Reprinted from

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Minute Mechanical-Excitation Wave-Front Propagation in Human Myocardial Tissue
Hiroshi Kanai and Motonao Tanaka

Jpn. J. Appl. Phys. 50 (2011) 07HA01# 2011 The Japan Society of Applied Physics

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Japanese Journal of Applied Physics 50 (2011) 07HA01
DOI: 10.1143/JJAP.50.07HA01

Minute Mechanical-Excitation Wave-Front Propagation in Human Myocardial Tissue
Hiroshi Kanai and Motonao Tanaka1
Graduate Schools of Biomedical Engineering and Engineering, Tohoku University, Sendai 980-8579, Japan
1
Cardiovascular Center, Tohoku Welfare Pension Hospital, Sendai 983-0005, Japan
Received January 18, 2011; accepted March 9, 2011; published online July 20, 2011
Complexity of the cardiac contraction sequence is still not fully understood because the dynamic mechanical excitation process, which directly
correlates with contraction, cannot be accurately measured based on the electro-magnetic phenomena. By developing a noninvasive novel
imaging modality with high temporal and spatial resolutions, the present study shows that the propagation of the mechanical wave-front occurs at
the beginning of cardiac contraction sequence for the first time (about 60 ms prior to the ordinarily accepted onset time of the contraction). From
the apical side of the interventricular septum, a minute velocity component with an amplitude of several tenth micrometers is generated andit propagates from the apex to the base of the posterior wall, and then from the base to the apex of the septum, with a propagation speed of 3–9
m/s. This dynamic measurement modality is also applicable to various tissues in biology. # 2011 The Japan Society of Applied Physics

to conﬁrm whether the detected velocity component
corresponds to the myocardial contraction or extension.

1. Introduction

Unlike the case of skeletal muscle, the direction of myocardial contraction does not coincide with the direction of work
necessary to eject the intraventricular blood, contributing togreat complexity of the wall deformation sequence of cardiac
contraction. Electrocardiography is an invaluable clinicaltool for the diagnosis of cardiac failure. Electrocardiographic
measurement1) has realized noninvasive imaging of thespatial distribution of action potentials, and magnetocardiography2) conducted inside a shielded room enables similar
imaging. By these electro-magnetic phenomena-based methods, however, mechanical properties of myocardial velocity
and contraction are not been directly measured. Other cardiac
imaging tools, namely, computed tomography (CT),3) magnetic resonance imaging (MRI),4,5) single photon emission
computed tomography (SPECT),6) and conventional echocardiography,7,8) enable visualization of two-dimensional(2D) or three-dimensional (3D) images, motion, torsional
deformation, asynchronous wall motion during acute myocardial ischemia,9) and the left ventricular inﬂow.10) The timeof peak contraction of the heart wall has been reported using
3D MRI tagging.11) With MRI tagging, the onset time of thecontraction has been reported.12,13) However, their visualization is restricted to static conﬁgurations or large and slow
motion due to contraction. Using the Doppler eﬀect of theultrasound, the velocity or displacement are measured,14,15)
but an accurate waveform for which the frequency analysis
is applicable is not obtained, and measurement of minute,rapid velocity waveforms at the beginning of the contractionin the heart wall has not been attempted.
We have previously found that the rapid response of theexcised heart muscle of a rat to electrical stimulations isminute (displacement of 30 m and velocity of 0.5 mm/s)16)
and that velocity measurement is superior to displacement
measurement since the displacement is the accumulation ofvelocity, that is, low-pass ﬁltering.17) To realize noninvasive
detection of such minute mechanical responses to the
propagation of the action potential in the human heart, wedeveloped a novel ultrasound-based noninvasive method18)
and we successfully measured such response as a velocity
waveform for human subjects for the ﬁrst time.19) In thepresent study, the regional change in length or wall thickness
was simultaneously measured with high temporal resolutionE-mail address: kanai@ecei.tohoku.ac.jp

