HLC 1701 No.

of Pages 10

Heart, Lung and Circulation (2014) xx, 1–10 REVIEW

1443-9506/04/$36.00
http://dx.doi.org/10.1016/j.hlc.2014.10.003

Tissue Doppler Imaging in

Echocardiography: Value and Limitations
Krishna K. Kadappu, MBBS, MD a,b,c, Liza Thomas, MBBS, PhD a,b*
a
South Western Sydney Clinical School, The University of New South Wales, University of Western Sydney, NSW, Australia
b
Cardiology Department, Liverpool Hospital, University of Western Sydney, NSW, Australia
c
Cardiology Department, Campbelltown Hospital, University of Western Sydney, NSW, Australia

Received 15 October 2014; accepted 15 October 2014; online published-ahead-of-print xxx

Tissue Doppler imaging (TDI) is a useful echocardiographic technique to evaluate global and regional
myocardial systolic as well as diastolic function. It can also be used to quantify right ventricular and left
atrial function. Recent studies have demonstrated its utility as a diagnostic as well as prognostic tool in
different cardiac conditions including coronary artery disease, heart failure (both systolic and diastolic),
valvular heart disease, cardiomyopathies as well as constrictive pericarditis. TDI measurements are also
helpful to identify patients who will benefit from cardiac resynchronisation therapy. Even though it is
reproducible and relatively easy to obtain, it is underutilised in routine clinical practice. TDI is readily
available on most commercially available echocardiographic systems, and we recommend that TDI be used
for routine clinical echocardiographic evaluation of patients.
Keywords Tissue Doppler imaging  Colour tissue Doppler imaging  Myocardial contraction velocity
 Left ventricular systolic function  Left ventricular diastolic function

Tissue Doppler imaging (TDI) for echocardiographic evalua-
tion of myocardial function was first described in 1989, [1] and
has revolutionised the quantitative evaluation of myocardial
function. Doppler ultrasound relies on detection of a fre-
quency shift of ultrasound signals reflected from moving
objects. In the heart, both blood flow and myocardial contrac-
tion result in velocity changes. Blood flow causes high fre-
quency, low amplitude signals that are obtained using
traditional Doppler. Tissue Doppler imaging is designed to
characterise low velocity, high amplitude signals from myo-
cardial motion [2], and are obtained by inverting the low pass
filter used in traditional Doppler to a high pass filter.
The myocardium has subendocardial and epicardial
layers, with the former having longitudinally arranged myo-
fibres [3]. During ventricular contraction, various layers
exert varying tension with the endocardium moving greater
distances. Tissue Doppler imaging examines the longitudi-
nal component of myocardial contraction throughout the
cardiac cycle.
Tissue Doppler imaging is obtained using pulsed wave
tissue Doppler or colour tissue Doppler imaging (CTDI).
Pulsed wave TDI measures peak longitudinal myocardial
velocity from a single segment, but has to be performed
‘on line’. Colour tissue Doppler imaging is performed ‘off
line’, and can interrogate velocities from multiple sites simul-
taneously [4]. However, CTDI represents the mean peak
velocity, and are 25% lower than pulsed wave Doppler
[5]. The two methods are therefore not interchangeable.
The major disadvantage of TDI is its angle dependence i.e.
if the angle of incidence exceeds 15 degrees, there is 4%
underestimation of velocity [6]. Accurate TDI imaging addi-
tionally requires high frame rates (>100fps) for image acqui-
sition with excellent temporal resolution.
TDI Measurement
The TDI signal over a cardiac cycle has three peaks, a positive
systolic peak and two negative diastolic peaks (Fig. 1A & B).

*Corresponding author. Cardiology Department, Liverpool Hospital, Elizabeth Street, Liverpool, NSW 2170, Australia Tel.: +61 2 87383070; fax: +61 2 87383054.,
Email: l.thomas@unsw.edu.au
© 2014 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier
Inc. All rights reserved.

