Stent thrombosis and restenosis: what have we learned and where are we going? The Andreas Grüntzig Lecture ESC 2014.
Stent thrombosis and restenosis: what have we learned and where are we going? The Andreas Grüntzig Lecture ESC 2014.
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DOI：
10.1093/eurheartj/ehv511
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发表时间：
2015-12-14
影响因子：
39.3
通讯作者：
Kastrati A
中科院分区：
文献类型：
--
作者：
Byrne RA;Joner M;Kastrati A
现代支架植入术利用了药物治疗和器械创新的进步。接受现代抗血小板药物、围手术期抗凝血酶治疗和新一代药物洗脱支架（DES）治疗的患者在短期至中期内结局良好。事实上，随着这些器械在大多数国家的成本降低，仍有极少数适应症患者应拒绝接受标准治疗DES治疗。支架失效的两个主要原因是支架内血栓形成（ST）和支架内再狭窄（ISR）。近年来，这两种疾病的发病率都大大降低。目前的临床登记研究和随机试验采用广泛的纳入标准，显示1年后ST发生率≤ 1%，此后每年发生率≤ 0.2-0.4%;临床ISR发生率分别为5%。大型队列中的血管造影监测研究显示，新一代DES的血管造影ISR发生率> 10%。高分辨率冠状动脉内成像的出现表明，在许多晚期支架失效病例中，支架段内的新动脉粥样硬化变化代表血栓形成和再狭窄事件的最终共同途径。在未来，更好地了解这一过程的发病机制可能会转化为改善后期的结果。此外，随访期间非支架相关疾病作为后续心肌梗死原因的优势突出了生活方式和药物干预的重要性，这些干预旨在改变基础疾病过程。最后，虽然最近的发展集中在策略，规避需要长期留置支架，如药物涂层球囊或完全生物可吸收支架，需要更多的数据之前，更广泛地使用这些疗法可以提倡。
Modern-day stenting procedures leverage advances in pharmacotherapy and device innovation. Patients treated with contemporary antiplatelet agents, peri-procedural antithrombin therapy and new-generation drug-eluting stents (DES) have excellent outcomes over the short to medium term. Indeed, coupled with the reducing costs of these devices in most countries there remain very few indications where patients should be denied treatment with standard-of-care DES therapy. The two major causes of stent failure are stent thrombosis (ST) and in-stent restenosis (ISR). The incidence of both has reduced considerably in recent years. Current clinical registries and randomized trials with broad inclusion criteria show rates of ST at or <1% after 1 year and ∼0.2–0.4% per year thereafter; rates of clinical ISR are 5% respectively. Angiographic surveillance studies in large cohorts show rates of angiographic ISR of ∼10% with new-generation DES. The advent of high-resolution intracoronary imaging has shown that in many cases of late stent failure neoatherosclerotic change within the stented segment represents a final common pathway for both thrombotic and restenotic events. In future, a better understanding of the pathogenesis of this process may translate into improved late outcomes. Moreover, the predominance of non-stent-related disease as a cause of subsequent myocardial infarction during follow-up highlights the importance of lifestyle and pharmacological interventions targeted at modification of the underlying disease process. Finally, although recent developments focus on strategies which circumvent the need for chronically indwelling stents—such as drug-coated balloons or fully bioresorbable stents—more data are needed before the wider use of these therapies can be advocated.