Influence of Postshock Epicardial Activation Patterns on Initiation of Ventricular
Fibrillation by Upper Limit of Vulnerability Shocks
Nipon Chattipakorn, Jack M. Rogers and Raymond E. Ideker
Circulation. 2000;101:1329-1336
doi: 10.1161/01.CIR.101.11.1329
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Influence of Postshock Epicardial Activation Patterns on
Initiation of Ventricular Fibrillation by Upper Limit of
Vulnerability Shocks
Nipon Chattipakorn, MD, PhD; Jack M. Rogers, PhD; Raymond E. Ideker, MD, PhD
Background—Shocks of identical strength and timing sometimes induce ventricular fibrillation (VFI) and other times do
not (NoVFI). To investigate this probabilistic behavior, a shock strength near the upper limit of vulnerability, ULV50,
was delivered to yield equal numbers of VFI and NoVFI episodes.
Methods and Results—In 6 pigs, a 504-electrode sock was pulled over the ventricles. ULV50 was determined by scanning
the T wave. S1 pacing was from the right ventricular apex. Ten S2 shocks of approximate ULV50 strength were delivered
at the same S1-S2 coupling interval. Intercycle interval (ICI) and wave front conduction time (WCT) were determined
for the first 5 postshock cycles. ICI and the WCT of cycle 1 were not different for VFI versus NoVFI episodes (P⫽0.3).
Beginning at cycle 2, ICI was shorter and WCT was longer for VFI than NoVFI episodes (P⬍0.05).
Conclusions—The first cycle after shocks of the same strength (ULV50) delivered at the same time has the same activation
pattern regardless of shock outcome. During successive cycles, however, a progressive decrease in ICI and increase in
WCT occur during VFI but not NoVFI episodes. These findings suggest shock outcome is (1) deterministic but
exquisitely sensitive to differences in electrophysiological state at the time of the shock that are too small to detect or
(2) probabilistic and not determined until after the first postshock cycle. (Circulation. 2000;101:1329-1336.)
Key Words: electrophysiology 䡲 fibrillation 䡲 shock
A
strong stimulus during the vulnerable period can induce
repetitive responses that either halt without inducing
ventricular fibrillation (VF) or degenerate into VF.1 Most
proposed mechanisms of VF induction based on this finding,
such as the nonuniform dispersion of refractoriness hypothesis,2 imply that activation immediately after the shock in a
successful VF induction (VFI) differs from that in a failed VF
induction (NoVFI).2– 4
Previous studies that used a range of shock strengths and
timings showed that the interval between the shock and the
first global postshock activation is shorter for VFI than for
NoVFI shocks.3,5 However, comparison of VFI and NoVFI
episodes after shocks of the same strength has not been
reported.
In this study, we determined activation patterns after
shocks of identical strength and timing. A shock strength near
the upper limit of vulnerability that induced VF in ⬇50% of
the trials (ULV50) was used. We tested the hypothesis that the
activation pattern immediately after VFI shocks differed from
that after NoVFI shocks.
capture. A shock at ULV50 produced a shock voltage of
498⫾112 V. The mean coupling interval (CI) at which VF
was induced with ULV50 shocks was used as the S1-ULV50 CI
(sCI); the sCI was 214⫾14 ms. To determine ULV50, 15⫾11
shocks were required. The diastolic pacing threshold (DPT)
was 0.2⫾0.1 mA. Heart weight was 154⫾45 g. For each
animal, delivered shock voltage for the 10 ULV50 shocks was
nearly constant (%SD of 0.1 to 0.3). Repeatability of the
shock potential distribution at the 504 electrodes was measured in 1 pig. The mean correlation coefficient of the
potentials was 0.995⫾0.004 for all 10 shocks.
The preshock interval and wave front conduction time
(WCT) of the last paced cycle before the shock was not
different between VFI and NoVFI episodes (Table 1). The
similarity of the last paced cycle before the shock (Table 2)
was not different, which suggests that the activation sequence
of the last paced cycle was constant for all 10 shock episodes.
Cycle 1 Site of Earliest Activation
Cycle 1 sites of earliest activation (SEAs) were always at the
anteroapical left ventricle (LV). While the cycle 1 SEA varied
slightly between animals, it was highly repeatable for each
animal (Table 3), showing that the first postshock cycle appeared
in the same epicardial region regardless of shock outcome.
