External Counterpulsation (ECP)

Number: 0262

Policy

  1. Aetna considers a course of up to 35 sessions of external counterpulsation (ECP) medically necessary for members who meet both of the following criteria:

    1. Members with disabling chronic stable angina (New York Heart Association Class III or Class IV angina) (see Appendix); 

      and

    2. Members are refractory to maximum medical therapy and not readily amenable to surgical intervention such as percutaneous transluminal coronary angioplasty (PTCA) or cardiac bypass due to any of the following:

      • Their condition is inoperable; or
      • They are at high-risk of operative complications or post-operative failure; or
      • Their coronary anatomy is not readily amenable to such procedures; or
      • They have co-morbid states that create excessive risk.

    There is no proven benefit to extending a course of ECP beyond 35 sessions.

  2. Aetna considers repeat courses of ECP medically necessary for persons with chronic stable angina if all of the following criteria are met:

    1. Member meets medical necessity criteria for ECP in section I above; and

    2. Prior ECP has resulted in a sustained improvement in symptoms, with:

      1. A significant (greater than 25 %) reduction in frequency of anginal symptoms; or
      2. Improvement by 1 or more anginal classes; and

    3. Three or more months has elapsed from the prior ECP treatment.

  3. Aetna considers the use of ECP for all other conditions (e.g., abnormal glucose tolerance, aortic insufficiency, arrhythmia, atherosclerosis obliterans of the lower extremity, chronic cerebrovascular occlusive disease, erectile dysfunction, fatigue/malaise, heart failure, hepato-renal syndrome, hypertension, improvement of exercise endurance in individuals with chronic obstructive pulmonary disease; peripheral vascular disease or phlebitis, restless leg syndrome, retinal artery occlusion, rotational vertebro-basilar insufficiency, stroke, sudden deafness, tinnitus, and unstable angina) experimental and investigational because its effectiveness for indications other than the one listed above has not been established.    

  4. Aetna considers hydraulic versions of these devices not medically necessary.

Background

External counterpulsation (ECP) is a non-invasive, outpatient treatment for coronary artery disease with angina refractory to medical and/or surgical therapy.  A series of 3 compressive air cuffs that inflate and deflate in synchronization with the patient's cardiac cycle via microprocessor-interpreted ECG signals are wrapped around each leg; one at calf level, another slightly above the knee and the third on the thigh.  The cuffs are larger versions of the familiar blood pressure cuff.  During diastole the 3 sets of air cuffs are inflated sequentially (distal to proximal) compressing the vascular beds within the muscles of the calves, lower thighs and upper thighs.  This action results in an increase in diastolic pressure, generation of retrograde arterial blood flow and an increase in venous return.  The cuffs are deflated simultaneously just prior to systole, which produces a rapid drop in vascular impedance, a decrease in ventricular work-load and an increase in cardiac output.

In the short-term, this method of therapy is thought to deliver more oxygen to the ischemic myocardium by increasing coronary blood flow during diastole, while at the same time reducing the demand for oxygen by diminishing the work requirements of the heart.  Long-term benefit is expected to result as coronary collateral flow to ischemic regions of the myocardium is increased.  A full course of ECP typically involves 5 hours of treatment per week, delivered in 1- to 2-hour sessions for 7 weeks, for a total of 35 hours of treatment (Arora et al, 1999; CMS, 2006).  The pivotal randomized controlled trial of ECP, the MUST-ECP trial, employed a 35-hour protocol (Arora et al, 1999).  There is no reliable evidence that clinical outcomes of ECP are improved with prolonged courses of treatment.  Michaels et al (2005) reviewed registry data to assess the frequency, efficacy, predictors, and long-term success of repeat ECP therapy in relieving angina in patients who had chronic angina and had undergone a full course of ECP.  Within 2 years of the initial course of ECP, the rate of repeat ECP was 18 %, which occurred at a mean interval of 378 days after initial ECP.  Of those who underwent repeat ECP, 70 % had a decrease of 1 or more angina classes at the end of repeat ECP with similar decreases in nitroglycerin use.  Although patients who underwent repeat ECP did benefit from the 2 courses of therapy, the symptomatic improvement was not sustained.  Of the patients who had repeat ECP, 59 % also had class 0 to II angina compared with 82 % of those who did not undergo repeat ECP (p < 0.001).  Nitroglycerin use was more common in patients who underwent repeat ECP (63 %) than in those who did not (45 %; p < 0.0001).

Clinical trials have demonstrated that the beneficial effects of ECP, including increased time until onset of ischemia and a reduction in the number and severity of anginal episodes.  These effects are not only sustained between treatments, but may persist for several months to 2 years after completion of a course of therapy.

While the Food and Drug Administration has granted Enhanced External Counterpulsation (EECP) 510(k) clearance for treating a variety of conditions, including stable or unstable angina pectoris, acute myocardial infarction and cardiogenic shock, the effectiveness of EECP for conditions other than stable disabling angina (e.g., heart failure and retinal artery occlusion) has not been established in the peer-reviewed medical literature.

