Ayman Mourad

Evidence for Multiple Mechanisms in Human Ventricular Fibrillation

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 (100×100 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.

Human Ventricular Fibrillation During Global Ischemia and Reperfusion Paradoxical Changes in Activation Rate and Wavefront Complexity

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 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.

Human Ventricular Fibrillation During Global Ischemia and ReperfusionClinical Perspective: Paradoxical Changes in Activation Rate and Wavefront Complexity

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 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.

Human Ventricular Fibrillation During Global Ischemia and ReperfusionClinical Perspective

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 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.

Epicardial mapping of ventricular fibrillation in the human heart during ischaemia and repercussion

The aim of this study was to map electrical activity over the ventricular epicardial surface during ventricular fibrillation (VF) in the human heart, and to document changes associated with ischaemia and repercussion. In 5 patients undergoing cardiopulmonary bypass VF was induced by burst pacing, and three 30 s episodes of epicardial activity were recorded at I kHz using an epicardial sock with 256 unpopular contact electrodes. The first episode of activity was recorded at the start of VF, the second after 2 minutes of ischaemia, and the third during coronary repercussion. Following 2 minutes of ischaemia the mean dominant frequency (DF) of the epicardial signals fell from 5.6 Hz to 4.5 Hz, and the mean number of epicardial phase singularities increased from 7.8 to 10.5. Following coronary repercussion the mean DF increased to 6.5 Hz, but there was no significant change in the mean number of epicardial phase singularities.