Results
Thirty of the 60 shocks in the 6 pigs were VFI episodes. One
VFI episode was excluded because the last S1 stimulus did not
Received February 16, 1999; revision received September 14, 1999; accepted October 7, 1999.
From the Departments of Medicine (N.C., R.E.I.), Physiology (N.C., R.E.I.), and Biomedical Engineering (J.M.R., R.E.I.), University of Alabama at
Birmingham.
The Methods section of this article can be found at http://www.circulationaha.org
Correspondence to Nipon Chattipakorn, MD, PhD, 1670 University Blvd, B140, Birmingham, AL 35294-0019. E-mail toon@crml.uab.edu
© 2000 American Heart Association, Inc.
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TABLE 1.
Preshock Interval and WCT of Last Paced Cycle
VFI
Preshock interval, ms
WCT, ms
TABLE 3.
NoVFI
203⫾14
203⫾13
60⫾6
59⫾5
TABLE 2. Mean Correlation and Temporal Lag of Last
Paced Cycle
Correlation of Potential
Temporal Lag, ms
VFI-VFI
0.9998⫾0.0002
1⫾1.5
VFI-NoVFI
0.9998⫾0.0006
1⫾1.5
NoVFI-NoVFI
0.9997⫾0.0009
1⫾1
Maximum first derivative (dV/dt) of activation at the cycle
1 SEA was not different for VFI and NoVFI episodes (Table
3). Mean dV/dt at the SEA of cycles 2 to 5 was less negative
than that of cycle 1 for VFI episodes (P⬍0.01). However, no
dV/dt differences were found among the first 5 postshock
cycles in NoVFI episodes. For VFI episodes, SEA repeatability for cycles 2 to 5 (Table 3) was slightly lower than for cycle
1 because the SEA of cycles 2 to 5 moved a short distance
(2⫾3 electrodes) away from the cycle 1 region of earliest
activation (REA). However, the SEA of cycles 2 to 5 in
NoVFI episodes moved a much greater distance away from
the cycle 1 REA, 9⫾4 electrodes (P⬍0.002 vs VFI episodes).
Propagation Pattern in VFI Episodes
A typical VFI episode is shown in Figure 1A (first cycle) and
Figure 2A (subsequent cycles). All 5 cycles began in the
anteroapical LV 36, 140, 229, 320.5, and 430 ms after the
Repeatability of SEA and dV/dt
SEA Repeatability, %
Postshock
Cycle
dV/dt, V/s
VFI
NoVFI
VFI
NoVFI
1
93⫾10
97⫾8
⫺2.6⫾0.9*
⫺2.6⫾0.9
2
60⫾33
50⫾50
⫺1.7⫾0.9
⫺2.8⫾1.4
3
44⫾29
0⫾0
⫺1.4⫾0.7
⫺2.7⫾2.0
4
33⫾29
0⫾0
⫺1.8⫾1.0
⫺2.0⫾0.2
5
16⫾24
0
⫺1.3⫾0.8
⫺2.5
*P⬍0.01 vs cycles 2 through 4 in VFI episodes.
shock, respectively. Cycle 1 initially propagated toward the
LV base, blocking at the right ventricular (RV) apex. It
continued bilaterally around the apex, rejoining on the posterior RV to complete activation. Subsequent cycles did not
block at the RV apex and activated both ventricles in a more
radial pattern from apex to base. WCTs increased progressively up to cycle 3, then slightly decreased (89, 161, 215,
170, and 160 ms, respectively). Cycle 2 did not overlap
temporally with cycle 1; however, subsequent cycles all
overlapped with their immediate predecessor.
Propagation Pattern in NoVFI Episodes
Cycle 1 after a NoVFI shock in the same animal (Figure 1B)
was nearly identical to cycle 1 of the VFI episode. This
first-cycle similarity is also apparent in the electrograms
(Figure 3). Because cycle 1 for both episodes blocked at the
RV apex, we paced from the anterobasal LV in the absence of
shocks to establish there were no anatomic or functional
barriers at the apex to cause the block (Figure 1C).
