Journal of Cardiology (2011) 58, 232—244

available at www.sciencedirect.com

journal homepage: www.elsevier.com/locate/jjcc

Original article

Physiological basis and clinical signiﬁcance of left
ventricular suction studied using echo-dynamography
Motonao Tanaka (MD, FJCC) a,∗, Tsuguya Sakamoto (MD, FJCC) b,
Shigeo Sugawara (MD, FJCC) a, Hiroyuki Nakajima (RMS) a,
Takeyoshi Kameyama (MD) a, Haruna Tabuchi (MD) 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, Japan
Hanzomon Hospital, Kojimachi 1-14, Chiyoda-ku, Tokyo 102-0083, Japanc
Institute of Medical Ultrasound Technology, Yokoham 2-12-15, Sagamihara 229-1122, Japand
Department of Electrical Engineering, Tohoku University, Aramaki-Aoba 6-6-05, Aoba-ku, Sendai 980-8579, Japanb

Received 22 June 2011; accepted 28 June 2011
Available online 27 August 2011

KEYWORDS
Ventricular suction;
Rapid ﬁlling phase;
Blood ﬂow structure;
Strain rate;
Third heart sound;Echo-dynamography

Summary
Background: The existence as well as the exact genesis of left ventricular suction during rapid
ﬁlling phase have been controversial. In the present study, we aimed at resolution of this problem using noninvasive and sophisticated ultrasonic methods. The clinical meaning was also
documented.
Methods: Ten healthy male volunteers were examined by 2D echocardiography and echodynamography which enables us to obtain detailed instantaneous data of blood ﬂow and wallmotion simultaneously from the wide range of the left ventricle. The correlation of blood ﬂow
and wall motion was also studied.
Results: Rapid ventricular ﬁlling was divided into 2 phases which had different physiology. The
early half (early rapid ﬁlling: ERF) showed the effect which was alike drawing a piston. Thiswas proved by the shape of the velocity of inﬂow and the basal muscle contraction which
actively assisted extension of the relaxed apical and central parts of the left ventricle, giving
the negative pressure which causes the ventricular suction.
The later half (late rapid ﬁlling: LRF) showed the turning of the fundamental ﬂow and thesqueezed basal part just like the sphincter in addition to the expansion of the apical and central
portions of the left ventricle, and all of these cooperatively augmented the suction effect.

∗ Corresponding author. Tel.: +81 022 719 5161; fax: +81 22 719 5166.

E-mail address: m.tanaka@jata-miyagi.org (M. Tanaka).
0914-5087/$ — see front matter © 2011 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.
doi:10.1016/j.jjcc.2011.06.011

Physiological basis and clinical signiﬁcance of left ventricular suction studied using echo-dynamography

233

Conclusion: Ventricular suction does exist to help ventricular ﬁlling. Simultaneous appearanceof the contraction in the basal part and the relaxation or extension in the apical part during thepost-ejection transitional period was made to occur the suction in the LV. And it can be said thatthe suction appeared in the late stage of systole as the one of the serial systolic phenomena.
© 2011 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

Introduction
Katz [1] speculated that ventricular suction during diastole
might exist, and later on, Wiggers [2] mentioned an aspiration force might be generated whenever the elastic stressduring contraction was released. Thereafter, the conceptof diastolic suction has been disputed by Brecher [3] andothers.
However, the previous studies dealt with only an excisedand isolated heart preparation [4,5] or, at most, anesthetized animals [6—9], Although human studies using acatheter-tip manometer [10—12] were able to measure pressure difference in the ventricle, the distinctive features,
genesis, and physiological signiﬁcance of the diastolic suction have been controversial. This was because these studies
did not clarify the data concerning the pressure differenceor transmitral ﬂow velocity. This was also true as to the onedimensional information of the ultrasonic Doppler method.
We attempted to clarify many facets of left ventricularsuction in terms of blood ﬂow structure and ﬂow dynamics,
regional wall dynamics, as well as their correlation using
echo-dynamography [13,14] as previously reported.

