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Remodeling des Altersherzens

Sinusknotendysfunktion und Vorhofflimmern

Remodeling of the aging heart

Sinus node dysfunction and atrial fibrillation

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Herzschrittmachertherapie + Elektrophysiologie Aims and scope Submit manuscript

Zusammenfassung

Sinusknotendysfunktion („sick sinus syndrome“, SSS) und Vorhofflimmern (AF) zeigen eine zunehmende Inzidenz im Alter. Beide Störungen sind assoziiert mit kardiovaskulären Erkrankungen und treten nicht selten gemeinsam auf. Tatsächlich findet man bei beiden Störungen gleichartige Pathomechanismen wie strukturelles Remodeling in Form einer degenerativen Fibrose und funktionelles Remodeling in Form eines gestörten Ca2+-Handlings. Als Mediator des Remodelings steht eine exzessiv aktivierte CamKII (Ca2+/Calmodulin-abhängige Proteinkinase Typ II) im Mittelpunkt. Im Sinusknoten führt das Remodeling zur Apoptose und als Folge zu Sinusknotenstillstand oder Reentry (Tachyarrhythmie-Bradykardie-Syndrom). Im Vorhofmyokard begünstig das Remodeling ebenfalls Reentry bzw. dessen Triggermechanismen, insbesondere getriggerte Aktivität aufgrund später Nachdepolarisationen (DAD). SSS und AF könnten somit unterschiedliche Phänotypen derselben Veränderung im Vorhof sein. Andererseits kann nach dem Henne-und-Ei-Prinzip SSS das Auftreten von AF oder umgekehrt bewirken.

Abstract

The incidence of both sinus node dysfunction (SND) and atrial fibrillation (AF) increases with age. SND and AF frequently coexist. Likewise, they are often associated with cardiovascular diseases. Both arrhythmias share similar pathomechanisms such as structural and functional remodeling, i. e., degenerative fibrosis and altered Ca2+ handling, respectively. A growing body of evidence suggests an important role for the CamKII (Ca2+/calmodulin-dependent protein kinase II) in structural as well as in functional remodeling. In the sinus node, remodeling leads to degenerative fibrosis and as a consequence to sinus node arrest or to reentry (brady/tachycardia). In the atrium, remodeling sets the conditions for reentry and its triggering mechanisms, especially the conditions for triggered activity on the basis of delayed afterdepolarizations (DAD). Thus, SND and AF seem to be different phenotypes of related pathophysiological mechanisms. On the other hand, it remains controversial as to whether SND causes AF or vice versa.

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  1. Institut für Physiologie, Abteilung II, Medizinische Fakultät, Albert-Ludwigs-Universität Freiburg, Hermann-Herder-Str. 7, 79104, Freiburg, Deutschland

    Jörg Weirich

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Correspondence to Jörg Weirich.

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Weirich, J. Remodeling des Altersherzens. Herzschr Elektrophys 28, 29–38 (2017). https://doi.org/10.1007/s00399-017-0485-3

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  • DOI: https://doi.org/10.1007/s00399-017-0485-3

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