4.6 Article

Six-Month Comparison of Coronary Endothelial Dysfunction Associated With Sirolimus-Eluting Stent Versus Paclitaxel-Eluting Stent

Journal

JACC-CARDIOVASCULAR INTERVENTIONS
Volume 1, Issue 1, Pages 65-71

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jcin.2007.11.002

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Objectives This study was designed to investigate whether endothelial dysfunction is related to drug-eluting stent (DES) implantation at 6 months after stenting. Background Current available DES could delay vessel healing and subsequently impair endothelial function. Methods Endothelial function was estimated at 6-month follow-up in 75 patients (31 men, mean age 62.1 years) with a DES (39 sirolimus-eluting stents [SES], 36 paclitaxel-eluting stents [PES]), and 10 patients with a bare-metal stent (BMS) to the left anterior descending artery, by incremental acetylcholine (Ach) infusion (20 mu g/min, 50 mu g/min, 100 mu g/min) and nitrate (200 mu g/min) into the left coronary ostium. Vascular responses were quantitatively measured in arterial segments 5 mm proximal and distal to DES and compared with corresponding segments in the BMS group and midsegments in the left circumflex artery as a reference nonstented artery. All antianginal agents were withheld for at least 72 h before coronary angiography. Results Greater vasoconstriction to Ach was observed in both the SES and PES groups than in the BMS group or control segments of left circumflex artery. Vasoconstriction to Ach was more prominent in arterial segments distal to stents in both SES and PES groups compared with those in the BMS group (p < 0.001). The degree of vasoconstriction to Ach was similar between the SES and PES groups. Endothelium-independent vasodilatation to nitrate did not differ significantly between the study groups. Conclusions Abnormal vasoconstriction to Ach was found in the SES and PES groups, especially in arterial segments distal to DES at 6 months after stenting, which suggests that DES has a potential long-term adverse effect on local coronary endothelial dysfunction. (J Am Coll Cardiol Intv 2008;1:65-71) 2008 by the American College of Cardiology Foundation

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