Subjects and methods
Subjects
Ten healthy male volunteers aged 30—50 years who provided
informed consent were the subjects.

Methods(2) Analysis by using the 2D ﬂow velocity vector distribution
As described previously [23—25], the Doppler velocity
vector was obtained at many points, and the two dimensional distribution was displayed on the same scanningplane together with color Doppler signal and 2D echocardiogram (Fig. 1(1) and (2)).
(3) Analysis by the spread of main ﬂow axis line
The meaning of the ridge line in the magnitude distribution of the ﬂow vector was described previously[26]. The ridge line represents a main ﬂow axis, andcentralization of the power produced by the motion of
the local ventricular wall and the transmission of theblood were shown. The wall function was evaluatedby the changes of the pattern during the cardiac cycle[18,19,27] (Fig. 1(3) and (4)).
(4) Analysis by using the velocity proﬁle along the main ﬂow
axis line
Displaying the ﬂow velocity vector distribution, themagnitude distribution along the ﬂow axis line wasobtained as a one-dimensional curvilinear graph. Then,the inclination of the graph indicates the one of theconvective acceleration of ﬂow, and the integration
indicates the ﬂow volume [25] (Fig. 2).
(5) Analysis by using the Doppler pressure distribution on
the scanning plane [14,18—20]
To deduce the inﬂuence of the dynamic pressurechange to the distribution of ﬂow velocity data, theNavier—Stokes’ equation of motion was applied for theprocessing of the data [19]. This ‘‘Doppler pressure’’
was displayed by color on the 2D echocardiogram. The
reference point was set at the area beneath the ﬁbrous
trigon (Fig. 3).

The details were described partly in the previous articles[13—24].
Analysis of the blood ﬂow structure in the left ventricle(LV) [13—18,23](1) Acquisition of ﬂow velocity information
Special designed ultrasonic equipment (Alola Co.,model 6500, Tokyo, Japan,) was used, and the recordings were made in the supine or lateral decubitus
position. The scanning plane of the two-dimensional(2D) echocardiogram included 3 points, i.e. center ofboth the aortic and mitral oriﬁces, and the ventricular apex. This plane had the advantage to analyze
the blood ﬂow ﬁeld in the LV as previously mentioned [25]. 2D Doppler velocity was measured by
apical approach and transferred to a personal computer. The data was processed off-line using thesoft-ware of echo-dynamography [14—16,19,23,24].
Furthermore, phonocardiogram using a crystal acceleration microphone placed around the cardiac apex
was recorded simultaneously with echocardiogrm andelectrocardiogram.

Analysis of the regional LV wall dynamics(1) Macroscopic analysis using 2D echocardiogramHigh speed sector scan of 66 frames/s was used tomeasure the thickness of the interventricular septum(IVS) and the posterior wall (PW) during cardiac cycle.
The LV internal diameter at the apical (A), central (C)and basal (B) parts, as well as the diameter (MRD)
and displacement (MRM) of the mitral ring were alsomeasured. The images of successive 24 echocardiograms were used every 30 ms. The LV movement during
one cardiac cycle was precisely analyzed as shown in
Fig. 4.
(2) Analysis using free angle M-mode method
Using the memory of 2D echocardiogram of several cycles, M-mode echocardiograms were depicted
to obtain the motion of the tissue of the oriented
directions, so as to measure accurately various tissue movements simultaneously (named as free angle
M-mode: FAM-mode). This method also enabled us to234

M. Tanaka et al.

Figure 1 Upper images 1 and 2: Two-dimensional mapping of the ﬂow velocity vector during rapid ﬁlling phase in the longitudinal
section plane of the left ventricle in a normal case. The cardiac phase recorded the vector mapping is shown by the yellow lineon the ECG. A reference size of the vector is shown by a yellow bar at the upper left corner of the mapping. A white arrow (E)shows the toroidal eddy ﬂow. Bottom images 3 and 4: Two-dimensional distribution of the main ﬂow axis line of the inﬂow into theventricle in ERF (3) and LRF (4) shown by the overlapped display with the color ﬂow imaging. White lines show the line for obtaining
the ﬂow velocity distribution along the main ﬂow axis line shown in Fig. 2. ERF, early stage of the rapid ﬁlling; LRF, late stage ofthe rapid ﬁlling; AO, aorta; LA, left atrium; LV, left ventricle.

