Journal of Cardiology 69 (2017) 462–470

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Journal of Cardiology
journal homepage: www.elsevier.com/locate/jjcc

Original article

Deformability of the pulsating left ventricular wall: A new aspect
elucidated by high resolution ultrasonic methods
Motonao Tanaka (MD, PhD, FJCC)a,*, Tsuguya Sakamoto (MD, PhD, FJCC)b,
Shigeo Sugawara (MD, PhD, FJCC)a, Yoshiaki Katahira (MD, PhD, FJCC)a,
Kaoru Hasegawa (MD)a, Hiroyuki Nakajima (RMS)a, Takafumi Kurokawa (RMS)a,
Hiroshi Kanai (PhD)c, Hideyuki Hasegawa (PhD)ca

Cardiovascular Center, Tohoku Pharmaceutical University Hospital, Sendai, Japan
Hanzomon Hospital, Tokyo, Japanc
Department of Electrical Engineering, Tohoku University, Sendai, Japanb

A R T I C L E I N F O

A B S T R A C T

Article history:
Received 2 November 2015
Received in revised form 6 January 2016
Accepted 1 February 2016
Available online 22 March 2016

Background: Although the deformability of the left ventricular (LV) wall appears to be important inmaintaining effective cardiac performance, this has not been debated by anyone, probably owing to the
difﬁculties of the investigation.
Objectives: This study applies a new technology to demonstrate how the LV wall deforms so as to adjustfor optimum cardiac performance.
Subjects and methods: Ten healthy volunteers were the subjects. Using echo-dynamography, an analysis
at the ‘‘microscopic’’ (muscle ﬁber) level was done by measuring the myocardial axial strain rate (aSR),
while the ‘‘macroscopic’’ (muscle layer) level contraction-relaxation/extension (C-R/E) properties of the
LV wall were analyzed using high frame rate 2D echocardiography.
Results: Deformability of the LV was classiﬁed into three types depending on the non-uniformity of both
the C-R/E properties and the aSR distribution.
‘‘Basic’’ deformation (macroscopic): The apical posterior wall (PW) thickness change was concentricand monophasic, whereas it was eccentric and biphasic in the basal part. This deformation was large in
the PW, but small in the interventricular septum (IVS). The elongation of the mitral ring diameter and the
downward movement of its posterior part were shown to be concomitant with the anterior extrusion of
the PW.
‘‘Combined’’ deformation (macroscopic and microscopic): This was observed when the basic
deformation was coupled with the spatial aSR distribution. Three patterns were observed: (a) peristaltic;(b) bellows-like; and (c) pouch-like.
‘‘Integrated’’ deformation: This was the time serial aSR distribution coupled with the combined
deformation, illustrating the rotary pump-like function.
The deformability of the LV assigned to the apical part the control of pressure and to the basal part,ﬂow volume. The IVS and the PW exhibited independent behavior.
Conclusions: The non-uniformity of both the aSR distribution and the macroscopic C-R/E property were
the basic determinants of LV deformation. The apical and basal deformability was shared in LV
mechanical function.
ß 2016 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

Keywords:
Deformability
Contraction-relaxation/extension property
Bellows action
Peristalsis
Pouch-like deformation

Introduction* Corresponding author at: Cardiovascular Center, Tohoku Pharmaceutical
University Hospital, Fukumuro 1-12-1, Miyagino-ku, Sendai 983-8512, Japan.
Tel.: +81 22 719 5161; fax: +81 22 719 5166.
E-mail address: m.tanaka@jata-miyagi.org (M. Tanaka).

The deformability of the left ventricular (LV) wall may be an
indispensable determinant of smooth and effective LV mechanicalperformance [1,2]. However, this concept was not noticed byprevious researchers. Although it might have been speculated, itwould have been difﬁcult to investigate because of the poor spatial

http://dx.doi.org/10.1016/j.jjcc.2016.02.009
0914-5087/ß 2016 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

