Japan Bangladesh Friendship Hospital

Japan Bangladesh Friendship Hospital


Cardiac and ECP Center

Photo: Cardiac and ECP center.


The ECP device offered by Cardiomedics, Inc. provides a non-invasive treatment for patients with Angina and/or Congestive Heart Failure. ECP treatment is typically provided on an outpatient basis in 35 one-hour sessions over a period of approximately seven weeks. Additional hours may be safely and effectively added to this standard regimen if the physician evaluation of the patient’s response to treatment will result in greater relief of angina symptoms. In certain circumstances, adjusting the patient’s treatment regimen to two hours per day can make it more comfortable for the patient to complete a course of ECP therapy.

To receive ECP therapy, the patient reclines on a treatment table. Three sets of comfortable, inflatable cuffs (similar to blood pressure cuffs) are snugly and securely wrapped around the patient’s calves, thighs and buttocks. The cuffs are inflated sequentially at the onset of diastole and deflated before the onset of systole. The inflation and deflation are specifically timed with the patient’s ECG to optimize therapeutic benefit. This sequence increases coronary perfusion pressure and venous return to the right heart (increasing preload and cardiac output). The simultaneous deflation, at the onset of systole, rapidly decreases cardiac afterload (creating systolic unloading) of the heart.


HEMODYNAMIC effects of ECP Therapy: Taguchi et al demonstrated that ECP therapy produces hemodynamic effects very similar to the Intra-Aortic Balloon Pump (IABP) in patients with Acute Myocardial Infarction. Michaels et al also demonstrated the hemodynamics of ECP in the cath lab. They determined that the therapy unequivocally and significantly increases central aortic and intracoronary diastolic pressure and intracoronary blood flow velocity. Mean aortic and intracoronary pressure is increased, and left ventricular systolic unloading occurs during the therapy. Schecter, Hod et al report that the mechanisms of action for ECP therapy are not yet definitely defined. Many clinical studies however, identify components of the hemodynamic, physiological and neurohormonal cascades that ECP initiates.

The many beneficial effects that ECP produces appear to emanate through arterial diastolic augmentation. The retrograde pressure wave increases coronary perfusion pressure, which creates a gradient between ischemic and nonischemic areas of the myocardium that can recruit latent conduits and increase myocardial perfusion. Increased nitric oxide (NO) and atrial natriuretic peptide (ANP), and decreased endothelin (ET-1) and brain natriuretic peptide (BNP) raise the possibility of peripheral benefits as well as restored coronary flow reserve. Increased endothelial shear stress releases growth factor, which can improve endothelial function.

Bonetti, et al have concluded that external counter pulsation is associated with an acute improvement in peripheral endothelial function, as is demonstrated by the acute increase in RH-PAT index observed in response to ECP during the first three days of treatment. By increasing coronary blood flow, ECP is thought to promote myocardial collateralization via opening of pre-formed collaterals. Increased blood flow and shear stress may also improve coronary endothelial function favoring vasodilation and myocardial perfusion.




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