Bme.sunysb.edu2
IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING, VOL. 51, NO. 2, FEBRUARY 2004
Nonlinear Analysis of the Separate Contributions of
Autonomic Nervous Systems to Heart Rate Variability
Using Principal Dynamic Modes
Yuru Zhong, Hengliang Wang, Ki Hwan Ju, Kung-Ming Jan, and Ki H. Chon*
, Member, IEEE
Abstract—This paper introduces a modified principal dynamic
the occurrence of life-threatening ventricular tachyarrhyth-
modes (PDM) method, which is able to separate the dynamics of
mias, whereas augmented vagal tone exerts a protective and
sympathetic and parasympathetic nervous activities. The PDM is
antifibrillatory effect Experimental evidence suggests that
based on the principle that among all possible choices of expansion
myocardial ischemia, acute myocardial infarction, and chronic
bases, there are some that require the minimum number of
basis functions to achieve a given mean-square approximation
heart failure all exhibit signs of autonomic function imbalance
of the system output. Such a minimum set of basis functions is
Consistent with autonomic imbalance, patients who have
termed PDMs of the nonlinear system. We found that the first
suffered a myocardial infarction have a marked decrease in HRV
two dominant PDMs have similar frequency characteristics for
due to a decrease in vagal and an increase in sympathetic neural
parasympathetic and sympathetic activities, as reported in the
activities. Power spectral analysis of HRV has been shown to
literature. These results are consistent for all nine of our healthy
human subjects using our modified PDM approach. Validation
be useful in risk stratification after myocardial infarction
of the purported separation of parasympathetic and sympathetic
Power spectra of human HRV can be divided into three main
activities was performed by the application of the autonomic
frequency zones: the power spectral density (PSD) below 0.04
nervous system blocking drugs atropine and propranolol. With
Hz is considered to be very low-frequency (VLF), between 0.04
separate applications of the respective drugs, we found a signifi-
and 0.15 Hz is the low-frequncy (LF), and between 0.15 and 0.5
cant decrease in the amplitude of the waveforms that correspond
to each nervous activity. Furthermore, we observed near complete
Hz is the high-frequncy (HF). The LF is found to be mediated by
elimination of these dynamics when both drugs were given to the
both the sympathetic and parasympathetic nervous influences
subjects. Comparison of our method to the conventional low-fre-
and the HF is unequivocally believed to be dominated solely
quency/high-frequency ratio shows that our proposed approach
by the parasympathetic nervous system The VLF has been
provides more accurate assessment of the autonomic nervous
proven to be related to factors other than the autonomic nervous
balance. Our nonlinear PDM approach allows a clear separation
system (ANS) (e.g., temperature, hormones, etc.) The ratio
of the two autonomic nervous activities, the lack of which has been
the main reason why heart rate variability analysis has not had
of the LF to HF power obtained from spectral analyses has been
wide clinical acceptance.
shown to be a good marker of the sympathovagal balance in
Index Terms—Autonomic nervous systems, heart rate vari-
assessing HRV For example, a large LF/HF ratio suggests
ability, parasympathetic, power spectrum, principal dynamic
predominantly sympathetic control, whereas a small LF/HF ratio
indicates predominantly vagal control. However, the LF/HFratio for clinical utility has not gained wide acceptance, mainlybecause it is an approximation of the autonomic balance and
does not truly reflect the balance of the two nervous influences.
and parasympathetic influences on the modulation of heart
mediated by the sympathetic nervous system, despite the pre-
rate. It is through efficient interactions between the parasym-
vailing understanding that the LF reflects both the sympathetic
pathetic and sympathetic nervous systems that homeostasis of
and parasympathetic nervous systems. Another deficiency of the
the cardiovascular system is properly maintained. Failure of the
LF/HF ratio is that the method is linear and does not properly
interactions may lead to sympathetic hyperactivity, promoting
account for nonlinear characteristics of the ANS. A plethora ofrecent studies have shown that the physiological mechanisms re-
Manuscript received January 27, 2003; revised May 26, 2003. This work was
sponsible for heart-rate fluctuations have nonlinear components
supported in part by the National Institutes of Health (NIH) through the Center
While the LF/HF ratio obtained via the PSD is inaccurate,
for Research Resource under Grant RR15217.
