Thirty-two tachyarrhythmia episodes were initiated and successfully mapped in 10 pig hearts (2–5 per heart). The VF0 sources resulting from S2 stimulation were either a single rotor, two counter-rotating rotors, or a fast breakthrough pattern consistent with an intramural rotor. We characterized global dynamics by computing the total number of compound rotors present on the epicardium after the S2 as a function of time. Figure shows three examples, each with a different type of VF0 source. Only rotors with lifetimes >100 video frames were counted to prevent the signal from being obscured by transient PSs caused by recording noise.
3.1. VF0 sources
In the 24 episodes in which the S2
site was precisely known (those resulting from epicardial S2
stimulation), the VF0 source site (see Supplementary material online
) was located 14 ± 8 mm from the S2
electrode. VF0 cycle length (see Supplementary material online
) progressively decreased from 202 ± 55 ms immediately after induction to 142 ± 26 ms in the last cycle before PST1 formation (P
< 0.01 by paired t
-test). In addition, the epicardial conduction time for waves leaving the source (see Supplementary material online
) progressively increased. The epicardial conduction time of the first VF0 wavefront was 78 ± 27 ms. By the last cycle before PST1 formation, this had significantly increased to 168 ± 32 ms (P
< 0.01 by paired t
-test). VF0 sources persisted for 6.6 ± 3.8 cycles before producing PST1s.
3.2. First wavebreak in the transition to fully developed VF
The predominant pattern we observed during the first wavebreak event was a wavefront propagating away from the VF0 source catching up to the waveback from the previous cycle as it crossed the ARVI. This resulted in wavebreak and the formation of PST1s. An example is shown in Figure
. This is the same episode shown in Figure A
and is also animated in the Supplementary material online, Video 1
. Two additional examples that correspond to the episodes shown in Figure B
are animated in the Supplementary material online, Videos 2 and 3
Figure 4 The first wavebreak event in the transition to developed VF. (A) Each subpanel displays a snapshot of wavefronts (black) and wavebacks (grey) on the ventricular epicardium using a Hammer map projection. The ARVI midline is white; the RV is to the left (more ...)
PST1 formation at the ARVI was predominant, but not universal (Table ). In 5 of the 10 hearts, in all episodes, PST1s formed in the ARVI region in a manner similar to Figure . In three additional hearts, this pattern was observed in most episodes (2/3 or 3/4). In the remaining two hearts, it occurred in only one episode.
VF initiation sites (S2), and number of episodes with PST1s in the ARVI region
Figure shows the sites of all PST1s relative to the ARVI region and S2 site in each heart. In three episodes, the wavefront broke in two places simultaneously. In these cases, all PST1s were registered. The 54 PST1s inside the ARVI region were 6 ± 4 mm from the ARVI midline. The 15 PST1s outside were 24 ± 5 mm from the midline. The ARVI region occupied 26 ± 2% of the area of the epicardial model. If PST1 formation was independent of location, the probability of 54/69 PST1s occurring in an area of this size by chance is <10−8 by χ2 analysis.
Figure 5 PST1 sites in all 10 hearts. Sites from all episodes in a heart are displayed on the common epicardial model for that heart (with a Hammer projection). In each model, the ARVI region is outlined. The RV is in the centre of each model, to the left, and (more ...)
3.3. APD analysis
The areas of the epicardial test sites for the ARVI, PRVI, LV, and RV were 67.4 ± 14.0, 67.3 ± 13.3, 67.0 ± 12.2, and 65.6 ± 9.9 mm2, respectively. The fastest pacing rate with 1:1 capture (rapid pacing) was 177.0 ± 33.3 ms. Rapid pacing APDs were 132.1 ± 25.3, 130.8 ± 24.5, 129.4 ± 23.0, and 129.7 ± 23.0 ms for the ARVI, PRVI, LV, and RV test sites, respectively. There was a significant difference among APDs at these sites by repeated measures ANOVA (P< 0.01). Post hoc analysis indicated that the APD was 2.2 ± 2.1 ms longer at the ARVI than the mean of the other sites.
||APD alternans|| during rapid pacing were 4.1 ± 2.1, 2.6 ± 1.4, 3.2 ± 1.7, and 3.0 ± 3.1 ms for the ARVI, PRVI, LV, and RV test sites, respectively. These values were not significantly different (P= 0.49). ||APD alternans|| for the signals in Figure B and C are 2.3 and 12.0 ms, respectively. To place these values in context, we randomly shuffled the APD values from each signal and recomputed ||APD alternans||. This should destroy any alternating structure present in the signals and yield values close to 0. ||APD alternans|| values after shuffling were 2.7 ± 1.1, 2.0 ± 0.7, 2.8 ± 1.6, and 2.1 ± 0.9 ms at the same sites, respectively. These values are significantly different from ||APD alternans|| in ordered beats (P< 0.01), but the size of the difference is small.
3.4. Wavefront conduction velocity during rapid pacing
Mean epicardial conduction speed during rapid pacing was highly variable across the epicardium. In addition, patterns of fast and slow regions were not consistent from heart to heart, probably partly due to the variation in pacing site among hearts. In four of the hearts, the paced wavefronts crossing the ARVI in the vicinity of the PST1 sites were relatively straight and parallel to the ARVI. In these hearts (hearts 3–6), all 24 PST1s that were located in the ARVI region were co-localized with regions with locally slowed conduction, although the regions were not necessarily the slowest on the epicardium. Figure A shows an example of one of these hearts (heart 6). In the remaining hearts, paced propagation across the ARVI near PST1 sites was more complex, typically involving collisions between the wavefront propagating from the pacing site and wavefronts breaking through to the epicardium from below. In these hearts, the activation sequence was likely a more important determinant of apparent epicardial conduction speed than tissue properties. Accordingly, the relationship between PST1 sites and conduction speed patterns was variable: PST1s in the ARVI region were co-localized with either locally slowed conduction (n= 10), locally elevated conduction (n= 11), or missing speed data (n= 9). An example of a heart with complex conduction at the ARVI is shown in Figure B (heart 8). Very similar results were obtained during 300 ms pacing (data not shown).
Figure 6 Relation between PST1 sites and conduction speed during the fastest pacing rate with 1:1 capture. A black outline identifies the ARVI region. Black asterisks indicate the pacing site (S1). The magenta line indicates the position of the paced wavefront (more ...)