conﬁrm the relationship between the minimal mitralvalve ring and the maximal valve opening (Fig. 5).
(3) Microscopic analysis using strain rate (SR) distribution
measured by the phase difference tracking method(PDT)
By switching beam direction at every 5◦ intervals(sparse scan), about 30◦ within the 90◦ sector angle
was scanned at the speed of 630 frame/s. The moving
velocity of the pulsating myocardium was measured, thethickness change in each direction was obtained at every
thickness interval of 0.82 mm by the PDT [21]. This was
based on the assumption that the sound speed in the
myocardium is 1600 m/s [28]. The SR thus obtained wasoverlapped on the M-mode and 2D images, respectively,
as a color corded information [22] (Figs. 6 and 7).
(4) Measurement of LV internal diameter

Using PDT, the change in the LV internal diameter wasexactly measured by looking the moving speed of the
2 target points set on the endocardium of the PW and
IVS. This was displayed by the curvilinear graph together
with electrocardiogram and phonocardiogram (Fig. 7).

Results
Blood ﬂow structure in the LV demonstrated by
ﬂow velocity vector
During rapid ﬁlling, two types of ﬂow velocity vector distribution widely spread in the longitudinal sector plane wereseen from the mitral valve (MV) oriﬁce to the apex as follows(Fig. 1):

Physiological basis and clinical signiﬁcance of left ventricular suction studied using echo-dynamography

235

Figure 2 Upper four graphs: Velocity distribution (red zigzag curvilinear lines) and velocity gradient (black lines) along the main
ﬂow axis line (shown in Fig. 1(3) and (4)) of the inﬂow into the left ventricle during the ERF, LRF, SF, and AC phases. Bottom graph:
Velocity gradient on the main ﬂow axis line in the ERF obtained from 10 normal cases. The black line indicates the mean value ofthe gradient. The inclination of the gradient is almost the same in all normal cases. The red line shows the mean value of that in
the AC. In AC, the inclination of the gradient was different in atrial side from that in apical side. ERF, early stage of the rapid ﬁlling;
LRF, late stage of the rapid ﬁlling; SF, slow ﬁlling; AC, atrial contraction; LA, left atrium; VR, mitral valve ring position; B, basal
part; C, central part; A, apical part; Abscissa shows velocity in mm/sec, and Ordinate, distance in mm.

(1) During ERF
The ﬂow velocity vector directed rather straight tothe apex with a minor zigzag pattern. Though thecircularly arranged vectors (E) due to the toroid-likeeddy probably resulting from the ﬂow separation wasobserved behind the MV tips, no reversal or reﬂected
ﬂow was observed at the inner surface of the LV (Fig. 1,
ERF).
The main ﬂow axis line was nearly straight from thecenter of the MV oriﬁce to the apex, and thereafter
3 branches of the axis line were observed behind thepapillary muscle area (Figs. 1—3). The velocity proﬁlealong the main ﬂow axis line showed ‘‘ups and downs’’of shape (Fig. 2-ERF; black lines), and the summit wasnear the center of the basal part at the maximal part of
the LV short-axis diameter. The velocity gradients in the
MV oriﬁce side (acceleration) and apical side (deceleration) were ca. 12.9 and ca. −10.4, respectively (blacklines).
The averaged velocity gradients from 10 subjects
were 13.3 (acceleration) and −11.1 (deceleration),
respectively (black lines in Fig. 2 bottom).

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M. Tanaka et al.

