Download Assessment of Diastolic Hemodynamics by Analyzing Left

241
St. Marianna Med. J.
Original Article
Vol. 29, pp.241 ~ 249, 2001
Assessment of Diastolic Hemodynamics by Analyzing Left Ventricular
Filling Flow Propagation Velocity in Patients with Hypertensive
Left Ventricular Hypertrophy
Shinichi Tokuoka, Sachihiko Nobuoka, Junzo Nagashima, and Fumihiko Miyake
（Received for Publication: August 17, 2001）
Abstract
Objectives: The purpose of this study was to assess the left ventricular (LV) filling flow propagation both in
early and late diastolic phases using the color M-mode Doppler technique, and to assess relation of diastolic hemodynamics to cardiac alterations in patients with hypertensive LV hypertrophy.
Methods: Subjects included 45 consecutive patients with hypertensive LV hypertrophy (HT group) and thirtyone subjects with no evidence of heart disease (Control group).
Echocardiographic and pulsed Doppler examinations were performed, and the data was analyzed to determine
the LV mass index (LVMI), relative wall thickness (RWT), and the maximal early (E) and late (A) transmitral
Doppler velocities. A color M-mode Doppler image of the LV filling flow was recorded and the flow propagation
velocity was measured during early (FPV-E) and late (FPV-A) LV filling phases. Then, 1) FPV-E/E, FPV-A/A
and the ratio of FPV-A/A to FPV-E/E (the FPV ratio) were compared between the two groups, 2) correlation
between FPV-E/E or FPV-A/A and LVMI or RWT was assessed in the HT group.
Results: 1) FPV-E/E and FPV-A/A were significantly lower in the HT group than in the Control group, and
the FPV ratio was significantly higher in the HT group than in the Control group. 2) There was a significant negative correlation between FPV-E/E and LVMI, and there was a significant negative correlation between FPV-A/A
and RWT in the HT group.
Conclusions: In patients with hypertensive LV hypertrophy, diastolic function was considered to be impaired
both in early and late diastolic phases, and this impairment was considered more severe in the early diastolic phase
than in the late diastolic phase. It was considered that LV diastolic dysfunction was more severe in patients with
hypertensive LV hypertrophy in cases having a higher RWT and larger LVMI.
Key words
hypertensive left ventricular hypertrophy, diastolic function, flow propagation, color M-mode Doppler method
Division of Cardiology (Director: Prof. Fumihiko Miyake), Department of Internal Medicine
St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae-ku, Kawasaki 216-8511, Japan
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Tokuoka S Nobuoka S et al
242
Table 1 Clinical characteristics of the study subjects
INTRODUCTION
HT Group
Impairment of the left ventricular (LV) diastolic
function occurs in the early stage of hypertension
and is considered to be an important factor contributing to hypertensive heart failure1)2). In view of the
importance of LV hypertrophy and associated myocardial fibrosis in the development of diastolic dysfunction3)4), it is meaningful to assess how LV
diastolic hemodynamics are related to cardiac alterations and geometric remodeling in patients with
hypertension.
The assessment of the blood flow propagation
of the LV filling phase by using a color M-mode
Doppler technique has recently attracted attention
as a new non-invasive method for assessing LV
diastolic function. Several reports5~7) have emphasized the advantages of the LV filling flow propagation for conventional non-invasive parameters
obtained by pulsed Doppler examination. However,
the LV filling flow propagation in patients with
hypertension has not been well examined, and
assessment of the flow propagation in the late
diastolic phase has not been studied.
The purpose of this study was to assess the
LV filling flow propagation both in early and late
diastolic phases using the color M-mode Doppler
technique, and to assess how LV diastolic hemodynamics are related to cardiac alterations in
patients with hypertensive LV hypertrophy.
Control Group P value
Number
45
31
Age (yr.)
64.8 ± 12.9
63.0 ± 9.8
20/25
19/12
Male/Female
BSA (m2)
1.65 ± 0.19
1.67 ± 0.16
NS
NS
SBP (mmHg)
150.2 ± 13.5
128.5 ± 9.4
p<0.01
DBP (mmHg)
85.9 ± 10.2
79.5 ± 9.0
p<0.01
MBP (mmHg)
107.2 ± 10.2
95.9 ± 7.2
p<0.01
HR (beats/min)
69.4 ± 8.2
68.7 ± 8.1
NS
Abbreviations: BSA=body surface area, SBP=systolic blood
pressure, DBP=diastolic blood pressure, MBP=mean blood
pressure, HR=heart rate
subjects (Control group) (Table 1).
