CORRESPONDENCE: LETTER TO THE EDITOR
The Effect of Drug-Eluting Stents on Collateral Coronary Flow
Carlo di Mario, MD, PhD, FACC* and
Konstantinos Dimopoulos, MSc, MD
* Clinical Cardiology, Royal Brompton Hospital and National Heart and Lung Institute, Imperial College, Sydney Street, SW3 6NP London, United Kingdom (Email: c.dimario{at}rbh.nthames.nhs.uk).
I read with great interest the article by Meier et al. (1) published in the previous issue of the Journal. The article seems to report another, previously unappreciated, adverse effect of the use of drug-eluting stents (DES): impairment of coronary collateral function. Despite the large study population and the elegant well-validated method of measurement of collateral flow (2), we remain very skeptical that this study truly proves its main conclusion.
After stent implantation, there is no stimulus for collateral development because the main factors promoting its growth (regional ischemia and the pressure gradient between poststenotic artery and other normal or prestenotic coronary arterial segments) are abolished. Conceptually, it is difficult to understand how an extremely small amount of antiproliferative/cytotoxic medication released downstream of the site of stent implantation can affect quiescent endothelial cells in collapsed vessels with no flow. The elution profile of the DES is so short that it is unconceivable to expect a persistent drug release months after implantation, when collateral neoformation may occur in response to severe restenosis.
A possible explanation for the difference observed and a suggestion for data reanalysis comes from a more careful observation of Figure 2: both groups seem to cluster at the bottom of the collateral flow index range, suggesting a non-normal distribution of the study population. Should a nonparametric test such as the Wilcoxon signed rank test for paired data be used, the results of the analysis could change.
The most likely reason for the high collateral flow index observed in some patients with bare-metal stents (BMS) is the presence of a more severe degree of restenosis in these patients. Even though a similar average percent diameter stenosis is reported on angiography, this is not sufficient to indicate an equivalent functional severity in the 2 populations. The typical pattern of in-stent restenosis after BMS implantation is diffuse proliferation, as opposed to focal restenosis in DES, often at the edges of the stent (3). If available, comparison of fractional flow reserve in the 2 groups at follow-up is a better marker of hemodynamic severity (4) and would greatly help to clarify the cause of the observed difference in collateral flow index.
Assuming that a "statistically significant" difference in collateral flow index between the BMS and the DES groups truly exists, this difference is unlikely to be clinically relevant. The collateral flow index was so low in the majority of patients regardless of the type of stent implanted, to be incompatible with myocardial viability in the territory of distribution of the stented artery should an acute occlusion, for instance a thrombosis, suddenly develop.
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References
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- Meier P, Zbinden R, Togni M, et al. Coronary collateral function long after drug-eluting stent implantation J Am Coll Cardiol 2007;49:15-20.[Abstract/Free Full Text]
- Vogel R, Zbinden R, Indermuhle A, Windecker S, Meier B, Seiler C. Collateral-flow measurements in humans by myocardial contrast echocardiography: validation of coronary pressure-derived collateral-flow assessment Eur Heart J 2006;27:157-165.[Abstract/Free Full Text]
- Colombo A, Orlic D, Stankovic G, et al. Preliminary observations regarding angiographic pattern of restenosis after rapamycin-eluting stent implantation Circulation 2003;107:2178-2180.[Abstract/Free Full Text]
- Pijls NH, Van Gelder B, Van der Voort P, et al. Fractional flow reserveA useful index to evaluate the influence of an epicardial coronary stenosis on myocardial blood flow. Circulation 1995;92:3183-3193.[Abstract/Free Full Text]
Related Article
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- Pascal Meier and Christian Seiler
J. Am. Coll. Cardiol. 2007 50: 561.
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