Norbert Jost

Norbert Jost

University of Szeged, Hungary

Title: Atrial remodeling in permanent atrial fibrillation. Mechanism and implications


Norbert Jost has completed his Ph.D. in theoretical medical sciences at the age of 29 years from Faculty of Medicine, University of Szeged, Hungary, and postdoctoral studies from Carl Gustav Carus Faculty of Medicine, Unicersity of Technology Dresden, Germany. He supervises the In Vitro Cardiac Electrophysiology Laboratory, Division of Cardiovasculary Pharmacology, Hungarian Academy of Sciences, a team that in the last one and half decades has published more than 40 papers in the fi eld of cardiac, cellular, electrophysiology and pharmacology. In these publications, they described the properties of various transmembrane currents focusing particularly on the modulating effect of several newly developed antiarrhythmic drugs or investigational compounds.


Atrial fi brillation (AF) is the most common arrhythmia in clinical practice. It can occur at any age, however, it becomes extremely common in the elderly, with a prevalence approaching more than 20% in patients older than 85 years. AF is associated with a wide range of cardiac and extra-cardiac complications and thereby contributes signifi cantly to morbidity and mortality. Present therapeutic approaches to AF have major limitations, which have inspired substantial eff orts to improve our understanding of the mechanisms underlying AF, with the premise that improved knowledge will lead to innovative and improved therapeutic approaches. Our understanding of AF pathophysiology has advanced signifi cantly over the past 10 to 15 years through an increased awareness of the role of “atrial remodeling”. Any persistent change in atrial structure or function constitutes atrial remodeling. Both rapid ectopic fi ring and reentry can maintain AF. Atrial remodeling has the potential to increase the likelihood of ectopic or reentrant activity through a multitude of potential mechanisms. Th e present lecture reviews the main novel results on atrial tachycardia-induced electrical, structural and contractile remodeling focusing on the underlying pathophysiological and molecular basis of their occurrence. Special attention is paid to novel strategies and targets with therapeutic signifi cance for atrial fi brillation.

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