Mazur Alexander, Iakobishvili Zaza, Kusniec Jairo, Strasberg Boris
Cardiology Department, Rabin Medical Center, Beilinson Campus, Petah-Tikva and Sackler School of Medicine, Tel Aviv University, Israel.
Ann Noninvasive Electrocardiol. 2003 Oct;8(4):352-5. doi: 10.1046/j.1542-474x.2003.08414.x.
A 55-year-old, previously healthy man presented with an episode of wide QRS tachycardia that had left bundle branch morphology and left superior axis. His electrocardiogram in sinus rhythm showed characteristic Brugada pattern with coved type ST-segment (J-point) elevation in leads V1-V2, mild QRS widening of 110 ms, and left axis deviation. The mechanism of the tachycardia was shown to be bundle branch reentry. Baseline H-V interval of 68 ms additionally lengthened to 119 ms after intravenous procainamide administration indicating significant conduction system disease. The tachycardia was no longer inducible after successful ablation of the right bundle branch.
一名55岁、既往健康的男性出现一次宽QRS心动过速发作,呈左束支形态及左上轴。他窦性心律时的心电图显示特征性的Brugada图形,V1-V2导联呈穹窿型ST段(J点)抬高,QRS轻度增宽至110毫秒,以及电轴左偏。心动过速的机制显示为束支折返。静脉注射普鲁卡因胺后,基线H-V间期68毫秒进一步延长至119毫秒,提示存在显著的传导系统疾病。成功消融右束支后,心动过速不再能被诱发。