Pending Policies - Medicine
Electrocardiographic Body Surface Mapping
*CAREFULLY CHECK STATE REGULATIONS AND/OR THE MEMBER CONTRACT*
Electrocardiographic body surface mapping is considered experimental, investigational and/or unproven for the diagnosis or management of cardiac disorders, including acute coronary syndrome.
Electrocardiographic (ECG) body surface mapping (BSM) uses multiple electrocardiography leads to detect cardiac electrical activity (generally >80 leads). It is postulated that multiple leads may improve the diagnostic accuracy of acute myocardial infarction or acute coronary syndrome compared with that of the standard 12-lead electrocardiography.
ECG BSM consists of an 80-lead disposable electrode array in the form of a vest and includes a conducting gel that is applied to the patient’s chest and back. The vest can be affixed to the patient in less than 5 minutes. This system displays clinical data in 3 forms: a colorimetric 3-dimensional (3D) torso image, an 80-lead single beat view, and the 12-lead ECG. The colorimetric torso images are said to allow the practitioner to scan the heart rapidly for significant abnormalities.
Currently, in patients presenting to the emergency department (ED) with symptoms suggestive of acute coronary syndrome, a standard 12-lead ECG is obtained. In the presence of ST segment elevation on the ECG, personnel are activated to respond promptly to open a presumed coronary artery occlusion, either by mechanical means through balloon angioplasty or medically, through intravenous thrombolytic drugs. The 12-lead ECG has a specificity of 94%, leading to relatively few erroneous interventions. However, the sensitivity is approximately 50%. These patients may be further stratified by scoring systems and time- sensitive cardiac enzymes, which may require up to 24 hours of monitored observation.
BSM is being considered as a method to assist in the rapid identification of patients who would benefit from earlier coronary artery intervention than is achieved using current standards of care.
In March 2002, the device PRIME ECG® (Verathon, Bothell, WA) was cleared for marketing by the U.S. Food and Drug Administration (FDA) through the 510(k) process. The FDA determined that the device was substantially equivalent to existing devices for use in recording of ECG signals on the body surface. To date, neither the PRIME ECG device nor its successor, the Heartscape™ 3D ECG System, is being marketed in the U.S. FDA product code: DPS.
This medical policy was created in 2007 and has been updated regularly with searches of the Medline database. The most recent literature review was performed through September 24, 2018.
Assessment of a diagnostic technology focuses on the following parameters: 1) technical performance; 2) diagnostic accuracy (sensitivity, specificity, positive predictive value [PPV], negative predictive value [NPV]) in relevant clinical populations; and 3) clinical utility (i.e., demonstration that the diagnostic information can be used to improve patient outcomes). The following is a summary of the key literature to date.
Electrocardiographic Body Surface Mapping (BSM)
Clinical Context and Proposed Clinical Utility
The proposed clinical utility of BSM evaluated in this review is to improve the accuracy of diagnosing acute coronary syndrome (ACS) to identify those patients who would benefit from a medical or surgical coronary artery intervention. The current standard intervention is a 12-lead electrocardiography (ECG), which has a relatively high specificity but a relatively low sensitivity. However, the sensitivity of the 12-lead ECG can be improved by incorporating information from clinical evaluation and cardiac enzyme analysis. Still, a test with a higher sensitivity could be clinically beneficial.
The question addressed in this medical policy is: In individuals with suspected or confirmed ACS that present in the emergency department (ED), does use of ECG BSM lead improve the identification of patients who would benefit from medical or surgical intervention and/or improve health outcomes compared with standard care?
The following categories were used to select literature to inform this policy.
The relevant population of interest is patients with symptoms suggestive of ACS.
The intervention is ECG BSM.
The comparator of interest is standard 12-lead ECG with or without cardiac enzyme testing.
The primary outcome of interest is overall survival. Other outcomes of interest are disease-specific survival, test accuracy and validity, and morbid events (e.g., myocardial infarction).
Overall survival, disease-specific survival, and morbid events would be measured both in the short term (i.e., hospital and within 30-days of discharge mortality) and long term (i.e., 6 months, ≥1 year).
Patients would be tested in the ED setting.
