Global systolic functional imaging

Displacement and velocity

Strain and strain rate

Top, mitral annular displacement curve, being the curve showing the longitudinal shortening of the left ventricle. Below, the tissue velocity curve, which is the temporal derivative of the displacement curve. Comparing to the volume/flow curve, it is evident that there is more complex motions, especially n elation to the isovolumic phases, than is evident from the mere volume diagram to the left.

Top, strain curve from mid septum, showing the deformation, below the strain rate (temporal derivative). The curves seem to be very similar to inverted motion and velocity curves, however, deformation will show more regional detail as discussed here. Remark also how the strain curve is similar to the volume curve, showing the same pattern, while the strain rate (temporal derivative of strain) is similar to the flow curve (temporal derivative of volume).

It has been established that the longitudinal shortening of the left ventricle, and thus the longitudinal measures is closest related to the stroke volume and EF, i.e. to the total left ventricular volume change (13, 30 - 35, 56, 59, 60, 64 - 67, 116). Thus, the longitudinal strain is the most important measure, and it is also closely related to the wall thickening and thus internal shortening as discussed here.


 
It is obvious that the LV shortening and the ejection are interrelated. In fact, the LV systolic shortening * the circumferential area should be aproximately equal to the stroke volume.

Stroke volume by Doppler flow velocity integral (VTI) and LVOT diameter. The diameter gives the area, and the velocity time integral gives the distance that an object travels if it follows that velocity curve (v =ds/dt, means that s =  v dt. Multiplied with each other, the area and VTI gives the volume of a cylinder, equal to the stroke volume.	Relation of stroke volume and LV shortening. The volume reduction is LV shortening * LV area at the mitral plane. As area is far higher, the distance is far smaller than the VTI.

Global systolic function measures

Peak systolic versus end systolic measures of ventricular function.

Peak systolic measures are the measures of peak ventricular performance, and are basically

• peak ejection velocity in the LVOT,
• peak annular systolic velocity, and
• peak global ventricular strain rate.

These occur early in systole, and may be less load dependent, as maximum afterload is reached later in systole. They all occur during the first part of systole, and thus are more closely related to contractility, and especially to contractility changes, as shown in studies (78, 79, 80, 223).

All such studies are really studies in contractility changes, and thus, useful to separate contractile states, rather than measure contractility direct.

However, they are not completely load independent, as increased load will result in a delayed and blunted development of force and velocity, as opposed to the pressure/volume relation.


End systolic measures on the other side, are measures of the total work performed by the left ventricle during ejection. This is influenced not only by force, but also by load (resistance), and the ejection time (HR). They are

• stroke volume,
• Ejection fraction (and fractional shortening)
• annular displacement and
• global strain

There is, however, little evidence directly comparing displacement / strain to velocity / strain rate at varying load, and the few and small studies that are published seems to indicate a very similar load response. However,  increased contractility will not to the same degree lead to increased stroke volume, if there is no concomitant increase in venous return, as in inotropic stimulation. Thus stroke volume wil be maintained, but at a lower end diastolic volume. This means end systolic measures will be less sensitive to  contractility increase as discussed above (223).

Peak systolic annular velocity (S'), which is early systolic,  compared to peak annular displacement (MAPSE), which is end systolic. S' is actually the peak rate of annular displacement, and is thus closer to contractility, while MAPSE is end systolic and thus closer to ejection fraction.	Peak strain rate, being early systolic,  compared to peak strain, which is mainly end systolic, and closer even, to ejection fraction.

Most of the indices above have been studied, and are established as indices of ventricular function. However, in addition to they all being only imaging indices, they have different shortcomings, and to some degree slightly different interpretation physiologically.

Even LV elastance is an end systolic measure, although it is taken as the real contractility. This may be only in relation to volume, in fact.

Peak systolic measures - contractility indices

Even though contractility per se cannot be measured by imaging alone, the measurement can be approximated, but early systolic measures come close (78, 79, 80, 223).

