Acoust. Sci. & Tech. 24, 1 (2003)

PAPER

Measurement and analysis of vibration in the myocardium telescopic motion
for novel echo-graphic diagnosis
Hiroshi Kanai1 , Shin-ichi Katsumata1 , Hideyuki Honda2 and Yoshiro Koiwa3
1

Graduate School of Engineering, Tohoku University,
Aramaki-aza-Aoba 05, Sendai, 980–8579 Japan
2
Faculty of Medical Science and Welfare, Tohoku Bunka Gakuen University,
Kunimi 6–45–16, Aoba-ku, Sendai, 981–8551 Japan
3
Graduate School of Medicine, Tohoku University,
Seiryou-machi 1–1, Aoba-ku, Sendai, 980–8574 Japan( Received 21 December 2001, Accepted for publication 10 July 2002 )Abstract: We have already developed a novel ultrasonic-based method, namely, the phased tracking
method, to measure the rapid velocity in the heart wall by accurately tracking the movement in theheart wall. By applying this method to in vivo experiments, the velocity signal of the heart wall withsmall amplitude, less than several micrometers on the large motion resulting from a heartbeat, can be
successfully detected. There are high frequency components of up to several hundreds Hertz, whichhave not been previously investigated at all. In this study, after the papillary muscle had been extracted
from an isolated rat heart, it was electrically stimulated, and the resultant muscular vibration was
directly measured in the frequency range up to 2 kHz using a laser Doppler velocimeter in order to
conﬁrm if the high frequency vibrations occur during contraction and relaxation. For the injured
myocardium, the power increase in the high frequency components becomes smaller. The
experimental results support the hypothesis that the high frequency components are included in thevelocity signal measured for the ﬁrst time in the human interventricular septum by the phase tracking
method using ultrasound.
Keywords: Phased tracking method, Myocardium vibration, Myocardium vulnerability
PACS number: 43.80.Qf, 43.80.Vj

1.

INTRODUCTION

We have already developed a novel ultrasonic-based
method, namely, the phased tracking method, to measure
the rapid velocity in the heart wall by accurately tracking
the movement xi ðtÞ of a point (i) in the heart wall by theconstraint least-squares method applied to both the phaseand magnitude of the quadrature-demodulated signals [1].
RF pulses are transmitted from an ultrasonic transducer at apulse repetition interval T, and the reﬂected ultrasonicwave is received by the same transducer and is multipliedby the original RF signal in quadrature-demodulation. By
synchronizing the pulse transmission timing and theacquisition timing in A/D conversion rigidly with theoriginal RF signal, the achieved lower limit jvmin j in theabove velocity measurement was 0.1 mm/s, which was
conﬁrmed in phantom experiments [2], using the developed
method and system [1]. The lower limit depends on thesmall dispersion in the above synchronization and on the

additive noise in the received signal. Since the lower limit
jvmin j is less than 1/2,000 of the upper limit jvmax j of themeasurable velocity, which is free from aliasing, thedynamic range of the velocity measurement is given by
20 log10 jvmax j=jvmin j ¼ 73 dB. In other phantom experiments [1], a vibration with small amplitude of 20 m
generated on the large motion with an amplitude of7:5 mm and a frequency of 1 Hz, which simulates theheartbeat, was successfully measured in the range from
1 Hz to 1 kHz.
By applying this method and system to in vivo
experiments, the velocity signal, vðt; xi Þ, of point i at a
depth of xi in the heart wall with small amplitude, less thanseveral micrometers on the large motion resulting from aheartbeat, can be successfully detected with reproducibility[1]. By applying frequency analysis to the resultant
velocity signal, vðt; xi Þ, of the heart wall, the Fourier
spectrum of vðt; xi Þ has been obtained for the ﬁrst time with
suﬃcient reproducibility in the frequency range up to17

Acoust. Sci. & Tech. 24, 1 (2003)

