Enhanced External Counterpulsation and Future DirectionsStep Beyond Medical Management for Patients With Angina and Heart Failure
Aarush Manchanda, MD* and
Ozlem Soran, MD, MPH, FACC, FESC ,1,*
* Department of Internal Medicine, The George Washington University, Washington, DC
Cardiovascular Institute, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
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Figure 1 Technique of EECP
Three pairs of pneumatic cuffs are applied to the calves, lower thighs, and upper thighs. The cuffs are inflated sequentially during diastole, distal to proximal. The compression of the lower-extremity vascular bed increases diastolic pressure and flow and increases venous return. The pressure is then released at the onset of systole. Inflation and deflation are timed according to the R-wave on the patient’s cardiac monitor. The pressures applied and the inflation–deflation timing can be altered by using the pressure waveforms and electrocardiogram on the enhanced external counterpulsation (EECP) therapy monitor.
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Figure 2 Possible Mechanisms Responsible for the Clinical Benefit Associated With EECP Therapy
Acute afterload reduction decreases myocardial demand. By increasing coronary blood flow, enhanced external counterpulsation (EECP) therapy is thought to promote myocardial collateralization via opening of preformed collateral vessels, arteriogenesis, and angiogenesis. Increased blood flow and shear stress also may improve coronary endothelial function, favoring vasodilation and myocardial perfusion. In addition, improvement in endothelial function may further promote collateral formation by arteriogenesis and angiogenesis. In addition to a peripheral training effect, a minor placebo effect is considered to contribute to the symptomatic benefit of EECP therapy. ET = endothelin; NO = nitric oxide.
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