Asterisk indicates corresponding
it shows great promise of being a useful noninvasive marker for
Y. Zhong, H. Wang, and K. H. Ju are with the Department of Biomedical
determining the state of the ANS, if a new method is developed
Engineering, State University of New York at Stony Brook, Stony Brook, NY
that can separate the dynamics of the two nervous systems. This
11794-8181 USA.
new method should also account for the nonlinear components
K.-M. Jan is with the Department of Cardiology, Columbia University, New
York, NY 10027-6902 USA.
of heart rate fluctuations, in order to more accurately represent
*K. H. Chon is with the Department of Biomedical Engineering and
the nonlinear properties of heart rate dynamics.
the Department of Physiology and Biophysics, HSC T18, Rm. 030, State
This paper aims to address the above problem of separating
University of New York at Stony Brook, Stony Brook, NY 11794-8181 (e-mail:
[email protected]).
the two nervous systems' dynamics by the use of principal
Digital Object Identifier 10.1109/TBME.2003.820401
dynamic modes (PDM). The PDM has been shown to be a novel
0018-9294/04$20.00 2004 IEEE
IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING, VOL. 51, NO. 2, FEBRUARY 2004
method for characterizing nonlinear physiological systems
and then the HR data were normalized to a unit variance. A
while reducing higher-order dimensions. The nonlinear PDM
total of 300 data points were used for analyses.
method was first introduced and applied in the analysis ofphysiological systems by Marmarelis –The PDMs are
calculated using Volterra-Wiener kernels based on expansionof Laguerre polynomials We have modified the PDM
The need for the input signal having broad-band character-
technique to be used with even a single output signal of HRV
istics has been well documented as a prerequisite for a general
data, whereas the original PDM required both input and output
methodology of nonlinear modeling of dynamic systems using
data. Our analyses will reveal that the first two dominant PDMs
functional expansion of kernels With recent advances,
obtained from the heart rate data of healthy human subjects
the strict requirement of input being white is alleviated using
correspond to the two autonomic nervous activities. This has
the Laguerre expansion of kernels approach However, it is
been demonstrated in both time and frequency domains. The
still necessary to have the input signal exhibit broad-band char-
application of the autonomic nervous blocking agents, propra-
acteristics to obtain accurate kernel estimates. The HR data is
nolol and atropine, corroborated our finding that the magnitude
far from broad-band, however. For example, significant power
of the waveforms corresponding to either sympathetic or
exists in the VLF of the HR data compared to LF and HF. The
parasympathetic nervous activities were significantly reduced.
spectral power bands of interest, the LF and HF, are dwarfed by
This technique allows a more in-depth analysis of the ANS and
the significantly high spectral power in the VLF band. An ap-
offers for the first time a more accurate measure of the balance
proach we took to reduce high spectral power in the VLF band
between the two autonomic nervous activities. Furthermore,
is the method introduced by Tarvainen with the aim of re-
the method specifically accounts for the inherent nonlinear
ducing VLF power to the level of the LF and HF bands. This
dynamics of heart rate control, which the PSD does not.
detrending method is briefly described in the Appendix.
We represent the heart rate data after detrending as HRc. The
PDM method requires both the input and output data, but since
II. DATA COLLECTION
we have only the output signal of HR recordings, we utilize the
The data analyzed in this investigation were obtained from
following steps to create an input signal. The goal is to create
a previously-published study Experimental methods are
an input signal that has broad-band characteristics. It is inappro-
described in detail in and will be only briefly summarized
priate to use white noise data as the input signal even though the
here. Data used in this study were collected from nine healthy
task was to create a broad-band signal because white noise has
male subjects between 19 and 38 years of age and consisted
no correlation to the dynamics of heart rate. We used HRc, de-
of the simultaneous recordings of surface electrocardiogram
layed by one unit, as the input, and undelayed HRc as the output
(ECG) and changes in instantaneous lung volume and arterial
signal to obtain PDMs. We used the first three PDMs to re-
blood pressure. In this study, our analyses were based on only
construct the output signal, which was then subtracted from the
ECG recordings. The data were collected for 13 min each for
original HRc signal to obtain estimation error, labeled HRe. The
both supine and upright positions with a minimum of 5 min
justification for using the first three PDMs is because they ac-
allocated for hemodynamic equilibration between changes in
counted for our set threshold value of 90% of the HR dynamics.
