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Journal of the American College of Cardiology
© 2005 by the American College of Cardiology Foundation
Published by Elsevier Inc.
Vol. 45, No. 2, 2005
ISSN 0735-1097/05/$30.00
doi:10.1016/j.jacc.2004.10.033
Heart Rhythm Disturbances
Heart Rate Turbulence After Atrial Premature
Beats Before Spontaneous Onset of Atrial Fibrillation
Saila Vikman, MD,* Kai Lindgren, MD,† Timo H. Mäkikallio, MD,† Sinikka Yli-Mäyry, MD,*
K. E. Juhani Airaksinen, MD,‡ Heikki V. Huikuri, MD, FACC†
Tampere, Oulu, and Turku, Finland
This study was designed to assess the temporal changes in vagal responses to atrial premature
beats before spontaneous onset of atrial fibrillation (AF).
BACKGROUND Enhanced vagal activity plays a major role in the onset and perpetuation of experimental AF,
but the role of vagal activation in the onset of clinical AF episodes is not so well established.
METHODS
We calculated heart rate turbulence after atrial premature impulses occurring 0 to 60 min
before the onset of AF (“prior to AF”) and compared it with the hourly means of the other
hours of the 24-h electrocardiogram recordings (“non-AF hours”) in 39 patients with
structural heart disease and 29 patients with lone AF. Traditional heart rate variability
measurements and approximate entropy (ApEn) were also analyzed.
RESULTS
Turbulence onset (TO) was significantly less negative during the 1 h preceding AF than
during the non-AF hours (0.71 ⫾ 1.76 vs. ⫺0.35 ⫾ 1.46, p ⬍ 0.00001). Less negative TO
before AF was observed among both the patients with structural heart disease (1.16 ⫾ 1.73
vs. 0.07 ⫾ 1.23; p ⬍ 0.0001) and those with lone AF (0.17 ⫾ 1.67 vs. ⫺0.85 ⫾ 1.56; p ⬍
0.0001). No significant difference was seen in the turbulence slope between the two periods,
and none of the traditional frequency and time domain measurements differentiated between
the periods; ApEn was significantly lower before AF than during the non-AF hours (p ⬍
0.01).
CONCLUSIONS Altered heart rate dynamics, suggesting transient enhancement of vagal outflow after
premature atrial excitation, are temporally related to spontaneous onset of clinical
AF. (J Am Coll Cardiol 2005;45:278 – 84) © 2005 by the American College of Cardiology
Foundation
OBJECTIVES
The pathophysiology of atrial fibrillation (AF) consists of
both a triggering focal activator and changes in the atrial
electrophysiologic properties capable of maintaining AF
(1,2). Ablation of the ectopic pulmonary venous focus
eliminates AF in many cases and emphasizes the importance of these triggers located in the muscular sleeves (3,4).
Such sleeves are also present in the normal heart, and the
reasons for the maintenance of triggering activity are largely
unknown. Experimental studies have shown that parasympathetic stimulation dramatically shortens the atrial effective
refractory period and, thereby, facilitates the onset and
perpetuation of AF (5–7). The role of the parasympathetic
nervous system in the genesis and maintenance of clinical
AF episodes is not equally evident, however (8).
Analysis of heart rate (HR) variability has commonly
been used to assess the cardiac autonomic regulation before
the onset of AF episodes (9 –14). Previous studies have
shown alterations in some measures of HR variability before
the occurrence of paroxysmal AF episodes, but the results
have been partly controversial (11,12,14,15). This controversy may partly be due to methodological problems related
From the *Heart Center, University Hospital of Tampere, Tampere, Finland;
†Division of Cardiology, Department of Medicine, University of Oulu, Oulu,
Finland; and ‡Division of Cardiology, Department of Medicine, University of Turku,
Turku, Finland. Supported by the Medical Research Fund of Tampere University.
Manuscript received June 3, 2004; revised manuscript received September 26, 2004,
accepted October 4, 2004.
to the assessment of changes in autonomic regulation by the
traditional HR variability methods. Frequent ectopic beats,
which often precede the onset of AF, cause a potential
methodological bias, particularly for spectral analysis of HR
variability (16).