Figure 3 Two dimensional distribution of the Doppler pressure (dynamic pressure) in the left ventricle in the four cardiac phases.
Cold colored area shows the negative pressure and warm colored area, the positive pressure. Pressure level is indicated in thecolor bar in the right column. Narrow white arrow, the negative pressure appeared in the area just behind the posterior wall during
the initial stage of the sucking action even during the systolic phase. Wide white arrow, the increasing negative pressure at the
beginning of the upward movement of the mitral valve ring. Green arrow, oscillation of the pressure wave indicating the originof the third heart sound. Bottom graphs are one dimensional display of the pressure distribution along the blue lines on the 2D
images. Oscillating pressure pattern are clearly observed (green arrow). LS, late systolic phase; ID, isovolumetric dilatation phase;
ERF, early stage of rapid ﬁlling; LRF, late stage of rapid ﬁlling; AO, aorta; LA, left atrium; LV, left ventricle.

(2) During LRF
The distribution of the velocity vector of the inﬂow
blood widely spread (Figs. 1—2 LRF). As to the toroidlike eddy and reversal or reﬂected ﬂow at the apicalarea, the same was true as in ERF.
The main ﬂow line was divided in 2 ways. The one
was main and curved anteriorly at the center of the LV,
and the other was divided into 3 branches directing toeither the apical or anterior or posterior areas behindthe papillary muscles (Figs. 1—4). The main ﬂow further
directed behind the anterior MV and collided with thereverse side of the leaﬂet, causing resonant oscillationof pressure wave. This was demonstrated as a pile of thecold and warm color strips (green arrow in Fig. 3; LRF).
The velocity vector proﬁle was also ‘‘ups and downs’’
shaped similar to that of ERF, and the summit was lower
about 50% than that of ERF (Fig. 2: LRF). The velocity
gradients were 10.7 in the acceleration side and −9.0
in the deceleration side, respectively. However, velocity
gradient at the beginning and ending points was slightly
greater than those of ERF.

2D Doppler pressure distribution
Even during late systolic phase (LS), negative pressure ofabout −0.04 mmHg was observed at the central and basal

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237

Figure 4 Top graph, Changes in thickness of the posterior wall (PW) and the inter-ventricular septum (IVS) measured at 3 parts ofbasal (B, blue line), central (C, red line), and apical part (A, green line) of the left ventricle during one cardiac cycle. Bottom graph,
Changes in the internal diameter of the left ventricle at the 3 parts of basal (B), central (C) and apical (A), and of the mitral ring
diameter (MRD, brown), and changes in distance of the upward displacement of the posterior part of mitral ring during one cardiac
cycle (MRM, yellow). The measurement was performed from the two-dimensional echo-cardiograms obtained in the longitudinal
direction of a normal left ventricle. The number shows a speed and distance of the change. IVS, Inter-ventricular septum; PW,
posterior wall; Is, 1st heart sound; IIs, 2nd heart sound; IC, isovolumetric contraction; Ej, ejection; ID, isovolumetric dilatation; SF,slow ﬁlling; AC, atrial contraction; ERF, early stage of rapid ﬁlling; LRF, late stage of rapid ﬁlling; Green shaded area; the phase inwhich the contracting and extending parts coexist in the ventricular wall.

areas near the inner surface of the PW (thin white arrow in
Fig. 3: LS).
During isovolumetric dilatation (isometric relaxation:
Fig. 3: ID), negative pressure areas appeared near the
inner surface of the LV wall and beneath the valve rings(thick white arrow). The measurement value was −0.07 and−0.13 mmHg beneath the aortic and mitral valve, respectively, and −0.03 mmHg at the apical area near the PW.
Therefore, the negativity of the basal area was 2—4 times
greater than those at the other areas.
During ERF (Fig. 3-ERF), such a widely spread negativity
and a resonance of the negative pressure were seen from
the MV oriﬁce to the apex along the LV long axis, and thelowest was −1.2 mmHg in the central and basal area. The
pressure gradient along the inﬂow axis line was about 0.46
in the oriﬁce side and was about 0.32 in the apical side.
During LRF (Fig. 3-LRF), positive pressure area spreadover the apical area, while negative one appeared widelyin the central and basal areas along the short axis. At thesame time, the minimal pressure (ca. −1.8 mmHg) was in thecenter of the outﬂow area near the IVS, and the pile of thepositive and negative pressure areas was seen behind theanterior mitral valve, resulting in the pressure oscillation(green arrow).

