Article Text

Non-invasive imaging
Imaging assessment of ventricular mechanics
  1. Thor Edvardsen,
  2. Kristina H Haugaa
  1. Department of Cardiology and Institute for Surgical Research, Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway
  1. Correspondence to Professor Thor Edvardsen, Department of Cardiology, Oslo University Hospital, Rikshospitalet, N-0027 Oslo, Norway; thor.edvardsen{at}medisin.uio.no

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One of the most important objectives in cardiology is to gain knowledge about the function of the left ventricle (LV). The patient's prognosis is closely related to LV function in nearly all cardiac diseases affecting myocardial function. The ventricular mechanics are complicated. LV mechanics consist of longitudinal and circumferential shortening and lengthening, radial thickening and thinning and twist. This means that every attempt to assess LV function by cardiac imaging will be a simplification of true LV deformation.1 The most recent imaging techniques from echocardiography have improved diagnostics considerably and will give the cardiologist valuable information on the diagnosis and prognosis of the patient.

This article describes the assessment of ventricular mechanics by echocardiographic techniques which are widely available to all cardiologists. The different deformation patterns and how the assessment of these can be used in the clinical setting are discussed.

Left ventricular anatomy

LV myocardial fibres are oriented mainly in three layers. Myocardial fibres in the mid LV wall are oriented mainly in the circumferential direction (0°). The fibres in the subendocardium have an approximately longitudinal orientation of about 80° to the circumferential direction. Fibres in the sub-epicardium are oriented in an oblique way of around 60° to the circumferential direction and rotated in the opposite direction from the subendocardial fibres. The subepicardial fibres form a left handed helix and subendocardial fibres form a right handed helix, which is essential for the development of ventricular torsion.w1–w5

Right ventricular anatomy

The normal right ventricle (RV) is relatively thin-walled compared to the LV. The RV has normally low pressures, but RV function will adapt quickly to changes in pre- and afterload due to the thin walls. Longitudinal function is a major contributor to RV performance.2

Techniques to assess detailed ventricular deformation

Echocardiography

Established echocardiographic techniques such as M mode, colour Doppler, pulsed Doppler, two dimensional greyscale loops and two dimensional colour Doppler flow images provide the cardiologist with important information regarding ventricular mechanics.

Tissue Doppler imaging (TDI) is a quantitative and more objective method for assessing myocardial function.w6 The different TDI modalities include myocardial velocity imaging, displacement imaging, strain rate and strain imaging. These methods give a detailed insight into the ventricular mechanics and provide additional and important information in many patients (box 1).

Box 1

Echocardiographic modalities for detailed ventricular function

  • Myocardial velocities (cm/s)

  • Strain (%)

  • Strain rate (1/s)

  • Displacement (mm)

  • Rotation (degrees or radians)

  • Torsion (degrees/cm or radians/m)

Myocardial velocities

The myocardial velocities towards and away from the transducer along the ultrasound beam are displayed as a specific velocity pattern through the cardiac cycle (figures 1 and 2).w7–w9 In a normal LV, the myocardial velocities increase from the apex towards the base (figure 1).w7 w8 Assessment of myocardial velocities by Doppler is limited to velocities along the long axis and the anterior and posterior walls from the short axis view. Radial velocities can be assessed from the anterior part of the septum and from the posterior wall, and circumferential velocities can be assessed from a small part of the lateral wall and septum from the parasternal short axis view.

Figure 1

Parameters from myocardial velocity and strain curves by tissue Doppler imaging in a healthy individual. Left panel displays myocardial velocity curves from basal, mid and apical part of the interventricular septum. Note that peak systolic velocity (S) is highest in the basal part of the left ventricle (yellow curve) and lowest in the apical part (red curve). a', diastolic annular velocity; e', early diastolic annular velocity; IVC, isovolumetric contraction; IVR, isovolumetric relaxation. Right panel displays a strain curve from a healthy individual. Peak systolic strain is normally a negative value, but can be positive if no segmental shortening occurs, as in infarcted tissue. AVC, aortic valve closure.

