Journal of Cardiology 64 (2014) 401–408

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

Original article

Non-uniform distribution of the contraction/extension (C–E) in theleft ventricular myocardium related to the myocardial function
Motonao Tanaka (MD, PhD, FJCC) a,∗ , Tsuguya Sakamoto (MD, PhD, FJCC) b ,Yoshiaki Katahira (MD, PhD, FJCC) a , Haruna Tabuchi (MD) a , Hiroyuki Nakajima (RMS) a ,Takafumi Kurokawa (RMS) a , Hiroshi Kanai (PhD) c , Hideyuki Hasegawa (PhD) c ,Shigeo Ohtsuki (PhD) da

Cardiovascular Center, Tohoku Pharmaceutical University Hospital, Sendai, Japan
Hanzomon Hospital, Tokyo, Japanc
Department of Electrical Engineering, Tohoku University, Sendai, Japand
Institute of Medical Ultrasound Technology, Yokohama, Japanba r t i c l e

i n f oArticle history:
Received 2 December 2013
Received in revised form 5 February 2014
Accepted 18 February 2014
Available online 16 May 2014
Keywords:
Contraction/extension property
Axial strain rate
Phase difference tracking method
Non-uniformity of the C–E
Myocardial functiona b s t r a c t
Objective: We attempted to disclose the microscopic characteristics of the non-uniform distribution of
the contraction and extension (C–E) of the left ventricular (LV) myocardium using a new methodology(echo-dynamography).
Methods: The distributions of the “axial strain rate” (aSR) and the intra-mural velocity in the local areas of
the free wall including the posterior wall (PW) and interventricular septum (IVS) were microscopicallyobtained using echo-dynamography with a high accuracy of 821 ␮m in the spatial resolution. The results
were shown by the color M-mode echocardiogram or curvilinear graph. Subjects were 10 presumably
normal volunteers.
Results:(1) Both the C–E in the pulsating LV wall showed non-uniformity spatially and time-sequentially.
(2) The C–E property was better evaluated by the aSR distribution method rather than the intra-mural
velocity distribution method.
(3) Two types of non-uniformity of the aSR distribution were observed: i.e. (i) the difference of its (+)SR(contraction: C) or (−)SR (extension: E) was solely the “magnitude”; (ii) the coexistence of both the (+)
SR and (−)SR at the same time.
(4) The aSR distribution during systole was either “spotted,” or “multi-layered,” or “toned” distribution,
whereas “stratiﬁed,” “toned,” or “alternating” distributions were observed during diastole.
(5) The aSR distribution in the longitudinal section plane was varied in the individual areas of the wall evenduring the same timing.
(6) To the mechanical function of the LV, there was a different behavior between the IVS and PW.
Conclusions: The aSR and its distribution were the major determinants of the C–E property of the LV
myocardium. Spatial as well as time-sequential uniformity of either contraction or extension did notexist. The myocardial function changed depending on the assemblage of the aSR distribution, and by thesynergistic effect of (+)SR and (−)SR, the non-uniformity itself potentially served to hold the smooth LV
mechanical function.
© 2014 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

Introduction∗ Corresponding author at: Cardiovascular Center, Tohoku Pharmaceutical
University Hospital, Fukumuro 1-12-1, Miyagino-ku, Sendai 983-0005, Japan,
Tel.: +81 022 719 5161; fax: +81 022 719 5166.
E-mail addresses: m.tanaka@jata-miyagi.org, shin@jcc.gr.jp (M. Tanaka).

The mechanical pump function of the left ventricle (LV) is
performed by the sacciform structure with thick walls. It is constituted from the following 4 steps of the contraction and extension(C–E) property: i.e. (1) a cellular step including sarcomere; (2) a

http://dx.doi.org/10.1016/j.jjcc.2014.02.024
0914-5087/© 2014 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

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M. Tanaka et al. / Journal of Cardiology 64 (2014) 401–408

multi-cellular step; (3) a ventricular wall step (deformability); andﬁnally (4) the step of the intra-ventricular ﬂow structure causedby the deformation of the LV. In this respect, it has been said thatthe non-uniformity at each step leads to the uniformity of function
at the next step [1,2]. However, the actual feature of the nonuniformity of the C–E distribution in the myocardium has been
obscure until now.
In this study, we attempted to disclose the actual feature of thisnon-uniformity of the C–E distribution in each step and its clinicalsigniﬁcance using non-invasive echo-dynamography. This method
was used because of the difﬁculty of in situ study using conventional
methodology [1–8].

