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.
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.
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.
Intracoronary tracing in catheterization lab showing gradual increase in cuff inflation pressure resulting in increased diastolic pressure, mean arterial pressure and decrease systolic pressure.
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.
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 |
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. |
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 |
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.
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
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.
(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.
Randomized, controlled multi center PEECH trail result supports the use of EECPtreatment in heart failure patients.
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 | ||
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Increases ejection fraction |
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