Kyohei Yamaji1, Yasushi Ueki2, Geraud Souteyrand3, Joost Daemen4, Jens Wiebe5, Holger Nef6, Tom Adriaenssens7, Joshua P Loh8, Benoit Lattuca9, Joanna J Wykrzykowska10, Josep Gomez-Lara11, Leo Timmers12, Pascal Motreff3, Petra Hoppmann13, Mohamed Abdel-Wahab14, Robert A Byrne5, Felix Meincke15, Niklas Boeder6, Benjamin Honton16, Crochan J O'Sullivan17, Alfonso Ielasi18, Nicolas Delarche19, Günter Christ20, Joe K T Lee21, Michael Lee22, Nicolas Amabile23, Alexios Karagiannis24, Stephan Windecker2, Lorenz Räber25. 1. Swiss Cardiovascular Center Bern, Department of Cardiology, Bern University Hospital, Bern, Switzerland; Division of Cardiology, Kokura Memorial Hospital, Kitakyushu, Japan. 2. Swiss Cardiovascular Center Bern, Department of Cardiology, Bern University Hospital, Bern, Switzerland. 3. Department of Cardiology, University Hospital of Clermont-Ferrand, CHU Clermont-Ferrand, Clermont-Ferrand, France. 4. Department of Cardiology, Thoraxcenter, Erasmus Medical Center, Rotterdam, the Netherlands. 5. Deutsches Herzzentrum München, Technische Universität München, Munich, Germany. 6. Department of Cardiology, University of Giessen, Giessen, Germany. 7. Department of Cardiovascular Medicine, University Hospitals Leuven, Leuven, Belgium, and Department of Cardiovascular Sciences, Catholic University Leuven, Belgium. 8. Department of Cardiology, National University Heart Centre, Singapore. 9. Department of Cardiology, University Hospital Caremeau, Nimes, France. 10. Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands. 11. Hospital Universitari de Bellvitge, Institut d' Investigació Biomèdica de Bellvitge, Universitat de Barcelona, L' Hospitalet de Llobregat, Barcelona, Spain. 12. Department of Cardiology, University Medical Center Utrecht, Utrecht, the Netherlands. 13. Klinik und Poliklinik Innere Medizin I, Klinikum rechts der Isar, Technische Universität München, Munich, Germany. 14. Heart Center, Segeberger Kliniken GmbH, Bad Segeberg, Germany. 15. Department of Cardiology, Asklepios Klinik St. Georg, Hamburg, Germany. 16. Department of Interventional Cardiology, Clinique Pasteur, Toulouse, France. 17. Department of Cardiology, Stadtspital Triemli, Zurich, Switzerland. 18. Cardiology Division, ASST Bergamo Est, Bolognini Hospital, Seriate (BG), Italy. 19. Department of Cardiology, CH F Mitterand, Pau Université Cedex, Pau, France. 20. 5th Medical Department with Cardiology, Kaiser Franz Josef Hospital, Vienna, Austria. 21. Swiss Cardiovascular Center Bern, Department of Cardiology, Bern University Hospital, Bern, Switzerland; Cardiology Division, Department of Medicine, Pamela Youde Nethersole Eastern Hospital, Chai Wan, Hong Kong. 22. Cardiology Division, Department of Medicine, Queen Elizabeth Hospital, Kowloon, Hong Kong. 23. Cardiology Department, Institut Mutualiste Montsouris, Paris, France. 24. CTU Bern, and Institute of Social and Preventive Medicine (ISPM), University of Bern, Bern, Switzerland. 25. Swiss Cardiovascular Center Bern, Department of Cardiology, Bern University Hospital, Bern, Switzerland. Electronic address: lorenz.raeber@insel.ch.
