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EECP© is a Non-Invasive treatment for patients with refractory angina and heart failure.


Treatment Regimen

Patients are usually treated with EECP one hour a day, six days a week for six weeks for a total of 35 hours. In some patients it can be offered two hours per day.

Patients Receiving EECP

Cuffs inflate sequentially from the calves to the upper thighs and buttocks to raise diastolic coronary perfusion pressure and increase venous return. Cuffs deflate at the onset of systole producing left ventricular unloading with an associated decrease to cardiac workload.


Acute Hemodynamic Effects.

The acute hemodynamic effects of external counterpulsation are similar to those seen with an intra-aortic balloon pump with the addition of increased venous return.


Inflation resulted in:


  • Increase central aortic diastolic pressure up to 92%
  • Increase intracoronary  diastolic pressure up to 93%
  • Increase in coronary perfusion pressure.
  • Increase coronary collateral flow velocity.
  • Increase venous return and therefore preload.
  • Increase in cardiac output up to 25%

Deflation resulted in:


  • Decrease central aortic systolic pressure up to 11%
  • Decrease intracoronary systolic pressure up to 15%
  • Decrease in LV end-diastolic pressure up to 25%
  • Reduce systemic vascular resistance.
  • Decrease Left ventricular workload and afterload.

Intracoronary tracing in catheterization Lab showing gradual increase in cuff inflation pressure resulting in increase diastolic pressure, mean arterial pressure and decrease systolic pressure




Must – EECP

The MUST – EECP trail is a randomized, controlled, double-blinded, multi-center trail undertaken at seven leading university hospitals in the United States. Patients in the active EECP group demonstrated significantly increased in exercise duration and statistically significant increased in time to exercise-induced ST-segment depression when compared to sham group from baseline.

Clinical Benefits.

  • Relief of anginal pain.
  • Reduction in the use of nitrates.
  • Improvements in Quality of life.
  • Improvements in Exercise tolerance.
  • Clinical benefits are sustained for up to 5 years following treatment.


International EECP Patient Registry (IEPR)

In 1998, the International EECP Patient Registry (IEPR) was established. The IEPR is a voluntary registry of consecutive patients open to provider members.
Additionally, an analysis of long-term outcomes suggests that the clinical benefits achieved are sustained up to two years following an initial course of treatment.

EECP has shown to improve the myocardial perfusion to the ischemic area. It is assessed by PET and SPECT Nuclear study. The Mechanism is believed to be increase pressure gradient and coronary blood flow velocity in coronary vascular bed. This will lead to formation of new vessels and opening of the dormant collaterals.
EECP treatment has shown to increase the plasma nitric oxide and decreases the Endothelin level. These changes were proportional to the treatment duration and were sustained even after completion of the treatment.

Mean Age


Prior Mi


Duration of CAD








2 years follow up study results from International EECP Registery


Long-term Benefit:



Number of patients


American Journal of Cardiology



3-year survival 100%
76% event free

Clinical Cardiology



5-years survival 88%
64 % event free

American Journal of Cardiology



2-year survival 91%
41% event free.
(32% heart failure, 43% DM, prior MI 68%)

Long term clinical follow up study on EECP.


C linical Benefit Summary




Agina (% >/ 1CCS)

Nitrate Use

Ex. Tolerance

Time to
ST Depression

Arora etal (MUST EECP)

J AM Coll cardiology 1999






Lawson et al.

Cardiology 2000


¯ 74%




Styes et al

Angiology 2001


¯ 88%




Barsness et al

Clinical Cardiology 2001


¯ 81%




Clinical improvement after EECP treatment N= Number of Patients
¯ = decreased, ­ = increased, N/A = Not available


Mechanism of action:

1. Improve Myocardial Perfusion to ischemic area

EECP has shown to improve the myocardial perfusion to the ischemic area. It is assessed by PET and SPECT Nuclear study. The Mechanism is believed to be increase pressure gradient and coronary blood flow velocity in coronary vascular bed. This will lead to formation of new vessels and opening of the dormant collaterals.





Perfusion Changes

Lawson et al

J. Am. Coll.
Cardiology 19992



78% pts ¯
(Maximal exercise)

Urano et all

J. Am. Coll Cardiology 2001



46% ¯ (sameworkload)

Masuda et al

Eu Heart J. 2001



23% ¯ (Overall 47%¯ (ischemic)

Stys, Ramasamy. S

2002. J. Am Coll Cardiology 2002

Thallium / Sestamibi


83% Pts ¯ (same workload)
54% Pts ¯ (Maximal Exercise)

Tartaglia, Ramayasamy. S
et al

Clin cardiology 2003



64% Pts (Maximal Exercise)

Long term clinical follow up study on EECP.


2. Improve Endothelial Function
Sustained Shear stress to Endothelium

EECP treatment has shown to increase the plasma nitric oxide and decreases the Endothelin level. These changes were proportional to the treatment duration and were sustained even after completion of the treatment.


3.Effect on Neurohormonal  system.

EECP treatment decreases the activation of Renin—angiotensin-aldosterone system (RAAS). Angiotensin II is a vasoconstrictor, and also responsible for myocardial hypertrophy and fibrosis. A course of EECP has shown to decrease the plasma rennin activity and Angiotensin II level significantly.


4.EECP on Ventricular function.

EECP decrease Left Ventricular End Diastolic pressure and increase peak filling rate. Plasma BNP (Brain Natriuretic peptide) level, which is an indicator of ventricular stretch significantly decreases after EECP treatment.




