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Transcript
Clinical Science (2002) 102, 515–522 (Printed in Great Britain)
Left ventricular long-axis changes in early
diastole and systole: impact of systolic
function on diastole
Gabriel W. YIP*, Yan ZHANG*, Peggy Y. TAN†, Mei WANG*, Pik-Yuk HO*,
L.-AH . BRODIN‡ and John E. SANDERSON*
*Division of Cardiology, Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Prince of Wales
Hospital, Shatin, N.T., Hong Kong SAR, China, †Department of Anaesthesia and Intensive Care, The Chinese University of Hong
Kong, Prince of Wales Hospital, Shatin, N.T., Hong Kong SAR, China, and ‡Department of Clinical Physiology, Karolinska
Institute, Huddinge University Hospital, SE-141 86, Huddinge, Sweden
A
B
S
T
R
A
C
T
Impaired long-axis motion is a sensitive marker of systolic myocardial dysfunction, but no data
are available that relate long-axis changes in systole with those in diastole, particularly in subjects with diastolic dysfunction and a ‘ normal ’ left ventricular (LV) ejection fraction. A total of
311 subjects (including 105 normal healthy volunteers) aged 20–89 years with variable degrees of
systolic function (LV ejection fraction range 0.15–0.84) and diastolic function were studied using
tissue Doppler echocardiography and M-mode echocardiography to determine mean mitral
annular amplitude and peak velocity in systole and early and late diastole. The LV systolic
mitral annular amplitude (SLAX, where LAX is long-axis amplitude) and peak velocity (Sm)
correlated well with the respective early diastolic components (ELAX and Em) and late diastolic
(atrial) components (ALAX and Am). A non-linear equation fitted better than a linear relationship
(non-linear model : SLAX against ELAX, r2 l 0.67 ; Sm against Em, r2 l 0.60 ; SLAX against ALAX and
Sm against Am, r2 l 0.42). After adjusting for age, sex and heart rate, linear relationships of early
diastolic (ELAX, r2 l 0.70 ; Em, r2 l 0.60) and late diastolic (ALAX, r2 l 0.61 ; Am, r2 l 0.64) longaxis amplitudes and velocities with the respective values for SLAX and Sm were found, even in
those subjects with apparently ‘ isolated ’ diastolic dysfunction. Long-axis changes in systole or
diastole did not correlate with Doppler mitral velocities. We conclude that ventricular long-axis
changes in early diastole are closely related to systolic function, even in subjects with diastolic
dysfunction. ‘ Pure ’ or isolated diastolic dysfunction is uncommon.
INTRODUCTION
Movement along the left ventricular (LV) long axis is due
to longitudinally oriented subendocardial myocardial
fibres, and constitutes an important part of global LV
performance [1–4]. It was recognized by Hamilton and
Romf in 1932 [5] that the heart is relatively fixed with
respect to the chest wall ; LV long-axis changes can,
therefore, be measured by changes in the position of the
atrio–ventricular plane, and the extent of shortening is
Key words: early diastole, echocardiography, long-axis function, systolic function.
Abbreviations: LV, left ventricular ; LVEF, left ventricular ejection fraction ; ARP, abnormal relaxation pattern in diastole ;
DT, deceleration time ; IVRT, isovolumic relaxation time ; LAX, long-axis amplitude ; S
, systolic mitral annular displacement ;
LAX
E
, early diastolic mitral annular displacement ; A
, late diastolic (atrial) mitral annular displacement ; S , systolic mitral annular
LAX
LAX
m
velocity ; E , early diastolic mitral annular velocity ; A , late diastolic (atrial) mitral annular velocity.
m
m
Correspondence : Professor J. E. Sanderson (e-mail jesanderson!cuhk.edu.hk).
# 2002 The Biochemical Society and the Medical Research Society
515
516
G. W. Yip and others
not modified by changes in the short (minor) axis.
Abnormal LV long-axis function has been reported to be
an early sign of ischaemia, and occurs in the absence of
other major disturbances of global LV performance [6–8].
Changes in the long axis in systole and diastole can be
readily quantified by M-mode echocardiography and
tissue Doppler echocardiography, which allow the amplitude as well as the velocity of the ring motion to be
measured. The mitral annular motion supplements the
use of mitral Doppler inflow patterns to assess LV
diastolic function, although the concordance between the
two is frequently disrupted, especially in various disease
states [9–13].