body position. The data were collected under three conditions:
This created signal, HRe, is considered to be the input signal,
1) control, 2) administration of a single autonomic blocking
which has the broad-band characteristics needed for accurate
agent, either 0.03 mg/kg of atropine (four of the nine subjects)
estimation of PDMs. The obtained input data, HRe, is then nor-
or 0.2 mg/kg of propranolol (five of the nine subjects), and 3)
malized to a unit variance (HRn). The input signal of HRn and
double blockade resulting from the subsequent administration
the output signal of HRc are used to calculate the final values
of the second blocking agent (all subjects). Selection of which
of the PDMs. Note that the PDM is based on the principle that
subjects initially received either atropine or propranolol as a
among all possible choice of expansion bases, there are some
single autonomic blockade agent was random. The interval
that require the minimum number of basis functions to achieve
between administration of the autonomic agents and data
a given mean-square approximation of the system output. The
collection was long enough (minimum of 5 min) to allow for
methodology of the PDM has been presented before and thus,
physiologic equilibration and to prevent transient nonstation-
we outline the detailed steps of calculating the PDM in the Ap-
arity in each condition. Doses of both atropine and propranolol
pendix section for the convenience of the reader
were selected to be sufficient for complete blockade of theparasympathetic or sympathetic system Measurements
of ECG signals recorded on the frequency-modulated taperecorder were sampled at 360 Hz to allow accurate detection
The PDM methodology outlined in the Appendix provided
and identification of QRS complexes in the ECG The
two PDMs (with time lag
, Laguerre coefficient
QRS complexes were used to identify beat locations. Once the
, and the number of Laguerre functions
timing of beats was determined, an instantaneous HR signal
correspond to the main frequency-response characteristics of
was created at a sampling rate of 4 Hz using the technique
the two ANSs, sympathetic and parasympathetic. We obtain
described in HR signals were down sampled to 1 Hz
fairly consistent waveforms corresponding to parasympathetic
after low-pass filtering at 0.5 Hz in order to concentrate on
and sympathetic nervous activities for all nine subjects, pro-
the frequency bands of interest, which are all below 0.5 Hz.
vided in Figs. 1–4 for the supine position and Figs. 5–8 for the
Furthermore, mean and trends were removed from the HR data,
upright position. The solid lines represent average waveforms
ZHONG
et al.: SEPARATE CONTRIBUTIONS OF ANSS TO HRV USING PRINCIPAL DYNAMIC MODES
Dynamics of (a) parasympathetic and (b) sympathetic during supine
Dynamics of (a) parasympathetic and (b) sympathetic during upright
Dynamics of (a) parasympathetic and (b) sympathetic during supine
Dynamics of (a) parasympathetic and (b) sympathetic during upright
position with application of atropine.
position with application of atropine.
Dynamics of (a) parasympathetic and (b) sympathetic during supine
Dynamics of (a) parasympathetic and (b) sympathetic during upright
position with application of propranolol.
position with application of propranolol.