Heart rate turbulence is a recently described method (17)
that characterizes the short-term oscillations of HR after a
premature impulse. In HR turbulence analysis, the presence
of premature beats is a prerequisite rather than a harmful
phenomenon in an analysis of temporal changes in autonomic regulation. Therefore, we set out to test the hypothesis that altered vagal responses to atrial premature beats
may precede the onset of paroxysmal AF by analyzing the
temporal changes in the measures of HR turbulence preceding the onset of AF.
METHODS
Patients. The 24-h electrocardiographic (ECG) recordings
of patients who had paroxysmal episodes of AF were
collected from the Tampere and Oulu University Hospitals
in Finland during 1991 to 2001. Only recordings containing
at least one episode of AF lasting ⬎10 s, with at least 60
min of sinus rhythm preceding the AF episode, were
included in the analysis. Patients ⬎60 years of age with
sinus pauses ⬎2.5 s were excluded. Patients who had
hypertension, coronary artery disease, or other structural
JACC Vol. 45, No. 2, 2005
January 18, 2005:278–84
Abbreviations and Acronyms
AF
⫽ atrial fibrillation
ApEn ⫽ approximate entropy
HF
⫽ high frequency
HR
⫽ heart rate
LF
⫽ low frequency
SDNN ⫽ standard deviation of all normal R-R intervals
TO
⫽ turbulence onset
TS
⫽ turbulence slope
heart disease were included in the group of patients with
structural heart disease, and patients who did not have
hypertension, diabetes, or structural heart disease but had
atrioventricular accessory pathways were included in the
group of patients with lone AF.
The study population consisted of 29 patients with lone
AF who underwent 33 24-h recordings, and 39 patients
with structural heart disease who underwent 40 24-h recordings. Five recordings from both patients with lone AF
and patients with structural heart disease were excluded
from the HR variability analyses because of signal artifacts.
Thus, HR variability analyses were made on 63 recordings.
Analysis of HR variability. All of the two-channel 24-h
recordings were analyzed both with the Medilog Excel
ECG software and manually, to detect and quantify arrhythmias and artifacts. The 24-h ECG data were sampled
digitally and transferred from the Oxford Medilog scanner
(version 4.1c, Oxford Medical Ltd.) to a microcomputer for
analysis of HR variability and HR turbulence. All R-R
interval time series were first edited automatically, to detect
all ectopic beats and artifacts, followed by careful manual
editing for details. After automatic and manual editing, the
artifacts and ectopic beats were deleted, and the gaps were
filled using an interpolation method described earlier
(16,18). All questionable portions were compared with
two-channel Holter electrocardiograms. Only recordings
with ⬎80% qualified sinus beats were included in the
analysis. The non-spectral and spectral measures of HR
variability were analyzed according to the methods recommended by the task force (19).
Analyses of HR variability were performed in 60-min
segments on the entire recording. The 1-h periods preceding the onset of an AF episode were compared with the
hourly means of sinus rhythm in the rest of the recording.
From the 1-h periods, HR variability was calculated in
segments of 512 beats. Heart rate variability was also
analyzed in 15-min segments from the hour preceding the
onset of the AF episodes; 15-min R-R interval data were
divided into two segments of equal size according to their
beat count, and a linear detrend was applied to these
segments of 400 to 1,000 samples to make the data more
stationary. Spectral power was quantified through fast
Fourier transform analysis over 15- or 60-min periods in
two frequency bands: 0.04 to 0.15 Hz (low frequency [LF])
and 0.15 to 0.40 Hz (high frequency [HF]) (19). The ratio
Vikman et al.
HR Turbulence Before AF
279
of LF to HF spectra was also calculated. The SD of the
normal R-R intervals (SDNN) and the mean length of the
R-R intervals were used as time domain measures of HR
variability (19).
To determine overall complexity, approximate entropy
(ApEn) was calculated from the same pre-edited data that
were used for the spectral and time domain analyses of HR
variability. The ApEn expresses the logarithmic likelihood
that the data points of a certain deviation over a defined
number of observations retain the same deviation in incremental comparisons. Details of this method have been
described previously (20 –22).
Identification of ectopic beats. Premature ectopic beats
were identified manually by checking simultaneously twochannel Holter recordings and R-R interval tachograms.