Please cite this article in press as: Kadappu KK, Thomas L. Tissue Doppler Imaging in Echocardiography: Value and
limitations. Heart, Lung and Circulation (2014), http://dx.doi.org/10.1016/j.hlc.2014.10.003
 HLC 1701 No. of Pages 10

2 K.K. Kadappu, L. Thomas

Figure 1 (A) Pulsed wave tissue Doppler Imaging from the apical 4 chamber view sampling from the septal mitral annulus
(B) Colour Tissue Doppler Imaging from the apical 4 chamber view sampling from the septal mitral annulus.

The positive systolic wave (s’ velocity, Sa or Sm) represents
myocardial contraction. The negative waves represent the
early diastolic myocardial relaxation (e’ velocity, Ea or Em)
and active atrial contraction in late diastole (a’ velocity, Aa or
Am) (Fig. 1 A & B). The time to peak s’ velocity can be
measured and segmental heterogeneity can be ascertained
using CTDI [7] (Fig. 2). Additionally, isovolaemic contraction
and relaxation periods can also be identified. (Fig. 3) Pulsed
wave TDI velocity measurements are obtained by placing the
sample volume at the mitral annular level (denoted Sa/s’ or
Ea/e’ or Aa/a’) or within the basal LV myocardial segment
(denoted Sm or Em or Am). Tissue Doppler imaging velocities
can be measured either from the septal or lateral annulus, but
the current recommendation is that e’ velocity is expressed as
the average of septal and lateral measurements [8]. The current
accepted nomenclature favours denoting TDI velocities as s’, e’
and a’, although the other abbreviations are also commonly
used. Normal pulsed TDI values are given in Table 1.
Normal ageing can alter TDI derived myocardial veloci-
ties. There is a decrease in s’ and e’ velocities with ageing,

Please cite this article in press as: Kadappu KK, Thomas L. Tissue Doppler Imaging in Echocardiography: Value and
limitations. Heart, Lung and Circulation (2014), http://dx.doi.org/10.1016/j.hlc.2014.10.003
 HLC 1701 No. of Pages 10

Tissue Doppler Imaging in Echocardiography 3

Figure 2 Colour tissue Doppler image from the apical 4 chamber view sampling from the septal and lateral mitral annulus
illustrating dyssynchronous contraction of the LV.

Figure 3 IVCT and IVRT measurements from pulsed wave TDI trace. IVCT = isovolumetric contraction time; IVRT = iso-
volumetric relaxation time.

with a corresponding increase in a’ velocity [8]. Nagueh and
colleagues have reported age-based normal cut-off values for
basal septal and lateral segments [8] (Table 2)
TDI measurements are reported in varying cardiac condi-
tions with validation as a marker of LV systolic dysfunction
[9,10], diastolic dysfunction [8,11], LV dyssynchrony [12–14],
right ventricular [15] and atrial function [16]. It is useful in the
evaluation of coronary artery disease [17] and has prognostic
implications [15,18–21]. Tissue Doppler imaging measure-
ments are more sensitive than conventional echocardiography

Please cite this article in press as: Kadappu KK, Thomas L. Tissue Doppler Imaging in Echocardiography: Value and
limitations. Heart, Lung and Circulation (2014), http://dx.doi.org/10.1016/j.hlc.2014.10.003
 HLC 1701 No. of Pages 10

4 K.K. Kadappu, L. Thomas

Table 1 Normal reference range of TDI values in healthy adults (mean  SD).

s’(cm/s) e’ (cm/s) a’ (cm/s) E/e’ e’/a’

Septal velocity 8.1  1.5 8.6  1.9 9.5  2.4 8.7  2.2 1  0.7
Lateral velocity 10.2  2.4 12.2  3 11.3  2.9 6.3  1.9 1.5  0.6
Average septal + lateral 9.2  1.7 10.4  2.2 10.4  2.7 7.5  1.9 1.3  0.7

Adapted from Chahal N.S, Lim T.K et al. Eur J Echocardiogr 2010, Garcia, M. J, Rodriguez L et al AHJ 1996, Pai R.G and Gill K.S JASE 1998.