Dynamics of (a) parasympathetic and (b) sympathetic during supine
Dynamics of (a) parasympathetic and (b) sympathetic during upright
position with application of atropine and propranolol.
position with application of atropine and propranolol.
based on nine subjects with dotted lines corresponding to the
peak centered at 0.03 Hz. The significance of these two peaks is
standard error bounds. Fig. 1(a) and (b) shows frequency re-
that many studies have shown that the parasympathetic nervous
sponses of the two PDMs obtained during the control condition;
system operates both in LF and HF bands. Therefore, this PDM
remarkably, they correspond to the dynamics of the parasym-
correctly exhibits both the low and high frequencies of the
pathetic and sympathetic nervous systems, respectively. The
parasympathetic nervous activity. Fig. 1(b) shows prominent
dominant peak of Fig. 1(a) is centered at 0.l7 Hz, which is in
peaks in the prescribed frequency band of the sympathetic
the prescribed frequency range of the parasympathetic nervous
nervous system, indeed an exciting finding. Therefore, we con-
system. Furthermore, this PDM also shows a prominent second
jecture that the two dominant PDMs correspond to sympathetic
IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING, VOL. 51, NO. 2, FEBRUARY 2004
and parasympathetic activities. This conjecture, if true, for thefirst time allows separation of the two nervous activities thatare known to interact nonlinearly.
To validate the aforementioned conjecture, we analyzed
PDMs of subjects under the influence of propranolol andatropine separately, as well as the application of both drugsto produce a complete blockade of the two nervous activities.
Figs. 2–4 show average frequency response characteristicsof the two PDMs for the application of atropine, propra-nolol, and the combination of atropine and propranolol,respectively. Since the power of HR under the influence ofa drug is different from the HR power of a normal case,we rescaled the PDMs of an abnormal case with:
Figs. 2 and 3, we observe similar waveforms to those of Fig. 1in which two PDMs exhibit characteristics corresponding tothe sympathetic and parasympathetic nervous activity. We notethe consistent and significant decrease in the magnitude of thewaveforms with application of the respective ANS blockingdrug. With atropine, which blocks parasympathetic activity, wenote the significant decrease in the amplitude of the PDM thatcorresponds to the parasympathetic activity. Similarly, withpropranolol, which blocks sympathetic activity, we observea significant reduction in the amplitude of the PDM that weconjecture to be the sympathetic activity. With double blockade(both atropine and propranolol), we correctly observe negligibleamplitudes corresponding to the two nervous activities. Thesephenomena are the very effects that atropine and propranololare expected to have on sympathetic and parasympathetic ac-tivities, respectively. Figs. 2–4 further corroborate the viabilityof our conjecture that the two PDMs correspond to the twonervous systems. It should be noted that with the applicationof atropine, we observe some changes in the waveform of thePDM corresponding to sympathetic dynamics. A similar effecton parasympathetic dynamics is also found with the applicationof propranolol. This is expected, since it has been shown thatthese two nervous activities interact in a nonlinear manner. Thechange in the waveform that is not directly targeted by the drugmay be the compensatory effect due to nonlinear interactionsbetween the two mechanisms.
PSD of (a) and (b)control, (c) and (d) application of atropine, (e) and
Similar waveforms and characteristics from those of the
(f) propranolol, and (g) and (h) atropine and propranolol. For all figures, left andright panels represent supine and upright positions, respectively.
supine position are found for the upright position, as shownin Figs. 5–8. Two dominant PDMs obtained from the controlcondition also correspond to parasympathetic and sympathetic
Fig. 9 shows the average spectra obtained from the control and
activities, as shown in Fig. 5. As with the supine position,
with the application of autonomic blockade drugs. A nonoverlap-
we observe a significant decrease in the magnitude values
ping Welch periodogram (with Hanning window and a frequency
of the PDM corresponding to parasympathetic activity with
resolution of 0.015 625 Hz) was used to obtain the spectra.
the application of atropine. Likewise for the PDM waveform
Fig. 9(a) and (b) represents supine and upright positions, respec-
corresponding to the sympathetic activity with the application
tively. The solid and dotted lines represent the mean and standard
of propranolol. In addition, we observe the significant reduction
error bounds, respectively. A general trend of decreasing power
in magnitude of the waveform [Fig. 7(b)] with the application
is seen with the application of a single blockade and nearly
of propranolol, but it has no significant affect on the PDM
complete elimination of the power is seen with application of the
that reflects parasympathetic activity, as shown in Fig. 7(a).
