JOEL
A.
I(IRSW,
STEVEN
MS,
SWIRYN,
Evanston,
ALAN
MD.
SAHAKIAN,
V.
i-‘,:
FACC
Illinois
Irregularity
patients
of the ventricuiar
with
irregularity
atrial
rhythm
fibrilIation,
is a hallmark
~/et tk
geuesis
is not yet fulky understuod.
atrioventricular
The
role oF :he
in detcrrkning
the irregularits
of the ventricular response to atriai fihrilla!ionnas in+Fs.
Ligated
atrial
(AV)
OF
~4 the
node
by comparing
(AA)
the frecpucncy
and the ventricular
distributions
(RR)
of lbe
intervals.
Atrial
electragrams
and surface eIPctrocardiograptic
leads were recorded during sastained atriai fibr&tion
in
12 patients with conductionovtr the .AV node. RIR xating
factor (mean RR interval/meanAA interval)quantifiedt%
ability
of the conduction
a slower ventricular
(mean
pathway
to scale the atrial
response and ranged
ZT SD 9.77 2 0.92).
mput to
fr+lm Z.5
to 5.92
The coeffici+:~rt of variatiorr
idD!
mean) measured the relative variabilityof the Ah and RR
intsrvaf distributions. The atrial and ventricutaa cnefiicients of variation were not significantlydifferent IO.20 T’C
0.04 Ve?MS0.21 * 0.03, p > 0.27A
Similar
irregularity
atrial
rerordings
of the
fibrillation
nation
remains
ventricular
unclear
conduction
(3-6)
and
statistical
have
been
undertaken,
factors
determining
cently.
studies
atrial
conducting
fibrillation
(2).
within
measures
with
the
relating
pathways
hav\:
analyzed
rhythm
has long been
concealed
AV
were
in six patknts
as a ctsn%quencc
studies
NU!?!CiWS
focusing
the atrmventricular
of the
ventricular
RR
(AV)
intervals
responLc
been
perform4
as to the
(71.
the electrophysiologic
More
rc-
propcrtw,
tit
response
(15-20).
on
node
~3.7-14)
conclusions
to the ventric&u
djf
I I ! yet;I\ cxph-
recognized
conflicting
with
~II!
during
ihere
KIRSH ET AL.
VENTRICULAR
JACC Vol. 12. No. 5
RESPONSE
Table 1. Clinical
-
TO ATRIAL
Characteristics
Patient
AgelyrY
Gender
I
2
3
WV1
72M
6nM
November 1988: 1265-72
FIBRILLATION
in 18 Patients
ax
4
7lF
5
6
7
58M
79M
SOM
CAD
CAD
CAD
CHD
CAD
CAD
CM
8
9
IO
II
‘.
13
Ir;
I5
tklM
25M
26M
30M
47M
19M
53F
25M
AS
WPW
WPW
WPW
WPW
WPW
WPW
WPW
16
I7
1g
65F
48M
28M
WPW
WPW
WPW
Pathway
Atrial
Fibrillation
AVN
AVN
AVN
AVN
AVN
AVN
AVIS
Chronic
Chronic
Chronic
Chronic
Chronic
Chronic
Chronic
AVN
AVN
AVN
AVN
AVN
AP
AP
AP
AP
AP
Chronic
induced
Induced
Induced
Induced
Induced
Induced
Induced
Induced
Induced
AP
Induced
Medications
None
None
Digoxin
Digoxin, verapamil
Digoxin
Diltiazem. metoprolol
Digoxin, verapamil
Digoxin. diltiazem
None
None
None
None
None
None
None
None
None
None
AP = accessory AV ptithway; AS = aortic stenosis; AVN = AV node; CAD = coronary artery disease: CHD
= conwnital heart disease: CM = cardiomyopathy: Dx = diagnosis; F = female: M = male: WPW =
Wotff-Parkinson-White syndrome.
pared with those from the paiionts with conduction over the
AV node.
Methods
Criteria for admission to the study. Patients undergoing
either hemodynamic cardiac catheterization or electrophysiologic study who demonstrated either chronic or induced
sustained atrial fibrillation were considered eligible for incluaion in this study, The study was limited to those patients
who cxhibired either type I or type II atrial fibrillation and
therefore had discrete atrial electrograms (25) with AV
conduction exclusively over the AV node or exclusively
over an accessory AV pathway. Patients with type 111
fibrillation (25) were excluded because of difficulty in accurately determining atria1 intervals in the absence of discrete
electrograms. The study was approved by the institution’s
committee on human research, and written informed consent
was obtiined from all patients before study.