LV wall dynamics macroscopically observed by 2D
echocardiography and FAM
Thickness of the IVS and the PW at the apical area decreased
during rapid ﬁlling phase (line A: green in Fig. 4), while theinternal LV diameter increased rapidly in ERF and then slowly
in LRF (Fig. 4 top).
At the mid-ventricular level (central area: line C: red),the PW thickness increased in the mid-ERP and decreased
rapidly in LRF, while the IVS thickness decreased. The LV

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M. Tanaka et al.

Figure 5 The free angle M-mode display of the left ventricular wall and mitral valve. M-mode display of the ventricular wall atbasal (B), central (C) and Apical (A) parts for measuring the time when the maximum inward displacement of the wall appeared.
AO, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.

internal diameter increased rapidly in ERF and then slowly
in LRF.
At the basal area (line B: blue), the PW thickness
increased until mid-LRF, while the LV diameter decreased
until the end of ERF and then gradually increased in LRF. No
apparent changes were seen in the IVS thickness.
The timing of the maximum thickness of the PW was
delayed in B compared to A by about 210msec, and thatof the minimal internal diameter of the LV was similarly
delayed in B. This indicated that contraction and extension
were transmitted dispersively, resulting in the peristalsis of
the LV wall [25].
After the maximal MRD (brown line) reached the endof ERF, it decreased rapidly in LRF. The FAM-mode image
showed time lag of about 18msec in the minimal size of the
MRD compared to the maximal MV opening (Fig. 5), while
the posterior part of the mitral ring (MR) moved toward theleft atrium (LA) (Fig. 4 bottom: MRM: yellow line). This indicated that LV predominantly dilated longitudinally at thebasal part of the LV.
During rapid ﬁlling phase, as indicated by the shaded areain Fig. 4 top, the muscle in basal area (B) was contracting,whereas the muscle in apical area (A) was in the reversed
behavior, i.e. the contracting and extending state occurredat the same time process. Also, the maximal thickness ofthe basal part of the PW coincided in time with the minimal
thickness of the apical and central parts of the PW, and further the boundary between ERF and LRF nearly coincided intime with the summit of E of Doppler velocity curve. These
facts indicated the basal muscle contraction tempted in therelaxed apical and central muscles to extend.

Microscopic LV wall dynamics analyzed by strain
rate (SR) distribution
In Fig. 6, positive SR (+) (cold color; blue) indicates contraction, and negative SR (−) (warm color), either relaxing (red)or extending (yellow) state.
(1) During ERF(a) PW (Fig. 6)
The apical endocardial side was in the relaxing
state (SR: nearly 0), and the epicardial side was inextending state (SR = ca. −4.0) (Fig. 6(3)). The central part showed a sandwitched pattern (Fig. 6(2)),
i.e. contracting and extending states were piled.
The contraction was mainly in endcardial side andthe extension was mainly in epicardial side as wellas in the mid-layer between these two sides. Furthermore, the string-like narrow contracting area
was seen near the epicardial side (vertical whitearrow C). The basal part (Fig. 6(1)) showed a large
contraction in the endocardial side during the ﬁrst
half of ERF, whereas it changed to large extension
in the second half of ERF. Extension was also seenin epicardial side and again string-like contraction
was observed.
(b) Interventricular septum (IVS)
Contraction and extension were mixed in the apical and central areas, and extension was seen in thebasal area. The tension state persisted in the apicaland central areas, whereas extension persisted in
the basal area.

Physiological basis and clinical signiﬁcance of left ventricular suction studied using echo-dynamography

239

Figure 6 M-mode images of the strain rate (SR) distribution in the time sequential change in the intra-ventricular septum (IVS)
and posterior wall (PW) measured by using the sparse scan and the phase difference tracking method on the longitudinal section
plane of the left ventricle (LV). The SR was obtained in the beam direction of 1—3 shown on the two dimensional echo-cardiogramin the right below. The cold color area shows an increment of the SR (contraction) and the warm color area shows a decrement of
the SR (extension) as demonstrated in the color bar. IC, isovolumetric contraction; Ej, ejection; ID, isovolumetric dilatation; ERF,
early stage of rapid ﬁlling; LRF, late stage of rapid ﬁlling; White arrow C, contracting muscle layer; Oblique white line, spreading
process of the extending area in the LV wall; AO, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.

