Knowledge Base

A Doctor's Guide to EECP

EECP Therapy 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, treatment can be offered two hours per day.

EECP Treatment Procedure

Cuffs inflate sequentially from the calves to the upper thighs and buttocks to raise diastolic coronary perfusion pressureand 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 EECP treatment procedure is similar to those seen with an intra-aortic balloon pump with the addition of increased venous return.

Inflation Resulted In
  • Increase in central aortic diastolic pressure up to 92%
  • Increase intracoronary diastolic pressure up to 93%
  • Increase in coronary perfusion pressure.
  • Increase in coronary collateral flow velocity.
  • Increase in venous return and therefore preload.
  • Increase in cardiac output up to 25%
Deflation Resulted In
  • Decrease in central aortic systolic pressure up to 11%
  • Decrease in intracoronary systolic pressure up to 15%
  • Decrease in LV end-diastolic pressure up to 25%
  • Reduced systemic vascular resistance.
  • Decrease in left ventricular workload and afterload.

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

Must – EECP

The MUST – EECP trail is a randomized, controlled, double-blinded, multi-center trial undertaken at seven leading university hospitals in the United States. Patients in the active EECP group demonstrated significantly increased capacity in exercise duration and statistically significant increase 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 Therapy® 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 duration and were sustained even after completion of the treatment.dormant collaterals. EECP treatment has shown to increase the plasma nitric oxide and decreasesthe Endothelin level. These changes were proportional to the treatment

Mean Age

66.9yrs

Prior Mi

67.6%

Duration of CAD

10.9yrs

CHF

31.7%

Prior PCI/CABG

85.7%

Diabetes

42.2%

2 years follow up study results from International EECPRegistery

Long-Term Benefit

Journal

Year

Number of patients

Result

American Journal of Cardiology

1995

18

3-year survival 100% 76% event free

Clinical Cardiology

2000

33

5-years survival 88% 64 % event free

American Journal of Cardiology

2004

1097

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

Long term clinical follow up study on EECP.

Clinical Benefit Summary

Authors

Journal

N

Agina (% >/ 1CCS)

Nitrate Use

Ex. Tolerance

Time to ST Depression

Arora et al (MUST EECP)

JAM Coll cardiology 1999

139

 

 

 

 

Lawson et al.

Cardiology 2000

2238

74%

N/A

N/A

N/A

Styes et al

Angiology 2001

395

88%

N/A

N/A

N/A

Barsness et al

Clinical Cardiology 2001

978

88%

 

N/A

N/A

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

Authors

Journal

N

Agina (% >/ 1CCS)

Nitrate Use

Ex. Tolerance

Time to ST Depression

Arora et al (MUST EECP)

JAM Coll cardiology 1999

139

 

 

 

 

Lawson et al.

Cardiology 2000

2238

74%

N/A

N/A

N/A

Styes et al

Angiology 2001

395

88%

N/A

N/A

N/A

Barsness et al

Clinical Cardiology 2001

978

88%

 

N/A

N/A

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

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. EECPon 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 EECPtreatment.

Conclusion

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

EECP Doctors Guide for Patient Selection
1. Chronic Cad

Primary utilization of EECP is those who no longer respond to medication.

(a) Surgery / PTCA not contemplated

Patients may not be amenable to PCI or CABG due to following:

(b) Preparation for Revascularization

2. Heart Failure
3. Microvascular Angina
4. Acute Coronary Syndrome
Contraindications Check List
Precautions

Precautions 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 obstruction 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.

Severe peripheral in patients with Congestive Heart failure.

SAFETY OF EECP SHOULD BE WITHHELD IF THERE IS EXACERBATION OF HEART FAIL-URE 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.

(GENERAL CARDIOLOGY 2001 LAWSON ET AL.). DURING TREATMENT ONLY 5.5% EXPERIENCED WOR-SENING 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.

Peechtmtrial Prospective Evaluation of EECP in Congestive Heart Failure
Conclusion

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

Possible Adverse Effects

EECPis 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 monitored 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 hyperemia , Peripheral artery tonometer
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