What is the clinical evidence from this study?

Study design: Editorial. Population: Cardiac Disease and Arrhythmias.

What does this research mean for the field?

Cardiac diseases trigger structural, mechanical, and electrical remodelling processes in the human heart. Novelty: ClaimNovelty.SYNTHESIS. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To synthesize molecular, cellular, and organ-level mechanisms underlying pathological electrical remodelling across cardiac diseases to advance arrhythmic risk prediction and therapeutic protection.

January 5, 2023CellsOpen Access

Electrical Remodelling in Cardiac Disease

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Key result

Electrical remodelling in cardiac disease involves complex molecular, cellular, and whole-organ changes that promote life-threatening arrhythmias, as summarized in this Special Issue.

Design

Editorial

Authors

URUrsula RavensElectrophysiology RPRémi PeyronnetUniversity of Freiburg

Discussion

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Implication

This special issue provides a comprehensive overview of the molecular, cellular, and macroscopic mechanisms underlying electrical remodeling and arrhythmogenesis in various cardiac diseases.

Key Points

To synthesize molecular, cellular, and organ-level mechanisms underlying pathological electrical remodelling across cardiac diseases to advance arrhythmic risk prediction and therapeutic protection.
Synthesized findings from experimental investigations spanning single-cell patch-clamp electrophysiology, ion channel trafficking, and tissue-level conduction velocity measurements.
Evaluated physiological and pathological data from human atrial and ventricular myocardial tissue slices, rodent knock-out models, and pig models of atrial fibrillation.
Abnormal intracellular calcium handling via ryanodine receptor leakage and transverse-axial tubule disruption triggers early and delayed afterdepolarizations through excessive sodium-calcium exchanger activation.
Two-pore potassium channel K2P3.1 (TASK-1) is upregulated in atrial fibrillation and downregulated in heart failure, whereas TRPM4 deficiency protects against aldosterone-induced afterdepolarizations.
Disrupted ion channel trafficking mediated by Rab GTPases and MAGUK scaffolding proteins impairs membrane excitability and slows myocardial conduction velocity, facilitating re-entry arrhythmias.

PICO

Population

Cardiac Disease and Arrhythmias

This special issue provides a comprehensive overview of the molecular, cellular, and macroscopic mechanisms underlying electrical remodeling and arrhythmogenesis in various cardiac diseases.

Cite This Study

Ravens et al. (2023) conducted an editorial in Cardiac Disease and Arrhythmias. Electrical remodelling in cardiac disease involves complex molecular, cellular, and whole-organ changes that promote life-threatening arrhythmias, as summarized in this Special Issue.

synapsesocial.com/papers/6a19342da0353395e958020e https://doi.org/10.3390/cells12020230

Topics

Heart failure HFrEF treatment

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Implication

This special issue provides a comprehensive overview of the molecular, cellular, and macroscopic mechanisms underlying electrical remodeling and arrhythmogenesis in various cardiac diseases.

Electrical Remodelling in Cardiac Disease

Discussion

Member takes

Implication

Key Points

PICO

Cite This Study

Topics

Electrical Remodelling in Cardiac Disease

Discussion

Member takes

Implication

Key Points

PICO

Cite This Study

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