Journal of Medical Ultrasonics (2019) 46:413–423
https://doi.org/10.1007/s10396-019-00943-5

ORIGINAL ARTICLE—CARDIOLOGY

Role of intra‑ventricular vortex in left ventricular ejection elucidated
by echo‑dynamography
Motonao Tanaka1 · Tsuguya Sakamoto2 · Yoshifumi Saijo3 · Yoshiaki Katahira4 · Shigeo Sugawara5 ·Hiroyuki Nakajima1 · Takafumi Kurokawa1 · Hiroshi Kanai6
Received: 27 November 2018 / Accepted: 18 March 2019 / Published online: 10 May 2019
© The Japan Society of Ultrasonics in Medicine 2019

Abstract
Purpose From the correlation between the blood flow dynamics and wall dynamics in the left ventriocle (LV) analyzed using
echo-dynamography, the ejection mechanisms and role of the intra-ventricular vortex in the LV were elucidated in detailduring the pre-ejection transitional period (pre-ETP), the very short period preceding LV ejection.
Methods The study included 10 healthy volunteers. Flow structure was analyzed using echo-dynamography, and LV wall
dynamics were measured using both high-frame-rate two-dimensional echocardiography and a phase difference tracking
method we developed.
Results A large accelerated vortex occurred at the central basal area of the LV during this period. The main flow axis velocity line of the LV showed a linearly increasing pattern. The slope of the velocity pattern reflected the deformity of the flowroute induced by LV contraction during the pre-ETP. The centrifugal force of the vortex at its junction with the main outflow
created a stepwise increase of about 50% of the ejection velocity.
Conclusion Ejection of blood from the LV was accomplished by the extruding action of the ventricular wall and the centrifugal force of the accelerated vortex during this period. During ejection, acceralated outflow was considered to create aspiral flow in the aorta with help from the spherical structure of the Valsalva sinus.
Keywords Echo-dynamography · Vortex · Wall dynamics · Flow structure · Axial strain rate

Introduction* Motonao Tanaka
m.tanaka@jata‑miyagi.org
1

Department of Cardiovascular Medicine, Tohoku Medical
and Pharmaceutical University Hospital, 1‑12‑1 Fukumuro,
Miyagino‑ku, Sendai, Miyagi 983‑8512, Japan

2

Hanzomon Hospital, 1‑14 Kojimachi, Chiyoda‑ku,
Tokyo 102‑0083, Japan

3

Graduate School of Biomedical Engineering, Tohoku
University, 4‑1 Seiryo‑machi, Aoba‑ku, Sendai,
Miyagi 980‑8575, Japan

4

Katta General Hospital, 36 Shimoharaoki, Kuramoto,
Fukuoka, Shiroishi, Miyagi 989‑0231, Japan

5

Nihonkai General Hospital, 30 Akiho‑machi, Sakata,
Yamagata 998‑8501, Japan

6

Department of Electronic Engineering, Tohoku
University, 6‑6‑05 Aramaki Aza Aoba, Aoba‑ku, Sendai,
Miyagi 980‑8579, JapanAs previously noted in the literature [1, 2], the blood flowfrom the left ventricle (LV) is an accelerated spiral flow withhigh velocity. Such a flow is not solely due to the pressure
difference between the LV and aorta alone; therefore, thedetails of the ejection mechanism have yet to be elucidated.
This has inspired us to clarify the detailed LV wall dynamics concomitant with the inseparable intra-ventricular bloodflow structure.
However, an investigative and noninvasive methodology
has not been developed to date, likely since no sufficientspatial resolution has been determined using any available
technique [3–9]. Accordingly, here we aimed to examine
the production mechanism of this accelerated flow and its
physiological function.
By using echo-dynamography including a new analytical intra-ventricular vortex method we have developed, we
attempted to elucidate the production mechanism of LV
ejection and the role of the vortex in ejection according

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to the correlation between the flow structure and the wall
dynamics from the onset of the apical contraction to justbefore LV ejection, which was defined as the pre-ejection
transitional period (pre-ETP) [10].