Table 2 Normal age related values for Doppler-derived diastolic measurements.

16-20(yrs.) 21-40 (yrs.) 41-60 (yrs.) >61(yrs.)

Septal é (cm/s) 14.9  2.4 15.5  2.7 12.2  2.3 10.4  2.1
Septal é/á ratio 2.4 1.6  0.5 1.1  0.3 0.85  0.2
Lateral é (cm/s) 20.6  3.8 19.8  2.9 16.1  2.3 12.9  3.5
Lateral é/á ratio 3.1 1.9  0.6 1.5  0.5 0.9  0.4

Modified from Nagueh, S. F., C. P. Appleton, et al. 2009. Eur J Echocardiogr 10(2): 165-193.

for detecting early myocardial alterations in primary myocar-
dial (eg hypertrophic and dilated cardiomyopathies) and sec-
ondary myocardial disorders (eg ischaemia) [18,19,22–28].
Hence TDI is useful for screening and detection of subclinical
myocardial dysfunction, and for evaluating the efficacy of
therapeutic interventions [23,29].
Quantitative Systolic Function
Assessment: s’ Velocity
s’ velocity measures longitudinal LV contraction and is a
surrogate of LV systolic function. s’ velocity (average of four
basal segments) demonstrated good correlation with LV
ejection fraction (LVEF) [30]; s’ 7.5 cm/s had a sensitivity
of 79% and a specificity of 88% in predicting LVEF  50%.
Similarly, s’ (average of six basal segments) > 5.4 cm/sec, had
a sensitivity of 88% and specificity of 97% for identifying
normal LVEF [31]. Endocardial longitudinal fibre contraction
is largely responsible for long axis function, which is suscep-
tible in a variety of cardiac conditions with either resultant
LV hypertrophy or dilatation. Early myocardial damage
often involves the subendocardial fibres, particularly in myo-
cardial ischaemia, with impairment in long-axis contraction
evident before changes in short-axis function. Hypertension,
coronary artery disease (CAD), cardiomyopathies and heart
failure have all been shown to alter subendocardial fibre
function with a reduction in s’ velocity [18,29], despite pre-
served LVEF. Fang and colleagues screened 101 asymptom-
atic patients with diabetes mellitus who underwent detailed
evaluation including echocardiography and exercise stress
testing, excluding those with cardiac dysfunction or ischae-
mia. Subclinical LV systolic dysfunction with a reduced s’
was noted in 24% [32]. In primary cardiomyopathic condi-
tions like hypertrophic cardiomyopathy (HCM), s’ velocity
was reduced in mutation positive individuals without LVH
[25].
Ischaemic heart disease constitutes a significant proportion
of patients reviewed in routine cardiology practice. The s’
velocity is reduced in ischaemic and infarcted segments [33].
Tissue Doppler imaging has been utilised in dobutamine
stress echocardiography (DSE), to objectively quantify
ischaemia and will be addressed in the stress echocardiogra-
phy section. [34,35]. However, TDI is limited by its inability
to differentiate active myocardial contraction from the teth-
ering effects of adjacent myocardium (i,e. TDI measures
tissue velocity in relation to the transducer rather than to
adjacent myocardium), thus lacking site specificity.[36]
Diastolic Function Assessment:
e’ Velocity
Aging, even in healthy adults, results in altered LV diastolic
relaxation [8]. Tissue Doppler imaging e’ velocity is a mea-
sure of LV relaxation in early diastole and is relatively load
independent [37]. e’ velocity can be measured from the septal
or lateral annulus in the apical four chamber view [2,8].
However, there is regional variation, and e’ is higher in
the lateral, inferior and posterior basal segments compared
to anterior and septal segments. e’ velocity correlates
inversely with early diastolic pressure (dP/dt) or tau (time
constant of LV relaxation) [38] thereby reflecting LV relaxa-
tion and elastic recoil. In adults, a lateral e’ velocity > 12 cm/s
represents normal LV diastolic function [39] and < 8 cm/s
indicates impaired LV diastolic function[5], while a septal e’
of > 8 cm/s is considered normal [40].
In normal subjects, transmitral E velocity is higher than A
velocity; this pattern reverses in early diastolic dysfunction
(DD). However, in advanced DD, E velocity again becomes

