Grants: This work was supported by Spanish Ministry of Science “Instituto de Salud Carlos III” Grants FIS PS09/02417 and RETIC REDINSCOR RD06/0003/0010, and by “Generalitat Valenciana” Grant PROMETEO 2010/093.
Ventricular Fibrillation Conduction through an Isthmus of Preserved Myocardium between Radiofrequency Lesions
Article first published online: 13 DEC 2012
©2012, The Authors. Journal compilation ©2012 Wiley Periodicals, Inc.
Pacing and Clinical Electrophysiology
Volume 36, Issue 3, pages 286–298, March 2013
How to Cite
CHORRO, F. J., IBAÑEZ-CATALÁ, X., TRAPERO, I., SUCH-MIQUEL, L., PELECHANO, F., CÁNOVES, J., MAINAR, L., Tormos, Á., CERDÁ, J. M., ALBEROLA, A. and SUCH, L. (2013), Ventricular Fibrillation Conduction through an Isthmus of Preserved Myocardium between Radiofrequency Lesions. Pacing and Clinical Electrophysiology, 36: 286–298. doi: 10.1111/pace.12060
- Issue published online: 5 MAR 2013
- Article first published online: 13 DEC 2012
- Manuscript Accepted: 23 OCT 2012
- Manuscript Revised: 14 OCT 2012
- Manuscript Received: 17 JAN 2011
- Spanish Ministry of Science “Instituto de Salud Carlos III”. Grant Number: FIS PS09/02417
- RETIC REDINSCOR. Grant Number: RD06/0003/0010
- “Generalitat Valenciana”. Grant Number: PROMETEO 2010/093
- Cardiac mapping;
- mechanical stretch;
- myocardial activation;
- spectral analysis;
- ventricular fibrillation
Selective local acceleration of myocardial activation during ventricular fibrillation (VF) contributes information on the interactions between neighboring zones during the arrhythmia. This study analyzes these interactions, centering the observations on an isthmus of myocardium between two radiofrequency (RF) lesions.
In nine isolated rabbit hearts, a gap of preserved myocardium was established between two RF lesions in the anterolateral left ventricle (LV) wall. Before, during, and after increasing the spatial heterogeneity of VF by local myocardial stretching, VF epicardial recordings were obtained.
Local stretch in the anterior LV wall decreased the excitable window (17 ± 7 ms vs 26 ± 7 ms; P < 0.05) and increased the dominant frequency (DFr; 18.9 ± 5.0 Hz vs 15.2 ± 3.6 Hz; P < 0.05) in this zone, without changes in the non-stretched posterolateral zone (25 ± 4 ms vs 27 ± 6 ms, ns and 14.1 ± 2.7 Hz vs 14.3 ± 3.0 Hz, ns). The DFr ratio at both sides of the gap was inversely correlated to the excitable window ratio (R = −0.57; P = 0.002). Before (31% vs 26%), during (29% vs 22%), and after stretch suppression (35% vs 25%), the wavefronts passing through the gap from the posterolateral to the anterior LV wall were seen to predominate. The number of wavefronts that passed from the anterior to the posterolateral LV wall was related to the excitable window in this zone (R = 0.41; P = 0.03).
The VF acceleration induced in the stretched zone does not increase the flow of wavefronts toward the non-stretched zone in the adjacent gap of preserved myocardium. The absence of significant changes in the electrophysiological parameters of the non-stretched myocardium limits the arrival of wavefronts in this zone.