AMIODARONE INSTILLED INTO THE CANINE PERICARDIAL SAC MIGRATES TRANSMURALLY TO PRODUCE ELECTROPHYSIOLOGIC EFFECTS AND SUPPRESS ATRIAL-FIBRILLATION

Pericardial Sac as Amiodarone Reservoir. Introduction: We investigated whether amiodarone delivered into the pericardial sac exerted an effe ct on atrial and ventricular refractoriness, impulse generation, and c onduction and on induced atrial fibrillation. Methods and Results: All animals were anesthetized with alpha-chloralose. After a sternotomy, the pericardium was opened and cradled to produce a ''container'' of a pproximately 75 mt. Part I experimental animals received amiodarone, 0 .5, 1.0, or 5.0 mg/mL, dissolved in 3 mL polysorbate 80 and 5% dextros e in water (D5W) instilled into their pericardial sac for 3-hour inter vals, Part II experimental animals received either 1.0 or 5.0 mg/mL of amiodarone, Control dogs received a pericardial solution of 3 mt poly sorbate 80 in D5W, Pre- and postinstillation electrophysiologic studie s were performed, In part I, the increase in sinus cycle length, 1:1 A V conduction, and effective refractory period (ERP) of atrium, right v entricular (RV) and left ventricular epicardium, and RV endocardium we re significantly greater in animals receiving amiodarone compared with controls, Amiodarone concentrations in the tissue samples were highes t in the superficial sites of the atria, sinoatrial node, and ventricu lar epicardial samples and lowest in the interventricular septum, Only trace concentrations of amiodarone and no desethylamiodarone were fou nd in the blood samples, In part II, atrial ERP significantly increase d in the animals receiving amiodarone, and the number of episodes of s ustained atrial fibrillation that could be induced decreased. Conclusi ons: Amiodarone instilled into the pericardial sac migrates transmural ly to produce significant electrophysiologic effects at superficial si tes and appears to suppress electrically induced atrial fibrillation.