Archived Policies - Medicine
Enhanced External Counterpulsation (EECP)
Enhanced External Counterpulsation (EECP) may be considered medically necessary for patients who meet all the following criteria:
• Have been diagnosed with disabling angina (New York Heart Association Class III or IV, or equivalent classification), and
• In the opinion of a cardiologist or cardiothoracic surgeon, are refractory to maximum medical therapy, and
• Are not readily amenable to surgical intervention, such as percutaneous transluminal coronary angioplasty (PTCA) or cardiac bypass because of any of the following:
o Their condition is inoperable, or at high risk of operative complications or postoperative failure; or
o Their coronary anatomy is not readily amenable to such procedures; or
o They have co-morbid states that create excessive risk.
NOTE: A full course of therapy usually consists of 35 one-hour treatments, which may be offered once or twice daily, usually 5 days per week.
The use of EECP is considered experimental, investigational and/or unproven for all other indications not noted above including but not limited to the following:
• Class II angina (New York Heart Association),
• Aortic Insufficiency,
• Peripheral vascular disease or phlebitis,
• Severe hypertension,
• Acute retinal artery occlusion,
• Acute myocardial infarction,
• Erectile dysfunction,
• Ischemic stroke,
• Cardiogenic shock, or
• Heart failure.
Enhanced external counterpulsation (EECP) is a noninvasive treatment used to augment diastolic pressure; decrease left ventricular afterload, and increase venous return. It has been studied primarily as a treatment for patients with refractory angina and heart failure, as well as for other indications such as erectile dysfunction and ischemic stroke.
Enhanced external counterpulsation (EECP) uses timed, sequential inflation of pressure cuffs on the calves, thighs, and buttocks to augment diastolic pressure, decrease left ventricular afterload, and increase venous return. Augmenting diastolic pressure displaces a volume of blood backward into the coronary arteries during diastole when the heart is in a state of relaxation and the resistance in the coronary arteries is at a minimum. The resulting increase in coronary artery perfusion pressure may enhance coronary collateral development or increase flow through existing collaterals. In addition, when the left ventricle contracts, it faces a reduced aortic pressure to work against, since the counterpulsation has somewhat emptied the aorta. EECP has been primarily investigated as a treatment for chronic stable angina.
Intra-aortic balloon counterpulsation is a more familiar, invasive form of counterpulsation that is used as a method of temporary circulatory assistance for the ischemic heart, often after an acute myocardial infarction (MI). In contrast, EECP is thought to provide a permanent effect on the heart by enhancing the development of coronary collateral development. The multiple components of the procedure include the use of the device itself, finger plethysmography to follow the blood flow, continuous electrocardiograms (EKGs) to trigger inflation and deflation, and optional use of pulse oximetry to measure oxygen saturation before and after treatment.
While EECP has been primarily researched as a treatment of chronic stable angina, it has also been used in patients with heart failure. The Vasomedical EECP® Therapy System Model has the following labeled indication under 510(k) clearance from the U.S. Food and Drug Administration (FDA):
"The EECP Therapy System Model TS3 with Pulse Oximetry is a non-invasive external counterpulsation device intended for the use in the treatment of patients with heart failure, stable or unstable angina pectoris, acute myocardial infarction, or cardiogenic shock."
Cardiomedics, Inc. has FDA 510(k) clearance to market the CardiAssist Counterpulsation System (K022107) and the CardiAssist ECP System (K010261) for the same indications as the Vasomedical EECP® systems.
New York Heart Association and Canadian Cardiovascular Society Functional Classifications
New York Heart Association and Canadian Cardiovascular Society Functional Classifications Class
New York Heart Association Functional Classification
Canadian Cardiovascular Society Functional Classification
Patients with cardiac disease but without resulting limitations of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.
Ordinary physical activity does not cause angina, such as walking and climbing stairs. Angina occurs with strenuous or rapid or prolonged exertion at work or recreation.
Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.
Slight limitation of ordinary activity. Walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in cold, in wind, or under emotional stress, or only during the few hours after awakening. Walking more than two blocks on the level and climbing more than one flight of ordinary stairs at a normal pace and in normal conditions.
Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary physical activity causes fatigue, palpitation, dyspnea, or anginal pain
Marked limitation of ordinary physical activity. Walking one to two blocks on the level and climbing one flight in normal conditions and at a normal pace.
Patient with cardiac disease resulting in inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.
Inability to carry on any physical activity without discomfort, anginal syndrome may be present at rest.
This policy was created in 1998 and has been updated regularly with searches of the MEDLINE database. The most recent literature search was performed through November 2013. The following is a summary of the key literature to date.
The literature base consists of a small number of randomized controlled trials (RCTs), some of which report relevant clinical outcomes and others that report intermediate, or physiologic, outcome measures. In addition to the small number of RCTs, there are a large number of observational studies, including publications from enhanced external counterpulsation (EECP) registries and case series, which generally report pre- and post-treatment measures of EECP effectiveness.
Chronic Stable Angina
The original literature review for this policy was based on a 1999 BCBSA Technology Evaluation Center (TEC) Assessment on EECP for chronic stable angina and updated with 2002 and 2005 TEC Assessments. These assessments concluded that the evidence was insufficient to determine whether EECP improved the net health outcome or is as beneficial as any established alternatives in patients with chronic stable angina.
Specifically, the 2005 BCBSA TEC Assessment offered the following observations and conclusions regarding EECP for chronic stable angina (1, 2):
• There is insufficient evidence to draw conclusions about the benefits of EECP.
• The results of the single randomized, controlled trial, the Multicenter Study of Enhanced External Counterpulsation (MUST-EECP), discussed further here, must be interpreted with caution, in view of the high subject dropout rate and uncertainty regarding the clinical significance of the reported improvement in physiologic measures, especially when intent-to-treat analysis is applied. (3, 4)
• Comparative studies of EECP do not address the hard outcomes of cardiac death or recurrent cardiac events such as myocardial infarction and revascularization procedures. (5, 6)
• Several case series and registry-based studies have reported the outcomes of large numbers of patients treated in a number of different institutions. There are several problems with this kind of evidence. These studies, while contributing to the body of knowledge of EECP, do little to address the efficacy or durability of EECP treatment. The lack of comparison groups makes it impossible to rule out either placebo effect or spontaneous recovery among patients with milder disease.
In 1999, Arora and colleagues presented results of the MUST-EECP trial. MUST-EECP applied a randomized, controlled, double-blinded protocol that compared active treatment to placebo (inactive counterpulsation [CP] sham treatment) among 139 patients with Canadian Cardiovascular Society (CCS) Classification Scales (a functional assessment tool based on the level of exertion that elicits symptoms) class I–III chronic, stable angina. (3) Four outcomes were examined:
• Self-reported frequency of angina, analyzed two ways;
• Self-reported use of on-demand nitroglycerin;
• Exercise duration tolerance testing; and
• Time to exercise-induced ischemia (defined as time to depression of ≥1mm in the ST segment on electrocardiogram).
All patients underwent the same 35-hour protocol, followed by an exercise tolerance test within 1 week of completion of therapy. Follow-up beyond the treatment period was not conducted.
Intention-to-treat analyses were reported for the angina count and nitroglycerin usage outcomes only. There was a statistically significant difference (p=0.01) between groups in the change in time to ≥1 mm ST segment depression. Patients in the EECP group had an average difference of 37 seconds longer time to ST segment depression compared to the sham-treated group. There was no significant difference between treatment groups in the change in exercise duration from baseline to the post-treatment period (p<0.31). In addition, there were no statistically significant differences between groups with respect to angina counts (p<0.09) or nitroglycerin use (p>0.1).
In addition to a number of methodologic limitations found in the design, execution, and reporting of this study, the magnitude of the benefit reported is not large. Of the 4 endpoints of interest, only the time to ST segment depression was statistically different in the EECP group compared to the sham-treated group. The clinical significance of a 37-second improvement in time to ST segment depression is unknown, but given that it occurred while the other 3 endpoints were statistically unchanged with therapy, does not suggest a marked improvement. That both groups showed increased exercise duration suggests a degree of placebo effect; exercise duration possesses a motivational component that time to ST segment depression does not.
In 2002, Arora and colleagues published a 12-month follow-up study to the MUST-EECP trial. (4) However, only 71 (54%) of the original 139 subjects were included in the study. Subjects treated with EECP reported greater improvement in several quality-of-life scales. However, such findings could not be correlated with treatment response reported in the first study (because of data limitations).