Please cite this article in press as: Kadappu KK, Thomas L. Tissue Doppler Imaging in Echocardiography: Value and
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 HLC 1701 No. of Pages 10
Tissue Doppler Imaging in Echocardiography
higher than the A wave (pseudonormal pattern), making it
difficult to use mitral inflow pattern to evalute DD [41].
However, e’ velocity is reduced even in subjects with early
DD, occurring almost 10-15 years prior to reduction of mitral
E velocity [42]. Its utility is evident from its inclusion in the
EAE/ASE guidelines for assessment of diastolic dysfunc-
tion [8].
Late Diastolic a’ Velocity
Late diastolic TDI a’ (a’/Aa/Am) velocity is useful in assessing
atrial function. The a’ velocity is a marker of global atrial
function [43]. a’ velocity increases with age [8], with no signif-
icant regional variation in a’ velocity (septum or lateral wall)
[44]. a’ velocity correlates with other measures of left atrial
function including transmitral peak A velocity, atrial fraction
and atrial ejection force [43,45]. Colour tissue Doppler imaging
a’ velocity permits evaluation of segmental atrial function [43].
Clinical Utility and Prognostic
Implications of TDI Velocities:
Systolic s’ Velocity
s’ velocity has been investigated in a variety of cardiac con-
ditions, including heart failure, cardiomyopathies, valvular
as well as coronary artery disease [9,23,28,35], for both diag-
nosis as well as for long-term prognosis. It is also useful to
identify patients with cardiac dyssynchrony [7].
Wang et al. reported that s’ was lower in non-survivors at
19 month follow-up in 252 patients with cardiovascular risk
[28]. A similar increase in adverse cardiovascular events was
seen in hypertrophic cardiomyopathy patients with a low s’
velocity [23]. The prospective SPHERE (multicenter proSPec-
tive study of ecHocardiography in hypERtEnsion) study [18]
enrolled 1556 patients with LVEF  50%; 286 (18%) had
LVDD (advanced LVDD in 128, less advanced in 158).
s’ velocity was reduced in LVDD and was an independent
predictor of advanced LVDD. Seo and colleagues evaluated
s’ velocity and its relation with dp/dt in experimental dogs
during dobutamine and esmolol infusion. s’ showed a dose-
dependent increase and decrease after dobutamine and
esmolol infusions, respectively. [46]. More recently a reduced
s’ velocity was demonstrated despite preserved LVEF, in
patients undergoing chemotherapy for breast cancer [47].
s’ velocity is useful in detecting and assessing prognosis in
CAD. Hoffmann and colleagues measured s’ from six annular
segments prior to coronary angiography [48]. Both s’ velocity
and E/e’ negatively correlated with vessels with significant
stenosis. s’ was reduced regionally and globally in patients
with three-vessel disease. In another study, 296 patients with
stable angina with normal LVEF were compared with 188
patients without significant CAD [49]; 108 had 70% stenosis
in at least one epicardial coronary artery. Average (six annular
segments) s’ remained an independent predictor of CAD
after multivariable analysis of exercise ECG and conventional
Please cite this article in press as: Kadappu KK, Thomas L. Tissue Doppler Imaging in Echocardiography: Value and
limitations. Heart, Lung and Circulation (2014), http://dx.doi.org/10.1016/j.hlc.2014.10.003
5
echocardiographic parameters. Tissue Doppler imaging s’ can
also diagnose early myocardial ischaemia [50]. Biering-Soren-
sen and co-workers also noted that a low s’ velocity after ST
elevation MI (STEMI) resulted in poor prognosis [51] in 391
patients treated with primary percutaneous coronary inter-
vention. Patients with low s’ at median follow up of 25 months
had >2 times risk for the composite end point of death, heart
failure, or recurrent myocardial infarction (hazard ratio, 2.60;
95% CI 1.64-4.13; P < .001).
Stress TDI
Stress echocardiography is an essential tool in the clinical