The criterion for prematurity was a minimum shortening of
20% in the R-R interval. An ectopic beat was considered an
atrial premature beat when there was conclusive evidence of
abnormal atrial depolarization in any of the Holter channels. Only isolated atrial ectopic beats (preceded and followed by ⱖ20 normal sinus beats) with a distinct postectopic pause were included. The prematurity index of
ectopic beats was defined as the coupling interval divided by
the mean of the two preceding sinus R-R intervals.
Analysis of post-ectopic HR turbulence. Heart rate turbulence was calculated as previously described (17). Briefly,
turbulence onset (TO) was defined as the difference between
the means of the first two sinus R-R intervals after a
compensatory pause and the last two sinus R-R intervals
before the ectopic beat divided by the mean of the last two
sinus R-R intervals before the premature beat. Turbulence
slope (TS) was calculated as the maximum slope of the
regression line over any sequence of five sinus R-R intervals
within the first 20 sinus beats after an ectopic beat. The
means of TO and TS for all atrial ectopic beats occurring
during the hour preceding an AF episode(s) were calculated.
From the rest of the 24-h recording, the means of TO and
TS for all ectopic beats were calculated by hour and
compared with the means of the 1-h periods preceding the
onset of AF.
To find out the possible correlation between the duration
of AF episodes and the TO values, the AF episodes were
divided into two groups based on their duration. The
duration of the episodes was calculated as previously described, and we used the same cutoff value (200 s) to
differentiate between short and long episodes of AF as in
our previous work (23).
Statistical analysis. The results are presented as mean
values ⫾ SD. In the Kolmogorov-Smirnov test (z value
⬎1), in addition to using the absolute values, a logarithmic
transformation to the natural base was performed on the
spectral components of HR variability, the SDNNh, and the
number of ectopic beats in the different periods, which
made the data normally distributed. The paired-samples
Student t test was used to evaluate the differences between
the values of the hour preceding AF and the values of the
280
Vikman et al.
HR Turbulence Before AF
JACC Vol. 45, No. 2, 2005
January 18, 2005:278–84
Table 1. Clinical Characteristics of the Study Population
Age (yrs)
Gender (M/F)
Structural heart disease, n (%)
Coronary artery disease
Hypertensive heart disease
Valvular or other heart disease
Diabetes mellitus
Cardiac medication during recording,
n (%)
Beta-blocking agents
Calcium-channel blockers
ACE inhibitor
Digitalis
Type IA antiarrhythmics
Type IC antiarrhythmics
Amiodarone
No medication
Lone AF
(n ⴝ 29)
Patients With
Structural
Heart Disease
(n ⴝ 39)
54 ⫾ 11
14/15
64 ⫾ 10
20/19
17 (44)
28 (72)
13 (33)
12 (31)
13 (45)
1 (3)
1 (3)
1 (3)
—
6 (21)
4 (14)
11 (38)
21 (54)
6 (15)
13 (33)
8 (21)
2 (5)
4 (10)
5 (13)
—
ACE ⫽ angiotensin-converting enzyme; AF ⫽ atrial fibrillation.
non-AF hours. Analysis of variance with repeated measures
was performed to compare the differences between the
15-min periods preceding AF. Student t test was used to
analyze the differences between the patients with structural
heart disease and those with lone AF. Pearson’s correlation
coefficients were used in the analysis of correlations between
the continuous variables. A p value ⬍0.05 was considered
significant.
RESULTS
The clinical characteristics of the study population are
presented in Table 1. The patients with lone AF were
younger, and 39% of them had no medication, whereas all
patients with structural heart disease had medication at the
time of the recording.
HR turbulence after atrial premature beats. Table 2
presents the HR variability measures, the number of ectopic
beats, the coupling interval, the prematurity index, and HR
turbulence during the 1-h period(s) preceding AF and the
hourly means of the rest of the recording. In the patients
with lone AF, the number of ectopic beats was higher before
AF than during the other hours of the recordings, and the
ectopic beats were more premature during the 1-h period(s)
preceding the AF episode(s) than during the rest of the
recordings. The mean value for TS was not significantly
different between the two periods. The mean values for TO,
both in the patients with lone AF and in the patients with
structural heart disease, were significantly less negative
during the 1-h period preceding AF than during the
non-AF hours of the recordings (Table 2, Fig. 1). The
patients with lone AF also had more negative values of TO
both during the 1 h before AF and during the other hours
than the patients with structural heart diseases (p ⬍ 0.05
and p ⬍ 0.01, respectively).
