Echocardiography: Useful indices of left ventricular systolic functionThe most frequently used methods for the assessment of left ventricular (LV) systolic function are LV ejection fraction (EF) and regional wall motion analysis. Two dimensional (and also M-mode) echocardiography is the most common technique used but other tests that can examine LV systolic function are tissue Doppler imaging (TDI), speckle tracking imaging, three-dimensional (3D) echocardiography, computed tomography (CT), and cardiac magnetic resonance imaging (CMR).
FS as an index of global LV function can be problematic when there is a marked difference in regional function, in patients with a previous myocardial infarction.
Two-dimensional (2D) echocardiography for the evaluation of LV systolic function
Stroke volume= the volume of blood ejected by a ventricle in systole= EDV-ESV.
Thus, EF= (EDV-ESV)/ EDV.
It is a measure of global LV systolic function, with established prognostic significance (the lower the EF, the worse the prognosis), but it is also influenced by preload, afterload, heart rate, and valvular function. (In patients with severe aortic or mitral regurgitation, conditions causing volume overload of the left ventricle, the normal value for the EF is ≥ 60%.) Systolic function of the left ventricle (LV) is considered as mildly reduced when EF is between 45 and 55 %, moderately reduced with EF between 30 and 45 % and severely reduced with EF< 30%.
Left ventricular EF is a strong predictor of clinical outcome and is widely used to make clinical decisions.
EF should be calculated from volumetric measurements
by 2D echocardiography. Even more accurate measurements of left ventricular volumes and EF are obtained with three dimensional (3D) echocardiography, or magnetic resonance imaging (MRI). The latter two techniques have similar accuracy.
Echocardiography quiz. Any abnormality in the systolic function of the left ventricle?
Parasternal long axis echocardiogram of a patient with dilated cardiomyopathy
A male patient (age 40 ) with symptoms of heart failure (nocturnal and exertional dyspnea). He was diagnosed with dilated cardiomyopathy. Parasternal long axis echocardiographic view: The left ventricle and the left atrium are dilated. The anteroseptal and the posterior left ventricular wall are severely hypokinetic. There is also a very small pericardial effusion.The coronary arteriography was normal. He was treated with ramipril (ACE inhibitor), carvedilol (beta-blocker), furosemide (loop diuretic) and eplerenone (aldosterone antagonist). On re-examination symptoms and left ventricular function showed improvement.
Doppler Echocardiography derived systolic indices (stroke volume)Doppler echocardiography also provides some indices of LV systolic function, such as the stroke volume (SV), i.e. the blood volume ejected per beat. For this measurement one obtains from the apical 5 chamber view the pulse wave doppler signal of the velocity in the left ventricular outflow tract (LVOT) and also measures the diameter of the LVOT (in the parasternal long axis view at the base of the aortic valve leaflets or immediately proximal to the aortic valve).
SV= VTI (LVOT) x area (LVOT)
VTI is the velocity time integral (also named time velocity integral-TVI) of blood flow through the LVOT during systole.
This formula is explained as follows: VTI is calculated as the area under the curve of the Doppler velocity signal (which displays velocity on the vertical axis and time on the horizontal axis). This area of the Doppler signal is automatically calculated by the machine software, after the examiner manually traces the doppler velocity signal. It mathematically represents a velocity time integral, i.e. the sum of many products of velocity x time, each corresponding to every small time interval in systole. Since in every small time interval the column of blood moves by a distance given by the product of blood velocity x time interval, the VTI as a sum represents the total distance the column of blood has "traveled" in systole. This distance multiplied by the area of the orifice through which blood has passed, is the volume of blood which passed through the orifice in systole= the stroke volume (SV). Assuming a circular LVOT with radius r and diameter D (=2r) :
LVOT area = πr2=3,14r2=3,14(D/2)2 = (3,14 D2)/4= 0,785D2
In the absence of aortic regurgitation, SV reflects the forward effective blood flow in a cardiac beat and multiplied by heart rate (beats per minute) it gives the cardiac output (= the volume of blood passing through the circulation per minute). Strictly speaking, the SV is the hemodynamic result of LV function and not a true index of systolic function. Normal values of SV: 55-80 mL.
