钙化病变经皮冠状动脉介入治疗中如何处理球囊夹闭“病例报告”

Zaoui Nassime, Boukabous Amina, Bachir Nadhir, I. Nabil, T. Ali
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引用次数: 0

摘要

经皮冠状动脉血管成形术是一种微创手术,旨在疏通冠状动脉,并发症发生率较低(严重并发症发生率为3%-7%,死亡率为1.2%)。PCI期间的装置卡夹是一种罕见但危及生命的并发症,发生在<1%的PCI中,球囊卡夹排在冠状动脉导丝之后。我们报告了一例68岁的男性、吸烟者、高血压和2型糖尿病患者,该患者在心肌断层扫描中表现出心绞痛,并有缺血的证据,其中放射状冠状动脉造影显示左前降支中部狭窄。在经皮冠状动脉介入治疗期间和用2.5×12的NC球囊扩张后,后者拒绝放气,仍被困在病变中,出现疼痛和ST段抬高,尽管多次尝试在充气机中稀释产品并通过过度扩张使其破裂。对球囊的牵引导致引导导管的深度插管,引导导管与被捕获的球囊接触,后者的海波管破裂,海波管在病变部位保持充气状态,并安装在0.014导丝上。我们在左前降支远端放置第二根0.014导丝,并与第一根导丝的远端扭转,然后在第二根导丝上引入第二个2.0×20的球囊,直到引导导管的远端并充气以捕获卡住的球囊。我们逐渐拆除了这个紧急集合,使我们能够取回被困的气球。对照注射显示左前降支血栓闭塞,通过血栓切除术和抗GPIIbIIIa治疗,然后放置DES 2.75×28。患者48小时后出院,LVEF良好。可能的球囊截留机制是高度钙化病变的急性反冲,压迫不完全放气的球囊,这似乎是我们患者的情况,如果在完全放气之前取出球囊,并使海波管破裂或弯曲,则引导导管会勒死球囊近端。如果发生不适球囊截留,解决方案是稀释充气机中的产品,通过过度膨胀使其爆裂,穿过坚硬的导丝(或穿过微导管或OTW球囊上的另一端),切开其外部并被动排空,引入第二根导丝并进行Buddy球囊或将患者转移到外科手术。材料包埋仍然是一种罕见但危及生命的并发症,其清除需要选择材料大小和温和的操作(钙化病变时为小气球),其管理使用不同的技术,其选择取决于临床和解剖情况。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
How to manage balloon entrapment during percutaneous coronary intervention of a calcified lesion “Case report”
Percutaneous coronary angioplasty is a minimally invasive procedure aimed at unclogging a coronary artery with a low complication rate (with a serious complication rate of 3% to 7% and a mortality rate of 1.2%). Device entrapment during PCI is a rare but life-threatening complication that occurs in < 1% of PCIs and balloon entrapment comes second after coronary guidewires. We present the case of 68-years-old man, smoker, hypertensive and type2 diabetic that presents angina with evidence of ischemia on myocardial tomoscintigraphy and in whom the radial coronary angiography reveals a tight calcified mid LAD stenosis. During his PCI and after dilatation with an NC balloon 2.5 × 12 the latter refuses to deflate and remains trapped in the lesion with the appearance of pain and ST-elevation despite several attempts to dilute the product in the inflator and to burst it by overexpansion. Traction on the balloon resulted in the deep intubation of the guiding-catheter, which comes in contact with the trapped balloon, and the rupture of the latter’s hypotube, which remains inflated at the site of the lesion and mounted on the 0.014 guidewire. We put a second 0.014 guidewire distally in the LAD and twisted with the distal part of the first guidewire, then we introduced a second balloon 2.0 × 20 over the second guidewire until the distal part of the guiding-catheter and inflated to trap the stucked balloon. We gradually removed this emergency assembly that allowed us to retrieve the trapped balloon. The control injection revealed a thrombotic occlusion of the LAD treated by thrombectomy and anti-GPIIbIIIa followed by a DES 2.75 × 28 placement. The patient was discharged 48 hours later with a good LVEF. The possible balloon entrapment mechanisms are an acute recoil of a highly calcified lesion with compression of the incompletely deflated balloon, which seems to be the case in our patient, strangulation of the proximal balloon end by the guiding-catheter if the balloon is removed before complete deflation and break or bend of the hypotube. The solutions in case of undeflatable balloon entrapment are to dilute the product in the inflator, to burst it by overexpansion, to pierce it through a stiff guidewire (or through its other end on a Microcatheter or OTW balloon), to cut its outer part and let it empty passively, to introduce a second guide-wire and perform a Buddy-Balloon or to transfer the patient to Surgery. Material entrapment remains a rare but life-threatening complication, its eviction requires the choice of material size and gentle manipulations (small balloons in the event of a calcified lesion) and its management uses different techniques, the choice of which depends on the clinical and anatomical situation.
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