Manchanda and Soran (2007) stated that numerous clinical trials in the last 2 decades have shown EECP therapy to be safe and effective for patients with refractory angina with a clinical response rate averaging 70 % to 80 %, which is sustained up to 5 years.  It is not only safe in patients with co-existing heart failure, but also is shown to improve quality of life and exercise capacity and to improve left ventricular function long-term.  Interestingly, EECP therapy has been studied for various potential uses other than heart disease, such as restless leg syndrome, sudden deafness, hepatorenal syndrome, and erectile dysfunction.  Moreover, Arora and Shah (2007) stated that EECP has been proven to provide symptomatic benefit in angina patients, but has not been proven to show an increase in life expectancy or decrease in cardiovascular events.  Furthermore, EECP in heart failure has been proven to be safe, but its effectiveness is still uncertain.

Alexandrov et al (2008) determined ECPs effect on middle cerebral artery (MCA) blood flow augmentation in normal controls as a first step to support future clinical trials in acute stroke.  Bilateral 2-MHz pulsed wave transcranial Doppler (TCD) probes were mounted by head frame, and baseline M1 MCA TCD measurements were obtained.  External counterpulsation was then initiated using standard procedures for 30 mins, and TCD readings were repeated at 5 and 20 mins.  Physiological correlates associated with ECP-TCD waveform morphology were identified, and measurable criteria for TCD assessment of ECP arterial mean flow velocity (MFV) augmentation were constructed.  A total of 5 subjects were enrolled in the study.  Pre-procedural M1 MCA TCD measurements were within normal limits.  Onset of ECP produced an immediate change in TCD waveform configuration with the appearance of a second upstroke at the dicrotic notch, labeled peak diastolic augmented velocity (PDAV).  Although end-diastolic velocities did not increase, both R-MCA and L-MCA PDAVs were significantly higher than baseline end-diastolic values (p < 0.05 Wilcoxon rank-sum test) at 5 and 20 mins.  Augmented MFVs (aMFVs) were also significantly higher than baseline MFV in the R-MCA and L-MCA at both 5 and 20 mins (p < 0.05).  The authors concluded that ECP induces marked changes in cerebral arterial waveforms and augmented peak diastolic and mean MCA flow velocities on TCD in 5 healthy subjects.  In this regard, Han and Wong (2008) stated that randomized, controlled trials with a large sample size are needed to further define the safety and effectiveness of ECP in acute stroke management.

A Cochrane systematic evidence review concluded that there is a lack of reliable and conclusive evidence that EECP can improve symptoms of angina in patients with chronic stable or refractory forms of the condition (Amin et al, 2010).  The authors identified 1 trial, with 139 participants, that met criteria for inclusion in the review.  The authors found that poor methodological quality, in terms of trial design and conduct, incompleteness in reporting of the review's primary outcome, limited follow-up for the secondary outcomes and subsequent flawed statistical analysis, compromised the reliability of the reported data.  The authors explained that this trial failed to address the characteristics of interest satisfactorily, in terms of severity of angina, for the participants in this review.  Participants with the most severe symptoms of angina were excluded; therefore the results of this study represent only a subsection of the broader population with the disorder, are not generalizable and provide inconclusive evidence for the effectiveness of EECP therapy for chronic angina pectoris.

Similarly, an assessment by the National Institute for Health Research Health Technology Assessment Programme found that although EECP is cost-effective if the observed quality of life benefits are assumed to continue throughout a patient's lifetime, there is insufficient evidence for its long-term clinical effectiveness in refractory stable angina (McKenna et al, 2009). 

Vertebro-basilar insufficiency (VBI) is a condition in which decreased blood volume of the vertebral artery and basilar artery results in insufficient blood supply to certain parts of the brain.  This will lead to a variety of syndromes (e.g. difficulty in talking, disequilibrium/dizziness/vertigo, gait disturbances, headache, impaired vision, position-related nystagmus, and weakness or numbness on one or both sides of the body).  Xin et al (2010) examined the effectiveness of EECP and traction therapy for patients with rotational VBI.  A total of 163 patients with clinically suspected rotational VBI caused by cervical spondylosis were enrolled in this study.  They were randomly assigned into 3 groups:

  1. EECP + traction,
  2. EECP, and
  3. traction. 
All patients and 50 healthy volunteers received transcranial color Doppler examination of the vertebral artery and basilar artery in both a neutral cervical spine position and a rotational position.  Within 3 days after treatment, 47 (84 %) patients in EECP + traction group, 32 (61 %) patients in EECP group, and 8 (15 %) patients in traction group achieved successful outcomes, while at 3 months' follow-up, 45 (80 %) patients in EECP + traction group, 34 (64 %) in EECP group, and 3 (6 %) in traction group achieved successful outcomes.  With head rotation, the percentage of reduction of blood flow velocities of the vertebro-basilar artery (VBA) in patients was much greater than that of the healthy volunteers (p < 0.01).  After treatment, rotational blood flow velocity reduction percentage of VBA in each treatment group was much lower than that of each group before treatment.  Patients in the EECP + traction group experienced the greater decrease of rotational blood flow velocity reduction percentage of VBA than patietns in the EECP group.  The authors concluded that EECP and traction therapy can relieve the symptoms of rotational VBI, improve the rotational reduction of vertebro-basilar blood flow, and reduce the increased arterial impedance.  Moreover, they stated that further long-term investigations are needed to confirm these findings.