100 Hz [1]. The developed method has already beenrealized in a real-time measurement system [3]. Moreover,from the diﬀerence of the resultant velocity signals
fvðt; xi Þg between point xi and its succeeding point xiþ1
preset along the ultrasonic beam, a minute change inthickness of several tens of micrometers has been detectedwith a spatial resolution of 0.5 m [4] as described above.
With the phased tracking method it is possible toaccurately detect small amplitude velocity signals of lessthan a few micrometers in the heart wall [1]. There are highfrequency components up to several hundreds Hertz [1]which cannot be recognized in standard B-mode echocardiography, M-mode echocardiography, or in conventional
tissue Doppler imaging (TDI). The clinical and physiological meanings and the mechanisms of such high frequency
vibrations have not been previously investigated. If themechanism of the high frequency components can beclariﬁed, it will oﬀer potential for novel quantitative
assessment of myocardial viability.
It is known that vibrations along the muscular ﬁbers
occur during contraction and relaxation of the skeletal
muscle [5–9]. In the literature, there have been many
reports of attempts to transcutaneously measure suchmuscle sounds originating from the muscle vibrations[5–9]. However, the muscle vibrations have been measured
only in the frequency range up to 100 Hz.
In this paper, after the papillary muscle was extracted
from the isolated rat heart, it was electrically stimulated
during perfusion with physiological solution, and theresultant muscle vibration was directly measured in thefrequency range up to 2 kHz using a laser Doppler
velocimeter. The detected vibrations were then analyzed
in the frequency domain in order to conﬁrm that highfrequency vibrations occur during contraction and relaxation of the heart muscle.

2.

IN VITRO EXPERIMENTS

A papillary muscle extracted from a rat heart was ﬁxed
in a water tank by two tungsten hooks and a force
transducer was employed to measure the generated tensionTðtÞ along the longitudinal axis of the myocardium asshown in Fig. 1. In order to maintain the physiologicalconditions close to in vivo conditions, Krebs-Henseleit
solution was circulated in the water tank by the peristaltic
pump and the temperature of the water tank was kept
constant at 25  0:2 degrees Celsius.
The myocardium was electrically stimulated throughtwo parallel platinum electrodes by rectangular wave eðtÞwith a duration of 1 ms and a repetition frequency of 1 Hz
as shown in Fig. 3(a). At the same time, the velocity
component vðtÞ generated in the direction normal to that of
the myocardium was measured at the center of the muscle
by a laser Doppler velocimeter (Ono Sokki LV-1300) as

18

work station

CRT

CCD camera

digitaloscilloscope

O2 95%+CO25%gas

laser Doppler
velocimeter

Krebs-Henseleit
solution

amplifierforce
transducer

drain

constant
temperature
circulator

peristaltic
pump

water

electric
stimulator

myocardium
tungsten hookelectrodewater bath (alminium plate)Fig. 1 Experimental setup for measuring the vibrationof the papillary muscle extracted from the isolated rat
heart, which is electrically stimulated during physiological solution perfusion.

shown in Fig. 3(b). The output TðtÞ of the force transducer
was obtained as shown in Fig. 3(d). These signals were
simultaneously A/D converted at a sampling frequency of
50 kHz. They were then transfered to a workstation via a
GPIB interface for further frequency analysis.
In order to detect the presence of contaminating noise
component nðtÞ in the measured velocity vðtÞ, the velocity
component nðtÞ at the arm of the tungsten hook was
simultaneously measured as shown in Fig. 3(c). By
integrating the velocity vðtÞ of the myocardium in theworkstation, its displacement xðtÞ was estimated as shownin Fig. 3(e).

3.

IN VITRO EXPERIMENTAL RESULTS

Each signal from Fig. 3(a) to Fig. 3(e) is divided into
the respective duration periods and is overlaid in Fig. 2(a)to Fig. 2(e), where the horizontal time axis is expanded.
From Fig. 2(b), the velocity vðtÞ of the myocardiumincluded two types of components: one is the low
frequency component which is synchronous with theelectrically stimulated signal eðtÞ in Fig. 2(a), and theother is the high frequency component which seems to be
similar to the noise component nðtÞ in the time domain ofFig. 2(c).
For detection of the change in power during one
duration period in the frequency domain, the velocity
signal vðtÞ of each duration period in Fig. 3(b) was divided
into 39 short-period signals fvðt; iÞg (i ¼ 1; 2; . . . ; 39) byshifting and multiplying the Hanning window with a lengthof 50 ms from the rising edge (T ¼ 0) of the electricalstimulation eðtÞ of each duration period, where half of thesucceeding windows overlapped. Then, the Fourier transform was applied to each signal of fvðt; iÞg(i ¼ 1; 2; . . . ; 39). The resultant power spectra fPðf ; iÞg up
to 2 kHz of the ith short-period signals fvðt; iÞg with the

H. KANAI et al.: VIBRATION IN THE MYOCARDIUM TELESCOPIC MOTION
change
in
power
[dB]
30
20
10
0
10

0.8

0

200

0.6
400

0.4

600

800
1000
fre
1200
que
1400
ncy
1600
[Hz
1800
]
2000

0.2
0
0.2

d]

con

se
e[

tim

Fig. 4 For the velocity signal vðtÞ in Fig. 3(b), thechange in the averaged power spectra compared withthat just before the contraction.