Patterns of electric potentials with additional ECG leads in normal subjects have been established, and the significance of abnormal signals has been explored over past several decades. (1, 2) A 2006 publication has described the use of the 80-lead technique in the evaluation of patients with chest pain in the ED. (3) The authors commented that use of this approach has been hampered by slow acquisition time and the complexity of interpretation but that technologic advances are overcoming these limitations. However, they added that the future of BSM in emergency medicine is unclear and that more research is needed to define its benefits and limitations.
In 2007, Lefebvre and Hoekstra described improvements in the technical performance and ease of use in BSM technologies. (4) A standardized vest improves lead placement, and changes to software direct clinicians’ attention to locations on the body mapping that may be significant, possibly reducing the amount of training needed.
In 2012, the Agency for Healthcare Research and Quality (AHRQ) published a technology assessment on the diagnostic utility of ECG-based signal analysis technologies for patients at low to intermediate risk of coronary artery disease (CAD). (5) Findings of the updated review were summarized in a 2013 publication by Leisy et al. (6) The AHRQ literature review focused on studies evaluating U.S. Food and Drug Administration?approved or cleared devices that are commercially available in the United States and can feasibly be used in most medical facilities. The AHRQ assessment combined data from 10 studies on the PRIME ECG that involved patients with chest pain. Six of 10 studies were published by the same research group in Northern Ireland. The studies from Northern Ireland may have included a patient population that was at higher than average risk because some patients were treated in mobile cardiac care centers. Using a bivariate, random-effects model, the summary estimate for sensitivity was 71.1% (95% confidence interval [CI], 45.6% to 87.8%); for specificity, it was 90.2% (95% CI, 83.2% to 94.4%). The summary estimate for the positive likelihood ratio was 6.3 (95% CI, 3.3 to 12.1), and the summary negative likelihood ratio negative was 0.30 (95% CI, 0.16 to 0.56). These combined summary estimates were compared with pooled estimates from the 10 studies reporting 12-lead ECG performance (8 of these 10 studies were also included in the analysis of PRIME ECG sensitivity, previously described.) The pooled sensitivity was 43.1% (95% CI, 25.8% to 62.2%), and the pooled specificity was 94.4% (95% CI, 88.4% to 97.4%). The difference in sensitivity between the PRIME ECG and the 12-lead ECG was not significantly different (p<0.078), nor was the difference in specificity (p<0.234).
Many individual studies have shown higher sensitivity for BSM, and some have shown lower specificity. For example, in a retrospective study conducted at 4 centers, Ornato et al. (2009) reviewed the cardiac enzyme-confirmed cases of acute myocardial infarction (AMI) against results of 12-lead ECG and BSM. (7) Due to a change in standard practice during the study, AMI was defined by either elevated troponin or heart-specific creatinine kinase levels. Of 647 patients, 58 (8.9%) were not analyzed due to lack of enzyme data. Sensitivity comparison between BSM and 12-lead ECG in the creatinine kinase group favored BSM (100% vs 72.7%, respectively, p=0.031; n=364), and likewise in the troponin group (92.9% vs 60.7%, respectively, p=0.022; n=225). Specificity for BSM did not differ significantly from 12-lead ECG in either group (96.5% vs 97.1 and 94.9 vs 96.4, both respectively).
A 2013 study from Northern Ireland retrospectively reported on 645 consecutive patients with sudden out-of-hospital cardiac arrest initially attended by a mobile cardiac care unit. (8) Eighty patients survived initial resuscitation, and 59 underwent ECG BSM and 12-lead ECG analysis by the physician leading the mobile unit. Twenty-four patients died prehospital and 35 were admitted to the hospital and underwent coronary angiography. Twenty-six (75%) of the 35 patients who received angiography acute occlusion of a main coronary artery. An ECG BSM post resuscitation showed ST segment elevation in 23 of 35 patients (66%) and had 88% sensitivity and 100% specificity for diagnosing acute coronary occlusion in these 35 patients. In contrast, the combination of either ST elevation myocardial infarction (STEMI) or ST segment depression on 12-lead ECG had a sensitivity of 46% and specificity of 100% for diagnosing acute coronary occlusion. A 2008 retrospective study from Northern Ireland included 755 patients presenting to the ED, mobile cardiac care, or hospital with symptoms of ischemic chest pain. (9) Each patient’s clinical course was guided by standard American College of Cardiology 12- lead ST segment criteria and subsequent cardiac enzymes if electrocardiographically negative. A cardiologist blinded to the clinical details measured BSM retrospectively. AMI was defined by elevated cardiac troponin levels. The standard 12-lead ECG demonstrated a sensitivity of 45% and a specificity of 92% for detecting troponin-positive ischemia. When non-ST electrographic changes were permitted as part of the criteria for AMI, sensitivity increased (51%-68%), but specificity decreased (71%-89%). In this study, BSM performed with a sensitivity of 76% and a specificity of 92%.
