Experimental atrial fibrillation
The current research of our group focuses on the variability of the mechanisms underlying the initiation and perpetuation of AF. In various animal models (atrial fibrillation, atrial dilatation, rapid atrial pacing, heart failure) we study electrical activation patterns during AF and correlate the results to the underlying tissue architecture to better understand the relation between atrial structural characteristics (e.g. bundle architecture, fibrosis, and fatty infiltrates) and the perpetuation of AF. The analysis of the activation pattern of fibrillation waves in the spatial domain provides important new insides in trigger mechanisms and the development of a substrate of the arrhythmia. The ultimate goal is to develop a classification of AF based on the spatio-temporal behavior of the fibrillation waves. Quantitative analysis of fibrillation waves will also allow better understanding the mode of action of anti-arrhythmic drugs. Besides the development of means to prevent structural remodeling of the atria, there is great need for new pharmaceutical agents that can more effectively and safely prolong atrial refractoriness without affecting ventricular electrophysiology. In various animal models, the ability of newly developed blockers of atrial-specific potassium channels to prolong atrial refractoriness, to cardiovert AF and to restore atrial contractility is investigated.
I coordinate studies on electrical, contractile, and structural remodeling in heart failure and atrial fibrillation. Main research topics are: Adaptation processes of excitation-contraction coupling in ventricular and atrial myocardium, cellular and integrated action of antiarrhythmic drugs, and the development of substrates for the perpetuation of atrial fibrillation.