Subjects and methods
Subjects
Ten presumably normal volunteers aged 30–50 (39.6 ± 10.4)
years who gave informed consent were investigated.

Methods
Measurement of the axial strain rate distribution of the
myocardium
In the 2D echocardiography, as described previously [9–11],
the LV “longitudinal” section plane was used to minimize acoustical measurement error [9,10]. Perpendicular to this plane was theshort-axis plane. As shown in Fig. 1 top, the range of the angle of 30◦
out of 90◦ was scanned at a high speed of 630–700 frame/s, transiently switching 5 beam directions evenly from the base to theapex (1–5: sparse scan). The echo signals from the wall for about
2–6 s were recorded in the memory and processed off-line by using
our software [12–16].
The axial strain rate (aSR) in the local myocardial tissue of821 ␮m thickness was obtained by the bottom equation (Fig. 1)
using “the phase difference tracking method” [13,14].
The serial aSR distribution was obtained by shifting the measuring point of aSR at every 200 ␮m from the endocardium (End)to the epicardium (Epi) (the distance is about 10 mm). The minimum range of changes in the thickness accuracy was about 2 ␮m.
The time serial aSR distribution is displayed in the color-coded Mmode images (Figs. 2 and 3). The magnitude of the aSR is shown by
the color bar. The increment of the (+)aSR (contraction) is indicatedby the cold color (dark to light blue tone) and that of the (−)aSR(extension), by the warm color (red to yellow tone). In between,
the black zone (B in Figs. 2 and 3) indicates the relaxation shownnear zero aSR.

Measurement of the contraction and extension velocity
distribution
To verify the sensitivity and/or accuracy of the aSR measurementcompared with that of the previous conventional methodology[13,14], the intramural velocity at many points in every 0.2 mm
distance on 5 ultrasonic beams was measured at the same time.
These speed data were overlapped for display in curvilinear graphs(Fig. 4). The thick velocity curves indicated that the velocities at
every measuring point were different and non-uniform, and thethin curves indicated muscle ﬁber movement with the same velocity. Plus (+) or minus (−) signal was used for the advancing orreceding movement.

Fig. 1. Measuring process of the high resolution axial strain rate (aSR) in the
myocardium by the phase difference tracking method. Upper ﬁgure: After conﬁrmation of the heart structure in the longitudinal section plane, 5 beam directions were
decided. Middle ﬁgure: In each beam direction, the measuring range is decided,
e.g. from endocardium (End) to epicardium (Epi) and then, the measuring width(821 ␮m) was set. The velocity data [v(x1i ; t), v(x2i ; t)] at two terminal pointsof the measuring width were calculated under the assumptive intramural velocity of 1600 m/s [16] and using difference in the distance between two points[x2i (t) − x1i (t)]. The aSR was obtained by the equation [Si (t)] at the bottom. Whenshifting the measuring width at every 200 ␮m from End to Epi, the aSR distribution
in the myocardium along the beam direction was obtained. LV, left ventricular wall;End, endocardium; Epi, epicardium.

Results
The results obtained were similar in all 10 subjects examined.
A minor difference was seen in the heart rate among the subjects,
but the general tendency was unequivocal.
The C-R/E property evaluated by the aSR distribution
Along the short-axis direction, the areas of (+) and (−)SR usuallycoexisted and uniform behavior was not observed. The following
two types of aSR distribution were observed (Figs. 2 and 3).
(1) The black area (B in the ﬁgures, aSR ≈ 0; relaxation area) at theboundary between (+) and (−)SR;(2) No black area between (+) and (−)SR.
In addition, two types of non-uniform distribution wereobserved.