We were interested to determine if disturbances of
early diastolic long-axis motion could occur independently of systolic function, i.e. whether ‘ isolated ’ diastolic dysfunction exists, at least in the long axis. We
reasoned that this was unlikely, because LV recoil in
early diastole, which creates the ‘ suction ’ effect, is
dependent on the stored energy from the previous
systole, and this is a major contribution to filling of the
ventricle in the normal heart. Impaired contraction of the
left ventricle during systole will lead to reduced recoil
and suction, and therefore reduced early diastolic filling.
Changes in ventricular compliance will affect function
more at end-diastole, changing the pressure–volume
relationship, rather than during early diastolic filling. We
investigated this hypothesis using spectral tissue Doppler
imaging, which is capable of high temporal resolution, to
measure apically directed myocardial velocities during
diastole, which were then related to the annular amplitude
and velocity in systole and other standard measurements
of global ejection fraction, in a large group of subjects
with a wide range of LV systolic function and diastolic
dysfunction.
These results were presented in part at the XXI
Congress of the European Society of Cardiology, Barcelona, Spain, on 29 August 1999.
METHODS
Study subjects
A total of 311 subjects (156 females and 155 males) aged
between 20 and 89 years (mean age 59.4 years) were
recruited, comprising 105 normal healthy volunteers
(mean age 47.6 years ; range 20–84 years) and 206 patients
with a wide range of values for LV ejection fraction
(LVEF) (mean 0.56 ; range 0.12–0.84). The healthy
volunteers had no history of cardiovascular symptoms,
or of hypertension, diabetes mellitus, hypercholesterolaemia or peripheral vascular disease, and had normal
findings on two-dimensional echocardiography. All subjects had normal sinus rhythm without bundle branch
block or significant valvular or pericardial disease. The
# 2002 The Biochemical Society and the Medical Research Society
Table 1
Major disease entities in 206 patients
Abbreviations : MI, myocardial infarction ; CVA, cerebral vascular accident ; TIA,
transient ischaemic attack ; PVD, peripheral vascular disease.
Prevalence
Disease
No.
%
Hypertension
Coronary artery disease
Diabetes mellitus
Dilated cardiomyopathy
History of previous MI
Previous history of CVA, TIA or PVD
Paroxysmal atrial fibrillation
End-stage renal failure
82
47
47
30
29
12
10
2
39.8
22.8
22.8
14.6
14.1
5.8
4.9
1.0
remaining 206 subjects had a variety of cardiac diseases
(Table 1).
Recording of echocardiograms
Echocardiograms were obtained using GE-VingMed
System 5 echocardiographic equipment (GE-VingMed Sound AB, Horten, Norway) and a 3.5 mHz multiphase-array probe. Subjects lay in the left lateral
decubitus position. Echocardiographic techniques and
calculations of the various cardiac dimensions were
performed according to the recommendations of the
American Society of Echocardiography [14–17].
Doppler mitral inflow velocities at the tip of the mitral
leaflets were recorded in the LV apical four-chamber
view. Diastolic parameters were measured for at least
three beats. These parameters included peak early mitral
valve filling velocity (E wave), peak atrial filling velocity
(A wave), E\A ratio and deceleration time (DT). The isovolumic relaxation time (IVRT) was measured by pulsewave Doppler sampled between the anterior mitral leaflet
and the LV outflow tract [18]. The LV diastolic mitral
flow pattern was characterized as a normal pattern, an abnormal relaxation pattern (ARP), a pseudonormal pattern
or a restrictive filling pattern, as described previously
[19–21]. An ARP was characterized by a prolonged DT
( 240 ms), a reversed E\A ratio and a prolonged
IVRT ( 100 ms). A restrictive filling pattern was
characterized by a short DT ( 140 ms), a large E\A
ratio ( 2) and a short IVRT ( 70 ms). A pseudonormal pattern was defined by a relatively normal DT
(140–240 ms), a reversed pulmonary venous flow pattern
with predominant systolic forward rather than diastolic
flow, and a pulmonary venous atrial reversal wave
duration that is 30 ms longer than the mitral A wave [22].