Study patients (Table I). A total of I8 patients were
studied, and their clinical diagnoses are summarized in Table
I. Twelve patients (I I men, I woman), ranging in age from
25 to 79 years (mean 551, had conduction over the AV node
during atrial fibrillation. Six patients (four men, two women),
ranging in age from I9 to 65 years (mean 40), with WolffParkinson-White syndrome had conduction over an accessory AV pathway during atria1 fibrillation. All IO patients
with induced atrial fibrillation, including 4 with conduction
over the AV node and 6 with conduction over an accessory
pathway, were free of all cardioactive medications for at
least five drug half-hves before study. Six of the eight
patients with chronic atrial fibrillation (all with conduction
over the AV node) were taking various negative dromotropic
medications.
Data acquisition. Continuous recordings of 2 to 5 (mean
4) min duration were made during atrial fibrilIation. A bipolar
high right atria1 electrogram with a I cm interelectrode
spacing (USCI), as well as surface electrocardiographic
(ECG) leads 1, II and V,, were amplified and filtered using a
physiologic recorder (Honeywell VR-16; Electronics for
Medicine, Honeywell Inc.) as previously described for our
laboratory (26.27). The intraatrial signals were filtered using
a passband of 30 to 500 Hz, whereas the surface leads were
filtered using a passband of 0.05 to 5,000 Hz. Signals were
recorded on frequency-modulated (FM) tape (Honeywell
101). In three cases the patients were studied at another
laboratory, and the signals were amplified and filtered using
a similar Honeywell VR-16 recorder, recorded on FM tape
using a Honeywell 56OOEand then rerecorded using a Vetter
mode1 B FM tape recorder (A. R. Vetter) for transport.
Preprecessing. One surface lead and the high right atrial
electrogram were played back simultaneously from tape
through an antialiasing filter with a cutoff frequency of 120
Hz. The signals were amplified and then digitized at 1,200 Hz
using a Masocomp MCS-563 computer system (Massachusetts Compute’). Thcsc signals wcrc then reduced to an
effective sampling rate of 240 Hz by extracting every fifth
data point while stiff satisfying the Nyquist sampling criterion (28).
JACC Vul. 12, No. 5
November 1988: 1265-72
vENTRlCULAR
generated
RESF’ONSE
on-line,
KlRSW ET AL.
FlBRlLLATION
TO ATRIAL
and each
detected
R wave
1267
was
manu&y
:onfirmed.
lnterva!
histograms. Frequency
distribution
histograms
generated for both atrial and ventricular cyck lengths,
with a class width of 20 and 50 ms. respectively
(Fig. 3. The
sJr”
I ’
T,ImV
rcl
IO
256
I83 196 192
t---t--+--t---i---+-+----+----l
254
t92
242
were
1
I
maximal
AA
percentile
bution
I
(IO).
appear
r.ccnr--+
adapted
from
as a straight
shape
factor,
rr.ean
Atrial and ventricular event detection. The digitized high
right atrial signals were scanned for discrete electrograms
with use of an adaptive threshold detection algorithm previously described by our laboratory (a), Patients in the study
were restricted to those exhibiting either type I or type II
fibrilation as described by Wells et al. (25). and :hus by
definition had discrete atriaJ electrograms.
Atrial cycle
lengths were measured as the intervals between successive
discrete complexes (Fig. !). A graphic display of the atrial
signal, with detected electrographic complexes marked, was
generated on-line and each detected complex was manually
confirmed.
R wu:les in the digitizedsrrrfaceECG lead were detected
algorithm
intervals
were
and
defined
as the
95th
ven!ricu!ar cycle !engah
result
w&d
cause
frequency
iine with
a plot
versus
a negative
of thi:
intmgai
slope.
nalural
length
To
to
quantify
of both the AA and RR
was plotted on a
semilogarithmic wale. Regession lines were caicula!ed relating the natural logarithm of mterval frequency to the
Interval len$h, and correlation coefficients were measured.
Scaling factors ru;d coe&ien& of variatii.
The scaling
the
during atrial fibrillation
with detected AA intervals marked. As defined by Wells et al, (25),
type I fibrillation (la) is characterized
by discrete complexes separated by an isoelectric baseline whereas type Ii fibrillation (lb) is
characterized
by discrete complexes
with perturbations
cf the
baseline between complexes.
Type I11 fibrillation fails to demonstrateeither discrete complexes or isoelectric intervals. and thus the
measurement
of AA intervals
is less certain. All AA interval
measurements
are in milliseconds.
a differentiation-squaring
This
of interval
of the
rigtit-hafid
the
normalized
distributions.
Figure I. High right atrial electrograms
using
RR
of the &iaI
distributions, respectively.
