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Manninger, M; Zweiker, D; van Hunnik, A; Alogna, A; Prassl, AJ; Schipke, J; Zeemering, S; Zirngast, B; Schönleitner, P; Schwarzl, M; Herbst, V; Thon-Gutschi, E; Huber, S; Rohrer, U; Ebner, J; Brussee, H; Pieske, BM; Heinzel, FR; Verheule, S; Antoons, G; Lueger, A; Mühlfeld, C; Plank, G; Schotten, U; Post, H; Scherr, D.
Arterial hypertension drives arrhythmia progression via specific structural remodeling in a porcine model of atrial fibrillation.
Heart Rhythm. 2018; 15(9):1328-1336 Doi: 10.1016/j.hrthm.2018.05.016
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Führende Autor*innen der Med Uni Graz
Manninger-Wünscher Martin
Co-Autor*innen der Med Uni Graz
Alogna Alessio
Antoons Gudrun
Brussee Helmut
Ebner Jakob
Heinzel Frank
Huber Stefan
Lueger Andreas
Pieske Burkert Mathias
Plank Gernot
Post Heiner
Prassl Anton
Rohrer Ursula
Scherr Daniel
Schönleitner Patrick
Schwarzl Michael
Trummer-Herbst Viktoria
Zirngast Birgit
Zweiker David

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Arterial hypertension (HT) contributes to progression of atrial fibrillation (AF) via unknown mechanisms. We aimed to characterize electrical and structural changes accounting for increased AF stability in a large animal model of rapid atrial pacing (RAP)-induced AF combined with desoxycorticosterone acetate (DOCA)-induced HT. Eighteen pigs were instrumented with right atrial endocardial pacemaker leads and custom-made pacemakers to induce AF by continuous RAP (600 beats/min). DOCA pellets were subcutaneously implanted in a subgroup of 9 animals (AF+HT group); the other 9 animals served as controls (AF group). Final experiments included electrophysiology studies, endocardial electroanatomic mapping, and high-density mapping with epicardial multielectrode arrays. In addition, 3-dimensional computational modeling was performed. DOCA implantation led to secondary HT (median [interquartile range] aortic pressure 109.9 [100-137] mm Hg in AF+HT vs 82.2 [79-96] mm Hg in AF; P < .05), increased AF stability (55.6% vs 12.5% of animals with AF episodes lasting >1 hour; P < .05), concentric left ventricular hypertrophy, atrial dilatation (119 ± 31 cm2 in AF+HT vs 78 ± 23 cm2 in AF; P < .05), and fibrosis. Collagen accumulation in the AF+HT group was mainly found in non-intermyocyte areas (1.62 ± 0.38 cm3 in AF+HT vs 0.96 ± 0.3 cm3 in AF; P < .05). Left and right atrial effective refractory periods, action potential durations, endo- and epicardial conduction velocities, and measures of AF complexity were comparable between the 2 groups. A 3-dimensional computational model confirmed an increase in AF stability observed in the in vivo experiments associated with increased atrial size. In this model of secondary HT, higher AF stability after 2 weeks of RAP is mainly driven by atrial dilatation. Copyright © 2018 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Atrial Fibrillation - etiology
Atrial Fibrillation - physiopathology
Atrial Fibrillation - therapy
Atrial Remodeling -
Blood Pressure - physiology
Computer Simulation -
Disease Models, Animal -
Electrocardiography -
Heart Atria - diagnostic imaging
Heart Atria - physiopathology
Heart Rate - physiology
Hypertension - complications
Hypertension - physiopathology
Pacemaker, Artificial -
Swine -

Find related publications in this database (Keywords)
Arterial hypertension
Atrial dilatation
Atrial fibrillation
Atrial fibrosis
Electrical remodeling
Structural remodeling
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