Arrhythmogenic Mechanisms of Novel Biomarkers in Cardiac Electrophysiology

TL;DR

This review explores new biomarkers for arrhythmia, highlighting their potential in diagnosis and treatment while addressing challenges in clinical use.

Contribution

The paper identifies novel biomarkers and their mechanisms in arrhythmia, emphasizing the need for standardized validation and clinical integration.

Findings

Novel biomarkers show promise in revealing arrhythmia mechanisms through inflammation, fibrosis, and electrical remodeling.

Clinical translation is hindered by assay standardization and lack of large-scale validation studies.

Combining multiple biomarkers and discovering subtype-specific markers could improve individualized antiarrhythmic therapy.

Abstract

Arrhythmia is an important cause of cardiovascular disease deaths and a serious threat to human health, but the current means of identification are limited. Biomarkers, with the advantages of easy access and rapid detection, have shown significant value in arrhythmia risk prediction, precision diagnosis, and prognosis assessment. In recent years, with the development of molecular biology and multiomics technology, some novel biomarkers have made great breakthroughs in revealing the pathological mechanisms of arrhythmia. However, clinical translation still faces challenges such as a lack of standardization of assays and insufficient clinical prospective validation. This review comprehensively searched studies published between 2010 and 2025 in PubMed, Web of Science, Embase, and CENTRAL databases, focusing on the mechanisms underlying the role of arrhythmia biomarkers in inflammation, fibrosis, autoimmunity, and electrical remodeling and clinical translation potential. Future research should focus on the combined application of multiple biomarkers and the discovery of subtype‐specific markers. Conducting large‐scale, multicenter studies to validate these biomarkers and ultimately integrate them into clinical practice is crucial for advancing biomarker‐guided individualized antiarrhythmic therapy.

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