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What's New
VasoHealthcare Holds Launch Summit 2010 In Greensboro, NC Vasomedical Releases iPhone Application for EECP® Therapy Vasomedical Announces Reorganization of Its Board of Directors Vasomedical Announces FDA 510(k) Clearance on the First Combined ECG Holter and Ambulatory Blood Pressure Monitoring System |
Clinical Data
Hemodynamic Effects of EECP® Therapy The counterpulsating action of EECP therapy increases venous return and cardiac output. During EECP therapy systolic unloading is improved by increasing blood flow and oxygen to the heart, while diastolic augmentation increases the energy supply to the heart thus reducing the workload of the heart. The hemodynamic effects of EECP also increase the pressure gradient as well as the release of vascular growth factors that enhance coronary collateral circulation. The increase of blood flow increases shear stress on the walls of the arteries and improves endothelial function. Studies have shown that the hemodynamics of EECP therapy closely resemble those of the intra-aortic balloon pump (IABP) long held as the "gold standard" for circulatory support of hemodynamically compromised patients. The magnitude of diastolic augmentation that can be achieved with EECP therapy was found comparable to that of the IABP, resulting in improved coronary blood flow with decreased cardiac workload. Michaels, et al, in a landmark cath lab study, demonstrated the hemodynamics of EECP" therapy in the central vasculature: "Treatment with EECP 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 EECP therapy." EECP therapy improves clinical outcomes including exercise capacity, quality of life and functional classes, reduces angina episodes and nitroglycerin usage in patients with ischemic heart disease including heart failure.
Michaels AD, Accad M, Ports TA, et al. Left ventricular systolic unloading and augmentation of intracoronary pressure and Doppler flow during enhanced external counterpulsation. Circulation. 2002 Sep 3:106(10);1237-42. Mechanisms of Action Though the specific mechanisms of action of EECP therapy have not as yet been defined, Clinical studies published in peer-reviewed journals suggest the possible mechanisms as they continue to identify components of the physiological, neurohumoral, and hemodynamic cascades initiated by the sequential cuff inflation and simultaneous cuff deflation during treatment. EECP therapy produces beneficial effects that appear mediated through arterial diastolic augmentation. The retrograde arterial pressure wave increases coronary perfusion pressure, creating a gradient between ischemic and non-ischemic areas of the myocardium that may recruit latent conduits and enhance myocardial perfusion. Increased endothelial shear stress releases growth factors. Increased nitric oxide (NO) and atrial natriuretic peptide (ANP) levels, and decreased endothelin (ET-1) and brain natriuretic peptide (BNP) levels, also ascribed to increased shear stress and improved endothelial function, raise the possibility of peripheral benefits as well as restored coronary flow reserve. The suggested mechanisms contributing to the clinical benefit of EECP therapy include improvement in endothelial function, promotion of collateralization, enhancement of ventricular function, and peripheral effects similar to those observed in response to regular physical exercise. In a study evaluating the effects of EECP therapy using reactive hyperemicperipheral arterial tonometry (RH-PAT) as a measure of peripheral endothelial function, Bonetti, et al conclude, "that EECP therapy 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 EECP therapy on the first three study days. Moreover, the significant difference between RH-PAT indices before the course of EECP therapy and at one-month follow-up suggests that EECP therapy also exerts a beneficial medium-term effect on endothelial function." 
Possible mechanisms responsible for the clinical benefit associated with EECP therapy. By increasing coronary blood flow, EECP therapy 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. Besides a peripheral training effect, a minor placebo effect is considered to contribute to the symptomatic benefit of EECP therapy. ET = Endothelin: NO = Nitric Oxide. Bonetti. et al16 Bonetti PO, Barsness GW, Keelan PC, et al. Enhanced external counterpulsation improves endothelial function in patients with symptomatic coronary artery disease. Journal of the AmericanCollege of Cardiology. 2003 May 21:41(10);1761-8. Long-term Follow-up Clinical studies and data from the International EECP Patient Registry (IEPR), coordinated by the Epidemiology Data Center at the University of Pittsburgh, continue to demonstrate that 70-80% of patients realize therapeutic benefit immediately upon completion of a course of EECP therapy. At patient follow-up, therapeutic benefit is enhanced at six months and sustained at 36 months post treatment. Quality-of-life measures from a randomized trial and registry studies show significant improvement in the patients' ability to resume activities of daily living, social interaction, and recreational pursuits. Duration of Clinical Benefit 
Source: Loh PH, Cleland JG, Louis AA, Kennard ED , et al. Enhanced external counterpulsation in the treatment of chronic refractory angina: a long-term follow-up outcome from the International Enhanced External Counterpulsation Patient Registry. Clinical Cardiology. 2008 Apr 10;31(4):159-164. Information about the IEPR and the complete IEPR bibliography can be found at www.edc.gsph.pitt.edu/iepr. |
