Zusammenfassung
Eine chronische Inflammation im Rahmen von Autoimmunerkrankungen ist mit einer erhöhten Rate an supraventrikulären und ventrikulären Arrhythmien vergesellschaftet, welche mit einer gesteigerten Morbidität und Mortalität assoziiert ist. Die Beteiligung des spezifischen Erregungsleitungssystems wird sehr häufig bei chronischen Autoimmunprozessen beobachtet, wenngleich die klinische Penetranz sehr unterschiedlich ist und therapiebedürftige Blockierungen nur selten auftreten. Für die Pathogenese tachykarder Arrhythmien scheint die Kombination aus der gesteigerten Prävalenz struktureller Herzerkrankungen und dem direkten Einfluss inflammatorischer Mechanismen auf die kardiale Elektrophysiologie ursächlich zu sein. Dabei werden vor allem die Fibroblastenaktivierung, eine gestörte Gap-Junction-Funktion durch Änderung der Connexin-Zusammensetzung sowie die Störung des intrazellulären Ca2+-Stoffwechsels angeführt. Als elektrokardiographische Marker eines erhöhten arrhythmogenen Risikos bei Patienten mit chronischen Autoimmunerkrankungen können eine verlängerte P‑Wellen-Dauer sowie eine abnorme QTc-Zeit und reduzierte Herzfrequenzvariabilität gelten. Die frühzeitige und konsequente inflammationshemmende Therapie rückt somit auch im Hinblick auf die Vermeidung von Arrhythmien in den Vordergrund.
Abstract
Chronic inflammation due to autoimmune diseases is associated with a higher rate of supraventricular and ventricular arrhythmias leading to an increased risk for cardiovascular morbidity and mortality. Involvement of the cardiac conduction system is common in patients with chronic autoimmune diseases, although the penetrance of clinical signs and symptoms is variable and complete heart block with need for therapy is rare. The combination of the increased prevalence of structural cardiovascular disease and the direct impact of inflammatory mechanisms on cardiac electrophysiology seems to be responsible for the higher rate of tachyarrhythmias. In particular, fibroblast activation, gap junction impairment via changes in connexin composition and abnormalities in intracellular calcium-handling are mentioned. Electrocardiographic markers of an increased arrhythmogenic potential in patients with chronic autoimmune disorders may include prolonged P‑wave duration as well as abnormal QTc interval and reduced heart rate variability. Thus, minimizing the inflammatory burden through tight control of disease activity may help reduce the arrhythmic load.
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M. Neef, K. Berndt, C. Spies, U. Laufs und M. Metze geben an, dass kein Interessenkonflikt besteht.
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Neef, M., Berndt, K., Spies, C. et al. Rhythmusstörungen bei chronischen Autoimmunerkrankungen. Herzschr Elektrophys 30, 240–244 (2019). https://doi.org/10.1007/s00399-019-00636-z
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DOI: https://doi.org/10.1007/s00399-019-00636-z