M. Tanaka et al. / Journal of Cardiology 64 (2014) 401–408

403

Fig. 2. M-mode images of the axial strain rate (aSR) distribution in the short-axis direction of the interventricular septum (IVS) and posterior wall (PW) measured on thelongitudinal section plane during systolic to early diastolic phase. These results were obtained in the beam directions 1–5. The cold color area shows an increment of the strain
rate [(+)SR; contracting] and the warm color area decrement [(−)SR; extending]. The black area (B, SR ≈ 0) shows relaxing or diastasis. The color bar demonstrates the gradeof the strain rate. IC, isovolumetric contraction; Ej, ejection; IR, isovolumetric relaxation; ERF, early stage rapid ﬁlling; LRF, late stage rapid ﬁlling; SF, slow ﬁlling; AC, atrial
contraction; pre-ET, pre-ejection transitional phase; post-ET, post-ejection transitional phase; white narrow oblique lines, beginning of the PW extension; white narrowvertical lines, beginning of the PW contraction; C, contracting muscle component (superﬁcial oblique muscle); i, Spotted D; ii, multi-layered D; iii, Toned D; iv, stratiﬁed D;
Alt 1, Alternating D1; Alt 2, Alternating D2; IVS, interventricular septum; PW, posterior wall; P,Q,R,S,T, ECG symbols.

(1) The magnitude of either the (+)SR or the (−)SR was unevenly
distributed(2) The non-uniform distribution produced by coexisting (+)SR and(−)SR during the same timing.
Non-uniformity in the spatial distribution of the aSR along theshort axis
Considering pre-ejection transitional (pre-ET), ejection (Ej),post-ejection transitional (post-ET), and slow ﬁlling (SF) phases,characteristics of the spatial aSR distribution at the apical, central,and basal parts in each cardiac phase displayed 5 varieties (Fig. 5
and Fig. 6).
Spotted distribution. Non-uniform distribution caused by dispersing the narrow and strong (−)SR as a spotted pattern in the basic

distribution of the (+)SR. Therefore, no black area was present. This
distribution was frequently observed during the Ej phase at the apical part of the free wall (PW) and inter-ventricular septum (IVS).
The (−)SR spot usually increased in the early ejection phase but
decreased in the late ejection phase (Fig. 5-i-1). In the rapid ﬁlling(RF) phase, the (+) and (−) were reversed (Fig. 5-i-2).

Multi-layered distribution. Non-uniformity was displayed by 2 or
3 layers, viz. (−)SR appeared in the endocardial side and (+)SR in
the epicardial side (Fig. 5-ii-1). Otherwise, (+)SR in the middle layer
was sandwiched by the endocardial and epicardial (−)SR (Fig. 5-ii2) during Ej. A three-layered pattern was usually observed at theapical and central parts and a two-layered pattern in the basal part404

M. Tanaka et al. / Journal of Cardiology 64 (2014) 401–408

Fig. 3. M-mode images of the axial strain rate (ASR) distribution in the short-axis direction of the interventricular septum (IVS) and posterior wall (PW) during diastolic
to systolic phase. These results were obtained in the beam directions 1–5 as shown in the 2D echo-cardiogram in the right middle ﬁgure. The cold color area shows anincrement of the strain rate [(+)SR; contracting] and the warm color area decrement [(−)SR; extending]. The black area (B, SR ≈ 0) shows relaxing or diastasis. The color bar
demonstrates the grade of the strain rate. Abbreviation: See Fig. 2.