Each 1-h period preceding an AF episode was divided
into four 15-min periods, and TO was analyzed for the
subgroup of patients who had at least one atrial ectopic beat
in each of the 15-min periods. There were 17 recordings (11
from patients with lone AF and 6 from patients with
structural heart disease) fulfilling these criteria. As shown in
Figure 2, TO during the last 15-min period before AF was
significantly less negative compared with the 60 to 45 min
preceding the AF episode (1.67 ⫾ 2.53 vs. ⫺0.41 ⫾ 2.46;
p ⬍ 0.05 tested with the paired-samples Student t test).
There were 87 short (⬍200 s) and 63 long (⬎200 s)
episodes of AF. In the whole group and in the patients with
structural heart disease, TO values were not significantly
different before short and long episodes (0.35 ⫾ 2.65 vs.
1.04 ⫾ 2.50, p ⫽ NS; and 1.15 ⫾ 2.46 vs. 0.86 ⫾ 2.41, p
⫽ NS, respectively). In the patients with lone AF, TO was
significantly more negative before short than long episodes
of AF (⫺0.39 ⫾ 2.62 vs. 1.24 ⫾ 2.63; p ⬍ 0.01).
HR variability measures. None of the traditional frequency and time domain measures showed any significant
differences between the two periods. Both in the patients
with lone AF and in the patients with structural heart
disease, the values of ApEn were significantly lower before
AF episodes than during the non-AF hours (Table 2).
No significant changes in HR variability measurements
were found when the 1-h period(s) preceding AF episode(s)
were divided into four 15-min periods and HR variability
analyses were performed on these data segments (Table 3).
Turbulence onset did not correlate with SDNNh or any
of the frequency domain measures of HR variability (r ⬍ 0.3
for all), with ApEn (r ⫽ ⫺0.19, p ⫽ NS), or with the
prematurity of the ectopic beats (r ⫽ 0.07, p ⫽ NS).
Turbulence onset correlated weakly with the mean length of
R-R intervals (r ⫽ 0.36, p ⬍ 0.01) and had a weak inverse
correlation with TS (r ⫽ ⫺0.31, p ⬍ 0.01).
DISCUSSION
This study demonstrates that the immediate R-R interval
responses to atrial premature impulses are blunted before
the onset of AF compared with the other hours of the
recordings in patients both with and without structural
heart disease. The normal response of R-R intervals to both
atrial and ventricular premature beats is a short-term acceleration of HR (i.e., a decrease of R-R intervals, which
creates a negative TO). This acceleration was blunted, or
even a slight deceleration of HR was observed after premature atrial beats during the 1-h period preceding the onset of
AF. These blunted HR responses to atrial premature beats
can be best explained by altered autonomic reflexes, such as
the transient enhancement of vagal outflow that reduces HR
changes in response to premature impulses in relation to the
onset of AF.
Traditional measures of HR variability and onset of
AF. Several studies have assessed the changes in cardiac
autonomic regulation before the onset of AF by analyzing
Vikman et al.