M. Tanaka et al. / Journal of Cardiology 69 (2017) 462–470463

resolution of past investigative methods [3–11], such as X-ray,magnetic resonance imaging (MRI), and conventional 2D echocardiography, including the speckle tracking method. Also, theexperimental studies [12–16] and artiﬁcial cardiac models[17,18] are not physiological, and cannot observe the phenomenaof the living heart moving under ‘‘negative pressure’’ in the thorax[19–24]. The present study attempts to challenge this difﬁcult
problem by using the high-resolution non-invasive methodology(echo-dynamography) to conﬁrm the signiﬁcance of the deformability for LV performance.
Objectives
We attempted to disclose LV wall deformability in situ using
echo-dynamography which has been heretofore repeatedly
described. The ‘‘microscopic’’ method (to the muscle ﬁber level)measured the axial strain rate (aSR) using the phase difference
tracking method [25–29]. The ‘‘macroscopic’’ method (to themuscle layer level) observed the morphology using high frame rate
2D echocardiography. In addition, the spatial and time serial
behaviors [7,8,30,31] were observed.
Subjects and methods
Ten presumably healthy volunteers aged 30–50 years(39.6  10.4 years) who had given informed consent were thesubjects. They are working in our laboratory, and volunteers with pastand present history of adult disease were not included in this study.
Acquisition of the information
The information of the wall dynamics was obtained using thespecially designed ultrasonic machine (Aloka 6500 model, Hitachi
Aloka Medical, Tokyo, Japan). While the examinee was in thesupine or left lateral decubitus position, a transthoracic parasternal
908 sector scan was passed through three points (center of both theaortic and the mitral oriﬁces and the LV apex) so as to include thecenter of the LV, the left atrium (LA), and both axis lines of theinﬂow and outﬂow. This plane was named ‘‘longitudinal section
plane [32]’’ and the LV structure was symmetrical with this plane(Fig. 1). The rectangular plane perpendicular to this was named‘‘short-axis plane’’ throughout which 3D measurement of the LV
was done from the apex to base precisely. Then, we measured theintra-ventricular blood ﬂow [30,31] and the LV mechanicalphenomena with minimum acoustical measurement error[8,33,34].
Measurement of the macroscopic (muscle layer level) dynamics of the
LV wallA high speed of 66 frame/s with 3.5 MHz in frequency and
4.5 KHz in repetition rate was used for 2D echocardiography[7,8,32]. A 908 scan from the base to the apex was performed.
During one cardiac cycle, the images of continuous 30 frames ofevery 30 ms were analyzed at each of the 3 points, that is, the apical(A: just above the papillary muscle level), basal (B: ca 10 mm apartfrom the mitral valve ring), and central (C: in the middle of A and B)(Fig. 1).
The thicknesses of the posterior wall (PW) and the interventricular septum (IVS), and the internal diameter of the LV were
measured, respectively. Mitral valve ring diameter (MRD) and themitral ring movement (MRM) were also measured.
Selected heart rate was about 70/min and the time course of the
cardiac cycle of each case was corrected by R–R interval after
Bazett’s equation to stabilize the data among the subjects.

Fig. 1. Measurement methods of the structure change of the LV wall by high frame
rate 2D echocardiography and of the high-resolution axial strain rate (aSR) by phasedifference tracking method. Cardiac structures conﬁrmed by 2D echocardiogram.
The 1–3 beam directions to parts A (apical), C (central), and B (basal) were decided
on the long-axis section plane. In the aSR method, the beam direction was decided
on the systolic maximum image. The received echo signals from the wall for about
6 s were stocked in the digital memory and processed off-line by using our own
developed software. The aSR at the point area on the beam was calculated by thebottom equation (strain rate). Details were shown in the previous papers[35,37]. MRD, mitral ring diameter; US beam, ultrasonic beam; LV, left ventricle;
End, endo-cardium; Epi, epicardium; v(x1i; t), velocity at the point of x1; v(x2i; t),velocity at the point x2.

Measurement of the microscopic (muscle ﬁber level) dynamics of the
LV wall by the aSR
For methodological reasons, we measured the myocardial ﬁber‘‘thickness’’ change instead of the change in the ﬁber ‘‘length’’. Thisis because the change in the pulsating myocardial ﬁber length is ininverse proportion to the thickness [21–23], which is easily andaccurately measured by the present methodology.
The ultrasound used was 3.75 MHz in frequency and 133 ms in
the pulse repetition interval. The limited angle of each 308 out of
908 was scanned at a high speed of 630 frame/s from the base to theapex (sparse scan) (Fig. 1A–C). The B point was decided from the
maximum systolic image. The thickness (821 mm) was measured
at the microscopic level with a high spatial resolution of 200 mm
by using the phase difference tracking method of ultrasound[26,27]. Furthermore, the non-uniformity of the contraction andextension in the local myocardium was estimated from the resultof the spatial aSR distribution [25–29,32,35].
The calculated aSR was displayed on the M-mode images. The
cold color indicates the increment of the aSR [contraction: aSR(+)]
and the warm color, the decrement [extension: aSR()]. In thisregard, the relaxation (B1) (no active movement) is indicated byblack color, where there is nearly no contraction nor extension (themuscle is completely relaxed either in systole or in diastole).