Figure 2

Echocardiographic modalities to assess detailed myocardial function in a healthy individual (left panels) and in a patient with a left anterior descending (LAD) myocardial infarction (MI) (right panels). Yellow curves are from the septal segments and blue curves from the lateral segments. Myocardial velocity by tissue Doppler imaging (TDI). The patient with an LAD MI and left ventricular remodelling has reduced systolic velocity in both walls and a pronounced post-systolic velocity in the septal wall. Myocardial velocities from mitral annulus by spectral Doppler. The post-systolic velocity is prominent in the patient with MI. Displacement traces. Note the different scales. The patient with MI has reduced septal and lateral displacement. Strain curves by TDI. The MI patient shows reduced strain in the septum with a typical initial stretch (lengthening) of the segment in addition to post-systolic shortening. Peak systolic and peak end-systolic strain occur during systole. Segmental shortening, which occurs after aortic valve closure, is defined as post-systolic shortening. Strain rate by tissue Doppler imaging. The yellow trace in the MI patient has low systolic and notable post-systolic strain rate (white arrow).

Regional myocardial velocities are generated by tethering effects from other myocardial segments and by translational motion of the entire heart, which could limit the ability of tissue Doppler imaging to quantify regional function.3 w7

There are two methods to acquire myocardial velocities: spectral Doppler and tissue colour Doppler (figure 2). Spectral Doppler depends on a fixed position and cannot be further processed, while tissue colour Doppler images can be post-processed. Velocities from spectral Doppler are absolute velocities, while velocities from tissue colour Doppler images are mean velocities and approximately 25% lower than the corresponding velocities from spectral Doppler.

Displacement, mitral and tricuspidal annuli excursions

Displacement of the mitral annulus (atrioventricular plane displacement) can be calculated by temporal integration of the corresponding myocardial velocity and correlates well with ejection fraction (figure 2).4 w10 Displacement of the mitral annulus will give the cardiologist a brief impression of LV long axis function (figures 2 and 3), but it is not as accurate as strain measurements and might ignore smaller areas of decreased function.4

Figure 3

Displacement curves in a healthy individual and displacement and strain curves from a patient with hypertrophic cardiomyopathy (HCM). Upper left panel shows displacement curves in a healthy individual from the basal (yellow curve), mid septal (blue curve), and apical (red curve) segment. Upper right panel shows impaired displacement from a patient with HCM (same colour codes). Note the different scales. Displacement is an easy and fast method to demonstrate reduced longitudinal function. Lower left panel shows reduced longitudinal strain and lower right panel shows preserved circumferential strain in a patient with HCM.

Similarly, RV function can be assessed by placing the M mode cursor at the lateral tricuspid annulus (tricuspid annular plane systolic excursion, TAPSE).w11

Myocardial strain and strain rate

Strain is a measure of how much an object has been deformed. This measure has been adapted in cardiology as a measure of myocardial deformation. Strain is produced by application of a stress (force per unit cross-sectional area of a material).w12 Strain is a dimensionless quantity and is defined as the relative change from end-diastolic dimension to end-systolic dimension. It expresses the myocardial shortening in negative values3 (figure 1) (box 2). Strain can therefore be regarded as the regional shortening fraction and relates to ejection fraction. Strain rate measures the time course of deformation and it seems to be a correlate of rate of change in pressure (dP/dt) which again reflects contractility.5

Box 2

Definitions: strain

Global left ventricular (LV) longitudinal strain=average peak systolic strain from 16 LV segments from the apical views. Conversion from 18 segments into a 16 segments model is achieved by averaging strain values in the equivalent apical segments from the apical long axis and four chamber views.

Global LV circumferential strain=average peak systolic strain from 16 LV segments from three short axes slices.

Global right ventricular (RV) strain=average peak systolic strain from the three RV lateral wall segments.

Strain=(L−L0)/L0

L=the instantaneous segment length; L0=the segment length at time 0 (end diastole).

