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Japanese Journal of Applied Physics 56, 07JF05 (2017)https://doi.org/10.7567/JJAP.56.07JF05

Ultrasound imaging of propagation of myocardial contraction
for non-invasive identiﬁcation of myocardial ischemia
Yuya Matsuno1*, Hirofumi Taki1,2, Hiroaki Yamamoto3, Michinori Hirano3, Susumu Morosawa3,
Hiroaki Shimokawa3, and Hiroshi Kanai2,1*
1

Graduate School of Biomedical Engineering, Tohoku University, Sendai 980-8579, Japan
Graduate School of Engineering, Tohoku University, Sendai 980-8579, Japan
3
Graduate School of Medicine, Tohoku University, Sendai 980-8574, Japan2*E-mail: kanai@ecei.tohoku.ac.jp
Received November 25, 2016; revised February 1, 2017; accepted February 20, 2017; published online June 6, 2017
Non-invasive identiﬁcation of ischemic regions is important for diagnosis and treatment of myocardial infarction. In the present study, ultrasoundmeasurement was applied to the interventricular septum of three open-chest swine hearts. The properties of the myocardial contraction responseof the septum were compared between normal and acute ischemic conditions, where the acute ischemic condition of the septum originated fromdirect avascularization of the left anterior descending (LAD) coronary artery. The result showed that the contraction response propagated from thebasal side to the apical side along the septum. The estimated propagation velocities in the normal and acute ischemic conditions were 3.6 and1.9 m/s, respectively. This ﬁnding indicates that acute ischemia which occurred 5 s after the avascularization of the LAD promptly suppressed the
propagation velocity through the ventricular septum to about half the normal velocity. It was suggested that the myocardial ischemic region could
be identiﬁed using the diﬀerence in the propagation velocity of the myocardial response to contraction.
© 2017 The Japan Society of Applied Physics

1.

Introduction

About 7.3 million people in the world, including 200,000
people in Japan, die from heart diseases every year.1,2) The
number of deaths due to heart diseases in Japan ranks second
only to malignant neoplasm and accounts for 15.8% of annual
deaths. Therefore, the prevention of heart diseases and theirprompt and appropriate treatment are essential, and there is acompelling need for development of diagnostic methods thatcan be applied repeatedly and promptly with a high degree of
accuracy.
Chest X-ray, computed tomography (CT),3) magnetic
resonance imaging (MRI),4,5) and medical ultrasound arecommonly used for the diagnosis of heart disease. Chest
X-ray and CT are suitable to diagnose pathological conditions, but repetition is not recommended due to radiation
exposure. Both morphological diagnosis by three-dimensional images and evaluation of coronary artery stenosis with
contrast agents are possible with MRI; however, it cannot beapplied to a patient with a cardiac pacemaker because MRI
uses strong magnetic ﬁelds. In contrast, the use of ultrasoundfor diagnosis is suitable for repeated and prompt application
because it is a non-invasive, low-cost, and real-time
diagnostic method.6–10)
Cardiac ischemia accounts for most heart diseases.
Figure 1 shows an illustration of myocardial infarction.
Myocardial ischemia originates from a decrease in blood ﬂow
caused by stenosis of a coronary artery. The prompt recoveryof blood ﬂow enables the ischemic region to avoid becoming
necrotic, that is, becoming an infarct region. For myocardialischemia, myocardial ischemia without pain (termed silent
myocardial ischemia) is especially dangerous because it isdiﬃcult to detect.11,12) Therefore, the development of a noninvasive, repeatedly applicable method of identifying a
myocardial ischemic region would be very useful in the
diagnosis and treatment of the early stage of myocardial
infarction, that is, myocardial ischemia.
Several researchers have focused on myocardial ischemia.13–18) Konofagou et al. reported that the propagation

Fig. 1. (Color online) Outline of three layers separated by progression of
myocardial infarction.