In a Cochrane review, Lin et al (2012) evaluated the safety and effectiveness of ECP for acute ischemic stroke.  These investigators searched the Cochrane Stroke Group Trials Register (June 2011), Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library, 2011 Issue 2), MEDLINE (1948 to June 2011), EMBASE (1980 to June 2011), CINAHL (1982 to June 2011), AMED (Allied and Complementary Medicine) (1985 to June 2011), China Biological Medicine Database (CBM) (1978 to June 2011), Chinese National Knowledge Infrastructure (CNKI) (1979 to June 2011), Chinese Science and Technique Journals Database (VIP) (1989 to June 2011) and Wanfang Data (1984 to June 2011).  They also searched ongoing trials registers, reference lists and relevant conference proceedings and contacted authors and manufacturers of ECP devices.  Randomized controlled trials (RCTs) in which ECP (started within 7 days of stroke onset) was compared with sham treatment or no treatment, or ECP plus routine treatment was compared with routine treatment alone, in patients with acute ischemic stroke.  Two review authors independently assessed trial quality and extracted data, checked for adverse events data and contacted trialists for missing information.  These researchers included 2 trials involving 160 patients.  Numbers of death or dependent patients at the end of at least 3 months follow-up were not reported in either of the included trials.  The outcome measure used in the included trials was only the number of participants with improvement of neurological impairment after treatment according to the Modified Edinburgh-Scandinavian Stroke Scale (MESSS) or self-making criteria.  External counterpulsation was associated with a significant increase in the number of participants whose neurological impairment improved (risk ratio (RR) 1.75, 95 % confidence interval (CI): 1.37 to 2.23).  Only 1 trial reported no adverse events.  The authors concluded that the methodological quality of the included studies was poor, and reliable conclusions could not be drawn from the present data.  They stated that high-quality and large-scale RCTs are needed.

May (2013) stated that enhanced ECP (EECP) is a non-invasive therapy offered to patients with angina pectoris who have unacceptable chest pain despite medical treatment and who have no operative options.  During EECP, 3 sets of pneumatic cuffs wrapped around the lower extremities are inflated to a pressure of 260 to 300 mm Hg in diastole.  This creates an augmented diastolic blood pressure and an increase in coronary blood flow.  The therapy is usually given for 1 hour 5 days a week in 7 weeks.  The author concluded that EECP is known to reduce the frequency of angina, increase the quality of life and reduce the frequency of hospitalization.

An UpToDate review on “Possibly effective emerging therapies for heart failure” (Colucci, 2015) states that “Trials and registries of EECP included some patients with HF, some of whom had improvements in their exercise capacity following EECP therapy.  The PEECH trial directly evaluated the possible benefit of EECP in patients with mild-to-moderate HF.  One hundred and eighty-seven patients were randomly assigned standard medical therapy with seven to eight weeks of EECP or standard medical therapy alone.  Patients assigned to EECP were slightly more likely to increase their total exercise time by more than 60 seconds (35 versus 25 percent with standard medical therapy).  However, EECP did not have any effect on peak VO2.  Thus, this study did not achieve positive results for its two primary endpoints.  In addition, the results of this single-blind trial are subject to placebo effect.  Further research will be necessary to define the impact of EECP in the treatment of HF”.

Martin et al (2014) stated that EECP improves resistance artery function in coronary artery disease patients.  However, whether EECP elicits similar effects in persons with abnormal glucose tolerance (AGT) is unknown.  These researchers provided novel evidence that EECP significantly improves resistance arterial function in the forearm of persons with AGT, whereas the calf only approached significance (p ≤ 0.10).  These improvements were coincident with greater glycemic control, providing further insight into the potential mechanisms of EECP-mediated alterations in glycemia.  These preliminary findings need to be validated by well-designed studies.

Erectile Dysfunction

Raeissadat and colleagues (2018) reviewed  the effectiveness of EECP in patients suffering from erectile dysfunction (ED).  PubMed, Medline, Google Scholar, Tripdatabase, Scopus, and Cochrane library databases were searched for articles with the following search terms: enhanced external counterpulsation and erectile dysfunction.  No restrictions with respect to study setting, date of publication, and language were imposed.  From an initial set of 208 records, 4 studies were selected after a final review.  A total of 177 patients with a mean age of 59.98 years were included in these studies, with 20 to 35 hours/week of EECP treatment; 3 studies used the International Index of Erectile Function questionnaire and 1 applied a four-item questionnaire and a peak systolic flow measurement.  All of these parameters were significantly improved after the EECP treatment.  The authors concluded that to the best of their knowledge, this was the first study reviewing the clinical effectiveness of EECP in patients with ED.  According to the articles reviewed in this study, an improvement in erectile function following EECP treatment courses has been observed in patients with and without coronary artery disease without any significant adverse effects.  Moreover, these investigators stated that since the safety and effectiveness of EECP were observed in non-controlled studies, there is a need for well-designed randomized clinical trial studies with larger sample sizes and long-term follow-up periods to evaluate this new and non-invasive therapeutic option in patients suffering from ED by excluding the confounders.