Strain rate=time derivative of strain = (L−Lo/Lo)/t

t=time

There are several non-invasive methods to assess myocardial strain: MRI tagging, TDI, and speckle tracking imaging (STI). The echocardiographic techniques are more practical methods for assessment of myocardial strain and several studies confirm that strain by TDI and STI correlates with strain by sonomicrometry and MRI tagging.3 6 w13 w14

Strain will increase after significant volume loading by a saline infusion, while the myocardial contractility itself does not change.3 Myocardial strain is therefore load dependent.w15 This fundamental association is probably less important for regional measurements than for global indices because regional differences are likely to persist despite load changes.

One important criticism of assessing myocardial strain from TDI has been that the technique is angle dependent. One way to partially avoid this objection is to align the ultrasound beam along the main fibre direction in the myocardial wall during acquisition of the datasets. The recent development of STI permits assessment of global myocardial deformation independently of insonation angle since STI is based on B mode greyscale images. Characteristic speckle patterns are created by interference of the ultrasound beams in the myocardium and can be followed by dedicated software during the heart cycle. STI can provide regional and global information about the myocardial deformationw16 (box 3).

Box 3

Strain by tissue Doppler imaging (TDI) and speckle tracking imaging (STI): advantages

  • Strain by TDI

    • An accurate parameter for quantification of myocardial function

    • Analogous to left ventricular ejection fraction, which quantifies global contractility, myocardial strain quantifies regional and global contractility

    • Not influenced by overall motion of the heart (translation) or by motion caused by contraction in adjacent segments

    • Better temporal resolution

  • Strain by STI

    • No angle dependency

    • Three possible deformation directions (longitudinal, circumferential, and radial strain)

    • Less time consuming, tracking is performed automatically

There are, however, technical limitations that need to be resolved (box 4). Important pitfalls are dropout artefacts and reverberations where normal myocardial function will appear as decreased. Poor tracking originating from the mitral annulus may also confuse the cardiologist. A complete flat strain curve around zero is likely to be erroneous and conclusions about myocardial function can therefore be wrong.

Box 4

Limitations of echocardiographic deformation imaging

  • Good image/speckle quality is needed

  • Reverberations are a major source of error

  • Avoid measurements of the pericardium

  • Optimal frame rate in speckle tracking imaging (STI): approximately 60–100 frames/s

  • Spatial smoothing in STI may influence strain values in neighbouring segments

  • An increase in time resolution will lead to a decline in spatial resolution

Strain rate has been shown to correlate very well with contractility.5 Its clinical use has, however, been limited due to demanding interpretation. Strain rate measurements need high temporal resolution. Strain rate should therefore be assessed from the TDI technique where frame rates of 150/s or more may be easily obtained. Strain and strain rate traces from the TDI technique can appear as noise, and a high level of training is therefore required to avoid accepting artefacts as real myocardial function.

Global LV function

Ejection fraction

The most widely used assessment of LV systolic function is LV ejection fraction (LVEF). This can be obtained relatively easily by non-invasive imaging techniques such as echocardiography, nuclear techniques, and MRI. LVEF and LV end-systolic volume (LVESV) provide important information about diagnosis, prognosis, and selection of treatment.w17 w18

LV volumes assessed by MRI have been more reproducible than LV volumes obtained by echocardiography.w19 w20 Fewer study participants are therefore required to detect changes in volumes and mass over time by MRI compared with echocardiography.

Global strain

Global longitudinal strain is a promising method to achieve measures of global LV function and is defined as the average peak systolic strain from all LV segments from the apical views (box 2).7 w21 Two of the apical segments can be assessed both from the apical four chamber and long axis views and therefore only 16 LV segments are usually averaged to obtain global longitudinal strain.

Recent studies have shown that LVEF was inferior to global strain for LV function when compared to infarct size by MRI.7 One possible explanation is that LVEF describes the global LV function, whereas the infarcted area and reduced function are regional and so are better assessed by global strain. A decrease in LVEF implies that several LV segments are involved.

Longitudinal function

The longitudinal fibres are oriented approximately parallel to the ultrasound beam when using apical views. Contraction in the longitudinal axis is mainly performed by subendocardial fibres and subendocardial strains therefore have a higher magnitude compared to subepicardial strains.w22

Spectral Doppler velocities are most commonly assessed at the mitral annulus to obtain a brief impression of LV function. Almost every significant loss of myocardial function will result in decreased velocities in the longitudinal direction. Decreased myocardial velocities are therefore a rather unspecific sign of myocardial dysfunction.