The diastolic flow patterns give a fair estimation of
increasing LV filling pressures in the presence of a stiffer
left ventricle. The ARP is seen early with impaired LV
relaxation, and is recognized by a decrease in early
Left ventricular long axis in diastole and systole
Table 2 Baseline echocardiographic characteristics of the 105 normal subjects and of the total study population of 311
subjects
LVEF(2D), LVEF measured by the two-dimensional modified Simpson’s method ; LVEF(avpd), LVEF measured by the atrio–ventricular plane method ; LVEDd, LV end-diastolic
diameter ; FS, fractional shortening.
Normal subjects (n l 105)
Total population (n l 311)
Parameter
Mean
S.D.
S.E.M.
Minimum
Maximum
Mean
S.D.
S.E.M.
Minimum
Maximum
Age (years)
Heart rate (beats/min)
LVEF
LVEF (avpd)
LVEDd (cm)
SLAX (cm)
ELAX (cm)
Sm (cm/s)
Em (cm/s)
FS
47.13
71.68
0.69
0.71
4.54
1.37
0.87
6.54
8.34
0.36
14.52
10.17
0.06
0.08
0.50
0.14
0.18
1.00
2.06
0.05
1.41
1.12
0.01
0.01
0.05
0.01
0.02
0.10
0.21
0.01
20
53
0.54
0.53
3.48
1.05
0.49
4.73
4.57
0.26
84
109
0.84
0.90
5.45
1.74
1.33
9.24
12.83
0.50
59.45
72.10
0.56
0.57
4.90
1.13
0.67
5.15
5.76
0.29
16.54
13.61
0.17
0.18
0.93
0.32
0.23
1.79
2.81
0.11
0.94
0.93
0.01
0.01
0.06
0.02
0.01
0.10
0.16
0.01
20
45
0.12
0.13
2.90
0.33
0.18
1.08
0.73
0.05
89
115
0.84
0.90
9.26
1.74
1.33
9.24
12.83
0.53
transmitral LV filling (E wave) and an increased proportion of filling during atrial contraction (A wave). As the
left ventricle becomes less compliant and the LV filling
pressure is high, the pseudonormal pattern is seen with a
relatively normalized DT. With further decrease in LV
compliance, LV filling has restrictive features characterized by rapid early filling with high filling pressures,
very little atrial contribution and a poor prognosis.
The mean mitral annular displacement in systole
(SLAX,where LAX is long-axis amplitude), early diastole
(ELAX) and late diastole due to atrial contraction (ALAX)
were obtained by M-mode echocardiography, by placing
a cursor at the septal, lateral, anterior and inferior aspects
of the mitral annulus in the apical view.
Similarly, pulsed-wave tissue Doppler echocardiography was performed with the same machine with a
sample volume located at four different positions of the
mitral annulus. Mean peak systolic (Sm), peak early
diastolic (Em) and late diastolic (atrial contraction) (Am)
mitral annular velocities were obtained.
All images were acquired during end-expiration. Attention was given to ensuring appropriate velocity range
settings (high enough pulse repetition frequency) to
avoid aliasing within the tissue Doppler images.
Each measurement of mitral annular motion was
recorded for three cardiac cycles, and corresponding
mean measurements were analysed with an off-line
Microsoft NT workstation.
LVEF was obtained using a modified biplane Simpson
method from apical two- and four-chamber views, and
also by using the atrio–ventricular plane displacement
method described by Willenheimer et al. [23].
Statistical analysis
Velocity, amplitude and timing comparisons were made
among all three types of recording of mitral Doppler
inflow patterns and longitudinal mitral annular amplitudes and velocities in the same patient. The mitral inflow
velocity indices and the mitral ring excursions and
velocities in whole cardiac cycle were also related to the
LVEF. The means were compared using Student’s t test
or ANOVA as appropriate. r# values were calculated
using multiple linear regression for a linear relationship
and the non-linear regression method for an exponential
relationship.
Inter- and intra-observer reliability were obtained for
analysis of the above parameters using results from 30
randomly chosen patients by inter- and intra-class
correlation and the Bland–Altman methods [24]. The
acquired images were analysed independently by two
blinded observers to obtain the inter-observer reliability.