Peak annular systolic velocity

Peak systolic velocity (S') was early validated as a measure of systolic function (37, 38, 39, 40). Peak annular velocity occurs early in systole, and may be less load dependent, as maximum afterload is reached later in systole. The peak velocity is taken as an average measure of two or four points around the mitral ring.

Pulsed tissue Doppler of the mitral ring.  These are the velocity traces of the longitudinal motion, while dividing by the end diastolic length results in an approximation to the Lagrangian strain rate .	Age dependent peak systolic, early and late diastolic velocity in normals from the HUNT study (165). The early diastolic velocities are higher than the systolic, and the decline is thus steeper, but the relation is evident.

The peak systolic annular velocity is useful in that it is a better marker of systolic function than EF, and that it offers a measure that allows direct comparison of systolic and diastolic function.
as they are measured by the same method.

But there are some slight limitations:

1: Peak systolic velocity is not a direct measure of peak rate of shortening.

Even though it seems intuitive, the comparison with peak strain rate shows that there is a velocity component in the peak that is a global translational motion toward the apex as discussed here. This is due to the recoil force from the ejected blood.

Peak velocities from the myocardial wall are shown in blue and green, showing parallel velocity curves at peak, thus identifying the velocity as translation, which do noe show in the difference (strain rate) curve (red).	Peak velocities along the septum, showing a slight blunting of the velocity peak in the apex. Even if there is a translational velocity, this will decrease in the apex where the myocardium is pressed into the chest wall. The strain rate curves corresponding to the regions between the velocity curves are shown below, indicating the this velocity is not the true deformation rate.

It might be argued that the recoil velocity is also generated by myocardial contraction, and represents a liberation of the work done during IVC. From this argument, peak velocity might be considered a fully legitimate measure of myocardial performance, maybe even more legitimate that peak rate of volume decrease.

2: Peak systolic velocity is not always simultaneous in all segments of the mitral annulus. 

The normal pattern of annular velocities varies in the normal subjects:

A fairly common pattern is a sharp peak in the lateral annulus (cyan), and a more rounded curve with a later peak velocity in the septum (yellow). Thus, the divergence of the curves in the initial ejection phase may represent a light tilting (rocking) of the apex toward the septum.	A slightly different normal pattern where the initial peak in the lateral wall decelerates slightly, the accelerates again, giving a later second peak. The septum shows an even curve, but with peak velocity between the two peaks of the lateral wall.	In this case peak annular velocity is early and simultaneous in both walls.

The varying timing of the peaks is most probably due to different impact of the recoil force from ejection, creating a slight rocking motion of the whole heart. AS in the example to the left, this will mean that the lateral peak is exaggerated due to rocking, while the early septal velocity is blunted, and the later peak is due to this blunting.



The impact of the recoil momentum on the septal and lateral annulus will, of course, depend on the angle between the momentum vector (velocity vector), and the ventricular long axis. As the aortic opening is situated in the septal part of the LV base, the angle deviation, if any, can be expected to be towards the septum, delivering the highest impact laterally. This is in accordance with clinical observation, the peak is most consistently present in the lateral wall. However, the ejection from the right ventricle must also be taken into consideration, being nearly simultaneous, and with the same stroke volume (mass), only the difference in velocities will account for the difference in momentum. The pulmonary ostium is also situated medially, in front of the aortic, but often with less of an angle deviation. However, the angle will be opposite, and may counteract the aortic momentum.

Thus, both the actual value and the timing of peak systolic velocity can be dependent on the site where it is measured as shown above. This, of course means that the peak annular systolic velocity which is used as a systolic functional parameter, measured either as one site, or as an average, is an approximation, as the timing may differ between sites.

The correlation with EF is weaker than for MAPSE, which is not unsurprising, EF and MAPSE being end systolic measures, and as such measures of the total systolic work, S' is peak systolic, measuring peak systolic performance.




One of the main advantages of tissue velocities is that systolic and diastolic function are measured by the same method. From the beginning, systolic function by EF was compared to diastolic function by mitral flow, equivalent to comparing apples with bananas. This lead to the concept of pure diastolic dysfunction, which has later been shown to be erroneous (202).

