Author + information
- Received October 28, 2014
- Revision received November 12, 2014
- Accepted November 19, 2014
- Published online April 20, 2015.
- Andrea Mangiameli, MD∗,
- Yohei Ohno, MD∗,
- Guilherme F. Attizzani, MD∗,†,
- Davide Capodanno, MD, PhD∗∗ ( and )
- Corrado Tamburino, MD, PhD∗,‡
- ∗Department of Cardiology, Ferrarotto Hospital, University of Catania, Catania, Italy
- †Harrington Heart and Vascular Institute, University Hospitals, Case Medical Center, Cleveland, Ohio
- ‡Excellence Through Newest Advances Foundation, Catania, Italy
- ↵∗Reprint requests and correspondence:
Dr. Davide Capodanno, Cardio-thoraco-vascular Department, Ferrarotto Hospital, University of Catania, Via Citelli 6, Catania 95124, Italy.
A 48-year-old man who underwent uneventful 3.0 × 28 mm bioresorbable vascular scaffold (BVS) implantation on the mid left anterior descending coronary artery for stable angina, presented 15 months later with unstable angina. Coronary angiography showed a critical in-scaffold restenosis with Thrombolysis In Myocardial Infarction flow grade 2 (Figures 1A and 1B). Optical coherence tomography assessment (Ilumien, St. Jude Medical, St. Paul, Minnesota) was performed to elucidate the mechanism of BVS failure, which revealed heterogeneous tissue coverage within the scaffold (Figure 1C, cross sections D to G), as follows: 1) neointimal rupture with mural white thrombus at the rupture site (Figures 1D and 1E); 2) a low signal-intensity scaffold coverage pattern with dorsal attenuation and marked shadowing of the scaffold struts (Figures 1E and 1F); and 3) a normal pattern of neointimal hyperplasia (i.e., high signal intensity) (Figure 1G). The minimal lumen area was 1.3 mm2. An excellent angiographic result was obtained after plain old balloon angioplasty and abciximab infusion.
Metallic stents fail to fully protect the vessel from late plaque progression or neoatherosclerosis. BVS eliminate permanent vessel caging and promote late lumen enlargement; in addition, they are supposed to promote plaque stability and passivation of vulnerable plaques by providing a uniform homogeneous neointimal layer (1). However, BVS have not eliminated the early- and mid-term presence of polymer and antiproliferative drugs, both previously associated with a pro-inflammatory milieu. The time course of neoatherosclerosis in the present case (i.e., 15 months after the index procedure) resembles that of metallic drug-eluting stents (2). Although it might be a rare event, neoatherosclerosis could be considered a potential cause of late failure even with BVS. Replication of this finding in BVS populations is warranted to determine the incidence and the potential long-term clinical implications of neoatherosclerosis in this setting.
Dr. Attizzani has received consulting fees from St. Jude Medical. Dr. Tamburino has received speaker’s honoraria from Abbott Vascular. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received October 28, 2014.
- Revision received November 12, 2014.
- Accepted November 19, 2014.
- American College of Cardiology Foundation