Method and materials
Subjects
The 10 healthy subjects aged 30–50 years (39.6 ± 10.4 years), all of whom were also included in our previous studies[10–14], provided informed consent.

Journal of Medical Ultrasonics (2019) 46:413–423

5. Doppler pressure (DP) [12, 17, 23] obtained from thevelocity vector distribution on the scanning plane as previously reported [11, 24] and corrected by the reference
pressure value at the fibrous trigone. Warm colors show
positive pressure and cold colors negative pressure.
6. Acceleration for changing the flow direction (ACFD) [2,
11, 22] to evaluate quantitatively the vortex’s rotation
power, the product of the vorticity (ω) and the velocity
vector (υ) defined as “ACFD (ω·υ)” was automaticallycalculated. Details can be evaluated from the profile ofthe vector distribution on the line passing through thecenter of the 2D distribution of the ACFD.

Methods

Analysis of LV wall thickness and dynamics

Measurement and analysis of blood flow structure in the LV

Changes in the thicknesses of the intra-ventricular septum(IVS) and posterior wall (PW) and those in the internal
diameter of the LV at the apical (A: just at the papillary muscle level), basal (B: approximately 10 mm from the mitralvalve ring), and central (C: in the midst of A and B) areas,
as well as those of the mitral valve ring diameter (MRD)
and displacement (MRM) during the cardiac cycle, were
measured from 30 successive 2D echocardiograms [10–12].

The ultrasonic equipment and measuring methods used in
the present study were identical to those in our previous
investigations [2, 10–14]. Two-dimensional (2D) echocardiographic data and 2D Doppler flow velocity data on
the longitudinal cross-section of the LV passing throughthree points (the center of the aorta, mitral orifices, and theapex) were obtained during 10–15 cardiac cycles with quiet
breathing and digitally recorded.
The Doppler flow velocity data were processed offline
using our own echo-dynamography software [15–18] toobtain the flow velocity vector distribution on the observation plane, which was then overlaid onto the 2D echocardiogram [2, 10–14].
From the 2D distribution of the velocity vector, the bloodflow structure appearing in the LV on the scanning planeat an arbitrary time point during the cardiac cycle, such as
straight, meandering, or vortex, was qualitatively estimated[10–14]. The flow volume [19–22], velocity gradient of theflow [2, 11], and distribution of the stream line (SL) [16,19–21] were also quantitatively estimated.
Furthermore, the following flow dynamic parameters ofthe vortex were obtained in the pre-ETP.
1. Vortex diameter (VD) determined from half the width ofthe maximum value of the stream function [16, 18].
2. Circumferential velocity (CV) obtained from the velocity
vector along the circumference of the vortex [11].
3. Velocity distribution on the SL of the vortex estimatedalong the arbitrary SL.
4. Vorticity (RT) to differentiate the “irrotational” fromthe “rotational” vortex and estimate the vortex scale,the vorticity (ω) was calculated from the rotation of thevector on the scanning plane [22]. The positive vorticity(clockwise rotation) was shown as a cold color and thenegative (counterclockwise rotation) as a warm color.

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Analysis of LV wall dynamics at the local myocardial level
On the longitudinal section plane scanned at a high speedof 630–700 frames/s, three beam directions of the basal(B), central (C) and apical (A) parts were selected by sparsescan. The echo signals of the LV wall during time intervals of 2–6 s were recorded and then processed offline
using our software [24–27]. The axial strain rate (aSR) at
the local myocardial tissue level was obtained using “thephase difference tracking method.” The aSR distribution was
acquired by shifting the measuring point every 200 μm. The
time serial aSR distribution was overlaid in a color-coded
M-mode image. A contraction was indicated by a cold color(+), while extension was indicated by a warm color (−).