These calculations were made using the statistical package
SPSS for Windows, version 9.0 (SPSS Inc.) for IBMcompatible computers. A P value of 0.05 was taken as
significant. Results are given as meanspS.E.M.
RESULTS
Baseline characteristics
Table 2 summarizes the clinical, Doppler, M-mode
echocardiographic, tissue Doppler and haemodynamic
parameters for all subjects. The range of LVEF values
varied from 0.18 to 0.88. Heart rate averaged 72.1p
0.9 beats\min. There was no significant difference in ages
between males and females in the whole cohort (males,
57.48p16.61 years ; females, 57.87p1.44 years ; P l
0.85). The mean LV end-diastolic diameter increased
progressively with worsening diastolic mitral inflow
patterns and LVEF (Table 3). There was a good correlation between LVEF measured by the modified
Simpson’s two-dimensional method and by the atrio–
# 2002 The Biochemical Society and the Medical Research Society
517
G. W. Yip and others
Table 3
Distribution of age, sex and LV end-diastolic dimension (LVEDd) of 311 subjects by Doppler mitral inflow pattern
RFP, restrictive filling pattern ; PN, pseudonormal pattern. Values for age and LVEDd are meanspS.E.M. The LVEDd for healthy controls and patients with a normal
inflow pattern was obtained by combining data for these two groups.
Patients
No. of subjects
Sex
Female
Male
Age (years)
LVEDd (cm)
Healthy controls
Normal pattern
ARP
PN
RFP
Overall
105 (33.7 %)
30 (9.6 %)
126 (40.5 %)
23 (7.4 %)
27 (8.7 %)
311
7 (4.5 %)
16 (10.3 %)
63.57p2.41
5.83p0.25
11 (7.1 %)
16 (10.3 %)
59.00p2.81
5.97p0.20
156
155
59.40p0.94
4.90p0.06
65 (41.6 %)
40 (25.8 %)
47.13p1.41
4.66p0.06
15 (9.6 %)
15 (9.7 %)
65.30p2.34
4.66p0.06
58 (37.2 %)
68 (43.9 %)
67.54p1.26
4.86p0.11
Table 4 Corrected r 2 values for different types of regression
analyses
Slax
Regression analysis was performed (a) for the relationships of SLAX with ELAX and
ALAX, and (b) for the relationships of Sm with Em and Am in 311 subjects, with and
without adjustment for age, heart rate and sex. Non-linear regression is in form
a[1kexp(bX )], where X is the independent variable ; a and b are constants.
(a)
r 2 versus SLAX
Elax
ELAX
ALAX
Linear regression without constant
Non-linear regression
Without
adjustment
With
adjustment
Without
adjustment
With
adjustment
0.5086
0.2955
0.6898
0.6076
0.6706
0.4160
0.6973
0.6125
(b)
r 2 versus Sm
Sm
518
Em
Am
Linear regression without constant
Non-linear regression
Without
adjustment
With
adjustment
Without
adjustment
With
adjustment
0.2470
0.3411
0.5787
0.6377
0.5983
0.4194
0.5992
0.6380
Em
Figure 1 Linear and non-linear correlations between SLAX
and ELAX (upper panel) and Sm and Em (lower panel) without
correction for age, sex and heart rate
ventricular plane displacement method (r# l 0.82,
P 0.001).
origin moderately with ALAX (r# l 0.42). When corrected
for age, sex and heart rate, similar but linear correlations
of ELAX (r# l 0.70) and ALAX (r# l 0.61) with SLAX were
observed (Table 4a).
Relationships between systolic and diastolic
LAX values
Relationships between systolic and diastolic
velocities (tissue Doppler
echocardiography)
In M-mode long-axis measurements, SLAX was correlated
through the origin well in a non-linear fashion with ELAX
(r# l 0.67) (Figure 1, upper panel), and through the
Sm was correlated non-linearly through the origin with
Em (r# l 0.60) (Figure 1, lower panel) and Am (r# l 0.42).
When corrected for age, sex and heart rate, similar but
# 2002 The Biochemical Society and the Medical Research Society
Left ventricular long axis in diastole and systole
Table 5 Relationships between parameters of mitral ring
motion and heart rate or LV end-diastolic diameter (LVEDd)
r 2 values were obtained by linear regression.