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Statistical analysis
The present study did not include a precise statistical analysis.
The reasons were as follows:
The inscribed graphs and the measurement values were nearly
identical throughout all subjects. There were no visible unavoidable
variations in most of the medical study. Mild heart rate variability
was present, but it was corrected by Bazett’s equation. It was truethat individual subjects had slightly different measurement values
in the wall thickness and internal dimension, etc., however, thevariations are dependent on and parallel to the individual size anddimension. So, to take a mean and deviation of all subjects ismeaningless or may be misleading in this study in which all theitems had the same changing direction. Essentially, this study was
rather ‘‘physical’’ but not physiological or medical, so that it may bequite difﬁcult to obtain the conclusion if there was variability of thedata as seen in the clinical study. The data once stored in the MO-discgave exactly the same results, whenever it was rechecked by any
collaborators, so there was no observer variation- or test-to-test
variability. This is the reason why the present article shows only one
example in the ﬁgures. The authors believe that the limited 10 cases
are sufﬁcient to discuss and conclude the results.
Results
When the heart rate was corrected by R–R interval, the timeserial changes in the wall thickness and displacement, and theinternal diameter during one cardiac cycle showed the sametendency in all cases. Therefore, one example is shown in Fig. 2, andthe ratio to the apical data is listed in Tables 1 and 2.

Fig. 2. The various time serial LV changes measured from the successive 30 frames at every 30 ms using long-axis section plane of the high frame rate 2D echocardiograms.
Out of the similar measurement values in 10 cases, a representative case is presented. Top: Changes in the IVS and PW thickness measured at three parts (A, apical: green
triangle; C, central: red square; B, basal: blue rhombus) during cardiac cycle. The numbers indicate the contracting speed of the myocardium (mm/s), the changes of the wall
thickness (mm) and the time interval (ms) between the peak point of the contraction in the three parts. The red thick vertical arrows indicate simultaneous contraction andextension (large arrow, apical contraction and basal extension coexisted; small arrow, basal contraction and apical extension coexisted). Bottom: Changes in the internal
diameter at the three parts (symbols are the same as the top ﬁgure), changes in the mitral valve ring diameter (MRD: brown dotted line), and changes in displacement of theposterior part of the mitral ring movement (MRM: yellow dotted line). The numbers are the same as those in the top ﬁgure. The area ﬁlled with the blue color shows the effectof the bellows-like deformation, and that with the orange color, the effect of the pouch-like deformation. PW, posterior wall; IVS, interventricular septum; Is, 1st heart sound;IIs, 2nd heart sound; IC, isovolumetric contraction; Ej, ejection; IR, isovolumetric relaxation; SF, slow ﬁlling; AC, atrial contraction; ERF and LRF, early and late rapid ﬁlling;
pre-ET, pre-ejection transition; post-ET, post-ejection transition; P,Q,R,S,T, ECG symbols.

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Table 1
Changes in wall thickness.
A

C

B

Minimum (D) (mm): (Min)Maximum (S) (mm): (Max)Max/Min(Max/Min) vs A
(Max  Min)/Min(Max  Min)/Min vs A
(Max  Min)
(Max  Min) vs A

7.5 (St)
12.0
1.60
1.00
0.60
1.00
4.50
1.00

6.7
12.0
1.79
1.12
0.79
1.32
5.30
1.17

4.8
11.0
2.29
1.43
1.29
2.15
6.20
1.37

Contracting velocity (mm/s)(St  Min) (mm)Velocity difference
Contracting velocity vs A

17
0.0
0
1.00

22
0.8
5
1.29

27
2.7
10
1.59

PW

IVS

A

C

B

Minimum (D) (mm): (Min)Maximum (S) (mm): (Max)Max/Min(Max/Min) vs A
(Max  Min)
(Max  Min)/Min(Max  Min)/Min vs A

7.5
12.0
1.60
1.00
4.5
0.60
1.00

7.3
11.2
1.53
0.96
3.9
0.53
0.88

6.1
9.5
1.56
0.98
3.4
0.55
0.92

Contracting velocity (mm/s)

19

16

12

Wall thickness in the posterior wall (PW) and the interventricular septum (IVS)
measured at the three parts [apical(A), central (C) and basal part (B)] in the
maximum [systole, Max(S)] and the minimum [diastole, Min(D)] points during
one cardiac cycle shown in Fig. 2.
Measurement data by the ratio (Max/Min), Max/Min vs A (i.e. Max/Min
compared with the same ratio in the Apex), and others are shown. The
contraction velocity is referred to estimate the contractility of the local LV wall.
St, standard value (7.5 mm: end-diastolic thickness).

