Ultrasonics 38 (2000) 405–411
www.elsevier.nl/locate/ultras

Onset of pulsatile waves in the heart walls at end-systole
Hiroshi Kanai a, *, Sachiko Yonechi a, Ikuko Susukida a, Yoshiro Koiwa b,
Hide-ichi Kamada b, Motonao Tanaka ca Department of Electrical Engineering, Graduate School of Engineering, Tohoku University, Sendai 980-8579, Japanb First Department of Internal Medicine, Tohoku University School of Medicine, Seiryou-machi, Aoba-ku, Sendai 980-8574, Japanc Tohoku Welfare Pension Hospital, Takasago 10, Fukumuro, Miyagino-ku, Sendai 983-8512, Japan

Abstract
We have previously developed a novel ultrasonic method, namely, the phased tracking method, for accurately tracking the
movement of the heart wall based on both the phase and magnitude of the demodulated signals to determine the instantaneous
position of an object. With this method, it is possible to accurately detect small-amplitude velocity signals of less than a few
micrometers of the heart wall that are superimposed on the motion of the heart wall due to the heart beat. There are several
remarkable pulsatile waves during one cardiac cycle in the resultant velocity signals, some of them being commonly obtained forboth healthy subjects and patients. These pulsatile waves cannot be recognized in standard echocardiography M-mode images. In
this paper, by focusing on one pulsatile wave that occurs around the end-systole, the physiological meaning of these is consideredbased on various in-vivo experiments. The pulsatile wave measured by this novel ultrasonic method will offer potential for aquantitative assessment of myocardial viability. © 2000 Elsevier Science B.V. All rights reserved.
Keywords: Cardiac cycle; Isovolumetric relaxation period; Myocardial viability; Phased tracking method; Pulsatile wave

1. Introduction
Though M-mode echocardiography offers an advantage in critically looking at the motion pattern of theleft ventricle (LV ), its spatial resolution along the ultrasonic beam is limited to a few wavelengths, namely,
only up to 1 mm for ultrasound of 3 MHz because an
M-mode image is displayed based on the amplitude of
the reflected ultrasound. However, numerous elaborate
techniques have been proposed for non-invasive measurement of the velocity of the blood flow in the heartor the arteries based on the Doppler effect [1]. Moreover,
several methods, including the phase-locked-loop (PLL)
techniques, have been proposed to measure roughchanges in the diameter of the arterial walls by tracking
arterial wall displacement in real time [2,3].
For the accurate detection of velocity signals, that is,
the instantaneous movement on or in the heart wall, we
have developed the phased tracking method [4], whichis briefly described in Section 2. This method has beenvalidated by experiments using a water tank and has* Corresponding author. Fax: +81-22-263-9444.
E-mail address: hkanai@ecei.tohoku.ac.jp (H. Kanai)

been applied to in-vivo detection of small velocity signals, with sufficient reproducibility, on the wall of thehuman heart [4]. The detected velocity signals show
rapid motion including high-frequency components withsmall amplitudes, which are difficult to recognize by
M-mode echocardiography.
Moreover, the method has been applied to multiple
points preset along an ultrasonic beam in the LV wall
so that the instantaneous object positions, {x (t)}, andithe velocity signals, {v(x ; t)}, can be obtained for theseimultiple points, {i}, in the LV wall [5]. The wall changes
position and thickness with time. By making the locationof the RV side of the interventricular septum (IVS ) thereference point, the thickness change during myocardial
contraction/relaxation can be detected. Then, their spatial distribution is obtained and is superimposed on the
M-mode image using color coding.
A spectrum analysis was first applied to the resultant
non-invasively detected signals to identify the frequency
band for the components from 25 to 90 Hz due to the
myocardial thickening and thinning. Such an analysis
shows the novel possibility of diagnosis of the regional
myocardium [4,5].
The top three panels of Fig. 1 show the typical

0041-624X/00/$ - see front matter © 2000 Elsevier Science B.V. All rights reserved.
PII: S0 0 4 1 -6 2 4 X ( 9 9 ) 0 0 11 7 - 1

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H. Kanai et al. / Ultrasonics 38 (2000) 405–411