velocity of myocardial contraction in response to electricalstimulation decreases in the ischemic region of open-chest
canine hearts,19,20) and it has been found that the contraction
response of the myocardium to electrical stimulation propagates at a speed of several meters per second.21–27)
Therefore, high temporal resolution is required for measurement of this response. However, the accuracy of in vivo
measurement for the human heart is still low, and imaging of
the relationship from the arrival of electrical stimulation to
the myocardial contraction response is challenging.
In the present study, the propagation of the myocardial
response to contraction along the interventricular septum(IVS) of an open-chest swine heart was measured withmedical ultrasound to develop a method for identifying theischemic region in the IVS. In the previous research,medium-sized hearts, such as canine and feline hearts, weremainly targeted,19,20) whereas in the present study, swine
hearts, whose circulatory construction function and size aresimilar to those of humans were used. Moreover, in the openchest swine heart, the depth of the object (IVS) is shallow sothat it is possible to keep a high frame rate to evaluate the
myocardial contraction response with a high degree of
accuracy. An ischemic condition was manually induced tocompare the properties of the myocardial contraction

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Y. Matsuno et al.

response at the septum between normal and ischemic
conditions. Results conﬁrmed that the ischemia promptly
suppressed the propagation velocity in the IVS to about 70%of the normal condition or less at 5 s after the avascularizationof the LAD.
2.

Materials and methods

2.1 Measurement of myocardial micro vibration
velocityIn the ultrasound measurement of the IVS of a swine
heart, ultrasound pulses (center angular frequency ω0 = 2πf0)
are transmitted to the myocardium. The displacement of
the myocardium at time t is calculated by the following
equation:xðtÞ ¼

c0 !ðtÞ
;2

ð1Þ

where c0 is the velocity of ultrasound in soft biological tissue,and τ(t) is the round-trip propagation time of ultrasoundbetween an ultrasonic probe and the myocardium.
When ultrasound pulses are transmitted at intervals of ΔT
in a certain beam, the phase diﬀerence !"ðx; tÞ between two
succeedingly received signals is given by!
"!T!" x; t þ
¼ "ðx; t þ !TÞ % "ðx; tÞ
2
2!0 !xðtÞ
¼
;
ð2Þ
c0
where Δx(t) is the displacement of myocardium during theinterval ΔT. Therefore, the minute vibration vðx; t þ !T=2Þ
during the interval ΔT at a depth x in the myocardium isobtained by!
"!T!" x; t þ
!
"
2
!T
c0
v x; t þ
:
ð3Þ
¼
2
2!T
!0
In the present study, the phase diﬀerence at the center
frequency f0 was calculated by using the phased-tracking
method,28,29) and the minute vibration velocity vij(t) was
estimated at a j-th depth along the i-th ultrasonic beam at eachtime step.
2.2 Time delay measurement of myocardial
contraction
In the present study, the vibration of the myocardium wasmeasured as a waveform, which corresponds to myocardial
contraction at various locations where the contraction is in
response to the propagation of electrical stimulation. In order
to visualize the propagation of the myocardial contraction
response, the delay time τij at a depth of j-th along the i-th
ultrasonic beam was determined from the cross-correlation
between the vibration velocity waveforms with large
amplitude around the beginning of the ejection period. The
width of the correlation window was set to be the same as thewidth of the vibration waveform and the search area waslimited to before and after about 23 ms of the correlation
window.
2.3 Propagation velocity estimation of myocardial
contraction
In order to estimate the propagation velocity cc of thecontraction response in the IVS, the delay times {τij} wereaveraged in the depth direction along the i-th ultrasoundFig. 2. (Color online) Conventional B-mode image obtained byultrasound measurement in an open-chest swine heart. For the velocity
measurement of Eq. (3) in the present study, sparse scanning was employed
and the 13 selected ultrasonic beams (beam 0 to beam 12) are overlaid on theconventional B-mode image.

