Journal of Cardiology (2008) 52, 86—101

ORIGINAL ARTICLE

Blood ﬂow structure and dynamics, and ejection
mechanism in the left ventricle: Analysis using
echo-dynamography
Motonao Tanaka (MD, FJCC) a,∗, Tsuguya Sakamoto (MD, FJCC) b,
Shigeo Sugawara (MD) a, Hiroyuki Nakajima (RMS) a, Yoshiaki
Katahira (MD) a, Shigeo Ohtsuki (PhD) c, Hiroshi Kanai (PhD) da Cardiovascular Center, Tohoku Welfare Pension Hospital, Fukumuro 1-12-1, Miyagino-ku,

Sendai 983-0005, Japanb Hanzohmon Hospital, Kojimachi 1-14, Chiyoda-ku, Tokyo 102-0083, Japanc Institute of Medical Ultrasound Technology, Yokoyama 2-12-15, Sagamihara 229-1122, Japand Department of Electrical Engineering, Tohoku University, Aramaki-Aoba 6-6-05 Aoba-ku,
Sendai 980-8579, Japan
Received 28 April 2008 ; received in revised form 15 May 2008; accepted 16 May 2008
Available online 16 July 2008
KEYWORDS
Echo-dynamography;
Flow velocity vector;
Blood ﬂow dynamics;
Ejection mechanism;
Flow axis line;
Ventricular wall
dynamics;
Velocity gradient

Summary Using our ‘‘echo-dynamography’’, blood ﬂow structure and ﬂow dynamics during ventricular systole were investigated in 10 normal volunteers. The velocity
vector distribution demonstrated blood ﬂow during ejection was laminar along theventricular septum. The characteristic ﬂow structure was observed in each cardiac phases, early, mid- and late systole and was generated depending on the wall
dynamic events such as peristaltic squeezing, hinge-like movement of the mitral ringplane, bellows action of the ventricle and dimensional changes in the funnel shapeof the basal part of the ventricle, which were disclosed macroscopically by using
the new technology of high speed scanning echo-tomography and microscopically by
the strain rate distribution measured by phase tracking method.
The pump function was reﬂected on the changes in the ﬂow structure represented
by the ﬂow axis line distribution and the acceleration along the ﬂow axis line. The
acceleration of the ejection had three modes, ‘‘A’’, ‘‘B’’ and ‘‘C’’, and generated by
the wall dynamic events. ‘‘A’’ appeared from the apical to the outﬂow area along
the main ﬂow axis line, ‘‘B’’ along the anterior mitral leaﬂet and the branched
ﬂow axis line, and ‘‘C’’ generated by the high speed vortex behind the mitralvalve. The magnitude of the acceleration was estimated quantitatively from thevelocity gradient along the ﬂow axis line. Macroscopic and microscopic asynchrony in∗ Corresponding author. Fax: +81 22 719 5166.

E-mail address: m.tanaka@jata-miyagi.org (M. Tanaka).
0914-5087/$ — see front matter © 2008 Japanese College of Cardiology. Published by Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.jjcc.2008.05.005

Blood ﬂow structure and dynamics

87

the myocardial contraction and extension appeared systematically in the local partof the ventricular wall, which was helpful for making the ﬂow structure and for
performing the smooth pump function.
© 2008 Japanese College of Cardiology. Published by Elsevier Ireland Ltd. All rights
reserved.

Introduction
All energy involved blood ﬂow within the cardiac
chambers is supplied by myocardial contractionand extension. In these circumstances, an effective
transformation of the regional part of the myocardial wall is supposed to offer the most appropriate
spatial pressure distribution, which helps threedimensional (3D) blood movement.
Up to the present time, cardiac pump function
has been evaluated by global pressure and volume
measurements, but the changes in the spatial distribution of the regional ﬂux and pressure (ﬂow
dynamics) have not been analyzed in detail becauseof the lack of the suitable measurement technology.
To solve this problem, we evaluate quantitatively the local ﬂow structure and dynamics
using ‘‘echo-dynamography’’, which enables us
to assess instantaneously ﬂow dynamics noninvasively [1—5], especially to obtain the mappingof the ﬂow velocity vector during individual cardiac
phases and also to visualize the cardiac function.

Subjects
Ten presumably healthy volunteers aged 30—50
were the subjects. In all, information within theleft ventricle (LV) was obtained as to the ﬂow velocity, ﬂow velocity vector, ﬂow axis line, wall motion
and other variables during each early, mid- and latesystole.