It is better to express the normal values of stroke volume per m2 of body surface area:
Normal values of SV(ml/m2): 26-54
Tissue Doppler Imaging (TDI)Measurement of mitral ring velocities or myocardial velocities of the basal segments (velocity of the movement of these tissues along the longitudinal axis of the heart) is a simple and sensitive method for the assessment of the left ventricular systolic and diastolic function. Both peak systolic (Sm) and early diastolic (Em) mitral annular or left ventricular basal velocities are nearly always reduced in patients presenting with the clinical syndrome of systolic heart failure.
The systolic annular velocity of the mitral valve (Sm) is a measure of left ventricular longitudinal contraction (contraction of the long axis oft the ventricle). It generally correlates well with the left ventricular EF. Normally Sm of the septal mitral annulus is > 6.5 cm/sec, and Sm of the lateral mitral annulus ≥ 8 cm/sec, when measured with pulse wave tissue doppler (PW-TDI). It is better to assess the mean Sm of the septal and lateral mitral annulus (normal value > 7.5 cm/sec). Note that myocardial velocities measured by the color TDI method are lower than velocities by pulsed Doppler (typically about 25% lower).
Early myocardial damage often involves the subendocardial fibres, with impairment in long-axis contraction occuring before changes in short-axis function. Thus, the Sm is a sensitive marker of mildly impaired left ventricular systolic function, even in people with apparently preserved systolic function and a normal EF, for example in those with diastolic heart failure, or in some diabetic patients without overt heart disease. Reduced annular TDI velocities are also present in subjects with hypertrophic cardiomyopathy, (even in people having the related gene mutations, who are at the stage of subclinical disease, with no cardiac hypertrophy).
Note that whereas the Sm velocity is an index of left ventricular systolic function, the Em or E΄velocity (the peak early diastolic mitral annular velocity, which is a negative wave) is an index of LV diastolic function and the Am or A΄velocity (an end-diastolic negative wave) is an index of the systolic function of the left atrium.
Kadappu KK, Thomas L. Tissue Doppler Imaging in Echocardiography: Value and Limitations.Heart, Lung and Circulation 2015;24:224-233
LINK Tissue Doppler Imaging in Echocardiography
Myocardial strain and strain rate imagingIn general, in myocardial segments with diminished systolic function, systolic velocities are typically reduced and there are also reductions in systolic strain and strain rate. Strain is the proportion (percentage) of change in length of the myocardium (units %) and it is negative in systole, since there is a negative change in length (shortening), and positive in diastole (because in diastole the length increases).
Strain = L-Lo /Lo, where L is the current length and Lo is the original length of a myocardial segment. Strain rate (SR) is the rate of change of the strain value= the proportional change in length per unit of time. SR units are s-1
SR is negative in systole (because it represents the rate of proportional decrease in myocardial length) and positive in diastole (because it represents the rate of increase in length). LV longitudinal velocities measured from an apical window increase progressively from the apical toward the basal myocardial segments. Longitudinal strain and strain rate, however, are essentially similar between apical and basal segments.
The normal value of the peak systolic strain (percentage of shortening) of the left ventricle during systole in the longitudinal axis is greater than 15%. To be more accurate, lets mention that normal peak systolic strain has a value more negative than -15%, usually between -15 and -25%. (The negative sign indicates a decrease in the length of the myocardium, i.e. shortening).
Peak systolic strain is influenced by preload (like the ejection fraction which is also influenced by the ventricular loading conditions) and can be used as an indicator of the total, and of the regional systolic function (when measured at a segment of the left ventricle).
The normal value for the peak systolic strain rate of the left ventricular myocardium is between - 1.2 and - 2 s-1 (sec-1=1/s).
In normal hearts the value of strain rate and strain is about the same in all myocardial segments from the base to the apex of the heart, (showing no significant difference). Conversely, myocardial velocity recorded by the tissue Doppler (in cm/s), and the displacement (change in position) of a given point of the myocardium (in mm) is greater in the basal portions and is getting smaller towards the apex.