Figure 1. Examples from same animal of postshock cycle 1 for VFI (A) and NoVFI episodes (B) and of paced cycle (C). Electrode sites
at which dV/dt was ⱕ⫺0.5 V/s at any time during a 10-ms interval are black. Numbers above frames indicate start of each interval in
milliseconds relative to start of shock. Sock orientation is shown in Figure 7D. Arrows indicate SEA for each cycle. A, Cycle 1 arose at
anteroapical LV, propagated toward anterobasal LV, and blocked over RV apex. B, Cycle 1 arose in same region as in A and propagated similarly. C, Activation initiated by pacing from anterobasal epicardial LV propagated without slowing across apex.
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Figure 2. Postshock cycles 2 to 5 for same VFI episode (A) and cycles 2 to 4 for same NoVFI episode (B) shown in Figure 1. A, SEA of
VFI cycle 2 (140 ms) was in REA of cycle 1, and activation propagated away in focal pattern. Third (229 ms), fourth (320.5 ms), and fifth
(434 ms) VFI cycles arose before activation from previous cycle disappeared. B1, NoVFI cycle 2 appeared at 169 ms and propagated in
focal pattern. B2, NoVFI cycle 3 arose at 826 ms on posterobasal RV and propagated across entire epicardium faster than cycle 2. B3,
NoVFI cycle 4 arose 1444 ms after shock and was a sinus cycle.
Cycle 2 from this NoVFI episode (Figure 2, B1) followed
a pathway similar to the VFI cycle 2 but began later and
conducted faster. Overlapping cycles were absent. Cycles 3
(B2) and 4 (B3) arose after long delays from different SEAs
and had fast WCTs (73 and 38 ms, respectively). Cycle 4 was
sinus and not analyzed.
Postshock Intercycle Intervals
The mean intercycle interval (ICI) (Figure 4A) of cycle 1 did
not differ between VFI (51⫾23 ms) and NoVFI episodes
(n⫽24, 68⫾78 ms). The SD of NoVFI episodes was high
because of 1 episode with an extremely long postshock
interval (461.5 ms). This episode had its SEA near the
posterobasal LV, whereas the SEAs from other episodes in
this animal were at the anteroapical LV. If this NoVFI
episode is excluded, the mean postshock interval for NoVFI
episodes becomes 54⫾23 ms (P⫽0.6 vs VFI). ICIs for VFI
episodes were significantly shorter than for NoVFI episodes
for cycle 2 (138⫾38 vs 387⫾312 ms) and cycle 3 (132⫾31
vs 389⫾193 ms) (n⫽12 and 10, respectively). For cycle 4,
the mean ICI for VFI (126⫾40 ms) was shorter than for
NoVFI (484⫾182 ms) episodes; however, the difference was
not significant, probably because there were only 5 NoVFI
episodes with a fourth ectopic cycle. ICIs of cycle 5 were not
compared because only 1 NoVFI episode had a cycle 5 (537
ms). ICIs of cycle 5 for VFI episodes were 128⫾41 ms.
Postshock WCTs
The WCT (Figure 4B) of cycle 1 did not differ between VFI
(116⫾19 ms) and NoVFI episodes (113⫾16 ms). The mean
WCTs of cycles 2 (172⫾51 vs 99⫾44 ms), 3 (203⫾51 vs
83⫾18 ms), and 4 (197⫾55 vs 59⫾25 ms) were significantly
longer for VFI than for NoVFI episodes (P⬍0.01). WCT of
the single cycle 5 for NoVFI episodes was 58 ms. WCT of
cycle 5 for VFI episodes was 210⫾53 ms.
In all VFI episodes, overlap occurred during cycles 2 to 3,
3 to 4, and 4 to 5 (overlapping index ⬎1) but not cycles 1 to
2 (overlapping index ⬍1) (Figure 4C). In contrast, there was
no overlap among the first 5 ectopic cycles in any NoVFI
episode.
Correlation of 504 Electrograms of Cycle 1
The similarity function, sij, and temporal lag, ␶m, were
compared for all possible combinations of first cycles in each
animal and divided into 3 groups: VFI versus VFI, VFI versus
NoVFI, and NoVFI versus NoVFI episodes (Table 4). There
were no differences in any group for either variable. The very
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Figure 3. Selected electrograms from episodes shown in Figure 1. A, Polar map with numbers 1 through 5 representing sites where 5
electrograms shown in B through D were recorded. Arrows represent direction of propagation of activation. B, Electrograms from
NoVFI episode. Multiple vertical lines are shock artifact. Activation was earliest in electrogram 1 and latest in electrogram 5. Second
deflection in electrogram 1 was an activation in cycle 2. C, Electrograms from VFI episode. Second deflection in electrogram 1 was
activation during cycle 2. D, Electrograms from B (dotted) and C (solid) superimposed.
