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J Am Coll Cardiol, 2007; 50:560-561, doi:10.1016/j.jacc.2007.02.075 (Published online 23 July 2007).
© 2007 by the American College of Cardiology Foundation
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CORRESPONDENCE: LETTER TO THE EDITOR

Drug-Eluting Stent Implantation and Coronary Collateral Growth Attenuation: Is Drug the Only Culprit?

Marie-Claude Parent, MD and Stéphane Rinfret, MD, MSc, FRCPC*

* Centre-Hospitalier de l’Université de Montréal, Interventional Cardiology, 1560, Sherbrooke Street East, Montreal, Quebec H2L 4M1, Canada (Email: s.rinfret{at}umontreal.ca).


In a recent issue of the Journal, Meier et al. (1) presented the results of a physiological study designed to compare coronary flow index in patients after bare-metal stent (BMS) or drug-eluting stent (DES) implantation. They concluded that collateral function, 6 months after coronary stenting, with a DES is 30% to 40% lower compared with a BMS. The authors hypothesized that their findings might be related, in part, to the antiangiogenic properties of DES through an inhibition of endothelial growth factors and cytokines. Globally, reduced collateral formation may have a negative influence on ischemic burden, particularly in the event of acute thrombosis.

Although this study highlights a potentially new and important downside of DES utilization, its results must be carefully analyzed and interpreted in a broader clinical context. In fact, the patient population selected in the DES group had a remarkably high degree of restenosis after 6 months, as evidenced by coronary angiographic data, showing an average of 45% in-stent diameter stenosis in the 2 matched groups. Such a high level of restenosis 6 months after DES implantation is rarely observed in clinical practice. Therefore, it can be hypothesized that by matching BMS and DES patients for in-stent stenosis severity, Meier et al. (1) have inadvertently selected a subpopulation of DES patients more prone to restenosis. Therefore, it seems that these patients exhibited resistance to the antiproliferative and immunosuppressive drugs released by DES. Consequently, it is plausible that this subpopulation expresses various biological factors that may also reduce the ability to generate collateral vessels. Hence, it may be premature to consider DES as the leading factor contributing to reduced collateral formation, until a study using widely patent DES and BMS confirms this.


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  1. Meier P, Zbinden R, Togni M, et al. Coronary collateral function long after drug-eluting stent implantation J Am Coll Cardiol 2007;49:15-21.[Abstract/Free Full Text]

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Pascal Meier and Christian Seiler
J. Am. Coll. Cardiol. 2007 50: 561. [Full Text] [PDF]




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