4.7 Article

Sirolimus-eluting stents associated with paradoxic coronary vasoconstriction

Journal

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Volume 46, Issue 2, Pages 231-236

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacc.2005.01.062

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OBJECTIVES The purpose of the present study was to assess coronary vasomotor response to exercise after sirolimus-eluting stent (SES) implantation. BACKGROUND Sirolimus-eluting stents have been shown to markedly reduce the incidence of angiographic and clinical restenosis. However, long-term effects of sirolimus on endothelial function are unknown. METHODS Coronary vasomotion was evaluated with biplane quantitative coronary angiography at rest and during supine bicycle exercise in 25 patients with coronary artery disease. Eleven patients were treated with a bare-metal stent (BMS) (control group) and 14 patients underwent SES implantation (sirolimus group) for de novo coronary artery lesions. Both groups were studied 6 +/- 1 month after the intervention. Minimal luminal diameter; stent diameter; and proximal, distal, and reference vessel diameter were determined. RESULTS The reference vessel showed exercise-induced vasodilation (+13 +/- 4%) in both groups. Vasomotion within the stented vessel segments was abolished. In controls, the adjacent segments proximal and distal to the stent showed exercise-induced vasodilation (+ 15 +/- 3% and + 17 +/- 4%, respectively). In contrast, there was exercise-induced vasoconstriction of the proximal and distal vessel segments adjacent to SESs (-12 +/- 4% and -15 +/- 6%, respectively; p < 0.001 vs. corresponding segments of controls). Sublingual nitroglycerin was associated with maximal vasodilation of the proximal and distal vessel segments in both groups. CONCLUSIONS Implantation of a BMS does not affect physiologic response to exercise proximal and distal to the stent. However, SESs are associated with exercise-induced paradoxic coronary vasoconstriction of the adjacent vessel segments, although vasodilatory response to nitroglycerin is maintained. These observations suggest (drug-induced) endothelial dysfunction as the underlying mechanism. (c) 2005 by the American College of Cardiology Foundation.

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