Methods
Measurement of ﬂow velocity and selectionof the plane for the analysis
Commercially available ultrasonic equipment(Alolka Co. model 6500) was applied in the supine
or left lateral recumbent position. The ultrasonicfrequency was 3 MHz with the repetition rateof 4 kHz. Apical or parasternal two-dimensional(2D) echocardiograms were obtained by 90◦ sector
scan.
For the most advantageous section plane, we
selected ﬂow axis plane passing through the center of the mitral and aortic oriﬁces and including

the centers of both the left ventricle (LV) andleft atrium and the apex. This plane includes bothinﬂow and outﬂow axes of the LV. We named this‘‘long axis’’ plane. Normal intra-ventricular ﬂow is‘‘plane symmetry’’ with respect to this plane, andthe rectangular ones are short axis planes.
Data obtained from both 2D echocardiogram and
2D Doppler ﬂow velocity processed off-line using
our own software of ‘‘echo-dynamography’’ weretransferred to the personal computer through MO
disk memory.

2D ﬂow velocity vector mapping obtained
from the Doppler ﬂow velocity
The ﬂow velocity vector mapping on the scanning plane was obtained by the use of echodynamography which has been developed by us
introducing the two hydrodynamic theories of thestream function [7] and the ﬂow function [8] andexplained in details in the literature [6]. This mapping shows a cross-section picture of the 3D bloodﬂow in the LV.
The magnitude of the ﬂow velocity vector isshown by the length of yellow line, and the standard
length as the reference is shown at the left corner of the screen. The direction is indicated by the
inclination and the head is marked by the red pointat the edge of the line (ref. Fig. 1 left column).

Quantitative evaluation of distribution
range of the velocity vector
To quantify distribution range of the velocity vector, the contour lines of the magnitude of absolutevalue (red area) of the vector was superimposed on
the 2D echocardiogram (ref. Fig. 1 right column).
Quantiﬁcation was made by measuring the interval
between two contour lines.

Display of ﬂow axis line for evaluating
centralization of the power produced by
the ventricular wall
The ridge line (ref. Fig. 1 right column; blue line)
representing the ﬂow axis line in the LV as well as
centralization of the power was obtained in thevelocity vector distribution. This ridge line was
depicted by the connection of positive peak points

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M. Tanaka et al.

Figure 1 Left: two-dimensional (2D) mapping of ﬂow velocity vector in systole in the longitudinal section plane of theleft ventricle (LV) in a normal adult. The timing is shown in the ECG by a yellow line, and standard size of the vector
by a yellow bar at the upper left corner. A white arrow (E) shows the eddy ﬂow. ES: early systole, MS: mid-systole, LS:late systole, AO: aorta, IA: left atrium, LV: left ventricle, E: eddy. Right: 2D distribution of absolute value of velocity
vector in the longitudinal plane expressed by a equi-level line (yellow line). The ﬂow axis line distribution (blue line)
during each ES, MS and LS is overlapped with the equi-level line map. An unit interval of the equi-level line is shownat the upper left side. A: acceleration A, B: acceleration B, C: acceleration C, D: deceleration.

Blood ﬂow structure and dynamics
in the absolute value of magnitude of the velocity vector and the change in the 2D pattern of theridge line indicates local ventricular wall function[9,10].

Analysis of the LV wall movement
High-speed (66 frames/s) 2D echocardiogram wasused for the analysis.
Changes in the septal and posterior wall
thickness, the internal diameters at the levelof each apical, central and basal area of the
LV, and the diameter and displacement of themitral valve ring (MRD and MRM) during cardiac cycle were measured macroscopically fromsuccessive 24 echocardiograms selected at every
30 ms.

89

Measurement of the Doppler pressure
distribution [16—19]
The 3D blood ﬂow greatly changes during ventricular contraction, particularly due to the dynamic,
rather than static, pressure change. To deduce thischange from the distribution of the ﬂow velocity
data on the scanning plane, the Navier—Stokes’
equation of motion was applied for processing
Doppler velocity data, and the theory of Helmholtz
was applied to transfer velocity information to thepressure information as a scalar value [19]. The
pressure depicted by the color image was overlapped on the 2D echocardiogram (ref. Fig. 7 rightcolumn). Positive and negative components are displayed as warm and cold color.

Results
Strain and strain rate in the LV wall using a
new scanning technique (high frame ratesparse scan)
Thirty degree sector scan at a speed of 630 frames/swith the switching beam direction of every 5◦ interval (sparse scan) was performed, and measured
wall thickness change microscopically in each beam
direction at every thickness interval of 0.82 mm by
the phase difference tracking method [11], and thus
the strain rate was obtained [12,13]. Then, thiswas displayed on the M-mode and 2D images ascolor-coded information. The cold or warm color
indicates wax or wane of the stain rate (ref.
Figs. 5 and 6).