2. Materials and Methods

In the present study, the minute propagation of thecontraction/relaxation was visualized for the ﬁrst time in
the human as follows: The ultrasonic beams transmitted by
the ultrasound probe attached to the chest wall scan the 2D
plane of the heart, and the RF reﬂective wave for eachultrasound transmission is acquired by the same probe as inconventional echocardiography. In this novel method,
however, the phase shift between the succeedingly acquired
RF signals in the same direction is determined accurately ateach point in the heart wall along the ultrasonic beam, andthe position of each point is tracked. Thus, the minutemotion at each point is measured as a velocity waveform sothat the Fourier transform is applicable.17,20) The six periods(atriosystolic phase, isovolumetric contraction period, ejection period, isovolumetric relaxation phase, period of rapid
ﬁlling, and period of slow ﬁlling) during one cardiac cycle
were characterized by the measured waveforms.21) Moreover, by restricting the number of directions of transmission
to maintain a high frame rate (500 Hz), the velocity
waveforms are simultaneously obtained at about 3,000
points set in the heart wall on the 2D plane.22) Spatial
distribution of the heart wall vibrations generated by remote
perturbation of the inner pressure was also noninvasively
measured by the method.23) By applying frequency analysis
to each velocity waveform,17) the phase of its 40-Hz
component is detected and its instantaneous 2D distribution
is reconstructed at every 2 ms, precisely revealing theminute-wave propagation in the heart wall22) by neglecting
the diﬀerences in the amplitude components. The achieved
lower limit in the velocity measurement has been validated
as being 0.1 mm/s,20) which corresponds to 0.2 m indisplacement during 2 ms. Since the wavelength is about
410 m for the typical frequency (3.75 MHz), 0.2 mcorresponds to about 1/2000 of the wavelength. Such aminute velocity component superimposed on the large
motion due to heartbeat cannot be noninvasively measured
by any other known method. At the same time, the regionalchange in length of thickness is accurately obtained fromthe spatial diﬀerence between the velocity waveform at theadjacent points (820 m apart) with 0.5-m accuracy.24) The
propagation of the contraction in the heart wall was detectedjust at the apical side of the interventricular septum.25)

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O (probe)
inferior
b
180
apex
a

ECG
PCG

j

c
PW

RV
IVS

LV

d

90
0
-90
phase

i
Mv g

h
Ao
superiorfeone cardiac cyclearapid filling slow filling
atrial contraction ejection
50 mm
LA

a
IVS j
i
Ao h
Ao g
f
a
apex
b
PW c
d
LA
e b
a: 0.25 mm
c: 1 mmtoward apex
b,d,i,j: 5 mm
displacement 0
c toward basea,c,j: 10 mm/s
b,d,i: 50 mm/s
velocity 0
PCG
ECG

P
-200
d (TP)

first
R
0
(TR)

d
i

j

c

b a
d
a
c

b

j

i

second
200

T

R
400
(TII)

600

800
time from R-wave [ms]Fig. 1. (Color online) Time sequence of velocity and displacement in the unfolded left ventricular wall based on the apical view. (a) Cross-sectional image
from apical view of the LV of a healthy young subject. The two colored lines passing through the walls show the phase of the 40-Hz component of thevelocity wave at each point at TR . Red and light blue correspond to the upward and downward movements, respectively. (b) Temporal changes in the phase of
40-Hz component of the velocity wave for one cardiac cycle along the two lines in (a). Vertical axis corresponds to the line in (a). (c) Displacement
waveform at points a–j in (a). (d) Velocity waveform at points a–j with electrocardiogram (ECG) and phonocardiogram (PCG). (Ao = aortic valve;
LA = left atrium; Mv = mitral valve; RV = right ventricle; PW = posterior wall.)

3. In vivo Experimental Results

By applying this novel method to the longitudinal-sectional
plane of a healthy human heart as shown in Fig. 1(a), thevelocity signal was measured as a waveform at each pointon the plane. The velocity waveforms measured at six points(a–j) in Fig. 1(a) and their integration, the displacement
waveform, are shown in Figs. 1(d) and 1(c), respectively,
for one cardiac cycle. The left ventricular (LV) contraction
during the ejection period is roughly shown in the upward
displacement (toward the apex) of Fig. 1(c). In the velocity
waveform of Fig. 1(d), from the time of the P-wave, TP , of the

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50 mm
a
IVS j
i
Ao h
Ao g
f
apex a
b
PW c
d
LA
e a
a: 0.1 (m/s)/mc,j: 2 (m/s)/m 0change in lengthba: 5 mm/s
toward apex
c,j: 10 mm/s
b: 25 mm/s 0d,i: 50 mm/s
toward basevelocity
PCG
P
ECG
c
-100
(TP)

contraction
atrialcontraction

cessation
ejection

first
Q R S
0
(TR)

200
100
time from R-wave [ms]Fig. 2. (Color online) Expanded version of Fig. 1 at the beginning of the contraction. (a) Temporal changes in the phase of the 40-Hz component of thevelocity wave in Fig. 1(b). (b) Temporal changes in thickness or length at points a–j in Fig. 1(d). (c) Velocity waveform at points a–j.