Results
Similar flow structures appeared in nearly in all cases in
the pre-ETP. The results obtained in one representative case
(Case 10) are shown in Figs. 1, 2, 3, and 4. Case 10 is representative because the values were in the middle range of allof the cases. Tables 1 and 2 show a summary of all cases.
The findings in the early stage (ES, vortex formation stage)
were compared to those in the late stage (LS, accelerated
vortex stage).

Journal of Medical Ultrasonics (2019) 46:413–423

415

Early Stage

Late Stage

IVS

LV

AO
40

22

(c䟝/s)(c䟝/s)

VD

20

15
(mm)

(mm)

LV
RT

-160.6

AO(mm)

Fig. 1  Comparison of the vortex characteristics in the left ventricle(LV) between the early stage (ES) and the late stage (LS). Left column: ES, right column: LS. Upper row: Two-dimensional distributionof the flow velocity vector on the longitudinal section plane of the
LV. Middle row: Contour display of the stream function and measurement of the vortex diameter (VD). The VD was obtained from half(rad/s)(rad/s)LA-169.8(mm)

the width of the stream function on the yellow line. The curvilinear
red graph shows the stream function distribution. Bottom row: Twodimensional distribution of the vorticity (RT) and one-dimensional
distribution of the RT on the line passing the center of the vortex. A
clockwise rotation is shown as a cold color, while a counterclockwise
rotation is shown as a warm color

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Journal of Medical Ultrasonics (2019) 46:413–423

Early Stage

Late Stage

IVS

LV
SL

AO

(cm/s)

38.0

51.8(cm/s)

50.9

(mm)

(mm)

AC

-25.6

(m/s2)(m/s2)

FD

(mm)

-72.6

(mm)

Fig. 2  Comparison of the vortex characteristics between the earlystage (ES) and the late stage (LS). Upper row: Two-dimensional distribution of the stream line (SL) on the longitudinal section plane andchanges in the velocity along the SL of the vortex (curvilinear graph).
The SL (blue) shows an equi-formed pattern in the ES and a spiralpattern in the LS. Bottom row: Two-dimensional distribution of theacceleration for changing the flow direction (ACFD) of the vortex.
Vector grade is shown by the length of the blue lines and direction isshown by the red mark put on the tip of the vector. A radial pattern isvisible in the vortex. Reference data are shown at the upper left corner of the figure. Curvilinear graphs show the data along the blue line
displayed on the two-dimensional distribution

Flow structure in the LV appearedon the longitudinal section plane

velocity was about 30 cm/s in the central area, while thegreatest velocity (about 51 cm/s) was seen in the basal area.
Thereafter, these vectors were directed backward in the area
under the aortic valve (AV). After passing under the mitralvalve, the vectors were directed downward and decelerated
to about 38 cm/s. The vectors were then directed forward
to the IVS at the papillary muscle level showing the double
structure and joined with the upward vector group. Thus alarge clockwise rotational flow (vortex) with uneven velocity distribution developed. The vortex’s diameter was about
40 mm.

Velocity vector distribution of the vortex in pre‑ETP
The upper row of Fig. 1 shows the velocity vector distributions of the vortex in the ES (left, 0–100 ms) and that in theLS (right, 100–220 ms) of the pre-ETP (0–220 ms).
In the vortex formation stage, the main velocity vector
gradually increased and became widely distributed along
the IVS from the apical posterior area to the basal area. The

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Journal of Medical Ultrasonics (2019) 46:413–423

417

DP
Early Stage
1

1st

Step

2nd

Step

Late Stage
3

LV
AO
LA

2

4

Fig. 3  Doppler pressure distributions in the longitudinal section
plane of the LV during the pre-ejection transitional period (pre-ETP)
displayed on the contour line. The warm color shows positive pressure, while the cold color shows negative pressure. The pressurelevel is shown on the color bar on the right. The timing of the pres-sure images is indicated by the yellow bar on the ECG. The white
narrow arrows show the changes in the width of the positive pressurearea during the pre-ETP. The large thick arrows show the supposedtransmitting direction of the positive pressure. LV left ventricle, LA
left atrium, AO aorta

