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

摘要

BackgroundArterial hypertension (HT) contributes to progression of atrial fibrillation (AF) via unknown mechanisms. ObjectiveWe 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. MethodsEighteen 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. ResultsDOCA 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 1 hour;P< .05), concentric left ventricular hypertrophy, atrial dilatation (119 ± 31 cm2in AF+HT vs 78 ± 23 cm2in AF;P?