The correlation between systolic function S' and diastolic function e* was found in an early study to be 0.6 over a wider range of ventricular function (201), and in the HUNT study (165)with a large number (N=1266) and limited to healthy subjects, the correlation was found to be 0.59.

The correlation reflects among other things, the physiological mechanism that much of the diastolic recoil is due to elastic stored energy from systolic contraction (restoring forces), but also, and most important: that systolic and diastolic function are closely related.


In another study (202) it was found that the systolic function by S' was reduced in patients with heart failure with normal ejection fraction. This led to a renaming of the state that up to then was called "diastolic heart failure" to "heart failure with normal ejection fraction". This, of course corrects the implied, but mistaken assumption that there existed a pure diastolic failure. However, it does not address the fundamental problem, which is one of methodology, that EF should not been used in normal sized or smaller ventricles.


The S' has been shown to be sensitive for reduced function in relatives who are mutation positive, of patients with manifest hypertrophic cardiomyopathy, despite having normal EF and no hypertrophy (203). The diastolic function by tissue Doppler was similarly decreased. It also correlates better with BNP in heart failure than the fractional shortening (204).

Thus, the peak systolic annular velocity is useful in that it is a better marker of systolic function, and that it offers a measure that allows direct comparison of systolic and diastolic function.

The point from a puristic view is that if the peaks are not simultaneous, the mean peak velocity doesn't exist in real time (cfr. the peak-to-peak gradient of invasive aortic stenosis measurement). Still, the method has been established as useful, and normal values for the averages has been established (165). And, as in the example above, while the early peak in the lateral wall is exaggerated due to the rocking, the early septal velocity is blunted. The true peak translational velocity is seen in the average curve, and the true peak velocity is the peak of the average curve, not the average of the peaks.

The varying timing of the peaks is most probably due to different impact of the recoil force from ejection, creating a slight rocking motion of the whole heart. AS in the example to the left, this will mean that the lateral peak is exaggerated due to rocking, while the early septal velocity is blunted, and the later peak is due to this blunting.

In some cases, the rocking of the apex, even if the ventricle is normal may become completely misleading.

Rocking heart with normal ventricular function.	Peak velocities have totally different timing, and much of both of the peak components are due to translation.The septal peak has a component of rocking to the right, the lateral peak a component of rocking to the right, both may be overestimates.

As discussed here. In this case, the peak velocities should be viewed with skepticism as functional measures. The mean curve might give a more correct estimate, although this is not validated, and is not available in standard analysis software.

Using pulsed wave tissue Doppler, this is not an option, and curve averaging is not standard analysis software.

Normal values for systolic velocities of the right and left ventricle from the HUNT study by age and gender. From  (165).

	Left ventricle, mean of 4 walls		Right ventricle (free wall)
	S' (pw TDI)	S' cTDI	S' (pwTDI)
Females
< 40 years	8.9 (1.1)	7.2 ( 1.0)	13.0 (1.8)
40 - 60 years	8.1 (1.2)	6.5 (1.0)	12.4 (1.9)
> 60 years	7.2 (1.2)	5.7 (1.1)	11.8 (2.0)
All	8.2 (1.3)	6.6 (1.1)	12.5 (1.9)
Males
< 40 years	9.4 (1.4)	7.6 (1.2)	13.2 (2.0)
40 - 60 years	8.6 (1.3)	6.9 (1.3)	12.8 (2.2)
> 60 years	8.0 (1.3)	6.4 (1.2)	12.5 (2.3)
All	8.6 (1.4)	6.9 (1.3)	12.8 (2.2)

Annular velocities by sex and age. Values are mean (SD).  pwTDI: Pulsed Tissue Doppler recorded at the top of the spectrum with minimum gain, c TDI: colour TDI.  Normal range is customary defined as mean ± 2 SD.

The study is based on 1266 healthy individuals from the HUNT study by Dalen et al (165). The age dependency of values is evident. Colour tissue Doppler gives mean values, which are consistently lower than pulsed wave values, as discussed here. It is evident that the systolic values decline with age, as do the early diastolic.

