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Mechanisms of Very Late Bioresorbable Scaffold Thrombosis
Journal of the American College of Cardiology ( IF 24.0 ) Pub Date : 2017-11-01 , DOI: 10.1016/j.jacc.2017.09.014
Kyohei Yamaji , Yasushi Ueki , Geraud Souteyrand , Joost Daemen , Jens Wiebe , Holger Nef , Tom Adriaenssens , Joshua P. Loh , Benoit Lattuca , Joanna J. Wykrzykowska , Josep Gomez-Lara , Leo Timmers , Pascal Motreff , Petra Hoppmann , Mohamed Abdel-Wahab , Robert A. Byrne , Felix Meincke , Niklas Boeder , Benjamin Honton , Crochan J. O’Sullivan , Alfonso Ielasi , Nicolas Delarche , Günter Christ , Joe K.T. Lee , Michael Lee , Nicolas Amabile , Alexios Karagiannis , Stephan Windecker , Lorenz Räber

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).

中文翻译:

极晚期生物可吸收支架血栓形成的机制

背景 与金属依维莫司洗脱支架相比,生物可吸收支架(Absorb BVS 1.1,Abbott Vascular,Santa Clara,California)植入后极晚期支架血栓形成 (VLScT) 发生的频率更高。目的 本研究的目的是阐明通过光学相干断层扫描 (OCT) 评估的 VLScT 的潜在机制。方法 INVEST(极晚期生物可吸收支架血栓形成的独立 OCT 注册)注册是一个国际研究人员联盟,他们使用 OCT 检查 VLScT 患者。结果 2013 年 6 月至 2017 年 5 月期间,36 名患有 38 个病灶的 VLScT 患者在 19 个中心接受了 OCT。VLScT 发生在植入后的中位时间为 20 个月(四分位距:16 至 27 个月)。在 VLScT 时,83% 的患者接受阿司匹林单药治疗,17% 接受双联抗血小板治疗。VLScT 的潜在机制是(按降序排列)支架不连续 (42.1%)、贴壁不良 (18.4%)、新动脉粥样硬化 (18.4%)、扩张不足或支架回弹 (10.5%)、未覆盖的支柱 (5.3%) 和边缘相关疾病进展(2.6%)。不连续性(比值比 [OR]:110;95% 置信区间 [CI]:73.5 至 173;p < 0.001)、贴壁不良的支架(OR:17.0;95% CI:14.8 至 19.7;p < 0.001)和未覆盖的支架(OR:7.3;95% CI:6.2 至 8.8;p < 0.001)在血栓形成的支架区域比非血栓形成的支架区域更常见。在 16 名支架不连续的患者中,有 2 名在 VLScT 之前并发 OCT 提供了圆形并列支架支柱与最小组织覆盖的证据。结论 VLScT 的主要机制是支架不连续,这表明不利的再吸收相关过程,其次是贴壁不良和新生动脉粥样硬化。支架设计的修改和优化的植入是否可以降低 VLScT 的风险仍有待确定。(关于极晚期生物可吸收支架血栓形成的独立 OCT 注册 [INVEST];NCT03180931)。
更新日期:2017-11-01
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