Right atrial mechanism contributes to atrial fibrillation in a canine model of pulmonary arterial hypertension

Abstract

AbstractObjectivesThe aim of this study was to investigate proarrhythmic substrates of atrial fibrillation (AF) in a canine model of dehydromonophylline (DMCT)-induced pulmonary arterial hypertension (PAH).MethodsAll cannines (n=12) underwent baseline echocardiographic and hemodynamic examinations, 7 of which were injected with DMCT (3.0mg/kg) to induce PAH via jugular vein cannulation. The control beagles (n=5) were given the same dose of normal saline. Then, both groups were monitored by insertable cardiac monitors. Hemodynamic, echocardiographic, electrophysiological and histological examinations were performed 8 weeks later.ResultsIn PAH group, 2 died after the injection (mortality 28.6%). Thus, 10 beagles (PAH group: 5, control group: 5) underwent all the examinations. The pulmonary artery pressure increased significantly while the right atrium (RA) and right ventricle expanded slightly. Spontaneous AF episodes were recorded in all PAH canines 1 week after the injection. The AF burden increased rapidly from 1 week (7.6±1.8%) and remained high after 2-3 weeks (32.0±4.9% at 8 weeks). Compared with the control group, the PAH group had abbreviated effective refractory periods (ERPs), increased atrial ERP dispersion, and slower conduction velocities. Notably, AF susceptibility and atrial remodeling in RA was more significant those in LA, such as increased WOV(39.0±6.5ms vs. 28.0±5.7ms, P=0.022), enlarged low voltage regions (7.66±0.46% vs. 4.40±0.55%, P<0.0001) and fibrosis (8.22±0.61% vs. 4.93±0.60%, P <0.0001).ConclusionsDMCT-induced canine PAH model increased the incidence of spontaneous and induced AF. The electrophysiological and structural remodeling of the RA facilitated the AF genesis.