At the crossroads of BRS development: food for thought
What determines long-term outcomes using fully bioresorbable scaffolds - the device, the operator or the lesion?
It is clear that we have reached a crossroads with the new technology which we call the "fully bioresorbable scaffold". Today, the community is somewhat insecure about the future of this new technology which is currently still in its early iterations.
Surely, in the near future, this technology will be improved; however, at present, the interventional community is wondering whether the device, the operator or the lesion is the key determinant of the long-term outcome in the use of this technology.
Stephan Windecker and colleagues have written an exceptional editorial, taking into account these three components - device, operator, lesion - and have consequently opened up new intellectual and clinical avenues for us to explore, providing the entire interventional community with "food for thought".
I cannot recommend highly enough that you take the time to read this remarkable editorial and the three associated papers by A. Tanaka, A. Colombo, et al; M. Ohya, T. Kimura, et al and Y. Sotomi, Y. Onuma, et al:
- Clinical outcomes of a real-world cohort following bioresorbable vascular scaffold implantation utilising an optimised implantation strategy. A. Tanaka, A. Colombo, et al.
- Impact of lesion calcification on angiographic outcomes after Absorb everolimus-eluting bioresorbable vascular scaffold implantation: an observation from the ABSORB Japan trial. M. Ohya, T. Kimura, et al.
- Possible mechanical causes of scaffold thrombosis: insights from case reports with intracoronary imaging. Y. Sotomi, Y. Onuma, et al.
Figure 1. Representative examples of scaffold thrombosis underlying mechanisms explored by optical coherence tomography. In acute and subacute ScT, strut malapposition (A), incomplete lesion coverage (B, possible ruptured plaque [white arrow], uncovered thrombu s [white asterisk]), and underdeployment (C) were the leading mechanical causes, followed by acute disruption (D) and overlap (E). In la te and very late ScT, malapposition (A), late discontinuity (F, white arrowhead), and peri-strut low-intensity area (G) were the leading fe atures, followed by uncovered struts (H) and neoatherosclerosis (I), mural thrombus (red asterisk) with highly attenuating area (white asterisk) . Panel B reprinted with permission from Wolters Kluwer Health, Inc., Copyright (2015)14. Panel F reprinted with permission from Elsevier, Copyright (2015)18. Panel I reprinted with permission from Elsevier, Copyright (2015)44.