Fig. 3. Schematic representation of the basic deformation. Top: Deformation of the
LV wall in the short-axis section planes. Schematic ﬁgures of Table 1 and Fig. 2,
illustrating the changes in the LV wall thickness and internal diameter. Large circles,
end-diastole; small circles, end-systole; IVS, interventricular septum; PW, posterior
wall; HL, horizontal line. Bottom: The time serial thickness change of the posteriorwall (PW) at the basal (B) and apical (A) parts. The yellow area shows the extension
and the brown, the contraction. AC, atrial contraction; IC, isometric contraction; Ej,ejection; IR, isometric relaxation; RF, rapid ﬁlling; SF, slow ﬁlling. (St), the standard
value (7.5 mm: end-diastolic thickness); pre-ET, pre-ejection transition; post-ET,
post-ejection transition.

LV wall dynamics macroscopically measured
The wall thickness change at the three parts (A, C, B) (Fig. 2 top,
Table 1)
The normal myocardial thickness was ca 11–12 mm in the
maximum systolic level (Max) in all parts.
Apical part (A) (Fig. 2 top, green line): The PW thickness
showed a 60% increase at the maximum from the enddiastolic minimum {i.e. (Max  Min)/Min = (12.0  7.5)/7.5 =0.60} (Table 1, Fig. 2 top, 7.5 = standard thickness; St). The change
in the IVS was nearly identical (ca 56%), so that the LV cylindricallyshrank, leading to the monotonously concentric wall thickening(see Fig. 3 top left).
Basal part (B) (Fig. 2 top, blue line): The PW thickness change
was not simple. It decreased 2.7 mm from 7.5 mm (St) to 4.8 mm
during ejection (Ej), although the dimension in this part was
enlarged (vide infra). Then it increased 3.5 mm (47% of the St) by
the contraction from the isometric relaxation (IR) to the rapid
ﬁlling (RF) (Fig. 3, bottom B). Thus the basal wall thickness change
was not monotonous but biphasic due to the initial thinningfollowed by the thickening during one cardiac cycle.
Central part (C) (Fig. 2 top, red line): Although the thickness
changes were nearly the same as those of the apical part, themaximum contraction to the extending deformation during the RF
was ca 3 times faster compared to that in the basal part.
Velocity of muscle contraction in each part (Table 1,
contracting velocity):
The increment of the wall thickness was less in the basal part
than that in the apical part (47% vs 60%). However, the contracting
velocity in the basal part (mm/sec) was greater than that in theapical part (27 mm/s vs 17 mm/s), reﬂecting the contracting powerin the basal part by the contraction added the preload [19,20].
The speed for recovering from 12 mm to the standard thickness
in the central part was faster than that in the apical part (67 mm/s

vs 19 mm/s; Fig. 2, top), indicating the rapid extending deformation in this part during the RF by a part of the bellows movement
and the pouch-like deformation with the late systolic basal
contraction.
Speciﬁcity of the IVS: The IVS thickness increase duringcontraction in all three parts (A, C, and B) was almost identical. Thiswas evidenced by the ratio of (Max/Min)/Ap (= from 1.00 to 0.96)(Table 1, bottom). Contrary to the PW, there was no biphasic
thickness change in the basal part. So, the behavior of the IVS wasconsiderably different from that of the free wall and was intrinsic
to the eccentric deformation in the basal part of the LV during Ej.
Time serial changes of the PW thickness (Fig. 2 top, Fig. 3)
The PW increase in thickness (contraction) at the apical part (A)started in the early pre-ejection transitional period (pre-ET)
coincident with the P wave of the electrocardiogram from theendocardial side of the LV wall and reached the maximum in the
middle of Ej (Fig. 3, bottom A). Then it decreased (extension)
gradually toward the late rapid ﬁlling (RF). Thus, the apical part
had its contraction up to the mid Ej followed by the extension.
Thereafter, there was no remarkable change (Fig. 3, bottom A: SF
period).
On the contrary, the thickness in the basal part (B)unexpectedly began to decrease (extension) from the early preET, and reached the minimum in the early Ej period (Fig. 3, bottom
B). The thickness increase, which was delayed, began in the late Ej
toward the late RF (LRF) and gradually returned to the initial
thickness.
Observing the correlation between the time serial changes, theapical contraction (thickness increase) and the basal extension(thickness decrease) of the PW occurred coincidentally during the
Ej phase (Fig. 2 top, large vertical red arrow), and further the apicalextension occurred simultaneously with the basal contraction

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466
Table 2
Changes in internal diameter.
ACB(B  A)Ej(B  A)RF

Maximum (D) (mm): (Max)Minimum (S) (mm): (Min)Max vs A
Min vs A(Max  Min)
(Max  Min)/Min(Max  Min)/Min vs A
Max/St(Max/St) vs A