Echocardiographic study
Echocardiograms were obtained using a
TOSHIBA SSH-160A equipped with a 2.5-MHz
transducer. A two-dimensional targeted M-mode
echocardiogram was recorded in each patient with
simultaneous recording of a II-lead electrocardiogram and phonocardiogram. All examinations were
performed in the 30˚ left-lateral decubital position.
On the M-mode LV echocardiogram, LV end-diastolic dimension (LVDd), LV end-systolic dimension
(LVDs), diastolic wall thickness of interventricular
septum (IVSTh), and posterior wall thickness
(PWTh) were measured. The LV internal dimension
and diastolic septal and posterior wall thickness
were measured at the peak of R wave of the electrocardiogram. The percentage of fractional fiber shortening (FS) (%) was calculated as (LVDd–LVDs/
LVDd) × 100. Relative wall thickness (RWT) was
calculated as 2 × PWTh/LVDd. LV mass (LVM)
was calculated using the following formula validated
by Devereux and Reichek9):
LVM (g) = 1.04 × {(LVDd + IVSTh + PWTh)3 –
(LVDd)3} – 13.6
LVMI (g/m2) was obtained by dividing LVM by
the body surface area.
Doppler study
Pulsed Doppler imaging was performed with
reference to a two-dimensional echocardiographic
image from an apical two-chamber view in each
patient. The pulsed Doppler sample was placed at
the mitral leaflet tips to obtain maximal transmitral
METHODS
Subjects
We studied 45 consecutive patients with hypertensive LV hypertrophy (HT group) who underwent routine echocardiographic examinations in
addition to conventional pulsed Doppler and color
M-mode Doppler examinations. The presence of
LV hypertrophy was established when the LV mass
index (LVMI) obtained from echocardiography was
>111 g/m2 for men and >106 g/m2 for women8).
All subjects had normal sinus rhythm. No patient
had evidence of valvular disease or myocardial
infarction determined clinically, by Doppler imaging, or by electrocardiography. Thirty-one patients
with no evidence of heart disease served as control
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Diastolic function of hypertenive heart
243
Table 2 Comparison of echocardiographic and Doppler
parameters between the two groups
HT Group
Control Group P value
(n=45)
(n=31)
LVDd (mm)
46.9 ± 4.8
42.7 ± 4.1
p<0.01
FS (%)
40.7 ± 9.5
38.3 ± 5.0
NS
A (cm/sec)
0.74 ± 0.20
0.73 ± 0.14
NS
E (cm/sec)
0.61 ± 0.21
0.67 ± 0.18
NS
A/E
1.16 ± 0.32
1.32 ± 0.45
p<0.01
Abbreviations: LVDd=left ventricular end-diastolic dimension, FS=fractional shortening, A=maximal late diastolic
transmitral flow velocity, E=maximal early diastolic transmitral flow velocity, A/E=the ratio of the maximal late (A)
Fig. 1 Measurement of LV filling flow propagation velocity.
LV filling flow was recorded in the early and late diastolic
phases, and flow propagation velocities in the early (FPVE) and late (FPV-A) diastolic phases were measured as the
slopes of the flow wave fronts during the early and late LV
filling, respectively.
to the early (E) diastolic transmitral flow velocities
Statistical analysis
Values were expressed as means ± SD, and
comparisons were assessed by the Student's paired
t-test. Differences were considered significant at p
values of <0.05. Simple regression analysis was
employed to test correlations.
flow velocities during the LV filling phase, and the
maximal early (E) and late (A) diastolic transmitral
velocities were measured. Color M-mode Doppler
images of the LV filling flow were recorded in the
early and late diastolic phases, and flow propagation velocities in the early (FPV-E) and late (FPVA) diastolic phases were measured as the slopes of
the flow wave fronts during the early and late LV
filling, respectively (Fig. 1). The ultrasound beam
was interrogated from the apex of the heart towards
the center of the mitral orifice as parallel to the LV
filling flow as possible. Measurements were obtained from an average of three consecutive cardiac
cycles.
Since the color Doppler flow signal may also
change due to relation in the angle between the
ultrasonic beam and flow, we calculated the following three ratios: FPV-E divided by E (FPV-E/E),
FPV-A divided by A (FPV-A/A), and FPV-A/A
divided by FPV-E/E (FPV ratio).