of PW. No black area was observed at the boundary between (+)
and (−)SR.
Toned distribution. As shown in the middle left of Fig. 5, the nonuniformity was displayed by either (+)SR or (−)SR. The differencein the magnitude was displayed by the changes in the color grade.
This pattern was frequently observed at the basal part of the PW
and IVS during Ej (Fig. 5-iii-1) or RF (Fig. 5-iii-2). This indicated thatthe contraction in the Ej and the extension in the RF were propagated from the epicardial side to the endocardial side. This indicatedthe process of transmission of the contraction or extension within
the myocardium, and thus the process of displacement of the ventricular wall. In addition, the black area (SR ≈ 0, relaxation) was
frequently observed at the boundary area between (+) and (−)SR.
Stratiﬁed distribution. This type was displayed by the alternately
stratiﬁed arrangement of both the narrow (+)SR and (−)SR. Thiswas observed at the PW and IVS during the SF phase. The (−)SR
component at the epicardial side was larger than that at the endocardial side in the PW (Fig. 5-iv-1,2). In the IVS, it was larger at theLV side than at the right ventricular side (Fig. 3).
The black area (aSR ≈ 0) was observed widely both in the IVS
and in the endocardial side of the PW as well as at the boundary
area between (+) and (−)SR in the SF phase. This indicated that theactive outward extension occurred at the epicardial side, whereas
the diastasis or cessation of the myocardial activity occurred widelyin the endocardial side during the SF phase.
Alternating distribution. The following two types of distribution
were observed.
(1) The special multi-layered distribution type (Fig. 5-v-1), in
which (+)SR at the endocardial side and (−)SR at the epicardial side alternate in timing with the opposite side. This

M. Tanaka et al. / Journal of Cardiology 64 (2014) 401–408

Fig. 4. Overlapped display of the curvilinear patterns of the intra-mural velocity atmany points in the posterior wall (PW) and interventricular septum (IVS) obtainedin the 5 beam directions at the same time. No. 1–5, beam direction. Narrow patternmeans that the moving velocity of the myocardial ﬁbers in the beam direction isalmost equal. Wide pattern means that the velocity of the ﬁbers is different within
the wall (non-uniformity). IC, isovolumetric contraction; Ej, ejection; IR, isovolumetric relaxation; ERF, early stage rapid ﬁlling; LRF, late stage rapid ﬁlling; SF, slow
ﬁlling; AC, atrial contraction.

was observed at the apical part of the IVS during the SF to
the IC phase. The black area (aSR ≈ 0) was present in the
mid-layer.
(2) The special toned distribution type (Fig. 5-v-2), in which large(−)SR and (+)SR appear successively. The large SR component
was observed at the basal part of both the IVS and PW during the pre-ET phase followed by the (−)SR component. The
black area was observed at the boundary between the twocomponents.

Spatial aSR distribution in the long-axis section plane
The characteristics was estimated by the aSR distribution
from the apex to the base at each of the 4 cardiac phases(Figs. 2, 3 and 6).
A different type of aSR distribution appeared in the apical, central, and basal parts of the LV wall at the same cardiac phase. For
example, during the Ej in the PW, the spotted distribution wasshown in the apical part, the multi-layered distribution with threelayered type in the central part and the double-layered type in thebasal part. During the pre-ET in the PW, when the (+)SR component was shown at the apical part, the alternating distribution 2
with large (−)SR component appeared at the basal part, but in the
post-ET phase, when the large extent of (+)SR component showedat the basal part, the large (−)SR component appeared at the apicalpart (Fig. 6).

405

Fig. 5. Classiﬁcation of the spatial distribution pattern of the axial strain rate in thewall displayed in the M-mode image. Non-uniformity of the (+) and (−)SR distribution appeared in the left ventricular wall and is classiﬁed as 5 types. The rightbottom ﬁgures show schematic display of the production mechanism of type (v),viz. thickness oscillation of the wall will occur as shown by blue and red arrows.
1 and 2 are different types in the oscillation mode. B, relaxing area; blue arrows,
contraction; red arrows, extension.

Estimation of the non-uniformity of the C–E property by the
intra-mural velocity distribution
The curvilinear graph of the intra-mural velocity distribution in the IVS and PW during one cardiac cycle is shown in
Fig. 4.
The widened (thick) velocity curve indicated that the moving
velocity of the local area was not uniform. The thin curve indicatednearly equal velocity.
The apical part in the IVS moved almost uniformly through one
cardiac cycle, whereas the basal part had the non-uniform velocity distribution. The velocity difference was about 20–30 mm/s
throughout the pre-ET and the early rapid ﬁlling (ERF), and about
30 mm/s in the RF. Throughout the SF and the anterior half of
the atrial contraction (AC), the moving velocity was almost uniform.
The velocity differences in the PW were observed in the entire
wall throughout the posterior half of the AC and the late rapid ﬁlling(LRF). The difference in the velocity was about 30 mm/s in the Ej andabout 65 mm/s in the RF.
However, the difference was small throughout the SF and anterior half of the AC. The difference occurred during systolic phase,but the extending velocity in the diastolic phase was nearly thesame and uniform.