39.0
32.0 (St)
1.00
1.00
7.0
0.22
1.00
1.22
1.00

42.5
33.0
1.09
1.03
9.5
0.29
1.32
1.33
1.09

49.0
35.5
1.26
1.11
13.5
0.38
1.73
1.53
1.25

10
3.5

12
3.5

2.9

3.4

Contracting velocity (mm/s)

52

54

26

Internal diameter changes of the left ventricle (LV) at the three parts (Table 1) inthe maximum [diastole, Max(D)] and the minimum [systole, Min(S)] points
during one cardiac cycle in Fig. 2.
A, apical data; St, standard value (32.0 mm: end-systolic diameter); (B  A)Ej,
difference between B and A at the IC phase; (B  A)RF, difference between B and
A at the end of the RF point.

during the LRF phase (Fig. 2 top, small vertical red arrow). This
indicated the non-uniform contraction of the PW.
Discrepant changes in the LV wall thickness and the concept of
peristalsis
As shown in Fig. 2 top, and schematically shown in Fig. 3
bottom, the wall contraction started from the apex and was
followed by the delayed basal contraction. Namely, the contraction
transmitted from the apical part to the basal part. The onset, themaximum, as well as the end of the contraction of the PW and IVS
occurred at the apical (A), central (C) and basal (B) parts in thisorder. This conﬁrmed the presence of the ‘‘peristalsis’’ of the PW
and the IVS.
The time discrepancy in the maximum thickening between theapical and the basal part in the PW was about 210 ms (A–C = 120 ms, C–B = 90 ms) and about 180 ms in the IVS (Fig. 2, top).

Fig. 4. Schema represents the deformability of the posterior wall and the mitral ringin the long-axis direction. A, B, and C, end-diastolic points at the apical (A), basal (B),and central (C) parts; B0 , C0 , end-systolic points (Apical point is ﬁxed); during cardiac
cycle, the points B (basal) and C (central) move to the points B0 and C0 . The change in
the internal diameter during systole is depicted by the distance between the paired
blue arrows in the Max and Min at points B and C (cf. Table 2). The percentage
numbers (%) are the changing ratios to the apical diameter (A). Red line is the mitralring diameter (long: systole, short: diastole), broken line: period of extension,+61% = increment of the ring diameter during systole compared with that at theendo-diastole. Ao, aorta; MV, mitral valve; LV, left ventricle; orange colored area, LV
wall and interventricular septum.

Changes in the LV internal diameter and the sequel (extruding
deformation)

beyond the IR, while the diameters of these parts were increasingat the same time.

Changes at the three parts of the LV (Fig. 2, bottom, Fig. 3, Table 2)
Another feature of LV deformability was the effects of thechanges in the internal diameter. The measured data for each partare shown in Table 2, where the Max(D) is the so-called maximum
end-diastolic, and the Min(S), the minimum end-systolic dimensions.
As each diameter changed concomitantly with the wall
thickness changes, the shape of the LV and also the mitral valve(vide infra) were obliged to change as schematically shown in
Fig. 4.
When compared with the apical part during so-called diastole,
the Max(D) in the central and basal parts was bigger by 9% and26%, respectively; however, the Min(S) during so-called systole
was smaller in C and B, i.e. only 3% and 11%, respectively (Fig. 2;
shaded blue area). This indicated much more dilatation in thecentral and basal parts during the apical end-systolic phase, theincrease of which was 32% (part C) and 73% (part B). Thus, thecontraction of the LV wall was not equal, indicating that the apicalcontraction promoted the rather ‘‘systolic’’ dilatation, particularlyin the basal part.
Moreover, central diameter [Min(S)] (Fig. 2, middle; red line)
was transiently less than that of the apical part (green line) during
the late systolic phase, indicating the ‘‘systolic extruding
deformation’’ toward the LV cavity. Also, it should be mentionedthat the central and basal PW were still continuing to thicken

Time serial change of the internal diameter in the LV (Fig. 2, bottom)
The difference in the diameter between the apical (green line)
and the basal parts (blue line) was about 10 mm in the IC period,
but it decreased rapidly to about 3.5 mm in the RF period (bluecolor area). The nearly parallel movement of these two lines wasdue to volume change and was regarded as the ‘‘bellows-likedeformation’’ during the LV contraction.
Thereafter, this difference rapidly increased toward the SF
period due to the LV ﬁlling (orange color area) followed by the
gentle expansion of all parts.
Among them, it is of note that there was a rather rapid increasein the diameter of part C, which indicated the prompt recovery
from the extruding deformation described above, which will be
related to the RF described below.
When the thickness in the basal part of the PW was at the
maximum during the LRF the apical and central parts were at theminimum (Fig. 2, top), indicating the inevitable expansion of theseparts.
Changes in the mitral valve ring diameter (MRD) and the valve ring
movement (displacement: MRM)
Changes in the diameter (brown line in Fig. 2, bottom; MRD)The MRD increased in average from ca 15.4 mm in the IC to ca
25.0 mm in the end of the early RF (ERF) during Ej (ca 61% increase).

