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Circulation. 2004;110:3430-3434
Published online before print November 22, 2004, doi: 10.1161/01.CIR.0000148371.53174.05
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(Circulation. 2004;110:3430-3434.)
© 2004 American Heart Association, Inc.


Coronary Heart Disease

Nonuniform Strut Distribution Correlates With More Neointimal Hyperplasia After Sirolimus-Eluting Stent Implantation

Hideo Takebayashi, MD; Gary S. Mintz, MD; Stéphane G. Carlier, MD, PhD; Yoshio Kobayashi, MD; Kenichi Fujii, MD; Takenori Yasuda, MD; Ricardo A. Costa, MD; Issam Moussa, MD; George D. Dangas, MD, PhD; Roxana Mehran, MD; Alexandra J. Lansky, MD; Edward Kreps, MD; Michael B. Collins, MD; Antonio Colombo, MD; Gregg W. Stone, MD; Martin B. Leon, MD; Jeffrey W. Moses, MD

From the Cardiovascular Research Foundation, Lenox Hill Heart and Vascular Institute, New York, NY.

Correspondence to Stéphane G. Carlier, MD, PhD, Cardiovascular Research Foundation, 55 E 59th St, 5th Floor, New York, NY 10022. E-mail scarlier{at}crf.org

Received June 2, 2004; revision received July 28, 2004; accepted September 9, 2004.

Background— Little is known about causes of intimal hyperplasia (IH) after sirolimus-eluting stent (SES) implantation.

Methods and Results— Intravascular ultrasound was performed in 24 lesions with intra-SES restenosis and a comparison group of 25 nonrestenotic SESs. To assess stent strut distribution, the maximum interstrut angle was measured with a protractor centered on the stent, and the visible struts were counted and normalized for the number of stent cells. In SES restenosis patients, minimum lumen site was compared with image slices 2.5, 5.0, 7.5, and 10.0 mm proximal and distal to this site. The minimum lumen site had a smaller IVUS lumen area at follow-up (2.7±0.9 versus 6.2±1.9 mm2; P<0.01), larger maximum interstrut angle (135±39° versus 72±23°; P<0.01), larger IH area (3.4±1.5 versus 0.6±1.1 mm2; P<0.01) and thickness (0.7±0.3 versus 0.1±0.2 mm; P<0.01) at maximum interstrut angle, and fewer stent struts (4.9±1.0 versus 6.0±0.5; P<0.01) even when normalized for the number of stent cells (0.78±0.15 versus 0.97±0.07; P<0.01). Compared with nonrestenotic SES, the restenosis lesions also had a smaller minimal lumen area, larger IH area, thicker IH at maximum interstrut angle, fewer stent struts, and larger maximum interstrut angle. Multivariate analysis identified the number of visualized stent struts normalized for the number of stent cells and maximum interstrut angle as the only independent IVUS predictor of IH cross-sectional area (P<0.01 and P<0.01), minimum lumen area (P<0.01 and P<0.01), and IH thickness (P<0.01 and P<0.01).

Conclusions— The number and distribution of stent struts affect the amount of neointima after SES implantation.


Key Words: restenosis • stents • ultrasonics




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