Abstract 2356: Induction of Postshock Triggered Activity in Purkinje Fibers: Possible Role of Inward Rectifying Potassium Currents
Introduction: Spontaneous ventricular tachycardia/fibrillation (VT/VF) episodes after initial successful defibrillation occur in 50% of patients during cardiopulmonary resuscitation and are associated with poor clinical outcome.
Hypothesis: We hypothesize that the postshock arrhythmias occur due to spontaneous sarcoplasmic reticulum Ca release, delayed afterdepolarization (DAD), and triggered activity from Purkinje fibers.
Methods: We simultaneously mapped intracellular Ca (Cai) and transmembrane potentials (Vm) on epicardial (n=14) or endocardial (n=14) surfaces of Langendorff-perfused rabbit ventricles.
Results: Spontaneous Cai elevation (SCaE) was defined by Cai elevation before Vm elevation. It was noted after defibrillation in 32% of VT/VF at baseline and 83% during isoproterenol infusion (0.01~1 μmol/L). SCaE was reproducibly induced by rapid ventricular pacing. The SCaE amplitude and slope increased while the coupling intervals decreased with increasing pacing rate, duration, and dose of isoproterenol. We found triggered activities arising from 6 of 14 endocardial surfaces but none from epicardial surfaces. The magnitude of SCaEs on endocardial and epicardial surfaces was the same, but the amplitude of DADs (with baseline action potential amplitude as 1 artificial unit, or AU) was larger on endocardial surface (0.057±0.037 AU) than epicardial surface (0.008±0.014 AU, P<0.001). In 2 hearts, Purkinje-like potentials were observed on the endocardial surface that developed triggered activity and VT. Ik1 suppression with CsCl (5 mmol/L, n=3) or BaCl2 (3 μmol/L, n=3) enhanced Vm responsiveness to SCaE and enabled the epicardium to also generate triggered activities. We observed 1 episode of bidirectional VT after Ik1 suppression. SCaE alternans led to alternating origin of triggered activities in that episode.
Conclusions: SCaE and triggered activities underlie the mechanisms of postshock arrhythmias, which originate exclusively from endocardial surface before Ik1 suppression but may occur in both endocardial and epicardial surfaces after Ik1 suppression. These findings are compatible with the hypothesis that Purkinje fibers (which have low Ik1 activity) are important sources of postshock ventricular arrhythmias.