Published online before print July 31, 2006, doi: 10.1161/CIRCULATIONAHA.105.602870
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(Circulation. 2006;114:536-542.)
© 2006 American Heart Association, Inc.
Arrhythmia/Electrophysiology |
Evidence for Multiple Mechanisms in Human Ventricular Fibrillation
From the Bioengineering Institute and Engineering Science, University of Auckland, New Zealand (M.P.N., A.M.); Department of Computer Science, University of Sheffield, UK (R.H.C.); Department of Physiology, Anatomy and Genetics, University of Oxford, UK (C.P.B., D.J.P.); and Departments of Cardiology and Cardiothoracic Surgery, University College Hospital, London, UK (P.M.S., M.H., P.T.).
Correspondence to Peter Taggart, Departments of Cardiology and Cardiothoracic Surgery, University College Hospital, 16-18 Westmoreland St, London W1G 8PH, UK. E-mail peter.taggart{at}uclh.org
Received November 21, 2005; revision received June 1, 2006; accepted June 6, 2006.
Background— The mechanisms that sustain ventricular fibrillation (VF) in the human heart remain unclear. Experimental models have demonstrated either a periodic source (mother rotor) or multiple wavelets as the mechanism underlying VF. The aim of this study was to map electrical activity from the entire ventricular epicardium of human hearts to establish the relative roles of these mechanisms in sustaining early human VF.
Methods and Results— In 10 patients undergoing cardiac surgery, VF was induced by burst pacing, and 20 to 40 seconds of epicardial activity was sampled (1 kHz) with a sock containing 256 unipolar contact electrodes connected to a UnEmap system. Signals were interpolated from the electrode sites to a fine regular grid (100x100 points), and dominant frequencies (DFs) were calculated with a fast Fourier transform with a moving 4096-ms window (10-ms increments). Epicardial phase was calculated at each grid point with the Hilbert transform, and phase singularities and activation wavefronts were identified at 10-ms intervals. Early human VF was sustained by large coherent wavefronts punctuated by periods of disorganized wavelet behavior. The initial fitted DF intercept was 5.11±0.25 (mean±SE) Hz (P<0.0001), and DF increased at a rate of 0.018±0.005 Hz/s (P<0.01) during VF, whereas combinations of homogeneous, heterogeneous, static, and mobile DF domains were observed for each of the patients. Epicardial reentry was present in all fibrillating hearts, typically with low numbers of phase singularities. In some cases, persistent phase singularities interacted with multiple complex wavelets; in other cases, VF was driven at times by a single reentrant wave that swept the entire epicardium for several cycles.
Conclusions— Our data support both the mother rotor and multiple wavelet mechanisms of VF, which do not appear to be mutually exclusive in the human heart.
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