Tachycardia-induced silencing of subcellular Ca2+ signaling in atrial myocytes

Greiser, Maura; Kerfant, Benoît-Gilles; Williams, George S.B.; Voigt, Niels; Harks, Erik; Dibb, Katharine M.; Giese, Anne Katrin; Meszaros, J. Gary; Verheule, Sander; Ravens, Ursula; Allessie, Maurits A.; Gammie, James S.; Velden, Jolanda van der; Lederer, W. Jonathan; Dobrev, Dobromir; Schotten, Ulrich

doi:10.1172/jci70102

Cited by 104 publications

(181 citation statements)

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“…Hiperfosforylacja różnych białek uczestniczących w gospodarce jonów wapniowych może się przyczyniać do zwiększenia incydentów samoistnego uwalniania jonów wapnia oraz wyzwalanej aktywności [97,98], wywołując w ten sposób ektopię i sprzyjając AF. Mimo że koncepcję niestabilności gospodarki jonów wapniowych ostatnio zakwestionowano [106,107], to czynnik ten może leżeć u podłoża AF w przedsionkach, które uległy przebudowie strukturalnej, i może tłumaczyć, w jaki sposób zmiany napięcia układu autonomicznego mogą generować AF [80,105].…”

Section: Elektrofizjologiczne Mechanizmy Migotania Przedsionkówunclassified

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

Kirchhof

Benussi

Kotecha³

et al. 2016

Kardiol Pol

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Section: Elektrofizjologiczne Mechanizmy Migotania Przedsionkówunclassified

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

Kirchhof

Benussi

Kotecha³

et al. 2016

Kardiol Pol

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“…96 Hyperphosphorylation of various Ca 2+ -handling proteins may contribute to enhanced spontaneous Ca 2+ release events and triggered activity, 97,98 thus causing ectopy and promoting AF. Although the concept of Ca 2+ -handling instability has been challenged recently, 106,107 it may mediate AF in structurally remodelled atria and explain how altered autonomic tone can generate AF. 80,105 …”

Section: Electrophysiological Mechanisms Of Atrial Fibrillationmentioning

confidence: 99%

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

Kirchhof¹,

Benussi²,

Kotecha³

et al. 2016

Eur J Cardiothorac Surg

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“…In the presence of AF, high atrial rates and early reactivation of cardiomyocytes elevate diastolic Ca 2+ and intracellular Ca 2+ storage 56,57 . Adaptation to this new situation results in profound changes in the ion channels controlling Ca 2+ reuptake and release by the sarcoplasmic reticulum 13,21 .…”

Section: Altered Calcium Homeostasismentioning

confidence: 99%

“…Increases in spontaneous electrical activity have been suggested to have a major role in abnormal intracellular Ca 2+ handling in the genesis of AF 59 . Although this theory has been challenged by reports demonstrating improved Ca 2+ -handling stability, and even Ca 2+ silencing, after AF 56,60 , increases in the sympathetic activity in the atrial tissue might still underlie the increase in the rate of ectopic activity during AF.…”

Section: Altered Calcium Homeostasismentioning

confidence: 99%

Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

et al. 2015

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Despite the important advances that have enabled better stroke prevention in atrial fibrillation (AF) and more effective maintenance of sinus rhythm over the past decades, a large unmet need to improve the prevention and treatment of AF remains. Mortality for AF remains at 3.5% per year, and death is often experienced as sudden death or as a result of heart failure 1,2 . Each year, approximately 20% of patients with AF need to be hospitalized 3,4 , and stroke occurs in 1.5% of patients with AF who are receiving anticoagulant drugs 5 . Furthermore, more than half of the patients with AF are symptomatic despite adequate anticoagulation and rate control 4,6 . In view of the projected increase in the incidence and prevalence of AF 7-9 , as well as the substantial burden of death and dis ability that is still associated with this condition 10 , the status quo is unacceptable.Current management of patients with AF comprises treatment of the accompanying cardiovascular conditions, oral anticoagulation, rate control -with medications that slow atrioventricular nodal recovery or, rarely, with atrioventricular nodal ablation -and rhythm-control therapy with antiarrhythmic drugs, electrical cardioversion, catheter ablation or, at times, AF surgery 11,12 . Unfortunately, most of these current approaches are disconnected from our understanding of the major mechanisms that cause AF 1,13,14 1,2,7,19,20 Abstract | Despite remarkable advances in antiarrhythmic drugs, ablation procedures, and stroke-prevention strategies, atrial fibrillation (AF) remains an important cause of death and disability in middle-aged and elderly individuals. Unstructured management of patients with AF sharply contrasts with our detailed, although incomplete, knowledge of the mechanisms that cause AF and its complications. Altered calcium homeostasis, atrial fibrosis and ageing, ion-channel dysfunction, autonomic imbalance, fat-cell infiltration, and oxidative stress, in addition to a susceptible genetic background, contribute to the promotion, maintenance, and progression of AF. However, clinical management of patients with AF is currently guided by stroke risk parameters, AF pattern, and symptoms. In response to this apparent disconnect between the known pathophysiology of AF and clinical management, we propose a roadmap to develop a set of clinical markers that reflect the major causes of AF in patients. Thereby, the insights into the mechanisms causing AF will be transformed into a format that can underpin future personalized strategies to prevent and treat AF, ultimately informing better patient care.230 | APRIL 2016 | VOLUME 13 www.nature.com/nrcardio CONSENSUS STATEMENT © 2 0 1 6 M a c m i l l a n P u b l i s h e r s L i m i t e d . A l l r i g h t s r e s e r v e d .

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Tachycardia-induced silencing of subcellular Ca2+ signaling in atrial myocytes

Cited by 104 publications

References 50 publications

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

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