Fig. 1. In-vivo experimental results firstly obtained by the novel method [4]. Left: waveforms of the vibration signal on the LV side of the IVS(several heartbeats overlaid ). The pulsatile wave interesting in this study is surrounded by an oval for each subject. Right: their average power
spectra. Upper three rows of plots: for three healthy young male volunteers. (n1) Healthy 22 year old male volunteer. (n2) Healthy 26 year old
male volunteer. (n3) Healthy 22 year old male volunteer. For each subject, the reproducibility is quantitatively confirmed up to 100 Hz. The
waveforms and power spectra of these volunteers are similar. Bottom four: for three patients, with acute lymphoblastic leukemia, who have beentreated with antracenadiones (mitoxantrone). (p1) A 32 year old male patient. The measurement was performed 2 months before his death. (p2)Same patient as (p1). The measurement was performed 3 months before the measurement of (p1). (p3) 23 year old male patient. (p4) 25 year old
female patient. The dotted lines overlaid show the power spectrum of the subject (n1).

waveforms of the vibration signals and their average
power spectra, measured by the phased tracking methodon the LV side of the IVS of three healthy young malevolunteers [4]. The waveforms of several heartbeats areoverlaid on each plot. For each subject, the reproducibility is quantitatively confirmed up to 100 Hz. The
bottom four panels of Fig. 1 show the waveforms forfour patients with cardiomyopathy induced by adriamycin injection. For all seven subjects, there are pulsatile
waves around the isovolumetric relaxation period, indicated by the ovals in Fig. 1. The waveforms of thepulsatile waves (marked by ovals) of the patients in
Fig. 1(p1), (p2), and (p4) are somewhat different fromthose for the healthy volunteers in Fig. 1(n1)–(n3).
In the right portion of Fig. 1, the average power
spectra of the vibration signals around the pulsatile
waves for several heartbeats are shown by solid curves.
The power of the vibration in the patients, except forpatient (p3), is decreased by at least several decibels ascompared with that of the healthy subjects, which shows

the possibility to diagnose the ventricular dysfunction.
It is well known that the second heart sound (II ) isradiated mainly by the closure of the aortic (Ao) valve.
However, the cause and mechanism of the pulsatile
waves in Fig. 1 remain unclear.
In this study, therefore, the novel method that wedeveloped is modified and applied to the IVS and theposterior wall of the LV of healthy young volunteers.
By comparing the timing of the pulsatile waves with thetiming of the Ao valve closure, new findings that characterize the pulsatile waves are obtained. Finally, thetiming of the pulsatile wave on the IVS is comparedwith the waveform of the LV inner pressure, which issimultaneously measured in an in-vivo experiment.

2. Principles of phased tracking method
Radio frequency pulses with an angular frequencyof v =2pf are transmitted with a repetition period of00H. Kanai et al. / Ultrasonics 38 (2000) 405–411

DT from an ultrasonic transducer. The ultrasonic pulse
reflected by the object (i) is received by the same
ultrasonic transducer. The output signal is amplified
and quadrature-demodulated. The resultant in-phaseand quadrature signals for each transmitted pulse are
simultaneously A/D-converted at a sampling frequencyof 1/T , and these two signals are combined into aS
complex signal, y(x; t), where x(t) and its simple expression x denote the depth from the ultrasonic transducer.
We assume that point i has only a velocity component
that is parallel to the direction of the beam if thedirection and position of the ultrasonic beam are appropriately selected so as to be perpendicular to the wall
during the cardiac cycle. The instantaneous depth,
x (t), of the object (i) from the ultrasonic transducer isigiven by the product of the acoustic propagation velocity, c , and the instantaneous period, t (t), required for0ione-way transmission from the ultrasonic transducer tothe object (i). The phase h(x ; t) of the signal y(x ; t) isiigiven by the angular frequency, v , multiplied by twice0
the delay time, t (t). Thus, the phase difference, Dh(x ;iit), between the analytic signals y(x ; t) and y(x ; t+DT )iiof the successively received signals in the interval DT isgiven byDh(x ; t)=h(x ; t+DT )−h(x ; t)iii2v=2v {t (t+DT )−t (t)}= 0 Dd (t),
(1)
0 i
i
i
c
0
where Dd (t)=x (t+DT )−x (t) is the instantaneousiiimovement of the object (i) in the period DT after a timet. Then, Dd (t) is given from the measured data by:i
Dh(x ; t)
i
(m).
(2)
2v
0
Since it is essential to accurately determine the phasechange Dh(x ; t) of Eq. (2) during the period DT, aicomplex correlation is employed in the determination
procedure of the instantaneous movement of the object
position, x (t) [4]. By dividing the estimate of theimovement, Dd (t), by DT, the velocity signal is given asifollows:
Dd (t)=ci0