2D distribution of the acceleration forchanging ﬂow direction [14,15]
The direction of blood ﬂow within the LV is greatlychanged whenever ventricular wall, papillary muscles, valves and other structures are forced todisplace and transform due to the wall contraction. Accordingly, measuring the ‘‘acceleration forchanging ﬂow direction’’ of the intra-ventricularblood ﬂow, the transmitting process of the ejecting
force produced by the wall contraction is possible
to estimate. Then, we deﬁned the product of thevorticity and velocity vector as the ‘‘acceleration
for changing ﬂow direction’’ [7]. This product was
obtained from 2D distribution, which showed radial
pattern in the eddy, and stratiﬁed pattern near thewall whenever the force is perpendicular to theblood from the ventricular wall [15] (ref. Fig. 7 left
column).

Flow velocity vector distribution in the left
ventricle
Typical 2D distributions of ﬂow velocity vector during systole is shown in Fig. 1.
Early systolic phase (ES)The distribution was wide in the basal area withlarge velocity gradient, while that of small gradient
was seen in the anterior half area near the septum in both central and apical areas (Fig. 1ES). The
vector directed from the apical area to the aorta
in the anterior half of the ventricular cavity adjacent to the septum and then shifted anteriorly at
the aortic area. A part of this vector separated at an
adjacent area to the anterior mitral leaﬂet and converted posteriorly. Thus the circular arrangement of
the vector was demonstrated (white arrow: E). The
magnitude of the vector was minimum at the posterior half of the apical area adjacent to the posteriorwall, whereas it increased rapidly toward the center of the outﬂow and was maximum just behind
the aortic valve.
The main ﬂow axis line (A in Fig. 1) showed anarrow ramiﬁed pattern at the apical and central
areas, and the velocity gradient along this ramiﬁed
ﬂow axis line was about 5.2 in average. The ﬂow
axis line in the basal area was conﬂuent at the outﬂow with the axis line (B in Fig. 1) along the anterior
mitral valve and the velocity gradient was about
18.6 (Acceleration B). This was greater at the aortic
area, reaching about 21.3 (Fig. 3ES). The velocities
of ejected blood ﬂow along the main ﬂow axis line
at the apical, central and basal areas were about
10, 40, and 100 cm/s, respectively. The calculated

90
velocity gradients in these three areas were about
4.5, 10.1 and 21.3 (Acceleration A) respectively,i.e., in the latter two areas, the velocity gradientwere about two to four times bigger than that of
the apical area.
Velocity vector distribution showed that the
blood in the postero-apical area was stationary,
while the blood ﬂow in another areas was accelerated toward the aorta along the septum. At thesame time, a part turned posteriorly, producing
strong eddy just behind the mitral valve (Acceleration C) (Fig. 1). This eddy ﬂow axis line (Cin Fig. 1) joined again the main ﬂow axis after
the circular motion. The eddy was about 22 mm
in diameter (D in Fig. 2), and about 56 cm/sin the circumferential speed (Fig. 2-1, bottom
graph). Thus, the centrifugal force was larger

M. Tanaka et al.
than that of the eddy in the isovolumetric phase[20].
The vector in the outﬂow rapidly directed anteriorly toward the septum. Passing through the aortic
valve, it directed posteriorly and then anteriorly
again.
Mid-systolic phase (MS)The velocity vector was observed in the anterior 2/3 areas near the left ventricular septum(Fig. 1MS) and the direction was almost straightfrom the apical area toward the aorta. The magnitude was extremely small in the postero-basal
area, whereas it became gradually larger in theantero-basal area near the septum toward the outﬂow (about 100 cm/s). In the apical area the vector
was about 25—30 cm/s. Circular arrangement seen

Figure 2 Measurement of the eddy in the early systolic phase—–1: the diameter of the eddy using the stream line
(blue line) method, which is represented by the circular stream line (D). Bottom graph shows the ﬂow velocity along
the stream line; 2: 2D distribution of the Doppler pressure (dynamic pressure) in the LV. Cold colored area shows anegative pressure and warm colored, a positive pressure. The pressure distribution on the line passing through thecenter of the eddy appeared in the area just behind the anterior mitral leaﬂet (E: white arrow) is demonstrated in thebottom graph. In a developing eddy, the pressure in a circumferential part (cf) of the eddy becomes lower than thatin the center (c) of the eddy nevertheless the pressure in the eddy is negative.

Blood ﬂow structure and dynamics
in the early systolic phase under the mitral valve
disappeared.
Level difference of the velocity gradient on
the main ﬂow axis line was 1.4 times greaterin the central area compared to that in the91
apical area, and further, 2.6 times greater inthe basal area compared to that of apical area.
Then, velocity difference between apical and outﬂow areas was smaller than that in early systole(Fig. 3MS).

