Abstract：
BACKGROUND: Takotsubo syndrome (TS) represents a form of nonischemic cardiomyopathy characterized by sudden and temporary weakening of the myocardium. Many data suggest a primary role for sympathetic overstimulation in its pathogenesis. Nevertheless, these correlates are less easily identified during anesthesia.
METHODS: A 50-year-old female patient with a 4-year history of drug-resistant left trigeminal neuralgia. She was scheduled for surgical microvascular decompression. In the operating room, after induction of general anesthesia and oral intubation, the electrocardiogram revealed a significant ST segment elevation along with a sudden decrease in systolic blood pressure and heart rate. Administration of atropine caused a conversion into ventricular tachycardia. The advanced cardiac life support protocols were applied with prompt defibrillation and rapid recovery at sinus rhythm. A transthoracic echocardiogram revealed apical akinesia with ballooning of the left ventricle with a reduction of systolic function. An emergency coronary arteriography was performed, showing normal epicardial coronary vessels. After 4 days, echocardiography revealed normalization of the left ventricular function with improvement of the ejection fraction.
CONCLUSIONS: In patients affected by trigeminal neuralgia, chronic pain can lead to a state of adrenergic hyperactivation, which can promote TS during the induction of general anesthesia, probably through the trigeminocardiac reflex.
METHODS: A 50-year-old female patient with a 4-year history of drug-resistant left trigeminal neuralgia. She was scheduled for surgical microvascular decompression. In the operating room, after induction of general anesthesia and oral intubation, the electrocardiogram revealed a significant ST segment elevation along with a sudden decrease in systolic blood pressure and heart rate. Administration of atropine caused a conversion into ventricular tachycardia. The advanced cardiac life support protocols were applied with prompt defibrillation and rapid recovery at sinus rhythm. A transthoracic echocardiogram revealed apical akinesia with ballooning of the left ventricle with a reduction of systolic function. An emergency coronary arteriography was performed, showing normal epicardial coronary vessels. After 4 days, echocardiography revealed normalization of the left ventricular function with improvement of the ejection fraction.
CONCLUSIONS: In patients affected by trigeminal neuralgia, chronic pain can lead to a state of adrenergic hyperactivation, which can promote TS during the induction of general anesthesia, probably through the trigeminocardiac reflex.
摘要：
背景：Takotsubo综合征（TS）代表一种非缺血性心肌病，其特征是心肌突然和暂时减弱。许多数据表明交感神经过度刺激在其发病机理中起主要作用。然而，这些相关性在麻醉期间不太容易识别.
方法：一名50岁女性患者，有4年耐药左三叉神经痛病史。她被安排进行微血管减压手术。在手术室里,全身麻醉诱导和口腔插管后，心电图显示明显的ST段抬高,同时收缩压和心率突然下降.阿托品的给药引起室性心动过速的转变。先进的心脏生命支持方案应用于快速除颤和窦性心律快速恢复。经胸超声心动图显示心尖运动障碍，左心室膨胀，收缩功能降低。进行了紧急冠状动脉造影，显示心外膜冠状血管正常.4天后,超声心动图显示左心室功能正常化，射血分数改善。
结论：在受三叉神经痛影响的患者中，慢性疼痛会导致肾上腺素能过度激活状态，在全身麻醉诱导过程中可以促进TS，可能是通过三叉神经心脏反射.
方法：一名50岁女性患者，有4年耐药左三叉神经痛病史。她被安排进行微血管减压手术。在手术室里,全身麻醉诱导和口腔插管后，心电图显示明显的ST段抬高,同时收缩压和心率突然下降.阿托品的给药引起室性心动过速的转变。先进的心脏生命支持方案应用于快速除颤和窦性心律快速恢复。经胸超声心动图显示心尖运动障碍，左心室膨胀，收缩功能降低。进行了紧急冠状动脉造影，显示心外膜冠状血管正常.4天后,超声心动图显示左心室功能正常化，射血分数改善。
结论：在受三叉神经痛影响的患者中，慢性疼痛会导致肾上腺素能过度激活状态，在全身麻醉诱导过程中可以促进TS，可能是通过三叉神经心脏反射.