electrocardiography, there is downward velocity component(toward the base), corresponding to the LV expansion due
to atrial contraction. After this, during systole, the upwardvelocity component (toward the apex) begins, which corresponds to the LV contraction, continuing until the time of thesecond heart sound, TII , the time of the aortic valve closure,which is followed by rapid ﬁlling and slow ﬁlling phases,
where these points moves downward (toward the base).
However, there are some diﬀerences among thesetransient times from downward to upward or from upward
to downward at the base-side points (d or i). To clearly showthese time diﬀerences regardless of the minuteness of thevelocity, by applying the moving short-time Fourier transform to each of the velocity waveforms, simultaneously
measured at all points set along the lines (a–b–c–d–e, g–f,
and a–j–i–h) in Fig. 1(a), the phase of the 40-Hz component
is color-coded, and its temporal change is shown in
Fig. 1(b). Red shows the upward velocity component toward
the probe (point O) in Fig. 1(a), and light blue shows its
reverse property. As shown in Fig. 1(b), the onset time of the
upward velocity (contraction) before time of R-wave of theelectrocardiography, TR , does not coincide at all points (a–j),
but there are some propagating components in the LV.
By expanding the time axis in Figs. 1(b) and 1(d), thetransition properties around TR are shown in Figs. 2(a) and2(c), respectively. At the same time, the instantaneouschange in length (shortening due to contraction or extension)
is obtained at the points (a, c, j) shown in Fig. 2(b). The
white dotted lines in Fig. 2(a) show the onset of thecontraction determined by conﬁrming whether the redcomponent of velocity is associated with the change inlength from extension to contraction as in Fig. 2(b). The
black dotted lines show the reverse phenomenon.
From TP , the atrial contraction begins and the LV volume
increases, corresponding to the downward velocity (lightgreen) in Fig. 2(a) to show the extension both in theposterior wall (b–c–d) and the interventricular septum (IVS)(a–j–i). Then, from the time 80 ms prior to TR , the upwardvelocity component is generated at the apical side (a), andthen from the time of 50 ms prior to TR , the upward
component propagates from the apex (b) to the base (e)along the LV posterior wall with a speed of about 9 m/s,
where it is accompanied by the transition from extension tocontraction. It then propagates along the IVS from point(i) to both the apex (a) and the base (h) at a speed of about
3 m/s. Just after passage of this component, the contraction
begins at each point. The starting point (a) of the velocity
component accompanying the contraction in Fig. 2(a) would
be close to the terminal of the Purkinje ﬁbers (special
electrical conducting cells which rapidly transmit anelectrical excitation).26) These velocity and change in length
are too minute to be identiﬁed by other methods.

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O (probe)
anterior

ECG
PCG

a

90

180

0

anterior

-90
phase

RV
IVS
b

d

LV
PW
c

a atrial contraction

ejection

posteriorrapid filling slow filling

50 mm a
IVS

b
c

PW
d
a
5 mm
0
displacementbcanteriorbdac posteriorcb

50 mm/s0velocity

a d
first

second

PCG
ECG

P

R

-200
d (T )
P

0
(TR)

T
200

P
400
(TII)

600

R

800
1000
time from R-wave [ms]Fig. 3. (Color online) Time sequence of velocity and displacement in the unfolded left ventricular wall made based on the short-axis view. (a) Short-axis
cross-sectional plane on the LV with the papillary muscle level. (b) For one cardiac cycle, the temporal changes in the phase of the velocity component.
Vertical axis corresponds to the colored line in (a). (c) Displacement waveform at points a–d in (a). (d) Velocity waveform at points a–d.

The ﬁrst heart sound following the QRS-complex istraditionally thought to be primarily associated withmechanical vibrations resulting from the closure of themitral value and the opening of the aortic valve.27) As shownin Fig. 2(a), after TR , two waves are generated and propagate

from the apex (a) to the base (e) along the LV posterior wall.
During the short period of 20 ms from the beginning of theﬁrst heart sound, the contraction property, which begins at
the above onset in Fig. 2(a), is reversed. This ‘‘cessation of
the contraction’’ would correspond to the LV expansion

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50 mm a atrial contraction
IVS

contraction

cessation

ejection

b
c

PW
d
a

a

2 (m/s)/mchange in0length b
30 mm/svelocity 0

bd

a
c
a

anteriordposterior

b c
first

PCG
ECG

P
c (T )
P

R

Q
-100

S

0
(TR)

100
200
time from R-wave [ms]Fig. 4. (Color online) Expanded version of Fig. 3 at the beginning of the contraction. (a) Temporal changes in the phase of the velocity component in
Fig. 3(b). (b) Typical waveforms of the change in thickness at point c and change in length at point b. (c) Velocity waveform measured at points a–d.

