The echocardiographic assessment of LV
systolic function plays a pivotal role in the diagnosis, risk
stratification and therapeutic guidance of proven medical and
interventional therapy in patients with suspected or known cardiac
disease. For example, an accurate assessment of LV function is now
recommended as part of the management of acute coronary syndrome
(ACS); it is mandatory before the initiation of proven medical
therapy in Heart Failure (e.g. ACE inhibitors and beta-blockers
etc.) and in the selection of those patients for complex pacing
devices ( Biventricular Pacing ± ICD). Furthermore is also vital in
monitoring LV function in response to cardio toxic medication (e.g.
The development of microbubble contrast and
3D echocardiography has resulted in the more precise
and reproducible assessment of LV function and even newer
techniques such as strain rate, velocity vector and speckle
tracking imaging are providing more sensitive and detailed
information on ventricular performance.
These measurements are relatively simple to perform,
reproducible with excellent temporal resolution.
Although the spatial resolution of a dedicated M-mode beam is
also superior to that of two-dimensional echocardiography, in
practice, the ability to visualize the entire left ventricle and to
ensure a true minor-axis dimension mitigates these potential
Linear measurements of LV size and function are listed
in Table 1.
Limitations of M-mode
assessment of LV function:
clear example concerns the fact that many forms of acquired heart
disease, especially coronary artery disease, will result in
regional dysfunction. As M-mode assessment provides
information regarding size and contractility along a single line
this may either underestimate the severity of dysfunction if only a
normal region is interrogated or overestimate the abnormality, if
the M-mode beam negotiates through the wall incorporating the
M-mode assessment may not reflect
the true minor-axis dimension. This is commonly
observed in elderly patients in whom there is angulation of the
M-Mode Assessment of Left Ventricular Size and
LV internal dimension in
LV internal dimension in
M-mode indicators of LV dysfunction
These markers include:-
The magnitude of opening of the mitral
valve (E-wave height), correlates with trans-mitral flow and with
left ventricular stroke volume (in absence of significant mitral
regurgitation and ventricular septal defect). The
internal dimension of the left ventricle correlates with diastolic
volume. Therefore, the ratio of mitral valve
excursion to left ventricular size reflects the ejection fraction.
Normally, the mitral valve E point (maximal early opening) is
within 6 mm of the left side of the ventricular septum (mitral
E-point to septal separation). In the presence of a
decreased ejection fraction, this distance is increased (Figure
Pattern of the aortic valve opening
can also provide indirect evidence regarding LV systolic function.
Low LV stroke volume may result in a gradual
reduction in forward flow in late systole, resulting in gradual
closing of the aortic valve in late systole. This
results in a rounded appearance of the aortic valve in late systole
M-mode echocardiograms recorded in
two patients with significant systolic
Left: An E-point septal
separation (EPSS) of 1.2 cm (normal, <6mm).
Recording in a patient with more significant left
in which the EPSS is 3.0 cm. Also note
the interrupted closure of the
valve with a B bump (top), indicating
an increase in the left ventricular end-
M-mode echocardiogram recorded through the aortic valve in a
cardiac function and
decreased forward stroke volume. Note
closure of the aortic valve, indicating
decreasing forward flow at the end of
Normal and abnormal aortic valve opening patterns are
superimposed on the
provides superior spatial resolution for determining left
ventricular size and function (Table 2). The most common method for
determining ventricular volumes is the Simpson Rule or the "method
of disks". This technique requires recording an
apical four- and two-chamber view from which the endocardial border
is outlined in end-diastole and end-systole. The
ventricle is then mathematically divided along its long axis into a
series of disks of equal height. Individual disk
volume is calculated as height multiplied by disk area where height
is assumed to be the total length of the left ventricular long axis
divided by the number of segments or disks. The
surface area of each disk is determined from the diameter of the
ventricle at that point. The ventricular volume is
then represented by the sum of the volume of each of the disks,
which are equally spaced along the long axis of the ventricle.
This methodology is illustrated in Figure 3.
If a ventricle is symmetrically contracting,
typically either the four- or two-chamber view will then reflect
the true ventricular volume. In any view,
foreshortening of the ventricular apex will result in
underestimation of the LV volumes and most often in overestimation
of the ejection fraction.
2. LV function assessment using
LV end-diastolic volume (LVEDV)
LV end-systolic volume
Stroke volume (SV)
Ejection fraction (EF)
Limitations of Simpson rule volume
- Myocardial drop-out is a potential issue.