A small unblinded RCT published in 2012 (7) addressed one health outcome, change after 7 weeks in CCS angina class, along with multiple intermediate outcomes. Twenty patients with refractory angina (CCS class III) were randomized to EECP or no EECP. Mean CCS class was significantly improved in the EECP group but not in the no EECP group. At 7-week follow-up, soluble interleukin-2 receptor measurements significantly increased in the EECP group and significantly decreased in the no EECP group. There were no differences between groups at 7 weeks in resting cutaneous microvascular blood flow or response to acetylcholine, sodium nitroprusside or local heating.
Some small RCTs have reported on intermediate, or physiologic, outcomes. One such RCT (n=20) was published in 2010 comparing intracoronary blood flows in patients treated with EECP against those treated with a sham procedure. (8) This trial was designed to detect statistically significant differences in collateral flow rates by angiography, not anginal symptoms. After 7 weeks of treatment, collateral flow index increased significantly in the EECP group compared to sham treatment. Similar findings were noted in a comparative study by Buschmann and colleagues of 23 patients published in 2009. (9)
Two publications from a single study reported on blood flow and other measures of arterial function. (10, 11). This study randomized 42 patients with coronary artery disease (CAD) and chronic angina to EECP or sham EECP. EECP improved flow-mediated dilation in the brachial and femoral arteries and improved numerous serum markers of blood flow and inflammation. The same study also reported that measures of arterial stiffness were improved in the EECP group. Martin et al. (12) randomized 18 patients with abnormal glucose tolerance to EECP or standard care and reported that measures of glucose tolerance, as well as measures of arterial function were improved in the EECP group.
A number of systematic reviews of the literature have been performed evaluating EECP for chronic stable angina. In 2010, Amin and colleagues published a Cochrane review of major databases through 2008 on evidence of the effectiveness of EECP for chronic angina pectoris. (13) The solitary RCT identified was the MUST-EECP trial. The authors of this review highlighted patient selection for this study. They comment that limiting the study population to patients with CCS class below IV diminishes the study’s generalizability to patients of interest, that is, patients with the most severe symptoms of chronic angina pectoris.
Also in 2010, Shah and colleagues published a meta-analysis of prospective studies, not limited to RCTs, of EECP in stable angina in which CCS class was adequately reported before and after treatment. (14) The MUST-EECP RCT was not included, as change in CCS class was not one of the reported outcomes. Thirteen studies met these inclusion criteria (n=949 patients). Overall, improvement of at least 1 level of angina class occurred in 86% of patients (95% confidence interval [CI]: 82-90%, p=0.008).
In a 2009 paper, McKenna and colleagues report on a systematic review and economic analysis of EECP for the treatment of stable angina and heart failure. (15) Four studies (1 RCT and 3 non-randomized comparative studies) comparing EECP treatment with no treatment in adults with chronic stable angina were included in the analysis. (3-6) The systematic review included a study by Barsheshet and colleagues in which 25 patients (15 EECP and 10 controls) were evaluated at the end of treatment. (16) Similar to the previously reviewed Schechter et al. study, (6) “CCS classification improved with EECP but not with usual care, however statistical analysis of between group differences was not reported and, for CCS classification, the data were treated as continuous data which is inappropriate for this four-category classification.”
Registry-based studies have been published that report on relatively large numbers of patients. In a registry-based study, 450 patients with left ventricular dysfunction (ejection fraction, EF ≤40) and refractory angina had 0.7 fewer emergency department visits and 0.8 fewer hospitalizations 6 months after treatment with EECP compared to the 6 months before EECP; 6-month data were available on only 81 patients. (17)
Another registry-based study (the International Enhanced External Counterpulsation Patient [IECP] Registry) reported long-term (3-year) results on patients with chronic refractory angina for patients in this registry. (18) The registry enrolled 5,000 patients from 99 U.S. and 9 international centers between 1999 and 2001. However, analysis was completed only for those centers that had at least 80% compliance with follow-up data submission; the study reported results on 1,427 patients. In this selective group, 220 patients (15.4%) died, while 1,061 patients (74.4%) completed their follow-up. Immediately post-EECP, the proportion of patients with severe angina (Canadian Cardiovascular Angina Classification [CCS] III/IV) were reduced from 89% to 25%, p<0.001. This was sustained in 74% of the patients during follow-up. More severe baseline angina and a history of heart failure or diabetes were independent predictors of unfavorable outcome.