Fermann et al. (2009) found very different performance characteristics for BSM and 12-lead ECG in other studies. (10) A convenience sample of 150 patients with chest pain presenting to the ED had BSM measured within 30 minutes of the standard ECG. Emergency physicians who had been trained in BSM interpreted both the BSM and the ECGs at the time of presentation. Both were stored electronically for review by a BSM expert; after the study had ended, a convenience sample of 135 BSMs was over read. Of 43 patients, 10 (23.3%) judged to have normal BSM by the emergency physicians had abnormal findings or frank infarction by the expert interpreter. The overall correlation between the emergency physicians and the expert reviewer was only fair (correlation coefficient κ=0.627; 95% CI, 0.530 to 0.724). The sensitivity of both standard ECG and BSM were low at 10.5% (95% CI, 1.8% to 34.5%) and 15.8% (95% CI, 4.2% to 40.5%), respectively. This low sensitivity likely reflects the Spectrum of patients in the study. Specificities were also comparable between the 2 groups at 90.1% (95% CI, 83.3% to 94.4%) and 86.3% (95% CI, 78.9% to 91.4%), respectively.
In 2010, O’Neil et al. published results from a secondary analysis of the Optimal Cardiovascular Diagnostic Evaluation Enabling Faster Treatment of Myocardial Infarction (OCCULT MI) trial. (11) A multicenter (10-site), prospective, observational study, the OCCULT MI trial enrolled 1830 subjects presenting to the ED with moderate- to high-risk chest pain. Patients were simultaneously tested with 12-lead and 80-lead ECGs, with clinicians able to access the 12-lead results only. The patients were treated using standard care based on 12-lead results or clinical suspicion. Off-site clinicians, who were not involved in patients’ care, reviewed the 80-lead ECG and made a diagnostic determination, validated through multiple reviewers.
In this analysis, 12-lead ECG was compared with 80-lead ECG mapping for detecting high-risk ECG abnormalities. Patients diagnosed with STEMI by 12-lead ECG (n=91) and patients with missing data (n=255) were excluded from the specificity and sensitivity analyses. When detecting myocardial infarction and ACS, the 80-lead ECG mapping sensitivity was significantly higher than the 12-lead ECG for myocardial infarction (19.4% vs 10.7%, p=0.0014) and ACS (12.3% vs 7.1%, p=0.001). The authors attributed these low sensitivity rates to the exclusion of STEMI patients in this analysis. The specificity of the 80-lead ECG mapping was significantly lower than the 12-lead ECG for myocardial infarction (93.9% vs 96.4%, p=0.001) and for ACS (93.7% vs 96.4%, p=0.001). Positive and negative predictive values and negative and positive likelihood ratios did not differ statistically between the lead groups. The 80-lead ECG mapping identified 18 additional myocardial infarction patients and 21 additional ACS patients who could potentially have benefited from more aggressive treatment. However, because the 80-lead ECG mapping results were not incorporated into treatment decision making, no conclusions can be made from this study on the impact of this technology on patient outcomes. Also, the authors did not explore the impact of decreased specificity and increased false-positive rates on patient outcomes. Other study limitations included lack of enrollment of low-risk ED patients and the lack of power to detect differences in ACS diagnosis.
