Skip to main content
Home
Zeitschriften
Zeitungen
Podcast
Gesundheitspolitik
Praxis
Allerlei
Jobs
Fachgebiete
Allgemeinmedizin Anästhesiologie & Intensivmedizin Apotheke Augenheilkunde Chirurgie Dermatologie Gynäkologie und Geburtshilfe HNO Innere Medizin Kinder & Jugendheilkunde Neurologie & Psychiatrie Orthopädie & Unfallchirurgie Pflege Urologie Zahnmedizin
Subfächer Innere Medizin
Diabetologie Gastroenterologie Infektiologie Kardiologie Onkologie und Hämatologie Pneumologie Rheumatologie
Fortbildungen
Überblick Fortbildungen DFP-Literaturstudium-Artikel DFP-Webcast Fortbildungen DFP-Podcasts
Erweiterte Suche
Anmelden
nach oben
Wiener Medizinische Wochenschrift
Erschienen in:

01.07.2012 | original article

Calcium handling and atrial fibrillation

verfasst von: Jordi Heijman, PhD, Niels Voigt, PhD, Stanley Nattel, MD, Univ.-Prof. Dr. med. Dobromir Dobrev, MD

Erschienen in: Wiener Medizinische Wochenschrift | Ausgabe 13-14/2012

Einloggen, um Zugang zu erhalten

Summary

Atrial fibrillation (AF) is the most prevalent sustained cardiac arrhythmia in the clinical setting. It is associated with substantial cardiovascular morbidity and mortality. Recent research has indicated that abnormal Ca2+ handling plays a critical role in the induction and maintenance of AF, contributing to ectopic activity, AF-maintaining reentry circuits and related prothrombotic atrial hypocontractility. The AF-specific Ca2+-handling abnormalities may constitute viable therapeutic approaches to treat AF. Here, we review the causes, consequences, and therapeutic implications of altered atrial Ca2+ handling for AF pathophysiology.
Vorheriger Artikel Calcium handling and ventricular tachyarrhythmias
Nächster Artikel Arrhythmia-associated cardiac Ca2+ cycling proteins and gene mutations
Literatur
1.
Lloyd-Jones DM, Wang TJ, Leip EP, et al. Lifetime risk for development of atrial fibrillation: the Framingham Heart Study. Circulation. 2004;110:1042–6.PubMedCrossRef
2.
Wakili R, Voigt N, Kaab S, et al. Recent advances in the molecular pathophysiology of atrial fibrillation. J Clin Invest. 2011;121:2955–68.PubMedCrossRef
3.
Dobrev D. Electrical remodeling in atrial fibrillation. Herz. 2006;31:108–12 (quiz 142-103).PubMedCrossRef
4.
Hove-Madsen L, Llach A, Bayes-Genis A, et al. Atrial fibrillation is associated with increased spontaneous calcium release from the sarcoplasmic reticulum in human atrial myocytes. Circulation. 2004;110:1358–63.PubMedCrossRef
5.
Dobrev D. Atrial Ca2+ signaling in atrial fibrillation as an antiarrhythmic drug target. Naunyn Schmiedebergs Arch Pharmacol. 2010;381:195–206.PubMedCrossRef
6.
Neef S, Dybkova N, Sossalla S, et al. CaMKII-dependent diastolic SR Ca2+ leak and elevated diastolic Ca2+ levels in right atrial myocardium of patients with atrial fibrillation. Circ Res. 2010;106:1134–44.PubMedCrossRef
7.
Bers DM. Calcium cycling and signaling in cardiac myocytes. Annu Rev Physiol. 2008;70:23–49.PubMedCrossRef
8.
Dobrev D, Voigt N, Wehrens XH. The ryanodine receptor channel as a molecular motif in atrial fibrillation: pathophysiological and therapeutic implications. Cardiovasc Res. 2011;89:734–43.PubMedCrossRef
9.
Walden AP, Dibb KM, Trafford AW. Differences in intracellular calcium homeostasis between atrial and ventricular myocytes. J Mol Cell Cardiol. 2009;46:463–73.PubMedCrossRef
10.
El-Armouche A, Boknik P, Eschenhagen T, et al. Molecular determinants of altered Ca2+ handling in human chronic atrial fibrillation. Circulation. 2006;114:670–80.PubMedCrossRef
11.
Vest JA, Wehrens XH, Reiken SR, et al. Defective cardiac ryanodine receptor regulation during atrial fibrillation. Circulation. 2005;111:2025–32.PubMedCrossRef
12.
Dobrev D, Nattel S. Calcium handling abnormalities in atrial fibrillation as a target for innovative therapeutics. J Cardiovasc Pharmacol. 2008;52:293–9.PubMedCrossRef
13.
Lenaerts I, Bito V, Heinzel FR, et al. Ultrastructural and functional remodeling of the coupling between Ca2+ influx and sarcoplasmic reticulum Ca2+ release in right atrial myocytes from experimental persistent atrial fibrillation. Circ Res. 2009;105:876–85.PubMedCrossRef