The frequency
of occurrence of RR intervals kmger than
the mean has previously been observed to Cdl off a;oongan
exponential decay curve reminiscent of the Poisson distri-
267
logarithm
t
and
points
that
of Hamilton and Tompkins (29). A graphic display of tb*
surface lead signal with detected R waves marked
which
atrial
was defined
cycle
kngth,
tail
histogram
as the ratii
quantified
of mean
the
ability
ventricular
of the
conduction pathway to transform its rapid atrial input into a
slower ver&icuiar response. To measure the relative vtiability of a distribution (i.e., ;lormafized to its mean), the
coeflicient of variation was caiculated as the ratio of the
standard deviation of the AA or RR interval distribution to
its n;can (13,14.30).
It was hypothesized that, if the rok of
the AV
conduction system during atrial fibrillation were
solely that of scaling the atria! input iu a slower ventricular
resprrdse, then the absolute variability inherent in the atrial
rhythm (SD,,,
the standard deviation of the AA interval
distribution) would be similarly scaled to produce the absolute variability in the ventricular rhythm (SD,,, the standard
deviation of the RR interval Bstribution), and the co&cients of variation would nof differ between the atria and
ventricles. Similarly, the maximal atrial intervals would be
scaled to produce the maxima! ventricular intervals.
T&z term “scaling” has been used by several mthors
,12,23.24)
to describe
the role of the AV node in determining
the ventricular response to atrial tibrilladon. In this study,
Figtare 2. Case 9. Atrial and ventricular interval histo.
grams. The ho&cntal
axes are not equivalent
but were
instead set such that the full scale RR interval is equal to the
scaling factor multiplied by the futl scale AA interval. The
verticaf scales were set autorzatlcaly
by the computer to
provide maximal vertical resolution. This choice of scales
demonstrates
the similarity in shape of the two distributions.
Ocl
to
AV
40
~120bo200240z8a
AA Interval lmsl
RR lnldrval (ms)
1268
T&k
Patient
I
2
4
KIRSH
JACC Vol. t.2. No. 5
til- At.
VEYiRltUL.&
RESPONSE
TO ATRIAL
t
November 1988: W-72
FtERtLLATtON
2. Xesults in 18 Patients
Mean AA
tins1
Mean RR
Pathway
AQN
AYN
AVN
AVN
Hi.3
i97.7
217.7
285.3
AVN
AVN
AYN
AVN
AVN
iVN
AVN
AVM
AP
974.0
252.3
163.5
246.4
146.2
140.5
147.2
160.0
AP
AP
hP
AP
AP
174.8
155.4
105.7
172.7
183.8
170.0
SD**
tms)
SDRR
(ms)
SF
CV**
CVFI,
895.0
794.2
811.7
857.3
23.1
36.5
3?.2
61.4
l86.9
148.7
118.5
205.6
5.92
4.02
3.73
0.153
0.209
0.187
0.146
llKi3.6
823.3
576.8
1151.8
461.2
3ZS.2
670.6
5117.4
38s.
169.8
369.2
259.9
29; 3
326.0
39.4
45.8
25.~
55.5
33.6
39. I
35.4
28.0
53.5
248.5
168.6
148.1
254.6
97.9
80.2
165.6
3.66
(ms\
1
CQ,, = SD,,/mean AA = atriai coefficient of variation; CV RI = S&,/mean
RRfmean AA = scaling factor. Other abbreviations
as in Table I.
the use of the term “scaling” is meant only to maintain
historical consistency rather than imply an assumption us to
the precise mechanism of AV node function.
Liif!ar regress~n and statistical tests of 6’best fit” lines.
Plots were drawn oftbe ventricular variability (SD,,) versus
the scaled atrial variability (scaling factor multiplied by
SD,&
ailJ of the maximal (95th percentile) RR interval
versus the scaled maximal BA interval (scaling factor multipled
by the 95th percentile
AA interval). Regression lines
were calculated using the method of least-squares. The slope
and intercept of the best fit line were then tested against the
slope and intercept of the identity line (I ,O and 0.0, respectively) using the Student’s f test (31).