In 2012, Daly et al. also compared 12-lead ECG with 80-lead ECG mapping in a retrospective review of 2810 consecutive patients admitted with ischemic-type chest pain. (12) All patients had coronary angiography and cardiac troponin levels measured at admission. The analysis was confined to patients with significant left main stem coronary stenosis (>70%), which was found in 116 (4.1%) patients. Of these 116 patients with left main stem coronary stenosis, 92 (79%) had AMI, diagnosed when cardiac troponin levels were 0.03 µg/L or higher. BSM was found to be more sensitive for diagnosing AMI in patients with LMS coronary stenosis than 12-lead ECG. BSM detected STEMI in 85 of 92 patients for an 88% sensitivity, 83% specificity, 95% positive predictive value, and 65% negative predictive value. The 12-lead ECG (using Minnesota 9-2 criteria) detected STEMI in 13 (11%) patients, for a 12% sensitivity and 92% specificity. The C statistic for the diagnosis of AMI in patients with left main stem stenosis by 12- lead ECG was 0.580 (95% CI, 0.460 to 0.701, p=0.088) compared with 0.800 (95% CI, 0.720 to 0.881; p<0.001) using physician interpretation of BSM or 0.792 (95% CI, 0.690 to 0.894, p<0.001) using the PRIME algorithm.
A report by Zeb et al. (2015) evaluated the 80-lead ECG mapping system (PRIME Delta) along with internally developed software to create a BSM Delta map. (13) The study included 49 patients who presented to the ED with cardiac-sounding chest pain. Using the final diagnosis
Of ACS as the reference standard, the sensitivity and specificity of the BSM Delta map for diagnosing ACS were 71% (22/31) and 78% (14/18), respectively. The sensitivity and specificity of the 12-lead ECG were 67% (21/31) and 55% (10/18), respectively. The authors did not analyze whether differences in diagnostic accuracy were statistically significant. Moreover, the BSM Delta mapping software, an important part of the diagnostic process in this study, is not currently available outside of the European research setting.
In 2017, Gage et al. (14) noted that electrical activation is important in cardiac resynchronization therapy (CRT) response. Standard electrocardiographic analysis may not accurately reflect the heterogeneity of electrical activation. These researchers compared changes in left ventricular size and function after CRT to native electrical dyssynchrony and its change during pacing. Body surface isochronal maps using 53 anterior and posterior electrodes as well as 12-lead electrocardiograms were acquired after CRT in 66 consecutive patients. Electrical dyssynchrony was quantified using standard deviation of activation times (SDAT). Ejection fraction (EF) and left ventricular end-systolic volume (LVESV) were measured before CRT and at 6 months. Multiple regression evaluated predictors of response. Changes in LVESV correlated with changes in SDAT (p = 0.007), but not with changes in QRS duration (p = 0.092). Patients with SDAT greater than or equal to 35 ms had greater increase in EF (13 ± 8 units versus 4 ± 9 units; p < 0.001) and LVESV (-34 % ± 28 % versus -13 % ± 29 %; p = 0.005). Patients with greater than or equal to 10 % improvement in SDAT had greater changes in EF (11 ± 9 units versus 4 ± 9 units; p = 0.010) and changes in LVESV (-33 % ± 26 % versus -6 % ± 34 %; p = 0.001). SDAT greater than or equal to 35 ms predicted changes in EF, while changes in SDAT, sex, and left bundle branch block predicted changes in LVESV. In 34 patients without class I indication for CRT, SDAT greater than or equal to 35 ms (p = 0.015) and changes in SDAT greater than or equal to 10 % (p = 0.032) were the only predictors of delta EF. The authors concluded that BSM of SDAT and its changes predicted CRT response better than did QRS duration. They stated that BSM may potentially improve selection or optimization of CRT patients. These preliminary findings need to be validated by well-designed studies.
Section Summary: Diagnostic Accuracy
Numerous published studies have compared the accuracy of BSM with standard 12-lead ECG for the diagnosis of ACS. These studies are mostly retrospective and did not enroll the ideal clinical populations (i.e., consecutive patients presenting with clinical signs or symptoms of ischemia). They also tended to compare the accuracy of BSM alone with the 12-lead ECG alone. This comparator is less clinically relevant because the 12-lead ECG is not used alone to diagnose ACS rather it is combined with the clinical presentation and the results of cardiac enzymes. The 2012 AHRQ technology assessment did not find a statistically significant difference in the diagnostic accuracy of BSM compared with a standard 12-lead ECG. Among the individual studies, the differences in sensitivity varied, and there was uncertain whether there is a higher sensitivity that is clinically significant. The specificity of BSM may be lower than that of the 12-lead ECG, because some studies reported lower specificity, but others not. Because of the uncertainty in the sensitivity and specificity in the available studies, it is not possible to estimate the tradeoff between additional cases of ACS detected and false-positive results leading to further unnecessary testing. Further prospective studies are needed that include relevant clinical populations and that compare the incremental value of BMS when used as part of the overall diagnostic workup for ACS.
