Diastolic Intracellular Calcium-Membrane Voltage Coupling Gain and Postshock Arrhythmias Role of Purkinje Fibers and Triggered Activity

Rationale: Recurrent ventricular arrhythmias after initial successful defibrillation are associated with poor clinical outcome. Objective: We tested the hypothesis that postshock arrhythmias occur because of spontaneous sarcoplasmic reticulum Ca release, delayed afterdepolarization (DAD), and triggered activity (TA) from tissues with high sensitivity of resting membrane voltage (Vm) to elevated intracellular calcium (Cai) (high diastolic Cai–voltage coupling gains). Methods and Results: We simultaneously mapped Cai and Vm on epicardial (n=14) or endocardial (n=14) surfaces of Langendorff-perfused rabbit ventricles. Spontaneous Cai elevation (SCaE) was noted after defibrillation in 32% of ventricular tachycardia/ventricular fibrillation at baseline and in 81% during isoproterenol infusion (0.01 to 1 μmol/L). SCaE was reproducibly induced by rapid ventricular pacing and inhibited by 3 μmol/L of ryanodine. The SCaE amplitude and slope increased with increasing pacing rate, duration, and dose of isoproterenol...