Loss of His-bundle and Right Ventricular Septal Capture Following Transcatheter Aortic Valve Replacement-A Case Report.

Abstract

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.