Department of Cardiology, Westmead Hospital, University of Sydney, Sydney, Australia; Westmead Applied Research Centre, University of Sydney, Sydney, Australia.
Department of Cardiology, Westmead Hospital, University of Sydney, Sydney, Australia.
JACC Clin Electrophysiol. 2021 Oct;7(10):1274-1284. doi: 10.1016/j.jacep.2021.06.001. Epub 2021 Aug 25.
This study describes the clinical and electrophysiological characteristics of basal-septal ventricular tachycardias (VTs) in patients with structural heart disease (SHD).
The basal septum is a common source of VT in patients with SHD.
Data from 312 consecutive patients with SHD undergoing catheter ablation of ventricular arrhythmias were reviewed.
Thirty-three basal-septal VTs in 31 patients (mean age 67.4 ± 14.2 years, mean left ventricular ejection fraction [LVEF] 42% ± 15%) were identified. Patients with VTs with left ventricular basal-septal breakthrough were more likely to have ischemic cardiomyopathy and lower LVEF; patients with right ventricular basal-septal VT were more likely to have sarcoidosis or right ventricular cardiomyopathy of unknown significance, with higher LVEF. Atrioventricular block was present in 45% of patients and intraventricular block including persistent biventricular pacing in 77%. Unipolar scar was larger than bipolar scar (area 18.8% ± 19.4% vs 12.7% ± 14.6%; P < 0.001). VTs with right bundle branch block configuration and S wave in lead V with positive V/V polarity consistently indicated left ventricular basal-septal breakthrough. Inferior limb-lead discordance with right bundle branch block configuration and "reverse pattern break in lead V" were identified in left ventricular basal inferior-septal origin in 3 patients. VT noninducibility was achieved in 55%, and VT recurred in 42% of patients after a single procedure, but VT burden was significantly reduced after ablation (59 episodes before vs 2 episodes after ablation; P = 0.02).
Basal-septal VTs in patients with SHD have a distinct clinical, electrocardiographic, and electrophysiological profile depending on the breakthrough site, accompanied by a deep intramural septal substrate that limits procedural success after catheter ablation.
本研究描述了结构性心脏病(SHD)患者中基底-间隔部室性心动过速(VT)的临床和电生理特征。
基底间隔是 SHD 患者 VT 的常见起源部位。
回顾了 312 例连续接受导管消融室性心律失常的 SHD 患者的数据。
31 例患者中有 33 例(平均年龄 67.4 ± 14.2 岁,平均左心室射血分数 [LVEF] 42% ± 15%)发生 33 例基底-间隔部 VT。左心室基底间隔突破的 VT 患者更可能患有缺血性心肌病和更低的 LVEF;右心室基底间隔 VT 患者更可能患有结节病或右心室原因不明的心肌病,LVEF 更高。45%的患者存在房室传导阻滞,77%的患者存在室内传导阻滞,包括持续性双心室起搏。单极瘢痕大于双极瘢痕(面积 18.8% ± 19.4%比 12.7% ± 14.6%;P<0.001)。具有右束支传导阻滞形态和 V 导联 S 波正向 V/V 极性的 VT 始终表明左心室基底间隔突破。在 3 例患者中,左心室基底下间隔起源时出现下壁导联不一致的右束支传导阻滞形态和“V 导联反向形态中断”。55%的患者 VT 不能诱发,单次消融后 42%的患者 VT 复发,但消融后 VT 负荷明显降低(消融前 59 次发作,消融后 2 次发作;P=0.02)。
SHD 患者的基底-间隔部 VT 具有独特的临床、心电图和电生理特征,取决于突破部位,并伴有限制导管消融后程序成功的深部室间隔基质。