Asreb Abdullah, Ahn Joon
Internal Medicine Residency, Northeast Georgia Medical Center, Gainesville, GA, USA.
Cardiac Electrophysiology, Northeast Georgia Medical Center, Gainesville, GA, USA.
J Innov Card Rhythm Manag. 2023 Feb 15;14(2):5332-5337. doi: 10.19102/icrm.2023.14022. eCollection 2023 Feb.
Conduction abnormalities following transcatheter aortic valve replacement (TAVR) are common. High-grade atrioventricular block (AVB) and new-onset left bundle branch block remain the most reported. These often require the placement of a permanent pacemaker (PPM). His-bundle (HB) pacing is increasingly being utilized as the preferred mode of ventricular pacing due to its more physiologic ventricular activation. In this case report, we present a case of a patient who developed loss of HB capture and experienced an increase in the local right ventricular (RV) capture threshold after TAVR that led to unrecognized intermittent loss of ventricular capture and symptoms. An 80-year-old man with severe aortic stenosis presented with symptomatic bradycardia due to typical atrial flutter (AFL) with a high-grade AVB and an underlying right bundle branch block. He underwent placement of a dual-chamber PPM (Medtronic, Inc., Minneapolis, MN, USA) with a HB pacing lead. HB mapping demonstrated a normal H-V interval, and the lead was fixated with non-selective HB capture. The R-waves measured 2.8 mV, the pacing impedance was 544 Ω, and the non-selective HB and local RV capture threshold was 0.5 V @ 1 ms. He underwent AFL ablation, and his atrial leads were normal. He subsequently underwent successful TAVR with a 29-mm Sapien 3 valve (Edwards Lifesciences, Irvine, CA, USA). Post-TAVR, PPM interrogation showed a loss of HB capture with a left bundle paced QRS morphology. Following discharge, he presented with stroke-like symptoms and was noted to have intermittent loss of RV capture with complete heart block (CHB) and a slow ventricular escape rhythm. PPM interrogation revealed an elevated pacing threshold, and his RV output was gradually increased to a maximum output of 7.5 V @ 1.5 ms. He also developed a fever and was found to have enterococcal bacteremia. Transesophageal echocardiography demonstrated vegetations on his prosthetic valve and pacemaker lead, without a perivalvular abscess. He underwent explantation of the pacemaker system and insertion of a temporary PPM. After intravenous antibiotic therapy with negative blood cultures, he underwent re-implantation of a new right-sided dual-chamber PPM, and an RV pacing lead was placed into the RV outflow tract. HB pacing is becoming the preferred mode of physiologic ventricular pacing. This case illustrates the potential risks of the TAVR procedure in patients with existing HB pacing leads. We observed a loss of HB capture and the development of CHB due to traumatic injury to the HB distal to the HB pacing lead after TAVR placement together with an increase in the local RV capture threshold. The depth of TAVR placement is an important aspect of the TAVR procedure that determines the risk of developing CHB and may also affect the HB and local RV pacing thresholds post-procedure.
经导管主动脉瓣置换术（TAVR）后传导异常很常见。高度房室传导阻滞（AVB）和新发左束支传导阻滞仍是报道最多的情况。这些情况通常需要植入永久起搏器（PPM）。希氏束（HB）起搏因其更符合生理的心室激动方式，越来越多地被用作心室起搏的首选模式。在本病例报告中，我们介绍了一例患者，该患者在TAVR后出现HB夺获丧失，并经历了局部右心室（RV）夺获阈值升高，导致未被识别的间歇性心室夺获丧失和症状。一名80岁严重主动脉瓣狭窄男性因典型心房扑动（AFL）伴高度AVB及潜在右束支传导阻滞出现症状性心动过缓。他接受了带有HB起搏导线的双腔PPM（美敦力公司，明尼阿波利斯，明尼苏达州，美国）植入。HB标测显示H-V间期正常，导线通过非选择性HB夺获固定。R波测量值为2.8 mV，起搏阻抗为544 Ω，非选择性HB和局部RV夺获阈值为0.5 V @ 1 ms。他接受了AFL消融，心房导线正常。随后他成功接受了29毫米Sapien 3瓣膜（爱德华兹生命科学公司，尔湾，加利福尼亚州，美国）的TAVR。TAVR后，PPM程控显示HB夺获丧失，出现左束支起搏QRS形态。出院后，他出现类似中风的症状，被发现存在间歇性RV夺获丧失伴完全性心脏传导阻滞（CHB）及缓慢的心室逸搏心律。PPM程控显示起搏阈值升高，其RV输出逐渐增加至最大输出7.5 V @ 1.5 ms。他还出现发热，被发现患有肠球菌菌血症。经食管超声心动图显示其人工瓣膜和起搏器导线上有赘生物，无瓣周脓肿。他接受了起搏器系统取出及临时PPM植入。在静脉应用抗生素治疗且血培养阴性后，他接受了新的右侧双腔PPM重新植入，一根RV起搏导线被置于RV流出道。HB起搏正成为生理性心室起搏的首选模式。本病例说明了在已有HB起搏导线的患者中TAVR手术的潜在风险。我们观察到在TAVR植入后，由于HB起搏导线远端的HB受到创伤性损伤，出现HB夺获丧失及CHB，同时局部RV夺获阈值升高。TAVR植入深度是TAVR手术的一个重要方面，它决定了发生CHB的风险，也可能影响术后HB和局部RV起搏阈值。