Fig. 2 Each signal from Fig. 3(a) to Fig. 3(e) is divided
the respective duration periods and overlaid. For
details, see the caption of Fig. 3.

change
in
power
[dB]
30
20
10
0
10

0.8

0

200

0.6
400
600

0.6

800

1000
fre
1200
que
1400
ncy
1600
[Hz
1800
]
2000

0
0.2

d]

on

0.4

e

tim

c
[se

Fig. 5 For the noise signal nðtÞ in Fig. 3(c), the change
in the averaged power spectra compared with that justbefore the contraction.

Fig. 3 For an uninjured heart muscle. (a) Rectangularpulse train eðtÞ with a duration of 1 ms and a repetition
frequency of 1 Hz for electrical stimulation of the
myocardium. (b) Measured velocity component vðtÞgenerated in the direction normal to that of the
myocardium measured by a laser Doppler velocimeter.
(c) Output TðtÞ of the force transducer. (d) Noise
component nðtÞ at the arm of the tungsten hook. (e)Displacement xðtÞ of the myocardium estimated fromvðtÞ in Fig. (b).

same delay time from the rising edge were averaged for the
5 duration periods and are plotted in Fig. 4. In Fig. 4, thetime origin (T ¼ 0) corresponds to the rising edge of theelectrical stimulation eðtÞ of each duration period in Fig.
3(a). Each averaged power spectrum was normalized by theaveraged power spectrum fP0 ðf Þg at the period 200 ms inlength just before the rising edge (T ¼ 0). Thus, the value
in Fig. 4 shows the change in the averaged power spectra

compared with that just before the contraction.
The same procedure was applied to the noise signal nðtÞin Fig. 3(c) and the change in power spectrum is shown in
Fig. 5. There did not seem to be any noteworthy change inpower in Fig. 5. In Fig. 4, however, for the contraction
period (0–200 ms) just after the electrical stimulation, there
were large increases in power both in the low frequency
component less than 25 Hz and in the wide frequency bandfrom 200 Hz to 2 kHz. For the relaxation period (200–500 ms) as well, there were large increases in power in bothof these frequency bands as above. The low frequency
component corresponds to the bending displacement of themuscle due to its contraction or the relaxation. For thehigher frequency band, the power increased.
For the contraction period of 50 ms around the time(Tc ) 75 ms after the rising edge T0 and for the relaxation
period with 50 ms around the time (Tr ) 350 ms after T0 , thechange in the averaged power spectrum compared with thatjust before the contraction in Fig. 4 are shown by red lines
in Figs. 6(a) and 6(b), respectively. For the noise vibrationnðtÞ of the hook arm, the results in Fig. 5 are shown by bluelines in these ﬁgures.

19Acoust. Sci. & Tech. 24, 1 (2003)30

myocardiumarmchange in power [dB]

25
20
15
10
5
0
-5
-10
0

200

400

600

(a)

800

1000 1200 1400 1600 1800 2000

frequency [Hz]30

myocardiumarmchange in power [dB]

25
20
15

Fig. 7 For the injured heart muscle. For details, see thecaption of Fig. 3.

10
5
0
-5
-10
0

(b)

200

400

600

800

1000 1200 1400 1600 1800 2000

frequency [Hz]Fig. 6 For the contraction period with 50 ms around thetime (Tc ) 75 ms after the rising edge T0 , and for therelaxation period with 50 ms around the time (Tr )350 ms after T0 , the change in the averaged power
spectrum compared with that just before the contraction in Fig. 4 are shown by red lines in the upper (a)and lower (b) portion of the ﬁgure, respectively. For
the noise vibration nðtÞ, the results in Fig. 5 areoverlaid by blue lines.

