4.5 Article

Impaired endothelial vasomotor function after sirolimus-eluting stent implantation

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CIRCULATION JOURNAL
卷 71, 期 2, 页码 220-225

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JAPANESE CIRCULATION SOCIETY
DOI: 10.1253/circj.71.220

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acetylcholine; endothelial vasomotor function; endothelium; sirolimus-eluting stent

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Background Sirolimus inhibits endothelial cell proliferation in vitro, but although the sirolimus-eluting stent (SES) is widely used because of the very low rates of in-stent restenosis, the influence of SES on coronary endothelial vasomotor function in humans is not well known. Methods and Results The present study included 21 patients treated with SES, and 12 patients treated with conventional bare metal stent (BMS). Endothelium-dependent vasomotor function was evaluated 6 months after stent implantation, using intracoronary acetylcholine infusion. Changes in diameter at the 5-mm proximal and distal edges of the stent, and at the control segment were assessed by quantitative coronary angiography. To evaluate native endothelial function, an intracoronary acetylcholine test was performed before stenting. In the 21 SES patients acetylcholine infusion at 10(-8) mol/L and 10(-7) mol/L produced significant vasoconstriction in the proximal stent segment (-11.3 +/- 10.3%, and -14.1 +/- 11.3%, respectively) and the distal stent segment (-13.7 +/- 9.3%, and -17.5 +/- 12.5%, respectively). In contrast, in the 12 BMS patients, acetylcholine infusion at the same concentrations did not produce a vasoconstrictive response in the proximal stent segment (5.0 +/- 8.2% and 4.9 +/- 9.1%, respectively) or the distal stent segment (4.2 +/- 7.6% and 5.1 +/- 7.7%, respectively). Intracoronary nitroglycerin induced a similar grade of vasodilation in the peri-stent area in both groups. Local endothelial function before SES implantation showed no vasoconstrictive response. Conclusions In contrast to vasodilation in BMS patients, SES implantation in the peri-stent area resulted in a vasoconstrictive response to acetylcholine. SES implantation may impair endothelial function in humans.

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