double blockade. It is apparent that application of atropine had
Finally, we observe a significant reduction in magnitude
greater effect on reducing spectral power for all frequencies than
of both waveforms in Fig. 8, with the application of both
did application of propranolol. Furthermore, atropine, which is
atropine and propranolol. These findings further corroborate
supposed to block parasympathetic activity, appears to signifi-
our conjecture that the two PDMs correspond to sympathetic
cantly reduce sympathetic power in the LF range. Therefore, it is
and parasympathetic nervous activity.
clear that based on only spectral analysis, it is difficult to examine
ZHONG
et al.: SEPARATE CONTRIBUTIONS OF ANSS TO HRV USING PRINCIPAL DYNAMIC MODES
SYMPATHETIC POWER/PARASYMPATHETIC POWER RATIO OBTAINED WITH PDMS
LF POWER/HF POWER RATIO OBTAINED WITH PSD
how each drug affected specific nervous activities. To quantita-
two more erroneous cases with spectral power decreasing as
tively compare the two methods for all nine subjects, we show in
the blocking agent is administered from the upright position.
Tables I and II the ratio of sympathetic/parasympathetic activity
With the PDM approach, we obtained a single incorrect result
obtained by PDMs and the LF/HF ratio obtained by the power
(patient 13) as the power decreased from supine control to the
spectral analyses, respectively. For the PSD analysis, the LF and
administration of atropine. The results obtained by the PDM
HF power were obtained in the frequency range of 0.04–0.15
are, therefore, far more accurate than the LF/HF ratio based
and 0.15–0.5 Hz, respectively. For the PDM, the ratios were
on spectral analysis. The better accuracy was obtained with
obtained by integrating the area of the waveforms corresponding
the PDM approach because the method is able to separate out
to the sympathetic and parasympathetic activities. The LF/HF
the dynamics of the two nervous activities, whereas the LF/HF
ratio provided three erroneous patterns as the power incorrectly
ratio suffers from its assumption that the LF power is solely
increased from supine control to supine single blockade and
due to sympathetic activity.
IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING, VOL. 51, NO. 2, FEBRUARY 2004
MEAN AND STANDARD DEVIATION OF
SIGNIFICANT EIGENVALUES
V. DISCUSSION AND CONCLUSION
PDM method is significant because we have adapted the methodfrom requiring both input and output data to be useful in the case
The past two decades of research in HRV have been mainly
of having only single output data. In addition, we utilized an ap-
based on analysis of the LF/HF ratio, which has been well docu-
proach by Tarvainen to reduce significant spectral power
mented not to be an accurate approach to assess autonomic ner-
in the VLF band, to enable better estimation accuracy with the
vous balance While recent nonlinear deterministic methods
PDM. The results we have obtained by the modified PDM are
have resulted in some promising results it is an unre-
physiologically meaningful and potentially exciting. The PDMs
solved question whether nonlinear deterministic methods could
in the control state, overall, reflect dynamics of the two ANSs.
be meaningfully applied to heart rate data. While the LF/HF
For example, with atropine (Figs. 2 and 6), we observe signifi-
ratio obtained via the PSD is inaccurate, it shows great promise
cant magnitude reduction in dynamics that reflect vagus nervous
of being a useful noninvasive marker for determining the state of
system and less effect on the dynamics that reflect the sym-
the ANS, if a new nonlinear method is developed that can sepa-
pathetic nervous system. Similarly, with propranolol (Figs. 3
rate the dynamics of the two nervous systems. Specifically, sym-
and 7), significant reduction in the magnitude reflecting sym-
pathovagal balance as calculated simply by taking the LF/HF
pathetic nervous system is seen while insignificant reduction in
ratio of the PSD relies on two major erroneous assumptions:
vagus nervous system is observed. While the PDM reflecting
that the parasympathetic nervous system dynamics are exhib-
the sympathetic nervous activity in the control state appears to
ited only in high frequencies, and that ANS control is linear. It
include some dynamics of the vagal activities, as notable mag-
has been well established that dynamics of the parasympathetic
nitude values are seen in high frequencies (
nervous system are not only reflected in high frequencies but
immaterial because of the aforementioned verifiable results ob-
they are also well represented in low frequencies A recent
tained with the application of autonomic blockades. With the
report corroborating this statement suggests that the low-fre-
PSD, however, it is impossible to delineate dynamics of the two
quency component results from an interaction of both the sym-
ANSs. For example, atropine appears to indiscriminately block
pathetic and parasympathetic nervous systems, and not solely
both low and high frequencies, and the effect of atropine is sim-
the sympathetic nervous activity Secondly, the LF/HF ratio
ilar to the double blockade case. Therefore, with the PSD ap-
is based on linear power spectral analysis, which itself is limited
proach, only general inferences can be made regarding the bal-
because it is widely recognized that control of ANSs involves
ance of the two ANSs.
