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(Circulation. 2004;109:2349-2356.)
© 2004 American Heart Association, Inc.
Basic Science Reports |
From the Department of Biomedical Engineering, University of Alabama at Birmingham.
Correspondence to Vladimir G. Fast, University of Alabama-Birmingham, 1670 University Blvd, VH B126, Birmingham, AL 35294. E-mail fast{at}crml.uab.edu
Received August 12, 2003; de novo received December 5, 2003; revision received February 5, 2004; accepted February 6, 2004.
Background Intramural virtual electrodes (IVEs) are believed to play an important role in defibrillation, but their existence in intact myocardium remains unproven. Here, IVEs were detected by use of optical recordings of shock-induced transmembrane potential (Vm) changes (
Vm) measured from the intact epicardial heart surface.
Methods and Results To detect IVEs, isolated porcine left ventricles were sequentially stained with a Vm-sensitive dye by 2 methods: (1) surface staining (SS) and (2) global staining (GS) via coronary perfusion. Shocks (2 to 50 V/cm) were applied across the ventricular wall in an epicardial-to-endocardial direction during the action potential plateau via transparent mesh electrodes, and shock-induced
Vm were measured optically from the same epicardial locations after SS and GS. Optical recordings revealed significant differences between
Vm of 2 types that became more prominent with increasing shock strength: (1) for weak shocks, SS-
Vm were larger and faster than GS-
Vm; (2) for intermediate shocks, cathodal GS-
Vm became multiphasic, whereas SS-
Vm remained monophasic; and (3) for strong shocks, cathodal GS-
Vm became uniformly negative, whereas SS-
Vm typically remained positive. The radical differences in the shape and polarity of SS and GS polarizations can be explained by the contribution of subepicardial IVEs to optical signals. Histological examination revealed a dense network of collagen septa in the subepicardium, which could form the IVE substrate.
Conclusions Intramural virtual electrodes are reflected in optical measurements of shock-induced
Vm on the intact epicardial surface. These IVEs could be a result of microscopic resistive discontinuities formed by collagen septa.
Key Words: arrhythmia defibrillation excitation mapping ventricles
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