BACKGROUND: The relationship between endothelial damage/dysfunction and coronary artery disease is well recognized. However, the effects of percutaneous coronary intervention (PCI) [stenting/angioplasty] on circulating markers of endothelial damage/dysfunction (eg, von Willebrand factor [vWF], soluble E-selectin [sEsel] levels, and more recently circulating endothelial cells [CECs]) has been less well defined. AIMS AND METHODS: We investigated the effects of both diagnostic coronary angiography (CA) [n = 15; blood sampling immediately before CA and 15 min after CA] and PCI (n = 38; blood sampling before PCI, 15 min after PCI, and 24 h after PCI) on levels of CECs, vWF, and sEsel across comparable patient groups. We also included a cohort of comparable healthy control subjects in order to compare baseline levels of three endothelial markers. RESULTS: There were no differences in baseline levels of CECs, vWF, or sEsel between the three study groups (healthy control subjects, CA, PCI; all p = not significant). Following CA (before to 15 min after), there were no significant changes in vWF and CECs (p = not significant). Following PCI, there were significant increases observed at 15 min after PCI and at 24 h after PCI (when compared with pre-PCI levels) in CECs (p = 0.0006), vWF (p = 0.007), and sEsel (p = 0.024). CONCLUSION: We observed significant increases in three endothelial markers (CECs, vWF, and sEsel) with elective PCI but not CA. This is in keeping with endothelial damage/dysfunction following PCI.
BACKGROUND: The relationship between endothelial damage/dysfunction and coronary artery disease is well recognized. However, the effects of percutaneous coronary intervention (PCI) [stenting/angioplasty] on circulating markers of endothelial damage/dysfunction (eg, von Willebrand factor [vWF], soluble E-selectin [sEsel] levels, and more recently circulating endothelial cells [CECs]) has been less well defined. AIMS AND METHODS: We investigated the effects of both diagnostic coronary angiography (CA) [n = 15; blood sampling immediately before CA and 15 min after CA] and PCI (n = 38; blood sampling before PCI, 15 min after PCI, and 24 h after PCI) on levels of CECs, vWF, and sEsel across comparable patient groups. We also included a cohort of comparable healthy control subjects in order to compare baseline levels of three endothelial markers. RESULTS: There were no differences in baseline levels of CECs, vWF, or sEsel between the three study groups (healthy control subjects, CA, PCI; all p = not significant). Following CA (before to 15 min after), there were no significant changes in vWF and CECs (p = not significant). Following PCI, there were significant increases observed at 15 min after PCI and at 24 h after PCI (when compared with pre-PCI levels) in CECs (p = 0.0006), vWF (p = 0.007), and sEsel (p = 0.024). CONCLUSION: We observed significant increases in three endothelial markers (CECs, vWF, and sEsel) with elective PCI but not CA. This is in keeping with endothelial damage/dysfunction following PCI.
Authors: Zsolt Fejes; Zsolt Czimmerer; Tibor Szük; Szilárd Póliska; Attila Horváth; Enikő Balogh; Viktória Jeney; Judit Váradi; Ferenc Fenyvesi; György Balla; István Édes; József Balla; János Kappelmayer; Béla Nagy Journal: PLoS One Date: 2018-06-11 Impact factor: 3.240