Division of Cardiology, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, Japan.
J Cardiol. 2011 Sep;58(2):84-91. doi: 10.1016/j.jjcc.2011.07.004. Epub 2011 Aug 11.
Although, the first-generation drug eluting stents (DES) have significantly reduced rates of restenosis compared to bare metal stents (BMS), an increased risk of late stent thrombosis (LST) has emerged as a major concern. Pathologic studies of patients dying from late DES thrombosis demonstrates delayed arterial healing characterized by persistent fibrin deposition and poor endothelialization as the primary substrate. However, recent thorough investigations revealed additional mechanisms of stent thrombosis such as hypersensitivity reaction, excessive fibrin deposit with malapposition, or neoatherosclerosis, which are associated with device-specific components and the majority of very late stent thrombosis is likely associated with these abnormal vascular responses. Therefore, although the incidence of stent thrombosis following DES implantation is similar in each period, the underlying mechanisms of this complication may vary. In the current review, the mechanisms of stent thrombosis in the DES era will be discussed using the data from autopsy studies that have been published.
尽管第一代药物洗脱支架 (DES) 与裸金属支架 (BMS) 相比,显著降低了再狭窄率,但晚期支架血栓形成 (LST) 的风险增加已成为一个主要关注点。对死于晚期 DES 血栓形成患者的病理研究表明,动脉愈合延迟,以持续的纤维蛋白沉积和不良的内皮化作为主要基质。然而,最近的深入研究揭示了支架血栓形成的其他机制,如过敏反应、支架贴壁不良导致的纤维蛋白过度沉积或新生动脉粥样硬化,这些与器械特定成分有关,大多数极晚期支架血栓形成可能与这些异常血管反应有关。因此,尽管 DES 植入后支架血栓形成的发生率在每个时期都相似,但这种并发症的潜在机制可能不同。在目前的综述中,将使用已发表的尸检研究数据讨论 DES 时代支架血栓形成的机制。