An advantage of the percentage of myocardial deformation (strain) and of the rate of the proportional change in deformation (strain rate) is the following: Strain and strain rate is not affected by the translational motion of the heart ("bouncing" movements in the chest during systole). In contrast, the myocardial velocities recorded with tissue Doppler (TDI) are affected by the translational motion of the heart within the chest and not only by the motion of myocardial shortening in systole or lengthening in diastole.
A diminished peak systolic strain or strain rate is a sensitive marker of an impairment in systolic function.
Need more information about these modern echocardiographic techniques? In that case, here is a link for you to click on (free review article with the option to download PDF) ...
Strain and Strain Rate Imaging by Echocardiography – Basic Concepts and Clinical Applicability
Dandel Μ ,Lehmkuhl H, et al. Strain and Strain Rate Imaging by Echocardiography – Basic Concepts and Clinical Applicability. Current Cardiology Reviews, 2009, 5, 133-148.
Assesment of left ventricular diastolic function (a summary)
Diastolic dysfunction can occur in many kinds of heart disease such as hypertensive heart disease, diabetes, hypertrophic cardiomyopathy, aortic stenosis with left ventricular hypertrophy, ischemic heart disease, restrictive cardiomyopathy, constrictive pericarditis, etc.
There are four key variables for a quick assessment of LV diastolic function. LV diastolic dysfunction is present if more than half of these parameters meet the abnormal cutoff values. These key parameters are:
►The peak early diastolic velocity of the mitral annulus e΄, obtained from the pulse wave tissue Doppler velocity tracing of the septal and lateral mitral annulus, in the apical 4 chamber view. The velocity e΄is a marker of myocardial relaxation and it is reduced in all stages of diastolic dysfunction. A normal e΄ is a strong indication that the diastolic function is normal, except in patients with constrictive pericarditis or significant mitral regurgitation.
The normal septal e΄ ≥ 8 cm/ s (centimeters per second). The lateral e΄ is normally higher than the septal (> 10 cm/s). Abnormal values suggestive of diastolic dysfunction: a septal e΄< 7 and a lateral e΄< 10 cm/s.
► The average E/e΄ ratio. This is the ratio of the peak early diastolic mitral inflow velocity E to the average of the e΄ velocities of the septal and lateral mitral annulus. Abnormal is a ratio E/e΄>14. The ratio E/e΄ is less age-dependent than other indices of LV diastolic function. A ratio > 14, regardless of the patient's age, is almost always abnormal, suggesting elevated LV diastolic pressures (and thus, an elevated mean left atrial pressure and pulmonary capillary wedge pressure)
► The LA volume index is the maximum volume of the left atrium (LA), measured at the end of ventricular systole, divided by the patient's body surface area (BSA). LA volume index > 34 ml/m2 is considered abnormal, indicating left atrial dilation. LA dilation in the absence of a chronic atrial arrhythmia (e.g. atrial fibrillation), or mitral valve disease, is an indication of increased LV filling pressures, resulting in chronically elevated left atrial pressures.
► The peak tricuspid regurgitation (TR) velocity measured with the continuous wave Doppler. A peak TR velocity > 2.8 m/s is suggestive of an elevated pulmonary arterial systolic pressure (with the exception of pulmonary stenosis). This can often result from elevated pulmonary venous pressures due to the elevated left atrial pressure caused by LV diastolic dysfunction (provided that there are no indications suggestive of another cause of pulmonary hypertension e.g. pulmonary arterial hypertension, lung disease, valvular heart disease, LV systolic dysfunction).
A more detailed discussion follows:
Evaluation of left ventricular (LV) diastolic function begins with M-mode and 2D echocardiography :
► Assessment of LV size, and wall thickness and
►Assessment of left atrial (LA) volume and anteroposterior dimension.
In patients with LV diastolic dysfunction, concentric or
eccentric LV hypertrophy can be found. Pathologic LV hypertrophy is usually associated with an increased left ventricular stiffness which results in diastolic dysfunction.
