Effects of enhanced counterpulsation on vascular cell release of coagulation factors

Abstract

Enhanced external counterpulsation (EECP), a noninvasive treatment for patients with angina pectoris, provides long-term benefits of decreased anginal frequency and improved exercise tolerance. Previous studies have suggested that shear stress may result in angiogenesis and alter endothelial hemostatic factor release. Whether EECP therapy effects an alteration in endothelial cell proliferation and function remains unclear. The level of vascular endothelial growth factor (VEGF) and four other endothelial hemostatic factors (tissue plasminogen activator, plasminogen activator inhibitor-1, von Willebrand factor, and D-dimers) were measured in patients before and after 35 hours of EECP treatment. Plasma levels of endothelial growth and hemostatic factors were assessed using the standard enzyme-linked immunosorbent method. No significant difference in the hemostatic factors and VEGF after EECP treatment was revealed; there was a trend toward an increase in VEGF levels posttreatment. Vascular endothelial cells play a critical role in the regulation of coagulation because they control the expression of tissue plasminogen activator, plasminogen activator inhibitor-1, von Willebrand factor, and D-dimers. Our results suggest EECP may not play a role in controlling coagulation in patients with coronary artery disease through release of endothelial hemostatic factors. Although there was a tendency for increased VEGF release, larger studies are necessary to confirm these observations.