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Submitted on December 19, 2007
Revised on March 12, 2007
Accepted on April 3, 2008
From the Division of Cardiovascular Disease (L.L., J.H., R.E.I.), Department of Medicine; Departments of Biomedical Engineering (R.E.I.), and Physiology (R.E.I.), University of Alabama at Birmingham; Shanghai Ruijin Hospital (Q.J.), Jiaotong University School of Medicine, China; and Peking Union Medical College Hospital (K.-A.C.), Beijing, China.
* To whom correspondence should be addressed. E-mail: rei{at}crml.uab.edu.
For more than 50 years, it has been assumed that ventricular fibrillation (VF) is maintained solely by reentry in the working myocardium. This hypothesis has never been tested by recording VF with electrodes spaced sufficiently close to map activation sequences in 3D. We recorded the first 10 minutes of electrically induced VF from the anterior left ventricular (LV) free wall near the insertion of the anterior papillary muscle in 6 pigs. A 3D transmural unipolar electrode array consisting of a 9x9 array of needles with 2-mm spacing and 6 electrodes 2 mm apart on each needle was used for recordings. Automatic analyses were performed to recognize 3D reentry and foci. Our results showed that intramural reentry is present early but not late during VF in the mapped region. The incidence of reentry in working myocardium decreases almost to 0 after 3 minutes of VF. In contrast, intramural foci are present during early VF and, as VF continues, increase in incidence, so that by 10 minutes of VF, 27% of wavefronts arise from intramural foci. These results suggest that, particularly after the first 3 minutes of VF, mechanisms other than local reentry in the working myocardium maintain VF in the anterior LV free wall near the root of the anterior papillary muscle. Intramural foci may play an important role in later VF maintenance. It remains to be determined if these foci arise from Purkinje fibers attributable to abnormal automaticity, afterdepolarizations, or reentry.
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