External Counterpulsation (ECP) a new paradigm for treating heart disease

June 17, 2002

Cardiovascular disease is the leading cause of death in the U.S., according to CDC statistics.1 Conventional treatment options typically include lifestyle modification, prescription drugs and surgery. While often effective at relieving symptoms such as chest pain or angina, these therapies have several drawbacks. They are frequently ineffective at extending life, are associated with numerous side effects and complications, and are expensive. Heart surgery carries a significant risk of death, and often leads to other morbid events.

In addition, a significant number of successfully treated patients become “treatment failures” over time. Following bypass surgery, it is estimated that only 75% of patients remain free of cardiac ischemia for five years, a figure that drops to 50% by ten years.2

Most new medical advances for treating heart disease are, for the most part, extensions of two existing therapies: prescription drugs and invasive surgical procedures. Any new therapy that could impact the leading cause of death in this country would represent a major advancement in anti-aging therapeutics. There is currently such a therapy, which is an entirely new paradigm for treating heart disease.3 This procedure is called either External Counterpulsation (ECP)4 or Enhanced External Counterpulsation (EECP)5 and has recently received FDA approval for treatment for ischemic heart disease.6

In development for almost 50 years, ECP is an ingenious method for treating angina that does not use drugs and is completely non-invasive.7 For the first time since the advent of bypass surgery, a unique therapeutic dimension has emerged for the treatment of patients with ischemic heart disease.8

The History of Counterpulsation

Kantrowitz and Kantrowitz were the first to describe the principle of “phase shift” diastolic augmentation in the 1950′s. Ten years later, Jacobey et al. provided the first evidence that counterpulsation could enhance the development of coronary collateral circulation. They suggested that counterpulsation might have value in the treatment of patients with coronary insufficiency and angina. At the same time, Birtwell and Clause working at Harvard developed the Intra-aortic Balloon Pump to help support blood circulation during cardiac surgery and in cases of cardiogenic shock.10

In 1983, Zheng and associates at Sun Yat Sen University in China designed a sequenced pneumatic external counterpulsation system, which produced excellent results in cases of coronary insufficiency.11 Long-term relief from symptoms of chronic angina were noted. These favorable results led a number of scientists in the U.S. to begin research into external counterpulsation. In 1995 an American company began importing the Chinese device following FDA market approval.

Mechanism of Action

Though a non-invasive device itself, we see that external counterpulsation had its origins in a very invasive device, the intra-aortic balloon pump. ECP has a similar mechanism to the intra-aortic balloon pump, but works on the outside of the body. A modern day ECP unit consists of a computer microprocessor, which triggers the sequential inflation with compressed air of cuffs that are wrapped around a patient’s calves, thighs and buttocks. Compression is triggered to occur during diastole (the resting phase of the heart rhythm). As the computer inflates the cuffs, blood is propelled from the lower body back into the heart. At the end of diastole, the ECP computer signals the sudden and simultaneous deflation of the cuffs, greatly reducing vascular resistance and assisting the heart with its next beat. This action also facilitates venous return of blood into the heart, increasing cardiac output.

ECP improves blood flow to the coronary arteries and helps treat angina, the indication for which it has received FDA approval. Most researchers feel that ECP helps angina by causing the release of a hormone known as vascular endothelial growth factor (VEGF). As ECP causes the heart to receive an unexpected surge of blood during diastole (when it is normally emptying), VEGF levels increase dramatically. VEGF promotes the development of collateral coronary vessels.12 In other words, ECP causes the heart to grow its own bypasses. For the past few years, doctors at The Texas Heart Institute have been involved in gene-therapy research, trying to develop an injectible form of VEGF as well.13

The Need for ECP

ECP fills a critical need because an increasing number of patients with refractory angina are either unwilling or unable to undergo invasive revascularization surgery. Many patients who have undergone bypass surgery are reluctant to undergo repeat surgery after their first (or even second) bypass has begun to fail. Additionally, thanks to better lifestyle choices, aggressive cardiac rehabilitation programs, and conventional medical and surgical therapies, many patients with cardiovascular disease are now living much longer lives. Many now live long enough that they reach a point where invasive therapies become too dangerous and/or medications are no longer effective.