Dd (t)
iv (t)=c(m/s).
i
0 DT(3)The velocity signal and the spectrum are effective indiagnosis of the regional myocardium [5].
The position x (t) of the object (i) in the heart wallichanges by more than 10 mm due to the heartbeat in
one cardiac cycle. It is, therefore, essential to track the
instantaneous object position, x (t). For this purpose,iby accumulating the estimate, Dd (t), of the instantani
eous movement in Eq. (2), the next object position,407

x (t+DT ), is estimated byix (t+DT)=x (t)+Dd (t) (m).
(4)
i
i
i
Thus, the instantaneous movement, Dd (t), and the nextiobject position, x (t+DT ), are simultaneously deteri
mined and are obtained as waveforms.
When the time interval, DT, of the transmission of
the r.f. pulses is about 200 ms, the maximum value ofthe instantaneous movement, Dd(t), of an object in theheart wall is about 20 mm during the time interval DT.
These values are much less than the wavelength of about
500 mm at 3 MHz. Since the quadrature-demodulated
signals are A/D-converted at a sampling interval, T , ofS
1 ms in this paper, the spatial resolution Dx =S
T ×c /2=750 mm in the direction of depth. However,S 0
the resultant estimate x (t) of the next object positioniof Eq. (4) in the above procedure is represented not by
a discrete value, which depends on the sampling interval,
T , but by the continuous value which is determinedSfrom the phase difference, Dh (x ; t). Thus, accurate
i itracking of the object is realized by this method, and asmall instantaneous movement in the order of several
microns is determined.
To accurately consider the difference between theradiation timing of the pulsatile wave and the closure
timing of the Ao valve, the ultrasonic pulse is alternatelytransmitted in two different directions, A and B, usinga phased array transducer; one direction includes theAo valve, and the other includes the IVS or the LV freewall. The velocity signals, v (t) and v (t), are simultaA
Bj
neously measured at points ii and j, eachof which is in
the direction of A and B of the ultrasonic beams,
respectively.

3. In-vivo experiments along the longitudinal axis
First, the proposed method is applied to the detectionof velocity signals on the wall of the aorta just anterior
to the Ao valve, the IVS and the free wall of the LV ofa healthy 24 year old male volunteer. The bottom right
portion of Fig. 2 shows the cross-sectional B-mode
images of these walls along the longitudinal axis, whichwere obtained by standard ultrasonic diagnostic equipment. The directions of the ultrasonic beams are set, asshown by the white lines A and B. Five points {A , A ,1 2
B , B , B } are set along these ultrasonic beams.
1 2 3
Since the results obtained by the proposed method
depend on the angle between the direction of the velocity
vector and the ultrasonic beam, the direction of theultrasonic beam passing through these walls is selected
so that the beam is almost perpendicular to each wall
during the A/D conversion of several cardiac cycles.
During the acquisition period, respiration is suspended.
Fig. 2(b) and (c) show the ECG and the phonocardiogram (PCG), respectively. Before applying the method

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H. Kanai et al. / Ultrasonics 38 (2000) 405–411

Fig. 2. In-vivo experimental results on (A) the Ao wall and (B) the IVS and LV posterior wall of a healthy 24 year old male volunteer. Right:
cross-sectional B-mode image with the longitudinal axis showing the directions, A and B, of the ultrasonic beams and five object points, A , A ,1 2
B , B , and B , set along the beams. (a) Tracking results {x (t)} and {x (t)} for the five points {A } and {B } are shown by white lines on the
1 2
3
Ai
Bj
i
j
M-mode images of the respective directions, A and B. From (a-A), the timing of the Ao valve closure is determined and is shown by the verticaldashed lines. (b) ECG. (c) PCG. (d ) Velocity signals {v (t)} and {v (t)} of the points {A } and {B }.
Ai
Bj
i
j

described in Section 2, by referring to the M-mode
image, which was reconstructed from the magnitude ofthe digitized signal of the analytic signals, the positionsof the multiple points along the ultrasonic beam aremanually preset in the workstation. The tracking results{x (t)} or {x (t)}, estimated by Eq. (4) of the pointsA
Bj{A }i or {B }, aresuperimposed on the M-mode imageijby white lines, as shown in Fig. 2(a-A) and (a-B). From
Fig. 2(a-A), the timing of the Ao valve closure is determined and is shown by the vertical dashed lines.
Fig. 2(d-A1), (d-A2), (d-B1) (d-B2), and (d-B3) show
the velocity signals {v (t)} or {v (t)} on the trackedAi
Bj
points {x (t)} or {x (t)}.
In orderto ease interpretaAi
Bjtion, the vertical axis of these figures is inverted so thatthe negative value of the velocity, which is shown above
the baseline, corresponds to the situation in which theobject moves in the direction of the ultrasonic transducer
on the chest wall. The resultant velocity signals are
reproducible for the heartbeat periods.