beam. The averaged delay time !" i along the i-th beam was
obtained by the following operation:
i %1
1 NX
!ij ;
ð4Þ
!" i ¼
Ni j¼0where Ni is the number of measurement points along the i-th
ultrasound beam.
Next, the propagation velocity cc was estimated byapplying the weighted least-square method to the averaged
delay time !" i along the i-th beam. The velocity within theregion of interest was assumed to be constant and inverse of
the standard deviation SDi of the delay time along eachultrasound beam was employed as the weight. The power pof error was deﬁned as follows:
N%1
X
ð"!i % # % $ & iÞ2
p¼
:
ð5Þ
SDi
i¼0
After determining α and β to minimize p of Eq. (5), thepropagation velocity cc was estimated from the value of β.
2.4 In vivo experiments
Ultrasound diagnostic equipment (Aloka SSD-6500) with aprobe having a center frequency of f0 = 3.75 MHz was
employed to acquire radio frequency (RF) data of the IVS inan open-chest swine heart. In this experiment, as shown in
Fig. 2, the number of beams was restricted to 13 to maintainthe frame rate 1=ΔT at 429 Hz, the angle between successive
beams was 5.6 degrees, and the sampling rate was 15 MHz.
Beam 0 was set at the cardiac apical side. The reference
position in the normal and ischemic conditions was set at a
depth of 50 mm along beam 5.
The measurement process was as follows. First, as acontrol (normal condition) an ultrasound echo was acquired
from the IVS in an open-chest swine heart (A), as shown in
Fig. 3(a). Next, the blood ﬂow of the left anterior descending(LAD) coronary artery was stopped manually to induce anacute ischemia condition at the IVS, and the same measurement as that applied to the normal condition was reapplied,
as shown in Fig. 3(b). By analyzing these measurements, thepropagation velocity was compared between normal and

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Y. Matsuno et al.

Fig. 5. (Color online) Minute vibration velocity waveform measured at
the reference position (beam 5, depth 50 mm) and at another position(beam 2, depth 50 mm).
Fig. 3. (Color online) (a) Conditions of ultrasound echo measurement atinterventricular septum in open-chest swine heart. (b) Protocol ofmeasurement.

Fig. 4. (Color online) Color ﬂow imaging of blood ﬂow in the case ofavascularization by compressing the LAD with a ﬁnger and then releasing it.

ischemic conditions to visualize the change in propagationof the myocardial contraction response caused by the acuteischemic condition.
3.

In vivo experimental results for swine hearts

The manual avascularization of the LAD was conﬁrmed bymeasurement of the blood ﬂow therein. As shown in Fig. 4,
the color ﬂow image of the LAD was darkened during
the period from −53 ms (avascularization) to 0 ms ( justreleased), when the blood ﬂow of the LAD was stopped. A
blue color then gradually appeared in the LAD from 53 ms
after the release, showing an acute ischemic condition in the
IVS.

Figure 5 shows minute vibration velocity waveforms
measured at the reference position (beam 5, depth 50 mm)
and at a measurement position (beam 2, depth 50 mm) in thenormal condition. The waveform of beam 2 (blue) was
delayed from that of beam 5 (red), showing that thecontraction response propagated from beam 5 (middle side)
to beam 2 (apical side).
Figure 6 shows color maps of the amplitudes of the minutevibration velocity waveforms {vij(t)} of 13 beams in thenormal and ischemic conditions. In Fig. 6(c), for each beam,
the velocity waveforms measured at 21 depths around thecenter point in the IVS along each beam, {vij(t)} (Ni=2 − 10 ≤ j ≤ Ni=2 + 10), are shown, Ni being the number ofmeasurement points along the i-th beam. At the beginning of
the ejection phase just after the QRS waves, the peak times ofthe minute vibration velocity waveforms are delayed backward as the beam number becomes small, as shown in
Fig. 6(a). On the other hand, as shown in Fig. 6(b), the delayin the ischemic condition was larger than that in the normal
condition. These ﬁndings show that the contraction response
propagates by a few m=s from the basal side to the apical sideand that the propagation velocity decreases in the ischemic
condition.
Figure 7 shows the delay time distribution {τij} at eachmeasurement point. The delay time increased from the basalside to the apical side in both the normal and ischemic
conditions, showing propagation of contraction from thebasal side to the apical side. The delay time diﬀerence fromthe basal side to the apical side in the normal condition was
about 15 ms, and that in the ischemic condition was about
20 ms. Thus, myocardial acute ischemia promptly suppressed
the propagation velocity of myocardial contraction.
Figure 8 shows the amplitude distribution of minutevibration velocity waveforms {vij(t)} obtained at eachmeasurement point superimposed on the B-mode image to
conﬁrm the estimation of the delay time distribution in Figs. 6
and 7. Each amplitude is shown by the maximum amplitude in
the search area of the correlation window in Fig. 5. It was
conﬁrmed that the amplitude of the minute vibration velocity
waveform was suﬃciently larger than noise.
Figure 9 shows the average delay time f"!i g with respect
to lateral distance x from beam 0. The solid line shows thestraight line determined by applying the weighted least-