It is important to realise that the peak values obtained by pw tissue Doppler are higher, due to the breadth of the spectrum, while colour tissue Doppler gives mean velocities, thus being modal velocities in the middle of the spectrum. However, peak values by spectral Doppler are affected by gain settings (increased gain - broader spectrum - higher peak values), while colour Doppler are affected by clutter (stationary reverberations - zero velocity - reduced average).

Same tissue Doppler recording with two different gain settings. We see that peak systolic velocity differs by 2 cm/s, and the lowest gain setting is closest to the modal velocity. However, the modal velocity itself, remains unchanged by the gain setting.	There is a band of clutter close to zero velocities, but as seen here, the spectral modality makes it very easy to separate the true and clutter velocities. However, the clutter affects the autocorrelation velocity (red line), giving lower velocities, but with clutter filter this effect is removed (blue line), and the peak value is substantially higher. Image modified from (268).

Peak acceleration (??)

As acceleration precedes velocity, and is at the time of peak rise of velocity, this should be slightly earlier than peak velocity, and thus even less load dependent, - at least afterload, preload dependency will still be present. Acceleration is also more closely related to peak force by Newton's second law (F = ma). In addition, if taking the peak velocity to be partly a function of the recoil, it is also caused by the pressure buildup, even more so than the peak velocity. Thus there are hypothetical advantages in relation to physics and physiology.

However, the concept is ill defined. Also, the temporal derivation of acceleration from velocity will result in a less favourable signal-to-noise ratio than the velocities.

Velocity curves from a normal subject. The initial peak acceleration may be defined by the slope of the tangent to the initial velocity curve. As illustrated, as the two curves from septum and lateral walls are different, this will result in different acceleration values. In addition, there can be different ways of defining the tangent: A: The steepest slope of the lateral curve B: The slope from nadir to the lateral curve peak C: The steepest slope of the septal curve D: The slope from nadir to the septal curve breakpoint E: The slope from nadir to septal curve peak All of them reasonable, but resulting in wildly different values (This is equal to a noise component as shown right)

Real-time temporal derivation of the two velocity curves. Due to the derivation, the curves are fairly noisy, especially taking into account the the velocity curves was somewhat smoothed at the outset. It is obvious that the peak values may be affected by the noise,  incorporating noise spikes. Averaging the septal and lateral points, still doesn't solve the noise problem. Also averaging can be done in two ways: Mean of peak values, which in this case will be 186, and Peak of mean curve, in this case 163 And in addition, curve derivation and averaging is not standard issue in analysis software.

At present, the peak acceleration is less useful, being

• Closely related to peak velocity, as the peak velocity is determined by the rate of velocity rise,
• In need of definition of concepts
• Dependent on heavy post processing, and not standard analysis software
  

- while especially pw Tissue Doppler in the standard mode is a quick, robust and online method.

Peak systolic strain rate

Peak systolic strain rate is the peak rate of shortening. As explained above, this peak occurs later during the ejection phase than peak velocity, as the strain  rate algorithm subtracts the initial velocty peak, being translation, not deformation:

Examining one normal subject with early velocity peak in the lateral annulus:	Looking at velocities within the wall in base an apex, the biphasic pattern with an early peak can be seen in both points in the lateral wall.	Examining the strain rate from the entire walls between the apical and basal points no sign of a biphasic shortening can be seen, indicating that the lateral peak is only due to translation, the peak being subtracted. The peak strain rate is much later than peak velocity in both walls.

The slight rocking motion affecting the timing of peak velocities, means that there is no fixed relation between the timing of peak strain rate and peak velocity:

Early peak velocity on both sides. Slightly later peak strain rate in both walls.	Early lateral peak velocity. late septal; early septal peak strain rate, later lateral, mean peak strain rate later than mean peak velocity	Early lateral and later septal peak velocity, earlier lateral than septal peak strain rate, mean peak strain rate later than mean peak velocity.

Thus, peak strain rate is the true measure of peak deformation rate, i.e. peak rate of shortening. However, this does not mean that it is a truer measure of peak systolic performance, as the peak velocity incorporates the ejection recoil due to the isovolumic pressure buildup.

