Delayed arterial healing and increased late stent thrombosis at culprit sites after drug-eluting stent placement for acute myocardial infarction patients - An autopsy study
Delayed arterial healing and increased late stent thrombosis at culprit sites after drug-eluting stent placement for acute myocardial infarction patients - An autopsy study
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DOI：
10.1161/circulationaha.107.762047
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发表时间：
2008-09-09
期刊：
影响因子：
37.8
通讯作者：
Virmani, Renu
中科院分区：
文献类型：
--
作者：
Nakazawa, Gaku;Finn, Aloke V.;Virmani, Renu
背景：药物洗脱支架（DES）治疗急性心肌梗死（AMI）的长期安全性仍不确定。利用尸检数据，我们评估了使用DES治疗AMI患者支架段的病理反应，并与稳定型心绞痛患者进行了比较。方法和结果：从138例DES尸检的CVPath登记处中，我们确定了25例AMI患者，并有潜在的坏死核心和纤维帽破裂。选择26例经DES治疗的稳定型心绞痛伴厚帽纤维粥样硬化患者作为对照。对支架放置时间为30d的患者进行组织形态学分析。我们比较了这两组在罪魁祸首部位和每个支架内的非罪魁祸首部位植入术的反应。稳定患者晚期支架血栓发生率（11%）明显低于AMI患者（41%,P = 0.04）。尽管在AMI的罪魁祸首网站大大减少新生内膜厚度(平均0.04毫米;四分位范围(差),0.02 - 0.09毫米),发现了struts的患病率(49%;差,16%到96%),纤维蛋白沉积(63 + / - 28%),和炎症(35%;差,27%到49%)明显更大而罪魁祸首网站稳定患者(血管内膜厚度:0.11毫米(差,0.07 - 0.21毫米),P = 0.008;发现了struts: 9%(差,0%到39%),P = 0.01;纤维蛋白:36 + / - 27%,P = 0.008;炎症，17% [IQR, 7% ~ 25%], P = 0.003)和每个支架内的非罪魁祸首部位。结论：与因稳定型心绞痛而接受DES治疗的AMI患者的罪魁祸首部位相比，接受DES治疗的AMI患者的罪魁祸首部位的血管愈合明显延迟，这强调了潜在斑块形态在动脉对DES反应中的重要性。我们的数据表明，接受DES治疗的AMI患者血栓并发症的风险增加。
Background-The long-term safety of drug-eluting stents (DES) for acute myocardial infarction (AMI) remains uncertain. Using autopsy data, we evaluated the pathological responses of the stented segment in patients treated with DES for AMI and compared with patients with stable angina.Methods and Results-From the CVPath Registry of 138 DES autopsies, we identified 25 patients who presented with AMI and had an underlying necrotic core with a ruptured fibrous cap. Twenty-six patients who had stable angina with thick-cap fibroatheroma treated by DES were selected as controls. Histomorphometric analysis was performed in patients with >30-day stent duration. We compared the response to stenting at the culprit site in these 2 groups and to nonculprit sites within each stent. Late stent thrombosis was significantly less frequent in stable (11%) than in AMI (41%; P = 0.04) patients. Although neointimal thickness in the AMI culprit site was significantly less (median, 0.04 mm; interquartile range [IQR], 0.02 to 0.09 mm), the prevalence of uncovered struts (49%; IQR, 16% to 96%), fibrin deposition (63 +/- 28%), and inflammation (35%; IQR, 27% to 49%) were significantly greater compared with the culprit site in stable patients (neointimal thickness: 0.11 mm [IQR, 0.07 to 0.21 mm], P = 0.008; uncovered struts: 9% [IQR, 0% to 39%], P = 0.01; fibrin: 36 +/- 27%, P = 0.008; inflammation, 17% [IQR, 7% to 25%], P = 0.003) and the nonculprit site within each stent.Conclusions-Vessel healing at the culprit site in AMI patients treated with DES is substantially delayed compared with the culprit site in patients receiving DES for stable angina, emphasizing the importance of underlying plaque morphology in the arterial response to DES. Our data suggest an increased risk of thrombotic complications in patients treated with DES for AMI.