This study was supported by NIH grant HL67748.
Role of Microscopic Tissue Structure in Shock-Induced Activation Assessed by Optical Mapping in Myocyte Cultures
Article first published online: 26 APR 2005
Journal of Cardiovascular Electrophysiology
Volume 16, Issue 9, pages 991–1000, September 2005
How to Cite
CHEEK, E. R., SHARIFOV, O. F. and FAST, V. G. (2005), Role of Microscopic Tissue Structure in Shock-Induced Activation Assessed by Optical Mapping in Myocyte Cultures. Journal of Cardiovascular Electrophysiology, 16: 991–1000. doi: 10.1111/j.1540-8167.2005.40342.x
Manuscript received 16 April 2004; Revised manuscript received 20 February 2005; Accepted for publication 22 February 2005.
- Issue published online: 31 AUG 2005
- Article first published online: 26 APR 2005
- virtual electrodes;
- optical mapping;
- cell cultures
Introduction: Termination of ventricular fibrillation by electric shocks is believed to be due to the direct activation of large tissue mass that may be caused by microscopic virtual electrodes formed at discontinuities in tissue structure. Here, microscopic shock-induced activation was measured optically in myocyte cultures; spatially averaged microscopic Vm measurements were compared with macroscopic measurements from left ventricular (LV) tissue.
Methods and Results: Experiments were performed in linear cell strands of different width (∼0.1 and 0.8 mm) and isolated porcine LV preparations. Uniform field shocks were applied across strands or LV preparations during diastole and action potential (AP) plateau. Depending on shock strength, three different types of activation were observed in cell strands. Weakest shocks produced “delayed make” activation that started on the cathodal strand side after long latency and rapidly spread to the anodal side. Stronger shocks caused “make” activation with short latency and rapid spread across strands. Strongest shocks caused nonuniform “make-break” activation where the cathodal side was activated with a short latency but activation of the anodal side was delayed until after the shock end due to a large negative shock-induced polarization. Spatial averaging of Vm responses across 0.1-mm (but not 0.8-mm) strands resulted in AP upstrokes and plateau polarizations that closely resembled the Vm responses measured in LV myocardium. The shock strength for the transition between fast and delayed activation in 0.1-mm cell strands and LV myocardium was similar as well.
Conclusion: These data provide evidence that microscopic tissue structures with dimensions of approximately hundred microns are responsible for shock-induced activation of ventricular tissue.