25 years of basic and translational science in EP Europace: novel insights into arrhythmia mechanisms and therapeutic strategies

Abstract

In the last 25 years, EP Europace has published more than 300 basic and translational science articles covering different arrhythmia types (ranging from atrial fibrillation to ventricular tachyarrhythmias), different diseases predisposing to arrhythmia formation (such as genetic arrhythmia disorders and heart failure), and different interventional and pharmacological anti-arrhythmic treatment strategies (ranging from pacing and defibrillation to different ablation approaches and novel drug-therapies). These studies have been conducted in cellular models, small and large animal models, and in the last couple of years increasingly in silico using computational approaches. In sum, these articles have contributed substantially to our pathophysiological understanding of arrhythmia mechanisms and treatment options; many of which have made their way into clinical applications. This review discusses a representative selection of EP Europace manuscripts covering the topics of pacing and ablation, atrial fibrillation, heart failure and pro-arrhythmic ventricular remodelling, ion channel (dys)function and pharmacology, inherited arrhythmia syndromes, and arrhythmogenic cardiomyopathies, highlighting some of the advances of the past 25 years. Given the increasingly recognized complexity and multidisciplinary nature of arrhythmogenesis and continued technological developments, basic and translational electrophysiological research is key advancing the field. EP Europace aims to further increase its contribution to the discovery of arrhythmia mechanisms and the implementation of mechanism-based precision therapy approaches in arrhythmia management.

In Silico TRials guide optimal stratification of ATrIal FIbrillation patients to Catheter Ablation and pharmacological medicaTION: the i-STRATIFICATION study

“…Computer modelling and simulation have been widely used for testing optimal ablation therapies of AF 33 in virtual cohorts. Early work by Hwang et al .…”

Genetic background determines the severity of age-dependent cardiac structural abnormalities and arrhythmia susceptibility in Scn5a-1798insD mice

“…These can, in part, be addressed using patient-specific induced pluripotent stem cell–derived cardiomyocytes (hiPSC-CMs), especially when combined with an isogenic cell line as control. However, given the limitations of these cell lines in studying various important features including the impact of aging and development of structural disease, 57 mouse models remain relevant for studying mechanisms underlying SCN5A -related cardiac dysfunction with the aim of identifying novel clinically relevant diagnostic, prognostic, and therapeutic tools. The current study also emphasizes the importance of using various mouse strains in such studies, as disease phenotype is strongly dependent on genetic background.…”

Safety and efficacy of long-term sodium channel blocker therapy for early rhythm control: the EAST-AFNET 4 trial

“… 10 This is even more important, considering that in the past decade no novel antiarrhythmic agent became available. 11 Sodium channel blocker remains underutilized, even in patients without structural heart disease, 12 , 13 most likely due to fear of proarrhythmia. 14 The Cardiac Arrhythmia Suppression Trial (CAST) observed proarrhythmic effects of flecainide and encainide in patients with prior myocardial infarction, frequent ventricular premature beats, and HF with reduced ejection fraction.…”