Table 7 Normal ranges for mitral annular amplitude and
velocity measurements in different age groups of adult
Chinese
DTLAX, deceleration time of ELAX ; IVRTm, IVRT in mitral annular velocity.
r2
ELAX
ALAX
Sm
Em
Am
0.0003
0.0053
0.0090
0.0089
0.1054
0.0099
0.1376
0.0382
0.0161
0.0074
0.2359
0.0032
SLAX (cm)
30
31–50
50
Overall
1.48
1.40
1.30
1.37
0.09
0.15
0.10
0.14
0.03
0.02
0.02
0.01
(1.42, 1.54)
(1.36, 1.44)
(1.27, 1.33)
(1.35, 1.40)
linear correlations of Em (r# l 0.60) and Am (r# l 0.64)
with Sm were observed (Table 4b).
ELAX (cm)
30
31–50
50
Overall
1.08
0.90
0.75
0.87
0.12
0.15
0.14
0.18
0.03
0.02
0.02
0.02
(1.00, 1.15)
(0.86, 0.95)
(0.70, 0.79)
(0.83, 0.90)
ALAX (cm)
30
31–50
50
Overall
0.45
0.53
0.55
0.53
0.05
0.08
0.07
0.08
0.02
0.01
0.01
0.01
(0.41, 0.48)
(0.51, 0.55)
(0.53, 0.58)
(0.51, 0.54)
DTLAX (s)
30
31–50
50
Overall
0.11
0.12
0.12
0.12
0.016
0.013
0.012
0.014
0.004
0.002
0.002
0.001
(0.10, 0.12)
(0.12, 0.12)
(0.12, 0.13)
(0.12, 0.12)
Sm (cm/s)
30
31–50
50
Overall
7.28
6.73
5.93
6.50
0.53
1.06
0.91
1.06
0.15
0.15
0.15
0.11
(6.95, 7.61)
(6.44, 7.03)
(5.63, 6.23)
(6.29, 6.71)
Em (cm/s)
30
31–50
50
Overall
10.77
8.88
6.76
8.32
1.09
1.69
1.65
2.09
0.32
0.24
0.27
0.21
(10.08, 11.47)
(8.41, 9.36)
(6.21, 7.31)
(7.91, 8.74)
Am (cm/s)
30
31–50
50
Overall
6.11
7.45
7.80
7.42
1.18
1.31
1.44
1.43
0.34
0.18
0.24
0.14
(5.36, 6.86)
(7.08, 7.82)
(7.32, 8.28)
(7.14, 7.70)
IVRTm (s)
30
31–50
50
Overall
55.50
66.15
72.10
67.07
9.63
12.37
16.42
14.55
2.78
1.73
2.70
1.46
(49.38, 61.62)
(62.67, 69.63)
(66.62, 77.57)
(64.18, 69.96)
Heart rate
LVEDd
Relationships between mitral inflow
velocities and LV long-axis variables
(Table 3)
Neither LV long-axis velocities nor amplitudes correlated
with their corresponding Doppler mitral inflow indices.
Approx. 85 % of patients were diagnosed with diastolic
dysfunction based on mitral inflow velocities and pulmonary vein patterns, as described above. The majority
(61 %) had an ARP with LVEF 0.45, i.e. within the
‘ normal ’ range. However, the relationship between
systolic and diastolic long-axis measurements (amplitude
and velocities) still held in this group, who therefore were
characterized by diastolic dysfunction and a ‘ normal ’
LVEF.
Age group (years)
Relationships between mitral ring motion
and age in healthy adults
Systolic and early diastolic mitral ring motion decreased
and late diastolic ring motion increased with advancing
age, but not with increasing heart rate or LV enddiastolic dimension ; gender had no effect (Table 5). The
age-related changes in the mitral annular parameters
between 20 and 84 years of age were calculated from
linear regression equations, and are shown in Table 6.
The normal ranges of these parameters in adult Chinese
are shown in Table 7.
Table 6
Mean
S.D.
S.E.M.
