Authors : Ashwin Shajith; Aparna Salimon

Volume/Issue : Volume 11 - 2026, Issue 7 - July

Google Scholar : https://tinyurl.com/mwr4whce

Scribd : https://tinyurl.com/4enrrf68

DOI : https://doi.org/10.38124/ijisrt/26jul457

Note : A published paper may take 4-5 working days from the publication date to appear in PlumX Metrics, Semantic Scholar, and ResearchGate.

Abstract : Hypothyroidism exerts wellcharacterised effects on myocardial calcium cycling, ion channel kinetics, connexin-43 (Cx43) gap junction expression, and interstitial fibrosis — each mechanistically relevant to conduction system capture and threshold stability in LBBAP. To our knowledge, no published study has specifically examined hypothyroidism as a modifier of LBBAP outcomes. This review synthesises published evidence to propose and support a clinical hypothesis: that hypothyroidism may adversely influence LBBAP by raising pacing thresholds, impairing reliable LBB engagement, widening paced QRS duration, and increasing susceptibility to pacing-induced cardiomyopathy (PICM) — through thyroid hormone-dependent alterations in SERCA2amediated calcium cycling, SCN5A and HCN4 expression, Cx43 localisation, and TGF-β1-driven septal fibrosis. Direct clinical validation is absent, and prospective studies are required. Routine pre-procedural thyroid function screening before elective LBBAP may represent a clinically actionable, low-cost intervention warranting formal evaluation, particularly in South Asian electrophysiology centres.

Keywords : Left Bundle Branch Area Pacing; Hypothyroidism; Conduction System Pacing; Pacing Threshold; Pacing-Induced Cardiomyopathy; Thyroid Dysfunction.

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