Permanent His bundle pacing: Electrophysiological and echocardiographic observations from long-term follow-up
Pugazhendhi Vijayaraman1, Gopi Dandamudi2, Daniel Lustgarten3
1Geisinger Wyoming Valley Medical Center, Wilkes-Barre, PA.
Insights
Permanent His bundle pacing (HBP) does not cause His-Purkinje conduction disease and maintains stable QRS duration. Long-term HBP does not impair left ventricular function or cause valve issues, even with high pacing burden.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiac Pacing
Background:
- Permanent His bundle pacing (HBP) offers a physiological alternative to traditional right ventricular pacing.
- The potential for HBP to induce His-Purkinje conduction (HPC) disease remains unclear.
Purpose of the Study:
- To evaluate His bundle capture and its long-term impact on left ventricular (LV) function.
- To assess for HPC abnormalities in patients with chronic HBP during pulse generator changes.
Main Methods:
- Recorded His bundle electrograms at implant and generator change.
- Compared His-ventricular (HV) intervals, pacing thresholds, and QRS duration (QRSd) pre- and post-generator change.
- Assessed His-Purkinje conduction (HPC) at various pacing cycle lengths and evaluated LV function via echocardiography.
Main Results:
- HV intervals and HBP QRSd remained stable over a mean follow-up of 70 months.
- Consistent 1:1 His-Purkinje conduction (HPC) was observed during HBP.
- No significant changes in left ventricular ejection fraction (LVEF) or new valve dysfunction were noted despite a high pacing burden.
Conclusions:
- His bundle pacing (HBP) does not appear to induce new His-Purkinje conduction (HPC) abnormalities.
- Long-term HBP is associated with stable pacing parameters and preserved left ventricular systolic function.
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.
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