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Integrative Physiology |
From the Departments of Biomedical Engineering (J.M.R., R.E.I.) and Medicine (J.H., S.B.M., R.E.I.), University of Alabama at Birmingham, Birmingham, Ala.
Correspondence to Jack M. Rogers, 1670 University Blvd, Volker Hall B140, Birmingham, AL 35294. E-mail jmr{at}crml.uab.edu
It has been proposed that ventricular fibrillation (VF) is driven by sustained reentry. However, mapping studies have not detected such "mother rotors" in large mammalian hearts. We mapped VF from three 21x12 unipolar electrode arrays in 6 pigs. Two of the arrays were adjacent to each other on the left-ventricular epicardium. Electrode spacing was 2 mm. The third array consisted of 21 needles (0.5-mm diameter, 12 electrodes, 1-mm spacing) inserted in a row (2-mm spacing) between the epicardial arrays. A total of 88 5-second VF epochs were analyzed with automatic reentry detection algorithms. Although intramural reentry was sporadically present (29 total occurrences), it was always short-lived with a mean life span of 127±57 ms. However, in 3 of the 6 animals, sustained epicardial reentry (ie, reentry persisting for more than a few cycles) was consistently present, often lasting for several seconds. For each epoch, we computed indices characterizing (1) the relative duration of reentry on the two epicardial arrays (R), (2) the flow of wavefronts between epicardial arrays (W), and (3) the relative activation rates of the two epicardial arrays (F). R did not correlate with either W or F indicating that rotor-containing regions did not produce a net outflow of wavefronts and were not faster than neighboring regions. Thus, sustained epicardial, but not intramural, rotors were consistently present in some large animal hearts during VF. However, we found no evidence that these rotors were responsible for sustaining VF through the mechanisms outlined in the mother rotor hypothesis.
Key Words: ventricular fibrillation rotor intramural reentry epicardial reentry mapping
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