Figure 3 Velocity distribution and velocity gradient in the main ﬂow axis line of the ejecting ﬂow in the LV in one
sample case. Left: ﬂow axis lines of the ejection are overlapped on the color Doppler imaging. Red, pink and bluelines indicate apical, central and basal part, respectively, and the color lines correspond with the velocity gradientshowing in the right column. Right: graphic display of the velocity distribution. Velocity gradient (a/b) in the threeparts is demonstrated. Abscissa shows velocity in mm/s, and ordinate, distance in mm.

92
As seen in early systole, the main ﬂow axis line
was ramiﬁed at the apical and central areas, andthe velocity gradient was about 17.2 in average.
This main ﬂow axis was parallel to the septum andgradually increased in width toward outﬂow area,and formed Y shape with branched line from thearea just under the mitral valve, and the velocity
gradient was 13.6 in average (Acceleration B).
The velocity vector of ejected blood directed
anteriorly at the outﬂow, and directed posteriorly
in the aorta (Fig. 1).
Late systolic phase (LS)The velocity vector distributed unevenly in theanterior half area of the ventricle near the septum(Fig. 1LS). The magnitude of ejected velocity vector was about 20 cm/s, and increased slightly at theaortic oriﬁce.
The direction of the vector was nearly parallelto the septum from the apical to basal areas, butsome parts in the outﬂow branched to posterior
direction. Then, about 1/3 to 1/6 of the ejected
ﬂow moved downward, and thereafter anteriorly,
to the apical area along the ventricular inner surface (Fig. 1LS).
The velocity gradient of the branched ﬂow axis
line (D in Fig. 1LS) was about −11.1 and that of
the other branched ﬂow axis line (B in Fig. 1) was
about 10.9. The velocity gradient from apical area
to outﬂow area was almost constant (Fig. 3LS).
Just under the aortic valve, blood was accelerated
slightly from about 20 to 50—60 cm/s, and blood
ﬂow markedly lost the velocity in late systole.
A part of blood turned backward from the basal
area toward the apical area, producing clockwise
rotation along the inner surface of the posteriorwall and small circular arrangement of the vector
was observed in the apical area, and resulted in the
deceleration of blood movement.

Displacement of the LV structures in systolic
phase measured by high-speed scanningtechnique
Mean value in 10 normal cases are shown in Fig. 4.
Changes in the thickness of LV wall during one
cardiac cycle
The thickness of the septum (IVS) increased justbefore the onset of the ﬁrst heart sound (S1) at
the apical part, whereas the increase delayed at
the central and basal parts. The maximum thickness appeared in the order of the apical, central
and basal part. The time difference between theapical and basal part was about 180 ms.

M. Tanaka et al.
The thickness of the posterior wall (PW)
increased about 4—6 mm during systolic phase. The
onset of the increase at the apical part coincided
in time with the R wave of ECG, whereas at theother two parts the increase was in early systole
after transient decrease. The maximum thickness
appeared in the order of the apical, central andbasal part. The time difference between the apicaland basal parts was about 210 ms.

Changes in internal diameter of the LV anddisplacement of the mitral valve structure
in systolic phase
The internal diameter decreased at almost thesame time of the onset of the S1 in all three parts,and the minimum was observed at apical, central
and basal part in this order, showing about 60—90 ms
in time differences between the apical and basal
parts. The largest of the change was in the central part. The downward movement of the lateralpart of the mitral valve ring (MRM) began with theonset of the S1 and continued to the end of isovolumetric relaxation. The mitral valve ring diameter(MRD) was minimal just before the onset of the S1
and increased about 10 mm during systole until theend of isovolumetric relaxation. Thus, the increasein the antero-posterior diameter of the mitral valve
ring was followed by the change in the shape fromoval to circular form, increasing the oriﬁce area
during systole, though the ring is ﬁbrous tissue withlittle extensibility.