In the accelerated vortex stage, the velocity vector in
the outflow tract increased rapidly from the apical to thebasal area along the IVS. The maximal velocity area shifted
antero-upward at the basal area. The vortex in this stage
was accelerated and its diameter decreased to about 22 mm(Fig. 1, right upper row). At the outflow tract area just under
the aortic valve, one part of the vector distribution was
directed to the aorta, while the other was directed posteriorly. After passing under the anterior mitral leaflet, the flow
was directed downward and rotated anteriorly. Thereafter, itjoined the upward flow components in the outflow tract area,
producing the accelerated vortex.
As shown in the middle row of Fig. 1, the vortex diameter (VD) calculated from the stream function was about
20 mm in the ES and about 15 mm in the LS, consequently

decreasing by about 25% in LS; the double structure disappeared. The RT was about 160.6 rad/s in the ES and about
169.8 rad/s in the LS, and a slight increase in RT appeared.
The maximum rotating velocity on the SL increased
from about 50.9 cm/s in the ES to about 51.8 cm/s in the
LS (Fig. 2, upper row). The rotation mode of the vortex
displayed by the SL showed a repetitive circular patternin the ES, whereas the revolution velocity increased in
the outer compared to the inner part of the vortex andthe accelerated vortex (spiral pattern) was observed in the
LS. Since the magnitude of the ACFD vector was about
25.6 m/s2 in the ES and about 72.6 m/s2 in the LS (Fig. 2,
lower row), the ACFD in the LS was remarkably increased
to about 2.8 times larger than that in the ES.

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Journal of Medical Ultrasonics (2019) 46:413–423− 0.8 mmHg and shifted from the area just under the mitralleaflets (Fig. 3b) to the antero-upward area of the outflow
tract (Fig. 3c). Moreover, the distribution pattern of thenegative pressure changed from a double circular pattern inthe central area (Fig. 3c) to a widely diffuse pattern in theoutflow area (Fig. 3d).
The positive pressure was widely distributed in the area
contacting the inner surface of the PW and IVS. The positive
pressure area (brown), as shown by the thick white arrow,gradually shifted upward from the apical area to the area
under the aortic valve together with a slight increase in thepositive pressure (0.1–0.2 mmHg). Also, as shown by thewhite thin arrows in Fig. 3a–d, the width of the positive
pressure area near the IVS changed reciprocally from wide
to narrow during the pre-ETP.
These results indicated that the changes in the pressure
distribution of the vortex yielded by the non-uniform distribution of the rotation speed, which knocked the IVS reciprocally, produced the mechanical oscillation of the IVS.

Late Stage

IVS
LV

AO

(cm/s)

53.0(mm)

Effect of the vortex on outflow blood(cm/s)

9.8
30.3
4.3

Ap Apilal

95.6
69.2 26.4
52%
19.2

Central

Basal

50.0

(mm)

AO

Fig. 4  Effect of the accelerated vortex on the main outflow in the latestage (LS). Upper row of the figure and red graph: The stream line
(SL) of the vortex and flow velocity distribution along the streamline of the vortex. Lower row of the figure and red graph: The SL of
the main outflow and flow velocity distribution along the SL. White
arrows: Positions of the 0 point in the distance scale on the curvilinear red graph (one dimensional velocity distribution) and rough junction area of the vortex and main outflow. AO aorta, Ap apex

Observing the changes in parameters of the vortex(Table 3) during the LS with the time duration of 120 ms,
the number of revolutions (Rev) increased about three times,
while centrifugal force (CRF) increased about two times.
These results indicated that the vortex in the LS was accelerated despite the diameter decreasing.