(2) During LRP(a) PWAt the apical area, there was a large extending part in the epicardial side, whereas a relaxing
part was present in the endocardial side. At thecentral area, a large extension was in the midlayer, but contraction was in the endocardial side,
and a string-like narrow contracting area was near
the epicardial side (Fig. 6(2), thick white symbolC) which continued from that of ERF. At the basal
area, a large area of extension continued from thatof ERF was shown in the mid-layer and epicardialside. Contracting area was seen in the mid-layer andendocardial side. During the second half, extension
was seen through endocardial to epicardial side.
Near the epicardial side, string-like narrow contracting area was again observed (Fig. 6(1), thickwhite symbol C).
(b) IVSA mixture of contracting and extending areas wasseen in the area from the apical to the basal part.
This indicated that the IVS was in tension state in
LRF.
(3) SR distribution

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M. Tanaka et al.

Figure 7 Upper 2 images show the two dimensional SR distribution in the time point of (a) and (b) on the ECG and PCG at the lower
graph. The contracting area (C) in ﬁgure b observed at the part near the epicardium was supposed to be the oblique muscle layer ofthe ventricular musculature, and (C) in ﬁgure a at the middle and endocardial parts near the valve ring at the basal part supposed
to be circumferential layer. Lower graph shows changes in the internal diameter of the left ventricle during systole through rapid
ﬁlling phase measured by the phase tracking method in the 5 beam directions (1—5) shown in the right upper side picture. Beams 1
and 2, basal part; Beams 3 and 4, central part; Beam 5, apical part; AO, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle;
III, third heart sound; ID, isovolumetric dilatation; ERF, early stage of rapid ﬁlling; LRF, late stage of rapid ﬁlling; SF, slow ﬁlling;
AVC, aortic valve closure; ECG, electrocardiogram; PCG, phonocardiogram.

As described above, SR distribution demonstrated
that contraction and extension of the myocardium
occurred simultaneously in the LV wall. Namely, a contracting area at the basal part of the LV near the valve
ring and remarkable extension in the short axis direction
at the central and apical areas in addition to dilatationof the apex were simultaneously observed.

LV expansion in short axis direction (Fig. 7)
During ERF, LV diameter increased slowly at the apical area
(red line) and center area (green line), whereas the change
was minimal at the basal part (black line). This indicatedthat LV volume during ERF increased predominantly along
the longitudinal axis.

Physiological basis and clinical signiﬁcance of left ventricular suction studied using echo-dynamography
On the other hand, LV diameter during LRF slowly
increased at the apical area (red line), slightly faster at
the central part (green line), and fastest at the basal part(black line). These results indicated that LV volume during
LRF increased predominantly along the shot axis.

The third heart sound (III)As shown in Fig. 7, the III was inscribed in the PCG coincided
in time with the rapid expansion along the short axis. Superimposition of Figs. 3 and 7 conﬁrmed that the III occurredcoinciding with the pressure oscillation within the LV (Fig. 3,
green arrow).