Strain rate distribution in the myocardium
measured by sparse scan method [14—16]
Strain rate of the IVS and PW measured to analyze
microscopically the myocardial mechanical events.
The results were shown in Figs. 5 and 6.
Strain rate distribution in the IVS (Fig. 5)
Remarkable differences in the distribution presented in the apex between right ventricular (RV)and LV sides at the beginning (about 100 ms) andending (about 100 ms) of systolic phase (Fig. 5-4,5).
Namely, at the beginning, it increased in the LV sideand decreased in the RV side, and the reverse wastrue at the end of systolic phase. In mid-systole,
both positive and negative strain rate areas weremixed in the apical part of the IVS. In the central and basal parts, the strain rate temporarily
decreased and the both parts expanded in earlysystolic phase. Thereafter, it increased throughout
systole, and the part having large strain rate moved
from RV side to LV side with the progress of sys-

Blood ﬂow structure and dynamics

93

Figure 4 Top: changes in thickness of the posterior wall (PW) and the septum (IVS) at the basal (B, blue line), central(C, red line), and apical area (A, green line) of the LV during one cardiac cycle. Bottom: changes in internal diameterof the LV at the basal (B), central (C) and apical (A) area as well as the mitral ring (MRD). MRM changes in the distanceof down ward displacement of the posterior part of mitral ring during one cardiac cycle. The number shows a speedof the change. Is: 1st heart sound, IIs: 2nd heart sound.

tole. In late systolic phase, this increased strain
rate rapidly decreased in both RV and LV sides simultaneously.
Strain rate distribution in the PW (Fig. 6)
In the apical part, the strain rate remarkably
increased in early systolic phase and the large stain
rate area spread from the epicardial side to theendocardial side, resulting in the progressive thickening from the early stage of systole from the outerside to the inner side of the PW. Up to just before
the end of systolic phase (judged by the second
heart sound: S2), there were mixed large and small
areas of the strain rate. There was a tendency toincrease in the inner half, whereas to decrease in
the outer half of the myocardium, indicating thepersisting contraction in the former and relaxation
or extension in the latter portion. The strain ratein the apical part decreased markedly in the end ofsystolic phase, resulting in the relaxation or dilatation. The strain rate in the central to basal parts
temporarily decreased markedly in the beginningof systolic phase, giving rise to the decrease in the
thickness of the myocardium and dilatation of the
LV cavity.
The increase in the strain rate in the basal
part spread to the isovolumetric relaxation beyond
the timing of the S2. From the end-systolic phaseto the isovolumetric relaxation period, the basal
part showed the inner half having increasing strain
rate and the outer half having decreasing strain
rate simultaneously, indicating the simultaneous
appearance of thickening of the inner half andextension or thinning of outer half. In the middleof central part, there was the area where neither
extension nor contraction occurred due to the stratiﬁed coexistence of increase and decrease in thestrain rate.

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M. Tanaka et al.

Figure 5 M-mode images of a time sequential change of the strain rate distribution in the interventricular septum(IVS) measured by sparse scan method on the longitudinal section plane of the LV during one cardiac cycle is shown.
The M-mode display of the strain rate of 1—5 correspond to those of 2D echo-cardiogram in the left row. Left middle
ﬁgure shows 2D strain rate image in the time point of the green line in the ECG.

Figure 6 M-mode images of a time sequential change in the strain rate distribution of the posterior wall (PW) measured
by the same method as in Fig. 5.

Blood ﬂow structure and dynamics

95

Figure 7 Left column: 2D distribution of the acceleration for changing the ﬂow direction in the LV in the early systole(ES), mid-systole (MS), and late systole (LS). The acceleration vector (blue line) is localized in the outﬂow area in
ES, and the eddy shows a radial pattern (E: white arrow). In MS, the stratiﬁed distribution appeared perpendicular to
the inner surface of the PW and IVS. In LS, the stratiﬁed distribution is seen perpendicular to the IVS and small radial
distribution (white arrow) indicating the eddy shows in the apical area. Right column: 2D distribution of the Doppler
pressure in the LV. Cold color area shows a negative pressure and warm color area, positive pressure. In ES, the negative
pressure caused by the eddy (E) appears in the basal area near the mitral valve. In LS, the negative pressure (whitearrow) spread and appeared at the area adjacent to the basal and central parts of the PW indicating the occurrenceof the premature dilatation and the beginning of the sucking action of the LV.

96

M. Tanaka et al.

Systolic ﬂow dynamics evaluated by 2D
distribution of the acceleration for changing
the ﬂow direction

extension of the ventricle indicating the beginningof the sucking action.

Distribution of the acceleration vector for changing
the ﬂow direction within the LV is demonstrated in
the left column of Fig. 7.
In the early systolic phase, stratiﬁed patternof acceleration appeared at the basal area near
the IVS. At the same time, radial pattern (E) of
acceleration caused by the eddy was observed justbehind of the anterior mitral valve (Fig. 7-ES). In
the mid-systolic phase, the direction of acceleration vectors showed perpendicular from the innersurface of the IVS and PW and the distribution wasobserved from apical to basal area indicating the
distribution of the force produced in the short-axis
direction by wall contraction (Fig. 7MS). In the midand late systolic phase, the line drawing with the
tip of the acceleration vector showed parallel tothe inner surface of the IVS and PW, showing thewave pattern. In the late systolic phase (Fig. 7LS),
two small radial patterns of the acceleration vector
were observed at the central and apical area near
the PW (white arrow) indicating production of thesmall eddy. At the same time, the arrangement of
the tip of the vector showed the ﬂat pattern parallel to the inner surface of the PW and the vectors
in the inﬂow tract area mainly directed to the PW
indicating the outward expansion of the PW nevertheless the direction of vectors in the adjacentarea to the IVS showed perpendicular from the innersurface of the IVS.