4. In-vivo experiments from the apex of the heart
Next, the proposed method is applied to the detectionof velocity signals on the IVS and the LV posterior wallof a healthy 26 year old female volunteer, as shown in
Figs. 3 and 4, respectively. The right panel of Fig. 3 andthat of Fig. 4 show the cross-sectional B-mode images ofthese walls from the apical view. The directions of
the ultrasonic beams are set as shown by the white lines
A and B. Six points from {B } to {B } in the IVS in
1
6
Fig. 3 and four points from {B } to {B } in the LV
1
4
posterior wall in Fig. 4 are set along the ultrasonicbeam B.
The tracking results {x (t)}, estimated by Eq. (4) ofBj
the points {B }, are superimposedon the M-mode imagejby white lines, as shown in Figs. 3(a) and 4(a). From
the M-mode image for the direction A of the ultrasonicbeam, the timing of the Ao valve closure is determined
and is shown by the vertical dashed lines. Figs. 3(d ) andH. Kanai et al. / Ultrasonics 38 (2000) 405–411

409

Fig. 3. In-vivo experimental results on (B) the IVS of a healthy 26 year old female volunteer. Right: cross-sectional B-mode image with the apicalview showing the directions, A and B, of the ultrasonic beams and six object points from B to B set in the IVS along the beam B. (a) Tracking
1
6
results {x (t)} for the six points {B } are shown by white lines on the M-mode image. From the M-mode image of the direction A, the timing ofBjj
the Ao valve closure is determined and is shown by the vertical dashed lines. (b) ECG. (c) PCG. (d) Velocity signals {v (t)} of the points {B }.
jBj

4(d ) show the estimates of the velocity signals {v (t)}Bjon the tracked points {x (t)}.
Bj
5. Simultaneous measurement of pulsatile wave and LV
inner pressure
Finally, we applied the developed method to the IVSof a 57 year old male patient with dilated cardiomyopathy (DCM ). The M-mode image, the ECG, and the
waveforms of the velocity signals of the IVS are shownin Fig. 5(a), (b), and (d ), respectively. In these measurements, the inner pressure of the LV is simultaneously
measured by catheterization. The pressure is shown in
Fig. 5(c). The two vertical dashed lines t and t show
1
2
the starting time of the pulsatile wave on the LV side of
the IVS and the location of the peak, respectively.

6. In-vivo experimental results and discussion
From the results in Fig. 2–5, which were all obtainedby the newly developed method, there are several new
findings, which cannot be recognized in the M-mode
image of standard echocardiography:

1. As shown by Fig. 2(d-B1) and (d-B2), there are clear
pulsatile waves on the IVS, each of which starts
about 20 ms prior to the closure of the Ao valve.
The velocity components in these figures are detectedin the direction of the ultrasonic beam B, which isalmost perpendicular to the IVS.
2. Similar results are obtained for a different subject, asshown in Fig. 3(d ), where the velocity components
are detected in the direction from the apex to thebase of the heart.
3. Specifically just before the Ao valve closure, thevelocity of the IVS is about 20 mm/s toward the rightventricle (RV ) and toward the base of the heart.
4. Thus, from the timing described above, the pulsatile
waves are not caused by the closure of the Ao valve.
However, in the latter half of the pulsatile waves on
the IVS, there are rapidly changing components,
which may correspond to the second heart soundcaused by the closure of the Ao valve.
5. As shown by Fig. 2(d-B3), the LV posterior wall has
a pulsatile wave slightly slower than those on the
IVS and it starts upon commencement of Ao valve
closure. Surprisingly, similar waveforms are obtained
for the different subjects in the apical view, as shownin Fig. 4(d-B3).

