, 2013

Established major risk factors for coronary heart disease (CHD) have been identified by the National Cholesterol Education Program (NCEP) Expert Panel.  These risk factors include elevated serum levels of low-density lipoprotein (LDL) cholesterol, total cholesterol, and reduced levels of high-density lipoprotein (HDL) cholesterol.  Other risk factors include a history of cigarette smoking, hypertension, family history of premature CHD, and age.  The third report of the NCEP Adult Treatment Panel (ATP III) establishes various treatment strategies to modify the risk of CHD, based in part on target goals of LDL cholesterol.  Pathology studies have demonstrated that levels of traditional risk factors are associated with the extent and severity of atherosclerosis.  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.  Therefore, there has been interest in identifying a technique that can measure and monitor atherosclerosis that reflects the pathogenic endpoint of CHD risk factors.  The carotid arteries can be well visualized by ultrasonography, and ultrasonographic measurements of the thickness of the carotid intimal medial (IMT) have been investigated as a technique to identify and monitor subclinical atherosclerosis.  B-mode ultrasound is most commonly used, and the intimal-medial thickness is measured and averaged over six sites in each carotid.


Each benefit plan, summary plan description or contract defines which services are covered, which services are excluded, and which services are subject to dollar caps or other limitations, conditions or exclusions.  Members and their providers have the responsibility for consulting the member's benefit plan, summary plan description or contract to determine if there are any exclusions or other benefit limitations applicable to this service or supply.  If there is a discrepancy between a Medical Policy and a member's benefit plan, summary plan description or contract, the benefit plan, summary plan description or contract will govern.


BCBSMT considers ultrasonographic measurement of carotid artery intimal-medial thickness (IMT) as a technique of identifying and monitoring subclinical atherosclerosis experimental, investigational and unproven.


This policy was originally created in 2012; this section of the current policy has been substantially revised, and has been updated with searches of the MEDLINE database through December 2011.  Following is a summary of the key literature to date.

Evaluation of a diagnostic technology typically focuses on the following three parameters:

  1. Technical performance.
  2. Diagnostic parameters (sensitivity, specificity, positive and negative predictive value); and
  3. Demonstration of clinical utility; the diagnostic information can be used to improve patient outcomes.

Literature Review

In the Atherosclerosis Risk in Communities (ARIC) study, the authors evaluated risk factors associated with increased carotid intima-medial thickness (CIMT) in 15,800 subjects.  CIMT had a graded relationship with increasing quartiles of plasma total cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides.  IMT was then also correlated with the incidence of CHD in a subgroup of patients enrolled in the trial after four to seven years of follow-up.  Among the 12,841 subjects studied, there were 290 incident events.  The hazard ratio (HR) rate for men and women, adjusted for age and gender, comparing extreme (CIMT) (i.e., ≤ 1 mm) to non-extreme CIMT (i.e., <1 mm) was 5.07 for women and 1.85 for men.  The strength of the relationship was reduced by including major CHD risk factors but remained elevated for higher measurements of CIMT.  The authors concluded that mean CIMT is a noninvasive predictor of future coronary heart disease (CHD) incidence.

The Rotterdam study was a prospective cohort study that started in 1989 and recruited 7,983 men and women aged 55 years and older.  The main objective of the Rotterdam study was to investigate the prevalence and incidence of risk factors for chronic diseases, including cardiovascular disease, in elderly individuals.  One aspect of the study sought to determine whether progression of atherosclerosis in asymptomatic elderly subjects is a prelude to cardiovascular events.  Measurements of CIMT were used to assess the progression of atherosclerosis.  Increasing CIMT was associated with increasing risks of stroke and myocardial infarction (MI).  O'Leary and colleagues performed CIMT in 4,476 asymptomatic subjects aged 65 years or older without clinical cardiovascular disease.  The incidence of cardiovascular events correlated with measurements of CIMT; this association remained significant after adjustment for traditional risk factors.  The authors concluded that increases in CIMT are directly associated with an increased risk of MI and stroke in older adults without a history of cardiovascular disease.

