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Critical inflammatory mechanisms underlying arrhythmias

  • N. Vonderlin
  • J. Siebermair
  • E. Kaya
  • M. Köhler
  • T. Rassaf
  • R. WakiliEmail author
Main topic
  • 47 Downloads

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.

Keywords

Atrial fibrillation Cardiac arrhythmogenesis Atherosclerosis C-reactive protein Cytokines 

Zugrundeliegende inflammtorische Mechanismen bei Herzrhythmusstörungen

Zusammenfassung

In den letzten Jahren rückte die Rolle von inflammatorischen Prozessen bei Herzkreislauferkrankungen immer mehr in den Vordergrund. Der wissenschaftliche Fokus lag hier primär auf Atherosklerose, aber auch die Assoziation mit kardialen Arrhythmien wurde intensiv untersucht. Neben der Rolle von Biomarkern, z. B. C-reaktives Protein (CRP) oder Zytokine, wurden auch gemeinsame pathophysiologische Mechanismen von Entzündungen und Arrhythmien evaluiert. Dieser Artikel gibt einen Überblick über die komplexen Zusammenhänge zwischen inflammatorischen Prozessen und verschiedenen kardialen Arrhythmien, insbesondere bei Vorhofflimmern. Ältere wissenschaftliche Arbeiten fokussierten sich primär auf das Auftreten von Fibrose und veränderten Eigenschaften des Aktionspotenzials. Neue Konzepte beschäftigen sich mit der kausalen Interaktion von Koagulationsmechanismen und Arrhythmien sowie intrazellulären Entzündungsprozessen in Kardiomyozyten. Es gibt verschiedene Faktoren, die aus einer akuten oder chronischen Entzündungsreaktion resultieren, welche die Entstehung von Herzrhythmusstörungen begünstigen können: eine gestörte Ionenkanal-Homöostase, frühe und späte Nachdepolarisationen, Fibrosierung und strukturelles Remodeling des Myokards. Als Folge wird das Auftreten von getriggerter ektoper Aktivität, kreisenden Erregungen (Re-entry) und damit die Entstehung und Aufrechterhaltung von kardialen Arrhythmien begünstigt. In der Zukunft werden weitere grundlagenwissenschaftliche sowie klinische Studien benötigt, um die zugrundeliegenden inflammatorischen Signalkaskaden und den exakten proarrhythmischen Effekt von interagierenden Biomarkern zu entschlüsseln. Auf dieser Grundlage könnten, analog zur Atherosklerose, neue Therapieansätze für inflammationsassoziierte Rhythmusstörungen etabliert werden.

Schlüsselwörter

Vorhofflimmern Kardiale Arrhythmogenese Atherosklerose C-reaktives Protein Zytokine 

Notes

Compliance with ethical guidelines

Conflict of interest

N. Vonderlin, J. Siebermair, E. Kaya, M. Köhler, T. Rassaf, and R. Wakili declare that they have no competing interests.

This article does not contain any studies with human participants or animals performed by any of the authors.

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Copyright information

© Springer Medizin Verlag GmbH, ein Teil von Springer Nature 2019

Authors and Affiliations

  • N. Vonderlin
    • 1
  • J. Siebermair
    • 1
  • E. Kaya
    • 1
  • M. Köhler
    • 1
  • T. Rassaf
    • 1
  • R. Wakili
    • 1
    Email author
  1. 1.Klinik für Angiologie und Kardiologie, Westdeutsches Herz- und Gefäßzentrum EssenUniversitätsklinikum der Universität EssenEssenGermany

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