Author + information
- Received July 12, 2017
- Accepted July 19, 2017
- Published online September 18, 2017.
- aDepartment of Cardiology, CHA Bundang Medical Center, CHA University School of Medicine, Seongnam-si, Gyeonggi-do, Korea
- bDepartment of Cardiology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea
- ↵∗Address for correspondence:
Dr. Won-Jang Kim, Department of Cardiology, CHA Bundang Medical Center, Department of Internal Medicine, CHA University School of Medicine, 59, Yatap-ro, Bundang-gu, Seongnam-si, Gyeonggi-do, 13496, Korea.
A 64-year-old man who underwent a successful 3.5 mm × 28 mm bioresorbable vascular scaffold (BVS) implantation on the mid left anterior descending artery for the treatment of stable angina presented with unstable angina 8 months later. Coronary angiography showed a critical in-scaffold restenosis with thrombolysis in myocardial infarction flow grade 2 (Figures 1A and 1B). Optical coherence tomography (Ilumien, St. Jude Medical, St. Paul, Minnesota) was performed to elucidate the mechanism of BVS failure. From the distal to mid portions of the BVS, the scaffolds were completely covered with neointima (Figures 1C and 1D). However, the proximal portion of the BVS had abundant neointima with a signal-poor region. At the minimal lumen area site, there was a large necrotic core with a fibrous cap thickness of <65 μm, suggesting the presence of thin-cap fibroatheroma (Figures 1E and 1F). An excellent angiographic result was obtained after implanting a zotarolimus-eluting stent (Resolute Onyx 4.0 × 18 mm, Medtronic Vascular, Minneapolis, Minnesota).
BVS eliminates permanent vessel caging and promotes late lumen enlargement. In addition, these scaffolds are supposed to promote plaque stabilization by providing a uniform homogeneous neointimal layer (1). Neoatherosclerosis, a time-dependent process, is an important mechanism for late or very late stent failure. Previous data suggested that thin-cap fibroatheroma–containing neointima and in-stent plaque rupture were identified within 2 years following the first-generation drug-eluting stent (DES) implantation and beyond 5 years after bare-metal stent placement (2). In this case, unstable intima was formed much earlier than in previously reported DES cases. Thus, even BVS implantations are not free from early and midterm effects of polymers and the toxic drugs associated with endothelial incompetence and proinflammatory action. Recent studies have reported a higher rate of target lesion failure after BVS implantation compared with the newer-generation DES (3,4). Longer-term follow-up studies are needed to clarify the incidence, time course, and clinical impact of neoatherosclerosis on late BVS failure.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received July 12, 2017.
- Accepted July 19, 2017.
- 2017 American College of Cardiology Foundation
- Nakazawa G.,
- Otsuka F.,
- Nakano M.,
- et al.
- Woudstra P.,
- Grundeken M.J.,
- Kraak R.P.,
- et al.
- Wykrzykowska J.J.,
- Kraak R.P.,
- Hofma S.H.,
- et al.