Oleg F Sharifov1, Vladimir G Fast. 1. Department of Biomedical Engineering, University of Alabama at Birmingham, 1670 University Boulevard, Birmingham, AL 35294, USA.
Abstract
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, Vm 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. Vm responses at the transmural surface were measured using optical mapping technique (resolution = 1.2 mm). Depending on shock strength, three types of Vm responses were observed. (1) Weak shocks (E approximately 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 DeltaVm during AP plateau. (2) Intermediate shocks (E approximately 4-23 V/cm) induced monophasic and biphasic upstrokes that were paralleled with predominantly negative plateau DeltaVm. 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 approximately 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 DeltaVm. 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 Vm responses and delayed activation.
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, Vm 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. Vm responses at the transmural surface were measured using optical mapping technique (resolution = 1.2 mm). Depending on shock strength, three types of Vm responses were observed. (1) Weak shocks (E approximately 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 DeltaVm during AP plateau. (2) Intermediate shocks (E approximately 4-23 V/cm) induced monophasic and biphasic upstrokes that were paralleled with predominantly negative plateau DeltaVm. 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 approximately 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 DeltaVm. 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 Vm responses and delayed activation.
Authors: M M Maleckar; M C Woods; V Y Sidorov; M R Holcomb; D N Mashburn; J P Wikswo; N A Trayanova Journal: Am J Physiol Heart Circ Physiol Date: 2008-08-15 Impact factor: 4.733
Authors: Flavio H Fenton; Stefan Luther; Elizabeth M Cherry; Niels F Otani; Valentin Krinsky; Alain Pumir; Eberhard Bodenschatz; Robert F Gilmour Journal: Circulation Date: 2009-07-27 Impact factor: 29.690