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Figure 3 Possible mechanisms responsible for the clinical benefit associated with enhanced external counterpulsation (EECP). Acute afterload reduction decreases myocardial demand. By increasing coronary blood flow, EECP is thought to promote myocardial collateralization via opening of preformed collaterals, arteriogenesis, and angiogenesis. Increased blood flow and shear stress may also improve coronary endothelial function favoring vasodilation and myocardial perfusion. In addition, improvement in endothelial function may further promote collateral formation by arteriogenesis and angiogenesis. Besides a peripheral training effect, a minor placebo effect is considered to contribute to the symptomatic benefit of EECP. ET = endothelin; NO = nitric oxide.
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