Results
Parknts With Conduction Uver the AV Node
(R&/e 2)
By study design, aB atria! clectrograms were indicative
of
either type 1 (n = 4) or type 11 (n = 8) fibrillation (25),
exhibiting discrete complexes of variable timing and configuration separated by either an isoelectric baseliae or one of
varying degrees of perturbation (Fig. I). The mean atrial
cycle length ranged from 140 to 286 ms (mean k SD I99 + 54
msj. In all patients, the ventricular response to atrial fibrillation was mtikedly irregular, with mean cycle lengths
W.?ing from 358 to 1,151 ms (743 f 234 ms).
lnlmal hist~rsms (Fig. 2). In all patients, both the AA
and RR intervals were &modally
distributed. Qualitatively,
ptiienls with longer mean ventricular cycle lengths were
observed to have wider interval histograms, reflecting an
35.0
2a.9
20.8
63.2
37.8
89.2
71.8
80.8
109.3
37.4
69.9
138.3
2.99
3.26
3.53
4.67
3.!5
2.55
4.55
3.17
2.26
1.54
2.37
2.46
I.69
I .77
0.165
0.171
0.214
0.144
0.182
0.156
0,225
0.230
0.279
0.240
0.175
0.315
0.200
0,186
0.197
0.366
0.205
0.240
0.248
0.205
0.257
0,221
0.212
0.224
0,247
0.176
0.186
0.300
0.2%
0.144
0.240
0.424
RR = ventricular coefficient of variation; SD = standard deviation; SF = mean
increase in the absolute variability of the RR intervals. The
semilogarithmic plots of the right-hand tail of the distributions were all linear, as demonstrated by correlation coefficients ranging from -0.907 to -0.996 (mean -0.%7) for the
AA interval distributions and correlation coefficients ranging
from -0.860 to -0,981 (mean -0.940) for the RR interval
distributions. All of the correlation coefficients were statisticalIy significant (all p < 0.005). This linearity demonstrated
that the right-hand tails of both the AA and RR interval
distributions had similar shapes, following an exponential
decay curve.
Wing
factors and cwiWeats of variation. The scaPng
factors (mean RR/mean AA) ranged from 2.55 to 5.92 (3.77 *
0.92) 2nd were found to relate both atrial variability and
maximal AA intervals to ventricular variability and maximal
RR intervals, respectively (see next section). The atrial
coefficients of variation (SD,,/mean
AA) ranged from 0. I4
to 0.21+ (0.20 f 0.04). The ventricular coefficients of variation
(SD&mean
RR) ranged from 0.14 to 0.26 (0.21 2 0.03).
There was no significant difference between the atrial and
ventricular coefficients of variation (p > 0.27) suggesting that
scaling of atria! variability can account for ventricular variability.
Maximal intervals. In the 12 patients, with conduction
over the AV node, the observed maximal RR interval ranged
from 508 to 1,634 ms (1,026 2 338 ms). The product of the
scaling factor and maximal AA interval ranged from 510 to
1,597 ms (988 4 313 ms). Similar to the comparison of
coefficients of variation described, these were not significantly different (p > 0.5), suggesting that scaling of the
Vol.12. No. 5
JACC
Novcmbcr
VENTKIC’U t AK RESPONSE
IYllR:lth5-72
maximal atrial intervals is sufficient to account
maximal ventricular intervals,
Patients Wirh Conduction
TO ATRIAL
KIRSHET AL..
FINRILLA?l0N
I269
for the
Over un Accrssory
Pathw,uy (Table 2)
To further investigate the role of the AV conduction
system in determining the irregularity of the ventricular
response to atrial fibrillation, the group of six patients with
conduction over an accessory pathway was examined and
Over the AV
compared with the patients with conduction
node. By study design, the atrial electrograms were all
indicative of either type I (n = 2) or type 11 (II = 4)
fibrillation. The mean atrial cycle length ranged from 106 to
I84 ms (I60 + 28 ms). This length was not significantiy
shorter (p > 0.15) than the mean atrial cycle length (I!39
2 54
ms) found in patients with conduction over the AV node.
The ventricular response was irregular, with mean cycle
lengths ranging from 260 to 385 ms (317 -c 52 ms).
Intenai hkbgmms. The frequency histograms of the
atria1 and ventricular cycle lengths were similar to those
found for the group with conduction over the AV node
except that in one patient the RR distribution was bimodal.
The semilogarithmic
plots of the right-hand tail of ihe
distributions were ail linear. The correlation coefficients of
these plots for the AA intervals ranged from -0.916 to
-0.991 (mean -0.9623, and those for the RR intervals ranged
from -0.834 to -0.984 (mean -0.915). All of the correlation
coefficiests were statistically significant (all p < 0.05). This
linearity again demonstrated that the right-hand tail of both
the AA and RR interval diskibutions had similar shapes,
following an exponential decay curve.