Doppler pressure distribution during pre‑ETP
As shown in Fig. 3, the negative pressure area (blue) at thecenter of the vortex decreased from about − 0.57 mmHg to

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The effect of the vortex on the LV outflow was estimatedfrom changes in the velocity distribution along the SL of
the main outflow. As shown in Fig. 4, the velocity in themain outflow was abruptly increased from about 19.2 cm/s
to about 69.2 cm/s by about 52% of the maximal ejection
velocity (95.6 cm/s) at the confluent area (white arrow) of
the vortex and the main outflow. The step-up increase invelocity was about 30.3 in the velocity gradient.
Consequently, the blood flow velocity of about 19.2 cm/sin the apical area was accelerated to about 95.6 cm/s in thebasal area. These results indicated that the accelerated vortex in the late stage during pre-ETP was very useful for LV
ejection and contributed greatly to the accelerated outflow
in the early ejection phase.

Wall dynamics measurement
Wall dynamics measured by 2D echocardiography
Figure 5 summarizes the results obtained from the 10 cases.
In the early stage (ES), the apical (A, green) and central (C,yellow) parts were in a contracting state that began at the
P of ECG; nevertheless, the basal part (B, blue) began toextend slightly, as shown in the change in thickness of theposterior wall (PWT) of the unshaded area in the upper row
of Fig. 5. The thickness change in the IVS was very small
compared with that in the posterior wall [10, 13].
In the late stage (LS), thickness of the apical part wasincreased, whereas the central and basal parts extended
under a contracting state. Although the internal diameterof the LV (LVD) showed temporal dilatation during atrial

Journal of Medical Ultrasonics (2019) 46:413–423

419

Table 1  Measurement data of the vortex appeared in the basal area of the LV in the early and late stages of pre-ETP in 10 normal cases
Case no.

1
2
3
4
5
6
7
8
9
10
Ave

SEX

F
F
M
M
M
M
F
F
F
F

Age

49
33
32
43
31
34
37
43
50
44
39.6

EF (%)

66
59
60
61
60
68
61
67
55
55
61.2

ES

LS

LVDd (mm)VD (mm)VD/LVDd

Vmax (cm/s)

OV (cm/s)

Vmax/OV (%)

VF ­(cm2/s)

46
42
46
54
45
49
48
53
48
50
48.1

20.8
22.2
19.3
20.3
20.5
22.2
19.9
19.2
23.1
20
20.8

0.45
0.53
0.42
0.38
0.46
0.45
0.41
0.36
0.48
0.40
0.43

37.2
31.8
66.8
37.6
52.2
48.7
35.9
32.5
34.7
44.1
42.2

95.1
93
85.7
94.5
71.5
94.5
108.5
76.5
99.6
95.6
91.5

39.1
34
78
40
73
51
33
42
35
46
47.1

36.7
32.6
43.2
38.9
31.6
30
28.1
41.2
32.9
53.7
36.9

EF ejection fraction, LVDd end-diastolic left ventricular diameter, VD diameter of the vortex, Vmax maximum velocity of the vector, OV outflow
velocity, and VF flux of the vortex
Table 2  Comparison of thecharacteristics of the vortex in
the early stage (ES) and that in
the late stage (LS) of the preETP in 10 cases

Case no.

1
2
3
4
5
6
7
8
9
10
AverageSD

Early Stage (Pre-ETP)

Late Stage (Pre-ETP)
2

RT (rad/s)

DP (mmHg)

ACFD (m/s )RT (rad/s)

DP (mmHg)

ACFD (m/s2)− 131.0− 90.9− 251.1− 101.8− 100.4− 88.5− 141.0− 108.0− 100.8− 160.6− 127.4
49.35− 0.95− 0.63− 1.40− 0.41− 0.65− 0.27− 0.70− 0.44− 0.86− 0.57− 0.69
0.32

29.3
22.6
21.0
23.4
26.0
24.2
15.7
30.6
22.3
25.6
24.1
4.23

− 137.7− 59.4− 158.1− 106.7− 80.4− 101.8− 101.4− 120.3− 104.1− 169.8− 114.0
33.71− 0.24− 1.01− 0.34− 0.47− 0.37− 0.26− 0.11− 0.46− 0.22− 0.67− 0.42
0.26

