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

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 pressure109.9 [100–137] mm Hg in AF+HT vs 82.2 [79–96] mm Hg in AF; P 1 hour; P 2 in AF+HT vs 78 ± 23 cm 2 in AF; P 3 in AF+HT vs 0.96 ± 0.3 cm 3 in AF; P Conclusion In this model of secondary HT, higher AF stability after 2 weeks of RAPis mainly driven by atrial dilatation.