Abstract 20790: The Relationship of Rotors to Scar Border Zones and Dominant Frequency Domains in Human Ventricular Fibrillation
Background: During VF there are regions of organized re-entry visualized as rotors using phase mapping of electrical activity. Physiological or anatomic determinants of the locale of these rotors, may provide a rationale for catheter based strategy for targeting rotors and thus modulating VF in humans.
Objective: We hypothesize that during human VF, rotors/phase singularities co-localize with dominant frequency (DF) and anatomical scar border zones.
Method: VF experiments were conducted in 3 isolated cardiomyopathic human hearts using a Langendorff setup. Previously published method was used to compute the regions of scar using the bipolar electrogram amplitudes (i.e. < 0.5 mv) during a pacing protocol. After the initiation of VF, unipolar electrograms from the epicardium were recorded and used to construct DF and phase maps. The phase maps were analyzed to identify the locations of phase singularities (PS) and the PS points were tracked over time to determine if they constitute a rotor (i.e. at least the PS should last for 400ms with 2 cycles of sustained phase pattern rotation). The number of tracks, duration of the rotor, chirality, and correlation with DF maps and scar maps were extracted for analysis.
Results: Figure 1 with subplots (a-e) demonstrates the correlation between rotor tracks, DF border zones, scar borders, and 4 instances of phase maps for a sample heart. The areas of interest are circled, pink tracks are anti-clockwise rotors and black tracks [subplot(c)] are clockwise. Based on our analysis of the 3 hearts we observed 5 rotors, 3/5 rotors were anticlockwise and 2/5 were clockwise, the mean number of continuous tracks per rotor to be 14, the mean duration of the rotors to be 7.2 s, and in all the 3 hearts rotors co-localized with DF border zones and scar borders.
Conclusions: Rotors co-localize with DF and anatomical scar border zones. These sites of co-localization may provide therepeutic targets for altering the substrate in human VF.
- © 2010 by American Heart Association, Inc.