Effects of stent coating on platelets and endothelial cells after intracoronary stent implantation
Open Access
- 1 February 2001
- journal article
- clinical trial
- Published by Wiley in Clinical Cardiology
- Vol. 24 (2), 159-164
- https://doi.org/10.1002/clc.4960240211
Abstract
Background: Adhesion molecules are known to be important in the regulation of endothelial cell and platelet functions. Increased platelets P‐selectin expression is a marker of stent thrombosis after uncoated stent placement. Hypothesis: The aim of this study was to compare the effects of intracoronary placement of phosphorylcholine (PC)‐coated, versus heparin‐coated, versus uncoated stents on platelets and endothelial activity. Methods: Thirty patients (age 55 ± 10, 27 men) with significant proximal left anterior descending coronary artery stenoses were randomized to elective implantation of PC‐coated. versus heparin‐coated. versus uncoated stents. Following stent placement, intravenous heparin and aspirin plus ticlopidine were administered. Venous plasma soluble E‐selectin, sP‐sclectin, and intercellular adhesion molecule‐1 levels were measured before the procedure and 24 and 48 h thereafter as markers of platelet and endothelial cell activation. Patients were excluded if they had a disease known to influence platelet and endothelial cell function. Results: Plasma sP‐selectin levels decreased significantly after implantation of PC‐ and heparin‐coated stents (p = 0.04), hut remained unchanged in patients randomized to uncoated stents. Plasma sE‐selectin levels increased significantly after uncoated stent placement (p = 0.04) and remained unchanged after coated stent implantation. Conclusion: In patients treated with combined antiplatelet therapy, implantation of PC‐ and heparin‐coated stents decreased platelet activity without activating endothelial cells, whereas placement of uncoated stents led to endothelial activation without changing platelet activity. These results suggest that PC‐coated and heparin‐coated stents may be advantageous in limiting thrombotic complications.Keywords
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