But basically, as volume change is generally are related to longitudinal shortening, peak strain rate must be close to peak rate of volume reduction, i.e. peak emptying rate.

For global strain rate measures, the strain length as well as the ROI should be as long as possible to reduce noise (331) as shown in the above examples and discussed in the measurements section.

Thus, the peak strain rate should be more related to peak force than to peak rate of force development. However, in an experimental invasive study, Greenberg (80) found a stronger correlation between both dP/dt and LV elastance with strain rate than with systolic annular velocities.

Normal values are necessary if measurements are to be used diagnostically. In addition, they will give additional information about physiology. In the north Tröndelag population (HUNT) study, 1266 subjects without known heart disease, hypertension and diabetes were randomly selected from the total study population of 49 827, and subjects with clinically significant findings on echocardiography (a total of only 30) were excluded. (153) This is the largest normal population study of echocardiographic strain and strain rate rate to date. End systolic strain and peak systolic strain rate was measured by the combined tissue Doppler / speckle tracking segmental strain application of the Norwegian University of Science and Technology, but the results were compared to other methods in a subset of subjects, showing small differences. The study consisted of  673 women with a mean BP of 127/71 ,mean age of 47,3 years and BMI of 25.8 and 623 men, with mean BP of 133/77, mean age of 50.6 and BMI of 26.5. Both sexes were normally distributed with an SD of 13.6 and 13.7 years, respectively. 20% of both sexes were current smokers. Basic echo findings  are in accordance with other studies, like the findings of Schirmer et al (156, 157), so the study population may be assumed to be representative.

While differences between septum and lateral wall was of the order of 10% in velocities, in deformation parameters (153), the same difference was on the order of 4% in strain rate and only 1% (relative) in strain.

Normal values for strain and strain rate per wall in the HUNT study. From (153).

	Anteroseptal	Anterior	(Antero-)lateral	Inferolateral	Inferior	(Infero-)septal
SR (s-1)	-0.99 (0.27)	-1.02 (0.28)	-1.05 (0.28)	-1.07 (0.27)	-1.03 (0.26)	-1.01 (0.25)
Strain (%)	-16.0 (4.1)	-16.8 (4.3)	-16.6 (4.1)	-16.5 (4.1)	-17.0 (4.0)	-16.8 (4.0)

Results from the HUNT study (153, 165) with normal values based on 1266 healthy individuals. Values are mean values (SD in parentheses).  The differences between walls are seen to be smaller in deformation parameters than in motion parameters, although still significant due to the large numbers.

Normal values for global strain and strain rate in the HUNT study by age and gender. From (153).

Normalised velocity(?)

As seen later, peak annular displacement can be normalised for left ventricular length to derive a measure of global longitudinal strain. But this doesn't necessarily mean that normalising velocity in the same way gives global strain rate. Assuming that annular velocity was the peak rate of ventricular shortening, normalising for end diastolic length would give peak Lagrangian strain rate, normalising for instantaneous systolic length would give the Eulerian strain rate. However, giving the difference in riming between the two curves, due to the translational velocity, this is not the case.

Basal velocity traces, and the velocity traces normalised for end diastolic ventricular length (Lagrangian normalisation), results in curves that resemble inverted velocity curves, with the same shape.	Comparing this with the real velocity / strain rate plots from the same subject, it is evident that strain rate curves have a different shape. (In fact, in this case the lateral strain rate curve is more rounded, the septal with an earlier and more defined peak, opposite of the velocity curves).

This means that in terms of curve shape and timing, there is no point in normalising the velocity curves, and the normalised velocity curves is still a slightly different measure than strain rate.


However, where there is a large variation in ventricular size, as in children it makes sense, giving age independent measures  (159, 214, 288). Strain rate is one form of size normalising, but using pulsed tissue Doppler, normalised velocity will make the velocity measurements useful in children of all ages.


