on July 5, 2005
Published online before print July 5, 2005, doi: 10.1161/CIRCULATIONAHA.104.503631
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Submitted on August 30, 2004
From the Department of Cardiology, Westmead Hospital, Westmead, and the University of Sydney, NSW, Australia. * To whom correspondence should be addressed. E-mail: stuartpt{at}yahoo.com.
Background--Studies of ventricular fibrillation (VF) in small mammals have revealed localized sustained stationary reentry. However, studies in large mammals with surface mapping techniques have demonstrated only relatively short-lived rotors. The purpose of this study was to identify whether sustained high-frequency activation with low beat-to-beat variability was present at intramural sites in a postinfarct ovine model of VF. Methods and Results--VF was induced in 12 sheep 77±40 days after anterior myocardial infarction. Electrical activation was recorded with 20 multielectrode transmural plunge needles. Unipolar electrogram frequency content and local cycle duration variability were studied in 30-second recordings beginning 5 seconds after the onset of VF. Higher mean beat frequency was associated with lower SD of the cycle duration intervals (r=-0.91, P<0.001). The mean beat frequency and the SD of cycle duration intervals of the highest-frequency electrode were 8.8±2.0 Hz and 17±11 ms. In 3 cases, a region with regular activation throughout the recording was identified (SD of the cycle duration interval, 6.0±0.7 ms). Two of these sites and 67% of all sites with low local cycle duration variability were intramural. They occurred within regions with a high dominant frequency as determined by fast Fourier transform of the unipolar electrogram. Conclusions--Regions with the highest frequency of activation during VF were always associated with a low local cycle duration variability and usually intramural in this chronic infarct model. In a minority of cases, a region of stable, rapid, and very regular activation could be identified. These findings support the hypothesis that relatively stable periodic sources form a component of the mechanism of VF in this model.
Revised on March 6, 2005
Accepted on March 10, 2005
Organization of Myocardial Activation During Ventricular Fibrillation After Myocardial Infarction. Evidence for Sustained High-Frequency Sources
Stuart P. Thomas BMed, PhD, FRACP*,
Key words: arrhythmia • death, sudden • fibrillation • ventricles
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