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Heart Rhythm. 2018 Sep;15(9):1328-1336. doi: 10.1016/j.hrthm.2018.05.016. Epub 2018 May 23.

Arterial hypertension drives arrhythmia progression via specific structural remodeling in a porcine model of atrial fibrillation.

Author information

1
Division of Cardiology, Department of Medicine, Medical University of Graz, Graz, Austria. Electronic address: martin.manninger-wuenscher@medunigraz.at.
2
Division of Cardiology, Department of Medicine, Medical University of Graz, Graz, Austria.
3
Department of Physiology, Cardiovascular Research Institute Maastricht, University of Maastricht, Maastricht, The Netherlands.
4
Department of Cardiology, Charité University Medicine, Campus Virchow-Klinikum, Berlin, Germany; Berlin Institute of Health (BIH), Berlin, Germany.
5
Institute of Biophysics, Medical University of Graz, Graz, Austria.
6
Institute of Functional and Applied Anatomy, Hannover Medical School, Hannover, Germany.
7
Department of Cardiothoracic Surgery, Medical University of Graz, Graz, Austria.
8
Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Hamburg, Germany; DZHK (German Centre for Cardiovascular Research), Partner site Hamburg/Kiel/Lübeck, Berlin, Germany.
9
Department of Cardiology, Charité University Medicine, Campus Virchow-Klinikum, Berlin, Germany; Department of Cardiology, Contilia Heart and Vessel Centre, St. Marien-Hospital Mülheim, Mülheim, Germany.
10
Division of Cardiology, Department of Medicine, Medical University of Graz, Graz, Austria; Department of Cardiology, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, The Netherlands.

Abstract

BACKGROUND:

Arterial hypertension (HT) contributes to progression of atrial fibrillation (AF) via unknown mechanisms.

OBJECTIVE:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSION:

In this model of secondary HT, higher AF stability after 2 weeks of RAP is mainly driven by atrial dilatation.

KEYWORDS:

Arterial hypertension; Atrial dilatation; Atrial fibrillation; Atrial fibrosis; Electrical remodeling; Structural remodeling

PMID:
29803020
DOI:
10.1016/j.hrthm.2018.05.016
[Indexed for MEDLINE]

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