Basically, peak strain rate is most useful for assessing regional function, where the motion due to tethering to neighboring segments needs to be subtracted n(although the effect of segment interaction remains). With uneven segmental contractility, the peak strain rate in different segments also becomes non simultaneous.

Peak ejection velocity

LVOT ejection velocity must be proportional to flow, as the LVOT diameter is considered constant. But this means that peak systolic velocity is actually a direct measure of peak volume reduction rate or peak emptying rate. And, as peak shortenoing rate (strain rate) is very close to peak emptying rate, this means that both measures are very close to measuring the same thing. THis was evident in a study where both measures did show a very similar change with chenges in contractile states (223).



Thus, both theoretically, empirically and experimentally, the peak LVOT flow and peak global strain rate seems to be measuring very much the same event, even though indifferent measures.

But should peak LVOT velocity be normalised for heart size? Probably not, AS strain arte already is a norlmalisation for heart size, the flow velocity is dependent on LVOT diameter, whic increases with heart sise. So, the LVOT velocity is in a way a normalisation of peak flow.

Normal peak ejection velocities from Doppler, by age and gender from the HUNT study (165)

	Females	Males
< 40 years	1.01 (0.17)	0.99 (0.17)
40 - 60 years	1.02 (0.16)	0.99 (0.18)
> 60 years	1.01 (0.17)	0.96 (0.18)
Over all	1.01 (0.16)	0.98 (0.18)

Values are given as mean ( SD). The customary definition of normal values as mean ± 2SD, giving about 95% of the normal population, results in wider normal limits than previously shown as cut off values in small patient studies.

The only difference is that peak values of peak ejection velocity do not decline with age. AS stroke volume gpoes down with ventricular volume by age, this must mean a corresponding reduction in LVOT diameter.



With the appearance of new methodology, a number of new methods for measuring left ventricular global function has emerged. Older measures has traditionally been measurements of the cavity function: Stroke volume, ejection fraction (and the M-mode equivalent shortening fraction). Newer methods include longitudinal measures of wall function, as annular displacement and velocity, as well as mean strain/strain rate, either based on segmental measurements, or a global averaging (as global strain form speckle tracking 2D strain). It should be of general interest to comment on the relationship between the methods. It is also important to realise that while strain and strain rate are measures of shortening per length unit, the annular velocity and displacement are also measures of the same, but in absolute values (i.e. not normalised for ventricular length). However, all measures that measure relations to changes, i.e. in paired experiments of load alterations, the normalisation will cancel out, and displacement will behave as strain, strain rate as velocity. Thus all experiments with systolic displacement and velocity in relation to global changes, will pertain also to strain and strain rate.

End systolic measures - systolic work indexes.

End systolic measures on the other side, are measures of the total work performed by the left ventricle during ejection. This is influenced not only by force, but also by load (resistance), and the ejection time (HR). They are

• stroke volume,
• Ejection fraction (and fractional shortening)
• annular displacement and
• global strain

There is, however, little evidence directly comparing displacement / strain to velocity / strain rate at varying load, and the few and small studies that are published seems to indicate a very similar load response. However,  increased contractility will not to the same degree lead to increased stroke volume, if there is no concomitant increase in venous return, as in inotropic stimulation. Thus stroke volume wil be maintained, but at a lower end diastolic volume. This means end systolic measures will be less sensitive to  contractility increase (223).

Cavity measurements of systolic function

Fractional shortening

As M-mode was the first echo modality, the fractional shortening of the LV cavity was the first LV systolic functional measure by echo. The fractional shortening is defined as FS = (LVIDD - LVIDS)/LVIDD thus, in fact being an one-dimensional version of EF. Diameter is conventionally measured to the endocardium, so the fractional shortening is more precisely the endocardional fractional shortening. It's less accurate than the EF when there is regional dysfunction, as the measured fractional shortening will be generalised to the whole ventricle. It is quite common to measure longitudinal strain, i.e. wall or segment shortening as a measure of longitudinal function. On the other hand the fractional shortening of the chamber diameter is a well established measure of global and radial function. But in the case of hypertrophy, this may lead to completely erroneous conclusions about the changes in radial versus global function, as shown in the theoretical treatment below.

