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Dynamics of rotational and focal drivers in persistent atrial fib | 53772
Clinical & Experimental Cardiology

Clinical & Experimental Cardiology
Open Access

ISSN: 2155-9880

Dynamics of rotational and focal drivers in persistent atrial fibrillation at cardiac fibrosis -A clinical mapping and simulation study


International Conference on Cardiovascular Medicine

August 01-02, 2016 Manchester, UK

Markus Rottmann, Ufuk Arslan, Viktor Markstein, Heiko Lehrmann, Jurgen Allgeier, Reinhold Weber, Wenzel Kaltenbacher, Farhan Rafdionza,Thomas Arentz, Olaf D�?¶ssel and Amir Jadidi

Karlsruhe Institute of Technology, Germany
University Heart center Freiburg-Bad Krozingen, Germany

Scientific Tracks Abstracts: J Clin Exp Cardiolog

Abstract :

Introduction: Persistent atrial fibrillation (AF) is associated with increased prevalence of atrial fibrosis. However, the role of fibrosis in arrhythmogenesis for AF is not well understood. Methods: Clinical data of 18 patients with persistent AF and AF termination by ablation were analysed with regard to spatial relationship of AF termination sites and low voltage areas (LVA<0.5mV). For the first time, numerical simulations in 3D human atrial models assessed the impact of variable size and degree of myocardial fibrosis (DoF) on development and stability of focal and re-entrant sources in AF. Conduction velocity (CV), fiberorientation, pacing frequency and repetition of sources were analyzed. Results: 14/18 (78%) of AF termination sites located to low voltage areas (0.5mV) and 4/18 (22%) to borderzones (<1cm distance to LVA). Simulations of persistent AF in a 3D-atrial model with regional fibrosis revealed stable (>20 AF cycles) anchoring of meandering rotational and focal sources within fibrosis (<5mm of borders). Rotational excitation wavefronts spread out from fibrosis area to healthy tissue, resulting in focal-like excitation patterns. However, the focal sources originated from variable locations around the fibrosis borders, potentially leading to beat-to-beat variabilities in the electrogram morphology. CV was 1 m/s within healthy tissue, 0.2 m/s at fibrosis > 40% and 0.4 m/s at fibrosis 30-40%. With increasing degree of fibrosis, electrogram amplitudes decreased but the cycle lengths, stability and consistency of sources increased. Conclusions: Region of increased atrial fibrosis display low voltage amplitudes and harbour rotational and focal sources responsible for AF.

Biography :

Markus Rottmann has completed his Master of Science degree from Karlsruhe Institute of Technology (KIT), Germany. Currently, he is pursuing PhD in Biomedical Engineering at the Institute of Biomedical Engineering, KIT. He is engaged in research on Computational Cardiology.

Email: markus.rottmann@kit.edu

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