As indicated by these blue lines, the noise vibration nðtÞdid not show a noteworthy increase in power. For thevibration of the myocardium, however, the power increased
by about 15–20 dB in the low frequency band less than
30 Hz and in the higher frequency band from 1 kHz to
2 kHz. As indicated by these results, due to the contractionor the relaxation, telescopic vibrations with high frequency
components in the frequency band from 1 kHz to 2 kHz,
which is other than the displacement, were certainly
generated.
Next, in order to compare the characteristics of theabove normal myocardium with those of an injured
myocardium, for the same papillary muscle after measurement of the signals in Fig. 3, the perfusion with the KrebsHenseleit solution was completely stopped for 120
seconds. Then, the same measurement and analysis wereapplied to the injured myocardium.
The results are shown in Figs. 7–11. As for themeasurement, the noise component nðtÞ in Figs. 7(c) or
8(c) was large. However, this erroneous component was a
low frequency component less than 40 Hz and was20

Fig. 8 For the injured myocardium, each signal from
Fig. 7(a) to Fig. 7(e) is divided into the respective
duration periods and overlaid. For details, see thecaption of Fig. 2.

change
in
power
[dB]
30
20
10
0
10
0
200

0.8
0.6
400
600
fre 8001000
que
ncy 12001400
[Hz
1600
1800
]
2000

0.4
0.2
0
0.2

d]

con

se
e[

tim

Fig. 9 For the velocity signal vðtÞ in Fig. 7(b), thechange in the averaged power spectra compared withthat just before the contraction.

H. KANAI et al.: VIBRATION IN THE MYOCARDIUM TELESCOPIC MOTION
change
in
power
[dB]
30
20
10
0
10
0

0.8
0.6

200
400
600

0.4

fre 8001000
que
ncy 12001400
[Hz
1600
1800
]
2000

0

d]

on

0.2

e

tim

c
[se

0.2

Fig. 10 For the noise signal nðtÞ in Fig. 7(c), the change
in the averaged power spectra compared with that justbefore the contraction.

30

myocardiumarmchange in power [dB]

25
20
15
10
5
0
-5

band component was detected during the contraction andrelaxation as shown in Figs. 9, 11(a), and 11(b). For the
injured myocardium, however, the power increase was only
about 10 dB, which is not so large in comparison with thoseof the normal myocardium in Figs. 6(a) and 6(b), and thefrequency band became lower at the point where the powerincreased.

4.

CONCLUSIONSIn this paper, by electrically stimulating the extracted
papillary muscle of rats, the vibration component in the
direction normal to the myocardial ﬁber was measured by alaser Doppler velocimeter. Then, it was analyzed in thefrequency domain. From the experimental results, thevibration during contraction and relaxation had a highfrequency component from 1 kHz to 2 kHz. For the injured
myocardium, the power increase in the high frequency
component during contraction or relaxation decreased. The
experimental results support the fact that the highfrequency component is included in the velocity signal
measured for the ﬁrst time for the human interventricular
septum (IVS) by the phase tracking method using
ultrasound [1]. Thus, the detection of the change in powerhas potential for diagnosis of the vulnerability of theregional heart muscle.

-10
0

200

400

600

(a)

800

1000 1200 1400 1600 1800 2000

frequency [Hz]30

myocardiumarmchange in power [dB]

25
20
15
10
5
0
-5
-10
0

(b)

200

400

600

800

1000 1200 1400 1600 1800 2000

frequency [Hz]Fig. 11 For the injured myocardium, in the contraction
period of 50 ms around the time (Tc ) 75 ms after therising edge T0 , and for the relaxation period of 50 ms
around the time (Tr ) 350 ms after T0 , the change in the
averaged power spectrum compared with that justbefore the contraction in Fig. 9 are shown by red lines
in the upper (a) and lower (b) portion of the ﬁgure,respectively. For the noise vibration nðtÞ, the results in
Fig. 10 are overlaid by blue lines.

cancelled out by the change in the power spectrum
component just before the contraction as shown in Fig. 10.
Also for the injured myocardium, a wide frequency

