Swiss Cardiovascular Center Bern, Department of Cardiology, Bern University Hospital, Bern, Switzerland; Division of Cardiology, Kokura Memorial Hospital, Kitakyushu, Japan.
Swiss Cardiovascular Center Bern, Department of Cardiology, Bern University Hospital, Bern, Switzerland.
J Am Coll Cardiol. 2017 Nov 7;70(19):2330-2344. doi: 10.1016/j.jacc.2017.09.014.
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.
The purpose of this study was to elucidate mechanisms underlying VLScT as assessed by optical coherence tomography (OCT).
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.
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.
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).
生物可吸收支架（雅培血管的 Absorb BVS 1.1）植入后发生非常晚期支架血栓（VLScT）的频率高于金属依维莫司洗脱支架。
本研究旨在通过光学相干断层扫描（OCT）阐明 VLScT 的发病机制。
INVEST（非常晚期生物可吸收支架血栓的独立 OCT 注册）注册研究是一个国际研究人员联盟，他们使用 OCT 检查了发生 VLScT 的患者。
2013 年 6 月至 2017 年 5 月，19 个中心的 36 名患者的 38 个病变发生了 VLScT。VLScT 发生在植入后中位数 20 个月（四分位距：16 至 27 个月）。VLScT 时，83%的患者接受阿司匹林单药治疗，17%的患者接受双联抗血小板治疗。VLScT 的发病机制依次为支架不连续（42.1%）、贴壁不良（18.4%）、新生动脉粥样硬化（18.4%）、支架扩张不全或回缩（10.5%）、裸支架（5.3%）和边缘相关病变进展（2.6%）。不连续（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）和裸支架（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 2 例支架不连续的患者中，VLScT 前的即时 OCT 检查提供了支架支架呈环形贴壁、组织覆盖最小的证据。
VLScT 的主要发病机制是支架不连续，这表明支架吸收相关过程不佳，其次是贴壁不良和新生动脉粥样硬化。目前尚不确定支架设计的改进和优化植入是否可以降低 VLScT 的风险。（非常晚期生物可吸收支架血栓的独立 OCT 注册 [INVEST]；NCT03180931）。