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M. Tanaka et al. / Journal of Cardiology 64 (2014) 401–408

thickness is in the fact that the thickness change is easy to measurewith a great accuracy. In this regard, the non-invasive measurementof the aSR distribution seemed to be an adequate methodology.
The non-uniformity in the mechanical performance of the LV
wall has been studied by many investigators utilizing ultrasonicmethods [19–29]. It was thought that the velocity gradient in the
myocardium [24] and the non-uniformity of the velocity [25,26],
as well as the strain of the ventricle [27–29] were valuable for
evaluating the myocardial function.
However, when comparing the measurement of the aSR distribution with the moving velocity distribution, it was disclosed thatthe latter was inadequate to evaluate the C–E property, though it
was able to evaluate the movability of the myocardium. This isbecause the parallel existence of the contraction [(+)SR] and extension [(−)SR] during the same time makes it difﬁcult to measure thechanges in the ﬁber length. Therefore, the aSR distribution method
seemed to be more useful in studying the C–E property of the LV
wall.
Correlation between the spatial distribution of the aSR and C–E
property in respect to the mechanical performance of the LV wallFig. 6. Classiﬁed table of the spatial distribution patterns of the aSR in the IVS and PW
displayed in Figs. 2 and 3. Vertical column; (1), (3), (5), beam directions; Bas, basal
part; Cent, central part; Ap, apical part; Comp., occupied component of the SR, viz.
(+)SR or (−)SR; Horizontal column; cardiac phases, Pre-ET, pre-ejection transition
phase; Ej, ejection phase; Post-ET, post-ejection transition phase; SF, slow ﬁllingphase; Alt 1 and 2, alternating distribution type 1 and type 2.

Correlation between the aSR distribution and the intra-mural
velocity distribution
The correlation between the two was as follows:In case of the “toned” distribution, the width of the velocity distribution was widened.
In case of the “multi-layered” distribution, it was either narrowor widened. The amount of the movement was known, but thedirection and changes in thickness were not known, so the differentiation between the contraction and the extension was difﬁcult.
In case of the “spotted distribution,” the width of the velocity distribution depended on the magnitude of the aSR distribution. The
above-mentioned differentiation was also difﬁcult.
In case of the “stratiﬁed or spotted distributions [coexistence ofsmall (−) and (+)SR],” the width of the velocity distribution was
narrow and ﬂat. Also, the same was true in the differentiation.
Discussion
Usefulness of the aSR distribution method
Brutsaert et al. [1,2] stated that the cardiac muscle function
is constituted from several steps of the contraction and relaxation/extension (C–E) property. The non-uniformity was supposed
to exist in the C–E property, and also, as a whole, such a nonuniformity at each small step leads to the uniformity of function
at the next large step. To evaluate such a mechanism in the LV wall,
it is necessary to estimate the non-uniformity of the C–E property
at the muscle ﬁber level [5,7,8]. However, it is difﬁcult to measureclinically the length of the muscle ﬁber or sarcomere. The change
in the ﬁber length is in inverse proportion to the thickness changeof the ﬁber or the wall [17,18]. The reason why we measure the

