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Pilsicainide-induced Brugada-type ECG and ventricular arrhythmias originating from the left posterior fascicle in a case with Brugada syndrome associated with idiopathic left ventricular tachycardia

机译:Bilsadainide引起的Brugada型ECG和源自左后束的室性心律失常,在Brugada综合征伴特发性左室心动过速的情况下

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摘要

The patient was a 50-year-old male in 2002, who was first suspected of having a Brugada-type electrocardiogram (ECG). A drug challenge test using pilsicainide was performed and unmasked a typical coved type ST elevation followed by ventricular arrhythmias (VAs) manifesting a QRS pattern with a right bundle branch block and left axis deviation. Three years later, he was transferred to the emergency room due to a wide QRS tachycardia with the same QRS morphology as the VA that previously occurred in the drug challenge test. An ECG just after the recorded termination of the tachycardia exhibited a typical Brugada-type ECG. In an electrophysiological study, ventricular fibrillation could be easily induced with reproducibility. Since the clinical tachycardia could not be sustained by an isoproterenol infusion, mapping and catheter ablation targeting the pilsicainide-induced VAs was performed. The successful ablation site was the left mid-lower septal wall where a Purkinje potential was recorded and a false tendon was attached just to it.
机译:该患者是2002年的50岁男性,最初被怀疑患有Brugada型心电图(ECG)。进行了使用比西卡尼的药物攻击试验,并揭露了典型的凹型ST抬高,随后出现室性心律失常(VA),表现为QRS模式,右束支传导阻滞和左轴偏离。三年后,他因广泛的QRS心动过速被转移到急诊室,其QRS形态与先前在药物激发试验中出现的VA相同。记录到的心动过速终止后的ECG表现出典型的Brugada型ECG。在电生理研究中,可容易地诱发心室纤颤并具有可重复性。由于异丙肾上腺素输注无法维持临床心动过速,因此针对比西卡尼德诱导的VA进行了标测和导管消融。成功的消融部位是左中间隔隔壁,记录有Purkinje电位,并在其上附着了假腱。

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