The scaling
Sc&isg factors and coefMents of variation.
factors ranged from 1.54 to 2.46 (2.02 k 0.39). This range
was significantly (p < 0.0005) lower than the mean scaling
factor (3.77 + 0.92) found in patients with conduction over
the AV node, consistent with the fact that the accessory
pathway is less effective at scaling down the atrial input than
is the AV node,
The arrial coejicients of variation ranged from 0. I3 to
0.37 (0,24 2 0.08). and the ventricular coefficients of variation from 0.14 to 0.42 (0.27 ? 0.10). As for parlents with
conduction over the A.V ncde, there was no significant
difference between the atrial and ventricular coefficients of
variation (p S- 0.6), suggesting that scaling of the atrial
variability can account for the ventricular variability regardless of the nature of the AV conduction pathway.
Maxhnd intervals. The maximal RR interval ranged from
329 to 571 ms (463 2 93 ms). As would be expected, this
interval was significantly (p < 0.0#05) shorter than the
maximal RR interval (1,026 ? 338 ms) observed in patients
with conduction over the AV node. Tile product of scaling
factor and maximal AA interval ranged from 327 to 565 ms
(444 + 90 ms). As was the case for patients with conduction
I’
L
Figure 3. Prediction of \cntriG ular variability KY&)
by ntrial VT!ability LSD,,,,) related by the scaling factor ISF). The regression line
k not significantly different from the line of identity tp Z 0.4,
sugge4ng that atrial variability during atrial fibrillation canaccount
for ventricular variability. AP = accessory AV pathway: AVN =
AV node: SD = standard deviation.
o :r the AV node, there was not a statistically significant
difference (p > 0.7) between the scaled maximal AA intervals and the maximal RR intervals, again suggesting that
scaling of the maximal atrial cycle lengths is sufficient to
account for the maximal RR intervals regardless of the
nature of the AV conduction pathway.
Atrial
variability
md
maxha
atria1 cyck
BS predicts
of
ventricular vrr&&l&y
and maximal ventricular
cycles. To
illustrate the relation between atrial and ventricular variability, a plot of the product of the scaling factor and the
standard deviation of the AA interval distribution versus the
standard deviation of the RR interval distributionfor both
groupsof patients is shown in Figure 3. The two quantities
are strongly correlated (r = 0.77, p < 0.0005) and the
regression line is not significantly different from the line of
identity (p r 0.4). This predictability reflects the equality of
the atrial and ventricular coeflkients of variation previously
described. In Figure 3 the data from both groups of patients
lie along the same line regardless of the nature of the AV
conductionpathway.
To illttsmte the relation between he tnnxitnal alrial and
~ettrrictrlrr cycles, a plot of the product of the scaling factor
and the maximal AA intervals versus the maximal RR
interval for both groups of patients is shown in Figure 4.
There is againa strongcorrelation(; = 0.98, p < O.ooO5) and
the regression line is not significantlydifferenrfrom the line
of identity (p > 0.4). Again, the data from both groups of
patients lie along the same line regardless of the nature of the
AV conduction pathway.
Discussion
Previous
Soderstrom
Early work by Arnoldi (32) and then
(7) focused on the existence of a number of
stud&
1270
KIRSH ET AL.
VENTRICULAR
I
"0
,
2#)
RESPONSE
,
5w
,
750
,
lcol
SF I mmm~m
TO ATRlAL
flRRILLATlON
,
,
,
1250
I500
1750
,
zoca
AA (ms)
Figure 4. Prediction of the maximal (95th percentile) RR interval by
the maximal (95th percentile)
AA interval related by the scaling
factor (SF). The regression line is not significantly different from the
line of identity (p > 0.4). suggesting that the long ventricuIar
“pauses”
associated with atrial fibriliation
can be atlributed
to
scaling of the maximal atrial cycle lengths. Abbreviations
as in
Figure 3.
“levels”
in the interval
tachogram (a plot of RR
interval against consecutive beat number) corresponding to a
set of evenly spaced modes in the interval histogram. SoderStrom sought IO explain the ordered structure of these modes
as being determined by multiples of the refractory period of
the AV node, which he was unable lo measure. However,
subsequent
work (8,10,12) failed to discern any such structure in the patterns of the ventricular
response.
In particular,
Bootsma
(12) and Meijler
(24) and their coworkers, using RR
interval analysis alone, concluded that the AV node, other
than scaling the atria1 impulses, did not play a primary role in
determining the irregularity of the ventricular response to
atrial fibrillation.