The relation between wall thickening and fractional shortening is ilustrated below:

In this theoretical M-mode of the LV, a normal ventricle has a wall thickness of 1 cm, an internal end diastolic chamber diameter (EDD) of 4 cm, resulting in an external diameter of 6 cm. As most of the wall thickening is inward, with little change in outward diameter (except in the case of differing filling pressures on the two sides), an end systolic wall thickness of 1.5 cm will result in a diameter shortening of 1 cm and an end systolic chamber diameter of 3 cm. Thus, wall thickening (WT, transmural strain) is (1.5 cm - 1 cm) / 1 cm = 50%, chamber diameter reduction is 1 cm, fractional shortening (FS) is (4 cm - 3 cm) / 4 cm = 25%. Thus, if wall thickening decreases due to reduced myocardial function, so do fractional shortening as seen in the middle figure. And if there is dilation as well, the denominator will increase, resulting in further reduction in FSas an inverse function of the diameter. In LV dilation, there is usually a combination of increased diameter and reduced wall thickening.

The erroneous comparison between longitudinal strain and fractional shortening:

The incompressibility principle tells us that as the wall shortens in the longitudinal and circumferential direction, it has to thicken in the transverse direction, and the relation is geometrically determined. Thus the longitudinal and transverse function as measured by strain should be interrelated. Reports about radial compensation of reduced longitudinal function is in direct opposition to the incompressibility principle.  The problem arises if we do not measure the same values for longitudinal and radial function.


From the reasoning above, any conclusions about radial function based on fractional shortening in the presence of hypertrophy may be erroneous, and the term radial function needs to be defined. The conclusion that there is radial compensation for reduced longitudinal function should be reserved to the cases where WT is increased (If this is possible, it seems theoretically impossible, as the reduced longitudinal shortening should correspond to reduced wall thickening due to incompressibility).

It is extremely important that if longitudinal and "radial function" are compared, care should be taken that the measurements are comparable. To compare for instance fractional shortening of the LV diameter with longitudinal strain (wall shortening), is comparing two different measures, and may lead to completely erroneous conclusions as shown above, where fractional shortening increases but wall thickening decreases.

 as the same erroneous results will be obtained by the fractional shortening as of EF, as shown below.

And this shows that fractional shortening is not a true measure of "radial function".

Wall thickness 17 mm, EDD 40 mm, Fractional shortening was 35%, however, wall thickening only 28%

Ejection fraction

Based on Nuclear or X-ray contrast studies, the first measures was measurements of cavity reduction in systole, i.e. the stroke volume. While this may be the most important result of cardiac pumping, it confers little information about the state of the heart itself. A dilated ventricle can maintain stroke volume, but it is reduced in terms of the left ventricle volume, and may have a severely reduced contractility. Thus stroke volume should be normalised for end diastolic volume, to obtain Ejection fraction:

The problem with both strain AND EF in eccentric hypertrophy

In eccentric hypertrophy, the problem reverses, but in this case it even affects strain. Basically, in eccentric hypertrophy, the VV mass increases, but hte wall cavity ratio remains normal (146). This means that the ventricle enlarges mainly outwards, but as a more or less normally thick wall (at least relative) surrounds a much larger cavity, the mass has to increase. This is seen in different states:

1. As compensation for volume load in valvular regurgitation. In this case, the end diastolic volume increases, but so does the total stroke volume. In this case the EF remains normal or even super normal. The strains can thus also be expected to remain normal as long as myocardial function is.
   
2. In athletes heart. In this case there is eccentric hypertrophy in response to endureance training, i.e. the demands on the ventricle during near maximal performance. The ventricle increases both in diameter and length, and hence, in end diastolic volume.
   

Thus, with an increased EDV and unchanged stroke volume, the EF and FS may be reduced, and so may strains, due to the larger ventricle.


However, athletes usually have downregulated heart rate as well,  which increases diastolic filling, and thus the stroke volume. In the intact body, the cardiac output is regulated according to the circulatory need, by both autonomic balance and other vasoactive and volume regulatory mechanisms affecting both filling and resistance, contractility and heart rate simultaneously.

