From the Centro Ricerche Cardiovascolari, CNR; Medicina Interna II e
Medicina Interna III (S.P.), Ospedale L. Sacco, Università di Milano;
Divisione di Cardiologia (S.D.), Ospedale Uboldo, Cernusco S/N; Medicina del
Lavoro (F.B.), Ospedale di Novara; and Dipartimento di Bioingegneria (A.B.,
L.M., S.C.), Politecnico di Milano, Milano, Italy.
Correspondence to Dr Raffaello Furlan, Medicina Interna II, Ospedale L. Sacco, Università di Milano, Via G.B. Grassi, 74, 20157 Milano, Italy. E-mail r.furlan{at}planet.it
Methods and Results—To evaluate the beat-by-beat modifications in
the neural control of heart period preceding a syncopal event, we
studied RR interval variability in 22 healthy subjects who experienced
fainting for the first time during a 90° head-up tilt and in 22
control subjects by means of time-variant power spectral
analysis. Sympathetic and vagal modulations to the sinoatrial
node were assessed by the normalized power of the low-frequency (LF,
Conclusions—Two different patterns may be recognized in the
cardiac autonomic changes preceding an occasional vasovagal event,
namely, one characterized by a progressive increase of the marker of
cardiac sympathetic modulation up to the onset of syncope, the other by
a sympathetic inhibition with an impending vagal predominance. The
recognition of different pathophysiological
mechanisms in fainters may have important therapeutic implications.
On the basis of experimental observations,2 it
has been hypothesized that a possible trigger mechanism in humans might
be the inappropriate mechanical activation of ventricular
vagal unmyelinated afferents in the presence of reduced
ventricular filling. In particular, the stimulation of
ventricular vagal receptors would be produced by an
enhancement of heart contractility due to an
exaggerated cardiac sympathetic activation.
The possibility that an initial cardiac sympathetic overactivity might
promote vasovagal reactions is supported by the clinical observation of
a transient rise in heart rate before syncope.3
In addition, it has been observed that the administration of exogenous
catecholamines4 or
nitroglycerin5 before a tilt test
promotes neurogenic fainting in susceptible subjects by eliciting a
direct or reflex increase in sympathetic activity.
However, the attempt to quantify sympathetic activity before syncope
has also furnished variable and sometimes opposite results. For
instance, plasma norepinephrine concentrations have been
found to be elevated3 6 or
diminished7 8 before syncope. Studies based on
conventional power spectral analysis of RR variability have
indicated increased,9 10
reduced,11 12 or
unchanged13 values of the markers of cardiac
sympathetic modulation before a vasovagal event. The
heterogeneity of the changes in the sympathetic drive
to the vessels before syncope was recently highlighted in a study that
used microneurography techniques.14 Indeed,
vasovagal events induced by a tilt test were preceded by either a
blunted increase (in habitual fainters) or a marked enhancement (in
occasional fainters) of the muscle neural sympathetic
discharge.14
However, the methodologies used in those studies could not continuously
assess the cardiac autonomic changes that precede neurogenic syncope.
This is of paramount importance, because the wide range of clinical
presentations of vasovagal reactions might reflect
different underlying cardiac pathogenetic mechanisms, which in turn
imply the necessity of differently tailored therapeutic approaches. In
fact, the actual onset of syncope can be abrupt, with only few and
transient symptoms, or slower, with presyncope signs such as nausea and
dizziness preceding the complete loss of consciousness by seconds or
even minutes. It is conceivable that these different clinical
presentations might be related to different cardiac neural
changes preceding the vasovagal event.
We addressed this hypothesis by evaluating RR interval variability in
the period preceding the onset of bradycardia in a group of young,
healthy subjects who fainted for the first time during a tilt test.
Time-variant autoregressive spectral analysis was used to
obtain markers of sympathetic and vagal cardiac modulation on a
beat-by-beat basis15 to evaluate continuously the
possible complex and rapid changes in the autonomic control of heart
rate before syncope.
A second group comprises 22 healthy control subjects (age, 20±1 years;
9 male, 13 female) who were asymptomatic on tilt and during
2 or more previous tilt tests.
None of the subjects had ever experienced a syncopal event. Informed
consent was provided by the subjects and their parents.
Recorded Variables
Protocol
The experimental protocol was approved by the Ethical Committee of our
hospital.
Definitions
Data Analysis
Time-variant spectral analysis of heart period variability
represents a development of usual autoregressive power spectral
analysis. It is based on a recursive least-squares-method
algorithm, which makes the autoregressive identification procedure
suitable to update the coefficients of the model every new beat.
