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

Figures

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  Figure 1. Chest radiograph and electrocardiogram at pacemaker implantation. (A) Chest radiograph obtained immediately after pacemaker implantation, demonstrating placement of the right ventricular lead at the His-bundle. (B) Two distinct pacing morphologies observed at implantation. The non-selective His-bundle pacing threshold was 2.25 V/0.4 ms, and the selective His-bundle pacing threshold was 1.25 V/0.4 ms.

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  Figure 2. Comparison of ventricular lead slack between immediately after implantation and standing chest radiographs obtained 1 week following the procedure. While the ventricular lead demonstrated a U-shaped slack configuration on chest radiography obtained in the supine position immediately after implantation, standing chest radiography performed 1 week after implantation revealed a reduction in lead slack.

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  Figure 3. Temporal changes in His-bundle and right ventricular myocardial pacing thresholds and lead impedance. (A) Serial changes in His-bundle pacing and right ventricular myocardial pacing thresholds of the ventricular lead from 3 months after implantation to lead extraction, assessed at a pulse width of 0.8 ms. The chronic-phase His-bundle pacing threshold deteriorated by 1 year after implantation. (B) Serial changes in ventricular lead impedance. No increase in impedance was observed throughout the follow-up period.

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  Figure 4. Fluoroscopic images during lead extraction. Adhesions in the left subclavian vein, superior vena cava, and right atrium were dissected using a 12-Fr laser sheath, followed by extraction of the ventricular lead using simple traction. The lead was successfully extracted without the lead tip entering the laser sheath. Based on this finding, the tissue adherent to the screw tip was considered to have originated from tissue adjacent to the His-bundle.

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  Figure 5. Tissue adherent to the extracted lead tip and histopathological evaluation. (A) Tissue adhesion was incidentally observed on the screw tip at the time of ventricular lead extraction. (B) Haematoxylin–eosin staining (4× magnification) demonstrated abundant fibrin-rich tissue without evidence of myocardial or conduction system tissue. At the interface between the lead and the adherent tissue, accumulation of inflammatory cells suggestive of chronic inflammation, including macrophages and monocytes, was observed. Granulation tissue was also identified in the outer layer. (C) CD31 immunohistochemical staining (10× magnification) demonstrated CD31-positive microvascular structures within the fibrin layer, suggesting angiogenesis. (D) CD68 immunohistochemical staining (10× magnification) demonstrated scattered to clustered infiltration of numerous CD68-positive macrophages within the fibrin layer and granulation tissue, suggesting ongoing tissue reactions related to chronic inflammation and fibrin organization and degradation.