Yet, the dilemma is that improving the quality of life with medication and surgery in elderly patients is more difficult due to the higher incidence of adverse side effects. For example, Taddei found that for every ten-year increase in age, the risk of death for patients undergoing balloon angioplasty increases 65%.14 Alexander found that octogenarians undergoing coronary artery bypass grafting had a 270% increase in mortality compared to younger patients and twice the incidence of postoperative stroke and renal failure.15

In addition to age, other reasons that often preclude angina patients from pursuing further treatment with drugs or surgery include: unavailability of grafts, comorbid situations such as diabetes or congestive heart failure, adverse coronary anatomy, and intolerance or ineffectiveness of medications. ECP is an excellent option for such patients and has been shown in numerous studies to be effective in cases where coronary angioplasty or bypass surgery has failed.16,17

Today’s patients are better educated about their diseases. They are more aware of treatment options and consequently seek safer and less invasive treatments. They understand that surgical procedures such as stent placement, angioplasty and bypass surgery are not free of risk. Even the newest surgical treatments, such as transmyocardial laser (where a laser beam is used to drill tiny holes in the wall of the heart), suffer the same drawbacks as their predecessors, being invasive, expensive, and associated with a high rate of complications.18

Advantages and Safety of ECP

A recent study of external counterpulsation involving patients from seven university hospitals, on the other hand, showed that ECP was both effective and without risk of serious side effects. (The only reported side effect to date from ECP is chaffing of the skin on the legs.) It was the conclusion of this study that “Enhanced external counterpulsation reduces angina and extends time to exercise-induced ischemia in patients with symptomatic coronary artery disease. Treatment was relatively well tolerated and free of limiting side effects in most patients.”19

ECP patients typically undergo one hour of treatment daily, five days a week for seven weeks. In more advanced cases of ischemic heart disease, such as severe triple vessel disease, it is not uncommon for additional ECP treatments to be needed.20

The Modern Bias Towards Invasive Procedures

However, ECP is a non-invasive procedure, while the current bias in conventional cardiology favors invasive therapies. Topol recently described the prevailing preoccupation of using surgery to open coronary arteries as nothing more than “coronary cosmetology.”21 This bias towards surgical therapies is difficult to understand when one considers that a procedure such as angioplasty, done over 500,000 times annually in the U.S., does not have the support of studies that prove that this procedure decreases the risk of heart attacks and death.22,23 Indeed, two major studies that compared angioplasty with medical therapies both showed angioplasties to be ineffective in preventing myocardial infarction and death. , A recent meta-analysis that compared angioplasty to medical treatment for non-acute coronary heart disease found angioplasty of value in reducing angina, but only at the cost of significantly increased rates of myocardial infarction, need for coronary artery bypass graft surgery and repeat angioplasties.24

The New Concept of Vulnerable Plaque– Have We Been Operating on the Wrong Lesions?

Cardiologists and cardiac surgeons typically operate on “high grade” occlusions of the coronary arteries (70-100% occlusions), while ignoring lower grade lesions. Yet, heart attacks are most commonly due to rupture of atherosclerotic plaque that occludes less than 50% of the vessel. Rupture of a 90% lesion with subsequent heart attack is much less common.25 Yet it is the 90% lesion that gets the angioplasty, while the more dangerous 10-50% lesions are ignored. The new concept of “vulnerable” atherosclerotic plaque posits that the smaller deposits of cholesterol along the walls of the arteries are far more dangerous than their larger, older and more obstructive cousins. The smaller lesions tend to be softer and more “vulnerable” to rupture upon exposure to free radicals, with subsequent heart attack or stroke.26

Due to the high failure rate of angioplasty alone, cardiologists have turned to angioplasty with stent placement. Stents (tubes made out of wire mesh that are inserted into arteries to help keep them open) did not come into wide use until 1995, so studies regarding their long-term effects do not exist. However, a recent study suggests that stents cause inflammation of the walls of arteries that “may have implications with respect to the progression of atherosclerosis in coronary arteries.”27 Interestingly, this lack of long-term research on stents has not decreased their use, and stent placement has grown over the past few years into a multibillion-dollar industry.28

The statistics for bypass surgery are sobering as well.29,30 The 22-year VA follow up study of coronary artery bypass surgery for stable angina found that patients who underwent bypass surgery experienced neither long-term survival or symptomatic benefit.31,32 It has been estimated that up to 44% of bypass surgeries are done unnecessarily or for equivocal reasons.33 Graboys found that, when second opinions were obtained prior to coronary artery bypass surgery, as many as 50% of the surgeries could be safely deferred or postponed indefinitely.34

One of the easiest determinants of cardiac function is measurement of the “ejection fraction,” the percentage of blood contained within the left ventricle that is pumped out with each heartbeat. Bypass surgery has been shown to be the most beneficial to those angina patients with an ejection fraction of less than 50%. For patients with an ejection fraction over 50%, there appears to be no benefit, yet the majority of patients undergoing bypass surgery have ejection fractions greater than 50%.

