| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Integrative Physiology |
From the Departments of Physiology and Biophysics, Medicine, and Biomedical Engineering, University of Alabama at Birmingham, Ala.
Correspondence to Raymond E. Ideker, MD, PhD, University of Alabama at Birmingham, B140 Volker Hall, 1670 University Blvd, Birmingham, AL 35294. E-mail rei{at}crml.uab.edu
We quantified ventricular fibrillation (VF) activation rate, conduction block, and organization transmurally in pigs and dogs, whose transmural Purkinje distribution differ. In six pigs and five dogs, 75 to 100 plunge needles, containing four electrodes for the right ventricle (RV) and six electrodes for the left ventricle (LV) and septum, were inserted in vivo. Six VF episodes were electrically initiated and allowed to last for 47 to 180 seconds. From the FFT power spectra, dominant frequency (DF), an estimate of activation rate, and incidence of double peaks (DPI), an estimate of conduction block, were calculated every 8 ms at each electrode. DF was highest at the epicardium and lowest at the endocardium, whereas DPI was highest at the endocardium and lowest at the epicardium for the entire LV and the RV base in both pigs and dogs for the first 70 seconds of VF. This distribution changed little throughout the first 3 minutes of VF in pigs but reversed in dogs by 2 minutes of VF. In conclusion, estimated activation rates and conduction block incidence during VF are not uniformly distributed transmurally. During the first minute of VF, the faster activating LV base epicardium exhibits less estimated block than the slower endocardium, raising the possibility that faster activating epicardium generates wavefronts that drive the endocardium early during VF. Constancy of this pattern in pigs but its reversal by 2 minutes in dogs is consistent with the hypothesis that activation during later VF is driven by Purkinje fibers.
Key Words: cardiac electrophysiology arrhythmia mapping ventricular fibrillation
This article has been cited by other articles:
![]() |
D. J. Dosdall, P. B. Tabereaux, J. J. Kim, G. P. Walcott, J. M. Rogers, C. R. Killingsworth, J. Huang, P. G. Robertson, W. M. Smith, and R. E. Ideker Chemical ablation of the Purkinje system causes early termination and activation rate slowing of long-duration ventricular fibrillation in dogs Am J Physiol Heart Circ Physiol, August 1, 2008; 295(2): H883 - H889. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. A. Trayanova The Long and the Short of Long and Short Duration Ventricular Fibrillation Circ. Res., May 23, 2008; 102(10): 1151 - 1152. [Full Text] [PDF] |
||||
![]() |
P. B. Tabereaux, G. P. Walcott, J. M. Rogers, J. Kim, D. J. Dosdall, P. G. Robertson, C. R. Killingsworth, W. M. Smith, and R. E. Ideker Activation Patterns of Purkinje Fibers During Long-Duration Ventricular Fibrillation in an Isolated Canine Heart Model Circulation, September 4, 2007; 116(10): 1113 - 1119. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. H.W.J. Ten Tusscher, R. Hren, and A. V. Panfilov Organization of Ventricular Fibrillation in the Human Heart Circ. Res., June 22, 2007; 100(12): e87 - e101. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Masse, E. Downar, V. Chauhan, E. Sevaptsidis, and K. Nanthakumar Ventricular fibrillation in myopathic human hearts: mechanistic insights from in vivo global endocardial and epicardial mapping Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2589 - H2597. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. P. Thomas, A. Thiagalingam, E. Wallace, P. Kovoor, and D. L. Ross Organization of Myocardial Activation During Ventricular Fibrillation After Myocardial Infarction: Evidence for Sustained High-Frequency Sources Circulation, July 12, 2005; 112(2): 157 - 163. [Abstract] [Full Text] [PDF] |
||||
|
Circulation Research Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2004 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |