Sirolimus-eluting stents associated with paradoxic coronary vasoconstriction

Mario Togni, Stephan Windecker, Rosangela Cocchia, Peter Wenaweser, Stephane Cook, Michael Billinger, Bernhard Meier, Otto M Hess, Mario Togni, Stephan Windecker, Rosangela Cocchia, Peter Wenaweser, Stephane Cook, Michael Billinger, Bernhard Meier, Otto M Hess

Abstract

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.

Source: PubMed

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