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J Am Coll Cardiol, 2005; 46:231-236, doi:10.1016/j.jacc.2005.01.062
(Published online 5 July 2005). © 2005 by the American College of Cardiology Foundation |
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Swiss Cardiovascular Center Bern, Bern, Switzerland
Manuscript received October 11, 2004; revised manuscript received December 27, 2004, accepted January 11, 2005.
* Reprint requests and correspondence: Dr. Otto M. Hess, Professor of Cardiology, Swiss Cardiovascular Center, Inselspital, CH-3010 Bern, Switzerland (Email: otto.hess{at}insel.ch).
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.
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