Chronic Cerebrovascular Occlusive Disease

Buschmann and associates (2018) noted that ECP improves cerebral perfusion velocity in acute stroke and may stimulate collateral artery growth.  However, whether (non-acute) at-risk patients with high-grade carotid artery disease may benefit from ECP needs to be validated.  In this study, a total of 28 patients (71 ± 6.5 years, 5 women) with asymptomatic unilateral chronic severe internal carotid artery stenosis (greater than 70 %) or occlusion were randomized to receive 20-min active ECP followed by sham treatment or vice-versa.  Cerebral blood flow velocity (CBFV) (measured bilaterally by transcranial middle cerebral artery Doppler), tissue oxygenation index (TOI) (measured over the bilateral prefrontal cortex by near-infrared spectroscopy) and cerebral hemodynamic parameters, such as relative pulse slope index (RPSI), were monitored.  Ipsilateral mean CBFV (ΔVmean +3.5 ± 1.2 cm/s) and tissue oxygenation (ΔTOI +2.86 ± 0.8) increased significantly during active ECP compared to baseline, while the sham had little effect (ΔVmean +1.13 ± 1.1 cm/s; ΔTOI +1.25 ± 0.65).  On contralateral sides, neither ECP nor sham control had any effect on either parameter.  During ECP, early dynamic changes in ΔRPSI of the ipsilateral CBFV signal predicted improved tissue oxygenation during ECP (odds ratio [OR] 1.179, 95 % CI: 1.01 to 1.51), while baseline cerebrovascular reactivity to hypercapnia failed to show an association.  The authors concluded that in patients with high-grade carotid disease, ipsilateral cerebral oxygenation and blood flow velocity were increased by ECP.  This is a necessary condition for the stimulation of regenerative collateral artery growth, and thus a therapeutic concept for the prevention of cerebral ischemia.  These researchers stated that the findings of this study provided a rationale for further investigations on the long-term effects of ECP on cerebral hemodynamics and collateral growth.  They stated that future studies in chronic carotid artery occlusion should examine if repetitive ECP can lead to persistent elevation in cerebral oxygenation and whether it can improve cerebral collateral flow.

The authors stated that this study had several drawbacks.  First, only a small number of participants (n = 28) were recruited.  In order to fully elucidate the potential of the techniques, data are needed for a higher number of clinically stable and asymptomatic patients, with mostly ipsilateral impaired auto-regulatory reserve.  Second, the majority of the study population was men; thus, it would be important to recruit a more gender‐balanced cohort for future investigations.  Furthermore, prospective long‐term and multi-center studies are needed in order to analyze whether ECP has a sustained effect on CBFV and TOI.  Finally, functional analyses following treatment with ECP are needed to evaluate any improvement in cognitive function and compensatory vascular re-modeling processes.

Improvement of Exercise Endurance in Individuals with Chronic Obstructive Pulmonary Disease

Zhao and colleagues (2020) noted that EECP is popular in China for the treatment of coronary heart diseases, but it may be an effective treatment for other populations.  In a pilot study, these researchers examined the effect of EECP on exercise endurance of healthy people and chronic obstructive pulmonary disease (COPD) patients and provided intervention measures to improve their physical condition.  Patients were randomly divided into the EECP and non-EECP groups.  According to their maximal oxygen uptake, the volunteers were also sub-grouped into the normal, low exercise endurance, and COPD subgroups.  Differences in exercise endurance were evaluated between the EECP and non-EECP groups before and after treatment.  Cardiopulmonary exercise testing included anaerobic threshold oxygen uptake (AT-VO2Kg), maximum oxygen uptake (Max-VO2Kg), anaerobic threshold pulse (AT-O2puls), anaerobic threshold metabolic equivalent (AT-Mets), and maximum metabolic equivalent (Max-Mets).  A total of 72 volunteers were enrolled.  The EECP and non-EECP groups were similar in terms of age, sex, body mass index (BMI), blood pressure, heart rate, breathing frequency, AT-VO2Kg, Max-VO2Kg, AT-O2puls, AT-Mets, and Max-Mets (p > 0.05) before treatment.  EECP significantly improved AT-VO2Kg, Max-VO2Kg, AT-O2puls, AT-Mets, and Max-Mets compared with the non-EECP group (p < 0.05).  When analyzed according to sub-groups, the AT-VO2Kg, Max-VO2Kg, AT-O2puls, AT-Mets, and Max-Mets of the normal, low exercise endurance, and COPD subgroups were all significantly increased after EECP (p < 0.05).  The authors concluded that EECP significantly improved the exercise endurance of normal adults, low endurance adults, and COPD patients.  Moreover, these researchers stated that these findings need to be validated using a large-scale, multi-center clinical trial.  The drawbacks of this trial included the small sample size (n = 13 in the EECP COPD-subgroup), and short-term follow-up.  Furthermore, stratified randomization was not used.