work-up of subjects with suspected CAD or latent ischaemia.
Wall motion scoring by visual assessment has improved
accuracy compared with stress electrocardiography, but
has high inter-observer variability [52]. Segmental TDI
velocities are reduced with ischaemia and recover with
reperfusion [53] and can differentiate transmural from non-
transmural infraction [53,54]. Yamada et al reported a smaller
increase in myocardial velocities in ischaemic segments with
dobutamine stress echocardiography (DSE); peak TDI s’
velocity of <12 cm/s had 80% accuracy for detecting ischae-
mic segments [55]. Cain et al combined TDI with wall motion
score and derived cut-off values of myocardial Doppler
velocities in 128 normal subjects [56]. s’ velocity for the septal,
anteroseptal and inferior basal segments was  7 cm/sec and
 5 cm/sec for the mid segments; s’ was  6 cm/sec for basal
and  4 cm/sec for mid segments of other walls. When
applied to 114 patients who underwent DSE and angiogra-
phy, a sensitivity of 83% and specificity of 73% was present
for detection of  50% coronary artery stenosis, but were not
significantly different to visual assessment.
Marwick and colleagues reported prognostic value of s’
velocity; patients with a lower s’ velocity had more adverse
events (average s’  4.9 +/- 1.7 cm/s versus 6.4 +/- 6.5 cm/s;
p < 0.001) [35]. s’ velocity can also be used with low dose DSE
to determine viability; the percentage increase in s’ velocity
in viable segments, four weeks after revascularisation was 45
+/-10%, versus 25+/-12% in non-viable segments. [34].
Both s’ velocity [24] and isovolumic acceleration [26] reflect
regional wall motion. Isovolumic acceleration is less affected
by ventricular loading compared to myocardial velocity. In
the Myocardial Doppler in Stress Echocardiography (MYD-
ISE) study, 149 patients had DSE before coronary angiogra-
phy. Both peak s’ velocity and isovolumic acceleration, at rest
and post stress, from basal and mid segments were compared
to angiographic results. Isovolumic acceleration velocity was
a better diagnostic marker for CAD and in combination with
peak s’ had an accuracy of 85-95% to diagnose coronary
stenosis [24,26]. Hence, combining TDI with DSE, may
improve accuracy for identifying ischaemic segments, reduce
inter observer variability and determine viability.
Measurements can also be performed during exercise
echocardiography [33]. A s’ velocity of <5 cm/s at peak stress
predicted exercise induced wall motion abnormality [57]
 HLC 1701 No. of Pages 10
6 K.K. Kadappu, L. Thomas
Valvular Heart Disease
Tissue Doppler imaging has been useful in identifying sub-
clinical myocardial dysfunction in patients with valvular
heart disease. Patients with aortic stenosis have reduced
mitral annular excursion despite normal LVEF [58]. LV lon-
gitudinal shortening, age and indexed aortic valve area, were
independent predictors of symptoms in patients with aortic
stenosis [59].
A reduction in longitudinal s’ velocity has also been dem-
onstrated in asymptomatic patients with severe aortic regur-
gitation [60].
In patients with chronic mitral regurgitation, LV function
appears ‘hyperdynamic’ but there is often subclinical dys-
function with reduced s’ velocity [20]. In 169 patients who
underwent mitral valve surgery s’ was the only independent
predictor of LV reverse remodelling. Haluska et al [61] fur-
ther demonstrated that s’ velocity was lower in mitral regur-
gitation patients without contractile reserve on exercise
echocardiography.
Cardiac Dyssynchrony
Patients with severe systolic dysfunction have evidence of
electromechanical dyssynchrony [62], with delayed propa-
gation of electrical activity from the LV septum to the lateral
wall. Prognostic value of LV dyssynchrony, was first
reported by Bader and co-workers [63], and TDI was consid-
ered one of the most useful echocardiographic dyssynchrony
measures [7,12]. Colour tissue Doppler imaging was consid-