The Carotid Atherosclerosis Progression Study (CAPS) was a longitudinal study of 4,904 subjects.  All subjects received a baseline CIMT measurement, as well as traditional risk factor analysis, and were followed over a 10-year period (mean follow-up 8.5 years, range 7.1-10.0 years).  Adverse outcome events were MI in 73 patients (1.5%), angina or MI in 271 patients (5.5%), and death in 72 subjects (1.5%).  Lorenz et al. have recently published a retrospective review of the data from CAPS.  The authors modeled the predictive value of CIMT on the cardiovascular adverse events within that decade.  Because the thresholds of CIMT measurements that would lead to reclassification of risk are unknown, the authors used 24 different models of reclassification and five statistical tests.  Each model compares the predictive value of traditional risk factors alone with those risk factors with the addition of CIMT.  The authors were unable to find significance in the reclassification models with the addition of CIMT measurements.  They concluded that this retrospective analysis does not support the use of CIMT as a clinically useful risk classification tool when used in conjunction with traditional risk factor analysis.

Several other studies have, in fact, used CIMT measurements as outcome measures.  In this setting, serial measurements of CIMT are performed, as opposed to a single measure.  For example, the Asymptomatic Carotid Artery Progression Study (ACAPS) was designed to evaluate the role of lovastatin (an HMG-CoA reductase inhibitor, i.e., a statin drug) in patients asymptomatic for cardiovascular disease and with LDL cholesterol levels at or below the limits established by the National Cholesterol Education Program.  A total of 919 asymptomatic men and women were randomly assigned to receive various combinations of lovastatin, warfarin, and placebo over a three-year period.  The principal outcome measurement was the progression of CIMT, tested at six sites in both carotid arteries.  Lovastatin treatment was associated with a reduction in the progression of mean maximum CIMT.  The Monitored Atherosclerosis Regression Study also included measurements of CIMT every six months for four years in a subset of enrolled subjects.  The authors concluded that lipid-lowering therapy resulted in a regression of CIMT.

CIMT is frequently being used in the research setting but application or widespread use is uncertain.  In the Multi-Ethnic Study of Atherosclerosis (MESA) trial, an ongoing cohort study of atherosclerosis, CIMT was found to be a modestly better predictor of stroke but a worse predictor of CHD than coronary artery calcium score at a median follow-up of 3.9 years among 6,698 adults asymptomatic at baseline.  In a 2010 article from MESA, CIMT results in 4,792 healthy, nondiabetic adults who were not on lipid-lowering medications were compared in six different lipid groups, including normolipemia and several types of common dyslipidemias.  The mean CIMT values were increased only for the combined hyperlipidemia (defined as any HDL-C level, LDL-cholesterol [C] >160 and triglyceride >150) and simple hypercholesterolemia (defined as any HDL-C level, LDL-C >160 and triglyceride <150) groups.  In another MESA report, in 2011, on 6,760 patients with elevated high-sensitivity C-reactive protein (hsCRP) as defined by the JUPITER study, CIMT increases correlated with obesity but only mildly with hsCRP.  In the Bogalusa Heart Study of 991 subjects, obesity along with overweight and elevated metabolic risk was also associated with increased CIMT.  In this study population, 41% of patients were found to have increased CHD risk.  In the CARDIA study, clotting factor VII was associated with increases in CIMT in 1,254 subjects.  CIMT is also used as a surrogate outcome measure in atherosclerosis treatment research studies.

In 2010, Raiko et al. compared cardiovascular disease risk scoring tools for identification of CHD risk to CIMT results in 2,204 healthy adults, aged 24-39 years, from the Cardiovascular Risk in Young Finns study.  The cardiovascular disease risk scoring tools evaluated included the Framingham, Reynolds Risk Score, Systematic Coronary Risk Evaluation (SCORE), PROCAM, and Finrisk cardiovascular risk scores.  In this population-based follow-up study, the authors found all of the cardiovascular disease risk scores performed equally in being able to predict subclinical atherosclerosis as measured by high CIMT six years later.

Mookadam and colleagues conducted a systematic review of the role of CIMT in predicting individual cardiovascular event risk and as a tool in assessing therapeutic interventions.  The authors 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, further studies are needed to identify the best approaches to screening and interventions to prevent progression of atherosclerosis.

Ongoing Trials

A search of the online site database in June 2011 identified three open, prospective, randomized trials.  Trials NCT00613158 and NCT00734123 will stratify subjects to treatment arms based on CIMT.  The end point in the first trial will be the course of atherosclerosis measured by both CIMT and carotid artery calcium score at two years and the incidence of cardiovascular disease at five years of follow-up.  The second study will follow the progression of atherosclerosis and cardiovascular disease in a treatment versus placebo trial.  At present, published intervention trials using this technology in clinical care are lacking.