Tissue harmonic imaging and contrast echocardiography
have largely overcome this problem (Figure 4).
- For accurate volume determination, the transducer
must be at the true apex and the ultrasonic cross-sectional beam
must be through the center of the left ventricle.
These conditions are frequently not met, resulting in artifactually
small left ventricular volumes.
3: Method for determining the left
ventricular volume from the rule of disks
or Simpson's rule.
The method assumes that the ventricle is
composed of a
stacked series of
elliptical disks of equal height. By
knowing the major and minor
diameters of each disk (measured
from the views shown), an ellipse can be
defined and the area of each ellipse
is then multiplied by the slice thickness.
When all the disks are
summated as shown by the
formula, the volume of the
whole ventricle can be determined.
A4C- apical four chamber; A2C- apical
chamber; EDV - end diastolic volume;
ESV - end systolic
Techniques to identify
the true apex:
In the normal ventricle, the apex
does not move from apex to base during filling or emptying of the
true apex is usually the thinnest area of the left ventricle.
If the visualized apex has the same thickness as the
surrounding walls and appreciable motion in systole, it is likely
to be a tangential cut through the left ventricle rather than a
true on-axis view.
An important technological advance in the
determination of ventricular volume involves the application of
Contrast echocardiography is
performed by injecting small volumes of microbubbles.
Microbubbles consist of a gas (e.g. perfluorocarbon, sulphur
hexafluoride) surrounded by a shell (phospholipids or protein etc)
which make the microbubbles stable enough to traverse the pulmonary
microvasculature and opacity of the left ventricle.
Contrast echocardiography results in not only improving the left
ventricular endocardial definition (Figure 4) but also in improving
assessments of LV volumes, LVEF and regional wall
4: Apical four-chamber view. (Right)
Left ventricular opacification with
agent outlines the normal smooth
endocardial border. The
image artefact is eliminated, thereby excluding
apical thrombus as
suggested on the
unenhanced image (left).
Regional wall motion
Echocardiography, with its high
spatial and temporal resolution, is an ideally suited non-invasive
method of assessing wall motion. In suspected acute
coronary syndrome (ACS) wall motion abnormality (WMA) precedes
changes on the ECG and symptoms and hence is extremely useful in
the early detection of ACS. Conversely in patients
with suspected ACS with inconclusive ECGs, normal WM excludes
ischaemia. In patients presenting with a prior
history of CAD, the presence and extent of regional WMA gives
valuable information regarding the site and severity of myocardial
damage. Improved image quality, particularly with
harmonic imaging and left ventricular opacification (LVO) with
ultrasound contrast agents enhances reproducibility of
The movement of a given myocardial segment is
influenced by the adjacent muscle to which it is attached.
For example, in a chamber with a dyskinetic ischaemic
segment, some of the adjacent normal tissue may appear hypokinetic
because its motion is influenced by the attached dyskinetic
segment. Conversely a vigorously contracting normal
muscle adjacent to a hypokinetic segment may mask the abnormal
segment. In general, wall motion abnormalities alone
tend to overestimate the degree of ischemia seen in the myocardium.
However, a more specific finding for ischaemic muscle
is a reduction of systolic wall thickening while a normal
myocardial muscle increases in thickness during systole.
During ischaemia, there may also be systolic thinning
during acute ischaemia, ie. wall thickening is greater in diastole
compared to systole. Situations in which wall motion
may be abnormal with preserved wall thickening include left bundle
branch block (LBBB), Wolf-Parkinson-White syndrome and when the
patient has a paced rhythm. The presence of preserved
systolic wall thickening in these conditions confirms that the wall
motion abnormalities are not due to underlying CAD.
Assessment of regional wall
Left ventricular wall motion is assessed in the
apical 4-, 2-, 3-chamber, parasternal long and short
axis views. This allows complete visualisation of all
the left ventricular walls, and hence all 3 vascular territories,
athough care must be taken to ensure clear endocardial border
definition. Clear visualisation of the endocardial
border is crucial for the full assessment of wall motion.
It is also important to remember that changes in the
left ventricle are not uniform, and thus it is preferable to obtain
different views of the same region to make an accurate assessment
of segmental wall function. This is usually done by
combining the use of the standard apical views with the parasternal
views, particularly in the short axis, where different levels of
function from base, through papillary muscle down to apex can be
The best way to assess wall motion in each of
these views is to consider the endocardial border and the
epicardium as a number of point targets. As normal
contraction occurs, the endocardium moves inwards (endocardial
excursion) and left ventricular cavity diminishes).