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H. Kanai et al. / Ultrasonics 38 (2000) 405–411

Fig. 4. In-vivo experimental results on (B) the IVS of the same volunteer as Fig. 3. Right: cross-sectional B-mode image with the apical view
showing the directions, A and B, of the ultrasonic beams and four object points from B to B set in the LV posterior wall along the beam B. (a)1
4Tracking results {x (t)} for the four points {B } are shown by white lines on the M-mode image. From the M-mode image of the direction A,
Bjj
the timing of the Ao valve closure is determined and is shown by the vertical dashed lines. (b) ECG. (c) PCG. (d ) Velocity signals {v (t)}Bjof the points {B }.
jFig. 5. In-vivo experimental results from the IVS of a 57 year old malepatient with dilated cardiomyopathy (DCM ). (a) M-mode image andthe tracking results x (t) and x (t). (b) ECG. (c) Inner pressure of
RV
LV
the LV. (d-1) Velocity signals {v(x ; t)} of the RV side of the IVS.
RV(d-2) Velocity signals {v(x ; t)} of the LV side of the IVS. The two
LVvertical dashed lines A and B show the starting time of the pulsatile
wave on the LV side of the IVS and the temporal location of the peakof this wave, respectively.

6. The direction of the pulsatile waves on the LV
posterior wall in Fig. 3(d-B3) is opposite that on the
IVS in Fig. 2(d-B1) and (d-B2). Thus, all the pulsatile

waves on the IVS in Fig. 2(d-B1) and (d-B2), and3(d ) and the LV posterior wall in Figs. 3(d-B3) and4(d-B3) have velocity components, indicating thatthe lumen of the LV expands upon commencementof Ao valve closure.
7. By comparing the amplitudes of the pulsatile waves{v (t)} in Fig. 3(d-B1) with those in Fig. 3(d-B6), itB
canj be seen that there are spatial distributions intheir velocity values and that the IVS near the basehas the highest velocity at the timing. Similar phenomena are obtained for the LV posterior wall, as
shown in Fig. 2(d).
8. The velocity signals at the wall of the orifice justbehind the Ao valve are measured in Fig. 2(d-A1)and (d-A2). The waveforms of the pulsatile waves
around the timing of the Ao valve closure are similar
to those obtained on the IVS in Fig. 2(d-B1) and(d-B2). However, the former is somewhat slower
than the latter, and there is some delay from thelatter to the former. These phenomena also support
the fact that the pulsatile waves on the IVS do not
originate from the closure of the Ao valve.
9. As shown by the vertical dashed line, t , in Fig. 5(c)1and (d-2), the onset of the pulsatile wave corresponds
to the point when the decrease in the LV innerpressure starts at the end of the ejection period.
10. At the point in time corresponding to the dashedline, t , in Fig. 5, the pulsatile wave on the LV side2

H. Kanai et al. / Ultrasonics 38 (2000) 405–411

of the IVS has reached its maximal velocity, and at
this point in time, the Ao valve has just closed, as
shown in Fig. 2(d-B1) and (d-B2).
Therefore, it seems very likely that the detectedpulsatile wave originates from the myocardial relaxationand that there is a close relationship between the pulsatile wave and decrease in the LV inner pressure, which
will be a direct cause of the Ao valve closure.

411

the latter half of the pulsatile waves on the IVS, however,rapidly changing components are included and they may
correspond to the second heart sound, which is causedby the closure of the Ao valve. Thus, further investigations, including experiments using animals, are needed
to confirm the the origin of these results.

Acknowledgements
7. Conclusions
The findings reported here show the timing difference
between the closure of the Ao valve and the pulsatile
waves on the IVS and the LV posterior wall, which werefirst able to be measured by the novel phased tracking
method. From the in-vivo experimental results, thepulsatile waves on the IVS and on the LV posterior wall
are caused just before and just after the closure of theAo valve, respectively. Thus, the pulsatile wave on the
IVS does not originate from the closure of the Ao valve
but originates in the myocardial contraction–relaxation
sequence. The waveforms and their power spectra in
Fig. 2 can be a significant clue for the diagnosis of the
myocardial viability. From the in-vivo experiments ofthis paper, the pulsatile wave on the IVS starts 20 ms
before the onset of the closure of the aortic valve. In

This work was supported in part by a Grant-in-Aid
for Scientific Research (No. 10555134, 10650400) from
the Ministry of Education, Science and Culture of Japan,
and in part by the Sound Technology Promotion
Foundation.

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