PO-01-180 MECHANISMS OF PULMONARY ARTERIAL HYPERTENSION-INDUCED ATRIAL FIBRILLATION IN THE RIGHT HEART: INSIGHTS FROM MULTI-SCALE MODELS OF THE HUMAN ATRIA

Pulmonary arterial hypertension (PAH) is one of the common conditions primarily affecting right heart and promoting atrial fibrillation (AF), but mechanisms are poorly understood. This study aimed to use multi-scale models investigate by which (RA) remodeling facilitates perpetuates arrhythmias. We have developed single-cell-to-tissue-level computer mimic control disease incorporating most recent experimental data on PAH-induced electrical structural (Hiram et al., JACC, 2019). The effects in both RA left atria (LA) action potential duration (APD), calcium transient (CaT), conduction velocity (CV), dynamics re-entrant excitation waves were assessed using models. Our simulation results suggested that at single cell level, although prolonged (ΔAPD: 49.6 ms vs. 41.6 LA) increased (ΔCaT: 7.5e-2 μM 0.9e-3 LA), heterogeneous susceptibility afterdepolarizations only (Fig. A). At tissue dramatically reduced CV (ΔCV: -0.5 m/s -0.05 abbreviated wavelength inthe not LA. In addition, repolarization dispersion promoted unidirectional block (Fig B). Finally, upregulated fibrosis chance breakdown sustained reentries C). These demonstrated AF mainly LA, due a higher degree cardiac remodeling. increases arrhythmias risk elevated afterdepolarizations, wavelength, heterogeneity upregulation fibrosis, together facilitate initiation maintenance circuits heart.