Therefore, power spectral analysis can be performed on a
beat-by-beat basis, permitting the evaluation of the changes in the
spectral components during unstable conditions like transient
ischemia15 and syncopal
events.17
The forgetting factor
In this study, we used an
Time-variant analysis of RR interval was performed on the whole
study session. In every subject, we considered as resting condition the
mean values obtained during the entire recumbent position.
In each subject, 2 nonoverlapped periods were identified during tilt:
early (T1) and late (T2)
tilt. T1 referred to the mean values obtained by
averaging all the spectra contained in 1 minute, starting from the
second minute of tilt. As to T2, in
symptomatic subjects, it referred to the last minute of
tilt preceding the onset of bradycardia, considered the cardiac
hallmark of syncope. In subjects who remained asymptomatic,
T2 values were computed on a 1-minute period of
tilt starting after the ninth minute. This period was chosen on the
basis of the mean duration of tilt (10±0.8 minutes) in the group of
subjects with syncope.
As already reported,16 18 19 2 major oscillatory
components can be identified in the power spectrum of RR variability: a
high-frequency (HF) component at
The power of the LF and HF oscillatory components is computed both in
absolute units (ms2) and in normalized units
(NU), obtained by dividing the absolute power of each oscillatory
component by total power minus the very-low-frequency component and
multiplying by 100.16 18 The LF/HF values were
calculated as a measure of the reciprocal changes of the sympathetic
and vagal modulation of the sinoatrial node discharge (sympathovagal
balance).16 18 19
Conventional spectral analysis was also performed on the
respiratory signal in the recumbent position and during
T1 and T2 to assess the
main respiratory frequency.
Statistics
The time course of changes during tilt of RR interval and of the
spectral markers of cardiac autonomic regulation, as obtained in an
asymptomatic control subject and in 2 subjects with
syncope, are illustrated in Figure 1
Of the 22 subjects who developed syncope, 13 showed a pattern similar
to the example of the central panels of Figure 1
Table 2
Figure 2
During tilt, subjects belonging to the sudden syncope group had a
progressive increase in the spectral marker of cardiac sympathetic
modulation LFNU, an inhibition of the vagal index
HFNU, and hence, an enhancement of LF/HF
indicating a shift of the sympathovagal balance toward sympathetic
predominance up to the syncopal episode.
Conversely, subjects with syncope with latency exhibited a progressive
increase of HFNU attended by a reduction of
LFNU and LF/HF, suggestive of an impending
predominance of the vagal modulation of the sinoatrial node
discharge.
It was found that individual spectral profiles preceding fainting could
be ascribed to 2 different patterns. One was characterized by a
progressive increase of cardiac sympathetic modulation up to the sudden
onset of bradycardia, and the second displayed a gradual inhibition of
sympathetic and a concomitant enhancement of vagal modulation of heart
period.
Autonomic Changes During Tilt
The possibility of performing spectral analysis on a
beat-by-beat basis allowed us to focus on the last 60 seconds preceding
the onset of bradycardia. Compared with asymptomatic
control subjects, in all subjects with syncope, the progression of tilt
was characterized by wide fluctuations of the indices of cardiac
autonomic control, suggestive of a marked instability of the cardiac
neural modulation. In addition, the time-variant approach permitted
highlighting of 2 different trends of the spectral markers of cardiac
autonomic modulation that might remain hidden10
when usual algorithms were used10 and that might
account for the conflicting findings in the evaluation of plasma
catecholamine levels reported in the period preceding
vasovagal events.3 6 7 8 The 2
representative patterns are discussed separately
below.
Progressive Sympathetic Activation
This pattern is in accordance with previous findings obtained by
conventional spectral analysis in patients with
isoproterenol-independent orthostatic
syncope9 and in trained
athletes.10 It must be pointed out that in the
group of asymptomatic control subjects of this study as
well, there was a slight increase of LFNU and
LF/HF and decrease of HFNU with the progression
of tilt. Thus, in subjects with occasional sudden syncope, the cardiac
neural changes attending passive orthostatism seem to be qualitatively
similar to those of normal subjects but quantitatively different.
A possible relationship between high values of LF and susceptibility to
neuromediated syncope can also be inferred from a study by Lipsitz et
al.24 These authors observed an increased rate of
syncopal attacks during passive orthostatism in young subjects, with
higher LF values compared with elderly subjects.