Increased LA volume reflects the effects of the increased LV filling pressures over time. Elevated left ventricular filling pressures can occur in patients with diastolic or systolic dysfunction. LA dilation can also occur in patients with mitral stenosis or regurgitation and in patients with chronic permanent atrial fibrillation. LA volume is measured at end-systole in the apical 4 chamber view with the same method (Simpson's method of summation of disks) used for the measurement of left ventricular volume.
E is the peak early diastolic velocity of transmitral flow and A is the peak late diastolic velocity at the time of atrial contraction. In adults with normal diastolic function E/A has a value between 0.8 and 2, but less than 2 (In younger people E>A and in middle-aged or older people E wave normally becomes lower and A increases and can be higher than A).
In adults with normal diastolic function (normal pattern) the E > A but is less than 2A (except in very young persons), or E may be a little smaller than A, but more than 0.8 A (the E wave can be lower than the A wave by less than 20 %). The deceleration time (DT) of the E wave (time from the peak of the E wave to its end at the baseline) is 150-200 ms (milliseconds). Isovolumic relaxation time (the time from the end of aortic flow to the beginning of mitral flow) is IVRT = 50-100 ms. Measure isovolumic relaxation time (IVRT) by placing the PW Doppler sample volume in- between LV inflow and outflow to simultaneously display the end of aortic flow and the onset of mitral E-wave velocity.
In very young people with normal diastolic function E/A can be >2, but this is not due to an increased LA pressure as in the restrictive pattern. This pattern in young people is normal and is due to a more active relaxation of the left ventricle (LV) in early diastole so that early diastolic flow velocity is increased. It is easy to distinguish this from the restrictive pattern because these are very young individuals with no heart disease, no symptoms of effort dyspnea, normal left atrial size and normal tissue Doppler velocities of the mitral annulus.
Mild (grade 1) diastolic dysfunction is characterized by the impaired relaxation (or delayed relaxation) mitral inflow pattern with E/A<0.8, E ≤ 50 cm/s and a prolonged deceleration time DT of the mitral flow E wave ( DT> 200 ms). DT is the time from the peak to the end of the E wave. There is also prolongation of isovolumic relaxation time, IVRT ≥ 100 ms. The IVRT is the time from the closure of the aortic valve (end of left ventricular ejection) to the opening of the mitral valve (onset of ventricular filling). In this time interval, left ventricular dimensions are constant and the mitral annulus does not move. So, the IVRT can be measured on the pulse wave tissue Doppler tracing of the mitral annulus as the time from the end of the systolic S wave to the onset of the e΄ (Ea) wave.
In grade 1 diastolic dysfunction the pulse wave Doppler of pulmonary venous flow shows S>D, where S is the peak velocity of the systolic flow in the pulmonary vein and D the peak velocity of the early diastolic flow.
In grade 1 diastolic dysfunction mean left atrial pressure and left ventricular filling pressure is not elevated.
An important point is that age should be taken into account when evaluating LV diastolic function since the LV filling pattern in healthy elderly individuals resembles that of younger people (e.g. 40-60 years old) with mild (grade 1) diastolic dysfunction. Indeed, healthy sedentary elderly people usually have a mild degree of diastolic dysfunction (grade 1) as a result of an increased left ventricular stiffness and a slower myocardial relaxation in comparison to younger individuals.
Moderate (grade 2) diastolic dysfunction shows the same transmitral flow pattern (0.8 < E/A <2), as that observed in people with normal diastolic function. It is called pseudonormal pattern.
In the pseudonormal pattern (as well as in the normal pattern),
150 <DT <200 ms and IVRT is <100 msec (range 60-100 msec).
This pattern can be distinguished from the normal pattern of diastolic inflow because at the peak of the Valsalva maneuver (which causes a reduction of preload = a reduction of ventricular filling) in people with grade-2 diastolic dysfunction, the pattern of mitral inflow takes the morphology of impaired relaxation (E< A). Other features of the pseudonormal pattern which allow its differentiation from the normal pattern are the following:
► A reduced mitral annular e΄ velocity (this is a simple way to distinguish it from normal diastolic function, which is characterized by a normal e΄). The normal and pseudonormal filling pattern have the same pattern of transmitral flow (generally E>A), but in case of a pseudonormal pattern, the e΄ velocity is reduced.