Discussion

2D Doppler pressure distribution in thesystolic phase
2D Doppler pressure distribution is demonstrated in
the right column in Fig. 7.
Throughout systole, high pressure area in the
LV was adjacent to the PW from the apical tobasal part, whereas low pressure area was in
the outﬂow tract and in the basal area of theaorta beyond the valve. The lowest Doppler pressure was about −11 mmHg just under the aortic
valve.
The pressure distribution in the eddy ﬂow behind
the anterior mitral leaﬂet in the early systolic phase
was about −0.3 mmHg at the center of the eddy and−0.8 mmHg at the circumferential part. Thus theeddy in the early systolic phase was in the developing stage (Figs. 7ES and 2-2). In the late systolic
phase, the negative pressure appeared again at thebasal to apical area adjacent to PW (white arrow
in Fig. 7-LS) due to the premature relaxation andSince the advent of modern cardiology, cardiac
function has been evaluated by global measurements, such as cardiac output, ejection fraction,
total ﬂux and pressure and many others [21—23].
However, these are inadequate because of the lackof the local information of the heart and blood ﬂow.
Using non-invasive technology, we need thefollowing three measurements for the clinical purpose. These are:(1) blood ﬂow structure and ﬂow dynamics in cardiac chambers,(2) mechanical events of cardiac structure during
pulsation,(3) local myocardial function of the LV.
For these purposes, several trials using computer
analysis [24—26] or X-ray ventriculography [10,27]
have developed, but these are not available atthe bedside. Recent clinical methodology, such as
ultrasonic method [28—30] or magnetic resonanceimaging (MRI) [31,32], has been proposed, but theformer has a difﬁculty to obtain the vector valueof blood ﬂow velocity and the latter is not enoughto analyze ﬂow dynamics because of the limited
spatial resolution.
Present report deals with the analysis ofabove-mentioned three informations using echodynamography, strain rate analysis with sparse scan
technique and high frame rate echo-tomography toclarify the following four systolic phenomena.
(1) characteristics of the blood ﬂow structure in
the LV and its generation mechanism,(2) correlation between the ﬂow structure andmechanical events of the ventricular wall,(3) correlation among the ﬂow structure, ﬂow
dynamics and pump function,(4) asynchronism in myocardial contraction forgenerating the ﬂow structure.

Characteristics of the ﬂow structure of theintra-ventricular ﬂow during the systolic
phase and its generation mechanism
Characteristics of the blood ﬂow structure in theintraventricular ﬂow during systole are summarized
as shown in Fig. 8. The blood ﬂow passing throughthe outﬂow tract area during systole was laminarand the ﬂowing structure showed a plane symmetry
to the longitudinal section plane which includes theBlood ﬂow structure and dynamics

97

Figure 8 Schematic representation of the ﬂow structure in the early, mid- and late systolic phase and summarized
correlation among the ﬂow structure, ﬂow dynamical changes and ventricular wall dynamics during systolic phase.
Gray arrow (F): ﬂow structure, Black arrow in ﬁgures: direction and magnitude of the wall movement, Blue arrow (P):dynamic pressure, Right under picture shows the Doppler ﬂow velocity curve obtained in the outﬂow tract of the LV,
and correlation between timing of the schematic ﬂow pattern and real ﬂow is represented.

long axis line of the LV. As demonstrated in Fig. 8,
the blood in the basal area in the early systolic
phase (ES) begin to move to the aorta, and at thesame time, a part of the blood in the basal area
moved toward posteriorly along the mitral valve

