Atherosclerotic plaque behind the stent changes after bare-metal and drug-eluting stent implantation in humans: Implications for late stent failure?
Name
nihms806345.pdf
Size
571.59 KB
Format
Adobe PDF
Checksum (MD5)
e20a5ff02d7a8ba8e13f8dd8e8039861
Author(s)
Takahashi, Saeko
Tsuda, Masaya
Shishido, Koki
Mizuno, Shingo
Coskun, Ahmet U.
Saito, Shigeru
Feldman, Charles L.
Stone, Peter H.
Andreou, Ioannis
Antoniadis, Antonios
Date Issued
July 2016
Journal
Atherosclerosis
Publisher
Elsevier
Citation
Andreou, Ioannis et al. “Atherosclerotic Plaque Behind the Stent Changes after Bare-Metal and Drug-Eluting Stent Implantation in Humans: Implications for Late Stent Failure?” Atherosclerosis 252 (September 2016): 9–14 © 2016 Elsevier Ireland Ltd
Version
Author's final manuscript
Abstract
Background and aims The natural history and the role of atherosclerotic plaque located behind the stent (PBS) are still poorly understood. We evaluated the serial changes in PBS following bare-metal (BMS) compared to first-generation drug-eluting stent (DES) implantation and the impact of these changes on in-stent neointimal hyperplasia (NIH). Methods Three-dimensional coronary reconstruction by angiography and intravascular ultrasound was performed after intervention and at 6–10-month follow-up in 157 patients with 188 lesions treated with BMS (n = 89) and DES (n = 99). Results There was a significant decrease in PBS area (−7.2%; p < 0.001) and vessel area (−1.7%; p < 0.001) after BMS and a respective increase in both areas after DES implantation (6.1%; p < 0.001 and 4.1%; p < 0.001, respectively). The decrease in PBS area significantly predicted neointimal area at follow-up after BMS (β: 0.15; 95% confidence interval [CI]: 0.10–0.20, p < 0.001) and DES (β: 0.09; 95% CI: 0.07–0.11; p < 0.001) implantation. The decrease in PBS area was the most powerful predictor of significant NIH after BMS implantation (odds ratio: 1.13; 95% CI: 1.02–1.26; p = 0.02). Conclusions The decrease in PBS area after stent implantation is significantly associated with the magnitude of NIH development at follow-up. This finding raises the possibility of a communication between the lesion within the stent and the underlying native atherosclerotic plaque, and may have important implications regarding the pathobiology of in-stent restenosis and late/very late stent thrombosis.
MIT Department
Massachusetts Institute of Technology. Institute for Medical Engineering & Science
Terms of Use
Creative Commons Attribution-NonCommercial-NoDerivs License
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1016/J.ATHEROSCLEROSIS.2016.07.914