In the third trial, the IMPRESS Study (NCT01330602) will randomly stratify 1,310 subjects with intermediate risk of cardiovascular events and family history of premature atherosclerosis to either a disease management program with intensive pharmacologic and behavioral interventions for primary prevention or usual health care management.  The study will evaluate whether the disease management program is effective and whether changes in CIMT over three years can determine atherosclerotic status and future cardiovascular events.

Practice Guidelines and Position Statements

In October 2009, the U.S. Preventive Services Task Force (USPSTF) published a systematic review of CIMT within the scope of a larger recommendation statement entitled “Using Nontraditional Risk Factors in Coronary Heart Disease Risk Assessment”.  On the basis of  fair- and good-quality studies, the USPSTF states that CIMT, independently of Framingham risk factors, predicts coronary heart disease (CHD) in asymptomatic patients.  These studies were longitudinal, population-based studies conducted in the U.S. and the Netherlands.  USPSTF reviewed the Atherosclerosis Risk in Communities (ARIC) study and concluded that CIMT measurement can result in risk prediction that is modestly improved, particularly in adult men.  However, the review cautions that the studies that did show an association were all done in a research setting, and therefore one cannot draw conclusions on the applicability of CIMT to the intermediate-risk population at large.

The Summary of Recommendation specific to CIMT is stated as: “The U.S. Preventive Services Task Force (USPSTF) concludes that the current evidence is insufficient to assess the balance of benefits and harms of using...[CIMT]…to screen asymptomatic men and women with no history of CHD to prevent CHD events.”  The USPSTF identifies the following research need:  “The predictive value…of carotid IMT…should be examined in conjunction with traditional Framingham risk factors for predicting CHD events and death.”

The 2010 American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines indicates: “Measurement of carotid artery IMT is reasonable for 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 treatment, 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 systems 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.”  Furthermore, “serial scanning of carotid IMT is challenging in individual patients across brief time horizons due to variability in measurement in relation to the rate of disease progression and is therefore not recommended in clinical settings.”

The American Society of Echocardiography Consensus Statement (2008) endorsed by the Society for Vascular Medicine, states that CIMT is a feature of arterial wall aging “that is not synonymous with atherosclerosis, particularly in the absence of plaque.”  The statement recommends measurement of both CIMT and carotid plaque by ultrasound “for refining CVD risk assessment in patients at intermediate cardiovascular disease risk (Framingham Risk Score 6–20%) without established CHD, peripheral arterial disease, cerebrovascular disease, diabetes mellitus, or abdominal aortic aneurysm.”  However, the authors acknowledge that, “More research is needed to determine whether improved risk prediction observed with CIMT or carotid plaque imaging translates into improved patient outcomes.”

The ATP III does not recommend using “emerging risk factors” in the assessment of persons for primary prevention.  It does state that “emerging risk factors” may be useful in certain patient-centered circumstances.


The existing data are insufficient to determine the impact of this technology on net health outcome.  At the present time, there appears to be no scientific literature that directly and experimentally 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.  Recent studies correlate increased CIMT with many other commonly used markers for risk of CHD but do not define how its use in clinical practice improves outcomes.


Disclaimer for coding information on Medical Policies           

Procedure and diagnosis codes on Medical Policy documents are included only as a general reference tool for each policy.  They may not be all-inclusive.           

The presence or absence of procedure, service, supply, device or diagnosis codes in a Medical Policy document has no relevance for determination of benefit coverage for members or reimbursement for providers.  Only the written coverage position in a medical policy should be used for such determinations.           

Benefit coverage determinations based on written Medical Policy coverage positions must include review of the member’s benefit contract or Summary Plan Description (SPD) for defined coverage vs. non-coverage, benefit exclusions, and benefit limitations such as dollar or duration caps. 

ICD-9 Codes

Experimental, investigational, and unproven for all diagnoses codes.

ICD-10 Codes

Experimental, investigational, and unproven for all diagnoses codes.