Present study. We found several descriptors of frequency
distribution histograms, including unimodality and the shape
of the right-hand tail, to be comparable for both atrial and
ventricular interval distributions in a group oi’ 12 patients
with atrial fibrillation. The predictability of both the ventricular variability and the maximal RR interval as scaled
functions of the corresponding atrial measures adds to
previous data derived from RR interval analysis alone,
suggesting that the nature of the distribution of the RR
intervals is primarily a consequence of the nature of the
This predictdistribution of the AA intervals (l&12,23,24).
ability would support the suggestion that the role of the AV
node during atrial fibrillation is predominantly confined lo
that of scaling the atrial activity. These relations were also
observed in six patients with atrial fibrillation and conduction over an accessory AV pathway, providing additional
evidence that the irregularity and maximal intervals of the
ventricular response to atrial fibrillation can be accounted
for by the irregularity and maximal intervals of the atrial
discrete
JACC Vol. 12, No. 5
Nnvcmhcr 19XR:1265-72
JACC Vol. 12. No. 5
Novcmhrr
:9lilt:lthS-72
the ventricular response IO atrial fibrillation with conduction
over an accessory AV pathway was Iimited to those patients
whose QRS complexes Appeared ccinsistently fully preexcited, refiecting an absence of fusion. and hence the
absence of any evident contribution to the ventricular response by the AV node. Under these conditions, repetitive
retrograde activation of the His bundle by way of the
accessory pathway might preclude the AV node from participating in any AV conduction (15.40,41).
Determining the inpuUoutpu1 of the AV conduction pathway. The R wave of the s&ace ECG lead identified the
output of the AV conduction pathway, but determining the
actual input to the pathway was more difficult. It: addition 10
the probable existence of multiple inputs to both the AV
rlode (3.42,43) and the accessory AV pathway (44). atrial
activity recorded in the +$II right strium is not necessarily
similar to activity simultaneously recorded at other atrial
sites (25). The eff& of muliip!e inputs impinging on the AV
conduction pathway is unclear; if the inputs respond independently with no consistent phase relation, then the apparent input rate to the conduction pathway would be much
more rapid than measured elsswhere in the atrium (3). If,
however, the separate inpu.., are not electrically independent, the effect of multiple inputs is less clear. The effects of
multiple inputs to the AV node or accessory pathway would
contribute to the behavior of the conducting pathway during
atrial fibrillation and would be reflected in the statistical
behavior of the output (i.e., the RR intervals). Thus. the
complication introduced by the multiple inputs was inseparable from other factors determining the behavior of the AV
conduction pathway and could not be examined mechanistically in this study.
Activity recorded in the high right atrium during atrial
fibrillation is not an instantaneous measure of tk input tc the
AV conduction pathway. However, there is no reasan to
believe that, over long periods of time, the staktical nature
of atrial activation intervals would differ between the high
right atrium and sites closer lo the atria1 insertion of the AV
conduction pathway because of the random nature of atrial
fibrillation (3,10,14.45). Therefore, for the purposes of this
study, the assumption was made that over a period of
minutes the statistical behavior of activation intervals measured in the high right atrium would provide an unbiased
estimate of the statistical behavior of activation intervals
closer lo the AV conduction pathway.
Conelusions. This study adds direct observation of arrial
events to a body of data that suggests lhdt the irregularity of
the ventricular response to atrial fibrillation is primarily a
conseqaence of the irregularity inherent in the atrial activity.
Ventricular variability and maximal RR intervals were related lo atnal variability and maximal AA intervals by the
scaling factor, and both the atrial and ventricular interval
histograms had shapes similar to the Pokon distribution.
This relation was observed in patients wi!h and without
VEN
rRI(‘U1.AR
RESPONSE
TO ATRIAL
KlRSH
ET AL..
FlBRILLATION
1271
acce\5ory AV pathways, further supporting the conclusion
that
no special prorzties
of the AV node need to be
considered lo account for the nature of tile RR inrerv;rl
distribution.
We sxpre$\
our dpprecialion
cnllec!ion.
Hahernan.
:o Jose
Galh~legu~.
for atzn~ance
MD
In data
Jo Ellen Womwn.
RN for technical
anintanre
and
PhD. Chairman.
Depanment
of SratiPticc. Nonhuc,tem
wily for advice regarding
revw
nf the maquxripi.
the ~!atls!ral
techmques
Shrl!.y J.
Univer-
in ihI,. #.dy
employed
and
References
I. Rolhherger
Wren
CJ, Winterberg
H. Vorh+lTimmern
Kim Wochenschr
Iw9:ZZ:839-U.
2. Brady
DA
Clrculallon
3.
Moe Gk.
arsoctated
Ventncular
IYirl:4l~i+5.
Ablldskov
with alaal
rate
panems
ud
Arhyrhmia
m arrial
fibnllahon
perpctua.
(editor&
JA. Observattonr
on the .ientricular
dyvhytnml.
fibnllatton
rn the do; hear!. Circ Res 1%4:lJ:447-
60.
J.
5.
h.
! angendorf R. Pick A. Kalr LN. Ventricular
timon. role of concealed
conduction
in Ihe
1%5X.6%75.