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467

Then, it rapidly deceased during the late RF (ca 18 mm; about 40%)
followed by the further decrease (about 20%) toward the next IC.
Systolic increment of the MRD resulted in the increase in thesurface area of the valve ring and then the volume of the left atrium(LA). The change in the ring conﬁguration from circular to oval andthe rapid upward movement of the ring during the RF caused theLV swallowing action to the intra-atrial blood. This is the ‘‘pouch
like’’ action (Fig. 4).

When the maximum PW contraction at the basal part appearedconcomitant with the relaxation at the central and apical parts(Fig. 2 top; LRF), the rapid MRD decrement and the rapid incrementof the MRM were observed (Fig. 2 bottom; LRF). These results were
reﬂected in the ‘‘sphincter-like action’’ surrounding the inﬂow
oriﬁce and the ‘‘pouch-like deformation’’ in the basal part together
with the hinge movement of the mitral valve ring (ca 15 mm)(Fig. 4).

Displacement of the posterior part of the mitral valve ring (MRM)

Correlation between the LV deformability and the non-uniformity ofthe myocardial C/E property

The mitral ring moved ca 15 mm downward during the Ej(yellow line in Fig. 2, bottom) and reached the lowest level at theearly RF (Fig. 4B–B0 , a part of the bellows action). At this time, themaximum contraction of the central part in the PW appeared.
When the muscle showed the maximal contraction in the basalpart, rapid upward movement of the ring accompanied with therapid expansion of the central part of the LV occurred during the RF(recovering from the extruding deformation of the LV) and reachedthe upper level at the end of the late RF. Then the maximum
displacement (ca 24 mm) was seen at the atrial contraction (AC).

Fig. 5 is a modiﬁcation of the ﬁgure from the previous paper[36]. It was demonstrated that the C/E property estimated by theaSR distribution spatially and time sequentially was unexpectedly
very complex. Myocardial contraction and extension were notalways cooperative and the synergism of the muscle ﬁbers was notnecessarily present in every muscle layer in the same location of
the LV wall.
The ‘‘toned’’ distribution (Fig. 5B, iii), where the ‘‘regional’’
myocardium had a different magnitude (intensity) of the aSR, wasFig. 5. M-mode aSR distribution images obtained at three points (B: basal, C: central and A: apical) during the slow ﬁlling (SF) through the ejection (Ej). The aSR distribution
data obtained simultaneously in the three beam directions (red lines on the 2D echocardiogram). i, ii, iii, iv, Bl, classiﬁcation of the spatial aSR distribution pattern; i, spotted;
ii, multi-layered; iii, toned; iv, stratiﬁed; Bl, relaxation; ES, early stage; LS, late stage; Alt 1, Alt 2, alternating 1, alternating 2; Ct, contracting superﬁcial cardiac muscle; AC,atrial contraction; IC, isometric contraction; Ej, ejection; IR, isometric relaxation; RF, rapid ﬁlling; SF, slow ﬁlling. (St), the standard value (7.5 mm: end-diastolic thickness).

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M. Tanaka et al. / Journal of Cardiology 69 (2017) 462–470

observed in the Ej, resulting in the monotonous deformation of thebasal PW and IVS.
The ‘‘multi-layered’’ distribution (Fig. 5C, ii) showed thesimultaneously contracting and extending muscles. Namely, theopposite aSR was piled up on the other. This was observed in theapical and central PW during the IC and the Ej.
Of the mixed pattern, the ‘‘spotted’’ distribution (Fig. 5A, i)appeared during the Ej in the apical part, and the ‘‘stratiﬁed’’
distribution (Fig. 5B, iv) was seen in the SF.
In between SR(+) and SR(), there was the widely spread
distribution Bl (black zone), where neither contraction nor
extension was observed. Namely, the muscle ﬁber was nearly orcompletely relaxed (real relaxation) during either diastole or evensystole. Thus the myocardial muscles essentially had non-uniform
activities.