HR Turbulence Before AF
JACC Vol. 45, No. 2, 2005
January 18, 2005:278–84
281
Table 2. Changes in Heart Rate Variability and Heart Rate Turbulence Before Spontaneous
Onset of AF
Period
All patients (n ⫽ 73)*
Average R-R interval (ms)†
HF power (ms2)†
LF power (ms2)†
LF/HF ratio†
SDNNh (ms)†
ApEn†
Turbulence onset (%)
Turbulence slope (ms/R-R interval)
Atrial ectopic beats (n)
Coupling interval (ms)
Prematurity index
Lone AF (n ⫽ 33)*
Average R-R interval (ms)†
HF power (ms2)†
LF power (ms2)†
LF/HF ratio†
SDNNh (ms)†
ApEn†
Turbulence onset (%)
Turbulence slope (ms/R-R interval)
Atrial ectopic beats (n)
Coupling interval (ms)
Prematurity index
Patients with structural heart disease
(n ⫽ 40)*
Average R-R interval (ms)†
HF power (ms2)†
LF power (ms2)†
LF/HF ratio†
SDNNh (ms)†
ApEn†
Turbulence onset (%)
Turbulence slope (ms/R-R interval)
Atrial ectopic beats (n)
Coupling interval (ms)
Prematurity index
Non-AF h
One h Before AF
p Value
969 ⫾ 135
261 ⫾ 235
484 ⫾ 431
2.0 ⫾ 1.3
79 ⫾ 27
1.05 ⫾ 0.22
⫺0.35 ⫾ 1.46
15.5 ⫾ 7.4
3.2 ⫾ 2.2
629 ⫾ 102
0.67 ⫾ 0.07
984 ⫾ 185
299 ⫾ 316
491 ⫾ 460
2.1 ⫾ 1.9
84 ⫾ 35
0.95 ⫾ 0.25
0.71 ⫾ 1.76
15.0 ⫾ 7.5
3.7 ⫾ 3.2
615 ⫾ 151
0.65 ⫾ 0.09
NS
NS
NS
NS
NS
⬍ 0.001
⬍ 0.00001
NS
NS
NS
NS
979 ⫾ 118
352 ⫾ 305
675 ⫾ 487
2.3 ⫾ 1.3
83 ⫾ 25
1.09 ⫾ 0.21
⫺0.85 ⫾ 1.56
18.8 ⫾ 8.2
2.9 ⫾ 2.2
611 ⫾ 80
0.64 ⫾ 0.08
968 ⫾ 182
376 ⫾ 391
657 ⫾ 528
2.5 ⫾ 1.8
91 ⫾ 34
0.97 ⫾ 0.25
0.17 ⫾ 1.67
17.0 ⫾ 8.3
4.2 ⫾ 4.2
560 ⫾ 129
0.61 ⫾ 0.09
NS
NS
NS
NS
NS
⬍ 0.01
⬍ 0.00001
NS
⬍ 0.05
⬍ 0.01
⬍ 0.05
961 ⫾ 148
192 ⫾ 128
337 ⫾ 317
1.8 ⫾ 1.2
76 ⫾ 28
1.02 ⫾ 0.23
0.07 ⫾ 1.23
12.8 ⫾ 5.5
3.4 ⫾ 2.0
644 ⫾ 115
0.69 ⫾ 0.06
996 ⫾ 188
239 ⫾ 232
363 ⫾ 356
1.9 ⫾ 1.9
78 ⫾ 36
0.94 ⫾ 0.26
1.16 ⫾ 1.73
13.5 ⫾ 6.5
3.3 ⫾ 2.0
660 ⫾ 155
0.68 ⫾ 0.08
NS
NS
NS
NS
NS
⬍ 0.05
⬍ 0.00001
NS
NS
NS
NS
*Number of recordings; †heart rate variability analyses obtained from 63 recordings (28 with lone atrial fibrillation [AF], 35 with
structural heart disease). Values are mean ⫾ SD. Statistical analysis made from the logarithmic transformation of HF and LF
power, SDNNh, and the number of atrial ectopic beats.
ApEn ⫽ approximate entropy; HF ⫽ high-frequency; LF ⫽ low-frequency; SDNNh ⫽ standard deviation of all R-R
intervals.
the spectral or non-spectral components of HR variability in
patients with structural heart disease and with idiopathic AF
(9 –14,24). According to these reports, most of the AF
episodes in patients with idiopathic AF are related to an
increase in vagal tone, whereas most patients with organic
heart disease are more sympathetically dependent (11,13,14).
In many reports, however, it has only been possible to categorize a minority of AF episodes to be solely vagally or sympathetically driven, and the mode of onset of AF has also been
inconsistent within individuals (24 –27).
Bettoni and Zimmermann (12) found a primary increase in
adrenergic tone followed by marked modulation toward vagal
predominance before AF episodes both in patients with structural heart disease and in patients with idiopathic AF. In the
present study, the power-spectral and time-domain measurements of HR variability were not different before the onset of
AF compared with the corresponding values during the
non-AF hours of the recordings. There are salient differences
between these studies, which may explain the divergent results.