ered superior to pulsed TDI, as multiple segments could be
measured from the same cardiac cycle. Systolic dyssyn-
chrony is the delay in time to peak s’ velocity between the
septal and lateral walls (Fig. 2). Bax and colleagues in their
meta-analysis concluded that TDI could predict responders
to resynchronisation therapy with 87-97% sensitivity and
55-100% specificity [14]; further, a septal to lateral delay
65 m/s, had prognostic value [7]. Systolic dyssynchrony
was further defined as the standard deviation of time to peak
s’ velocity from 12 segments; a value  33ms, was an inde-
pendent predictor of reverse remodelling [12].
While dyssynchrony determined by TDI showed great
promise early on, more recent trials demonstrated that QRS
duration >150m/sec with a left bundle branch block pattern is
the best determinant of responders to resynchronisation ther-
apy [64]. However, the prevalence of systolic dyssynchrony is
more marked in patients with a wide QRS (51% in the narrow
QRS group versus 73% in the wide QRS group)[13].
In summary, systolic myocardial velocity (s’/Sa/Sm) mea-
sured at the mitral annulus or basal myocardial segment
correlates with LVEF and dP/dt. s’ detects subclinical myo-
cardial dysfunction in various cardiac disorders including
CAD, CHF, hypertension, diabetes and primary cardiomy-
opathies. The s’ velocity can be used in stress echocardiog-
raphy [35] for improved identification of ischaemia and
viability and also has prognostic value.
Please cite this article in press as: Kadappu KK, Thomas L. Tissue Doppler Imaging in Echocardiography: Value and
limitations. Heart, Lung and Circulation (2014), http://dx.doi.org/10.1016/j.hlc.2014.10.003
Early Diastolic (e’) Velocity
Although s’ velocity is a good predictor of long term cardio-
vascular outcome, e’ appears superior [21]. Reduction in e’
velocity had prognostic significance in 518 subjects, who
were followed for two years. Reduction in e’ velocity and
increased left atrial dimensions were the strongest predictors
for cardiac mortality [65]. In 182 patients with LV systolic
impairment, e’ <3 cm/s emerged as the best prognostic
marker for cardiac mortality at long term follow-up [10].
Comparable results were reported in hypertensive patients
with LV hypertrophy [28]. e’ velocity was also reduced in
patients with hypertrophic cardiomyopathy who had pul-
monary oedema versus stable patients [27]. Hence e’ velocity
is a sensitive marker of LV DD and a prognostic predictor of
cardiovascular outcomes.
E/ e’ Ratio
Mitral inflow E velocity increases with higher LV filling
pressure (LVFP) with a corresponding reduction in e’ veloc-
ity [66]. The ratio of E/e’ correlates well with LV end diastolic
pressure or pulmonary capillary wedge pressure [66]. An E/
e’ > 15 using septal e’ or E/e’ >12 using lateral e’ velocity, is a
surrogate marker of elevated LVFP. In a cohort with dilated
cardiomyopathy with similar systolic function, patients with
an elevated E/e’ were more symptomatic [21]. Additionally,
the independent predictive value of E/e’> 15 for cardiac
mortality and heart failure has been documented [16] and
subsequently confirmed by Dokainish and co-workers [67].
Hillis and colleagues examined E/e’ ratio as a prognostic
indicator after myocardial infarction in 250 unselected
patients followed for a median of 13 months. Seventy-three
patients (29%) with an E/e’ >15, had an associated increased
mortality (log-rank statistic 21.3, p < 0.0001); moreover E/e’
was the most powerful independent predictor of survival
(risk ratio 4.8, 95% CI 2.1 - 10.8, p = 0.0002) [68]. The same
group also reported that E/e’ ratio >15 was a useful predictor
of LV dilation after infarction [69].
In another study, 417 patients admitted with heart failure
were followed for a median of 306 days [70]; an increase in E/
e’ was linearly associated with increased all-cause mortality.
