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Biological effects of drug-eluting stents in the coronary circulation


Steffel, Jan; Tanner, Felix C (2007). Biological effects of drug-eluting stents in the coronary circulation. Herz, 32(4):268-273.

Abstract

Drug-eluting stents (DES) are designed to release pharmacological agents into the vessel wall in order to inhibit the response to injury causing restenosis, i.e., vascular smooth muscle cell migration and proliferation. Once deployed, however, these substances exert many biological effects in the coronary circulation; their action is indeed not confined to inhibition of vascular smooth muscle cells, but extends to other cell types such as endothelial cells. Both rapamycin and paclitaxel decrease endothelial cell migration and proliferation; moreover, they induce tissue factor expression through specific interaction with signal transduction mediators. As both effects would lead to an increased thrombogenic potential of DES, they appear particularly important in light of a possibly increased risk for stent thrombosis with DES as compared to bare-metal stents. This aspect is further highlighted by the observation that DES also decrease proliferation, differentiation, and homing of endothelial progenitor cells, which are believed to contribute to reendothelialization after stent implantation. Furthermore, both rapamycin and paclitaxel have been demonstrated to induce endothelial dysfunction in the coronary vasculature distal to the stent. Finally, the polymer used for DES may be associated with hypersensitivity reactions, which may, at least in some cases, favor stent thrombosis. This review will discuss the biological effects of DES in the coronary vasculature

Abstract

Drug-eluting stents (DES) are designed to release pharmacological agents into the vessel wall in order to inhibit the response to injury causing restenosis, i.e., vascular smooth muscle cell migration and proliferation. Once deployed, however, these substances exert many biological effects in the coronary circulation; their action is indeed not confined to inhibition of vascular smooth muscle cells, but extends to other cell types such as endothelial cells. Both rapamycin and paclitaxel decrease endothelial cell migration and proliferation; moreover, they induce tissue factor expression through specific interaction with signal transduction mediators. As both effects would lead to an increased thrombogenic potential of DES, they appear particularly important in light of a possibly increased risk for stent thrombosis with DES as compared to bare-metal stents. This aspect is further highlighted by the observation that DES also decrease proliferation, differentiation, and homing of endothelial progenitor cells, which are believed to contribute to reendothelialization after stent implantation. Furthermore, both rapamycin and paclitaxel have been demonstrated to induce endothelial dysfunction in the coronary vasculature distal to the stent. Finally, the polymer used for DES may be associated with hypersensitivity reactions, which may, at least in some cases, favor stent thrombosis. This review will discuss the biological effects of DES in the coronary vasculature

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:National licences > 142-005
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Health Sciences > Cardiology and Cardiovascular Medicine
Language:English
Date:1 June 2007
Deposited On:17 Dec 2018 16:45
Last Modified:31 Jul 2020 02:45
Publisher:Springer
ISSN:0340-9937
OA Status:Green
Publisher DOI:https://doi.org/10.1007/s00059-007-3000-5
Related URLs:https://www.swissbib.ch/Search/Results?lookfor=nationallicencespringer101007s0005900730005 (Library Catalogue)

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