Then, we 1) compared FS, the ratio of A to E
(A/E), FPV-E/E, FPV-A/A and the FPV ratio
between the HT and Control groups; 2) assessed
the correlation of LVMI with FPV-E/E or FPVA/A in the HT group; 3) and assessed the correlation of LVMI with FPV-E/E or FPV-A/A in the
HT group.
RESULTS
Comparison of echocardiographic and Doppler
parameters between the two groups
1) LVDd was significantly larger in the HT
group than in the Control group (p<0.01).
2) There was no significant difference in FS,
used as the parameters of LV systolic function,
between the two groups. A/E, which was conventional Doppler derived index of LV diastolic function was significantly higher in the HT group than
in the Control group (p<0.01) (Table 2).
3) FPV-E/E and FPV-A/A were significantly
lower in the HT group than in the Control group
(p<0.01, p<0.01, respectively) (Fig. 2).
4) The FPV ratio was significantly higher in
the HT group than in the Control group, demonstrating impairement of diastolic function is more
severe in the early diastolic phase than in the late
diastolic phase (p<0.01) (Fig. 3).
Flow propagation velocity in the HT group
1) FPV-E/E was lower in cases having larger
LVMI, and there was a significant negative correlation between FPV-E/E and LVMI (r=–0.427,
p<0.001) (Fig. 4). There was no significant cor23
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Tokuoka S Nobuoka S et al
Fig. 2 Comparison of FPV-E/E and FPV-A/A between the
two groups.
FPV-E/E and FPV-A/A were significantly lower in the HT
group (HT) than in the Control group (control) (p<0.01,
p<0.01, respectively).
Fig. 3 Comparison of FPV ratio between the two groups.
The FPV ratio was significantly higher in the HT group
(HT) than in the Control group (control) (p<0.01).
Fig. 4 Correlation between FPV-E/E and LVMI.
There was a significant negative correlation between FPV-E/E and LVMI (r=–0.427, p<0.001).
relation between FPV-E/E and RWT (r=–0.168).
2) FPV-A/A was lower in cases having RWT
and there was a significant negative correlation
between FPV-A/A and RWT (r=–0.411, p<0.001)
(Fig. 5). There was no significant correlation
between FPV-A/A and LVMI (r=–0.137).
DISCUSSION
LV flow propagation and the color M-mode
Doppler technique
In the LV diastolic phase, the inflow of blood
from the left atrium to the left ventricle results in a
propagation of the blood flow from the mitral orifice
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Diastolic function of hypertenive heart
245
Fig. 5 Correlation between FPV-A/A and RWT.
There was a significant negative correlation between FPV-A/A and RWT (r=–0.411, p<0.001).
toward the apex. Assessment of the LV blood flow
propagation in the LV filling phase using color Mmode Doppler imaging has recently attracted attention as a new non-invasive method for assessing
LV diastolic function.
Pulsed Doppler measurement of the transmitral
flow velocity pattern has been widely used to assess
the LV diastolic function10)11). However, as previously discussed, the transmitral flow velocity pattern is
influenced by many factors other than primary
diastolic function indices, including left atrial pressure, age, and heart rate12)13). Indeed, patients who
have diastolic dysfunction and markedly elevated
pulmonary venous pressure can also have a normal
pattern of transmitral flow velocity14).
Regarding the difference between the pulsed
Doppler transmitral flow velocity pattern and the
flow propagation velocity, the pulsed Doppler
technique displays the velocity spectrum at a single
location, whereas the color M-mode Doppler technique displays the spatiotemporal distribution of
the velocity. Several published studies5~7) on the
LV flow propagation velocity using the color Mmode Doppler technique emphasized its usefulness
for assessing diastolic dysfunction. Brun et al.5)
demonstrated that the velocity of flow propagation
during early filling reduced in patients with LV
hypertrophy and seemed to be highly dependent on
the LV relaxation rate. Based on their findings,
they suggested that flow propagation velocity
could be an important tool in studying diastolic
function. In addition, Takatsuji et al.6) demonstrated
that FPV was free of pseudonormalized transmittal
flow velocity pattern, and Nagueh et al.7) reported
that the flow propagation velocity was useful as a
noninvasive parameter of LV diastolic function in
patients with atrial fibrillation.
Furthermore,
several reports6)15~17) demonstrated that the ratio of
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Tokuoka S Nobuoka S et al
FPV-E to E was appropriate for evaluating LV
diastolic function by the preload effect on the early
tramsmitral flow velocity.
