MANAGING ANGINA AND RISK VIA IMPROVED ENDOTHELIAL FUNCTION: THE EECP MODEL


Gregory Barsness, M.D., Mayo Clinic, Rochester, MN, USA

Enhanced external counterpulsation (EECP) is an outpatient therapy for the treatment of stable ischemic heart disease, angina and heart failure. Although a non-invasive therapy, EECP treatment produces a marked acute hemodynamic effect similar to that produced by the invasive intra-aortic balloon pump. The safety and efficacy of EECP therapy for angina and heart failure treatment have been well documented. Recently, investigators have studied the mechanisms of action of EECP therapy, including improvement in endothelial function caused by increased systemic blood flow velocity and beneficial vascular shear effects. Our group and others have demonstrated a reproducible global endothelial function improvement that is associated with an observed dose-dependent increase in the release of endothelial nitric oxide synthase (eNOs) and the vasodilator nitric oxide (NO), as well as reduction of the vasoconstrictor endothelin (ET-1). Others have shown that EECP therapy is associated with an increase in vascular endothelial growth factor levels and, together with the mechanical pressure gradient generated during EECP, may promote coronary collateral flow, improve coronary flow dynamics and increase microcirculatory density. We have also documented an association between EECP-derived improvements in endothelial function and decreased circulating levels of inflammatory cytokines and activated endothelial progenitor stem cells. In this way, EECP has been proposed as a modality to promote vascular homeostasis through replacement and repair of the endothelium, thereby enhancing endothelial function and modifying the atherosclerotic process and progression of cardiovascular disease.