82.8
56.9
42.0
43.1
38.6
93.1
93.9
97.8
85.5
72.6
70.6
23.45

RT vorticity (-, clockwise rotation), DP Doppler pressure, and ACFD acceleration for changing the flow
direction
Table 3  Changes incharacteristics of the vortex
accompanied by changes in the
diameter of the vortex during
the late stage

VD (mm)Circ. (mm)Vmax (cm/s)

TD (msec)

Distance (mm)

Rev

CFR

20
15
10
5

62.8
47.1
31.4
15.7

52
52
42
35

ES: 100
LS: 120
LS: 120
LS: 120

51.0
62.4
50.4
42.0

0.8
1.3
1.6
2.7

1.0
1.4
1.4
1.9

VD vortex diameter, Circ circumference, Vmax maximum velocity, Distance revolutionary distance (distance/Circ), TD time duration, ES early stage of pre-ETP, LS late stage of pre-ETP, Rev the number of revolutions of the vortex under the assumption that the duration of the TD was 100 ms in ES and 120 ms in LS,
CFR ratio to the centrifugal force of the vortex

contraction, it was almost unchanged at the apical part (A,black) and increased at the basal part (B, red) during preETP. These results show the coexistence of wall contractionand extension in this period.

Wall dynamics measured at the local myocardiallevel
As shown in the middle of Fig. 5, throughout the ES, in the

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Journal of Medical Ultrasonics (2019) 46:413–423

Pre-ETP((+)SR) and extension ((−)SR) appeared repeatedly in the
myocardium, was seen at the central and basal parts of the
IVS [13].

Ej

Accelerated
VortexEjec on

5mm

LVD

FS

VortexForma onb

Discussion

PWT

a
a
c
b
RV

EXTENDIVS aSRA䡈䡐1ac

CONTRACTECGa

PW aSREXTENDbc

CONTRACT

LV

A䡈䡐2

End.

b

EXTEND

Epi.

CONTRACTEXTEND

R
P

Q

T
S

1st Step 2nd Step

1st Step 2nd Step

Early Stage

Late Stage

Fig. 5  Schematic representation of the correlation among left ventricular wall dynamics, axial strain rate (aSR) distribution, and flow
structure (FS) during the pre-ETP (unshaded area) and the ejection
period (Ej). Curvilinear graph: Changes in thickness of the posteriorwall (PWT) and that of the internal diameter of the LV (LVD) at theapical (a, green or black line), basal (b, blue or red line), and central(c, yellow line) parts. Color bar graph: Changes in timing and duration of myocardial contraction (blue color) and extension (yellow
color) observed in the apical (a), central (c), and basal (b) parts in the
IVS (IVS aSR) and PW (PW aSR). Pre-ETP pre-ejection transitional
phase, Ej ejection, FS flow structure, LVD left ventricular diameter,
PWT posterior wall thickness, IVS aSR interventricular septum aSR
distribution, PW aSR posterior wall aSR distribution, Alt1 bending
oscillation, Alt2 thickness oscillation, ECG electrocardiogram, End
endocardium, Ep epicardium, RV right ventricle, LV left ventricle

apical part (A) of the PW (PW aSR) and IVS (IVS aSR),
both the extension ((−)SR, orange) in the epicardial side andthe contraction ((+)SR, blue) in the endocardial side beganat the P wave of the ECG. In the basal part (B), the extension((−)SR) from the endocardial to epicardial side was seen in
the PW and IVS.
In the LS, the apical part (A) of the PW was in the contracting state ((+)SR). At the basal (B) and central (C) partsof the PW, after the temporal contraction ((+)SR), the extension ((−)SR) appeared, followed by the contraction ((+)SR). These changes indicated that the thickness vibration
appeared in the PW.
In the IVS, alternating distribution 1 (bending oscillation), in which contraction ((+)SR) and extension ((-)SR)
appeared reciprocally in the endocardium and epicardium,was seen at the apical part. On the other hand, alternating
distribution 2 (thickening oscillation), in which contraction

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To elucidate the ejection mechanism, it is necessary tosimultaneously measure LV wall dynamics during the
cardiac cycle and accompanied flow structure dynamics
together with the hemodynamics. Changes in both the LV
wall and the flow dynamics can be easily estimated fromthe velocity information obtained by the echo methods. In
the present study, the ejection mechanism was elucidated
noninvasively using echo-dynamography in addition to thedetailed analytical method of the vortex in the LV. Understanding of the ejection mechanism may lead to very early
prediction of heart failure.

