BACKGROUND: Ischemic ventricular fibrillation in experimental models has been shown to progress through a series of stages. Progression of ischemic VF in the in vivo human heart has not been determined. METHODS AND RESULTS: We studied 10 patients undergoing cardiac surgery. Ventricular fibrillation was induced by burst pacing. After 30 seconds, global myocardial ischemia was induced by aortic cross-clamp and maintained for 2.5 minutes, followed by coronary reflow. Epicardial activity was sampled (1 kHz) with a sock that contained 256 unipolar contact electrodes. Dominant frequencies were calculated with a fast Fourier transform with a moving window. The locations of phase singularities and activation wavefronts were identified at 10-ms intervals. Preischemic (perfused) ventricular fibrillation was maintained by a disorganized mix of large and small wavefronts. During global myocardial ischemia, mean dominant frequencies decreased from 6.4 to 4.7 Hz at a rate of -0.011±0.002 Hz s(-1) (P<0.001) and then increased rapidly to 7.4 Hz within 30 seconds of reflow. In contrast, the average number of epicardial phase singularities increased during ischemia from 7.7 to 9.7 at a rate of 0.013±0.005 phase singularities per second (P<0.01) and remained unchanged during reflow, at 10.3. The number of wavefronts showed a similar time course to the number of phase singularities. CONCLUSIONS: In human ventricular fibrillation, we found an increase in complexity of electric activation patterns during global myocardial ischemia, and this was not reversed during reflow despite an increase in activation rate.
BACKGROUND: Ischemic ventricular fibrillation in experimental models has been shown to progress through a series of stages. Progression of ischemic VF in the in vivo human heart has not been determined. METHODS AND RESULTS: We studied 10 patients undergoing cardiac surgery. Ventricular fibrillation was induced by burst pacing. After 30 seconds, global myocardial ischemia was induced by aortic cross-clamp and maintained for 2.5 minutes, followed by coronary reflow. Epicardial activity was sampled (1 kHz) with a sock that contained 256 unipolar contact electrodes. Dominant frequencies were calculated with a fast Fourier transform with a moving window. The locations of phase singularities and activation wavefronts were identified at 10-ms intervals. Preischemic (perfused) ventricular fibrillation was maintained by a disorganized mix of large and small wavefronts. During global myocardial ischemia, mean dominant frequencies decreased from 6.4 to 4.7 Hz at a rate of -0.011±0.002 Hz s(-1) (P<0.001) and then increased rapidly to 7.4 Hz within 30 seconds of reflow. In contrast, the average number of epicardial phase singularities increased during ischemia from 7.7 to 9.7 at a rate of 0.013±0.005 phase singularities per second (P<0.01) and remained unchanged during reflow, at 10.3. The number of wavefronts showed a similar time course to the number of phase singularities. CONCLUSIONS: In humanventricular fibrillation, we found an increase in complexity of electric activation patterns during global myocardial ischemia, and this was not reversed during reflow despite an increase in activation rate.
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