nonlinear interactions. It is through efficient interactions be-
Note that magnitudes obtained by the PDM do not corre-
tween vagal and sympathetic nervous systems that homeostasis
spond directly to the PSD values, as PDMs are based on eigen-
of the cardiovascular system is properly maintained. The inter-
values. Furthermore, magnitudes between the PDMs that repre-
actions are believed to be nonlinear because physiological con-
sent sympathetic and parasympathetic nervous systems do not
ditions would most likely involve ANS regulation based on dy-
correspond in a direct manner since these PDMs are based on
namic and simultaneous activity of the vagal and sympathetic
different eigenvalues. However, comparison of PDMs that rep-
nervous systems in response to physical environmental stress.
resents either vagal or sympathetic nervous activity from the
A recent report suggests a quadratic nonlinearity between HRV
control state to the application of autonomic blockade is valid
and vagal effect rather than a linear relationship If the
since PDMs have been normalized by dividing, drug-influenced
LF/HF ratio is linear and LF and HF truly reflect sympathetic
eigenvalue by the control states eigenvalue.
and parasympathetic nervous activities, respectively, then an au-
With a sampling frequency of 1 Hz or a Nyquist frequency
tonomic blockade such as atropine should increase the LF/HF
of 0.5 Hz, as there is no significant power in the spectrum
ratio. Clearly this is not the case, as also evident in our PSD
beyond 0.4 Hz, one would expect eigenvalues corresponding
plot shown in the second row of Fig. 9; with atropine, we obtain
to the first two PDMs to have the greatest values among the
significant power reduction in both low and high frequencies.
possible 61 eigenvalues
. Indeed, this is the finding, as
Therefore, it is not surprising that the LF/HF ratio based on the
presented in Table III. For every condition, the ratio between
PSD, as shown in Table II, does not truly reflect sympathovagal
the sum of the two most significant PDMs and the sum of the
rest of the PDMs are calculated. For most cases, the two most
We introduced a modification of the PDM approach for the
significant PDMs together account for more than 90% of the
analysis of autonomic nervous activity. The modification of the
total dynamics. Therefore, given the fact that ANSs span most of
ZHONG
et al.: SEPARATE CONTRIBUTIONS OF ANSS TO HRV USING PRINCIPAL DYNAMIC MODES
the frequencies examined, the finding of the two most significant
Expansion of the Volterra kernels on a complete basis
PDMs reflecting more than 90% of the total dynamics is highly
transforms (1) into the multinomial expressions
In conclusion, two PDMs have been consistently identified
in all nine subjects examined, with each PDM correspondingto the sympathetic or parasympathetic nervous activities. Ourconjecture of the two PDMs reflecting the ANS activities was
corroborated by the administration of ANS blocking agents,after which the PDMs were significantly reduced. When bothblocking agents were administered, the PDMs were completely
obliterated. This analysis allows accurate and physiologicallymeaningful quantification of the separate contributions of sym-
pathetic and parasympathetic activities of HRV.
is the number of Laguerre functions used.