The IECP data have also been examined to determine the safety and efficacy of the use of this device in patients with peripheral arterial disease. Peripheral arterial disease, while a common comorbidity of coronary artery disease, has been regarded as a relative contraindication to EECP due to concerns of compression on peripheral blood flow and a potentially greater risk of aortic rupture. Thakker and colleagues compared registry data in patients with peripheral arterial disease to those without. (19) Based on a reduction of one or more CCS angina classes, patients with peripheral arterial disease had a similar rate (76.6% vs. 79.0%, respectively; p=0.27) of improvement as did the group without peripheral arterial disease. Rates of hospitalization for all cardiac causes (6.1% vs. 4.4%, respectively; p=0.17) and for unstable angina (5.4% vs. 3.5%, respectively; p=0.25) were also similar between groups.
Numerous individual observational studies have been detailed in previous reviews and are included in systematic reviews described above. (4-6, 9, 16, 20) For example, 2 prospective cohort studies (n=55 and n=61) with 1-year outcomes have been reported. (21, 22) Improved CCS classification was the main reported outcome, which persisted for 1 year in 79% and 78% of patients in the respective studies. Both studies had higher rates of treatment completion and follow-up than the previously reported (registry) studies of long-term outcomes.
The FDA510(k) approval of the Vasomedical devices states that objective measures such as peak oxygen consumption, exercise duration, and pre-load-adjusted maximal left ventricular power are improved following EECP therapy, as well as subjective measures of patient response to therapy, such as quality of life and functional ability measures. (15) However, no clinical details of these studies are provided in the FDA summary, and these data are not from controlled trials.
The 2005 TEC Assessment (1) included heart failure in the analysis and concluded the evidence supporting the role of EECP as an effective treatment for heart failure is lacking in both quantity and quality. A single randomized, multicenter study of EECP compared to usual care in 187 optimally medically managed patients with New York Heart Association (NYHA) functional class II/III heart failure with EF ≤35% of ischemic or idiopathic etiology, the “Prospective Evaluation of EECP in Congestive Heart Failure” (PEECH trial), was mostly inconclusive. (23) The design and methods of the PEECH trial were published by Feldman and colleagues. (24) The results of the PEECH trial found statistically improved, but modest, changes in exercise duration and improved functional classification but not in quality of life or peak oxygen uptake. (23)
A subgroup analysis from the PEECH trial for heart failure was published. (25) It showed that subjects aged 65 years and older treated with EECP (n=41) were more likely to meet the exercise duration (35% vs. 25% increased by ≥60 seconds) and peak VO2 (30% vs. 11% increased by ≥1.25 ml/kg per min) improvement thresholds compared to those undergoing sham treatment (n=45); there was no difference at 6 months in NYHA class. This post-study analysis must be viewed as a preliminary result.
Registry studies for heart failure use angina outcomes and contribute little to the body of evidence. (26-29) The single-arm study by Soran et al. (30) indicates that patients respond with some improvements, but the lack of a comparison arm precludes inference about the true effects of therapy. Treatment durability for either angina or heart failure has yet to be addressed with long-term studies. Therefore, the evidence is insufficient to determine whether EECP improves the net health outcome or is as beneficial as any established alternatives in patients with chronic stable heart failure.
The previously described 2009 review by McKenna and colleagues (15) included the single trial of EECP for heart failure included in the systematic review, the PEECH study. (23) The authors conclude that the studies do not provide firm evidence of the clinical effectiveness of EECP in refractory stable angina or in heart failure and that high quality studies are required to investigate the benefits of EECP and whether these outweigh the common adverse effects.
In summary, evidence for the use of EECP in heart failure is insufficient to form conclusions on efficacy. The single RCT that includes clinical outcomes reported modest improvements on some outcomes and no improvement on others. The observational studies add little to the evaluation of efficacy due to the variable natural history of heart failure, the multiple confounding variables for cardiac outcomes, and the potential for a placebo effect. Further high-quality RCTs are needed to determine whether EECP is a useful treatment for heart failure.
