Scaffold discontinuity, malapposition and neoatherosclerosis were found to be the leading mechanisms behind very late scaffold thrombosis (VLScT) in cardiac patients implanted with bioresorbable devices, investigators from the INVEST registry have reported.
VLScT is more common in patients whose heart stent is bioresorbable rather than a conventional metallic everolimus-eluting stent, first author Kyohei Yamaji, MD, PhD, and colleagues wrote in a new study published in the Journal of the American College of Cardiology. While fully bioresorbable vascular scaffolds (BVS) were first introduced to the market to circumvent risks like restenosis and thrombosis, recent studies of long-term results—especially those of Abbott Vascular’s Absorb BVS—have suggested bioresorbable devices can actually increase a patient’s risk of stent thrombosis.
The AIDA trial, which compared the BVS with metallic drug-eluting stents in an all-comer population, showed a higher risk of target-vessel myocardial infarction and early, late and very late device thrombosis an average of two years after implantation, Yamaji et al. explained, and though clinicians have a good understanding of what causes early scaffold thrombosis, the underlying mechanisms of very late thrombosis are unclear.
“As a result, the translation of mechanistic insights into modifications of the implantation procedure or device iterations to address specific components in scaffold design, polymer composition and degradation is lacking,” the authors wrote. “VLScT is a clinical manifestation of particular concern because it is responsible for a considerable proportion of device-related myocardial infarctions and could impact the need for extended-duration dual-antiplatelet therapy.”
Yamaji and co-authors studied 36 VLScT patients with 38 lesions between June 2013 and May 2017. The patients underwent optical coherence tomography (OCT) before emergency percutaneous coronary intervention at 19 medical centers across Europe and Asia. OCT has become a field favorite for the investigation of coronary device failures due to its high spatial resolution abilities.
In the study group, VLScT occurred an average of 20 months after BVS implantation. As an immediate treatment, 83 percent of patients received aspirin monotherapy, while 17 percent received dual-antiplatelet therapy.
The researchers found the greatest underlying mechanism of VLScT in these patients was scaffold discontinuity, which suggests an unfavorable resorption-related process, according to the paper. Just over 42 percent of the cohort experienced discontinuity, while 18.4 percent had malapposition and 18.4 percent developed neoatherosclerosis. Less evident markers included underexpansion or scaffold recoil, uncovered struts and edge-related disease progression.
“The data presented by Yamaji et al. are extremely valuable because they remind us that it is hard to make improvements in anything without first understanding in detail its shortcomings,” Renu Virmani, MD, and co-authors wrote in a JACC editorial accompanying the study. “Although it is likely some of the increased risk of ST after Absorb implantation can be mitigated by post-implant techniques to decrease the frequency of malapposition and perhaps by a longer duration of dual antiplatelet therapy, it is also likely that the residual risks of increased thrombotic events remain.”
Virmani and colleagues said the next steps likely include re-engineering the scaffold entirely.
“Although potential long-term benefits, such as resuming native coronary vasomotion, seem attractive, they remain unproven and thus the fate of BVS remains at the current moment uncertain,” they wrote.