the Laguerre functions calculated with Laguerre coefficient
can be constructed with the estimated kernels
A. Calculation of PDMS
in the following way:
The estimation of PDMs using Volterra-Wiener kernels was
first introduced in We will briefly describe the steps
involved in calculation of PDMs. For further details, the readeris referred to and
In discrete time, the general input-output relation of a stable
Laguerre functions are chosen as an appropriate orthonormal
(finite-memory) nonlinear time-invariant dynamic system is
basis because they exhibit exponential decaying properties that
given by the discrete-time Volterra series
make them suitable for physiological systems modeling. In ad-dition, due to basis function expansion, the estimation accuracyis maintained even with a small data length. We have previouslyshown that a data length of 250 points is sufficient for accuratekernel estimation using Laguerre expansions
is a real symmetric square matrix, it can always
be decomposed in the following way:
eigenvector matrix
will always be an orthonormal matrix.
is the output of the system.
the diagonal eigenvalue matrix. We select the significant eigen-
is the memory of the system. The Volterra kernels
and the corresponding orthonormal eigenvectors
describe the dynamics of the system from a
define the PDMs of this system.
hierarchy of system nonlinearities.
For each significant eigenvalue
, the values of the corre-
The kernel values obtained up to a maximum lag
sponding eigenvector
memory) are combined to form a real symmetric
) define the th PDM
square matrix (shown in (2) at the bottom of the page)
that can be used to express the second-order Volterra model re-
, in a quadratic form
The obtained th PDM generates the th mode via convolutionwith the input
. The second-order model estimation
denotes "transpose" and the
is composed of the input
-point epoch at each time n and a
constant 1 that allows incorporation of the lower order kernel
The nonzero values
give rise to the contribution of
contributions in (3).
linear terms.
IEEE TRANSACTIONS ON BIOMEDICAL ENGINEERING, VOL. 51, NO. 2, FEBRUARY 2004
B. Detrending Method
[18] M. S. Houle and G. E. Billman, "Low-frequency component of heart
rate variability spectrum: A poor marker of sympathetic activity," Amer.
The detrending method we utilized is based on smoothness
J. Physiol., vol. 276, pp. 215–223, 1999.
priors approach and operates like a time-varying FIR filter. The
[19] J. J. Goldberger, S. Challapalli, R. Tung, M. A. Parker, and A. H. Kadish,
Matlab source code as provided in for applying the de-
"Relationship of heart rate variability to parasympathetic effect," Circu-lation, vol. 103, pp. 1977–1983, 2001.
trending method to a signal,
Yuru Zhong received the B.E. degree from the
Department of Automation, the University of
Science and Technology of China, Hefei, China,
in 2001. Currently, she is a Ph.D. degree student inthe Department of Biomedical Engineering, State
The lambda controls the degree of detrend desired. For our anal-
University of New York at Stony Brook. Currently,
ysis, the value of lambda was adjusted so that the mean power
she is a Ph.D. degree student in the Department of
of the VLF was close to the mean power of the LF and HF
Biomedical Engineering, State University of NewYork at Stony Brook.
without affecting the power in the LF. The value of lambda dif-
Her research interests include biomedical signal
fered for each subject with the range of values varying from 500
processing and modeling of physiological systems.
Hengliang Wang received the B.S. and M.S. degrees Department of Automa-
[1] "Heart rate variability: Standards of measurement, physiological inter-
tion, the University of Science and Technology of China, Hefei, China, in 1997
pretation, and clinical use," in Circulation: Eur. Soc. Cardiol. North
and 2000, respectively.
Amer. Soc. Pacing and Electrophysiology, 1996, vol. 93, pp. 1043–1065.
His research interests include biomedical signal processing and medical in-
[2] H. V. Huikuri, M. J. Koistinen, S. Yli-Mayry, K. E. Airaksinen, T. Sep-
panen, M. J. Ikaheimo, and R. J. Myerburg, "Imparied low-frequencyoscillations of heart rate in patients with prior acute myocardial infarc-tion and life-threatening arrhythmias," Amer. J. Cardiol., vol. 76, pp.
56–60.
Ki Hwan Ju received the M.Sc.E.E. degree in
[3] J. M. Tapanainen, P. E. Thomsen, L. Kober, C. Torp-Pedersen, T. H.
electrical engineering from Yonsei University, Seoul,
Makikallo, A. M. Still, K. S. Lindgren, and H. V. Huikuri, "Fractal anal-
Korea, in 1984 and the Ph.D. degree from the School
ysis of heart rate variability and mortality after an acute myocardial in-
of Science and Engineering, Keio University, Tokyo,
farction," Amer. J. Cardiol., vol. 90, pp. 347–52, 2002.