The use of EECP for other conditions of ischemia has been investigated. In 2009, Fraser and Adams produced a Cochrane review on interventions for central retinal artery occlusion (CRAO). (31) One of the 2 RCTs identified compared hemodilution with EECP against hemodilution without further intervention. In this case, the EECP intervention was a single, 2-hour treatment. According to the reviewers, in this study (n=20), patients were randomized but not blinded; no sham treatment was given. Primary outcomes were Doppler flowmetry of retinal perfusion and visual acuity. (32) While acknowledging the relative safety of the technique, the authors’ remark, “The small size of the stud[y], potential for bias and the lack of data on final vision mean that we do not have convincing evidence at present to support the routine use of…EECP in patients with CRAO.”
Published registry studies also demonstrated improvements in erectile function. (33) Erectile function was improved in a study of 120 men prospectively enrolled from 16 centers. Three of 5 domains of the International Index of Erectile Function were statistically improved with EECP treatment (erectile function, intercourse satisfaction, and overall satisfaction), and the total score improved from 28 to 32, a statistically significant improvement. (33) The non-comparative design of this study makes it difficult to draw conclusions on treatment efficacy. This indication is added as investigational due to lack of adequate data on clinical outcomes. Preliminary studies from Asia are also reporting early results on use of EECP to the lower extremities in the treatment of acute ischemic stroke. (34) A 2012 Cochrane review of 2 RCTs of EECP in acute ischemic stroke (35) concluded that the methodologic quality of the studies was poor and reliable conclusions could not be reached from this evidence.
Practice Guidelines and Position Statements
The 2012 American College of Cardiology/American Heart Association (ACC/AHA) guidelines on the management of patients with stable ischemic heart disease chronic stable angina indicate EECP “may be considered for relief of refractory angina.” This recommendation is based on Class IIb, Level of Evidence: B. (36)
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1. Blue Cross and Blue Shield Technology Evaluation Center (TEC). External Counterpulsation for Treatment of Chronic Stable Angina Pectoris and Chronic Heart Failure. TEC Assessments 2005; 20(Tab 12).
2. Luo C, Liu D, Du Z et al. Short-term effects of enhanced external counterpulsation on transthoracic coronary flow velocity and reserve in patients with coronary slow flow. Int. J. Cardiol. 2012; 154(1):84-5.
3. Arora RR, Chou TM, Jain D et al. The multicenter study of enhanced external counterpulsation (MUST-EECP): effect of EECP on exercise-induced myocardial ischemia and anginal episodes. J Am Coll Cardiol 1999; 33(7):1833-40.
4. Arora RR, Chou TM, Jain D et al. Effects of enhanced external counterpulsation on Health-Related Quality of Life continues 12 months after treatment: a substudy of the Multicenter Study of Enhanced External Counterpulsation. J Investig Med 2002; 50(1):25-32.
5. Holubkov R, Kennard ED, Foris JM et al. Comparison of patients undergoing enhanced external counterpulsation and percutaneous coronary intervention for stable angina pectoris. Am J Cardiol 2002; 89(10):1182-6.
6. Shechter M, Matetzky S, Feinberg MS et al. External counterpulsation therapy improves endothelial function in patients with refractory angina pectoris. J Am Coll Cardiol 2003; 42(12):2090-5.
7. Bondesson SM, Edvinsson ML, Pettersson T et al. Reduced peripheral vascular reactivity in refractory angina pectoris: Effect of enhanced external counterpulsation. Journal of geriatric cardiology: JGC 2011; 8(4):215-23.
8. Gloekler S, Meier P, de Marchi SF et al. Coronary collateral growth by external counterpulsation: a randomised controlled trial. Heart 2010; 96(3):202-7.
9. Buschmann EE, Utz W, Pagonas N et al. Improvement of fractional flow reserve and collateral flow by treatment with external counterpulsation (Art.Net.-2 Trial). Eur J Clin Invest 2009; 39(10):866-75.
10. Braith RW, Conti CR, Nichols WW et al. Enhanced external counterpulsation improves peripheral artery flow-mediated dilation in patients with chronic angina: a randomized sham-controlled study. Circulation 2010; 122(16):1612-20.
