医学
北京
中国
Brugada综合征
内科学
印度
家庭医学
儿科
心脏病学
法学
政治学
作者
Jing Yang,Rong He,Ping Zhang
标识
DOI:10.1093/eurheartj/ehae921
摘要
A 32-year-old male patient was admitted to the emergency department following loss of consciousness. The patient experienced recurrent syncope over the past nine years. His prior electrocardiogram (ECG) demonstrated a coved-type Brugada pattern wave in lead V2 (Panel A). Genetic testing revealed a nonsense mutation in the SCN5A gene, specifically c.664C>T (p.Arg222Ter) (Panel B), confirming the diagnosis of Brugada syndrome (BrS). However, the patient declined to receive an implantable cardioverter-defibrillator. Upon admission, the emergency ECG revealed ventricular fibrillation (Panel C). Rapid intervention was initiated, including external electrical defibrillation, cardiopulmonary resuscitation, and epinephrine administration. The post-resuscitation ECG showed a combination of atrial tachycardia (arrows, Panel D) and monomorphic wide QRS tachycardia, along with a right bundle branch block (RBBB) pattern. Notably, there was a significant increase in the J-wave amplitude in lead V2, with the J point marked in leads V2–V3 (line, Panel D). Given the patient’s haemodynamic instability, synchronized electrical cardioversion was performed. The following ECG revealed sinus tachycardia with a QRS morphology resembling the prior tachycardia (see Supplementary data online, Figure S1A). The blood pressure increased to 85/60 mmHg, and the RBBB aberration was no longer present when the heart rate decreased to 95 beats per minute (see Supplementary data online, Figure S1B). The presence of atrial tachycardia complicates the differentiation between true RBBB and ventricular tachycardia in BrS patients. Rate-dependent RBBB pattern may represent a transient conduction abnormality.1,2 Additionally, the increased J-wave amplitude underscores the arrhythmic potential of BrS. Close monitoring and timely intervention to manage life-threatening arrhythmias in BrS patients are essential. Supplementary data are available at European Heart Journal online. All authors declare no disclosure of interest for this contribution. No data were generated or analysed for this manuscript. This research was funded by Beijing Hospitals Authority Clinical medicine Development of special funding support (grant no. ZLRK202518), Beijing Municipal Administration of Hospitals Incubating Program (grant number: PX2024036), and Beijing Tsinghua Changgung Hospital Fund (no. 2024YNRC01).
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