► The increased E/e΄
► The pulse wave Doppler signal of the pulmonary venous flow showing S<D (S/D <1). The peak velocity of the end systolic pulmonary vein reverse flow wave at atrial systole (AR) is elevated ( > 35 cm/s) and the duration of AR wave is increased:
AR wave duration-mitral A wave duration ≥ 30 msec.
The pseudonormal mitral inflow pattern can change to a delayed relaxation pattern by reducing preload with diuretic treatment.
Severe diastolic dysfunction is characterized by the restrictive left ventricular ﬁlling pattern, where the markedly elevated left atrial pressure causes an increased early transmitral pressure gradient (pressure difference between the left atrium and the left ventricle) in early diastole. This causes the following findings:
E/A ratio >2, a short deceleration time (DT <150 ms) and also a short IVRT < 60 ms. Due to the severe impairment of diastolic function, mitral annular e΄ velocity is usually severely reduced, the ratio E/e΄ is increased and pulmonary venous flow shows S<<D (the peak velocity of the S wave is much lower than the peak velocity of the D wave). The peak velocity of the end systolic pulmonary vein reverse flow wave at atrial systole (AR) is elevated ( > 35 cm/s) and AR wave duration-mitral A wave duration ≥ 30 msec.
The restrictive pattern is called stage 3 diastolic dysfunction if it can change, by reducing preload with diuretic treatment, to a pattern of stage 1 or 2 diastolic dysfunction. If treatment cannot change the restrictive pattern of left ventricular filling, then there is stage-4 diastolic dysfunction which carries a severe prognosis.
Regarding the tissue Doppler examination of the velocities of the mitral annulus, the early diastolic peak velocity of the mitral annulus (e΄ or Ea) is generally a good index of diastolic function. It is higher at the lateral mitral annulus than at the septal annulus. An indication of diastolic dysfunction is an e΄ < 7 cm/s at the septal annulus, or <10 cm/sec at the lateral annulus. Moreover, e΄ has a reasonable accuracy in identifying patients with diastolic dysfunction and pseudonormal LV ﬁlling.
In people with cardiac disease, an increased E/e΄ ratio can provide an indication of the presence of an elevated left ventricular filling pressure and pulmonary capillary wedge pressure,
Assessment of the dimensions and function of the right ventricle with echocardiographyEvaluation of right ventricular (RV) function is important because RV dysfunction has been associated with increased morbidity and mortality in patients with valvular heart disease, congenital heart disease, pulmonary hypertension, heart failure and coronary artery disease.
.Normally the right ventricular wall is thinner and more compliant than the left ventricular wall. Right ventricular wall thickness in diastole can be measured in the subxiphoid echocardiographic view. Normally it is < 5 mm.
Myocardial performance index MPI= (IVRT + IVCT) / RVET
An elevated (abnormal) MPI indicates reduced right ventricular global function (either diminished right ventricular diastolic or diminished right ventricular systolic function or more commonly both) and is associated with a worse prognosis.
Abnormal tissue Doppler MPI ≥ 0.54
Abnormal pulsed Doppler MPI ≥ 0.43
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Bibliography and links
Guideline ASE -2016 : Echocardiographic evaluation of diastolic function
Cardiology free e-book online
Lang, R. M., Badano, L. P., Mor-Avi, et al. Recommendations for Cardiac Chamber Quantification by Echocardiography in Adults: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovasc Imaging 2015; 16 (3 ), 233-271. https://doi.org/10.1093/ehjci/jev014
Horton, K. D., Meece, R. W., & Hill, J. C. (2009). Assessment of the Right Ventricle by Echocardiography: A Primer for Cardiac Sonographers. Journal of the American Society of Echocardiography 2009;22: 776-792. https://doi.org/10.1016/j.echo.2009.04.027