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Figure 4. ICIs (A), WCTs (B), and overlapping
index (C) of first 5 postshock cycles. Only 1
cycle 5 occurred in NoVFI episodes; therefore,
there is no SD for this cycle, and no comparison was made with VFI episodes. *P⬍0.05 vs
VFI for given cycle.
high similarity and short temporal lag among different episodes indicate that first postshock cycles were nearly identical whether or not VF was initiated.
Cycle 2 in NoVFI Episodes
In NoVFI episodes, cycle 2 could be divided into 2 distinct
subgroups. Subgroup 1 (n⫽7) had a short ICI, long WCT, and
same REA as cycle 1. Subgroup 2 (n⫽6) had a long ICI, short
WCT, and different REA than cycle 1.
ICIs in subgroup 1 were all ⬍200 ms (142⫾27 ms) but
were all ⬎400 ms (672⫾228 ms) in subgroup 2 (P⬍0.002).
Although the cycle 2 ICI of subgroup 1 was not different from
that in the VFI episodes, in subgroup 2 it was significantly
longer than in the VFI episodes (P⬍0.002). Subgroup 1 all
TABLE 4. Mean Correlation and Temporal Lag of Postshock
First Cycles
Correlation of Potential
Temporal Lag, ms
VFI-VFI
0.9987⫾0.0019
1⫾4
VFI-NoVFI
0.9989⫾0.0017
1⫾3
NoVFI-NoVFI
0.9993⫾0.0011
0.4⫾2
had WCTs ⬎100 ms (135⫾21 ms), whereas subgroup 2 all
had WCTs ⬍80 ms (56⫾12 ms, P⬍0.01). WCTs of both
subgroups were significantly shorter than WCTs of cycle 2 in
VFI episodes (P⬍0.004).
Cycle 2 SEA repeatability in subgroup 1 (63⫾48%) was
different (P⬍0.04) from subgroup 2 (0⫾0%) in NoVFI episodes. Cycle 2 SEA repeatability in VFI episodes (60⫾33%)
was different from that of subgroup 2 (P⬍0.007) but not
subgroup 1. Thus, cycle 2 SEAs in the No-VFI subgroup with
longer ICIs (subgroup 2) moved to a different site, whereas in
the NoVFI subgroup with shorter ICIs (subgroup 1), as well as
in VFI episodes, they mostly remained in the REA of cycle 1.
The mean dV/dt for cycle 2 in VFI episodes also differed from
that of subgroup 2 (⫺3.2⫾1.7 V/s) but not of subgroup 1
(⫺2.2⫾0.6 V/s) in the NoVFI episodes.
Thus, episodes could be distinctly divided into 3 groups:
(1) VFI, (2) NoVFI subgroup 1, and (3) NoVFI subgroup 2.
The propagation patterns (Figure 5) as well as electrograms
(Figure 6) of cycle 1 from these 3 groups were nearly
identical. Cycle 2 for groups 1 and 2 were also similar but not
quite identical (Figure 5). Group 3 had a different REA and
shorter WCT than did groups 1 and 2.
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Figure 5. Examples from same animal of first 2 cycles in VFI (A), NoVFI with short ICI
(B), and NoVFI with long ICI (C) episodes. A1, B1, and C1: Cycle 1. SEAs (arrows) were
all in same region and started 45, 48, and 49 ms after shock, respectively. Activation
patterns are all similar. WCTs in A1, B1, and C1 were 122, 120, and 116 ms, respectively. A2, B2, and C2: Cycle 2. ICI in C2 was longer (454 ms) than in A2 (132 ms) and
B2 (146 ms), whereas WCT in C2 (77 ms) was shorter than in A2 (154.5 ms) and B2
(118 ms). SEAs in A2 and B2 but not C2 were in same region as cycle 1. Overlapping
cycle was present only for VFI episode (A2, cycle 3 begins at 297 ms).