In keeping with the possible existence of a cardiac sympathetic
overactivity immediately before syncope is the observation of
echocardiographic signs of sympathomediated enhancement
of cardiac inotropism during the 1 to 4 minutes preceding the
syncope.25
The data obtained in our group of subjects with sudden syncope lend
further support to the experimental findings by Oberg and
Thoren,2 who reported that the activation of
vagal ventricular receptors and the consequent reflex
bradycardia could be observed only when a pronounced
tachycardia at the beginning of hemorrhage had
indirectly suggested the presence of a remarkable sympathetic
activation to the heart.
However, the activation of vagal ventricular afferents by
sympathetic overactivity is likely to be only one of the mechanisms
involved in the genesis of vasovagal episodes with cardioinhibition.
Central influences elicited by emotional stress or severe pain can also
generate neural mechanisms leading to syncope.1
Furthermore, low-pressure cardiopulmonary baroreceptors have
been hypothesized to be more sensitive to orthostatic
stress in habitual fainters.26 Finally, the
occurrence of vasoinhibitory fainting in patients with
heart transplants27 28 further suggests the
existence of mechanisms different from the activation of vagal
ventricular receptors. Among them,
Dickinson29 proposed the anomalous activation of
venoatrial stretch receptors as a possible trigger of the sequence of
events occurring in vasovagal fainting.
Progressive Sympathetic Inhibition
This pattern suggests that neuromediated syncope in occasional fainters
may be promoted by an alternative
pathophysiological mechanism independent of an
exaggerated enhancement of sympathetic activity to the
heart.2
Indeed, in a group of fainters, Morillo et al12
found reduced values of LF and LF/HF during the first 5 minutes of a
60° tilt, suggestive of a failure in vagal withdrawal and a blunted
sympathetic activation. Similarly, another
study11 based on time-frequency mapping of RR
variability concluded that subjects prone to vasodepressor syncope were
characterized by an elevated cardiac parasympathetic activity that
persisted during orthostatic stress.
A failure to enhance the sympathetic tone to the vasculature or to
maintain it during standing,30 long-lasting
tilt,14 or lower-body negative
pressure31 maneuvers has been reported in
patients with both occasional and recurrent orthostatic
syncope by use of microneurographic techniques. Moreover, a decreased
cardiac norepinephrine spillover was observed in
patients who experienced a vasovagal syncope during cardiac
catheterization.7 Finally, an
overall diminished cardiovascular sympathetic activity,
as inferred from reduced plasma norepinephrine levels, has
been documented before syncope in patients undergoing both passive
orthostatism8 and lower-body negative
pressure.32
Limitations of the Study
Moreover, we focused on a highly selected population, that is, on a
group of otherwise healthy subjects who fainted for the first time
during a gravitational stress. Thus, our findings might not be directly
extendable to other types of vasovagal reactions, such as emotional
syncope, or to patients with recurrent syncope.
Conclusions
We hypothesize that if these occasional fainters should develop
recurrent vasovagal reactions, the capability of recognizing different
cardiac pathophysiological mechanisms underlying
neurogenic syncope might help to select between different drug classes,
such as ß-adrenergic receptor antagonists or
Received April 7, 1998;
revision received June 19, 1998;
accepted June 23, 1998.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Cardiac Autonomic Patterns Preceding Occasional Vasovagal Reactions in Healthy Humans
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—The wide range of
clinical presentation of orthostatic vasovagal
syncope suggests different underlying changes in the cardiac
autonomic modulation. 
0.1-Hz) and high-frequency (HF, 0.25-Hz) oscillatory components
of RR variability. When the patients were supine, no differences were
observed in the hemodynamic and spectral
parameters of the 2 groups. During the tilt procedure, RR,
LFNU, and HFNU (NU=normalized units) values
were relatively stable in control subjects. During early tilt
(T1), subjects with syncope had reduced RR intervals
compared with control subjects. In 13 subjects with syncope, RR
decreased while LFNU and LF/HF increased in the last minute
of tilt before syncope (T2). Conversely, in the remaining 9
fainters, LFNU and LF/HF decreased from T1 to
T2 and HFNU increased slightly.
Key Words: syncope • nervous system, autonomic • spectroscopy
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Vasovagal syncope is a common clinical event, the
pathogenetic mechanisms of which are still poorly
understood.1
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Study Population
This study includes a group of 22 subjects (age, 16±1 years; 11
male, 11 female) who experienced a vasovagal reaction during a 90°
head-up tilt test. They were part of a population of healthy volunteers
recruited by our laboratory to study the effects of the tilt maneuver.