11. Casey DP, Beck DT, Nichols WW et al. Effects of enhanced external counterpulsation on arterial stiffness and myocardial oxygen demand in patients with chronic angina pectoris. Am. J. Cardiol. 2011; 107(10):1466-72.
12. Martin JS, Beck DT, Aranda JM, Jr. et al. Enhanced External Counterpulsation (EECP) Improves Peripheral Artery Function and Glucose Tolerance in Subjects with Abnormal Glucose Tolerance. J. Appl. Physiol. 2011.
13. Amin F, Al Hajeri A, Civelek B et al. Enhanced external counterpulsation for chronic angina pectoris. Cochrane Database Syst Rev 2010; (2):CD007219.
14. Shah SA, Shapiro RJ, Mehta R et al. Impact of enhanced external counterpulsation on Canadian Cardiovascular Society angina class in patients with chronic stable angina: a meta-analysis. Pharmacotherapy 2010; 30(7):639-45.
15. McKenna C, McDaid C, Suekarran S et al. Enhanced external counterpulsation for the treatment of stable angina and heart failure: a systematic review and economic analysis. Health Technol Assess 2009; 13(24): iii-iv, ix-xi, 1-90.
16. Barsheshet A, Hod H, Shechter M et al. The effects of external counter pulsation therapy on circulating endothelial progenitor cells in patients with angina pectoris. Cardiology 2008; 110(3):160-6.
17. Soran O, Kennard ED, Bart BA et al. Impact of external counterpulsation treatment on emergency department visits and hospitalizations in refractory angina patients with left ventricular dysfunction. Congest Heart Fail 2007; 13(1):36-40.
18. Loh PH, Cleland JG, Louis AA et al. Enhanced external counterpulsation in the treatment of chronic refractory angina: a long-term follow-up outcome from the International Enhanced External Counterpulsation Patient Registry. Clin Cardiol 2008; 31(4):159-64.
19. Thakkar BV, Hirsch AT, Satran D et al. The efficacy and safety of enhanced external counterpulsation in patients with peripheral arterial disease. Vasc Med 2010; 15(1):15-20.
20. Kumar A, Aronow WS, Vadnerkar A, et al. Effect of enhanced external counterpulsation on clinical symptoms, quality of life, 6-minute walking distance, and echocardiographic measurements of left ventricular systolic and diastolic function after 35 days of treatment and at 1-year follow up in 47 patients with chronic refractory angina pectoris. Am J Ther 2009; 16(2):116-8.
21. Pettersson T, Bondesson S, Cojocaru D et al. One year follow-up of patients with refractory angina pectoris treated with enhanced external counterpulsation. BMC Cardiovasc Disord 2006; 6:28.
22. Loh PH, Louis AA, Windram J et al. The immediate and long-term outcome of enhanced external counterpulsation in treatment of chronic stable refractory angina. J Intern Med 2006; 259(3):276-84.
23. Feldman AM, Silver MA, Francis GS et al. Enhanced external counterpulsation improves exercise tolerance in patients with chronic heart failure. J Am Coll Cardiol 2006; 48(6):1198-205.
24. Feldman AM, Silver MA, Francis GS et al. Treating heart failure with enhanced external counterpulsation (EECP): design of the Prospective Evaluation of EECP in Heart Failure (PEECH) trial. J Card Fail 2005; 11(3):240-5.
25. Abbottsmith CW, Chung ES, Varricchione T et al. Enhanced external counterpulsation improves exercise duration and peak oxygen consumption in older patients with heart failure: a subgroup analysis of the PEECH trial. Congest Heart Fail 2006; 12(6):307-11.
26. Soran O, Kennard ED, Kelsey SF et al. Enhanced external counterpulsation as treatment for chronic angina in patients with left ventricular dysfunction: a report from the International EECP Patient Registry (IEPR). Congest Heart Fail 2002; 8(6):297-302.
27. Lawson WE, Kennard ED, Holubkov R et al. Benefit and safety of enhanced external counterpulsation in treating coronary artery disease patients with a history of congestive heart failure. Cardiology 2001; 96(2):78-84.