Primum non nocere – “First of all, do no harm”

Throughout their training, medical students are cautioned again and again: Primum non nocere — “first of all, do no harm.” This cardinal rule of medicine dates back to the days of Hippocrates35 and Galen. With regard to coronary artery disease, this fundamental principle would seem to dictate that physicians should look first to treatments that are safe, simple and affordable before proceeding with others that are dangerous, painful and costly. Perhaps residency programs train cardiologists to focus on invasive procedures, leading to patients not being adequately screened prior to undergoing angioplasty and surgery.36

There is ample evidence of bias towards more dangerous and invasive therapies as first-line treatments for angina. One of my former professors from medical school and an excellent cardiologist, Dr. Richard Conti, exemplifies this bias as he notes that external counterpulsation has great potential, but should not be first line therapy. He encourages physicians to aggressively pursue revascularization therapies first.37

ECP is recognized among many cardiology experts as a valid treatment, and many cardiology groups around the country have ECP machines in their offices. But the prevailing sentiment is that ECP should be reserved for those patients who are not candidates for invasive therapy or for cases where such surgery has been done and subsequently failed. If ECP is safe and effective in cases where pharmacological and surgical revascularization has failed, imagine its potential in treating patients with less advanced or severe ischemic heart disease.

Involving Patients in Treatment Decisions

Primum non nocere, first of all, do no harm — the role of physicians is to foster informed participation and allow patients to become actively involved in the treatment decisions. Current trends in medicine are away from paternalistic informed consent and towards informed decision-making, which emphasizes meaningful dialogue between the patient and physician.38 Patients who are truly informed and take part in their treatment decisions are more likely to be compliant. Let physicians inform patients of all the treatment options available for ischemic heart disease.

Lifestyle modifications such as diet, exercise, and stress management should be tried first. Then if additional therapy is needed, present the full spectrum of approved treatment options: prescription medications, angioplasties, stents, bypass surgery and ECP, and let the patient decide. ECP should not be treated as an ugly stepchild selected only as a last resort.

Some might argue that in cases of angina, the stakes are too high and there is no room to allow patients their choice of treatment. Nease et al recently studied this issue of patient attitudes toward treating their chronic angina.39 Considerable variability was found in patients’ willingness to tolerate anginal symptoms. The researchers concluded that management of ischemic heart disease should not be based on the strict use of practice guidelines or the severity of symptoms alone, but rather should take into account the feelings and preferences of the patient.


While ECP is not a panacea and is not suitable for all patients, there are many patients who could benefit from this safe and novel treatment and would indeed request it, if only they were informed that it was available. When physicians discuss treatment options for angina patients, they need to provide balanced presentations and include full explanations of the pros and cons of all available alternative therapies, not just the pros of one therapy and the cons of another.

The optimal treatment plan should take into account the best available scientific data as well as the preferences of the individual patient in a shared decision-making process. The time has come to include discussion of ECP with cardiac patients as a safe, painless, inexpensive alternative to invasive therapy.

Terry Grossman M.D., M.D. (H), N.M.D, has offices in the Denver CO area and can be reached at [email protected]. His office phone is toll-free 877-548-4387.



2Foster ED. Reoperation for coronary artery disease. Circulation. 1985; 72((Suppl V)): V57-V64.

3Amsterdam EA. Enhanced external counterpulsation: Chronicle of a new approach to the therapy of angina pectoris. CR&R.18:15-19.

4One major company representing counterpulsation devices, Cardiomedics, uses the term ECP for external counterpulsation. See http://www.cardiomedics.com/index.cfm.

5The other major American supplier of these devices, Vasomedical, uses the name EECP. See http://www.eecp.com


7Soroff H, Hui JCK, Giron F. Historical review of the development of enhanced external counterpulsation technology and its physiologic rationale. CVR&R. 1997;18:34-40.

8Strobeck J, Baklajian R, Hannon J. The emerging role of enhanced external counterpulsation in cardiovascular disease management. CR&R. 1997;18:20?25.


10Soroff HS, Cloutier CT, Birtwell WC, Begley LA, Messer JV. External counterpulsation. Management of cardiogenic shock after myocardial infarction. JAMA. 1974; 229(11): 1441-50.

11Zheng ZS, Li TM, Kambic H, Chen GH, Yu LQ, Cai SR, Zhan CY, Chen YC, Wo SX, Chen GW, et al. Sequential external counterpulsation (SECP) in China. Trans Am Soc Artif Intern Organs. 1983; 29(599): 599-603.

12Ozlem S, Crawford L, Schneider V, Feldman A. Enhanced external counterpulsation in the management of patients with cardiovascular disease. Clin. Cardiol. 1999;22:173-178.


14Taddei CF, Weintraub WS, Douglas JS Jr, et al. Influence of age on outcome after percutaneous transluminal coronary angioplasty. Am J Cardiol. 1999;84:245-51.

15Alexander KP, Anstrom KJ, Muhlbaier L, et al. Outcomes of cardiac surgery in patients age >80 years: results from the National Cardiovascular Network. J Am Coll Cardiol. 2000;35:731-8.