Procedural Codes: 0126T
  1. Probstfield, J.L., Margitic, S.E., et al.  Results of the primary outcome measure and clinical events from the Asymptomatic Carotid Progression Study.  American Journal of Cardiology  (1995)  76(9):47C-53C.
  2. Hodis, H.N., Mack, W.J., et al.  Reduction in carotid arterial wall thickness using lovastatin and dietary therapy: a randomized controlled clinical trial.  Annals of Internal Medicine (1996) 124(6):548-56.
  3. Chambless, L.E., Heiss, G., et al.  Association of coronary heart disease incidence with carotid arterial wall thickness and major risk factors: the Atherosclerosis Risk in Communities (ARIC) study, 1987-1993.  American Journal of Epidemiology (1997) 146(6):483-94.
  4. Bots, M.I., Hoes, A.W., et al.  Common carotid intimal-media thickness and risk of stroke and myocardial infarction: the Rotterdam Study.  Circulation (1997) 96(5):1432-7.
  5. Hodis, H.N., Mack, W.J., et al.  The role of carotid arterial intimal-media thickness in predicting clinical coronary events.  Annals of Internal Medicine  1998)  128(4):262-9.
  6. Dobs, A.S., Nieto, .F.J, et al.  Risk factors for popliteal and carotid wall thickness in the Atherosclerosis Risk in Communities (ARIC) study.  American Journal of Epidemiology (1999) 150(10):1055-67.
  7. O’Leary, D.H., Polak, J.F., et al.  Carotid-artery intimal and media thickness as a risk factor for myocardial infarction and stroke in older adults.  Cardiovascular Health Study Collaborative Research Group.  New England Journal of Medicine (1999) 340(1):14-22.
  8. Byington, R.P., Evans, G.W., et al.  Effects of lovastatin and warfarin on early carotid atherosclerosis: sex-specific analyses.  Asymptomatic Carotid Artery Progression Study (ACAPS) Research Group.  Circulation (1999) 100(3):e14-7.
  9. National Cholesterol Education Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults.  2003
  10. Wagenknecht, L.E., Zaccaro, D., et al.  Diabetes and progression of carotid atherosclerosis; the insulin resistance atherosclerosis study.  Arteriosclerosis, Thrombosis, and Vascular Biology (2003) 23(6):1035-41.
  11. Anand, S., Gerstein, H., et al.  Relationship of metabolic syndrome and fibrinolytic dysfunction to cardiovascular disease.  Circulation (2003) 108(4):420-5.
  12. Singh, T.P., Groehn, H., Kazmers, A.  Vascular function and carotid intimal medial thickness in children with insulin-dependent diabetes mellitus.  Journal of the American College of Cardiology (2003) 41(4):661-5.
  13. McNeill, A.M., Rosamond, W.D., et al.  Prevalence of coronary heart disease and carotid arterial thickening in patients with the metabolic syndrome (the ARIC study).  American Journal of Cardiology (2004) 94(10):1249-54.
  14. van der Meer IM, Bots ML, Hofman A et al. Predictive value of noninvasive measures of atherosclerosis for incident myocardial infarction: the Rotterdam Study.  Circulation 2004; 109(9):1089-94.
  15. U.S. Preventive Services Task Force.  Screening for Coronary Heart Disease: Recommendation Statement.  Agency for Healthcare Research and Quality, Rockville, MD.  (February 2004) .
  16. Fernandes, V.R., Polak, J.F., et al.   Subclinical atherosclerosis and incipient regional myocardial dysfunction in asymptomatic individuals: the Multi-Ethnic Study of Atherosclerosis (MESA). Journal of the American College of Cardiology (2006) 47(12):2420-8.
  17. Naghavi, M., Falk, E., et al.  From vulnerable plaque to vulnerable patient – Part III: Executive summary of the Screening for Heart Attack Prevention and Education (SHAPE) Task Force report.  American Journal of Cardiology (2006) 98(2A):2H-15H.
  18. Lorenz, M.W., Markus, H.S., et al.  Prediction of clinical cardiovascular events with carotid intimal-media thickness: a systematic review and meta-analysis.  Circulation (2007) 115(4):459-67.
  19. Roman, M.J., Moeller, E., et al.  Preclinical carotid atherosclerosis in patients with rheumatoid arthritis.  Annals of Internal Medicine (2006) 144(4):249-56.
  20. Manolio, T.A., Arnold, A.M., et al.  Ethnic differences in the relationship of carotid atherosclerosis to coronary calcification: the Multi-Ethnic Study of Atherosclerosis.  Atherosclerosis (April 2007):Epub ahead of print.
  21. Kanwar, M., Rosman, H.S., et al.  Usefulness of carotid ultrasound to improve the ability of stress testing to predict coronary artery disease.  American Journal of Cardiology (2007) 99(9):1196-200.