14.
Grandi E, Pandit SV, Voigt N, et al. Human atrial action potential and Ca2+ model: sinus rhythm and chronic atrial fibrillation. Circ Res. 2011;109:1055–66.PubMedCrossRef
15.
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(17):2059–70.PubMedCrossRef
16.
Qi XY, Yeh YH, Xiao L, et al. Cellular signaling underlying atrial tachycardia remodeling of L-type calcium current. Circ Res. 2008;103:845–854.PubMedCrossRef
17.
Christ T, Boknik P, Wohrl 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.PubMedCrossRef
18.
Wang Z, Lu Y, Yang B. MicroRNAs and atrial fibrillation: new fundamentals. Cardiovasc Res. 2011;89:710–21.PubMedCrossRef
19.
Dobrev D, Friedrich A, Voigt N, et al. The G protein-gated potassium current IK, ACh is constitutively active in patients with chronic atrial fibrillation. Circulation. 2005;112:3697–3706.PubMedCrossRef
20.
Makary S, Voigt N, Maguy A, et al. Differential protein kinase C isoform regulation and increased constitutive activity of acetylcholine-regulated potassium channels in atrial remodeling. Circ Res. 2011;109:1031–43.PubMedCrossRef
21.
Pandit SV, Berenfeld O, Anumonwo JM, et al. Ionic determinants of functional reentry in a 2-D model of human atrial cells during simulated chronic atrial fibrillation. Biophys J. 2005;88:3806–21.PubMedCrossRef
22.
Ellinor PT, Lunetta KL, Glazer NL, et al. Common variants in KCNN3 are associated with lone atrial fibrillation. Nat Genet. 2010;42:240–4.PubMedCrossRef
23.
Schotten U, Ausma J, Stellbrink C, et al. Cellular mechanisms of depressed atrial contractility in patients with chronic atrial fibrillation. Circulation. 2001;103:691–8.PubMedCrossRef
24.
Nattel S, Burstein B, Dobrev D. Atrial remodeling and atrial fibrillation: mechanisms and implications. Circ Arrhythm Electrophysiol. 2008;1:62–73.PubMedCrossRef
25.
Yue L, Xie J, Nattel S. Molecular determinants of cardiac fibroblast electrical function and therapeutic implications for atrial fibrillation. Cardiovasc Res. 2011;89:744–53.PubMedCrossRef
26.
Wang YJ, Sung RJ, Lin MW, et al. Contribution of BK(Ca)-channel activity in human cardiac fibroblasts to electrical coupling of cardiomyocytes-fibroblasts. J Membr Biol. 2006;213:175–85.PubMedCrossRef
27.
Dobrev D, Nattel S. New antiarrhythmic drugs for treatment of atrial fibrillation. Lancet. 2010;375:1212–23.PubMedCrossRef
28.
Hwang HS, Hasdemir C, Laver D, et al. Inhibition of cardiac Ca2+ release channels (RyR2) determines efficacy of class I antiarrhythmic drugs in catecholaminergic polymorphic ventricular tachycardia. Circ Arrhythm Electrophysiol. 2011;4:128–35.PubMedCrossRef
29.
Zhou Q, Xiao J, Jiang D, et al. Carvedilol and its new analogs suppress arrhythmogenic store overload-induced Ca2+ release. Nat Med. 2011;17:1003–9.PubMedCrossRef
30.
Li N, Wang T, Wang W, et al. Inhibition of CaMKII phosphorylation of RyR2 prevents induction of atrial fibrillation in FKBP12.6 knockout mice. Circ Res. 2012;110:465–70.PubMedCrossRef
Metadaten
Titel
Calcium handling and atrial fibrillation
verfasst von
Jordi Heijman, PhD
Niels Voigt, PhD
Stanley Nattel, MD
Univ.-Prof. Dr. med. Dobromir Dobrev, MD
Publikationsdatum
01.07.2012
Verlag
Springer Vienna
Erschienen in
Wiener Medizinische Wochenschrift / Ausgabe 13-14/2012
Print ISSN: 0043-5341
Elektronische ISSN: 1563-258X
DOI
https://doi.org/10.1007/s10354-012-0109-9

Weitere Artikel der Ausgabe 13-14/2012

Calcium is omnipresent in the physiology and pathophysiology of heart disease

  • editorial

Calcium handling in human heart failure—abnormalities and target for therapy

  • Kalzium in der kardialen Pathophysiologie

Calcium handling and ventricular tachyarrhythmias

  • Kalzium in der kardialen Pathophysiologie

Odontogene Infektionen – Teil I

  • original article

Arrhythmia-associated cardiac Ca2+ cycling proteins and gene mutations

  • Kalzium in der kardialen Pathophysiologie

Calcium antagonists in myocardial ischemia/reperfusion—update 2012

  • Kalzium in der kardialen Pathophysiologie