PDF(Pubmed)
Abstract：
Brugada syndrome is a rare cardiac condition characterized by distinctive electrocardiogram patterns, predisposing individuals to fatal arrhythmias. While primarily linked to a loss-of-function mutation in the SCN5A gene, acquired forms of the syndrome have been associated with various factors, including drug use. We present a case of a 31-year-old female who presented to the emergency department unresponsive following cocaine use and developed type 1 Brugada ECG patterns alongside an incomplete right bundle branch block in V1-V3, ST elevations with biphasic waves, and diffuse repolarization abnormalities with J point deviations while in the intensive care unit. This study aimed to discuss the complexity of managing drug-induced Brugada-like findings and highlights the need for further research into the mechanisms underlying cocaine-induced cardiac effects. We aimed to discuss potential mechanisms for the impact of cocaine as its role as a sodium channel blocker and its potential effects on connexin 43 in the context of Brugada syndrome. This study also reinforced the importance of differentiating between true Brugada syndrome and other similar ECG changes for appropriate care management.
摘要：
Brugada综合征是一种罕见的心脏病，其特征是独特的心电图模式。易患致命心律失常的个体。虽然主要与SCN5A基因的功能缺失突变有关，该综合征的获得性形式与各种因素有关，包括吸毒。我们介绍了一例31岁的女性，该女性在使用可卡因后无反应地到急诊科就诊，并在V1-V3中出现不完整的右束支传导阻滞，ST抬高并伴有双相波，和弥漫性复极化异常与J点偏差，而在重症监护病房。这项研究旨在讨论管理药物诱导的Brugada样发现的复杂性，并强调需要进一步研究可卡因诱导的心脏效应的机制。我们旨在讨论可卡因作为钠通道阻滞剂的作用及其在Brugada综合征中对连接蛋白43的潜在影响的潜在机制。这项研究还加强了区分真正的Brugada综合征和其他类似ECG变化对于适当护理管理的重要性。