The 2012 AHRQ assessment (5) did not identify any studies in patients at low to intermediate risk of coronary artery disease that provided evidence on whether findings from ECG-based technologies other than the standard 12-lead ECG had an impact on patient management or health outcomes. The OCCULT MI trial (discussed earlier) addressed patient outcomes in a population at moderate to high risk for coronary artery disease. The main results of the OCCULT MI trial were published in 2009 and 2010 by Hoekstra et al. (11, 15) The primary outcome of the OCCULT MI trial was a door-to-sheath time in 12-lead STEMI patients vs a door-to-sheath time in patients with ST elevations noted on 80-lead testing. The secondary clinical outcomes were 30-day and angiographic data. Of the 1830 subjects, 91 had a discharge diagnosis of STEMI, 84 of whom underwent cardiac catheterization with a mean door-to-sheath time of 54 minutes. Twenty-five subjects (1.4% of the study population) met criteria for ST elevation in the 80-lead alone, 14 of whom underwent cardiac catheterization with a mean door-to-sheath time of 1002 minutes (estimated treatment difference, 881 minutes; 95% CI, 181 to 1079 minutes). Neither 30-day clinical outcomes nor adverse events differed significantly in the identified at-risk groups. These 25 patients were in addition to the 91 STEMI patients identified on 12-lead, leading reviewers to conclude that the additional leads identified 27.5% (25/91) more AMI patients than 12-lead alone. However, a distinction was made between those patients for who it is well established that early intervention is beneficial (i.e., STEMI on standard 12-lead ECG) and those for who BSM is positive but 12-lead is not. It is not known whether these patients benefit from early intervention. An editorial, accompanying publication of the OCCULT MI study, suggested that the patients identified have more in common with the non-STEMI patients based on peak troponin levels reported in the Hoekstra study (15) and that identification of these patients would not change treatment. (16)
In 2016, Ueoka et al. (17) stated that clinical and experimental studies have shown the existence of an arrhythmogenic substrate in the right ventricular outflow tract (RVOT) in patients with Brugada syndrome (BrS). These researches evaluated the activation pattern of induced ventricular tachyarrhythmias using BSM in patients with BrS. They examined 14 patients with BrS in whom ventricular tachyarrhythmias were induced by programmed electrical stimulation. The 87-lead BSM was recorded during induced ventricular tachyarrhythmias, and an activation map and an isopotential map of QRS complexes every 5 ms were constructed to evaluate the activation pattern of ventricular tachyarrhythmias. BSM during 20 episodes of ventricular tachyarrhythmias induced at the RVOT showed that repetitive excitation was generated at the RVOT and propagated to the inferior RV and left ventricle, and then returned to the RVOT. Polymorphic QRS change during ventricular tachyarrhythmias was associated with migration of the earliest activation site and rotor. BSM during 4 episodes of ventricular fibrillation (VF) showed that the excitation front moved randomly with formation of multiple wave-fronts. The authors concluded that programmed stimulation initiated repetitive firing from the RVOT. Migration and competition of the earliest activation site and rotor and local conduction delay changed the QRS morphology. Degeneration of the re-entrant circuit into multiple wave-fronts resulted in VF.
Section Summary: Clinical Utility
No studies have demonstrated how BSM can be used to change clinical management in ways that improve health outcomes. Indirect evidence suggests that BSM might be used in a subset of patients presenting with suspected ACS to reduce the time to diagnosis and thereby to provide revascularization more expediently. Whether or not this strategy improves outcomes has yet to be shown. The ideal study design that effectively demonstrates clinical utility is a randomized controlled trial in which patients are allocated to BSM or standard 12-lead ECG and patients are followed for changes in management and clinical outcomes.
