Furui Koichi, Morishima Itsuro, Kanzaki Yasunori, Tsuboi Hideyuki
Department of Cardiology, Ogaki Municipal Hospital, Ogaki, Japan.
J Cardiol Cases. 2019 Aug 27;20(6):221-224. doi: 10.1016/j.jccase.2019.08.010. eCollection 2019 Dec.
Coronary vasospasm is an emerging potentially lethal complication of catheter ablation for atrial fibrillation (AF), however, its mechanism in this setting has not been well elucidated. A 55-year-old man with symptomatic paroxysmal AF underwent pulmonary vein isolation under sedation with propofol. The procedure was completed without any complications. Fifteen months later, a repeated session was performed because of AF recurrence. Initially, a high-dose infusion of dexmedetomidine instead of propofol was administered to introduce sedation. Then, an ST-segment elevation developed in the inferior leads and the diagnosis of coronary vasospasm was made by urgent coronary angiography. A comparison of the procedural details between the first and second sessions identified dexmedetomidine, an α-2 adrenergic agonist with a short distribution half-life, as a potential cause of coronary vasospasm seen only in the second session in the same individual. Since it has been shown that α-2 adrenoreceptor-mediated vasoconstriction can involve the coronary circulation, it is thus possible that a stimulation of α-2 adrenergic receptors induced by dexmedetomidine caused a coronary vasospasm. The present case provides new insights into dexmedetomidine-induced vasospasm. Physicians should be aware of this potentially lethal side effect of dexmedetomidine which is increasingly used in the current AF ablation practice. < Dexmedetomidine has become widely used during catheter ablation for atrial fibrillation since it is generally regarded as a safe drug for sedation and analgesia with fewer respiratory depressant effects compared to other agents. However, it should be noted that dexmedetomidine may cause a coronary vasospasm, especially at the time of an initial high loading-dose infusion. Physicians should be aware of this potentially lethal side effect of dexmedetomidine.>.
冠状动脉痉挛是导管消融治疗心房颤动（房颤）新出现的一种潜在致命并发症，然而，其在这种情况下的机制尚未完全阐明。一名55岁有症状的阵发性房颤男性在丙泊酚镇静下接受了肺静脉隔离术。手术顺利完成，无任何并发症。15个月后，因房颤复发进行了再次手术。最初，给予高剂量右美托咪定而非丙泊酚进行镇静。随后，下壁导联出现ST段抬高，紧急冠状动脉造影诊断为冠状动脉痉挛。对比两次手术的操作细节发现，右美托咪定这种分布半衰期短的α-2肾上腺素能激动剂，可能是同一患者仅在第二次手术时出现冠状动脉痉挛的原因。由于已有研究表明α-2肾上腺素受体介导的血管收缩可累及冠状动脉循环，因此右美托咪定诱导的α-2肾上腺素受体刺激可能导致了冠状动脉痉挛。本病例为右美托咪定诱导的血管痉挛提供了新的见解。医生应意识到右美托咪定这种在当前房颤消融治疗中越来越常用的药物可能存在的致命副作用。<自右美托咪定被普遍认为是一种用于镇静和镇痛的安全药物，与其他药物相比呼吸抑制作用较少以来，它已在房颤导管消融术中广泛使用。然而，应注意右美托咪定可能导致冠状动脉痉挛，尤其是在初始高负荷剂量输注时。医生应意识到右美托咪定的这种潜在致命副作用。>