The distance between the endocardium and epicardium increases (wall
thickness). In patients with ischaemia, there is a
reduction in the degree of endocardial excursion together and a
decrease in the amplitude of wall thickening. This
can be seen clearly when compared to adjacent, normally contracting
areas of myocardium. Of the two parameters, the
degree of endocardial thickening is the most reproducible and
reliable method of wall motion assessment. It is also
important to emphasize at this point that one must be careful to
take into account translatory and rotatory motion of the left
ventricle which may give a false impression of preserved wall
motion. However, the absence of endocardial excursion
effectively rules out any significant wall thickening. Wall motion
and wall thickening assessments are described in Table 3.
Methods for Evaluation of Regional Wall Motion
normal, hypokinetic, akinetic, dyskinetic
WMS or WMSI
= hypokinetic, i.e. reduced endocardial excursion and wall
= akinetic, absent endocardial excursion and
= dyskinetic, systolic bulging with no
WMSI = Total score of segments/Total number of
wall motion score; WMSI, wall motion score index
The changes seen in regional wall
motion correlate closely with the blood supply to that area of
myocardium. Several methods have been described to
anatomically describe the left ventricle (LV) in order that
regional wall motion can be accurately assessed but the basic
principles remain the same. The ventricle is divided
into 3 sections: base, mid-ventricular cavity and the apex.
Each section is then divided into segments that
correspond to areas in the LV wall. The most recent
recommendations from the American College of Cardiology (ACC) and
American Heart Association (AHA) are to use a 17-segment model
(Figure 5). This divides the base and mid-ventricular cavity into 6
segments each, with the apex section having 4 segments.
A final segment is a very distal apical "cap" which
is best assessed in the apical 2- and 4- chamber views.
5: Regional wall motion is generally assessed
qualitatively based on a 16-
17-segment model. See text
for details: LA- left atrium; LAA- left atrial
LAD- left anterior descending; LCx- left
circumflex; MV- mitral valve;
artery; RCA/PDA- right coronary artery / posterior
artery; SVC- superior
Commonly a "bulls-eye" plot (Figure 6) of
all of these segments is used to note the individual segment
scores, with the basal segments on the outside, followed by the
mid-cavity and then the apex at the center. This
allows a clear localisation of any defect on a single report with
an indication of the corresponding vascular supply (Figure 7).
Table 4 outlines causes of non-ischemic
6: Bull's eye" polar plot
depicting specific regions from the various views
shown in Figure
7: The coronary territories corresponding to
the segmental model (Figure 5
are shown but it should be noted that
there may be considerable overlap in
4. Non-ischaemic regional wall motion
Left bundle branch
Right ventricular volume
Right ventricular pressure
After cardiac surgery
Congenital absence of the
Endocardial Border Tracking
Analysis of two-dimensional grey scale
images obtained during 2-dimensional imaging tend to be subjective,
qualitative and dependant on the experience of the observer.
When an image is acquired, the backscatter
information along the scan line is analysed and each pixel
classified as either blood or tissue. There is
sufficient difference between the energy returned from the blood in
the LV (low) and the endocardium (high) for this distinction to be
made. Once this interface has been established along
the whole of the endocardium, it can then be tracked.
Each pixel is colour coded and is superimposed onto the
2-dimensional image. The construction is then
integrated with the original scan image and this can be performed
on-line. This leads to real-time tracking of the
endocardial border which is continually updated frame-by-frame.
Colour coded endocardial tracking (Colour Kinesis and
A-SMA) is an extension of this automated process (Figure 8).
Once the endocardial border has been defined on the
basis of the backscatter from the blood and tissue, the inward
(systolic) and outward (diastolic) movement is colour-coded.
Each pixel is given a specific colour dependant on
its movement which is then compared to the previous frame so that
an accurate measurement of systolic function and regional motion is
8: Colour coded endocardial tracking (Colour
Kinesis and A-SMA) is an
an automated border detection
The colour overlays are superimposed onto
the grey scale images which are updated on a frame by frame basis.