Summary of Evidence
For individuals who have suspected or confirmed acute cardiac syndrome who receive electrocardiographic (ECG) body surface mapping (BSM), the evidence includes a number of studies on the association between ECG BSM and acute myocardial infarction. Relevant outcomes are overall survival, disease-specific survival, test accuracy and validity, and morbid events. No prospective trials using BSM to guide treatment were identified. Results of published studies have been variable, and an Agency for Healthcare Research and Quality review did not find statistically significant differences between the diagnostic accuracy of BSM and 12-lead ECG. Under ideal conditions, it is possible that BSM has a higher sensitivity than a 12-lead ECG for acute coronary events. However, studies have reported lower specificity with ECG BSM compared with 12-lead ECG, which may lead to false-positive results. There is no evidence demonstrating that ECG BSM leads to changes in management that improve health outcomes. The evidence is insufficient to determine the effect of the technology on health outcomes.
Practice Guidelines and Position Statements
The 2007 joint guidelines from the American College of Cardiology Foundation, American Heart Association, and Heart Rhythm Society on electrocardiography standardization and interpretation recognized that, although the studies of body surface maps from large electrode arrays have provided useful information on localization of electrocardiographic information on the thorax, at that time their complexity precluded their use as a substitute for the standard 12-lead electrocardiography for routine recording purposes. (18)
Ongoing and Unpublished Clinical Trials
A search of ClinicalTrials.gov did not identify any ongoing or unpublished trials that would likely influence this medical policy.
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.
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.
The following codes may be applicable to this Medical policy and may not be all inclusive.
0178T, 0179T, 0180T, 93799, [Deleted 1/2018: 0178T, 0179T, 0180T]
ICD-9 Diagnosis Codes
Refer to the ICD-9-CM manual
ICD-9 Procedure Codes
Refer to the ICD-9-CM manual
ICD-10 Diagnosis Codes
Refer to the ICD-10-CM manual
ICD-10 Procedure Codes
Refer to the ICD-10-CM manual
The information contained in this section is for informational purposes only. HCSC makes no representation as to the accuracy of this information. It is not to be used for claims adjudication for HCSC Plans.
The Centers for Medicare and Medicaid Services (CMS) does not have a national Medicare coverage position. Coverage may be subject to local carrier discretion.
A national coverage position for Medicare may have been developed since this medical policy document was written. See Medicare's National Coverage at <http://www.cms.hhs.gov>.
1. Gulrajani RM. The forward and inverse problems of electrocardiography. IEEE Eng Med Biol Mag. Sep-Oct 1998; 17(5):84-101, 122. PMID 9770610
2. Thivierge M, Gulrajani RM, Savard P. Effects of rotational myocardial anisotropy in forward potential computations with equivalent heart dipoles. Ann Biomed Eng. May-Jun 1997; 25(3):477-498. PMID 9146803
3. Self WH, Mattu A, Martin M, et al. Body surface mapping in the ED evaluation of the patient with chest pain: use of the 80-lead electrocardiogram system. Am J Emerg Med. Jan 2006; 24(1):87-112. PMID 16338516
4. Lefebvre C, Hoekstra J. Early detection and diagnosis of acute myocardial infarction: the potential for improved care with next-generation, user-friendly electrocardiographic body surface mapping. Am J Emerg Med. Nov 2007; 25(9):1063-1072. PMID 18022503
5. Coeytaux RR, Leisy PJ, Wagner GS, et al. Systematic review of ECG-based signal analysis technologies for evaluating patients with acute coronary syndrome (Technology Assessment Report). Rockville, MD: Agency for Healthcare Research and Quality; 2012. PMID 25834876
6. Leisy PJ, Coeytaux RR, Wagner GS, et al. ECG-based signal analysis technologies for evaluating patients with acute coronary syndrome: a systematic review. J Electrocardiol. Mar-Apr 2013; 46(2):92-97. PMID 23273746
7. Ornato JP, Menown IB, Peberdy MA, et al. Body surface mapping vs 12-le2009; 27(7):779-784. PMID 19683104