Discussion
The left ventricular relaxation process in diastolic ﬁlling was
ﬁrst described by Katz [1], and Wiggers [2] discussed the roleof diastolic suction.
Experimental studies were done by Brecher [3], but thepressure variation during rapid ﬁlling is so small that it
is unable to explain a large amount of ventricular bloodinﬂow during a very short time, particularly in animals withvery rapid heart rate and extremely short diastolic ﬁlling time [4,5]. Furthermore, many physiological conditions
including even the atmospheric pressure may change, sothat the results of animal experiments may not be worthy of evaluation. The similar results using intracardiac
pressure evaluation [6,7,9,12] or ultrasonic Doppler method[9—11] were not reliable, because spatial structure of intraventricular blood ﬂow, pressure distribution within the LV,
local ventricular wall dynamics and their correlation were
all difﬁcult to estimate by these methods. The present study
suggested that left ventricular suction involved a complicated mechanism, and that only noninvasive method such as
our echo-dynamography might resolve the above-mentioned
difﬁculties.
We have already pointed out that the ventricular suction
started at the late stage of the systole [25], and the distinctive feature of suction appeared in the ERF phase. As
Courtois [7] reported using pressure measurement methodthat this ﬁlling consisted of 2 phases, and further veriﬁed theboundary of these two phases coincided in time with the E
wave of the Doppler velocity curve. We proved further thatthese 2 phases contributed differently to the ventricularsuction during rapid ﬁlling phase.
As to the ERF phase, we disclosed that the inﬂow occurredwith less resistance and less inertia to draw the blood into
the LV, because of the correspondence of the direction ofventricular dilatation and inﬂow. This is such that a piston
effect along the long axis without the commitment of shortaxis dilatation.
On the other hand, ventricular ﬁlling during LRF phase
was quite different in terms of division of ﬂow direction.
Such a division was caused mainly by the active dilatationof the central and basal areas of the LV along the short axis,
so as to increase the LV volume and was also helpful to pourthe inﬂow blood into the outﬂow tract which was just like adead space during ERF.
The previously advocated theory of ventricular suction
was based on the assumption of myocardial elastic recoil

241

during diastole [6,9,12,29—31], which was caused by therelease of potential energy accumulated within the muscle during systole [32—34]. This assumption has several
ambiguous points. For example, they did not consider the
discordant movements of the local LV wall, instantaneousgeometric changes of the LV and intraventricular ﬂow structure within the LV.
Certainly, LV suction may require active negative pressure during diastole and the present study proved the widely
spread negativity which was spatially changing in time withthe wall dynamics. All facts considered, the correlation
between the wall and ﬂow dynamics is schematically summarized as shown in Fig. 8.
Sengupta et al. [35] stated that the mechanical shortening of the LV propagated from apex to base, as did theelectrical transmission.
However, our study disclosed that this delay was due tothe peristalsis [25], and at the end of systole, muscular
contraction propagated to the basal part near the mitralvalve ring, whereas the apical and central parts of the
PW were in the completely relaxed and extended state (asdemonstrated by green shadow in Fig. 4). Important facts
were that, during ERF, these relaxing (SR = 0) and extending(SR = −) parts were pulled rapidly parallel to the long axis
direction along with the upward movement of the mitralvalve ring. There was no simultaneous extension along theshort axis. On the other hand, LV extension at the central andapical parts appeared along the short axis direction during
LRF.
We postulated that these wall dynamics might have arelationship to the anatomy of the ventricular muscles. As
well known, myocardium has 3 muscle layers, including middle circular muscle which is thick, and internal and external
oblique muscles which are running along each other in the
opposite direction [36—40]. The upper margin of the muscle fuses tightly with the ﬁbrous aortic and mitral valve
rings which are also tightly fastened to each other at theﬁbrous trigon, and thereby the mitral ring has a hinge-likemobility.
When this anatomy was compared with our SR data, it
is not difﬁcult to speculate that symbol C in Figs. 6 and 7b
are both oblique muscle group, while symbol C in Fig. 7ais that of circular muscle. This means whenever the basal
muscle layer is in the contracting state (SR+), the central
and apical muscles are in either relaxing (SR 0) or extending(SR−) state. Namely, the contracting and extending areas
co-exist separately in the LV wall.
This phenomenon is illustrated in the bottom of Fig. 8,
and this makes it easy to understand the underlying mechanism of ventricular suction.
With the strong contraction of the circular muscle (Cir)(thick and blue arrow), the posterior part of the mitral valve
ring is vigorously pulled toward the interventricular septum of high tension and is further pulled up toward theleft atrium (vertical blue arrow) by the hinge-like motionof the ﬁbrous trigon as a fulcrum (black arrow). And then,
the narrowed mitral valve oriﬁce causes shortening of theantero-posterior diameter of the valve (thin horizontal blue
arrow), and the already relaxing and extending central andapical parts of the PW remain almost unchanged. Thus, thisis the reason of LV volume increase due to the suction during
ERF.

