Optical mapping of transmural activation induced by electrical shocks in isolated left ventricular wall wedge preparations

Introduction: It is believed that electrical shocks interrupt fibrillation by directly stimulating the bulk of ventricular myocardium in excitable states, but how shocks activate intramural tissue layers is not known. In this study, V. responses and transmural activation patterns induced by shocks during diastole were measured in isolated coronary perfused preparations of porcine left ventricle. Methods and Results: Rectangular shocks (duration 10 ms; field strength, E 1-44 V/cm) were applied across preparations (thickness = 14.9 +/- 2.5 mm, n = 9) via large mesh electrodes during diastole or action potential (AP) plateau. V-m responses at the transmural surface were measured using optical mapping technique (resolution = 1.2 mm). Depending on shock strength, three types of V. responses were observed. (1) Weak shocks (E similar to 1-4 V/cm) applied in diastole induced APs with simple monophasic upstrokes. The latency and time of transmural activation (TTA) rapidly decreased with increasing shock strength. Earliest activation occurred predominantly at the cathodal side of preparations in the areas that exhibited maximal DeltaV(m) during AP plateau. (2) Intermediate shocks (E similar to 4-23 V/cm) induced monophasic and biphasic upstrokes that were paralleled with predominantly negative plateau AV(m). Activation was initiated at multiple transmural sites and rapidly spread across the myocardial wall (TTA = 0.6 0.2 ms). (3) Very strong shocks (E similar to 23-44 V/cm) could cause triphasic upstrokes, likely reflecting occurrence of membrane electroporation, and delayed activation (TTA = 6.7 +/- 3.8 ms) at sites of largest negative plateau DeltaV(m). Conclusion: Shocks applied during diastole cause direct and rapid (within 1 ms) activation of ventricular bulk over a wide range of shock strengths, supporting the excitatory hypothesis of defibrillation. Very strong shocks can cause multiphasic V-m responses and delayed activation.