LV diastolic function in patients with hypertension
Congestive heart failure is a common and
often lethal complication of systemic hypertension,
and evaluation of LV function is important for the
management of hypertensive heart disease. For these
reasons, LV function has been thoroughly examined
in patients with hypertension18)19). Phillips et al.18)
reported that the early detection and prevention of
cardiac dysfunction is an important goal in the management of hypertensive patients.
According to previous evaluations of hypertensive subjects, their systolic function is similar to
normal subjects, and their LV diastolic abnormalities
tend to precede systolic dysfunction19)20). In the
present study, there was no significant difference in
FS between the two groups, whereas the pulsedDoppler-derived index A/E was significantly higher
in the HT group than in the Control group. These
findings are in agreement with the observations of
several previous studies20)21). Papademetriou et al.20)
demonstrated that indexes of systolic LV function
were similar in patients with mild hypertension and
normal persons, whereas indexes of diastolic function were abnormal in patients with mild hypertension. Based on this finding, they concluded that
subtle abnormalities of diastolic LV function may
be present in patients with mild hypertension when
LV systolic function remains normal. Soufer et al.21)
found that slowing of the maximal LV filling rate
was common in hypertensive patients, even before
signs of decreased systolic performance. While
these studies have drawn recent attention to the
evaluation of diastolic LV function in patients with
hypertensive LV hypertrophy, there have been no
thorough investigations of the LV filling flow
propagation in patients with hypertension or the
flow propagation velocity in the late diastolic phase.
Accordingly, we considered that the flow propagation velocity obtained by the color M-mode Doppler
technique should be assessed as a parameter of
diastolic function in patients with hypertension.
LV flow propagation in patients with hypertensive
LV hypertrophy
The main findings of the present study are
that; 1) FPV-E/E and FPV-A/A, were significantly
lower in the HT group than in the control group; 2)
the FPV ratio was significantly higher in the HT
group than in the control group; 3) there was a
significant negative correlation between FPV-E/E
and LVMI; and 4) there was a significant negative
correlation between FPV-A/A and RWT.
A delay in LV blood flow propagation in patients
with dilated cardiomyopathy was first described by
Jacobs et al.22). Several recent studies15)23)24) have
shown a decrease in the flow propagation velocity
in the early diastolic phase in patients with diastolic
dysfunction.
Two mechanisms have been proposed as
determinants of the flow propagation velocity16).
One is the presence of intraventricular pressure
gradient, and the other is the formation of vortexes.
In the early diastolic phase, rapid LV relaxation
generates a dynamic pressure gradient in the left
ventricle. This pressure gradient generates the driving force to pump the blood deep into the left
ventricle, resulting in a propagation of blood flow
from the mitral orifice towards the apex. In states
of diastolic dysfunction such as myocardial ischemia,
impairment of rapid filling leads to a decrease in
intraventricular pressure gradient, thereby decreasing the flow propagation velocity. Courtois et al.25)
showed that early diastolic intraventricular pressure
gradient decreased after coronary artery occlusion
in dogs. Flow propagation velocity is also determined by an intraventricular vortex formation.
Garcia et al.16) observed that vorticity is generated
by shear stress between inflowing blood and the
stationary blood already in the ventricle. Since the
shear stress correlates with the area in which inflowing blood contacts the stationary blood already in
the ventricle, vortex formation could increase the
incidence of dilated ventricles. Therefore, vortex
formation increases the size of the smaller mitral
orifices and dilated ventricles, thereby resulting in
a slower FPV. In summary, it is suggested that
abnormal relaxation and a higher relative mitral
orifice size leads to a slower FPV.
26
Diastolic function of hypertenive heart
In view of the importance of LV hypertrophy
and associated myocardial fibrosis in the development of diastolic dysfunction, we considered that it
was meaningful to assess the relation between
diastolic hemodynamics and cardiac alterations or
geometric remodeling in patients with hypertension. In the present study, we used LVDd, LVMI,
and RWT as the parameters of cardiac alterations
and geometric remodeling, and we assessed the
relation between ventricular LV filling flow propagation and these parameters in patients with hypertensive LV hypertrophy.
In the present study, FPV-E/E were significantly lower in the HT group than in the control
group. This result indicates diastolic dysfunction
in the early diastolic phase in patients with hypertensive LV hypertrophy. This result also suggests
that the slower FPV-E in patients with hypertensive
LV hypertrophy could be related to an increase of
LVDd. In addition, there was a significant negative correlation between FPV-E/E and LVMI. It is
suggested that FPV-E/E could be a useful parameter
for evaluating LV diastolic dysfunction associated
with LV hypertrophy in patients with hypertensive
LV hypertrophy.