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Figure 8 Schematic representation of the correlation among the ﬂow structure, wall dynamics and Doppler ﬂow velocity during
the rapid ﬁlling phase (upper two images), and of the correlation between the muscle orientation and the contraction process inthe basal part of the ventricle (lower image). E, toroidal eddy produced by the separation of ﬂow at the edge of the mitral valve
leaﬂets; Gray large arrows F, main inﬂow; Black arrows, direction and magnitude of the extension and contraction of the moving
ventricular muscle; Green arrows, extending direction; Blue arrows, direction of the muscle contraction; FRF, early stage of rapid
ﬁlling; LRF, late stage of the rapid ﬁlling; Cir, circumferential muscle layer; Obl, oblique muscle layer.

The mechanism of ventricular suction during LRF is asfollows: when both inner and outer oblique muscles contract efﬁciently (thin vertical blue arrow positioned laterally
in the ﬁgure), the basal part of the PW further displaces
upward and posteriorly. Then, the antero-posterior diameter of the mitral valve ring diminishes and the valve ring
becomes oval-shaped. This narrowing of the valve ring is
caused by the sphincter action of the circular muscle.

Furthermore, the central and a part of the basal areas arefurther extended in the short axis direction (green arrows),
resulting in the suction during LRF.
In fact, ventricular suction described herein is thought
to be one step of a series of ventricular systolic action. Theenergy required for such suction might be supplied by thecontraction of the basal myocardium. Many previous clinicalreports [10,12,29] suggested that myocardial contractility

Physiological basis and clinical signiﬁcance of left ventricular suction studied using echo-dynamography
was improved whenever ventricular suction was restored.
This was thought to be consistent with the previous experimental results [7—9,11].
Ventricular suction had some connections to the mechanism of heart sound production. In the present study, thethird heart sound is thought to be generated by the vibrationof either mitral valve or ventricular muscle coincident withthe sudden decrease or halt of the rapid ventricular ﬁlling[41—43]. Courtois [7] suggested that the place of production
was the apical ventricular wall, because pressure reversalof a high degree was observed around the apex. However,the present study disclosed that actively extending apicalarea causes inﬂow without resistance, so that the vibrationof the apex is unbelievable. Actually, the third heart sound
was recorded consistent in time with LRF. During this period,
blood inﬂow passed the outﬂow and reached the reverse sideof the mitral valve and collided with this valve. The pressure was reﬂected and transmitted to the IVS, resulting in
the oscillation of blood of back-and-forth between the valve
and the IVS. Thus, alternate positive and negative pressure
areas were seen in the outﬂow area (green arrow in Fig. 3LRF). This indicated that the occurrence of low frequency
vibration might be the resonance of the pressure wave inaccord with the vibration theory of the cardiohemic system[42,44].

Conclusion
Using echo-dynamography newly developed, physiologicaland clinical features of left ventricular suction during rapid
ﬁlling phase were investigated.
The suction developed by inhaling inﬂow blood by two
ways. One was the ERF, during which the apical part was
expanding along the long axis of the left ventricle, causing
the suction by the piston effect. The second was the LRF,
which was separated from ERF by the summit of the E waveof Doppler velocity curve, and during which blood supply of
inﬂow was due to the expansion in the short axis of the basal
part toward the outﬂow, causing additional volume increasein the left ventricle.
In these manners, both contraction and extension coexist
within the left ventricle during rapid ﬁlling phase and theeffectiveness of suction was thus enhanced.
For these mechanisms, systolic contraction of the basal
part during ERF phase, which was followed to the late stageof ventricular contraction, played an important role. Theenergy of suction was supplied by this basal muscle contraction.
The possible relationship of the mechanism of suction andthe structure of the ventricular muscle layer was discussed
in detail.
Clinically, the mechanism of generation of the third heartsound was thought to be derived from the resonance ofpressure between the anterior mitral valve and the intervenricular septum.

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