What is the mechanism of chronic threshold elevation after His-bundle pacing? A histopathological case report suggesting the involvement of fibrin fibrosis

His-bundle pacing (HBP) enables physiological ventricular activation and has been associated with superior clinical outcomes compared with conventional pacing. Nevertheless, chronic threshold elevation remains a major limitation, often leading to early battery depletion or lead revision. The pathological mechanisms underlying chronic threshold elevation have not been fully elucidated.

A 76-year-old man with symptomatic 2:1 atrioventricular block underwent successful HBP implantation, achieving selective His-bundle capture. One week after implantation, both His-bundle and right ventricular pacing thresholds increased markedly. Although the His-bundle capture threshold transiently improved during follow-up, it deteriorated again by 1 year and stabilized. After 5 years and 5 months, early battery depletion prompted extraction of the ventricular lead and re-implantation using left bundle branch pacing. Histopathological examination of the extracted lead tip revealed fibrin-rich tissue with fibroblast proliferation and CD31-positive microvessels. Numerous CD68-positive macrophages were present at the lead–tissue interface. No myocardial or conduction system tissue was identified, which may be consistent with development of a physical barrier between the lead tip and the His-bundle.

This case raises the hypothesis that early fibrin deposition followed by organization may contribute to chronic HBP threshold elevation by increasing the separation between the lead tip and the His-bundle. We speculated that fibrotic tissue interposed between the screw and the His-bundle progressively enlarged, leading to micro-dislodgement and subsequent threshold elevation. To our knowledge, this is one of the first reports describing the histopathological findings of a case with chronic threshold deterioration following HBP.