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Neue zelluläre und molekulare Erkenntnisse

Pathopysiologie des Vorhofflimmerns

  • Fortbildung_Kardiologie
  • Published:
CardioVasc Aims and scope

Es wird angenommen, dass Vorhofflimmern durch zwei Grundmechanismen entsteht: ektope (getriggerte) Aktivität und kreisende Erregungen. Das Auslösen und Aufrechterhalten von Vorhofflimmern ist auf elektrophysiologische und strukturelle Veränderungen zurückzuführen, die als „Remodelling“ bezeichnet werden. Die Remodelling-Vorgänge schränken die Ansprechbarkeit der therapeutischen Interventionen stark ein und erhöhen die Wahrscheinlichkeit des Wiederauftretens von Vorhofflimmern nach erfolgreicher Kardioversion. Dieser Übersichtsartikel fasst neuere Erkenntnisse zur zellulären und molekularen Pathophysiologie von Vorhofflimmern zusammen und zeigt potenzielle neue therapeutische Ansätze auf.

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Literatur

  1. Andrade J, Khairy P, Dobrev D et al. The clinical profile and pathophysiology of atrial fibrillation: relationships among clinical features, epidemiology, and mechanisms. Circ Res 2014;114:1453–68

    Article  CAS  PubMed  Google Scholar 

  2. Wakili R, Voigt N, Kääb S et al. Recent advances in the molecular pathophysiology of atrial fibrillation. J Clin Invest 2011;121:2955–68

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  3. Dobrev D, Carlsson L, Nattel S. Novel molecular targets for atrial fibrillation therapy. Nat Rev Drug Discov 2012;11:275–91

    Article  CAS  PubMed  Google Scholar 

  4. Camm AJ, Lip GY, De Caterina R et al. Focused update of the ESC Guidelines for the management of atrial fibrillation: an update of the 2010 ESC Guidelines for the management of atrial fibrillation. Developed with the special contribution of the European Heart Rhythm Association. Eur Heart J 2012;33:2719–47

    Article  PubMed  Google Scholar 

  5. Dobrev D. Electrical remodeling in atrial fibrillation. Herz 2006;31:108–12; quiz 142-3

    Article  PubMed  Google Scholar 

  6. Nattel S, Burstein B, Dobrev D. Atrial remodeling and atrial fibrillation: mechanisms and implications. Circ Arrhythm Electrophysiol 2008;1:62–73

    Article  PubMed  Google Scholar 

  7. Heijman J, Voigt N, Nattel S et al. Cellular and molecular electrophysiology of atrial fibrillation initiation, maintenance, and progression. Circ Res 2014;114:1483–99

    Article  CAS  PubMed  Google Scholar 

  8. Voigt N, Li N, Wang Q et al. Enhanced sarcoplasmic reticulum Ca2+ leak and increased Na+-Ca2+ exchanger function underlie delayed afterdepolarizations in patients with chronic atrial fibrillation. Circulation 2012;125:2059–70

    Article  CAS  PubMed  Google Scholar 

  9. Voigt N, Heijman J, Wang Q et al. Cellular and molecular mechanisms of atrial arrhythmogenesis in patients with paroxysmal atrial fibrillation. Circulation 2014;129: 145–56

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  10. Christ T, Boknik P, Wöhrl S et al. L-type Ca2+ current downregulation in chronic human atrial fibrillation is associated with increased activity of protein phosphatases. Circulation 2004;110:2651–7

    Article  CAS  PubMed  Google Scholar 

  11. Wagoner DR Van, Pond AL, Lamorgese M et al. Atrial L-type Ca2+ currents and human atrial fibrillation. Circ Res 1999;85:428–36

    Article  PubMed  Google Scholar 

  12. Voigt N, Trausch A, Knaut M et al. Left-to-right atrial inward rectifier potassium current gradients in patients with paroxysmal versus chronic atrial fibrillation. Circ Arrhythm Electrophysiol 2010;3:472–80

    Article  PubMed  Google Scholar 

  13. Narayan SM, Krummen DE, Shivkumar K et al. Treatment of atrial fibrillation by the ablation of localized sources: CONFIRM (Conventional Ablation for Atrial Fibrillation With or Without Focal Impulse and Rotor Modulation) trial. J Am Coll Cardiol 2012;60:628–36

    Article  PubMed Central  PubMed  Google Scholar 

  14. Schmidt C, Wiedmann F, Voigt N et al. Upregulation of K2P3.1 K+ Current Causes Action Potential Shortening in Patients with Chronic Atrial Fibrillation. Circulation 2015;132:82–92

    Article  CAS  PubMed  Google Scholar 

  15. Harada M, Luo X, Qi XY et al. Transient receptor potential canonical-3 channel-dependent fibroblast regulation in atrial fibrillation. Circulation 2012;126:2051–64

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  16. Luo X, Pan Z, Shan H et al. MicroRNA-26 governs profibrillatory inward-rectifier potassium current changes in atrial fibrillation. J Clin Invest 2013;123:1939–51

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  17. Qi X-Y, Diness JG, Brundel BJJM et al. Role of small-conductance calcium-activated potassium channels in atrial electrophysiology and fibrillation in the dog. Circulation 2014;129:430–40

    Article  CAS  PubMed  Google Scholar 

  18. Chatelier A, Mercier A, Tremblier B et al. A distinct de novo expression of Nav1.5 sodium channels in human atrial fibroblasts differentiated into myofibroblasts. J Physiol 2012;590:4307–19

    Article  PubMed Central  CAS  PubMed  Google Scholar 

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Authors and Affiliations

  1. Institut für Pharmakologie, Westdeutsches Herz- und Gefäßzentrum, Medizinische Fakultät, Universität Duisburg-Essen, Essen, Deutschland

    Shokoufeh Ghezelbash

  2. Inst. für Pharmakologie, Westdeutsches Herz- und Gefäßzentrum, Medizinische Fakultät, Universität Duisburg-Essen, Hufelandstrasse 55, 45122, Essen, Deutschland

    Dobromir Dobrev

Authors
  1. Shokoufeh Ghezelbash
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  2. Dobromir Dobrev
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Corresponding author

Correspondence to Dobromir Dobrev.

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Danksagung

Die Forschung von Dr. Dobrev ist durch das European Network for Translational Research in Atrial Fibrillation (EUTRAF: 261057) und DZHK (Deutsches Zentrum für Herz- und Kreislauf-Forschung) gefördert.

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Ghezelbash, S., Dobrev, D. Pathopysiologie des Vorhofflimmerns. CV 15, 36–40 (2015). https://doi.org/10.1007/s15027-015-0685-x

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  • DOI: https://doi.org/10.1007/s15027-015-0685-x

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