Critical inflammatory mechanisms underlying arrhythmias
Abstract
During the past few decades, cardiovascular research has increasingly focused on systemic inflammatory mechanisms, particularly in the field of atherosclerosis but also in association with cardiac arrhythmogenesis. Objective inflammatory markers including C‑reactive protein and cytokines, also called "biomarkers," seem to serve as predictors of onset and prognosis of cardiac arrhythmias. This review gives an overview of potential mechanisms underlying inflammatory processes and arrhythmias, especially atrial fibrillation, which is the most common sustained arrhythmia in daily clinical routine. The association between inflammatory pathways and cardiac arrhythmia is highly complex and includes direct as well as indirect pathways. While past research into arrhythmia focused on fibrosis, altered action potential properties, and ischemia, novel concepts include coagulation and inflammation in cardiac tissue. The underlying mechanisms are altered electrophysiological properties, including ion channel disturbance, early and late afterdepolarizations, as well as enhanced fibrosis and structural remodeling in cardiomyopathies. These pathophysiological factors favor the occurrence of ectopic pacemakers as well as re-entry tachycardia. Further studies are essential to better understand the main inflammatory signal cascades and the exact proarrhythmic effect of interacting key mediators. This will facilitate the evaluation of future anti-inflammatory therapeutic approaches for arrhythmias, analogous to recent developments in atherosclerosis.
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Prolonged exposure to reactive oxygen species from oxidative stress has been associated with vascular and cardiac myocyte dysfunction, which may lead to cardiac arrhythmias through cardiac fibrosis, ion-channel conduction disturbances, and early and late depolarisations.
“Prolonged exposure to reactive oxygen species from oxidative stress has been associated with vascular and cardiac myocyte dysfunction, which may lead to cardiac arrhythmias through cardiac fibrosis, ion-channel conduction disturbances, and early and late depolarisations. 38,39”
From Risk of cardiovascular outcomes among women with endometriosis in the United Kingdom: a retrospective matched cohort study (2021) · cites this paper as [39]
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- Authors
- Vonderlin, N., Siebermair, J., Kaya, E., Köhler, M., Rassaf, T., & Wakili, R.
- Affiliations
- Essen University Hospital (DE)
- Corresponding author
- Wakili, R.
- Venue
- Herz
- Published
- 2019-02-07
- Volume
- 44
- Issue
- 2
- Pages
- 121-129
- ISSN
- 0340-9937 (ISSN-L)
- 1615-6692
- OpenAlex
- W2912836197
- Cited by
- 41
- References
- 78
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 6 · 2023: 8 · 2022: 13 · 2021: 4 · 2020: 5 · 2019: 1
- FWCI
- 1.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Herz (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Atrial Fibrillation Management and Outcomes
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- cardiac arrhythmias, inflammation, atrial fibrillation, C-reactive protein, cytokines, inflammatory markers, arrhythmogenesis, myocardial fibrosis, structural remodeling, afterdepolarizations, coagulation, anti-inflammatory therapy
- MeSH terms
- Atrial Fibrillation, Fibrosis, Humans, Inflammation, Tachycardia
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