Discussion
Since the era of M-mode echocardiography, we have noticed
that the timings of the maximal systolic contraction of either the
IVS or the PW are not simultaneous [36] and usually the peak of
intrusion of the PW into the LV is slightly delayed. Such a nonuniform change in the length or thickness of the myocardial ﬁber
was veriﬁed in the present study. In fact, this induces the distortionof the myocardial tissue [35,36] and so deforms the wall [1,2].
This deformation is three-dimensional, therefore, the numerous
short-axis sections perpendicular to the long-axis plane were three
dimensionally stocked from the apex to the base and these
constituted the fundamental measurement source of the present
study. The study of the macroscopic (muscle layer) and themicroscopic (muscle ﬁber) levels afore-mentioned [8,27,30]
disclosed three types of deformation named (1) basic, (2)combined, and (3) integrated deformations which constitute the
LV wall dynamics.
The signiﬁcance of the basic deformation (Figs. 3 and 4)
The macroscopic study included the change in the LV wall andthe mitral valve deformity. First, the thickness change in the IVS
was slight, whereas change in the free wall (represented by thePW) was quite different.
Namely, the wall thickening was concentric and monotonous at
the apical part, while it was biphasic in the basal part (Fig. 3,
bottom). Furthermore, the behavior of the central part was in
between them, i.e. the extruded deformation toward the LV cavity
during systole followed by the brisk rebound during diastole.
It is of note that, contrary to expectation, the ‘‘systolic
thickening’’ and the ‘‘diastolic thinning’’ of the LV wall do notnecessarily indicate the classically deﬁned ‘‘systole’’ and ‘‘diastole’’, respectively. At the time of the apical thickening, whichstarted prior to the classical systole, the basal part showedthinning even during classical systole. Also, the division of thecontraction and the extension differs depending on the part of the
LV wall. During classical systole, both contraction and extension
in the LV wall coexisted. Also during classical diastole, the same
was true, i.e. the LV extension and contraction co-existed.
Therefore, the division of the systole and diastole in a sense ofclassic cardiac physiology is nothing but the clinical use, i.e.
electrocardiogram, direct or indirect pressure tracings or heartsounds and phonocardiogram.
The simultaneous LV internal diameter change observed in thelong-axis section was also important. Concomitant with thesystolic downward displacement of the lateral side of the mitralring and the enlarged circular deformation, there was the extruded
PW deformation of the central part toward the LV cavity (Fig. 4).

This was associated with the greatly enlarged internal diameterof the basal part which helped the bellows action described below.
In the late systole, the decreased valve ring diameter and theabrupt upward displacement (sphincter movement) caused thepouch-like deformation.
The basal part played an important role. Combined with thelarge change in the internal diameter on the one hand andrelatively small thickness change on the other hand, this partworks just like the controller for blood ﬂow volume and structurewith high mechanical efﬁciency regarding the LV function. This
importance, however, has not been discussed yet by anyone.
The apical part played an important role as the generator andcontroller of the intra-ventricular pressure. This was evidenced by
the big thickness change and relatively small diameter change.
The work of the central part (mid-ventricular portion) was justlike the hinge of the PW movement. In between the apical andbasal parts, the accelerating ejection was enhanced by its ‘‘bellows
like’’ effect, and also the suction effect [36] for the mitral inﬂow
was introduced by the extrusion during the RF phase.
The signiﬁcance of the combined deformation
This is just like an extended spectrum of the basal deformation
by adding the microscopic C-R/E properties using the aSR.
Peristaltic deformation
This peristaltic deformation is conﬁrmed by the apical to basaltransition of the contraction with the appropriate time lag (210 ms
in the normal case) (Fig. 2). This is reasonable to understand thesqueezing effect of the LV during the systolic phase [32] and thesuction effect in the diastolic phase [36].
Bellows-like deformation
The aSR study disclosed that in the Ej phase, the contraction of
the PW progressed from the epicardial side to the endocardial sideand that of the IVS, from the right ventricular (RV) side to the LV
side. The extrusion of the central PW into the LV cavity and thevarious mitral ring movements, both assist the eccentric deformation (Fig. 6, Ej), resulting in the bellows-like movement which gives
the forceful LV ejection [32] (the area ﬁlled with the blue color in
Fig. 2).
Pouch-like deformation
In the late Ej and post-ET period (basal contraction and apicalextension coexist), the special form of the deformation named‘‘pouched-like’’ was seen [35,36] (Fig. 6 LS-ERF, LRF). Thereafter,
the rapid LV dilatation occurs by the movement of the apical andthe central parts (Fig. 6 LRF-SF). Meanwhile, the paravalvular
muscle acts as the sphincter to the inﬂow oriﬁce which occurs withthe elliptical deformation of the mitral ring. This rather uniquepouch-like deformation is valuable to swallow the mitral inﬂow by
the sucking effect of the LV [37] during the RF (Fig. 6 SF).
The integrated deformation
As previous reports stated [35,37], the cardiac cycle iscomposed of four phases. The overlap of the contraction and theextension exists, and in total, the length of contraction andextension is equal. The overall deformation is the integrated
deformation, as schematically shown in Fig. 6, and which isbrought up en bloc on the right column.
Fig. 6 shows the sequence of the wall movement due to thedeformation. In the right column, blue arrows indicate theM. Tanaka et al. / Journal of Cardiology 69 (2017) 462–470