The present study disclosed that contracting [(+)SR], extending[(−)SR] and relaxing (SR ≈ 0; B) areas always coexisted in the pulsating myocardium. The grade of the contraction or extension was
decided by the magnitude and extent of the basal (+)SR or (−)SR
components in comparison with those of the antagonistic component, which is adequately evaluated by the spatial non-uniform
distribution of the aSR.
This spatial distribution pattern of the aSR was classiﬁed into
5 patterns (Figs. 5 and 6): spotted, multi-layered, toned, stratiﬁed,
and alternating distribution patterns.
The “spotted,” “multi-layered,” and “toned” distribution patterns were observed in the systolic phase, whereas “toned,”“stratiﬁed,” and “alternating” distribution patterns were seen in
the diastolic phase. The genesis and the plausible physiologicalsigniﬁcance of each are as follows:
The “spotted distribution” pattern was observed at the apicalpart during the Ej and is thought to be produced by either the preor afterload provided by the muscle ﬁber contraction in its earlyand mid stages.
Firstly, the contraction of the LV wall begins at the epicardial sideof the apical part and propagates toward both the endocardial sideand the basal part [30]. At this time, the initially contracted muscle
tissue may induce the extension of the relaxed adjacent muscle tissues [31]. As a result, the adjacent muscle tissue is given the preload
and shows the (−)SR. Thereafter, the muscle tissue produces larger
power in the contraction stage and shows the (+)SR. Likewise, (−)SR
may appear whenever this contracting muscle extends to the next
adjacent muscle tissue, but, in turn, the next adjacent muscle tissue
will begin to contract and (+)SR will appear, owing to the stronger
contracting power. When such a phenomenon occurs successively,
the larger contracting power is produced in the apical part [3] andthe area of (+) or (−)SR is inscribed as a spot.
Secondly, in the multi-cellular cardiac muscle tissue, the direction and arrangements of the ventricular muscle ﬁber and bundle
are more complicated, particularly at the apical part [8,32–34].
Whenever the intra-ventricular pressure rises during the contracting state, pressure load sensitivity in the multi-cellular cardiac
muscle inevitably changes depending on the direction of the muscle
ﬁber or muscle bundle.
The myocardial stress induced by the pressure load (afterload)
may also change [35], where the high load will extend ﬁbers despite
being in the contracting state, so the (−)SR will be recorded. Whileat the low loading part, the ﬁbers may be exclusively in the contracting state without extension, so (+)SR is inscribed and thus theM. Tanaka et al. / Journal of Cardiology 64 (2014) 401–408

Fig. 7. Schematic representation of the extension produced in the epicardial andendocardial sides of the left ventricular wall during systole in the type ii axial strain
rate (aSR) distribution. (1) Early ejection phase: The extension [(−)SR] along the circumferential direction in the epicardial side (black curved arrow) was produced by
the decrement of the internal diameter with the increment of the intra-ventricularpressure and thickness (increasing the afterload). (2) Mid ejection phase: The
extension [(−)SR] in the endocardial side (black long arrow) was produced in thelongitudinal direction by the inward extrusion of the endocardial side of the posterior wall (PW), with the downward movement of the mitral ring and shortening of
the long-axis direction in the PW during systole. AV, aortic valve; MV, mitral valve.

spotted (−)SR distribution is shown in the myocardium. In thesesituations, the extension of the muscle ﬁber occurs even under thecontracting state, and the relaxing condition [black area (SR ≈ 0)]
does not appear at the boundary area between (+) and (−)SR components. When the muscle tissue load increases during contracting
state, large contracting power might be produced compared withthat at the low load state [3,4]. The spotted distribution signiﬁesthat the apical part greatly contributes to the pressure productionin the LV.
The “multi-layered distribution” was observed at the apical andcentral parts of the LV during the Ej. Whenever the curvature of
the endocardial surface on the cross-section of the apical and central parts during contraction decreases together with incrementof the thickness and intra-ventricular pressure (increment of theafterload), the circumferential stress in the muscle layer near the
epicardium increases and the tension develops in the epicardialside (Fig. 7-1) [35]. Thus the (−)SR will appear near the epicardium
in the circumferential direction despite being in the contracting
state.
In the longitudinal section plane, as shown in Fig. 7-2, whenever the shortening of the PW in the longitudinal direction occurs
during contraction together with increment of the thickness, theextrusion of the PW will occur in the internal direction together
with the downward movement of the mitral valve ring. Thus, thestress (afterload) in the longitudinal direction (meridian direction)[35] may increase in the endocardial side, and the (−)SR may appear
in the endocardial part. Only the middle layer was in the contracting
state ((+)SR). As a result, the three-layered pattern is produced in
the PW. In this situation, the extension of the muscle layers occurs
during contracting state of the Ej. Therefore, the relaxing area (blackarea, SR ≈ 0) does not appear at the boundary area.
During contracting state, the (−)SR component may act as theafterload to the myocardium, then the contracting muscle may produce stronger power than that in the case without extension [3,4].
In the case where the “multi-layered distribution” appears only inthe endocardial side, the same effects will be produced.
From these results, the apical and central parts seemed tocontribute to produce the large contracting power and to act as
the controller for producing and maintaining the intra-ventricularpressure.
The “toned” distribution appeared at the basal part of the LV
wall in both the systolic and diastolic phases. The magnitude of407