and produced an accelerated eddy at the area adjacent to the ventricular surface of the MV. In the
mid-systolic phase (MS), the ﬂow speed in the apical and central area gradually increased while being
gathered the blood in the inﬂow area near the PW to98
the outﬂow area near the IVS. The ﬂow velocity inthe inﬂow tract area remarkably decreased. In thelate systolic phase, the speed of the ejected ﬂow
was obliged to decelerate. At this time, some partof the blood ﬂow separated from the main ﬂow atthe basal area and moved downward to the apicalarea along the PW and a rotating ﬂow appeared in
the posterior half area of the LV together with small
eddies at the apical area. Thus, the ﬂow structurein the systolic phase had respective characteristics
in the early, mid- and late systolic period, respectively.
The ﬂow structure is produced by the changes in
the regional wall motion and wall dynamics during
ventricular pulsation. The investigation disclosed
the following characteristics concerning mechanical phenomena; i.e.
(1) The LV short-axis transformation occurred
together with deduction of the internal diameter, and the increase in the predominant PW
thickness propagated from the apical to basal
region (peristaltic squeezing).
(2) The LV long-axis transformation occurred
together with the anterior displacement of thePW with protrusion of the papillary muscle. The
plane encircled by the mitral ring had hinge-likemovement. The ﬁbrous trigone act as a fulcrum
and downward movement of the posterior partof the ring changed the shape from elliptic tocircular with an increment of the surface area.
(3) Diminished volume and short-axis diameter ofthe LV caused by (1) and (2) modes was followedby the shift of the main ﬂow axis line toward the
IVS during systole. This is a bellows action.
(4) Dimensional changes of the funnel-shaped outﬂow tract which was formed by the basal IVS,
the anterior leaﬂet of the mitral valve and thebasal PW.
Based on the ﬂow structure and the mode of wall
dynamics above-mentioned, the possible mechanism of ventricular ejection is as follows:As summarized in Fig. 8, at the beginning of ventricular contraction, peristaltic motion (mode (1))
starts at the apical part with mode (2) ventriculartransformation, high pressure at the apical area istransmitted the basal area and ejects the blood.
Simultaneously, the basal part of LV is expanded
posteriorly in a short period following isovolumetriccontraction, and consequently some parts of blood
move posteriorly along the mitral valve. The bellows action of the mode (3) helps the developmentof the forceful accelerated vortex with equal dispersion of the centrifugal force, which causes thesmooth closure of the mitral valve as pointed by
Bellhouse [33] and Reul [34].

M. Tanaka et al.
In mid-systole and later on, bellows action isemphasized. Namely, the ejected ﬂow is generated
by mechanical events (mode (3) and (4)).
At the later half of ejection period, myocardial thickness successively increased from apical tobasal part as shown in the data of wall dynamics andstrain rate distribution. Furthermore, the greater
displacement of the wall occurred at the PW rather
than IVS in the short-axis direction, all contribute
blood ﬂow toward outﬂow tract. Such a wall motion
seems to maintain the completeness of ejection andproceeds to the closure of the aortic valve.
Rushmer [35] and Sakuma [36] described theimportant role of bellows action to the effective
right ventricular ejection, while our present data
indicated that the combined role of peristaltic
action as well as bellows action of the ventricularwall is important for the completeness of systolic
ejection in the LV.
In late systole, progressing the increment of the
myocardial thickness at the basal part of the PW
accompanying with the inward displacement, theposterior part of the mitral ring is made to moveantero-upward and the antero-posterior diameterof the mitral ring diminish. At the same time, tension in the myocardium at the apical and central
area is relieved in spite of the ejection period,
and the premature relaxation and extension of
myocardium begin and the LV tends to dilate (beginning of the sucking action).
The premature relaxation and extension produce
the negative pressure in the area adjacent to the
PW. At the same time, the negative pressure will
act not only for generating the small eddies at theapical area but also for dragging posteriorly about
one-thirds to one-sixth of the maximal ﬂux during early phase of ejection, and gives rise to therotating ﬂow at the central area, which works asa brake to the ejecting force along the main ﬂow
axis line. Thus the velocity vector of the ejecting
ﬂow becomes nearly the same size from the apical to basal area and the successive ejecting ﬂow is
obliged to be moved solely by inertia.

