Amiodarone Instilled Into the Canine Pericardial Sac Migrates Transmurally to Produce Electrophysiologic Effects and Suppress Atrial Fibrillation

Publisher Website
Google Scholar
Abstract
Pericardial Sac as Amiodarone Reservoir. Introduction: We investigated whether amiodarone delivered into the pericardial sac exerted an effect on atrial and ventricular refractoriness, impulse generation, and conduction and on induced atrial fibrillation. Methods and Results: All animals were anesthetized with α‐chloralose. After a sternotomy, the pericardium was opened and cradled to produce a “container” of approximately 75 mL. Part 1 experimental animals received amiodarone, 0.5, 1.0, or 5.0 mg/mL, dissolved in 3 mL polysorbate 80 and 5% dextrose in water (D5W) instilled into their pericardial sac for 3‐hour intervals. Part II experimental animals received either 1.0 or 5.0 mg/mL of amiodarone. Control dogs received a pericardial solution of 3 mL polysorhate 80 in D5W. Pre‐ and postinstillation electrophysiologic studies were performed. In part I, the increase in sinus cycle length, 1:1 AV conduction, and effective refractory period (ERP) of atrium, right ventricular (RV) and left ventricular epicardium, and RV endocardium were significantly greater in animals receiving amiodarone compared with controls. Amiodarone concentrations in the tissue samples were highest in the superficial sites of the atria, sinoatrial node, and ventricular epicardial samples and lowest in the interventricular septum. Only trace concentrations of amiodarone and no desethylamiodarone were found in the blood samples. In part II, atrial ERP significantly increased in the animals receiving amiodarone, and the number of episodes of sustained atrial fibrillation that could he induced decreased. Conclusions: Amiodarone instilled into the pericardial sac migrates transmurally to produce significant electrophysiologic effects at superficial sites and appears to suppress electrically induced atrial fibrillation.