REFERENCES[1] H. Kanai, M. Sato, Y. Koiwa and N. Chubachi, ‘‘Transcutaneous measurement and spectrum analysis of heart wall
vibration,’’ IEEE Trans. Ultrason. Ferroelectr. Freq. Control,
43, 791–810 (1996).
[2] H. Kanai, H. Hasegawa, N. Chubachi, Y. Koiwa and M. Tanaka,‘‘Noninvasive evaluation of local myocardial thickening and its
color-coded imaging,’’ IEEE Trans. Ultrason. Ferroelectr.
Freq. Control, 44, 752–768 (1997).
[3] H. Kanai, Y. Koiwa and J. Zhang, ‘‘Real-time measurements oflocal myocardium motion and arterial wall thickening,’’ IEEE
Trans. Ultrason. Ferroelectr. Freq. Control, 46, 1229–1241(1999).
[4] H. Kanai, K. Sugimura, Y. Koiwa and Y. Tsukahara, ‘‘Accuracy
evaluation in ultrasonic-based measurement of microscopicchange in thickness,’’ Electron. Lett., 35, 949–950 (1999).
[5] C. Orizio, R. Perini, B. Diemont, M. M. Figini and A.
Veicsteinas, ‘‘Spectral analysis of muscular sound duringisometric contraction of biceps brachii,’’ J. Appl. Physiol., 68,
508–512 (1990).
[6] F. V. Brozovich and G. H. Pollack, ‘‘Muscle contraction
generates discrete sound bursts,’’ Biophys. J., 41, 35–40 (1983).
[7] D. T. Barry, ‘‘Acoustic signals from frog skeletal muscle,’’Biophys. J., 51, 769–773 (1987).
[8] D. T. Barry and N. M. Cole, ‘‘Muscle sounds are emitted at theresonant frequencies of skeletal muscle,’’ IEEE Trans. Biomed.
Eng., 37, 525–531 (1990).
[9] J. V. Frangioni, T. S. Kwan-Gett, L. E. Dobrunz and T. A.
McMahon, ‘‘The mechanism of low-frequency sound production in muscle,’’ Biophys. J., 51, 775–783 (1987).

21

Acoust. Sci. & Tech. 24, 1 (2003)
Hiroshi Kanai was born in Matsumoto,Japan, on November 29, 1958. He received aB.E. degree from Tohoku University, Sendai,
Japan in 1981, and M.E. and the Ph. D. degrees,
also from Tohoku University, in 1983 and in
1986, both in Electrical Engineering. From 1986
to 1990 he was with Processing, Tohoku
University, as a research associate. From 1990
to 1992 he was a lecturer in the Department of ElectricalEngineering, Faculty of Engineering, Tohoku University. From1992 to 2001 he was an associate professor in the Department ofElectrical Engineering, Faculty of Engineering, Tohoku University.
Since 2001 he has been a professor in the Department of Electronic
Engineering, Graduate School of Engineering, Tohoku University.
His present interests are in ultrasonic measurement and digital signal
processing for diagnosis of heart diseases and arteriosclerosis.
Shin-ichi Katsumata was born in Sendai,
Japan, in 1977. He received a B.E. degree inElectrical Engineering from Tohoku University,
Sendai, Japan in 2000. Since 2000, he has beena student of the Department of Electrical andCommunication Engineering, Graduate Schoolof Engineering, Tohoku University. His research interests are ultrasonic measurementand digital signal processing for myocardial
tissue characterization.

22

Hideyuki Honda was born in Matsushima,
Japan, on June 9, 1953. He received a bachelorof Science Degree from Tohoku University,
Sendai, Japan in 1977. He received MD degree
and Ph.D. from Tohoku University School of
Medicine, in 1985 and in 1992, respectively.
From 1985 to 1987, he was a resident fellow at
Takeda general hospital, Aizuwakamatu, Japan.
From 1992 to 1995 and 1995 to 1997, he was a Research Associate
and Clinical Fellow at Tohoku University School of Medicine. From1998 to 1999, he was a Research Associate at the University of
Illinois at Chicago. Since 1999, he has been an associate professor at
Tohoku Bunka Gakuen University. His present interests are basic
characteristics of muscles.
Yoshiro Koiwa was was born in Sendai,
Japan, in 1944. He graduated from Tohoku
University, Sendai, Japan, in 1969. He received
the M.D. degree from Tohoku University in
1977. He is presently Associate Professor ofInternal Medicine of Tohoku University. His
main research interest is cardiovascular disease,especially cardiac function and heart failure. Dr.
Koiwa is member of American Federation for
Clinical Research, the Japanese Circulation Society, and the Japan
Society of Medical Electronics and Biological Engineering.