OBJECTIVEThe cardiac action potential (AP) and the intracellular Ca(2+) transient (CaT) are closely associated under normal physiological conditions, but not during ventricular fibrillation (VF). The purpose of this study was to determine whether this dissociation is directly related to the higher activation rate during VF.

METHODSWe optically mapped AP and CaT simultaneously in nine isolated rabbit hearts. Pinacidil, a K(ATP) channel opener, was used to shorten the action potential duration (APD) in order to capture tissue at fast pacing rates or to induce ventricular tachycardia (VT) comparable to VF activation rates. Mutual information (MI) was used to calculate the degree of AP and CaT coupling.

RESULTSPinacidil (40 micromol/L) infusion significantly shortened APD. The averaged cycle length (CL) of VF without Pinacidil was (77 +/- 13) ms, whereas the shortest CL achieved during VT under Pinacidil infusion was 76 ms. MIs during fast pacing (1.13 +/- 0.15) bits and fast VT (0.88 +/- 0.18) bits were higher than those during baseline VF (0.39 +/- 0.11) bits, VF with Pinacidil infusion (0.21 +/- 0.07) bits and VF after Pinacidil washout (0.36 +/- 0.15) bits. MIs during fast pacing or fast VT were higher than those of VFs at comparable dominant frequencies.

CONCLUSIONSCaT is closely associated with the AP during fast pacing and fast VT, but not during VF. The reduced MI during VF is not secondary to the fast rate of ventricular activation.