28. Lawson WE, Silver MA, Hui JC et al. Angina patients with diastolic versus systolic heart failure demonstrate comparable immediate and one-year benefit from enhanced external counterpulsation. J Card Fail 2005; 11(1):61-6.
29. Vijayaraghavan K, Santora L, Kahn J et al. New graduated pressure regimen for external counterpulsation reduces mortality and improves outcomes in congestive heart failure: a report from the Cardiomedics External Counterpulsation Patient Registry. Congest Heart Fail 2005; 11(3):147-52.
30. Soran O, Fleishman B, Demarco T et al. Enhanced external counterpulsation in patients with heart failure: a multicenter feasibility study. Congest Heart Fail 2002; 8(4):204-8, 27.
31. Fraser SG, Adams W. Interventions for acute non-arteritic central retinal artery occlusion. Cochrane Database Syst Rev 2009; (1):CD001989.
32. Werner D, Michalk F, Harazny J et al. Accelerated reperfusion of poorly perfused retinal areas in central retinal artery occlusion and branch retinal artery occlusion after a short treatment with enhanced external counterpulsation. Retina 2004; 24(4):541-7.
33. Lawson WE, Hui JC, Kennard ED et al. Effect of enhanced external counterpulsation on medically refractory angina patients with erectile dysfunction. Int J Clin Pract 2007; 61(5):757-62.
34. Han JH, Leung TW, Lam WW et al. Preliminary findings of external counterpulsation for ischemic stroke patient with large artery occlusive disease. Stroke 2008; 39(4):1340-3.
35. Lin S, Liu M, Wu B et al. External counterpulsation for acute ischaemic stroke. Cochrane Database Syst Rev 2012; 1:CD009264.
36. Fihn SD, Gardin JM, Abrams J et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol 2012; 60(24):e44-e164.
37. Enhanced External Counterpulsation (EECP) for Chronic Stable Angina or Congestive Heart Failure. Chicago, Illinois: Blue Cross Blue Shield Association Medical Policy Reference Manual (2014 January) Medicine 2.02.06.
|6/1/2015||Reviewed. No changes.|
|8/1/2014||Document updated with literature review. Coverage unchanged.|
|8/15/2013||Document updated with literature review. The following was added: Enhanced External Counterpulsation (EECP) may be considered medically necessary for patients who meet all the following criteria: 1) Have been diagnosed with disabling angina (New York Heart Association Class III or IV, or equivalent classification) 2) In the opinion of a cardiologist or cardiothoracic surgeon, are refractory to maximum medical therapy, and 3) Are not readily amenable to surgical intervention, such as PTCA or cardiac bypass because of any of the following: Their condition is inoperable, at high risk of operative complications or postoperative failure, their coronary anatomy is not readily amenable to such procedures, or they have co-morbid states that create excessive risk. In addition, the following was added: The use of EECP is considered experimental, investigational and unproven for all other indications including but not limited to class II angina, arrhythmia, aortic insufficiency, peripheral vascular disease or phlebitis, severe hypertension, acute retinal artery occlusion, acute myocardial infarction, erectile dysfunction, ischemic stroke, cardiogenic shock, or heart failure.|
|8/15/2010||Revised/Updated Entire Document. Document updated with literature review. Coverage unchanged and remains experimental, investigational and unproven for all indications. An additional two indications (erectile dysfunction and ischemic stroke) added under examples of experimental, investigational, and unproven indications.|
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|Title:||Effective Date:||End Date:|
|Enhanced External Counterpulsation (EECP)||10-15-2018||07-31-2019|
|Enhanced External Counterpulsation (EECP)||08-15-2017||10-14-2018|
|Enhanced External Counterpulsation (EECP)||10-01-2016||08-14-2017|
|Enhanced External Counterpulsation (EECP)||06-01-2015||09-30-2016|
|Enhanced External Counterpulsation (EECP)||08-01-2014||05-31-2015|
|Enhanced External Counterpulsation (EECP)||08-15-2013||07-31-2014|
|Enhanced External Counterpulsation (EECP)||08-15-2010||08-14-2013|
|Enhanced External Counterpulsation (EECP)||06-15-2008||08-14-2010|
|Enhanced External Counterpulsation (EECP)||04-15-2006||06-14-2008|
|Enhanced External Counterpulsation (EECP)||12-01-2003||04-14-2006|