In the present study, FPV-A/A was significantly lower in the HT group than in the control group.
Several studies18)26)27) have shown an increase of A
in patients with hypertensive LV hypertrophy, suggesting atrial hypercontractility due to compensation of early diastolic dysfunction. Our result seems
to contradict the results of the these recent reports.
However, Thomas et al.23) found that the peak
velocity of early diastolic phase reached its maximum value closer to the apex, whereas the highest
peak velocity of late diastolic phase occurred near
the mitral leaflet tips. We speculated that the peak
flow velocity in the late diastolic phase at the
mitral orifice was higher in patients with hypertensive LV hypertrophy, whereas the flow propagation
velocity in the late diastolic phase was decreased.
Thus, patients with hypertensive LV hypertrophy
seem to have impaired LV function in the late
diastolic phase. Moreover, since the FPV ratio was
significantly lower in the HT group, diastolic function seemed to be impaired in both the early and
247
late diastolic phases in patients with hypertensive
LV hypertrophy, especially in the early diastolic
phase.
There was a significant negative correlation
between FPV-A/A and RWT in the present study,
whereas there was no correlation between FPVA/A and LVMI. Phillips et al.18) reported that
abnormality of the peak velocity of late filling
phase in patients with hypertension may be independent of LV hypertrophy. However, flow
propagation velocity has never been examined in
patients with hypertension. Our results suggest
that the impairment of diastolic function in the late
diastolic phase was related not to the extent of LV
hypertrophy, but to the geometric remodeling of
LV hypertrophy. Further, among patients with
hypertensive LV hypertrophy, the LV diastolic
dysfunction was more severe in cases having a
higher RWT and larger LVMI.
CONCLUSION
In patients with hypertensive LV hypertrophy,
diastolic function is considered to be impaired both
in early and late diastolic phases, this impairment
considered is more severe in the early diastolic phase
than in the late diastolic phase. It was considered
that the LV diastolic dysfunction was more severe
in patients with hypertensive LV hypertrophy in
cases having a higher RWT and larger LVMI.
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抄 録
左室内血流伝播速度の解析による高血圧性心肥大例の
拡張期血行動態の検討
とくおか
しんいち
のぶおか
さちひこ
ながしま
じゅんぞう
み やけ
ふみひこ
徳岡
伸一
信岡
祐彦
長嶋
淳三
三宅
良彦
【目的】本研究は，カラー M モード Doppler 法を用いて，高血圧性心肥大例の左室内血流伝播
速度を解析し，高血圧性心肥大例の拡張期血行動態と心臓形態との関連を検討することを目的と
した。
【方法】対象は高血圧性心肥大（HT 群）45 例で，健常者 31 例を対照（コントロール群）とし
て用いた。
心エコー・超音波 Doppler 法により，左室心筋重量係数（LVMI），相対的左室壁厚，（RWT），
および拡張早期最大左室流入血流速度（E）および拡張後期（心房収縮期）同速度（A）を測定し
た。カラー M モード Doppler 法を用いて拡張期左室流入血流を記録し，拡張早期左室流入血流伝
播速度（FPV-E），拡張後期（心房収縮期）同伝播速度（FPV-A）を記録した。次いで 1）FPVE/E， FPV-A/A，およびその比（FPV-A/FPV-E: FPV 比）を HT 群とコントロール群とで比較し
た。2）HT 群において，FPV-E/E， FPV-A/A と LVMI，RWT とのそれぞれの相関を検討した。
【結果】1）FPV-E/E， FPV-A/A はコントロール群に比し，HT 群でいずれも有意に低値を示し，
FPV 比は HT 群で有意に高値を示した。2）FPV-E/E と LVMI との間に有意な負の相関がみられ，
FPV-A/A と RWT との間に有意な負の相関がみられた。
【結論】高血圧性心肥大例の左室拡張機能は，拡張早期，拡張後期のいずれにおいても低下し
ており，その程度は拡張早期に強いと考えられた。また高血圧性心肥大例では，左室心筋重量係
数が大きく，かつ相対的左室壁厚が厚いものほど左室拡張機能障害の程度が強いと考えられた。
（聖マリアンナ医大誌, 29: 241-249, 2001）
聖マリアンナ医科大学 内科学教室（循環器内科）
（教授 三宅良彦）
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