Abstract
BACKGROUND: Very late scaffold thrombosis (VLScT) occurs more frequently after bioresorbable scaffold (Absorb BVS 1.1, Abbott Vascular, Santa Clara, California) implantation than with metallic everolimus-eluting stents. OBJECTIVES: The purpose of this study was to elucidate mechanisms underlying VLScT as assessed by optical coherence tomography (OCT). METHODS: The INVEST (Independent OCT Registry on Very Late Bioresorbable Scaffold Thrombosis) registry is an international consortium of investigators who used OCT to examine patients with VLScT. RESULTS: Between June 2013 and May 2017, 36 patients with 38 lesions who had VLScT underwent OCT at 19 centers. VLScT occurred at a median of 20 months (interquartile range: 16 to 27 months) after implantation. At the time of VLScT, 83% of patients received aspirin monotherapy and 17% received dual-antiplatelet therapy. The mechanisms underlying VLScT were (in descending order) scaffold discontinuity (42.1%), malapposition (18.4%), neoatherosclerosis (18.4%), underexpansion or scaffold recoil (10.5%), uncovered struts (5.3%), and edge-related disease progression (2.6%). Discontinuity (odds ratio [OR]: 110; 95% confidence interval [CI]: 73.5 to 173; p < 0.001), malapposed struts (OR: 17.0; 95% CI: 14.8 to 19.7; p < 0.001), and uncovered struts (OR: 7.3; 95% CI: 6.2 to 8.8; p < 0.001) were more frequent in the thrombosed than the nonthrombosed scaffold regions. In 2 of 16 patients with scaffold discontinuity, intercurrent OCT before VLScT provided evidence of circularly apposed scaffold struts with minimal tissue coverage. CONCLUSIONS: The leading mechanism underlying VLScT was scaffold discontinuity, which suggests an unfavorable resorption-related process, followed by malapposition and neoatherosclerosis. It remains to be determined whether modifications in scaffold design and optimized implantation can mitigate the risk of VLScT. (Independent OCT Registry on Very Late Bioresorbable Scaffold Thrombosis [INVEST]; NCT03180931).
BACKGROUND: Very late scaffold thrombosis (VLScT) occurs more frequently after bioresorbable scaffold (Absorb BVS 1.1, Abbott Vascular, Santa Clara, California) implantation than with metallic everolimus-eluting stents. OBJECTIVES: The purpose of this study was to elucidate mechanisms underlying VLScT as assessed by optical coherence tomography (OCT). METHODS: The INVEST (Independent OCT Registry on Very Late Bioresorbable Scaffold Thrombosis) registry is an international consortium of investigators who used OCT to examine patients with VLScT. RESULTS: Between June 2013 and May 2017, 36 patients with 38 lesions who had VLScT underwent OCT at 19 centers. VLScT occurred at a median of 20 months (interquartile range: 16 to 27 months) after implantation. At the time of VLScT, 83% of patients received aspirin monotherapy and 17% received dual-antiplatelet therapy. The mechanisms underlying VLScT were (in descending order) scaffold discontinuity (42.1%), malapposition (18.4%), neoatherosclerosis (18.4%), underexpansion or scaffold recoil (10.5%), uncovered struts (5.3%), and edge-related disease progression (2.6%). Discontinuity (odds ratio [OR]: 110; 95% confidence interval [CI]: 73.5 to 173; p < 0.001), malapposed struts (OR: 17.0; 95% CI: 14.8 to 19.7; p < 0.001), and uncovered struts (OR: 7.3; 95% CI: 6.2 to 8.8; p < 0.001) were more frequent in the thrombosed than the nonthrombosed scaffold regions. In 2 of 16 patients with scaffold discontinuity, intercurrent OCT before VLScT provided evidence of circularly apposed scaffold struts with minimal tissue coverage. CONCLUSIONS: The leading mechanism underlying VLScT was scaffold discontinuity, which suggests an unfavorable resorption-related process, followed by malapposition and neoatherosclerosis. It remains to be determined whether modifications in scaffold design and optimized implantation can mitigate the risk of VLScT. (Independent OCT Registry on Very Late Bioresorbable Scaffold Thrombosis [INVEST]; NCT03180931).
Authors: Yanping Cheng; Marco Ferrone; Qing Wang; Laura E L Perkins; Jennifer McGregor; Björn Redfors; Zhipeng Zhou; Richard Rapoza; Gerard B Conditt; Aloke Finn; Renu Virmani; Grzegorz L Kaluza; Juan F Granada Journal: JACC Basic Transl Sci Date: 2020-06-03