Systolic Function of LV

Introduction

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. Herceptin chemotherapy).

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.

M-mode linear measurements:

  • 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 advantages.
  • Linear measurements of LV size and function are listed in Table 1.

Limitations of M-mode assessment of LV function:

  • One 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 localised abnormality.
  • 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 ventricular septum.

Table 1. M-Mode Assessment of Left Ventricular Size and Function1

Parameter

Formula

Abbreviation

Values (range)

LV internal dimension in diastole (cm)

LVIDd

3.6-5.6

LV internal dimension in systole (cm)

LVIDs

2.3-3.9

Fractional shortening (%)

(LVIDd - LVIDs)/LVIDd

FS

27-42

Other 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 1).
  • 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 (Figure 2).

Fig 1

M-mode echocardiograms recorded in two patients with significant systolic

dysfunction. Left: An E-point septal separation (EPSS) of 1.2 cm (normal, <6mm).

Right: Recording in a patient with more significant left ventricular systolic

dysfunction in which the EPSS is 3.0 cm. Also note the interrupted closure of the

mitral valve with a B bump (top), indicating an increase in the left ventricular end-

diastolic pressure.1

Fig 2

Figure 2: M-mode echocardiogram recorded through the aortic valve in a patient

with reduced cardiac function and decreased forward stroke volume. Note the

rounded closure of the aortic valve, indicating decreasing forward flow at the end of

systole. Normal and abnormal aortic valve opening patterns are noted in the

schematic superimposed on the figure.1

Two-dimensional measurements

Two-dimensional echocardiography 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.

Table 2. LV function assessment using Simpson's method1

Parameter

Formula

Value (range)

LV end-diastolic volume (LVEDV) ml/m2

49-85

LV end-systolic volume ml/m2

17-37

Stroke volume (SV) ml/m2

LVEDV-LVESV

26-54

Ejection fraction (EF) (%)

SV/LVEDV

49-71


Limitations of Simpson rule volume estimation

  • 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.

Fig 3

Figure 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 two

chamber; EDV - end diastolic volume; ESV - end systolic volume.2

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 chamber.
  • 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.

Microbubble Constrast Echocardiography

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 motion.3

Fig 4

Figure 4: Apical four-chamber view. (Right) Left ventricular opacification with

intravenous contrast agent outlines the normal smooth endocardial border. The

apical image artefact is eliminated, thereby excluding apical thrombus as

suggested on the unenhanced image (left).

Regional wall motion assessment

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 echocardiography.

Limitations

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 motion

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 visualised.

 

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.

 

Table 3. Methods for Evaluation of Regional Wall Motion Abnormalities

 

Visual/subjective

normal, hypokinetic, akinetic, dyskinetic

Semiquantiative

WMS or WMSI

1. = normal

2. = hypokinetic, i.e. reduced endocardial excursion and wall thickening

3. = akinetic, absent endocardial excursion and thickening

4. = dyskinetic, systolic bulging with no thickening

WMSI = Total score of segments/Total number of segments.

WMS, 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.

Fig 5

Figure 5: Regional wall motion is generally assessed qualitatively based on a 16-

or 17-segment model. See text for details: LA- left atrium; LAA- left atrial

appendage; LAD- left anterior descending; LCx- left circumflex; MV- mitral valve;

PA- pulmonary artery; RCA/PDA- right coronary artery / posterior descending

artery; SVC- superior vena cava.4

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 WMA.

Fig 6

Figure 6: Bull's eye" polar plot depicting specific regions from the various views

shown in Figure 5.4


Fig 7

 

Figure 7: The coronary territories corresponding to the segmental model (Figure 5

& 6) are shown but it should be noted that there may be considerable overlap in

coronary vascular supply.4

Table 4. Non-ischaemic regional wall motion abnormality

Conduction disorder

Left bundle branch block

Ventricular pacing

Premature ventricular contractions

Ventricular preexcitation (Wolf-Parkinson-White syndrome)

Abnormal ventricular interaction

Right ventricular volume overload

Right ventricular pressure overload

Pericardial constriction

Miscellaneous

After cardiac surgery

Congenital absence of the pericardium

Posterior compression

Ascites

Hiatal hernia

Pregnancy

Automated 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 possible.

Fig 8

Figure 8: Colour coded endocardial tracking (Colour Kinesis and A-SMA) is an

extension of an automated border detection process.4

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.

Doppler evaluation of global left ventricular function

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.

Fig 9
Figure 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 is progressive 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 wall.4

Fig 10

Figure 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). Cardiac

output (CO) can be calculated as the product of stroke volume and heart rate.1

Myocardial Performance Index

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 ) / ET

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).

Fig 11

Figure 11: Myocardial performance index, also known as the "Tei" index, is a

dimensionless index based on the sum of the isovolumic contraction and

relaxation times (ICT, IRT) divided by the ejection time (ET). This index

incorporates assessmentof both systolic and diastolic function and has been

related to prognosis in a variety of disease states.2

Left ventricular dP/dt

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 (seconds).

Limitations

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 reduced contractility.

Fig 12

 

Figure 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 mitral

regurgitation (MR), estimates of dP/dT can be derived from the time interval it

takes for 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 Doppler

velocities.2

Tissue Doppler Velocity Imaging (TDI)

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.

 

Fig 13

 

Figure 13: Doppler tissue imaging of the medial mitral annulus recorded from an

apical four-chamber 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 imaging

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.

 

Fig 14

Figure14: 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

rate at which this change occurs is strain rate (SR). Strain measures the actual

extent of shortening (negative strain) or lengthening (positive strain) relative to

its original length, whereas SR is the speed at which this occurs.2

Tissue tracking

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 15).

Although currently lacking clinical evidence to show its prognostic significance, this method may become a robust sensitive marker in LV dysfunction.

Fig 15

 

Figure 15: 2-D speckle tracking. In this technique, displacement is measured by

tracking a speckle over the cardiac cycle. Speckles are unique acoustic shadows

that are detected by the software. The individual speckle patterns are located at

end-diastole and then tracked to their new position in end systole. The

displacement is then integrated in order to derive the strain. The advantage of

this technique is that itis not angle independent.

3D Echocardiography

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 echocardiography.

 

Fig 16

 

Figure 16: 3-D volumetric echocardiography can accurately and reproducibly assess

regional and global LV systolic function and has shown excellent correlation with

gold standard methods such as MRI


References

1.  Echocardiography, ed. Feigenbaum, 6th Edition, Lippincotts, Williams & Wilkins

2. Atlas Of Echocardiography, ed S.D. Solomon 2nd Edition, Springer.

3. Senior 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. Eur J  Echocardiogr. 2009;10:194-212.

4. Jeetley P, Senior R Coronary Artery Disease: Assessing Regional Wall Motion: in Echocardiography Eds: P Nihoyannopoulos, J Kisslo, Springer-Verlag 2010; Chapter 15: 313-324

Last Updated (Fri 08 November 2013)

Copyright © 2011 British Society of Echocardiography