Respiratory activity (nasal thermistor; Nikon Kohden TR611) and
ECG were continuously recorded on an FM tape recorder (Racal
Store 7DS). Arterial pressure was measured at rest and 3
times during tilt by a mercury sphygmomanometer. In subjects with
syncope, blood pressure was also assessed, when possible, at the onset
of symptoms.
After an adequate period of adaptation on the tilt table, data
recording was initiated for the resting condition (15 minutes).
Thereafter, all subjects underwent a 90° head-up tilt, which was
maintained for 15 minutes. The tilt procedure was interrupted whenever
criteria for the onset of a vasovagal episode were satisfied.
A vasovagal episode was defined as the occurrence of loss of
consciousness or the onset of presyncopal signs and symptoms, together
with an increase of RR interval >80% of early tilt values and a
decrease of systolic pressure >40% of early tilt
values.
Analog data were analyzed off-line after
analog-to-digital conversion at 300 samples per second per channel. The
principles of the software for data acquisition and time-variant
spectral analysis have been escribed
elsewhere.15 16 17 
weighs the prediction error terms
exponentially, thus permitting focus on the most recent data out of the
window of interest. This latter is defined by , according to the
formula n=1/(1-), where n=number of beats. value of 0.98, that is, a window of
interest of 50 beats. The use of a high-pass IIR filter on RR series
before time-variant identification accounts for the reduction of total
RR interval variance and of the absolute power of the single
oscillatory components (see Tables). Moreover, a further
reduction in the power of the above-mentioned variables is probably
due to the shorter window of interest (ie, 50 beats when =0.98)
compared with the conventional spectral analysis usually
performed on longer segments of data. 0.25 Hz, considered a marker of
vagal modulation of the sinoatrial node,18 19 20
and a low-frequency (LF) component at 0.10 Hz, considered, when
normalized, a marker of sympathetic
modulation.16 18 21 22
Data are expressed as mean±SEM. Two-way ANOVA for repeated
measures and 1-way ANOVA with the Student-Newman-Keuls test for
multiple comparisons and Student's t test for paired
observations were used whenever appropriate. Differences were
considered significant at values of P<0.05.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
As summarized in Table 1
, at rest,
no differences in hemodynamic and spectral
parameters were observed between control subjects and
subjects who developed a syncopal attack. During tilt, RR interval
decreased in both groups, reaching lower values in subjects with
syncope. The frequency-domain analysis assessed a significant
increase of LFNU and LF/HF and a concomitant
decrease of HFNU in the 2 groups.
View this table:
[in a new window]
Table 1. Hemodynamic and Spectral Profiles of Control
Subjects and Subjects With Syncope at Rest and During the Early Phase
of
Tilt .
These examples of syncope represent the 2 most remote types of
patterns in the spectral components observed in subjects who fainted.
In the control subject, LFNU and
HFNU values remained stable along tilt. The
subject with "sudden syncope" had a slight decrease of RR and a
progressive increase of LFNU paralleled by a
reduction of HFNU before syncope that was
accompanied by a sudden rise of RR and HFNU and a
drop of LFNU. Of interest,
LFNU exhibited large fluctuations during the
entire tilt period. In the example depicted in the right panels of
Figure 1, the LFNU index, after an initial
plateau, underwent a slow decrease, with a final reduction at the time
of syncope. In addition, a marked progressive increase in
HFNU was evident in the period preceding the
maximal bradycardia. Thus, in this case, the period before syncope was
characterized by a slow, progressive inversion of the pattern of the
spectral markers LFNU and
HFNU, the reduction of the former being
accompanied by a gradual increase of HFNU.
Consequently, a latency between the maximum of
LFNU and the onset of bradycardia could be
identified in the example on the right side of Figure 1.
View larger version (21K):
[in a new window]
Figure 1. Examples of beat-by-beat changes of RR interval
and spectral markers of cardiac autonomic modulation LFNUand HFNU, as observed during tilt procedure in a
control (left) and in 2 subjects who suffered from syncope (center and
right). Latency (L) is arbitrarily defined as time lag between maximum
reached by LFNU component during tilt and onset of
bradycardia. Notice in example with sudden syncope that
LFNU drops abruptly and concomitantly with bradycardia.