8. Daly MJ, Finlay DD, Scott PJ, et al. Pre-hospital body surface potential mapping improves early diagnosis of acute coronary artery occlusion in patients with ventricular fibrillation and cardiac arrest. Resuscitation. Jan 2013; 84(1):37-41. PMID 22986067
9. Owens C, McClelland A, Walsh S, et al. Comparison of value of leads from body surface maps to 12-lead electrocardiogram for diagnosis of acute myocardial infarction. Am J Cardiol. Aug 1 2008; 102(3):257-265. PMID 18638583
10. Fermann GJ, Lindsell CJ, O'Neil BJ, et al. Performance of a body surface mapping system using emergency physician real-time interpretation. Am J Emerg Med. Sep 2009; 27(7):816-822. PMID 19683110
11. O'Neil BJ, Hoekstra J, Pride YB, et al. Incremental benefit of 80-lead electrocardiogram body surface mapping over the 12-lead electrocardiogram in the detection of acute coronary syndromes in patients without ST-elevation myocardial infarction: Results from the Optimal Cardiovascular Diagnostic Evaluation Enabling Faster Treatment of Myocardial Infarction (OCCULT MI) trial. Acad Emerg Med. Sep 2010; 17(9):932-939. PMID 20836773
12. Daly MJ, Adgey JA, Harbinson MT. Improved detection of acute myocardial infarction in patients with chest pain and significant left main stem coronary stenosis. QJM. Feb 2012; 105(2):127-135. PMID 21890878
13. Zeb M, Nagaraj N, Curzen N. Detection of multiregional transient myocardial ischaemia using a novel 80- electrode body surface Delta map [letter]. Int J Cardiol. Feb 15 2015; 181:114-116. PMID 25497532
14. Gage RM, Curtin AE, Burns KV, et al. Changes in electrical dyssynchrony by body surface mapping predict left ventricular remodeling in patients with cardiac resynchronization therapy. Heart Rhythm. 2017; 14(3):392-399. PMID 27867072
15. Hoekstra JW, O'Neill BJ, Pride YB, et al. Acute detection of ST-elevation myocardial infarction missed on standard 12-Lead ECG with a novel 80-lead real-time digital body surface map: primary results from the multicenter OCCULT MI trial. Ann Emerg Med. Dec 2009; 54(6):779-788 e771. PMID 19766352
16. Hollander JE. The 80-lead ECG: more expensive NSTEMI or Occult STEMI [editorial]. Ann Emerg Med. Dec 2009; 54(6):789-790. PMID 19766356
17. Ueoka A, Morita H, Watanabe A, et al. Activation pattern of the polymorphic ventricular tachycardia and ventricular fibrillation on body surface mapping in patients with Brugada syndrome. Circ J. 2016; 80(8):1734-1743. PMID 27319581
18. Kligfield P, Gettes LS, Bailey JJ, et al. Recommendations for the standardization and interpretation of the electrocardiogram: part I: the electrocardiogram and its technology a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol. Mar 13 2007; 49(10):1109-1127. PMID 17349896
19. Electrocardiographic Body Surface Mapping-Archived. Chicago, Illinois: Blue Cross Blue Shield Association Medical Policy Reference Manual (2017 July) Medicine 2.02.23.
|11/15/2018||Document updated with literature review. Coverage unchanged. Added references 14, 17.|
|10/15/2017||Reviewed. No changes.|
|11/1/2016||Document updated with literature review. Coverage unchanged.|
|10/15/2015||Reviewed. No changes.|
|4/15/2014||Document updated with literature review. Coverage unchanged. CPT/HCPCS code(s) updated.|
|4/15/2013||Document updated with literature review. Coverage unchanged.|
|6/15/2011||Document updated with literature review. Coverage unchanged. Description and rationale substantially revised.|
|9/15/2009||Policy reviewed with literature review; no changes to coverage statement.|
|7/1/2007||New medical document.|
|Title:||Effective Date:||End Date:|
|Electrocardiographic Body Surface Mapping||10-15-2017||11-14-2018|
|Electrocardiographic Body Surface Mapping||11-01-2016||10-14-2017|
|Electrocardiographic Body Surface Mapping||10-15-2015||10-31-2016|
|Electrocardiographic Body Surface Mapping||04-15-2014||10-14-2015|
|Electrocardiographic Body Surface Mapping||04-15-2013||04-14-2014|
|Electrocardiographic Body Surface Mapping||06-15-2011||04-14-2013|
|Electrocardiographic Body Surface Mapping||09-15-2009||06-14-2011|
|Electrocardiographic Body Surface Mapping||08-15-2007||09-14-2009|
|Electrocardiographic Body Surface Mapping||07-01-2007||08-14-2007|