TY - JOUR
T1 - German Cardiac Society Working Group on Cellular Electrophysiology state-of-the-art paper
T2 - impact of molecular mechanisms on clinical arrhythmia management
AU - Thomas, Dierk
AU - Christ, Torsten
AU - Fabritz, Larissa
AU - Goette, Andreas
AU - Hammwoehner, Matthias
AU - Heijman, Jordi
AU - Kockskaemper, Jens
AU - Linz, Dominik
AU - Odening, Katja E.
AU - Schweizer, Patrick A.
AU - Wakili, Reza
AU - Voigt, Niels
N1 - Funding Information:
Acknowledgements The authors work was supported in part by research grants from the German Heart Foundation/German Foundation of Heart Research (Josef Freitag Foundation to A.G., F/08/14 to D.T., F/03/15 to D.L.), from the Else Kröner-Fresenius-Stiftung (2014_A242 to D.T., 2014_A306 to D.L., 2016_A20 to N.V.), from the Joachim Siebeneicher Foundation (to D.T.), from the Deutsche Forschungsgemeinschaft (German Research Foundation; TH 1120/7-1 and TH 1120/8-1 to D.T., KFO 196 to D.L. et al., BR2107/4-1 and OD 86/6-1 to K.E.O., SCHW 1611/1-1 to P.A.S., VO 1568/3-1 and IRTG1816 RP12 and SFB1002 TPA13 to N.V.), from the Ministry of Science, Research and the Arts Baden-Wuerttemberg (Sonderlinie Medizin to D.T.; Wrangell Programme to K.E.O.), from the Josef-Freitag-Stiftung (to A.G.), and from the German Cardiac Society (DGK0914 to D.L.). D.T. and N.V. were supported by the German Center for Cardiovascular Research (DZHK). A.G. and J.K. were supported by European Union Seventh Framework Programme (EUTRAF-261057). J.H. was supported by the Netherlands Organization for Scientific Research (ZonMW Veni 91616057) and the Young Talent Program of the CardioVascular Onderzoek Nederland (CVON) and Netherlands Heart Foundation PREDICT project, D.L. was supported by a Beacon Research Fellowship from the University of Adelaide. P.S. received support from the Molecular Medicine Partnership Unit, Heidelberg (Senior Career Fellowship).
Publisher Copyright:
© 2018, Springer-Verlag GmbH Germany, part of Springer Nature.
PY - 2019/6
Y1 - 2019/6
N2 - Cardiac arrhythmias remain a common challenge and are associated with significant morbidity and mortality. Effective and safe rhythm control strategies are a primary, yet unmet need in everyday clinical practice. Despite significant pharmacological and technological advances, including catheter ablation and device-based therapies, the development of more effective alternatives is of significant interest to increase quality of life and to reduce symptom burden, hospitalizations and mortality. The mechanistic understanding of pathophysiological pathways underlying cardiac arrhythmias has advanced profoundly, opening up novel avenues for mechanism-based therapeutic approaches. Current management of arrhythmias, however, is primarily guided by clinical and demographic characteristics of patient groups as opposed to individual, patient-specific mechanisms and pheno-/genotyping. With this state-of-the-art paper, the Working Group on Cellular Electrophysiology of the German Cardiac Society aims to close the gap between advanced molecular understanding and clinical decision-making in cardiac electrophysiology. The significance of cellular electrophysiological findings for clinical arrhythmia management constitutes the main focus of this document. Clinically relevant knowledge of pathophysiological pathways of arrhythmias and cellular mechanisms of antiarrhythmic interventions are summarized. Furthermore, the specific molecular background for the initiation and perpetuation of atrial and ventricular arrhythmias and mechanism-based strategies for therapeutic interventions are highlighted. Current hot topics in atrial fibrillation are critically appraised. Finally, the establishment and support of cellular and translational electrophysiology programs in clinical rhythmology departments is called for to improve basic-science-guided patient management.
AB - Cardiac arrhythmias remain a common challenge and are associated with significant morbidity and mortality. Effective and safe rhythm control strategies are a primary, yet unmet need in everyday clinical practice. Despite significant pharmacological and technological advances, including catheter ablation and device-based therapies, the development of more effective alternatives is of significant interest to increase quality of life and to reduce symptom burden, hospitalizations and mortality. The mechanistic understanding of pathophysiological pathways underlying cardiac arrhythmias has advanced profoundly, opening up novel avenues for mechanism-based therapeutic approaches. Current management of arrhythmias, however, is primarily guided by clinical and demographic characteristics of patient groups as opposed to individual, patient-specific mechanisms and pheno-/genotyping. With this state-of-the-art paper, the Working Group on Cellular Electrophysiology of the German Cardiac Society aims to close the gap between advanced molecular understanding and clinical decision-making in cardiac electrophysiology. The significance of cellular electrophysiological findings for clinical arrhythmia management constitutes the main focus of this document. Clinically relevant knowledge of pathophysiological pathways of arrhythmias and cellular mechanisms of antiarrhythmic interventions are summarized. Furthermore, the specific molecular background for the initiation and perpetuation of atrial and ventricular arrhythmias and mechanism-based strategies for therapeutic interventions are highlighted. Current hot topics in atrial fibrillation are critically appraised. Finally, the establishment and support of cellular and translational electrophysiology programs in clinical rhythmology departments is called for to improve basic-science-guided patient management.
KW - ACTION-POTENTIAL DURATION
KW - ATRIAL-FIBRILLATION
KW - Antiarrhythmic therapy
KW - Arrhythmogenesis
KW - BRUGADA-SYNDROME
KW - CONDUCTION SYSTEM DISEASE
KW - Cellular electrophysiology
KW - HEART-RATE
KW - III ANTIARRHYTHMIC AGENT
KW - Ion channels
KW - LONG-QT
KW - PLURIPOTENT STEM-CELLS
KW - Pathophysiology
KW - RENAL DENERVATION
KW - VENTRICULAR-ARRHYTHMIAS
KW - NODE DYSFUNCTION
U2 - 10.1007/s00392-018-1377-1
DO - 10.1007/s00392-018-1377-1
M3 - (Systematic) Review article
C2 - 30306295
SN - 1861-0684
VL - 108
SP - 577
EP - 599
JO - Clinical research in cardiology
JF - Clinical research in cardiology
IS - 6
ER -