Conversely, in example of syncope with latency, bradycardia is preceded
by a slower decay of LFNU, suggesting progressive
sympathetic inhibition with continuous increase of vagally related
oscillatory component HFNU (bottom right). In this example,
L corresponds to 77 seconds. RR indicates RR interval; LF, LF
component; and HF, HF component. 
and were grouped as
sudden syncope. The 9 remainders, who displayed a time lag between the
maximum of LFNU and the onset of bradycardia
(range, 12 to 167 seconds), were considered to be "syncope with
latency." summarizes the differences among
groups during early tilt (T1), when all subjects
were asymptomatic. Only RR interval was lower in the
syncope with latency group than in control subjects. Conversely, during
the period of tilt immediately preceding the loss of consciousness
(T2), the 2 groups of patients with syncope both
had lower RR interval values than control subjects (Table 3). In addition, the syncope with latency
group was characterized by reduced values of LFNU
and of LF/HF in comparison with the sudden syncope subjects (Table 3).
In the 3 groups, RR interval decreased during T2
compared with T1. A reduction of blood pressure
values from T1 to T2 was
present in both groups of patients with syncope.
View this table:
[in a new window]
Table 2. Hemodynamic and Spectral Profiles of Control
Subjects and of the Two Groups of Subjects With Syncope During the
Early Phase of
Tilt
View this table:
[in a new window]
Table 3. Hemodynamic and Spectral Profiles of Control
Subjects and of the Two Groups of Subjects With Syncope During the Late
Phase of Tilt shows the individual and mean
changes observed in spectral markers by comparing
T1 and T2 in the 3 groups.
View larger version (18K):
[in a new window]
Figure 2. Time course of individual and mean changes in
spectral markers of cardiac autonomic modulation as assessed during
initial phase of tilt (T1) and in period of tilt
before syncope (T2). In control group, T2
corresponds to minute 10 of tilt. Values of LF and HF are in NU. In
group of subjects who developed sudden syncope, index of cardiac
sympathetic modulation LFNU increases from beginning to end
of tilt. Enhancement of LF/HF ratio indicates shift of cardiac
sympathovagal modulation toward sympathetic predominance. In group of
fainters with latency, progressive sympathetic inhibition is suggested
by decrease of LFNU and LF/HF and by concomitant increase
of vagal-related index HFNU. Abbreviations as in Figure 1 .
*P<0.05 vs T1; **P<0.01 vs
T1.
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
In this study, we addressed the hypothesis that the wide variety
of clinical presentations of vasovagal events may somehow
reflect different or even opposite changes in the cardiac autonomic
profile of the fainting subjects.
Our results show that both asymptomatic control
subjects and subjects who developed syncope exhibited similar
hemodynamics and spectral indices of cardiac autonomic
modulation in resting conditions. During the early phase of tilt, when
all the subjects of the study were still asymptomatic, the
subjects who would develop syncope had similar blood pressure but
reduced RR values compared with asymptomatic control
subjects (Table 1). This finding is in keeping with a recent
observation by Mallat et al23 indicating that a
marked increase of heart rate during the first 6 minutes of tilt may
predict the occurrence of vasovagal events.
In 13 subjects with syncope, the spectral marker of sympathetic
modulation, LFNU, suddenly dropped to nearly zero
concomitantly with the onset of bradycardia, thus suggesting a
persistent predominance of the sympathetic drive to the heart up to the
vasovagal event. In those subjects, the neural control of the
sinoatrial node activity followed a peculiar time course characterized
by an increase of cardiac sympathetic modulation in the early phase of
tilt compared with the recumbent position and, in most cases, by its
further enhancement in the period immediately preceding the onset of
fainting. The vagal modulation of heart period, as inferred from the
power of the HFNU component, decreased during the
last minute that preceded syncope.
In 9 of the fainters of our study, the autonomic profile during
tilt was characterized by an initial marked predominance of
LFNU, which, after having reached a maximum,
slowly decreased before dropping down at the onset of bradycardia.
Therefore, the period between the maximum sympathetic activation and
the onset of the vagal inhibitory reflex seemed to be
distinguished by a slow, progressive inversion of the sympathovagal
modulation with a consequent cardiac sympathetic inhibition.
This study was restricted to spectral analysis of heart
rate variability. Important neural control mechanisms known to be
altered in patients with syncope, such as high- and low-pressure
baroreceptor reflex control of heart
rate,13 14 33 were not directly addressed.
This study showed that in a group of healthy subjects, a marked
cardiac sympathetic activation may precede a vasovagal event induced by
gravitational stress. It also reported, in other cases, a slow
inversion of the cardiac sympathovagal balance with progressive
sympathetic inhibition. 
-adrenergic receptor agonists.
Acknowledgments
We gratefully acknowledge the typing assistance of Isabella
Ghirardelli.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
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