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Y. Matsuno et al.

Fig. 7. (Color online) Delay time distribution of myocardial contraction
response in (a) normal and (b) ischemic conditions.

Fig. 6. (Color online) Temporal change of myocardial minute vibration
velocity in 13 beams. Dotted lines show the delay of the peak times of theminute vibration velocity waveforms. (a) Normal (control), (b) ischemia,(c) outline of displayed region.

square method, as described in Sect. 2.3. As shown in Fig. 9,
the propagation velocities in the normal and ischemic
conditions were 3.6 and 1.9 m=s, respectively. These results
show that the ischemia caused by the avascularization of the
LAD promptly suppressed the propagation velocity along the
IVS to about half the normal velocity. By applying the samemeasurement to two other swine hearts (B and C), theestimated propagation velocity values in the normal condition
were 3.4 and 3.3 m=s, and for the ischemic condition thevalues were 2.0 and 2.4 m=s. These results show that theischemia promptly suppresses the propagation velocity toabout 70% of the normal condition or less.
In order to examine the inﬂuence on the propagation
velocity of the myocardial contraction response while theischemic condition continues, data for each beat during theavascularization for the swine heart (A) were compared.
Figure 10 shows the transient response of the impaired
propagation velocity due to ischemia. Each propagation

Fig. 8. (Color online) Amplitude distribution of minute vibration velocity
waveform obtained for (a) normal and (b) ischemic conditions.

velocity for the period from the ﬁrst beat to the fourth beat
5 s after the measurement for the normal condition gradually
decreased from 1.90, 1.81, 1.76 to 1.69 m=s, respectively, as
shown in Fig. 10(b). These results show that the progressionof the ischemic condition suppressed the propagation
velocity.

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Fig. 9. (Color online) Approximate line estimated by the weighted leastsquare method considering the standard deviation in normal and ischemic
conditions.

Fig. 11. (Color online) Temporal change of myocardial minute vibration
velocity in another swine heart. Dotted lines show the delay of the peak timesof the minute vibration velocity waveforms. (a) Normal and (b) ischemia.

Fig. 10. (Color online) (a) Transient response of impaired propagation
velocity due to ischemia. (b) Temporal change of the propagation velocity of
myocardial contraction.

Since the procedure employed in the present study caneasily produce ischemia, it will be helpful in elucidating not
only the properties of myocardial contraction in normal andischemic regions but also disease progression from thenormal region to the ischemic region. The proposed method
also has potential for use in non-invasive diagnosis of aregion with reentry causing abnormal cardiac rhythm using
the diﬀerence from the normal delay distribution and toevaluate the extent of the lesion quantitatively based on thediﬀerence of delay time between normal, ischemic and infarct
regions.
4.