Moore
Clrc Re\
EN. Ohrervutions
1967.?1:201-8.
on concealed
Yamada
K. Okajima
M. Hori
venrricutar arrhylhmiaassocialed
707-r.s.
7. Soderstrom
of duruxlar
rerponx
m alrial Cbrifla.
!V junction.
Circulatton
conduztron
fibnllation.
K. el al. On !he gene+
of rhe absolute
with slrial fibrillalion.
Circ Res t968:??:
N. What is the reason for the venlricular
fibrillation?
Am Head I 1950;40:?1?-23.
K. Braunuein
JR. Franke EK. Autocorrelalron
alnal Abnllahon,
Circ Res PX&9:3&%4.
9. Hem LG. Kinder JC. Study
Circ Re\ I9hl.%3OI-I
I.
m atnal
of ventricular
arrhythmia
of vemrxular
response
in Casey
recpon<e
III alnal
In
fibrdlatmn.
IO. Goldcrein
RE. Barnelr GO. A rI&lical
larity of atrial fibrillation.
Comp Biomed
study of rhe vemrrcular
Res 1967;l:i46-61.
irregu-
II.
Urbach
JR. Grauman
JJ. &us
SH.
recognitloo
of alriovenlricular
junchonnl
Clrcolialion
1969:39:803-17.
Quanlilahve
methods
for the
rhylhmc
in atria1 fibrillation.
i2.
Boolsma
BK. Hoelen
AJ. Slrdckee
J. Meljler
FL. Analys~r of R-R
intervals
tn palienls wilh atrIal fibrlllalion
at reel and during exercise.
Circularion
1970;41:783-94.
13. Exudero
EM. lveli CA. Moreyra
AE. Lorenle
H. Cingolani
HE.
pulce in patlenls wilh atria1 fibrtllalion:
iIs irregularity
and inequalily.
J Cardiol 1976:451-8.
The
Eur
I4
Cohen PJ. Berger RD. Dushane
TE.
A quannlauve
model for the
ventncular
response during atrial fibrillation.
IEEE Trans Biomed Eng
1983.3O:WLMll.
IS
Wellens HJ, Durrer D. Wolff-Parkinson-Whue
syrdrome
sod atrral fibrilIanon: relatton between
refrclory
period of accessory
palhwny
and
venmcular
wte during alrial lihrillaian.
Am J Cardiol 1974:34:777-8?.
Ih.
B~lletle J. Nadeau RA, Roberge F. Relalion between
the mimmum
RR
inbxvial durme atria! tibrdlallon
and the functIonal refraclorv
uenod nf Ihe
AV Juncllon.?ardiovasc
Res 1974:8:347-51
.
17. BIHeae
J.
Roberge
FA.
Nadeau
RA.
Pole>
of
the
delerminlngIhe ventricularresponseto alrfal fibrdlalion.
AV junction
III
Can J Phyriol
Phdrmitcul 1‘475;53:57!-84.
II!.
Rowland E. Curry P. Fox K. Krlkler D. Relarlon between alnovenlriLular
pslhway\
and venlncular
rerponse durtngarrral
fihnllation
and Ruller Rr
Heart J lY!ll:JS:HF7.
1272
KIKSH
JACC Vol. 12. No. 5
ET AL.
VENTRICULAR
KESPONSE
TO ATRIAL
FIBRILLATION
IY, Klein GJ. Ycc R. Sharma AD. Concealed conduction in accessory
afriovcntricular pathways: an important dctcrminanl
of the expression of
in patients with Wollf-Parkinson-White syndrome. Circulaarrhythmias
lmn 1984;70:402-3 I.
20. Milstein S, Klein GJ. Raltes MF. Sharma AD, Yce R. Comparison of the
ventricular response during atrial fibrillation in patients with enhanced
arrioventncular node conduction and Wolff-Parkinson-White syndrome. J
Am Cdl Cardiol 1987;10:1244-8.
November 1988~1265-72
33. Willkamof FHM. de Joneste MJL. Lie HI. Meiiler FL. Effect of riaht
ventricular pacing on ve&icular rhythm duringgtrial fibrillation. J Am
Coil Cardiol 1988;11:53~5.
34. Dreifus LS. Mazgalcv T. “Atria] paralysis”: does it explain the irregular
ventricular rate during atrial fibrillation (editorial)? J Am Coil Cardiol
1988:11:546-7.
21. Meijler FL. Alrial fibrillation: a new look al an old arrhythmia (editorial).
J Am Coll Cardicl l*Q’+791-3.
