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Issue title: Selected papers of the 38th Conference of the German Society for Clinical Microcirculation and Hemorheology, 21-23 November 2019, Braunschweig, Germany
Guest editors: P. Wiggermann, A. Krüger-Genge and F. Jung
Article type: Research Article
Authors: Ullrich, Helena; b | Gori, Tommasoa; b; *
Affiliations: [a] Zentrum für Kardiologie, Kardiologie I, Universitätsmedizin Mainz, Johannes Gutenberg- University Mainz, Germany | [b] Deutsches Zentrum für Herz-Kreislauferkrankungen (DZHK), Standort Rhein-Main, Partnereinrichtung Mainz, Germany
Correspondence: [*] Corresponding author: Tommaso Gori, Zentrum für Kardiologie, Kardiologie I, Universitätsmedizin Mainz, Johannes Gutenberg-Universität Mainz, Langenbeckstraße 1, 55131 Mainz, Germany. E-mail: tommaso.gori@unimedizin-mainz.de.
Abstract: Percutaneous coronary intervention is the most often used method for coronary revascularization. Stenting restores blood perfusion to ischemic areas, but it also causes mechanical disruption of the atheromatous plaque and the nearby endothelium, stimulating the activation of platelets. In a similar way, platelets are activated by thrombin exposure in the setting of plaque rupture. The interaction between platelets, oxidative stress and inflammation is an important factor determining the extent and severity of vascular dysfunction observed in these settings. Platelets activated by the vessel trauma release inflammatory and mitogenic mediators into the vascular microenvironment, activating leukocyte chemotaxis and switching the endothelial phenotypefrom a quiescent to an activate one. The increased bioavailability of reactive oxygen species from the vessel wall, from leukocytes and from platelets, and the subsequent decreased bioavailability of nitric oxide, further stimulates platelets, which are otherwise inhibited by this endothelial mediator. Thus, inflammation, oxidative stress and platelet activation cooperate in a feed-forward mechanism leading to vascular dysfunction and possibly compromising the effect of stenting. Inhibitors of platelet function have thus important ancillary effects beyond their antithrombotic ones, which will be discussed in the present short review.
Keywords: Endothelium, thrombosis, acute coronary syndromes, stent
DOI: 10.3233/CH-199214
Journal: Clinical Hemorheology and Microcirculation, vol. 73, no. 1, pp. 29-34, 2019
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