This means that athletes at rest (having no need of increased resting cardiac output - only of increased cardiac output reserve) will have unchanged cardiac output, a larger LV, with lower heart rate and increased stroke volume. But as this is a result of a lower sympathetic tone, the ejection fraction and strains may still be reduced, although to a lesser degree than if HR was unchanged, and may be unpredictable.

For evaluation of systolic myocardial function in eccentric hypertrophy, myocardial systolic velocities or strain rate would be more appropriate, although the litterature is fairly scarce, at least in comparing with normals. At least, the rate of shortening should be less affected by the total stroke volume, but afterload may still be a confounder, in general athletes may have lower blood pressure, but also a lower sympathetic tone.

Wall measurements - long axis systolic function.

Wall thickening measured in M-mode, however, is only available in limited segments, and can only be generalised to global measures if the ventricle is symmetric. In addition,  the wall thickening is mainly a function of the long axis shortening, due to the incompressibility of the heart muscle.




The systolic long axis function is measured by any means of any longitudinal motion or deformation. I.e. Long axis shortening measured by mitral annulus motion or global strain, or shortening velocity / rate by mitral annulus velocity or global strain rate.

Mitral annular systolic displacement (MAPSE)

Mitral annular plane systolic displacement or excursion (MAPSE), and mitral annular systolic velocities, are measurements of total ventricular shortening and shortening velocity:

Mitral annular dexcursion can be measured by B-mode, M-mode or tissue Doppler:

MAPSE by M-mode. In this case the MAPSE was 14 mm in the septal site and 16 mm in the lateral, giving an average of 15.	MAPSE by tissue Doppler showing an MAPSE of about 15 mm.

The annular measurements reflect the total shortening of the ventricle, and are thus measures of global longitudinal function.

The mitral annular systolic descent has had many names: The mitral annular excursion (MAE) (31, 35, 37, 40) has been used for a long time. Atrioventricular plane descent (AVPD) (30, 32, 34, 36) is incorrect, as the term also comprises the tricuspid part, and while tricuspid displacement and velocity can be measured (and is higher than in the left ventricle) , it is usually measured only in one point, and the relative weights for the measurements is unclear.

However, the term TAPSE for the tricuspid systolic annular excursion has been firmly established. In order to remain consistent in nomenclature, the corresponding term MAPSE for Mitral Annular Plane Systolic Excursion is in increasing use. Thus, it might be the best term, and it still retains the specificity that AVPD lacks.

The longitudinal shortening has been shown to be very closely related to ejection fraction when comparing different patients with normal or reduced left ventricular function (30, 31, 32, 34, 35, 36, 40, 64), as illustrated below:


In a later study (417) in the same material, we calculated normalised MAPSE as generic, or linear strain, as has been done later as well (444):

Normal values for global systolic left ventricular generic (linear) strain from the HUNT study

	Women	Men	All
Age	Strain (%)	Strain (%)	Strain (%)
< 40	-18.1 (2.0)	-16.5 (2.0)
40 - 60	-17.0 (2.2)	-15.4 (1.9)
> 60	-14.8 (2.1)	-14.9 (1.9)
All	-17.0 (2.5)	-15.5 (2.0)	-16.3 (2.4)

MAPSE in the septal and lateral mitral points from the four chamber view. The averaged value is the most representative for the global.	Different denominators for strain calculation. The straight line is the most robust, using clear anatomical landmarks, as well as having the same angle as the M-mode.

The results were very close to the segmental method (-16.3 vs -16.7%). This is an attractive method in the meaning that the strain is derived by generic measurements, and thus are applicable across methods like ulttrasound, MR (445) or CT.




However, the actual numbers rest on the assumption of using the straight line distance from apex to base as a proxy for wall length. Using the actual length of the curved wall would give a larger denominator, and thus a lower numerical strain value, using the midwall ventricular length would give a smaller denominator, and thus a larger numerical strain value. This is illustrated in the example below:


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