Treatment with EECP increases myocardial perfusion in association with improved regional wall motion and afterload reduction has resulted in significant improvement in both the systolic and diastolic ventricular function.


5. Peripheral Training Effect.

EECP treatment has shown to decrease the total peripheral resistance, heart rate and systolic blood pressure, which are similar to what observed during active exercise training. This peripheral vascular conditioning may be responsible for benefit in the patients whose improvement in myocardial perfusion is not demonstrated.



Patient Selection

1.Chronic CAD

Primary utilization of EECPis those  who no longer respond to medication.
(a) Surgery / PTCA not contemplated
Patients may not be amenable to PCI or CABG due to following:

  • Patients who refused for invasive procedure.
  • Diffuse distal disease.
  • Target lesion is inaccessible.
  • Co-morbid states create high risk.
  • LV dysfunction—High risk CABG.
  • Restenosis after PTCA.
  • CABG graft occlusion.

(b)Preparation for Revascularization

  • Severe LV Dysfunction with lot of hibernation to Stabilize Heart Function.
  • Waiting due to some other reason.


2.Heart Failure

  • Non-Ischemic cardiomyopathy.
  • Ischemic Cardiomyopathy.
  • Patient with LV Dysfunction.
  • Patient with moderate to severe levels of CHF.


3.Microvascular Angina

Cardiac syndrome X


4. Acute Coronary Syndrome

  • Unstable Angina.
  • Acute MI.
  • Cardiogenic shock.



Contraindications Check List

  • Significant AR.
  • DVT/active thrombophlibities.
  • Congenital Heart Disease.
  • Gross CHF.
  • Uncontrolled arrhythmia AF, VT, Frequent VPC’s.
  • Extreme Hypertension (BP>180/110mmHg).
  • Extreme Tachycardia (HR>120 BPM).
  • Cardiac Cath in Prior 1-2 weeks.
  • Bleeding Diathesis.
  • Pregnancy.




In some patients with a history of congestive heart failure (CHF) or low ejection fraction, left ventricular function may be insufficient to compensate for increased venous return during EECP. These patients should have their fluid balance closely monitored. Cuff pressure and deflation timing should be optimized for achieving maximum after load reduction and reducing the possibility of pulmonary congestion.

EECP should be withheld if there is exacerbation of heart failure symptoms and may be resumed once the patient has been stabilized. In patient with manageable edema with LVEF>35% continuous monitoring of oxygen saturation should be initiated.

Severe peripheral vascular disease including significant ileofemoral arterial obstruciton may limit the effectiveness of EECP treatment due to decreased blood flow.

Patient suspected of having an abdominal aortic aneurysm should be evaluated for its clinical significance prior to treatment with EECP.


EECP in heart failure patients

Patient with LVD with history of heart failure a course of EECP treatment has shown to decrease the Endothelin and nitric oxide ratio. This shift results in vasodilatation, which is persistent even after 3 months of completion of treatment. EECP thus benefits the patient with both ischemic and idiopathic cardiomyopathy independent of effect on Angiogenesis and collateral formation.


Safety of EECP in patients with Congestive Heart failure.

(General Cardiology 2001 Lawson et al.).

During treatment only 5.5% experienced worsening of their congestive heart failure. In six months follow up study of 444 patents with history of CHF with EF less than 39%, 88% with multiple vessel disease only 19% where re-hospitalize for CHF, which is only 1/3 rd of the expected re-hospitalization when compare to other randomize study with similar patient group.





PEECH stuty design and protocol



EECP significantly improve Exercise capacity up to 6 months compared to control group.

EECP significantly improves functional capacity and quality of life compared to control group.






Randomized, controlled multi center PEECH trail result supports the use of EECP treatment in heart failure patients.


EECP is well tolerated in heart failure patient
Results suggest that EECP provides adjunctive therapy in patients with NYHA II-III heart failure receiving optimal pharmacologic therapy

Possible Adverse Effects

EECP is shown well tolerated over a wide range of patient types and age span. Few patients do not complete the prescribed course of therapy. The most common adverse effect has been skin irritations and muscle pain.
In patients with history of heart failure EECP is safe when it is given to patients with stable condition with minimal edema. The patients are continuously monitor during the treatment for drop in oxygen saturation.

Clinical Summary

Clinical Improvements

Objective Improvements

Biochemical changes

Reduction in anginal episodes

Increases time to ST-Segment depression

Decreases in Endothelin level

Reduction in use of Nitrates

Increases treadmill exercise time

Increases in nitric oxide level

Improvement in exercise tolerance

Improves stress myocardial perfusion

Decreases oxidateive stress

Improvement in overall quality of life

Improves PET scan myocardial perfusion

Decreases in BNP Level

All outcomes sustained for longer-term

Improvement in peak oxygen consumption

Increases in VEGE level


Improves wall motion abnormality



Increases cardiac output



Increases ejection fraction



Possible Mechanism of action to clinical improvement in Chronic angina & heart failure patients




·  TMPG - Trans Myocardial Pressure gradient
·  VEGF - Vascular endothelial growth factor
·  HGF - Hepatocyte Growth factor
·  FGF - Fibroblast Growth factor
·  No - Nitric oxide
·  LVEF - Left ventricular ejection fraction
·  FMD - Flow mediated vasodilatation
·  RH(PAT) - Reactive hyoperemia, Peripheral artery tonometer



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