Author + information
- Received July 28, 2015
- Accepted August 1, 2015
- Published online January 25, 2016.
- Akihito Tanaka, MD∗,†,
- Neil Ruparelia, MBBS, DPhil∗,†,‡,
- Hiroyoshi Kawamoto, MD∗,†,
- Azeem Latib, MD∗,† and
- Antonio Colombo, MD∗,†∗ ()
- ∗Interventional Cardiology Unit, EMO-GVM Centro Cuore Columbus, Milan, Italy
- †Interventional Cardiology Unit, San Raffaele Scientific Institute, Milan, Italy
- ‡Department of Cardiology, Imperial College, London, United Kingdom
- ↵∗Reprint requests and correspondence:
Dr. Antonio Colombo, EMO-GVM Centro Cuore Columbus, 48 Via M. Buonarroti, 20145 Milan, Italy.
A 78-year-old man underwent percutaneous coronary intervention with implantation of a 2.5 × 28-mm Absorb bioresorbable scaffold (BRS) (Abbott Vascular, Santa Clara, California) in the mid-left anterior descending coronary artery, and treatment with a drug-coated balloon for recurrent metallic stent restenosis in the proximal segment (Figures 1A and 1B) (1).
Follow-up angiography at 7 months demonstrated no restenosis at the BRS site (Figure 1C). After 34 months, the patient returned with a recurrence of angina and underwent angiography, which demonstrated restenosis at the BRS site as well as recurrent metallic stent restenosis (Figure 1D). Intravascular ultrasound was performed at baseline, showing some residual scaffold struts. Although the vessel area was similar to that at the index procedure, the minimal lumen area was 1.73 mm2 with a lumen loss of 3.68 mm2, likely caused by simultaneous external compression (1.97 mm2) and intrascaffold tissue growth (1.71 mm2) (Figure 2).
By virtue of its bioresorption, the Absorb BRS begins to lose its radial strength approximately 6 months after implantation, and completely loses it by 12 months (2,3). Taking these processes into account, the mechanisms of BRS restenosis may be different to those in the setting of metallic stents, especially restenosis occurring in the very late phase.
On the basis of reports describing BRS restenosis (3,4), in the short-term, scaffold restenosis seems to be a result of intrascaffold tissue growth similar to that seen with metallic stents, and would be reasonable because the scaffold still maintains some degree of its radial strength during the period. On the other hand, little data are available regarding scaffold restenosis occurring in the very late phase. Although a case series suggested very late restenosis could be also attributed to intrascaffold tissue growth (3), data remain sparse.
In our case, very late restenosis appeared to be a result of the simultaneous external compression of the scaffold and intrascaffold tissue growth. This may suggest another potential mechanism of very late scaffold restenosis with progression of plaque behind incompletely resorbed scaffold struts.
Dr. Latib serves on the advisory board for Medtronic; and receives honoraria from Boston Scientific and Abbott Vascular. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received July 28, 2015.
- Accepted August 1, 2015.
- American College of Cardiology Foundation
- Onuma Y.,
- Serruys P.W.,
- Muramatsu T.,
- et al.