Pugazhendhi Vijayaraman1, Gopi Dandamudi2, Daniel Lustgarten3, Kenneth A Ellenbogen4. 1. Geisinger Wyoming Valley Medical Center, Wilkes-Barre, PA. 2. Indiana University, Indianapolis, IN. 3. University of Vermont Health System, Burlington, VT. 4. Virginia Commonwealth University Health System, Richmond, VA.
Abstract
BACKGROUND: Permanent His bundle pacing (HBP) is a physiological alternative to right ventricular pacing. It is not known whether HBP can cause His-Purkinje conduction (HPC) disease. The aim of our study is to assess His bundle capture and its effect on left ventricular (LV) function in long-term follow-up and to determine HPC at the time of pulse generator change (GC) in patients with chronic HBP. METHODS: HB electrograms were recorded from the pacing lead at implant and GC. HBP QRS duration (QRSd), His-ventricular (HV) intervals, and HB pacing thresholds at GC were compared with implant measurements. HPC was assessed by pacing at cycle lengths of 700 ms, 600 ms, and 500 ms at GC. LV internal diameters, ejection fraction (EF), and valve dysfunction at baseline were compared with echocardiography during follow-up. RESULTS: GC was performed in 20 patients (men 13; age 74 ± 14 years) with HBP at 70 ± 24 months postimplant. HV intervals remained unchanged from initial implant (44 ± 4 ms vs 45 ± 4 ms). During HBP at 700 ms, 600 ms, and 500 ms (n = 17), consistent 1:1 HPC was present. HBP QRSd remained unchanged during follow-up (117 ± 20 ms vs 118 ± 23 ms). HBP threshold at implant and GC was 1.9 ± 1.1 V and 2.5 ± 1.2 V @ 0.5 ms. Despite high pacing burden (77 ± 13%), there was no significant change in LVEF (50 ± 14% at implant) during follow-up (55 ± 6%, P = 0.06). CONCLUSIONS: HBP does not appear to cause new HPC abnormalities and is associated with stable HBP QRSd during long-term follow-up. Despite high pacing burden, HBP did not result in deterioration of left ventricular systolic function or cause new valve dysfunction.
BACKGROUND: Permanent His bundle pacing (HBP) is a physiological alternative to right ventricular pacing. It is not known whether HBP can cause His-Purkinje conduction (HPC) disease. The aim of our study is to assess His bundle capture and its effect on left ventricular (LV) function in long-term follow-up and to determine HPC at the time of pulse generator change (GC) in patients with chronic HBP. METHODS: HB electrograms were recorded from the pacing lead at implant and GC. HBP QRS duration (QRSd), His-ventricular (HV) intervals, and HB pacing thresholds at GC were compared with implant measurements. HPC was assessed by pacing at cycle lengths of 700 ms, 600 ms, and 500 ms at GC. LV internal diameters, ejection fraction (EF), and valve dysfunction at baseline were compared with echocardiography during follow-up. RESULTS: GC was performed in 20 patients (men 13; age 74 ± 14 years) with HBP at 70 ± 24 months postimplant. HV intervals remained unchanged from initial implant (44 ± 4 ms vs 45 ± 4 ms). During HBP at 700 ms, 600 ms, and 500 ms (n = 17), consistent 1:1 HPC was present. HBP QRSd remained unchanged during follow-up (117 ± 20 ms vs 118 ± 23 ms). HBP threshold at implant and GC was 1.9 ± 1.1 V and 2.5 ± 1.2 V @ 0.5 ms. Despite high pacing burden (77 ± 13%), there was no significant change in LVEF (50 ± 14% at implant) during follow-up (55 ± 6%, P = 0.06). CONCLUSIONS: HBP does not appear to cause new HPC abnormalities and is associated with stable HBP QRSd during long-term follow-up. Despite high pacing burden, HBP did not result in deterioration of left ventricular systolic function or cause new valve dysfunction.
Authors: Marin Nishimura; Gregory M Marcus; Paul D Varosy; Haikun Bao; Yongfei Wang; Jeptha P Curtis; Jonathan C Hsu Journal: J Interv Card Electrophysiol Date: 2019-04-19 Impact factor: 1.900