Japan, in 1991.
[4] C. Yang and T. Kuo, "Assessment of cardiac sympathetic regulation by
He was a Postdoctoral Fellow with the Sports
respiratory-related arterial pressure variability in the rat," J. Physiol.,
Medicine Research Center, Keio University, and a
vol. 515, pp. 887–896, 1999.
Research Associate with the University of Tokyo.
[5] A. M. Bianchi, L. T. Mainardi, C. Merloni, S. Chierchia, and S. Cerutti,
He was a Visiting Scientist with the City College of
"Continuous monitoring of the sympatho-vagal balance through spectral
The City University of New York. He is Research
analysis," IEEE Eng. Med. Biol., vol. 16, pp. 64–73, Sept./Oct. 1997.
Director of the Institute of Bio-Cybernetics, Tokyo,
[6] A. Zaza and F. Lombardi, "Autonomic indexes based on the analysis of
and a Research Scientist with the Department of Biomedical Engineering, The
heart rate variability: A view from the sinus node," Cardiovasc. Res.,
State University of New York at Stony Brook. His main areas of interest are
vol. 50, pp. 434–442, 2001.
system modeling of intergrative physiology in human and genetic targeted
[7] V. Z. Marmarelis, K. H. Chon, and D. J. Marsh, "Nonlinear analysis
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Kung-Ming Jan, photograph and biography not available at the time of publi-
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, "Identification of nonlinear biological systems using Laguerre ex-
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tion analysis of autonomic regulation—I: Respiratory sinus arrhythmia,"
Ki H. Chon (M'96) received the B.S. degree
Amer. J. Physiol., vol. 256, pp. H153–H161, 1989.
in electrical engineering from the University of
[12] A. D. Jose and R. R. Taylor, "Autonomic blockade by propranolol and
Connecticut, Storrs; the M.S. degree in biomedical
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engineering from the University of Iowa, Iowa City;
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and the M.S. degree in electrical engineering and
[13] R. D. Berger, S. Akselrod, D. Gordon, and R. J. Cohen, "An efficient
the Ph.D. degree in biomedical engineering from the
algorithm for spectral analysis of heart rate variability," IEEE Trans.
University of Southern California, Los Angeles.
Biomed. Eng., vol. BME–33, pp. 900–904, 1986.
He spent three years as a National Institutes
[14] N. Wiener, Nonlinear Problems in Random Theory.
of Health (NIH) Postdoctoral Fellow at the
Technol Press MIT and Wiley, 1958.
Harvard-MIT Division of Health Science and Tech-
[15] K. H. Chon, R. Cohen, and N.-H. Holstein-Rathlou, "Compact and accu-
nology, Cambridge, MA, one year as a Research
rate linear and nonlinear autoregressive moving average model param-
Assistant Professor in the Department of Molecular Pharmacology, Physiology,
eter estimation using Laguerre functions," Ann. Biomed. Eng., vol. 25,
and Biotechnology at Brown University, Providence, RI, and four years as an
pp. 731–738, 1997.
Assistant and Associate Professor in the Department of Electrical Engineering
[16] M. Tarvainen, P. Ranta-Aho, and P. Karjalainen, "An advanced
at the City College of the City University of New York. Currently, he is an
detrending method with application to HRV analysis," IEEE Trans.
Associate Professor in the Department of Biomedical Engineering at State
Biomed. Eng., vol. 49, pp. 172–175, Feb. 2002.
University of New York at Stony Brook. His current research interests include
[17] D. L. Eckberg, "Sympathovagal balance: A critical appraisal," Circula-
medical instrumentation, biomedical signal processing, and identification, and
tion, vol. 96, pp. 3224–3232, 1997.
modeling of physiological systems.
Source: http://www.bme.sunysb.edu/people/faculty/docs/kchon/1zhong.pdf
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