95 % Confidence
interval for mean
SLAX
Changes between 20 and 84 years of age for some LV dimensions calculated from linear regression equations
Change between 20 and 84 years
Parameter
Expected at age 20
Expected at age 84
Absolute
%
Linear correlation
with age (r )
SLAX (cm)
Sm (cm/s)
ELAX (cm)
Em (cm/s)
ALAX (cm)
Am (cm/s)
1.49
7.48
1.09
10.99
0.48
6.57
1.22
5.22
0.56
4.82
0.60
8.53
k0.28
k2.26
k0.53
k6.17
0.12
1.96
k18
k30
k49
k56
25
30
k0.44
k0.49
k0.67
k0.67
0.35
0.31
P value
0.001
0.001
0.001
0.001
0.001
0.002
# 2002 The Biochemical Society and the Medical Research Society
519
520
G. W. Yip and others
Reliability of mitral annular displacement
and velocity measurements
The intra-class correlations for various mitral annular
motion parameters by the same observer were between
0.8 and 0.9. The inter-observer correlations for same
parameters were between 0.7 and 0.9. Using the Bland–
Altman method, the mean difference between observations was 5 % of the mean value of the observations for
measurements of amplitude, duration and velocity.
DISCUSSION
Our results support a close link between contraction and
relaxation, especially during early diastole. They illustrate
that the heart, as a muscular pump, functions in the same
way as an isolated cardiac muscle ; a decrease in the force
of shortening and re-lengthening during relaxation of an
afterloaded twitch are parts of one activity cycle, i.e. part
of one contraction–relaxation cycle (or ‘ systole ’) [25].
Both experimental and clinical studies suggest that the
normal left ventricle contracts to a volume less than its
equilibrium volume, hence compressing elastic cardiac
elements, which creates early diastole-restoring forces
that produce a ‘ suction ’ effect that lowers LV minimal
pressure and increases early filling [26]. Active relaxation
is an important component, like its systolic counterpart
contraction ; it is an active, energy (ATP)-dependent
process that depends on systolic and diastolic loads, the
non-uniformity of the load, and the passive elastic
characteristics of the ventricle. However, the restoring
forces (among other factors), stored as potential energy
generated during contraction, also influence diastolic
relaxation. These restoring forces are related to the
amount of systolic deformation. Of course, it is impossible from the results of the present study to determine the relative contributions of active relaxation and
elastic recoil to early diastolic filling. It is likely that both
are dependent on the extent of systolic function. In
disease states, LV filling is generated predominantly by
the increased pressure gradient from the left atrium to the
left ventricle due to increased left atrial pressure and also
stiffness, rather than by LV elastic recoil and active
relaxation. This explains the discordance between the
long-axis and mitral inflow velocities ; the former reflects
systolic function, while the latter reflects the left atrium–
left ventricle pressure gradient. In our study, a non-linear
equation fitted better than a linear one for both long-axis
amplitudes and velocities. However, when corrected for
age, sex and heart rate, a linear relationship was seen.
Furthermore, the fact that heart rate had little influence
on long-axis mitral annular velocities indicates that
myocardial velocities are less dependent on preload, as
suggested by previous studies [4–10]. Short-axis shortening, as reflected by fractional shortening, does not
# 2002 The Biochemical Society and the Medical Research Society
compensate fully for the long-axis change in patients
with declining LVEF.
Our results also provide an explanation for observations from previous studies, which have used tissue
Doppler echocardiography to differentiate restrictive
cardiomyopathy from constrictive pericarditis [8,9], and
normal from pseudonormal Doppler mitral inflow patterns [10]. The differences are in fact related to the degree
of systolic LV dysfunction rather than to individual
absolute myocardial velocities. Patients with restrictive
cardiomyopathy tend to have poorer (albeit within the
‘ normal ’ range) systolic function, as do those with a
pseudonormal diastolic mitral pattern. The most common cause of a decrease in the early diastolic lengthening
rate is a low overall amplitude of the ring motion, which
is characteristic of systolic LV disease [13]. Our results
also question the notion of ‘ diastolic ’ heart failure. It
appears unlikely that a pure abnormality of diastolic
function will exist, or alternatively that the majority of
those with abnormal filling will also have some degree of
systolic dysfunction that can be detected by analysing the
long axis, but not the LVEF. This distinction is important,
as diastolic heart failure is the commonest form of heart
failure in many communities [27,28].
Clearly, the total excursion of the mitral valve annulus
during systole must equal that which occurs in diastole,
as the mitral valve ring returns to the same position with
every beat. However, this does not hold for the velocities
or for the relative balance between early and late diastole.