16Cohn P, Lawson W, Burger L, Hui JCK. Enhanced external counterpulsation: A new therapeutic option for patients who have failed coronary angioplasty and/or bypass surgery. CR&R. 1997;18:10?17.

17Lawson W, Hui JCK, Guo T, Burger L, Cohn P. Prior revascularization increases the effectiveness of enhanced external counterpulsation. Clin Cardiol. 1998;21:841-4.

18Hillis L, Lange R. Transmyocardial laser revascularization. N Engl J Med. 1999;341:1075-6.

19Arora RR, Chou TM, Jain D, Fleishman B, Crawford L, McKiernan T, Nesto RW. 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;33:1833-40.

20Lawson WE, Hui JC, Oster ZH, Zheng ZS, Cabahug C, Katz JP, Dervan JP,Burger L, Jiang L, Soroff HS, Cohn PF. Enhanced external counterpulsation as an adjunct to revascularization in unstable angina. Clin Cardiol. 1997;20:178-80.

21Topol EJ, Nissen SE. Our preoccupation with coronary luminology. The dissociation between clinical and angiographic findings in ischemic heart disease. Circulation. 1995;92:2333-42.

22Coronary angioplasty versus medical therapy for angina: the second Randomised Intervention Treatment of Angina (RITA-2) trial. RITA-2 trial participants. Lancet. 1997;350:461-8.

23Pitt B, Waters D, Brown WV, Van Boven AD J., Schwartz L, et al. Aggressive lipid-lowering therapy compared with angioplasty in stable coronary artery disease. N Engl J Med. 1999;341:70-76.

24Bucher HC, Hengstler P, Schindler C, Guyatt GH. Percutaneous transluminal coronary angioplasty versus medical treatment for non-acute coronary heart disease: meta-analysis of randomised controlled trials. BMJ. 2000;321:73-7.

25Ambrose JA, Fuster V. Can we predict future acute coronary events in patients with stable coronary artery disease? JAMA 1997;277:343-4.

26Fuster V. The Vulnerable Atherosclerotic Plaque: Understanding, Identification and Modification. Amonk NY: Futura Publishing, 1999.

27Caramori PR, Lima VC, Seidelin PH, Newton GE, Parker JD, Adelman AG. Long-term endothelial dysfunction after coronary artery stenting. J Am Coll Cardiol 1999;34:1675-9.

28Topol EJ Coronary-artery stents–gauging, gorging, and gouging N Engl J Med. 1998;339:1702-4.

29Alderman EL, Bourassa MG, Cohen LS, et al. Ten-year follow-up of survival and myocardial infarction in the randomized Coronary Artery Surgery Study. Circulation 1990;82:1629-46.

30Bourassa MG, Enjalbert M, Campeau L, Lesperance J. Progression of atherosclerosis in coronary arteries and bypass grafts: ten years later. Am J Cardiol. 1984;53:102C-107C.

31Cooperative Studies Program. Eighteen-year follow-up in the veterans affairs cooperative study of coronary artery bypass surgery for stable angina. The VA coronary artery bypass surgery cooperative study group. Circulation. 1992;86:121-30.

32Peduzzi P, Kamina A, Detre K. Twenty-two-year follow-up in the VA Cooperative Study of CoronaryArtery Bypass Surgery for Stable Angina. Am J Cardiol. 1998;81:1393-9.

33Winslow CM, Kosecoff JB, Chassin M, Kanouse DE, Brook RH. The appropriateness of performing coronary artery bypass surgery. JAMA. 1988;260:505-9.

34Graboys TB, Headley A, Lown B, Lampert S, Blatt CM. Results of a second-opinion program for coronary artery bypass graft surgery. JAMA. 1987;258:1611-4.

35Hippocrates. Epidemics, Book I, Section XI.

36Topol EJ, Ellis SG, Cosgrove DM, Bates ER, Muller DW, Schork NJ, Schork MA, Loop FD. Analysis of coronary angioplasty practice in the United States with an insurance-claims database. Circulation. 1993;87:1489-97.

37Conti CR. EECP-Enhanced External counterpulsation. J Am Coll Cardiol. 1999;33:1841-1842.

38Braddock CH, Edwards KA, Hasenberg NM, Laidley TL, Levinson W. Informed decision making in outpatient practice: time to get back to basics. JAMA.1999;282:2313-2320.

39Nease RF Jr, Kneeland T, O’Connor GT, Sumner W, Lumpkins C, Shaw L, Pryor D, Sox HC. Variation in patient utilities for outcomes of the management of chronic stable angina. Implications for clinical practice guidelines. Ischemic Heart Disease Patient Outcomes Research Team. JAMA. 1995;273:1185-90.

Copyright © 2002 by Terry Grossman. Used with permission.