Contribution of LV wall dynamics to ejection
The dynamic change of the LV wall during the pre-ETP isconsidered to appear as the ejected blood flow occurs along
the main outflow axis line of the LV, which is connected by
the apex to the center of the aortic valve ring [11, 14]. The
maximum flow velocity distribution along the outflow axis
line in the late stage is shown in the bottom row of Fig. 4.
As shown in the upper row of Fig. 5 and in the apical area
(Fig. 6a), change in the wall thickness was large, but that in
the internal diameter of the ventricle was small during the
pre-ETP. In the basal area (Fig. 6b), the internal space ofthe ventricle dilated, but change in the wall thickness was
small, whereas the outflow tract area was funnel-shaped andwide in the central area and narrow in the area just under theaortic valve. Changes in the velocity distribution along themain flow axis line caused by LV wall deformation will bereflected in the changes in the flow route shape, especiallyin route width.
As a result, the maximum blood flow velocity in the LV
during pre-ETP will be shown as a linearly increasing pattern for which the gradient will be small in the apical areaand large in the basal area. As shown in the bottom row ofFig. 4, the distribution showed a linearly increasing patternwith a gradient of about 9.8 and about 26.4 cm/s in velocity at the basal area, and a gradient of about 4.3 and about
19.2 cm/s in velocity at the apical area. These results were
thought to reflect the changes of the flow route shape caused
by deformation of LV contraction during the pre-ETP.
However, at the central area, a rapidly increasing curvewith a gradient of about 30.3 and about 50.0 cm/s in increment velocity was seen despite the wide flow route. These
increments are thought to be caused by another energy
supply other than transformation of the flow route. AfterJournal of Medical Ultrasonics (2019) 46:413–423

Aorta

4
SV
3

AV

LA
MV

IVS

b

2
PW

1

a

Fig. 6  Schematic representation of the correlation between the flow
structure of the vortex in the left ventricle (LV) displayed by the presumptive path line and wall dynamics of the LV appearing during
the pre-ETP. Brown area: contracting part of the wall, Yellow area:
extending part, Thick black arrows in the wall: moving direction andgrade, Thick gray arrows: path line of the intra-ventricular flow during pre-ETP, 1: residual flow due to the atrial contraction (AC), 2:
large rotating flow during the ES, 3: accelerated rotating flow during
the LS and main flow from the apical area, 4: the spiral flow in theaorta, Upper right figure (b): schematic representation of the LV wall
deformation appearing on the short axis cross-section at the basal part
during the LS, Lower right figure (a): that at the apical part during
the LS. LA left atrium, MV mitral valve, AV aortic valve, IVS interventricular septum, SV sinus Valsalva, PW posterior wall

observing the blood flow structure, we suspect that this rapid
increase in the velocity was caused by the kinetic energy ofthe vortex in the central area.

