Objectives: Single electrical field shocks are able to induce ventricular fibrillation (VF) if applied during the vulnerable period. During this period, a shock can either prolong the action potential duration or induce a new action potential. Whether the occurrence of different shock responses contributes to the induction of VF has not been investigated directly in the intact heart.
Methods: In 12 isolated Langendorff-perfused rabbit hearts seven monophasic action potentials (MAPs) were recorded simultaneously during the application of 838 T-wave shocks. Post-shock repolarization was assessed by classifying the shock-induced response in each MAP recording either as a full action potential or an action potential prolongation. Heterogeneity of post-shock repolarization was defined if both response patterns were present in different MAP recordings at the same time. The heterogeneity of post-shock activation was measured as the dispersion of the post-shock activation time (PS-AT). The arrhythmogeneity of a shock was quantified as the number of rapid shock-induced repetitive responses.
Results: Shocks inducing nonuniform repolarization were associated with greater arrhythmogeneity than shocks inducing uniform repolarization (17.6 +/- 30.0 versus 1.6 +/- 1.1 shock-induced repetitive responses, p < 0.001). The severity of the induced arrhythmia increased gradually with increasing nonuniformity of repolarization (p < 0.01 for a 10% increase), being maximal when the shock initiated near equal numbers of both full action potentials and action potential prolongations. The induction of severe arrhythmias by T-wave shocks was also associated with a higher dispersion of PS-AT (29 +/- 14 ms for the induction of VF, 19 +/- 12 ms for non-sustained arrhythmia, and 12 +/- 8 ms for no arrhythmic response, all p < 0.001). For VF inducing shocks, an increase in shock strength towards the upper limit of vulnerability decreased the dispersion of PS-AT from 34 +/- 15 ms to 23 +/- 11 ms (p < 0.001).
Conclusions: Nonuniform post-shock repolarization and dispersed post-shock activation contribute to the induction of VF by T-wave shocks. A decreasing dispersion of PS-AT towards higher shock strengths may contribute to the decreased or abolished inducibility by shocks above the upper limit of vulnerability.