Treatment of Individuals with Atherosclerosis Obliterans of the Lower Extremity

Badtieva and colleagues (2019) examined the effectiveness of EECP in the treatment and rehabilitation of patients with stages I to IIB obliterating atherosclerosis of the lower extremities (OALE).  A total of 68 patients aged 50 to 78 years with stages I to IIb OALE in the presence of clinical symptomatology of arterial insufficiency were examined and treated.  According to the method of treatment, patients were divided into 2 groups: 32 people received a standard drug therapy (a control group), and 36 patients had an EECP therapy cycle during the standard therapy (a study group).  The frequency of characteristic complaints, pain-free walking distance, peripheral hemodynamics, and the ankle-brachial index (ABI) were assessed.  Post-treatment leg pain on walking persisted in 11 (30.6 %) and 25 (78.1 %) patients in the study group and in the control one, respectively.  There were leg cramps in 9 (25.0 %) and 14 (43.8 %) people and cold feet in 5 (13.9 %) and 25 (78.1 %) patients, respectively (p < 0.05).  In the study group, the considerable increase in pain-free walking distance as compared to baseline values averaged 250 ± 31.2 m (p < 0.05), while that in the control group was only 64.5 ± 25.1 m (p > 0.05).  The post-treatment increase in the leg and foot rheographic indices averaged 23.9 and 23.2 %, respectively, in the study group and 11.9 and 12.3 %, respectively, in the control group.  The increases in ABI in the anterior and posterior tibial arteries were 31.4 and 35.2 %, respectively, in the study group (p < 0.05), and 16.0 and 13.0 %, respectively, in the control group (p > 0.05).  The authors concluded that the findings of this study suggested that the use of EECP in the combination therapy of patients with stages I to IIb OALE was safe and effective.  These preliminary findings need to be validated by well-designed studies.

Appendix

New York Heart Association Functional Classification of Cardiac Disability

Class I

Patients with cardiac disease but without resulting limitations of physical activity.  Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.

Class II

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.

Class III

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.

Class IV

Patients 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.

Source: Adapted from Goldman et al (1981).

Table: CPT Codes / HCPCS Codes / ICD-10 Codes
Code Code Description

Information in the [brackets] below has been added for clarification purposes.   Codes requiring a 7th character are represented by "+":

Other CPT codes related to the CPB:
93922 Limited bilateral non-invasive physiologic studies of upper or lower extremity arteries, (eg, for lower extremity: ankle/brachial indices at distal posterior tibial and anterior tibial/dorsalis pedis arteries plus bidirectional, Doppler waveform recording and analysis at 1-2 levels, or ankle/brachial indices at distal posterior tibial and anterior tibial/dorsalis pedis arteries plus volume plethysmography at 1-2 levels, or ankle/brachial indices at distal posterior tibial and anterior tibial/dorsalis pedis arteries with transcutaneous oxygen tension measurements at 1-2 levels)
93923 Complete bilateral non-invasive physiologic studies of upper or lower extremity arteries, 3 or more levels (eg, for lower extremity: ankle/brachial indices at distal posterior tibial and anterior tibial/dorsalis pedis arteries plus segmental blood pressure measurements with bidirectional Doppler waveform recording and analysis at 3 or more levels, or ankle/brachial indices at distal posterior tibial and anterior tibial/dorsalis pedis arteries plus segmental volume plethysmography at 3 or more levels, or ankle/brachial indices at distal posterior tibial and anterior tibial/dorsalis pedis arteries plus segmental transcutaneous oxygen tension measurements at 3 or more level(s), or single level study with provocative functional maneuvers (eg, measurements with postural provocative tests or measurements with reactive hyperemial)

HCPCS codes covered if selection criteria are met:
G0166 External counterpulsation, per treatment session

ICD-10 codes covered if selection criteria are met:
I20.0 - I20.9 Angina pectoris [disabling, refractory to maximum medical therapy and not readily amenable to surgical intervention]