the aSR showed the level of either the contraction or the extensionof the myocardium. Whenever the level of the (+)SR is larger inthe endocardial side, the increment of the thickness is large in thisside, and thus the displacement increases toward the inner side,
so the internal diameter of the LV decreases. When the level of(−)SR is larger in the epicardial side than that in the endocardialside, the latter will displace toward the outer side (dilatation) andproduce an increment of the LV volume, thus the basal part acts
as the controller of the ﬂow volume in the LV. The relaxing area
(SR ≈ 0) appeared at the boundary between (+) and (−)SR.
The “stratiﬁed” distribution appeared in the SF phase. In the PW,
the (−)SR component near the epicardial side was usually larger
than that along the endocardial side, and the (+)SR component near
the epicardial side was also large. The (+)SR component acts as anextender to the relaxing area, inducing a (−)SR component. Thus thegentle contraction may induce the gentle extension in the adjacenttissue. It is considered that the gentle active expansion (dilatation)
may occur toward the epicardial side during the SF. Therefore, therelaxing area (black area; SR ≈ 0) is widely observed in the IVS and
the PW during SF.
Based on the observation of the “toned” and “stratiﬁed” distributions, the basal part is considered to act as the controller of theﬂow volume in the ventricle.
The “alternating” distribution was observed in the IVS during the
RF and pre-ET phases. Considered together, these ﬁndings indicatethat the thickened muscle oscillation may occur during extending
state by the power of the eddy ﬂow [36,37] as shown in the rightbottom schema in Fig. 5.
Type (1) may be produced by multiple small eddies under thenegative or low pressure condition [36], and type (2) by the large
rotating ﬂow occurring under the high pressure condition [11,37]
during the pre-ET phase.
On the other hand, the aSR distribution in the longitudinal section plane showed a different type of distribution in each part of
the apex, center, and base at the same cardiac phase. This indicatedthat a synergistic effect of the function is produced in the LV wall as
seen in the Ej phase. The producing effect of the intra-ventricularpressure in the apical part, the maintaining effect of the increased
pressure in the central part and the volume controlling effect in thebasal part may all cooperate with each other, and thus an effective
ejection may be accomplished.
Limitations
Several limitations need to be mentioned. First, the number ofcases was rather small, precluding a statistical study. Second, thetechnology of “phase difference tracking method in ultrasonics” isnot widely used because it was developed in our own laboratory,
and is not familiar to other investigators at the present time.
Finally, we have to obtain clinical feasibility by investigating therelationship between the C–E property in the local myocardium
and the deformability of the LV, and further to obtain the related
pump function in cases with various pathological states. Therefore,
further observation is mandatory.
Conclusions
The C–E property of the local ventricular muscle was investigated using high-resolution aSR measurement. Analysis was madeon the characteristics of the C–E property in the PW and IVS, andthe correlation between the non-uniformity of the SR distribution
and the LV wall function was also obtained.
The C–E property was not so simple compared with the theory of
the previous investigators. Our investigation showed that the nonuniformity of the contraction and extension in the LV myocardium

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M. Tanaka et al. / Journal of Cardiology 64 (2014) 401–408

and its spatial distribution were the determinants of LV performance. From the standpoint of the aSR distribution, the myocardial
function changed depending on the assemblage of the aSR distribution and the cooperation, each area of the LV seemed to sharean individual role in maintaining pump function. The non-invasive
measurement of the aSR is thought to be foresighted and useful toinvestigate the myocardial function as a whole.
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