35. Klein GJ. Prystowsky EN. Pritchett ELC, Davis D, Gallagher JJ.
Atypical patterns of retrograde conduction over accessory atrioventricutar pathways in the Wolff-Parkinson-White
syndrome. Circulation
1979;ho: 1477-86.
22. Urbach JR. Ventn’cular response to atrial fibrillr+ion (letter). J Am Coil
Cardiol 1984:3:lIOS-6.
36. Ward DE. Camm AJ. Ventriculo-atrial conduction over accessory pathways exhibiting decremental properties. Eur Heart J 1982;3:267-75,
. .,.A.._.<
23. Scher AM, Heethaar RM. Zimmcrmun ANE. MeiJler FL. Alrral rhylhm
during ventricular fibrillation in the dog. Circ Res 1976:38:41-5.
24. Mcijler FL. Kronemau J, Van der Tweell. Herbschleb JN. Hcethaar RM.
Borsl C. Nonrdndom ventricular rhythm in horses with atrial fibrillation
and its significance fnr pa&Is.
J Am Coll Cardiol 1984;4:316-23.
25. Wellr II,, Karp RB. Kouchoukos NT. Maclean WAH, James TN, Waldo
AL. Chanctcrizaticln of atria1 fibrillation in man: sludies following open
hean surgery. PACE 1976;1:426-38.
26. Slocum J. Sahakian A. Swirvn S. Comoutcr discrimination of atrial
fibrillation and regular atrial-rhythms from intra-atrial electrograms.
FACE lL88:ll:61C-21.
37. Bauemfeind RA, Ayres BF, Wyndham CC, et al. Cycle length in
atrioventricular nodal reentrant paroxysmal lachycardia .Gth observations on the LownGanong-Levine
syndrome. Am J Cardiol 1980;45:
1148-53.
38. Jackman WM. Prystowsky EN, Naccarelli GV. et al. Reevaluation of
enhanced atrioventricular nodal conduction: evidence IO suggest a continuum of normal alriovenlricular nodal physiology. Circulation 1983;67:
441-8.
39. Meljler FL. An “account” of digitalis and atrial fibrillation. J Am Coil
Cardiol 1985;5(suppl A):6OA_8A.
40. Durrer D. Wcllcns HJ. The Wolff-Parkinson-White
Eur J Cardiol 1974;1:347-67.
syndrome anno 1973.
27. Ropella KM. Sahakian AV. Baerman JM. Swiryn S. The effects of
procainamidc on intro-atrial electrograms during atrial fibrillation: implications for detection algorithms. Circulation 1%8;77:1047-54.
41. Bolli R, Magro SA. Wyndham CRC. Concealed antidromic re-entrance
during rapid atrial pacing in the Wolff-Parkinson-While syndrome. PACE
1983;&385-91.
28. Jackson LB. IX&al Filters and Signal Processing. Wnnvell. MA: Kluwer
Academic Publishers, 1986:70.
42. James TN. Movhology of the human atriovenlricular node, with remarks
pertinent lo its electrophysiology. Am Heart J !%1;62:756-71.
29. Hamilton PS. Tompkins WJ. Yet another real-time QRS detection aigorithm. Proceedings of the Association for the Advancemcbi of Medical
Instrumentation (AAMI) 2ist Annual Meeting. Chicago: Associalion for
the Advancement of Medical instrumentation, 1988:36.
43. Morady F, Scheinman MM. Winston SA, DiCado LA, Davis JC. Dissociation ofatrial clcctrograms by right and left atrial pacing in patients with
alriovenlricular reciprocating tachycardia. J Am Coil Cardiol 1984;4:
1283-9,
30. Spiegel MR. Theory and Problems of Statistics. New York: Schaum
Publishing, 1%1:73.
Engineering Statistics.
44. Batchelder JE, Miles WM, Mahomed Y. et al. Presence of a broad
activation front in Wolff-Parkinson-White patients suggesting arborizing
atrial insertion of accessory pathways (abstr). J Am Coil Caniiol 1988:l t:
IOA.
32. Amoldi W. Die Ermittlung von dominierenden Rhythmen sowie der
Schwcre der Rhythmussti+ung bei Kranken mit Arhythmia perpetua.
KIin Wochenschr 1927;h:1846-8.
45. Mcilcr FL, Van dcr Tweel 1. Herbschleb JN, Hauer RNW, Roblcs de
Medina EO. Role of atria1 fibrillation and atrioventricular conduction
(including Wolff-Parkinson-White syndrome) in sudden death. 1 Am Call
Cardio! 1985;51suppl B1:178_22B.
31. Gullman
I. Wdks SS, Hunter JS. Inlroductory
New York: John Wiley & Sons. 1982360.
I