469

Fig. 6. Schematic representation of the LV deformability in the longitudinal section plane during a cardiac cycle. Left column shows the propagating process of the contraction(blue thick arrows), and middle column, the extension (red thick arrows) propagate from the apical to the basal parts. Yellow area, extending area; brown area, contracting
area; orange area, tension area; blue thick arrows, magnitude of contraction; red thick arrows, magnitude of extension; black arrows, direction and magnitude ofdisplacement of the wall; thick black arrow T, circumferential tension; light blue arrow P, local pressure change; black arrow F, ﬂow direction; AC, atrial contraction; IC,
isometric contraction; Ej, ejection; SF, slow ﬁlling; LS-ERF, late systole-early rapid ﬁlling; LRF, late rapid ﬁlling. Right column: En bloc diagram is the overlapping display of the
LV in the early systole and diastole showing the integrated deformation of the LV wall during a cardiac cycle. Periodical and reciprocal deformations between the apical andthe basal parts are demonstrated. The horizontal dotted line passing through the center signiﬁes an imaginary boundary line of the reciprocal deformation. Details: see thetext. Yellow area; extending area, brown area, contracting area; red arrow, deforming direction and magnitude of the LV wall in diastole; blue arrow, deforming direction andmagnitude of the LV wall in systole; LV, left ventricular; PW, posterior wall; IVS, inter-ventricular septum; horizontal dotted line, imaginary boundary line; AV, aortic valve;
MV, mitral valve.

simultaneous apical contraction and the basal extension duringsystole, and red arrows, the simultaneous basal contraction andthe apical extension during diastole. In between, the dotted line
indicates the imaginary boundary zone crossing the central part.
In total, the concrete results of the present study substantiallydiffer from the ordinary physiological concept of LV wall motion.
The LV pressure (P) develops by contraction when the internal
diameter decreases (Fig. 6 IC). Simultaneously, however, the basal
part dilates producing a large eddy ﬂow in the basal area [32](symbol F in Fig. 6 IC). Successively, the contractions of the central
and basal parts (extruding of the PW) conduct LV ejection (Fig. 6Ej), and also result in the apical extension (Fig. 6 LS-ERF). The
progressive LV dilatation (pouch-like deformation) (Fig. 6 LRF) isfollowed by the successive and gentle extension (Fig. 6 SF) and thenthe atrial contraction (Fig. 6 AC).
Whenever this reciprocal deformation occurs periodicallyduring a cardiac cycle, the proﬁle of the LV dynamics will be justlike that of a rotary pump with continuous circular movement
without any pause or any overload in any speciﬁc part. It mightplay an important role in preventing sudden changes in LV functionin either pressure, volume, or heart rate. A disorder of thisdeformation may produce various mechanical dysfunctions justlike the takotsubo cardiomyopathy, although further studies arenecessary to obtain clinical implications.

Study limitationsFirst, the small number of subjects makes it impossible togeneralize our results and precludes strong statistical conclusions,although a self-controlled design in this study may have made theresults more reliable. The subjects are presumably healthy adults,
but a small effect from age differences may not be excluded. Also, it
may be more accurate to present high-resolution movie images tobetter understand the results.
Second, both of the present technologies of ‘‘phase difference
tracking method in ultrasound’’ and ‘‘high frame rate 2D
echocardiography’’ have not been widely used because they weredeveloped in our laboratory. Therefore, the present results might
not be easy to acknowledge particularly to those who adhere to the
traditional physiological concept, although the present study does
not necessarily deny the previous noninvasive studies.
Third, we did not refer to or compare with the large amount ofliterature, and could not refer to a comparative study. We postpone
our ﬁnal conclusions.
Conclusions
By using the high frame rate 2D echocardiography and the aSR
distribution developed by us, the deformability of the LV

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470

throughout the cardiac cycle was investigated. We found that the
non-uniformity of the myocardial contraction and the axial strain
rate (aSR) distribution of the myocardial ﬁbers were the principal
determinants of LV deformability. Based on these observations, thefollowing three types of deformations were established, i.e. basic,
combined, and integrated deformations. The integrated deformation seemed to have the identical mechanism to a rotary pump andwas regarded as the ﬁnal feature of the smooth, tireless, and quite
efﬁcient cardiac beat.
Funding
This research received no grant from any funding agency in the
public, commercial, or not-for-proﬁt sectors.
Conﬂict of interest
The authors declare that there is no conﬂict of interest.
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