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on July 22, 2002

Circulation. 2002
Published online before print July 22, 2002, doi: 10.1161/01.CIR.0000027103.54792.9C
A more recent version of this article appeared on August 20, 2002
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Right arrow Arrythmias-basic studies

Submitted on February 12, 2002
Revised on May 22, 2002
Accepted on May 23, 2002

Intramural Virtual Electrodes During Defibrillation Shocks in Left Ventricular Wall Assessed by Optical Mapping of Membrane Potential

Vladimir G. Fast PhD*, Oleg F. Sharifov PhD, Eric R. Cheek MS, Jonathan C. Newton PhD, and Raymond E. Ideker MD, PhD

From the Department of Biomedical Engineering (V.G.F., O.F.S., E.R.C., R.E.I.) and Department of Medicine (J.C.N., R.E.I.), University of Alabama at Birmingham, Birmingham, Ala.

* To whom correspondence should be addressed. E-mail: fast{at}crml.uab.edu.

Background—It is believed that defibrillation is due to shock-induced changes of transmembrane potential ({Delta}Vm) in the bulk of ventricular myocardium (so-called virtual electrodes), but experimental proof of this hypothesis is absent. Here, intramural shock-induced {Delta}Vm were measured for the first time in isolated preparations of left ventricle (LV) by an optical mapping technique.

Methods and Results—LV preparations were excised from porcine hearts (n=9) and perfused through a coronary artery. Rectangular shocks (duration 10 ms, field strength E {approx}2 to 50 V/cm) were applied across the wall during the action potential plateau by 2 large electrodes. Shock-induced {Delta}Vm were measured on the transmural wall surface with a 16x16 photodiode array (resolution 1.2 mm/diode). Whereas weak shocks (E{approx}2 V/cm) induced negligible {Delta}Vm in the wall middle, stronger shocks produced intramural {Delta}Vm of 2 types. (1) Shocks with E>4 V/cm produced both positive and negative intramural {Delta}Vm that changed their sign on changing shock polarity, possibly reflecting large-scale nonuniformities in the tissue structure; the {Delta}Vm patterns were asymmetrical, with {Delta}V-m>{Delta}V+m. (2) Shocks with E>34 V/cm produced predominantly negative {Delta}Vm across the whole transmural surface, independent of the shock polarity. These relatively uniform polarizations could be a result of microscopic discontinuities in tissue structure.

Conclusions—Strong defibrillation shocks induce {Delta}Vm in the intramural layers of LV. During action potential plateau, intramural {Delta}Vm are typically asymmetrical ({Delta}V-m>{Delta}V+m) and become globally negative during very strong shocks.


Key words: arrhythmia • defibrillation • excitation • mapping




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