E/e’ ratio is also useful in detecting early LV DD in patients
with untreated early onset hypertension and hyperinsulinae-
mia [71].
Diastolic Stress Testing
In heart failure with preserved ejection fraction (HFpEF), it is
diastolic dysfunction that precipitates symptoms; HFpEF is
the cause for  50% of all heart failure cases [72]. Symptoms
of diastolic dysfunction are often exertional, due to elevated
LVFP during exercise [73]. As discussed earlier, E/e’ ratio is a
surrogate for LVFP. E/e’ was evaluated during exercise in 45
patients presenting with exertional dyspnoea with normal
 HLC 1701 No. of Pages 10
Tissue Doppler Imaging in Echocardiography
LVEF by Ha and colleagues, with supine bicycle exercise;
patients with normal resting E/e’, that increased with exer-
cise, had significantly shorter exercise duration [74]. In a
recent study of 522 patients referred for stress echocardiog-
raphy [75], the relative contributions of exercise E/e’ and
ischaemia to cardiovascular outcomes was assessed. E/e’
was obtained at rest and after exercise. Patients with a normal
exercise E/e’ and those without exercise induced ischaemia,
had better prognosis than those with ischaemia (with or
without raised exercise E/e’). Importantly cardiovascular
outcomes were similar in patients with increased exercise
E/e’ without ischaemia, to those who developed exercise
induced ischaemia. Additionally, patients with normal rest-
ing E/e’ but elevated exercise E/e’ had worse outcomes than
those with normal exercise E/e’. Thus exercise induced
elevations in E/e’ was associated with increased cardiovas-
cular hospitalisation, independent of inducible ischaemia
[75]. E/e’ correlates with exercise LVFP [76], and latent
diastolic dysfunction can be unmasked with exercise
E/e’ ratio.
e’ Velocity and CAD
Reduction of TDI e’ occurs early in myocardial ischaemia
[50]. As mentioned earlier, Hoffmann and colleagues studied
E/e’ along with s’ in patients with CAD [48]. Similar to s’
velocity, E/e’ negatively correlated with the number of ves-
sels with significant stenosis. e’ velocity was reduced in the
segments supplied by a stenotic artery. Average e’ velocity
remained an independent predictor of CAD, after adjustment
for baseline exercise ECG and conventional echocardio-
graphic parameters [49].
Biering-Sorensen and co-workers also noted a low e’ veloc-
ity after STEMI resulted in greater risk for the composite of
death, heart failure, or a new myocardial infarction (hazard
ratio, 2.26; 95% CI 1.44-3.55; P < .001) [51].
e’ Velocity in Cardiomyopathy
and Constrictive Pericarditis
Diastolic TDI velocities are reduced in inherited cardiomy-
opathies and could be used to detect the condition at a
preclinical stage. Reduced e’ velocity has been demonstrated
in genotype positive patients with hypertrophic cardiomy-
opathy prior to the development of LV hypertrophy [22].
Similarly, e’ velocities were reduced in Fabry patients before
they developed LVH [19], and stratified patients based on
severity in primary AL amyloidosis [77].
It is often difficult, both clinically and using traditional
echocardiography, to differentiate pericardial constriction
from restrictive cardiomyopathy; TDI is useful in differenti-
ating these two conditions. Septal e’ velocity is reduced in
restrictive cardiomyopathy whereas it was normal or ‘supra
normal’ in constrictive pericarditis (septal vs lateral e’: 12.3 vs
5.1 cm/s, p < 0.001). A septal e’  8 cm/s resulted in 95%
Please cite this article in press as: Kadappu KK, Thomas L. Tissue Doppler Imaging in Echocardiography: Value and
limitations. Heart, Lung and Circulation (2014), http://dx.doi.org/10.1016/j.hlc.2014.10.003
7
sensitivity and 96% specificity for the diagnosis of constric-
tive pericarditis [78]. Further, because of pericardial adhesion
to the lateral LV wall in constriction, the LV and RV lateral e’
velocities are not significantly different, and often reduced