This allows real time assessment of systolic function
and regional wall motion using a visual colour scale (Figure
9).However, the accuracy and reproducibility of this technique
depends on good image quality.
evaluation of global left ventricular
One of the more clinically useful
methods for following left ventricular function is to evaluate the
velocity time integral (VTI) of the left ventricular outflow tract
or ascending aorta.
The principle states that if the cross-sectional area of the
chamber is known, then the product of that cross-sectional area and
the mean flow velocity equates to the volumetric flow.
As the heart is a pulsatile flow system, in which the
flow velocity occurs during systole, the volume calculated equals
the forward LV volume in the aorta. This forward
stroke volume can then be multiplied by the heart rate to obtain
the cardiac output (Figure 10).
Typically, the areas evaluated for
determination of systolic flow and hence global left ventricular
performance have been the left ventricular outflow tract, with the
Doppler interrogation taking place from the apex of the heart.
In the absence of aortic regurgitation, the
calculated stroke volume should accurately reflect the actual flow
volume per heart beat.
9: Demonstration of automated endocardial
tracking with colour coding(Colour
Kinesis™) in the apical 4-chamber
view. At the beginning of systole (A),
athin rim of colour delineates the
endocardium. During systole (B) there
change in colour to demonstrate wall thickening.
In a patient suffering
acute myocardial infarction,
there is failure of wall thickening in the
septum and hence no change in
colour (C), whereas normal wall motion
is represented in the lateral
10: Schematic representation of the method
for determining volumetric
flow. This method
is applicable for any laminar flow for
which the cross-sectional
area (CSA = p r 2) of the
flow chamber can be determined.
The product of cross-
sectional area and the time velocity
integral (TVI) is stroke volume (SV).
output (CO) can be calculated as the
product of stroke volume and heart rate.1
The myocardial performance index (MPI, also
known as "Tei" index) is an expression of global ventricular
performance. It is a simple calculation that includes both systolic
and diastolic parameters and can be applied to either the left or
right ventricle. The MPI incorporates three basic time intervals
that are readily derived from Doppler recordings: the ejection time
(ET); isovolumic contraction time (IVCT) and the isovolumic
relaxation time (IVRT). From these values, the MPI can be
calculated from the following formula:-
MPI = ( IVCT +
IVRT ) /
Systolic dysfunction is associated with a
prolongation of IVCT and a shortening of the ET. Therefore, this
will result in an increase in the MPI, the normal range is 0.39 ±
0.05, and values above 0.50 are considered abnormal (Figure
11: Myocardial performance index, also known
as the "Tei" index, is a
dimensionless index based
on the sum of the isovolumic contraction
times (ICT, IRT) divided by the ejection time (ET).
assessmentof both systolic and diastolic
function and has been
related to prognosis in
a variety of
This represents the rate of increase
in pressure within the left ventricle. During
isovolumic contraction, this is a relatively load-independent
measure of ventricular contractility (Figure 12). The method by
which this is performed is to record the mitral regurgitation
spectral profile at a high sweep speed (typically 100 mm/sec).
Examination of the upstroke of the velocity curve can
then be used to derive instantaneous measurements:
To determine the dP/dt, one calculates the time (T)
difference in milliseconds from the point at which the velocity is
at 1 m/sec and 3 m/sec. The time between these two
points represents the time that it takes for a 32 mm Hg change to
occur within the left ventricular cavity.
dP/dt is then calculated as dP/dt = 32 mm Hg ÷ time T
In the presence of marked mechanical
dysynchrony i.e. LBBB, RV pacing and WPW syndrome, dP/dt may be
reduced as a consequence of contractile dysynchrony and not due to
12: The rate of LV pressure rise (dP/dT)
during isovolumic contraction (IVC)
phase of systole is a
useful measure of LV contractility. In patients with
regurgitation (MR), estimates of
dP/dT can be derived from the time interval it
V pressure to rise by 32 mmHg (i.e. from 1 m/s to 3
m/s). The Bernoulli
equation is used
to estimate LV pressures from the MR CW spectral
Tissue Doppler Velocity
Doppler velocities arising from relatively
dense, slow-moving targets such as the myocardium and cardiac
annulus may be imaged by altering receiver gains and frequency
filters. TDI can be displayed as a colour display,
saturating the typical anatomic structural information (Figure 13).
A pulsed Doppler sample volume is placed in either
the subendocardial or subepicardial regions and differential
velocities in adjacent wall segments can thereby be determined.
TDI demonstrates regional variation based on which
area of the mitral annulus is interrogated (septal vs. lateral).