  22. Touboul, P.J., Hennerici, M.G., et al.  Mannheim Carotid Intimal-Media Thickness Consensus (2004–2006) - Consensus Statement.  Cerebrovascular Disease (2007) 23:75–80.
  23. Folsom AR, Kronmal RA, Detrano RC et al. Coronary artery calcification compared with carotid intimal-media thickness in the prediction of cardiovascular disease incidence: the Multi-Ethnic Study of Atherosclerosis (MESA).  Arch Intern Med 2008; 168(12):1333-9.
  24. Prati P, Tosetto A, Vanuzzo D et al. Carotid intimal media thickness and plaques can predict the occurrence of ischemic cerebrovascular events. Stroke 2008; 39:2470-6.
  25. Stein JH, Korcarz CE, Hurst RT et al. Use of carotid ultrasound to identify subclinical vascular disease and evaluate cardiovascular disease risk: a consensus statement from the American Society of Echocardiography Carotid Intimal-Media Thickness Task Force. J Am Soc Echo 2008; 1(2):93-111.
  26. Adolphe A, Cook LS, Huang X.  A cross-sectional study of IMT, ethnicity, metabolic syndrome, and cardiovascular risk in 2268 study participants. Mayo Clin Proc 2009; 84(3):221-8.
  27. Bots MD, Palmer MK, Dogan S et al.; METEOR Study Group. Intensive lipid lowering may reduce progression of carotid atherosclerosis within 12 months of treatment: the METEOR study. J Intern Med 2009 Feb 28.
  28. Dobs AS, Nieto FJ, Szklo M et al. Risk factors for popliteal and carotid wall thicknesses in the Atherosclerosis Risk in Communities (ARIC) Study. Am J Epidemiol 1999; 150(10):1055-67. Minino AM, Heron MP, Murphy SL et al. Deaths: final data for 2004. Natl Vital Stat Rep 2007; 55(19):1-119.
  29. Bots ML, Palmer MK, Dogan S et al. Intensive lipid lowering may reduce progression of carotid atherosclerosis within 12 months of treatment: the METEOR study.  J Intern Med 2009; 265(6):698-707.
  30. Using nontraditional risk factors in coronary heart disease risk assessment: U.S. Preventive Services Task Force recommendation statement.  Ann Intern Med 2009; 151(7):474-82.
  31. 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 2010: 2041-2048.
  32. Greenland P, Alpert JS, Beller GA et al. 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. J Am Coll Cardiol 2010; 56(25):e50-103.
  33. Green D, Foiles N, Chan C et al. An association between clotting factor VII and carotid intima-media thickness: the CARDIA study. Stroke 2010; 41(7):1417-22.
  34. Paramsothy P, Knopp RH, Bertoni AG et al. Association of combinations of lipid parameters with carotid intima-media thickness and coronary artery calcium in the MESA (Multi-Ethnic Study of Atherosclerosis).  J Am Coll Cardiol 2010; 56(13):1034-41.
  35. 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 2010; 17(5):549-55.
  36. Mookadam F, Moustafa SE, Lester SJ et al. Subclinical atherosclerosis: evolving role of carotid intima-media thickness. Prev Cardiol 2010; 13(4):186-97.
  37. Camhi SM, Katzmarzyk PT, Broyles ST et al. Subclinical atherosclerosis and metabolic risk: role of body mass index and waist circumference.  Metab Syndr Relat Disord 2011; 9(2):119-25.
  38. 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 2011; 31(6):1430-8.
  39. Ultrasonographic Measurement of Carotid Intimal-Medial Thickness (IMT) as an Assessment of Subclinical Atherosclerosis. Chicago Illinois:  Blue Cross Blue Shield association Medical Policy Reference Manual (2011 July) Medicine 2.02.16.
August 2012  New Policy for BCBSMT: Policy statement is investigational.
September 2013 Policy formatting and language revised.  Policy statement unchanged.  Removed CPT code 93880. 
®Registered marks of the Blue Cross and Blue Shield Association, an association of independent Blue Cross and Blue Shield Plans. ®LIVE SMART. LIVE HEALTHY. is a registered mark of BCBSMT, an independent licensee of the Blue Cross and Blue Shield Association, serving the residents and businesses of Montana.
CPT codes, descriptions and material only are copyrighted by the American Medical Association. All Rights Reserved. No fee schedules, basic units, relative values or related listings are included in CPT. The AMA assumes no liability for the data contained herein. Applicable FARS/DFARS Restrictions Apply to Government Use. CPT only © American Medical Association.
Ultrasonographic Measurement of Carotid Intimal-Medial Thickness (IMT) as an Assessment of Subclinical Atherosclerosis