ICD-10 codes not covered for indications listed in the CPB (not all-inclusive):
G08 Intracranial and intraspinal phlebitis and thrombophlebitis
G25.81 Restless legs syndrome
H34.00 - H34.9 Retinal vascular occlusion
H91.20 - H91.23 Sudden idiopathic hearing loss
H93.11 - H93.19 Tinnitus
H93.A1 - H93.A9 Pulsatile tinnitus
I06.1 Rheumatic aortic insufficiency
I10 - I16.2 Hypertensive disease
I11.0, I13.0 - I13.2
I50.1 - I50.9		 Heart failure
I20.0 Unstable angina
I35.0 - I35.9 Nonrheumatic aortic valve disorder
I47.0 - I47.9 Paroxysmal tachycardia
I60.00 - I69.998 Cerebrovascular disease [stroke] [rotational vertebro-basilar insufficiency]
I70.201 - I70.799 Atherosclerosis of native arteries, unspecified type of bypass graft(s), autologous vein bypass graft(s), nonautologous biological bypass graft(s), nonbiological bypass graft(s) and other type of bypass graft(s) of the extremities [atherosclerosis obliterans of the lower extremity]
I73.00 - I73.9 Other peripheral vascular disease
I80.00 - I80.9 Phlebitis and thrombophlebitis
I82.1 Thrombophlebitis migrans
I83.10 - I83.12 Varicose veins of lower extremities with inflammation
J44.0 - J44.9 Other chronic obstructive pulmonary disease [improvement of exercise endurance]
K76.7 Hepatorenal syndrome
N28.0 Ischemia and infarction of kidney
N52.01 - N52.9 Male erectile dysfunction
R53.0 - R53.83 Malaise and fatigue
R73.09 Other abnormal glucose [abnormal glucose tolerance]

The above policy is based on the following references:

  1. 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):307-311.
  2. Alexandrov AW, Ribo M, Wong KS, et al. Perfusion augmentation in acute stroke using mechanical counter-pulsation-phase IIa: Effect of external counterpulsation on middle cerebral artery mean flow velocity in five healthy subjects. Stroke. 2008;39(10):2760-2764.
  3. Amin F, Al Hajeri A, Civelek B, et al. Enhanced external counterpulsation for chronic angina pectoris. Cochrane Database Syst Rev. 2010;(2):CD007219.
  4. Arora RR, Chou TM, Jain D, et al. Effects of enhanced external counterpulsation on Health-Related Quality of Life continue 12 months after treatment: A substudy of the Multicenter Study of Enhanced External Counterpulsation. J Investig Med. 2002;50(1):25-32.
  5. 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):1833-1840.
  6. Arora RR, Shah AG. The role of enhanced external counterpulsation in the treatment of angina and heart failure. Can J Cardiol. 2007;23(10):779-781.
  7. Badtieva VA, Voroshilova DN, Sichinava NV. Use of enhanced external counterpulsation in the treatment and rehabilitation of patients with atherosclerosis obliterans of the lower extremity. Vopr Kurortol Fizioter Lech Fiz Kult. 2019;96(4):5-11.
  8. Barsness GW. Enhanced external counterpulsation in unrevascularizable patients. Curr Interv Cardiol Rep. 2001;3(1):37-43.
  9. BlueCross BlueShield Association (BCBSA), Technology Evaluation Center (TEC). External counterpulsation for treatment of chronic stable angina pectoris. TEC Assessment Program. Chicago, IL: BCBSA; October 2002;17(15).
  10. BlueCross BlueShield Association, Technology Evaluation Center (TEC). External counterpulsation for the treatment of chronic stable angina pectoris and chronic heart failure. TEC Assessment Program. Chicago, IL: BCBSA; January 2006;10(12).
  11. 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):1612-1620.
  12. Buschmann EE, Hillmeister P, Bondke Persson A, et al. Short-term external counterpulsation augments cerebral blood flow and tissue oxygenation in chronic cerebrovascular occlusive disease. Eur J Neurol. 2018;25(11):1326-1332. 
  13. Caceres J, Atal P, Arora R, Yee D. Enhanced external counterpulsation: A unique treatment for the "no-option" refractory angina patient. J Clin Pharm Ther. 2021 Jan 7 [Online ahead of print].
  14. California Technology Assessment Forum (CTAF). Enhanced external counterpulsation for the treatment of heart failure. Technology Assessment. San Francisco, CA: CTAF; October 16, 2002.
  15. Canadian Agency for Drugs and Technologies in Health (CADTH). Putting the squeeze on heart disease. Health Technology Update. Issue 4. Ottawa, ON: CADTH; September 2006.
  16. Centers for Medicare and Medicaid Services (CMS). External counterpulsation therapy. Medicare Coverage Issues Manual Section 35-74, Issue #CAG-00003. Baltimore, MD: CMS; February 5, 1999.
  17. Centers for Medicare and Medicaid Services (CMS). NCD for external counterpulsation (ECP) for severe angina (20.20). Medicare Coverage Database. Baltimore, MD: CMS; effective March 20, 2006.
  18. Clapp JC, Banas JS, Stickley LP. Evaluation of sham and true external counterpulsation in patients with angina pectoris. Circulation. 1974;50:108-111.
  19. Cohn PF, Lawson WE. Role of enhanced external counterpulsation in angina treatment. J Myocard Ischemia. 1994;6(10):25-29.
  20. Cohn PF. Enhanced external counterpulsation for the treatment of angina pectoris. Prog Cardiovasc Dis. 2006;49(2):88-97.
  21. Colucci WS. Investigational and emerging therapies for heart failure. UpToDate [online serial]. Waltham, MA: UpToDate; reviewed January 2016.
  22. Colucci WS. Possibly effective emerging therapies for heart failure. UpToDate [online serial]. Waltham, MA: UpToDate; reviewed December 2014.
  23. Conti CR. Medical device therapy for chronic stable angina. Clin Cardiol. 1998;21(2):71.
  24. Conti CR. Ongoing and planned studies of enhanced external counterpulsation. Clin Cardiol. 2002;25(12 Suppl 2):II26-II28.
  25. Dery V. Agence D'Evaluation des Technologies et des Modes D'Intervention en Sante (AETMIS). Effectiveness of enhanced external counterpulsation for the treatment of chronic angina. AETMIS 03-08. Montreal, QC; AETMIS; March 2004.
  26. El-Sakka A, Morsy A, Fagih B. Enhanced external counterpulsation in patients with coronary artery disease-associated erectile dysfunction. Part I: Effects of risk factors. J Sex Med. 2007;4(3):771-779.
  27. 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):240-245.
  28. Feldman AM, Silver MA, Francis GS, et al; PEECH Investigators. Enhanced external counterpulsation improves exercise tolerance in patients with chronic heart failure. J Am Coll Cardiol. 2006;48(6):1198-1205.
  29. Goldman L, Hashimoto B, Cook EF, et al. Comparative reproducibility and validity of systems for assessing cardiovascular functional class: Advantages of a new specific activity scale. Circulation. 1981;64(6):1227-1264.
  30. Han JH, Wong KS. Is counterpulsation a potential therapy for ischemic stroke? Cerebrovasc Dis. 2008;26(2):97-105.
  31. 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):1182-1186.
  32. Kaluski E, Gabara Z, Uriel N, et al. The benefits and safety of external counterpulsation in symptomatic heart failure. Isr Med Assoc J. 2006;8(10):687-690.
  33. Kim MC, Kini A, Sharma SK. Refractory angina pectoris: Mechanism and therapeutic options. J Am Coll Cardiol. 2002;39(6):923-934.
  34. Kronhaus KD, Lawson WE. Enhanced external counterpulsation is an effective treatment for Syndrome X. Int J Cardiol. 2009;135(2):256-257.
  35. Lawson WE, Hui CK, Zheng ZS, et al. Can angiographic findings predict which coronary patients will benefit from enhanced external counterpulsation? Am J Cardiol. 1996;77:1105-1109.
  36. Lawson WE, Hui JC, Cohn PF. Long-term prognosis of patients with angina treated with enhanced external counterpulsation: Five-year follow-up study. Clin Cardiol. 2000;23(4):254-258.
  37. Lawson WE, Hui JC, Guo T, et al. Prior revascularization increases the effectiveness of enhanced external counterpulsation. Clin Cardiol. 1998;21(11):841-844.
  38. Lawson WE, Hui JC, Kennard ED, et al; International Enhanced External Counterpulsation Patient Registry Investigators. Two-year outcomes in patients with mild refractory angina treated with enhanced external counterpulsation. Clin Cardiol. 2006;29(2):69-73.
