Abstract
The mechanisms accounting for the salutary benefits of enhanced external counterpulsation (EECP) remain largely unknown. Emerging data now point to three possible hypotheses to explain its efficacy. These possible explanations include enhanced diastolic flow, changes in the neuro‐hurmoral milieu, and changes in ventricular function independent of changes in cardiac load. While each of these three hypotheses may help explain the mechanism behind EECP's effects, more clinical studies are required to refine these proposed explanations.
Keywords: angiogenic growth factors, atrial natriuretic peptide, brain natriuretic peptide, endothelian, enhanced external counterpulsation, MCP‐1, nitric oxide, vascular endothelial growth factor
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