目的:分析颈内动脉(ICA)转位到颈外动脉(ECA)的外侧壁的长期结果。
方法:在3.10.2017年至28.12.2020年期间,784例孤立的血液动力学显著ICA孔口狭窄患者被纳入本回顾性多中心开放比较研究“俄罗斯桦树”。根据实施的手术技术,形成组:第1组(n=517)-外翻颈动脉内膜切除术(eCEA);第2组(n=193)经典CEA,植入用二环氧化合物治疗的异心包膜补片;第3组(n=74)-ICA移位到ECA的侧壁中。将ICA换位到ECA的侧壁中如下进行。颈总动脉,分离ECA和ICA,然后用血管钳夹住它们。同时将ICA和ECA夹在孔口上方4cm处。将ICA在孔口上方2.5cm处切割。然后用聚丙烯缝合线缝合孔口中具有局部狭窄的ICA部分。同时,由于在ICA孔处存在颈动脉窦的受体,因此无法切除多余的无功能的ICA残端。因此,这种操作可能会损伤鼻窦,导致术后难以控制的动脉高血压。然后,在孔口上方2.5厘米的ECA侧壁中,使用手术刀和成角度的血管剪刀形成0.5cm直径的圆孔。然后,使用聚丙烯缝合线进行ICA的切断部分与ECA的侧壁中形成的圆形开口之间的端到侧吻合。移除血管夹并开始血流。
结果:在术后住院期间未发现并发症。在长期随访期间,第3组没有发现不良心血管事件。用双环氧化合物治疗的经典CEA组植入异心包膜贴片显示出急性脑血管意外(CVA)的致命结局最高(第1组:0.2%,n=1;第2组:2.6%;n=5;p=0.008);非致死性缺血性CVA(第1组:0.6%,n=3;第2组:14.0%,n=27;p<0.0001);需要重复血运重建的ICA再狭窄(超过60%)(第1组:0.8%,n=4;第2组:16.6%,n=32;p<0.0001)。经典CEA后所有CVA的原因是由于新生内膜增生引起的ICA再狭窄;外翻CEA和动脉粥样硬化进展后。在经典CEE后,复合终点在统计学上更为频繁,采用二环氧处理的异心包膜补片对重建区域进行成形术(第1组:1.0%,n=5;第2组:17.7%,n=33;p<0.0001)。在分析无ICA再狭窄的生存曲线时,已确定,在植入双环氧化合物处理的异心包膜补片的经典CEA组中,所有需要血运重建的ICA再狭窄的绝大多数患者早在术后6个月就被诊断出来.在外翻CEA组中,血管腔的丢失通常是在介入治疗后一年多的时间。比较存活曲线时(Logrank检验),已确定,在植入双环氧治疗的异心包膜补片的经典CEA后,ICA的再狭窄发生在统计学上更频繁(p<0.0001)。
结论:由于在动脉内膜切除术后没有内动脉壁炎症,ICA转位进入ECA侧壁并不伴随ICA再狭窄的风险。因此,该技术可作为CEA的替代方案,可用于ICA口局部血流动力学显著狭窄的常规应用.由于在中期和长期随访中ICA再狭窄的风险很高,经典的CEA与贴片植入是最不优选的手术。
To analyze the long-term results of transposition of the internal carotid artery (ICA) into the lateral wall of the external carotid artery (ECA) in the presence of hemodynamically significant stenosis of the ICA. During the period from 3.10.2017 to 28.12.2020, 784 patients with isolated hemodynamically significant ICA orifice stenosis were included in the present retrospective multicentric open comparative
study \"Russian Birch.\" Depending on the implemented surgical technique, groups were formed: group 1 (n = 517) -
eversion carotid endarterectomy (eCEA); group 2 (n = 193) classic CEA with implantation of a xenopericardium patch treated with di-epoxy compounds; group 3 (n = 74) - transposition of the ICA into the lateral wall of the ECA. Transposition of the ICA into the lateral wall of the ECA is performed as follows. The common carotid artery, ECA, and ICA are isolated and then they are clamped with vascular clamps. At the same time, the ICA and ECA are clamped 4 cm above the orifice. The ICA is cut 2.5 cm above the orifice. Then the section of the ICA with local stenosis in the orifice is sutured with a polypropylene suture. At the same time, the redundant nonfunctioning ICA stump is not resected due to the fact that there are receptors of the carotid sinus at the ICA orifice. Thus, such manipulation may damage the sinus, causing arterial hypertension that is difficult to control in the postoperative period. Then, in the lateral wall of the ECA 2.5 cm above the orifice, a 0.5 cm diameter round hole is formed using a scalpel and angled vascular scissors. Then an end-to-side anastomosis between the severed section of the ICA and the rounded opening formed in the lateral wall of the ECA is performed using a polypropylene suture. Vascular clamps are removed and blood flow is started. No complications were detected in the hospital postoperative period. No adverse cardiovascular events were registered in group 3 in the long-term follow-up period. The group of classic CEA with implantation of a xenopericardium patch treated with di-epoxy compounds showed the highest number of fatal outcomes from acute cerebrovascular accident (CVA) (Group 1: 0.2%, n = 1; group 2: 2.6%; n = 5; p = 0.008); nonfatal ischemic CVA (group 1: 0.6%, n = 3; group 2: 14.0%, n = 27; p < 0.0001); ICA restenosis (more than 60%) requiring a repeat revascularization (group 1: 0.8%, n = 4; group 2: 16.6%, n = 32; p < 0.0001). The cause of all CVAs after classical CEA was restenosis of the ICA due to neointimal hyperplasia; after
eversion CEA and progression of atherosclerosis. The composite end point was statistically more frequent after classical CEE with plasty of the reconstruction area with a diepoxy-treated xenopericardium patch (group 1: 1.0%, n = 5; group 2: 17.7%, n = 33; p < 0.0001). When analyzing the survival curves free of ICA restenosis, it was determined that the overwhelming number of all ICA restenosis requiring revascularization in the group of classical CEA with implantation of a diepoxy-treated xenopericardium patch is diagnosed as early as 6 months after surgery. In the group of
eversion CEA, the loss of the vessel lumen is most often visualized more than a year after the intervention. When comparing the survival curves (Logrank test), it was determined that restenosis of the ICA develops statistically more frequently (p < 0.0001) after classical CEA with implantation of a diepoxytreated xenopericardium patch. Transposition of the ICA into the lateral wall of the ECA is not accompanied by the risk of ICA restenosis due to the absence of inflammation of the internal artery wall after endarterectomy. Thus, this technique can be an alternative to CEA and be routinely used in case of local hemodynamically significant stenosis of the ICA orifice. Classical CEA with patch implantation is the least preferable operation due to the high risk of ICA restenosis in the mid-term and long-term follow-up.