The degree of motion during atrial systole will depend
both on the extent of the excursion during ventricular
systole, which stretches the pectinate muscles, and the
amount of movement during early diastole. The balance
between early diastolic and late diastolic amplitudes and
velocities will vary with different disease states and with
the strength of systolic function. In addition, the effect of
atrial systole is to draw the mitral valve ring around the
blood in the atrium, which is thereby transferred into
the ventricle. In contrast, during systole the movement
of the mitral valve ring downwards will increase the
atrial volume, creating a suction effect, which draws
blood from the pulmonary veins [29]. Thus atrial filling
is also dependent on ventricular systolic function. Indeed,
in our study there was a correlation between the systolic
component and the atrial component of mitral ring
motion.
Age has a marked effect on the balance between early
and late diastolic filling. Previous studies have shown that
LVEF at rest in adults is unchanged or increased slightly
with advancing age [30–32]. However, the long axis, as
reflected by mitral ring motion, decreases by up to 20 %,
whereas the short axis increases by up to 18 %, with
increasing age in normal adults [33]. These changes are
independent of systolic blood pressure, LV wall thickness, heart rate or sex. Our study showed similar results,
with decreases of approx. 18 % in SLAX and 30 % in Sm. A
Left ventricular long axis in diastole and systole
similar diminution was seen in the early diastolic motion,
with 49 % and 56 % decreases in ELAX and Em respectively, but with an increase in the atrial component of
mitral ring motion (25–30 %).
Study limitations
All previous known limitations of Doppler echocardiography will apply to the present study. These include the
following. (1) Tissue Doppler echocardiography measures myocardial velocity relative to the ultrasound beam.
Thus the smaller the angle between the Doppler beam
and the incident surface, the greater the accuracy of the
velocity measurement that is obtained. Further, the
direction of movement measured in the present study
was longitudinal from the base towards the LV apex, the
latter being relatively fixed throughout the cardiac cycle
[23]. (2) The velocity data acquired with colour Doppler
echocardiography are mean velocities. They are only
slightly different from temporal data obtained over
several cycles. The mean velocities have the additional
advantage of reducing the noise effect during measurement. The noise effect is reduced further by taking an
average of multiple measurement of a similar heart rate.
(3) Artefacts caused by thickening, translational motion
of the heart, and motion caused by breathing are
inevitably present. Breathing artefacts can be minimized
by image acquisition during expiration. The issue of
translational movement is still unresolved. The Doppler
sample site was fixed and did not track the myocardium
being sampled, and hence the same portion of the
myocardium was not sampled throughout the cardiac
cycle. However, as the sampled myocardium moved up
to just more than 10 mm, it is very likely that the
adjoining myocardium sampled at different parts of the
cardiac cycle with a fixed sample volume would move at
similar velocities, especially in the longitudinal direction.
Although the healthy volunteers included in the
present study had no evidence of cardiac disease, a small
possibility of incipient subclinical myocardial or coronary ischaemia in this control population cannot be
excluded. The heart rates of the whole group were fairly
constant (mean 72.6p1.1 beats\min), and the effect of
heart rate on the measurements was minimal. However,
the effect of loading conditions on myocardial velocities
has not been addressed in this within-patient study, as
comparisons were made using instantaneous recordings.
ated predominantly by the increased left atrium–left
ventricle pressure gradient due to increased left atrial
pressure and also stiffness, rather than by LV elastic
recoil and active relaxation. Early diastolic function is
therefore tightly coupled to the previous systole, even in
those subjects with an apparently normal LVEF and
evidence of diastolic dysfunction from Doppler mitral
flow studies. Isolated early diastolic dysfunction in the
presence of truly normal systolic function is probably
very rare.
ACKNOWLEDGMENTS
This research was funded by a Direct Grant for Research,
Faculty of Medicine, Chinese University of Hong Kong,
Hong Kong SAR, China. We thank Dr Derek Gibson for
his help and advice, and we are grateful to Mr K. K.
Wong, Centre for Clinical Trials and Epidemiological
Research, Chinese University of Hong Kong, for statistical advice and helpful assistance.
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Received 18 June 2001/9 October 2001; accepted 22 November 2001
# 2002 The Biochemical Society and the Medical Research Society