Discussion

The myocardial minute vibration velocity shown after the
QRS-wave of the electrocardiogram in Fig. 6(b) had
bimodality in the ischemic condition. As shown in Fig. 11,

similar results were obtained for another swine heart, but thecause of this phenomenon has not been ascertained and it isnecessary to measure more swine hearts in the future.
The velocity amplitude of the apical side was larger thanthat of the basal side for the normal condition, as shown in
Fig. 8(a). In the present study, the myocardial response to
the arrival of the action potential rather than the propagationof the mechanical vibration along the IVS was measured.
Moreover, since the beam direction and the IVS were notorthogonal at the basal side, the obtained velocity amplitudeof the IVS was smaller than that on the apical side. On theother hand, the velocity amplitude of the basal side for theischemic condition in Fig. 8(b) was larger than that in thenormal condition. This is due to the diﬀerence in measurement position between the normal and ischemic conditions
because the open-chest swine heart moves intensely. In thepresent study, the propagation of myocardial contraction was
evaluated even when the amplitude at each position was
diﬀerent because only the delay in the propagation of theminute vibration velocity was considered.
In the ischemic myocardium, just after the time of coronary
occlusion, it is known that the decrease of resting membranepotential (polarization failure) occurs because the concentration of potassium ions in the cell is decreased.30) Reductionof the resting membrane potential leads to the inactivationof the Na channel and the sodium current is reduced so thatthe upstroke of the action potential becomes slow. Therefore,

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Y. Matsuno et al.

side. In addition, the estimated propagation velocity values in
the normal and ischemic conditions were 3.6 and 1.9 m=s,respectively. These results show that ischemia caused byavascularization of the LAD promptly suppresses the
propagation velocity along the IVS to about half the normal
velocity. By applying the same measurement to two otherswine hearts, the estimated propagation velocity values in thenormal condition were found to be 3.4 and 3.3 m=s, whereas
those in the ischemic condition were 2.0 and 2.4 m=s. These
results show that ischemia promptly suppresses the propagation velocity along the IVS to about 70% of the normal
condition or less. Therefore, regarding myocardial contraction caused by acute ischemia, a prompt decrease inpropagation velocity was conﬁrmed by measurement andvisualization in the present study.

Fig. 12. (Color online) Two variables employed to calculate thewavelength λ0 of the phenomenon to be measured. (a) ΔT; period of the
myocardial minute vibration and (b) Δx; beam interval in the lateral direction
at the middle level of the IVS.

the propagation velocity of myocardial contraction was
decreased in the ischemic condition, as shown in Fig. 9.
In order to develop measurement technology as the basisof a method for identifying the ischemic region, the depth ofthe object (IVS) was shallow in this measurement. As shownin Fig. 12(a), the period ΔT of the minute vibration was
about 50 ms, and the dominant frequency f0 was about 20 Hz.
Since the measured propagation velocity v of the myocardial
contraction was estimated to be about 2 m=s, the wavelength
λ0 (mm) of the phenomenon was determined as%0 ¼

v
ffi 100:f0

ð6Þ

Since 13 beams were employed in the measurement, thebeam interval Δx in the IVS was 4.0 mm, as shown in
Fig. 12(b), which was much shorter than the wavelength λ0of the phenomenon to be measured. When the number ofbeams is reduced from 13 to 4, that is, only 0th, 4th, 8th, and12th beams in Fig. 12(b) are selected and a sparser scan is
performed, Δx is 12 mm, which is still suﬃciently shorter
than the wavelength λ0. Thus, the measurement with suchsparse scanning is consistent for estimating the propagation
velocity. Therefore, when applying the measurement to thehuman heart, it is possible to identify the myocardialischemic region even if the number of beams is reduced tokeep a high frame rate.
5.

Conclusions

In the present study, the propagation of myocardial
contraction along the IVS of open-chest swine hearts wasmeasured by medical ultrasound. The properties of the
myocardial contraction response in the IVS were compared
between normal and acute ischemic conditions, where theacute ischemic condition of the IVS originated from theavascularization of the LAD. As a result, delay time
distribution of the myocardial contraction response wasvisualized. These results show that the myocardial contraction response propagated from the basal side to the apical

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