Characteristics of wave fronts during ventricular fibrillation in human hearts with dilated cardiomyopathy: role of increased fibrosis in the generation of reentry
Tsu-Juey Wu, MD*,a,
James J. C. Ong, MD, FACCa,
Chun Hwang, MD, FACCa,
John J. Lee, MD, FACCa,
Michael C. Fishbein, MD, FACCa,
Lawrence Czer, MD, FACCa,
Alfredo Trento, MDa,
Carlos Blanche, MD, FACCa,
Robert M. Kass, MD, FACCa,
William J. Mandel, MD, FACCa,
Hrayr S. Karagueuzian, PhD, FACCa and
Peng-Sheng Chen, MD, FACCa
a Division of Cardiology, Department of Medicine and Department of Pathology, Burns and Allen Research Institute, Cedars-Sinai Medical Center and University of California Los Angeles School of Medicine, Los Angeles, California, USA
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Figure 1 The reentrant wave fronts initiated by epicardial breakthrough with a line of conduction block parallel to the epicardial fiber orientation (data from heart no. 1). Panels A to K are selected frames from the dynamic display of the activation patterns during VF. Panel L shows the trajectory of the tip of the reentrant wave fronts, demonstrating the meandering nature of the core. Numbers 1 and 2 indicate the first and second cycles of reentry. The time of each frame is shown in parentheses above the panels. The beginning of the data acquisition was taken as time zero. The myocardial fiber orientation is displayed by the double-headed arrow at the right lower border of the figure.
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Figure 2 The actual activations registered in Figure 1. The numbers on the left edge of each panel indicate the electrode numbers and the location in the electrode array. Numbers 0.8 and 1.6 indicate the times in seconds, with the onset of data acquisition as time zero. In panel A, the activations of epicardial breakthrough (long arrow with asterisk) failed to travel across the site between channels 237 and 219, leading to conduction block and the initiation of reentry. The activations with corresponding activation times (ms) from channels 222 to 257 (solid circle followed by short arrows) illustrate part of the first cycle of the reentrant loop. Note that conduction delay (1208 – 1176 = 32 ms) was present when the wave front propagated through the site between channels 219 and 237. In panel B, these activations show that the reentrant excitations (long arrows) persisted for two rotations. Numbers 1 and 2 indicate the first and second reentrant cycles.
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Figure 3 The reentrant wave front initiated by perpendicular intersection of two wave fronts (data from heart no. 5). Panel A shows that waves "a" and "b" interact at a right angle. The asterisk in panel B indicates the point of wave break. The wave break was then followed by one rotation of counterclockwise reentry (panels B to F). The reentry was terminated owing to collision of wave fronts (arrows in panel F). The myocardial fiber orientation is displayed by the double-headed arrow at the left lower border of the figure.
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Figure 4 The actual activations registered in Figure 3. Wave "b" collided with the tail of wave "a" at or near channel 304, and initiated reentry. The activations recorded at channel 304 show that wave "b" propagated to this area 75 ms (i.e., intersection interval) after it was activated by wave "a". The arrows with an asterisk indicate parts of a reentrant loop.
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Figure 5 An example of incomplete rotating circuit (data from heart no. 5). Panel A shows a wave front propagating through the area of conduction block, which is shown in panels B and C. After conduction block occurred, a rotating wave front was initiated (panels D to G) but had spontaneous termination (panels H and I). At the time of termination, the line of block was parallel to the fiber orientation. The myocardial fiber orientation is displayed by the double-headed arrow at the right lower border of the figure.
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Figure 6 Isochronal maps demonstrating transmural scroll waves during VF from the right ventricle of heart no. 5. Times of activation are colored-coded according to the color bar above the panels. The numbers in the electrode arrays indicate the location and the numbers of the bipolar recording electrodes. From epicardium, subepicardium, subendocardium to endocardium (panels A to D), there were only small differences in the transmural distribution of activation patterns. The filament of this scroll wave (line connecting white circles near channels 217, 218, 219 and 220) was perpendicular to the surface of the ventricular wall. The white arrow in each panel indicates the rotating direction of the scroll wave.
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Figure 7 Histologic findings corresponding to activations shown in Figure 1. Panels A, C, D and E show sections of the left ventricular myocardium parallel to the epicardium in heart no. 1. With trichrome stain, small veins with perivascular fibrosis (blue areas) were clearly seen in panel C (arrows). The magnified view (panel E) also showed interstitial and replacement fibrosis. The areas of fibrosis in panels C and E corresponded to the line of conduction block in panel B (same frame as Fig. 1B). However, in the areas without conduction block, histologic examination showed either normal tissue (panel A) or mild fibrosis (panel D). Original magnification 10x, panels A, C and D; 100x, panel E. Calibration lines 1 mm.
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Figure 8 Histologic findings corresponding to activations shown in Figure 5. Panels A, C and D show sections of the subepicardial myocardium from the left ventricle of heart no. 5. With trichrome stain, significant interstitial fibrosis (blue area) was demonstrated in panel C. The area of fibrosis corresponded to the line of conduction block in panel B (same frame as Fig. 5C). In the areas without conduction block, however, histologic examination showed less fibrous tissue (panels A and D). Original magnification 10x, panels A, C and D. Calibration lines 1 mm.
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