Landiolol, electrical remodeling, and the emerging biology of ventricular arrhythmia control

Table 1 Summary of molecular and electrophysiologic changes in sepsis and with landiolol

Domain	Sepsis (typical direction)	Landiolol in Hu et al[13] (direction)	Why this matters for ventricular arrhythmias
Inflammation (e.g., TNF-α, IL-6)	↑	↓	Cytokines and oxidative stress can destabilize myocardial electrophysiology and promote remodeling
Myocardial fibrosis/structural remodeling	↑	↓	Fibrosis increases conduction discontinuity and re-entry susceptibility
Cx43 remodeling	Context-dependent (often disordered localization; variable expression)	↓ (reported)	Altered coupling/hemichannel behavior and heterogeneity can widen dispersion and sustain re-entry
NaV1.5 remodeling	Variable; dysfunction/redistribution linked to conduction slowing/heterogeneity	↓ (reported)	Sodium current supports conduction reserve; disordered regulation can increase vulnerability to conduction block and re-entry
Conduction heterogeneity/dispersion	↑	↓	Dispersion is a substrate for re-entrant ventricular arrhythmias
Ventricular arrhythmia burden	↑	↓	Captures the clinically salient endpoint: Fewer malignant rhythms

TNF-α: Tumor necrosis factor-alpha; IL: Interleukin.