Abstract

Introduction: It is not clear why persistent (AF) is less trigger dependent than paroxysmal AF and responds less well to pulmonary vein isolation (PVI). We hypothesized that structural remodelling may flatten left atrial APD restitution, reducing the ability of a trigger to cause APD oscillations in persistent AF patients. Methods: Monophasic action potentials (MAP) were recorded in 47 patients (61 ± 9 years, LA 44 ± 6mm, 52% persistent AF) near the PV antra during pacing. We plotted MAP duration restitution cycle length (CL) dependence of APD90, i.e. the time from monophasic action potential (MAP) upstroke to 90% repolarization, as a restitution curve, and calculated its maximum slope. ERP was defined routinely. Both factors were related to LA size to assess structural remodelling. Results: Dynamic ERP tracked APD in remodelled human LA (Fig A; p < 0.05). Fig B shows an AF trigger engaging steep APD restitution (C) to initiate AF. Fig D shows that APD restitution slope correlated negatively with LA diameter (p < 0.05). Compared to patients with paroxysmal AF, those with persistent AF (remodelled atria) had shorter APD90 (236 ± 35 vs 284 ± 46ms, p < 0.01), flatter APD restitution (0.67 ± 0.2 vs 1.5 ± 0.4, p < 0.001) and shorter ERP (204 ± 28 vs 241 ± 38ms, p = 0.01).

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