Correlation between the blood ﬂow
structure and pump function of the heart
Acceleration process for ejecting blood from the
LV is essential for evaluating myocardial function,
however, it is difﬁcult to understand the mechanism of acceleration using sole pressure gradient
between the LV and aorta. We have to know spatial
distribution of the force and magnitude of the force
generated. The spatial distribution of the force inthe LV will be reﬂected in the centralization of theBlood ﬂow structure and dynamics
blood ﬂow in the ventricle. The centralization of
the ﬂow is evaluated in the ﬂow axis distribution.
The magnitude of the force will be reﬂected in themagnitude of the acceleration of the blood ﬂow andthe acceleration mode. In this study, we analyzed
acceleration mechanism, ventricular wall dynamics
and their correlation based on the four items, i.e.
(1) two-dimensional distribution of the ﬂow axis
line of the ejecting blood ﬂow,(2) the velocity vector distribution on the main
ﬂow axis line and the velocity gradient along
the main ﬂow axis line,(3) their transition (time course) during the systolic
phase,(4) two-dimensional distribution of the acceleration for changing the ﬂow direction.
Summarized results demonstrated in Figs. 1 and 8.
We found three kinds of acceleration modes along
the ﬂow axis lines; accelerations A, B and C. The
ventricular ejection is accomplished by the combination of these three modes acceleration generated
along the blood ﬂow axes (Figs. 1 and 3).
Acceleration A was produced along the main ﬂow
axis line from the apical to outﬂow tract area of
the LV. Two kinds of branched ﬂow axes joined at
the central and basal areas. The velocity gradientalong the main ﬂow axis line in the central area
was about twice than that in the apical one and thegradient in the basal area about four times further
than that in the apical ones. Thus, the acceleration
increased at the central area, and further at thebasal area (Fig. 3). This type of acceleration was
generated by the wall dynamical mode 3.
Acceleration B, which appeared at the basal
area parallel to the anterior leaﬂet of the mitralvalve and generated by passing though the funnel
structure constructed by the IVS, mitral leaﬂet andposterior wall, joined to the main ﬂow axis line.
Because of the extremely large antero-posterior
diameter at the basal area compared with thatof the aortic ostium, the convective acceleration
generated becomes very large. This type of acceleration was generated by the wall dynamics modes
2 and 4.
Acceleration C, which observed along the circular ﬂow axis line just behind the anterior mitralleaﬂet joined with the main ﬂow axis line at thecentral area is essentially due to the high speed
rotating ﬂow. The centrifugal force is proportion
to square of the rotation speed and is inverse
proportion to the radius of rotation. Accordingly,
accompanying decrease in the radius of rotation as
in the early systolic period, the centrifugal force
caused will be increased remarkably. The blood in
the adjacent area is dragged into the accelerated

99
rotation ﬂow and thus the accelerated outﬂow is
produced in the central area.
In the early systolic phase, all three modes work,and the acceleration increase about two times in
the central area and about four times in the basal
area compared with that in the apical area along
the main ﬂow axis line. In the mid-systolic phase,the acceleration A and B work, and the velocity gradient is about 1.3 times in the central area andabout 3 times in the basal area compared withthe velocity gradient in the apical area. In thelate systolic phase, only B is active, so that thevelocity gradient decreases and the ﬂow velocity keeps nearly the same level according to theinertia.
From the 2D distribution of the ﬂow axis line andthe velocity gradient and acceleration distribution
on the ﬂow axis line, it is concluded that the pumpfunction including the local function can be evaluated from the non-invasive information of blood
ﬂow structure.

Signiﬁcance of the asynchronism in the
myocardial contraction and extension forgenerating the ﬂow structure
As indicated by the distribution of the velocity vector and the main and branched ﬂow axis lines, bothcontracting and relaxing states coexisted simultaneously during ventricular systole, as indicated by
the simultaneously contracting the apical part andrelaxing basal part at the early systole and thereverse was true in the late systole.
The time difference of the wall thickness andinternal diameter of the LV, and also the peristaltic
squeezing and bellows action indicated that the
myocardial contraction and relaxation in the local
part have time discrepancy and also myocardialasynchrony always exist even during systole in the
microscopic point of view by the strain rate distribution.
Furthermore, the strain rate distribution indicated that the reverse strain rate occurred in earlysystole, resulting contraction of the apical part andrelaxation of the basal part. Even though, myocardial wall has laminar layer, positive strain rate in
the inner half of contraction accompanied with negative rate in the outer half of relaxation and thus
the wall thickness change propagated from epicardial to endocardial side.
From these facts, asynchronism of myocardial contraction and the time discrepancy of theasynchrony among local parts seems to play animportant roll in the smooth intra-ventricular blood
ﬂow and the effective pump function of the LV.

100Conclusions
Systolic blood ﬂow in the left ventricle analyzed
by using the echo-dynamography was the laminar ﬂow along the interventricular septum. The
ﬂow structure is quite different in its characterin such cardiac phases as early, mid- and late systole and was produced by the wall dynamic events
such as peristaltic squeezing of the ventricularwall, hinge-like movement of the mitral valve ringplane, bellows action and dimensional change inthe funnel shape of the basal part of the LV. Concerning the correlation between the ﬂow structure
and pump function, distribution of the force inthe LV is reﬂected on the ﬂow axis line distribution, and the ﬂow acceleration composed of threevarieties, i.e., A: from apex to outﬂow along themain ﬂow line, B: along the mitral leaﬂet, and
C: vortex at the mitral valve. Even during systole, macroscopic and microscopic asynchronous
contraction and relaxation in local part of the wall
contribute to not only the generation of the ﬂow
structure but also the smooth and effective pumpfunction.

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