Bettoni and Zimmermann (12) used 5-min periods for analysis, and the most marked changes in cardiac vagal regulation
were observed within the last 5-min period before the onset of
AF. Because of the random occurrence of atrial premature
beats before the onset AF, the shortest time interval we could
analyze here was 15 min. Thus, the lack of differences in
spectral components between the periods may not exclude the
occurrence of significant changes in the autonomic modulation
of HR during the last few minutes before the onset of AF.
Furthermore, the different numbers of premature complexes
may partly explain the divergent results: there may be a
potential bias caused by the replacement of ectopic beats and
compensatory pauses by any of the interpolation methods in
282
Vikman et al.
HR Turbulence Before AF
Figure 1. Heart rate turbulence onset (TO) after spontaneous atrial
premature beats. The value of TO is significantly less negative during the
1 h preceding atrial fibrillation (AF) than the hourly mean values of the
non-AF hours of the recording both in patients with lone AF (left) and in
patients with structural heart diseases (right).
the spectral analysis of HR variability (16). The frequency of
premature atrial beats often increases before the onset of AF, as
also observed here among the patients with lone AF.
Nonlinear HR variability and onset of AF. Methods of
analysis derived from nonlinear dynamics have been developed to describe the features of HR dynamics that are not
detectable with traditional methods (21,28,29); ApEn is a
measurement that quantifies the regularity and predictability of time series data. Reduced complexity of HR dynamics
has been seen in many cardiovascular disorders (19,30 –32).
Consistent with the present observation, reduced ApEn has
been shown to precede AF episodes in patients after
coronary artery bypass grafting and in patients without
structural heart disease (10,26). The physiologic determinants of ApEn have not been well defined, however.
HR turbulence. Heart rate turbulence was first described
to occur in response to ventricular premature beats with a
typical short-term early acceleration and subsequent deceleration of HR after premature beats. Early acceleration has
been shown to result from transient vagal withdrawal caused
by baroreflex-mediated inhibition of vagal outflow (33–35).
Recent pacing and Holter studies have shown that the
modulation of R-R interval sequences is also present after
atrial premature impulses (36,37). However, there are quantitative differences in the HR dynamics after ventricular and
atrial premature complexes, the latter showing blunted early
acceleration of HR immediately after the compensatory
pause. A similar phenomenon was also observed here after
atrial premature complexes. However, significant interindividual and time-dependent intraindividual differences were
observed in these responses. The patients with structural
heart disease tended to have even a more blunted acceleration of HR after the compensatory pauses than the patients
with lone AF.
In accordance with a previous study (37), TO after atrial
premature complexes was not related to the other HR
JACC Vol. 45, No. 2, 2005
January 18, 2005:278–84
variability indexes and correlated only weakly with TS,
suggesting that mechanisms other than autonomic effects
alone may also be involved in the modulation of R-R
interval dynamics immediately after premature atrial impulses. One plausible mechanism is the sinus node resetting,
which has been described to occur in response to atrial
premature complexes (38). However, TO was not related to
the prematurity of atrial impulses, suggesting that the
changes in the resetting of sinus activity may not be the
predominant factor influencing the temporal changes of
TO. Most likely, vagal effects, which have short latency and
duration, and the electrophysiologic resetting phenomenon
together determine the immediate R-R interval length after
premature atrial complexes.
The mechanism explaining the temporal relationship
between the altered TO after atrial premature beats and the
onset of AF could be explained by changes in vagal
responses. It can be assumed that sinus node automaticity
and its resetting after premature beats remain relatively
stable in a given individual. Thus, enhanced vagal activity in
response to premature excitation of the atrium could explain
both the onset of AF and the prolongation of the first R-R
intervals after the premature impulses shortly preceding the
onset of AF.
Study limitations. All the patients with structural heart
disease and many of the patients with lone AF were
receiving medication at the time of the Holter recordings,
which may have influenced the measurements of autonomic
tone. However, the patients served as their own controls,
and the results remained unchanged (data not shown) in the
subgroup of patients with lone AF who were not receiving
medication, which suggests that the cardiac medication
itself had no major effect on these observations. The group
of patients was relatively small, and the results should
naturally be confirmed in larger patient series before they
can be generalized.