in the pre-ejection period that is necessary to cause themitral valve closure.28) This cessation is terminated by the
beginning of the second component of the above two waves,and after this cessation, all the points have the upwardvelocity components [red in Fig. 2(a)], that is, the contraction restarts, which constitutes the substantial LV contraction in the ejection period.
For the same subject, the position and the direction of theultrasonic probe are changed so that the velocity and change
in thickness are measured in the parasternal short-axis crosssectional plane of the LV, as shown in Fig. 3(a). Figures 3(d)and 3(b) respectively show the velocity waveforms at four
points (a–b–c–d) in Fig. 3(a) and temporal changes in thephase of the velocity waveform for one cardiac cycle.
Figure 3(c) shows the displacement waveforms at thesepoints. Roughly, during the ejection period, the LV
contraction is associated with the downward displacement(to posterior) at point (a) and upward displacement (toanterior) at points (b, c), while point (d) is almost motionless.
By expanding the time axis in Fig. 3, the mechanicalexcitation is shown in Fig. 4 around TR . From a time 120 ms

prior to TR , the response propagates from the IVS (a), to theposterior wall (b–c–d) with a speed of about 6 m/s in the
counterclockwise direction when viewed from the apicalside. The propagation is unidirectional, that is, the contraction propagates in one direction (counterclockwise), not inboth directions. The passage of the component [blue in
Fig. 4(a)] is accompanied by thickening (at a and c) or
contraction (at b and d) along the ultrasonic beam; bothcorrespond to the contraction.
4. Discussion

Previous studies have deﬁned the pre-ejection period28,29) as
the interval from the onset of the QRS-complex to the timeof the aortic valve opening. It has been shown thatmyocardial acceleration during isovolumic contraction(IVA), which onset coincides with the initial upstroke of
the LV pressure and the R-wave of the ECG, is clinicallyuseful to measure LV contractile function that is unaﬀectedby preload and afterload changes.30,31) The importance of thepresent study is not to measure the pre-contraction or the
IVA but to measure the spatial and temporal distribution of

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the onsets of the IVA to show its excitation propagation. The
end of the cessation in Figs. 2(a) and 4(a) corresponds to the
traditionally accepted onset time of the contraction.12,13)
However, the minute contraction propagation occurring
prior to the onset time was found in the present study.
Physiologically, it is well known that the depolarized action
potentials, cyclically generated at the sino-atrial node,
propagate to the Purkinje ﬁbers, which form interweaving
networks on the endocardial surface of both ventricles
and transmit the impulse to the ventricular endocardium.
Their conduction velocity is 2.0–4.0 m/s in the normal
human.32,33) Around the time of the Q-wave, based on cellto-cell connections, the action potential starts to propagate
with a lower speed of 0.3–1.0 m/s in humans33) to the entire
wall from the Purkinje ﬁber-myocyte junctions on the IVS
surface, where the Purkinje ﬁbers are in contact with the
myocardium. In the present study, however, the measured
propagation velocity regarding the minute contraction isabout 9 m/s, which is much faster than those electricalconduction velocities in the previous studies. These differences suggest that the measured propagation components
prior to TR would be ‘‘pre-contraction’’ prior to the fullcontraction of the ejection period. Since the physiologicalbasis of the observed contraction sequence remains unclear,further mechanistic details will be necessary to better
substantiate these ﬁndings.
In the present study, the heart walls were manually
identiﬁed before applying the measurement method. For
applying the analysis in the present study to a lot of subjects
and animals, it is essential to develop a reliable method forthe automated identiﬁcation of the heart wall.34–37)
In the present study, the measurement of the velocity
components was restricted to the direction of the ultrasonicbeam. Alternatively, the measurement has been expanded
into the two-dimensional (2D) space recently.38–41) It is,however, still diﬃcult to measure the rapid and minutevelocity components in the heart wall by these methods.
For thorough analysis of the propagation of the minutemechanical-excitation wave-front, the heart wall velocity
distribution should be measured in the 2D space with hightemporal and spatial resolutions.42)
With the novel echocardiography in the present study, theminute-contraction sequences of the myocardium wereconﬁrmed noninvasively. These results show great potential
for thorough understanding of the principles of the cardiac
contraction mechanism, as well as for noninvasive assessment of myocardial tissue damage in early stage of
cardiomyopathy and myocardial infarction since it is known
that myocardial isotonic velocity for the contraction isdecreased in failing hearts.43) The biological implications ofthese observations also remain unclear. In order to elucidate
the role of these contractions in the ventricular remodeling,similar experiments should be performed in infracted hearts.
Moreover, investigation of methods to modulate thesecontractions should be performed to determine any potential
therapeutic value with biventricular pacing.

Graduate School of Engineering, Tohoku University andthe healthy subjects gave informed consent. This study waspartly supported by a Grant-in-Aid for Scientiﬁc Researchfrom the Japan Society for the Promotion of Science (2008–2010, No. 20360181).

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