when compared to septal e’ [79]. The reduction in lateral e’
velocity is termed ‘annulus reversus’ [80]. By combining
ventricular septal shift with a septal e’ 9 cm/s, 87% sensi-
tivity and 91% specificity for detection of constriction was
demonstrated [81].
a’ Velocity in Clinical Practice
The a’ velocity represents atrial contractile function, and is
useful in evaluating atrial dysfunction. Wang and co-work-
ers, using tertiles of a’ velocity (<4, 4 to 7, and>7 cm/s)
observed that a’ <4 cm/s and a’  4 but <7 cm/s, had an
increased hazard ratio for cardiac death compared with a’ >
7 cm/s (HR: 11.53, 95% CI: 4.1- 32.39 and HR: 4.28, 95% CI:
1.54 - 11.9 respectively) [65]. a’ velocity was also found to be
reduced in ventricular [82] and atrial dysfunction [83].
The duration from onset of the P-wave on electrocardiogram
to peak TDI a’-velocity of the lateral left atrial wall (PA-TDI
duration) has been proposed as an independent predictor of
AF recurrence post cardioversion [84], and can also predict
maintenance of sinus rhythm. Reports on the utility of a’
velocity are limited and require validation in larger groups.
Right Ventricular Function
Echocardiographic quantification of right ventricular (RV)
function is under-reported due to the difficulty in accurate
evaluation given its retrosternal position, making imaging
more challenging. Similar to the LV, pulsed TDI velocities of
the right ventricle demonstrate a base to apex gradient [85]
with lateral RV s’ being greater than the LV lateral s’ velocity.
Colour tissue Doppler imaging is also useful in assessing
segmental RV velocities offline [86]. In normal individuals,
RV s’ velocity is 14  2 cm/s [87]. Meluzin and co-workers,
reported good correlation between RV s’ velocity and RV
ejection fraction (r = 0.648, P < 0.001); RV s’ velocity <
11.5 cm/s predicted RV dysfunction (EF < 45%) with a sen-
sitivity of 90% and specificity of 85% [15]. Reduced s’ is seen
in posterior myocardial infarction, chronic pulmonary
hypertension [15] and chronic airway limitation [88]. More
recently, RV dysfunction has been reported in elite athletes
[89], while Bos and co-workers, reported a reduced RV s’
velocity in asymptomatic patients with congenitally cor-
rected transposition of the great arteries [90] and in tetralogy
of Fallot [91]. Hence TDI is a useful tool to assess early RV
dysfunction.
Limitations
Although TDI measurements are relatively robust, there is a
learning curve for acquisition and analysis of TDI data.
 HLC 1701 No. of Pages 10
8 K.K. Kadappu, L. Thomas
Commercially available machines may use varying algo-
rithms that may provide different TDI velocities [92]. It is
also not clear where in the spectral trace of the pulsed Dopp-
ler envelope to measure tissue velocity; a recent study rec-
ommends measurement at the mid portion of the spectral
trace [93] (Fig. 1A). Tissue Doppler imaging is angle depen-
dent and if the angle of interrogation exceeds 20 degrees, then
the velocity may be underestimated. Even though TDI sig-
nals are robust, it is not unusual to have some variation in
signal amplitude and timing by minimal alterations in posi-
tion of the sample volume. This is particularly important in
dyssynchrony studies as cursor position may alter timing.
Sometimes interpretation of pulsed TDI traces may be chal-
lenging, as there are multiple peaks.
Conclusion
Tissue Doppler imaging is a robust echocardiographic
technique for quantification of global and regional myocar-
dial contractile function as well as left ventricular relaxa-
tion and E/e’ is a surrogate for LVFP. Tissue Doppler
imaging measurements are powerful prognostic markers
in a variety of cardiovascular conditions. As it is relatively
easy to obtain and is reproducible, its incorporation in
routine clinical echocardiographic evaluation should be
considered.
Conflict of interest
There are no conflicts of interest.
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