  39. Lawson WE, Hui JC, Kennard ED, et al; IEPR Investigators. Effect of enhanced external counterpulsation on medically refractory angina patients with erectile dysfunction. Int J Clin Pract. 2007;61(5):757-762.
  40. Lawson WE, Hui JC, Lang G. Treatment benefit in the enhanced external counterpulsation consortium. Cardiology. 2000;94(1):31-35.
  41. Lawson WE, Hui JC, Oster ZH, et al. Enhanced external counterpulsation as an adjunct to revascularization in unstable angina. Clin Cardiol. 1997;20(2):178-180.
  42. Lawson WE, Hui JC, Zheng ZS, et al. Improved exercise tolerance following enhanced external counterpulsation: Cardiac or peripheral effect? Cardiology. 1996;87(4):271-275.
  43. Lawson WE, Hui JC, Soroff HS, et al. Efficacy of enhanced external counterpulsation in the treatment of angina pectoris. Am J Cardiol. 1992;70:859 -862.
  44. Lawson WE, Hui JC, Zheng ZS, et al. Three-year sustained benefit from enhanced external counterpulsation in chronic angina patients. Am J Cardiol. 1995;75:840-841.
  45. 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):61-66.
  46. Lin S, Liu M, Wu B, et al. External counterpulsation for acute ischaemic stroke. Cochrane Database Syst Rev. 2012;1:CD009264.
  47. Manchanda A, Soran O. Enhanced external counterpulsation and future directions: Step beyond medical management for patients with angina and heart failure. J Am Coll Cardiol. 2007;50(16):1523-1531.
  48. Martin JS, Beck DT, Braith RW. Peripheral resistance artery blood flow in subjects with abnormal glucose tolerance is improved following enhanced external counterpulsation therapy. Appl Physiol Nutr Metab. 2014;39(5):596-599.
  49. Masuda D, Nohara R, Hirai T, et al. Enhanced external counterpulsation improved myocardial perfusion and coronary flow reserve in patients with chronic stable angina. Evaluation by (13)N-ammonia positron emission tomography. Eur Heart J. 2001;22(16):1451-1458.
  50. May O. Enhanced external counterpulsation therapy for patients with angina pectoris. Ugeskr Laeger. 2013;175(3):116-119.
  51. 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.
  52. Michaels AD, Barsness GW, Soran O, et al; International EECP Patient Registry Investigators. Frequency and efficacy of repeat enhanced external counterpulsation for stable angina pectoris (from the International EECP Patient Registry). Am J Cardiol. 2005;95:94-97.
  53. Michaels AD, Kennard ED, Kelsey SE, et al. Does higher diastolic augmentation predict clinical benefit from enhanced external counterpulsation? Data from the International EECP Patient Registry (IEPR). Clin Cardiol. 2001;24(6):453-458.
  54. Michaels AD, Linnemeier G, Soran O, et al. Two-year outcomes after enhanced external counterpulsation for stable angina pectoris (from the International EECP Patient Registry [IEPR]). Am J Cardiol. 2004;93(4):461-464.
  55. Michaels AD, Raisinghani A, Soran O, et al. The effects of enhanced external counterpulsation on myocardial perfusion in patients with stable angina: A multicenter radionuclide study. Am Heart J. 2005;150(5):1066-1073.
  56. Ohman EM, Nanas J, Stomel RJ, et al. Thrombolysis and counterpulsation to improve survival in myocardial infarction complicated by hypotension and suspected cardiogenic shock or heart failure: Results of the TACTICS Trial. J Thromb Thrombolysis. 2005;19(1):33-39.
  57. Ontario Ministry of Health and Long-Term Care, Medical Advisory Secretariat. Literature review of enhanced external counterpulsation. Health Technology Scientific Literature Review. Toronto, ON: Ontario Ministry of Health and Long-Term Care; February 2003.
  58. Ontario Ministry of Health and Long-Term Care, Medical Advisory Secretariat (MAS). Enhanced external counterpulsation (EECP). Health Technology Policy Assessment Update. Toronto, ON: MAS; March 2006.
  59. Qin X, Deng Y, Wu D, et al. Does enhanced external counterpulsation (EECP) significantly affect myocardial perfusion?: A systematic review & meta-analysis. PLoS One. 2016;11(4):e0151822.
  60. Raeissadat SA, Javadi A, Allameh F. Enhanced external counterpulsation in rehabilitation of erectile dysfunction: A narrative literature review. Vasc Health Risk Manag. 2018;14:393-399.
  61. Shea ML, Conti CR, Arora RR. An update on enhanced external counterpulsation. Clin Cardiol. 2005;28(3):115-118.
  62. Soran O, Kennard ED, Kfoury AG, Kelsey SF; IEPR Investigators. Two-year clinical outcomes after enhanced external counterpulsation (EECP) therapy in patients with refractory angina pectoris and left ventricular dysfunction (report from The International EECP Patient Registry). Am J Cardiol. 2006;97(1):17-20.
  63. Soran O. A new treatment modality in heart failure enhanced external counterpulsation (EECP). Cardiol Rev. 2004;12(1):15-20.
  64. Soroff HS, Hui J, Giron F. Current status of external counterpulsation. Critical Care Clinics. 1986;2(2):277-295.
  65. Suresh K, Simandl S, Lawson WE, et al. Maximizing the hemodynamic benefit of enhanced external counterpulsation. Clin Cardiol. 1998;21(9):649-653.
  66. Urano H, Ikeda H, Ueno T, et al. Enhanced external counterpulsation improves exercise tolerance, reduces exercise-induced myocardial ischemia and improves left ventricular diastolic filling in patients with coronary artery disease. J Am Coll Cardiol. 2001;37(1):93-99.
  67. Wang Y, Xu D. The effect of enhanced external counterpulsation on platelet aggregation in patients with coronary heart disease. Cardiovasc Drugs Ther. 2021 Jan 21 [Online ahead of print].
  68. 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):541-547.
  69. Xin W, Fangjian G, Hua W, et al. Enhanced external counterpulsation and traction therapy ameliorates rotational vertebral artery flow insufficiency resulting from cervical spondylosis. Spine. 2010;35(15):1415-1422.
  70. Xiong L, Lin W, Han J, et al. Enhancing cerebral perfusion with external counterpulsation after ischaemic stroke: How long does it last? J Neurol Neurosurg Psychiatry. 2016;87(5):531-536.
  71. Zhang C, Liu X, Wang X, et al. Efficacy of enhanced external counterpulsation in patients with chronic refractory angina on Canadian Cardiovascular Society (CCS) angina class: An updated meta-analysis. Medicine (Baltimore). 2015;94(47):e2002.
  72. Zhao M, Huang Y, Li L, et al. Enhanced external counterpulsation efficacy on exercise endurance in COPD patients and healthy subjects: A pilot randomized clinical trial. Int J Chron Obstruct Pulmon Dis. 2020;15:25-31.