Contribution of the vortex in the ventricle
to ejection
As shown in LVD and PWT of Figs. 5 and 6a, under the LV
wall dynamics in the early stage of the pre-ETP, the pressure gradient appeared to flow from the apical area of the
LV wall to the IVS, as shown by the white thick arrows in
Fig. 3. The positive pressure (brown in Fig. 3) was transmitted from the apical area to the basal area. At this time,
as shown by the brown and yellow circles in Fig. 6b, theinternal diameter increased, but the wall thickness increased
little or decreased in spite of the contracting state. Thus, the421large vortex appeared at the central and basal areas in theearly stage (Fig. 1, left upper row).
In the subsequent LS, the apical part and the papillarymuscles gradually extruded antero-upward into the ventricle with thickness (thick black arrows at the apical partof Fig. 6). Not only was the center of the vortex displaced
from just under the anterior mitral leaflet to the outflow area
but also the vortex was spherical, the double structure had
disappeared, and the diameter was remarkably diminished(Fig. 1, right upper row). Both the rotating velocity and thenumber of revolutions of the vortex increased by about two
times higher than those in the ES. The ACFD increased
about three times higher than that in the ES (Tables 1, 2),
and that was in almost total agreement with the changes invelocity distribution (about 50.0 cm/s) shown in the lowest row of Fig. 4. The rotation velocity increased further
outside than inside the vortex. Thus, the vortex accelerated
with a large centrifugal force. When this accelerated vortex joined the blood flow in the outflow tract, the outflow
blood velocity was increased from 19.2 to 69.2 cm/s [about
52% of the ejected velocity (95.6 cm/s)] by the centrifugal
force of the accelerated vortex. These facts suggest that theaccelerated vortex in the pre-ETP produces almost half ofthe ejection velocity and plays an important role in the LV
ejecting function.

Contribution of the accelerated vortex to cardiac
function
1. The maximum velocity area of the main outflow wasmade to shift in the antero-upward direction just under
the aortic orifice by the accelerated vortex. At the beginning of the ejection, the spiral ejecting flow was produced in the aorta by aid of the spherical shape of the
Valsalva sinus (Figs. 4, 5, 6).
2. The accelerated vortex caused equalization of the intraventricular pressure just under the mitral leaflet and contributed to pushing up and evenly straining the mitralvalve leaflets from the ventricular side (Fig. 4). Accordingly, the valve leaflets closely contacted each other anduniform tension appeared.
3. The velocity vector distribution pattern near the IVS
showed a wave pattern, as seen in the ES in Fig. 1. Additionally, as shown in Fig. 3, the width of the positive
pressure area near the IVS (interval between the two
white thin arrows in Fig. 3) was reciprocally wide andnarrow. These results indicated that the power producedby the predominant contraction of the myocardium in
the PW was given to the IVS via the vortex within theventricle. Thus, the thickness changed such that oscillation in the IVS occurred and the alternated distribution 1 (bending oscillation) and alternated distribution 2
of aSR (thickening oscillation) appeared in the septum

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Journal of Medical Ultrasonics (2019) 46:413–423(IVS aSR) [13]. These changes in IVS thickness indicate
the genesis of the low-frequency components of the firstheart sound [28, 29].

Limitations
The present study had several limitations. First, the numberof cases was rather small, precluding a statistical analysis.
Second, the technology used here was developed in our laboratory and is not currently accessible by other investigators.
Finally, we must validate the clinical feasibility by investigating cases of various pathological conditions. Therefore,
further observations are essential.

Conclusions
1

2

The vortex with a double structure and uneven velocity
distribution appeared at the central to basal areas of the
LV in the ES of the pre-ETP. This vortex transformed toan accelerated one at the basal area in the LS.
Ejection of blood from the LV was accomplished by a
combination of the following two mechanisms:
1. Extruding action of the ventricular wall producedby narrowing of the LV chamber due to myocardial
contraction.
2. The centrifugal force of the accelerated vortex developed by spatial deformation of the LV structures.

	  These two mechanisms contributed at nearly similar
rates (50%) at the same time.
3. This accelerated vortex acted as a promoter of the spiralflow in the aorta and oscillated the IVS. This oscillationis thought to participate in the genesis of the first heartsound.
4. From a clinical and pathophysiological point of view, theaccelerated vortex in the pre-ETP played a very important role in the pump function, especially for the effective blood ejection from the LV.

Compliance with ethical standards
Conflict of interest There are no financial or other relations that could
lead to a conflict of interest.
Ethical aprroval All procedures followed were in accordance with thestandards of the Ethics Committee for Human Research (institutionaland national) and with the Helsinki Declaration of 1975, as revisedin 2008.

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