Figure 2. Heart rate turbulence onset (TO) after spontaneous atrial
premature beats in 15-min periods during the 1 h preceding atrial
fibrillation (AF) episode(s). In the subgroup of patients (n ⫽ 15; 17
recordings) with at least one atrial ectopic beat in each 15-min period
during the hour preceding an AF episode, TO is significantly less negative
during the 0- to 15-min period before AF than during the 45- to 60-min
period preceding AF.
Vikman et al.
HR Turbulence Before AF
JACC Vol. 45, No. 2, 2005
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283
Table 3. Changes in R-R Dynamics Before Spontaneous Onset of AF
Period Before AF
All patients (n ⫽ 63)*
Average R-R interval (ms)
HF power (ms2)
LF power (ms2)
LF/HF ratio
SDNN15min (ms)
ApEn
Lone AF (n ⫽ 28)*
Average R-R interval (ms)
HF power (ms2)
LF power (ms2)
LF/HF ratio
SDNN15min (ms)
ApEn
Patients with structural heart disease
(n ⫽ 35)*
Average R-R interval (ms)
HF power (ms2)
LF power (ms2)
LF/HF ratio
SDNN15min (ms)
ApEn
60–45 min
45–30 min
30–15 min
15–0 min
997 ⫾ 189
358 ⫾ 584
556 ⫾ 608
2.2 ⫾ 1.8
64 ⫾ 31
1.00 ⫾ 0.21
1,000 ⫾ 181
308 ⫾ 395
522 ⫾ 535
2.2 ⫾ 2.0
71 ⫾ 30
0.97 ⫾ 0.20
998 ⫾ 192
262 ⫾ 249
473 ⫾ 460
2.3 ⫾ 1.9
60 ⫾ 26
0.99 ⫾ 0.23
972 ⫾ 201
289 ⫾ 334
471 ⫾ 496
2.2 ⫾ 2.1
70 ⫾ 34
0.96 ⫾ 0.23
982 ⫾ 189
464 ⫾ 803
692 ⫾ 513
2.5 ⫾ 1.8
66 ⫾ 25
1.02 ⫾ 0.19
991 ⫾ 185
398 ⫾ 526
702 ⫾ 608
2.5 ⫾ 1.7
70 ⫾ 27
0.96 ⫾ 0.20
995 ⫾ 189
312 ⫾ 281
666 ⫾ 570
2.6 ⫾ 1.9
65 ⫾ 24
1.00 ⫾ 0.16
960 ⫾ 197
360 ⫾ 387
651 ⫾ 610
2.6 ⫾ 2.2
75 ⫾ 35
0.99 ⫾ 0.21
1,008 ⫾ 191
274 ⫾ 306
448 ⫾ 661
1.9 ⫾ 1.8
62 ⫾ 35
0.98 ⫾ 0.23
1,007 ⫾ 180
236 ⫾ 229
379 ⫾ 424
2.0 ⫾ 2.2
56 ⫾ 31
0.98 ⫾ 0.21
1,000 ⫾ 197
222 ⫾ 217
319 ⫾ 268
2.0 ⫾ 1.9
56 ⫾ 27
0.98 ⫾ 0.27
982 ⫾ 206
231 ⫾ 277
327 ⫾ 324
2.0 ⫾ 2.1
65 ⫾ 83
0.93 ⫾ 0.24
*Number of recordings. Values are mean ⫾ SD. Statistical analysis made from the logarithmic transformation of HF power, LF
power, and SDNN15min. p ⫽ NS for all.
AF ⫽ atrial fibrillation; ApEn ⫽ approximate entropy; HF ⫽ high-frequency; LF ⫽ low-frequency; SDNN15min ⫽ standard
deviation of all R-R intervals.
Conclusions. The R-R interval dynamics immediately after atrial premature impulses are blunted near the onset of
spontaneous AF episodes compared with the dynamics
during the non-AF hours of the recordings. The data
suggest that vagal inhibition in response to premature atrial
excitation is absent, or even that transient enhancement of
vagal outflow occurs before AF. The documentation of a
direct causal relationship between these phenomena warrants more experimental work.
Reprint requests and correspondence: Dr. Saila Vikman, Heart
Center, University Hospital of Tampere, Biokatu 6, PL 2000,
33521 Tampere, Finland. E-mail: [email protected].
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