Discussion
Similarity of First Postshock Cycle Regardless of
Shock Outcome
Our major finding is that the first cycle after a ULV50
shock that induces VF cannot be distinguished from that
after a shock of identical strength and timing that does not
induce VF. This finding was apparent in the activation
sequence animations and in the similarity of the following
first-cycle variables: (1) SEA repeatability, (2) postshock
interval, (3) WCT, (4) dV/dt at the SEA, (5) similarity
function, and (6) temporal lag.
Most studies reporting differences of activation sequences and dispersion of refractoriness between VFI and
NoVFI episodes used multiple shock strengths and coupling intervals.6,7 Those studies found that NoVFI episodes
correlated with a lower dispersion of refractoriness immediately after the shock, whereas VFI episodes correlated
with a greater dispersion of refractoriness. However, in
those studies the shock strengths of NoVFI episodes were
higher than those of VFI episodes. Thus, absence of VF
induction may not have been secondary to a lower dispersion of refractoriness; rather, both lack of VF induction
and a lower dispersion of refractoriness could have been
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Activation Pattern After T-Wave Shocks
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led to the overlap of wave fronts also probably caused
action potential duration to shorten and dV/dt to slow in
the second to fifth cycles,13 possibly leading to unidirectional block, wave front fractionation, and reentry. In
addition, the degeneration from the first postshock activation to VF could also be due to the nonuniform recovery of
excitability of cardiac muscle after the premature stimulation of the first few postshock cycles.14
Study Limitations
Figure 6. Selected electrograms from VFI (A), NoVFI with short
ICI (B), and NoVFI with long ICI (C) episodes shown in Figure 5.
All electrograms were taken from same site, began 10 ms after
shock, and were 600 ms in duration.
Although we did not observe epicardial reentry, intramural
reentry cannot be ruled out because we did not record
transmurally. The similarity of the first postshock cycle
was based on epicardial recordings; therefore differences
may have existed intramurally. The first postshock cycles
could have differed in ways too small to be detected in our
maps. Epicardial reentry may have been missed because it
was too small to be detected by electrodes 4 mm apart or
because part of the pathway consisted of activations that
were so slow and small that the recordings did not meet our
activation criterion.
Conclusions
secondary to higher shock strength. To evaluate this
possibility, we kept shock strength and timing constant.
Our results suggest that when shock strength and timing
are constant, differences in the dispersion of refractoriness
are not large enough to cause measurable differences in
postshock activation sequences and potentials. However,
differences may exist immediately after the shock that are
too small to be detected. These very small differences,
according to the Chaos theory,8 could cause prominent
differences after several cycles.
Association of Overlapping Cycles With VFI
Although differences between VFI and NoVFI episodes
were first seen at cycle 2, a prominent distinction was not
universally seen until cycle 3. This is because cycle 2 in 1
NoVFI subgroup behaved similarly to cycle 2 in the VFI
episodes. However, no overlapping cycles were present in
either No-VFI subgroup, whereas they were always present
in the VFI group. Overlapping cycles may not be the direct
cause of VF induction but may be a marker for short ICIs
and long WCTs that are responsible for unstable reentry
and VF induction. However, these results imply that at
least 3 ectopic cycles with overlap by the third cycle may
be required to initiate VF. If so, a method to halt the
initiation of ectopic cycles in the REA could prevent VF
even if it is applied as late as the third postshock cycle.
Recent defibrillation9 and VF induction studies10 support
this hypothesis.
Implications for Mechanism of VF Induction
It has been proposed that VF occurs by 2 mechanisms, an
initiating mechanism that may involve ectopic unifocal
impulses11,12 and a maintaining mechanism that involves
reentry.13 Our results are consistent with reentry as a
consequence of the initial accelerating, overlapping cycles
observed in the VFI episodes. The rapid activation rate that
The first postshock cycle has the same epicardial activation
sequence regardless of shock outcome (VFI vs NoVFI),
which suggests that large global differences in conduction or
tissue refractoriness caused by the shock are not always the
primary factors determining VF induction. Unidirectionally
propagating epicardial activation followed by several ectopic,
radially spreading impulses precedes VF. A progressive
decrease in ICI and increase in WCT, resulting in overlapping
cycles, heralds VF initiation.
Acknowledgments
This study was supported in part by National Institutes of Health
research grants HL-28429 and HL-42760.
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