Most laboratories standardize clinical measurements
to either the septal or lateral annulus to maximize efficiency
(Figure 13). The annular velocity in systole has shown a good
correlation with the left ventricular ejection fraction over a wide
range of ventricular function. It has been demonstrated that in
symptomatic patients with apparently normal LVEF, this technique
can detect impaired longitudinal systolic function (Sm < 4.4
m/s) and thus provide superior prognostic ability than the standard
measurements such as LVEF.
Doppler tissue imaging of the
medial mitral annulus recorded from an
view. Note the systolic motion of the
annulus toward the apex
(Sm) and the biphasic
diastolic motion (Ea and Aa),
which correspond to the mitral
valve E- and A-waves.
Strain and strain rate
TDI suffers from tethering and
translational motion artifact whereby the movement of the entire
heart is recorded in the tissue motion of a specifically measured
segment. This limitation can be overcome by Strain
imaging which measures actual deformation (Figure 14). Strain and
strain rate imaging is a variation of TDI that provides a
high-resolution evaluation of regional myocardial function. In this
method, TDI is used to simultaneously determine velocities in two
adjacent points as well as the relative distance between those two
points. Strain rate is defined as the instantaneous
rate of change in the two velocities divided by the instantaneous
distance between the two points. Positive strain rate
represents relaxation or lengthening and negative values relate to
active contraction between the two points (Figure 15).
As with the endocardial-epicardial velocity gradient,
strain rate has been demonstrated to be a more sensitive and
earlier indicator of regional dysfunction than many routine
techniques. Strain rate imaging has excellent
temporal resolution and can be used to demonstrate subtle phenomena
such as postsystolic contraction. However, strain and
strain rate derived from TDI is angle-dependent and may not be
reproducible enough for routine clinical applications.
Schematic representation of the definition of myocardial
strain or strain
rate. Strain is defined as
a change in length normalised to the
original length. The
which this change occurs is strain rate (SR).
Strain measures the actual
shortening (negative strain) or lengthening (positive
strain) relative to
original length, whereas SR
is the speed at which this occurs.2
The aforementioned TDI methods are still
limited by angle dependency and problems with evaluating regional
LV torsional dynamics (rotational LV contraction). Newer techniques
such as speckle
tracking involve the detection of multiple unique patterns of
echocardiographic pixel intensity that can be tracked throughout
the cardiac cycle. The angular displacement of these pixels can
then be plotted over time for basal, mid and apical LV segments
thereby providing a measure of rotational movement (Figure
Although currently lacking clinical
evidence to show its prognostic significance, this method may
become a robust sensitive marker in LV dysfunction.
15: 2-D speckle tracking. In this technique,
displacement is measured by
tracking a speckle over
the cardiac cycle. Speckles are unique
detected by the software. The individual speckle
patterns are located at
end-diastole and then tracked
to their new position in end systole. The
then integrated in order to derive the strain. The
this technique is that
itis not angle
With the advent of new martix array
transducers, full volume data sets to allow real-time imaging, this
technique is highly accurate and reproducible in the global and
regional assessment of LV size and function as compared with MRI
(Figure 16) . Three-dimensional imaging or reconstruction obviously
reduces the limitation on single or biplane imaging, which has the
potential to either disproportionately represent or underestimate a
wall motion abnormality. By creating a
three-dimensional image set, all regions of the ventricular
myocardium will be incorporated in the volume determination.
In addition, this method does not rely on geometric
assumptions and therefore provides more precise LV size and
function assessment. The latest development now allows the
acquisition of a full volume data set within a single heart beat
that may prove to be a particularly powerful technique in stress
16: 3-D volumetric echocardiography can
accurately and reproducibly assess
regional and global LV
systolic function and has shown excellent correlation
standard methods such as MRI
1. Echocardiography, ed.
Feigenbaum, 6th Edition, Lippincotts, Williams &
2. Atlas Of
Echocardiography, ed S.D. Solomon 2nd Edition,
R, Becher H, Monaghan M, Zamorano JL, Agati L, Nihoyannopoulos P.
Contrast echocardiography: Evidence
based contrast echocardiography for clinical use
recommend by European Association of Echocardiography.
4. Jeetley P,
R Coronary Artery
Disease: Assessing Regional Wall
Eds: P Nihoyannopoulos, J Kisslo,
Chapter 15: 313-324
Last Updated (Fri 08 November 2013)