Normal LV longitudinal function

The average peak LV longitudinal systolic strain assessed by speckle tracking technique was found to be −18.6±0.1% in healthy individuals in a recent multicentre studyw23 and −22.9% (95% CI −17.0% to −28.9%) in a TDI based studyw24 (box 3). There were significant variations in regional strain measurements by STI and the authors advocated site-specific normal ranges. Longitudinal strains have slightly higher amplitudes at the LV apex compared to base.w25 Segmental strain values greater than −14% should be regarded as pathological. Averaged longitudinal LV systolic strain rate in a general population was found to be 1.3/s (0.9–1.7/s). Peak systolic velocity at the mitral annulus should be approximately 6 cm/s or higher and atrioventricular plane displacement should be >10 mm.

Circumferential function

Strain along the circumferential axis is easily obtained by STI (figure 3). Circumferential strain is predominantly a measure of mid LV wall fibres and should therefore theoretically be more affected in patients with extended transmural infarcts. Only minor differences have, however, been demonstrated between the different strain directions and their ability to separate between decreased and normal myocardial function is similar.

Systolic function in the healthy elderly appears normal as indicated by maintained LVEF.w26 LVEF is maintained in old age by a compensatory increase in circumferential shortening while there is an age dependent decrease in longitudinal systolic shortening.w27 w28

Normal LV circumferential function

A small but significant non-uniformity in circumferential function is probably caused by differences in regional LV architecture and local stress.w29 There are sparse reports about normal ranges of circumferential strain by speckle tracking strain and normal values seem to be in the same range as longitudinal function (approximately −20% to −22%).

Radial thickening and thinning

LV mass is constant during systole and diastole. The systolic shortening in the longitudinal and circumferential direction results in a thickening in the radial direction and will therefore be displayed in positive values. The cardiac shearing deformation increases from the epicardium towards the sub-endocardium which results in higher amplitude of thickening strains in the subendocardium and >40% radial LV wall thickening in a normal heart.w30

Twist/torsion

The subendocardial LV fibres are arranged in a right handed helix and the subepicardial fibres in a left handed helix.8 w31 This helical arrangement can explain the simultaneous twisting motion, long axis and radial shortening of the LV during systole and untwisting during diastole.9 w32 w33 The LV apex rotates in a clockwise direction and the base rotates in a counterclockwise direction, when viewed from the apex. The mid LV level is relatively stationary (box 5).

Box 5

Definitions: rotation and torsion

Rotation=Rotation of short axis sections of the left ventricle as viewed from the apical end and defined as the angle (degrees or radians) between radial lines connecting the centre of mass of that specific cross-sectional plane to a specific point in the myocardial wall at end-diastole and at any other time during systole

Torsion=Base-to-apex gradient in the rotation angle along the longitudinal axis of the left ventricle (degrees/cm or radians/m)

Left ventricular (LV) twist angle/net LV torsion angle=The absolute apex-to-base difference in LV rotation (degrees or radians)

The net LV twist increases gradually from infancy to adulthood. Counterclockwise apical rotation is constant in its magnitude during childhood and increases during adulthood. The basal rotation changes over age, initially from a counterclockwise pattern in infancy to the adult clockwise pattern.w34

How to measure LV twist?

STI can measure LV rotation and torsion with great accuracy.8 w35 The basal rotation should be assessed from a standard short axis parasternal transducer position. This view may be complicated by out-of-plane motion when the base descends towards the apex in systole. LV rotation from the apical level should be assessed from a more distal anterior position. An easy way to access this position would be to start from a standard apical four chamber view while tilting and moving the transducer along the long axis to a short axis view at the apical level. Apical rotation represents the dominant contribution to LV twist.w36 This implies, however, that even small deviations from a correct echocardiographic apical position will lead to erroneous assessments of LV twist.

Normal LV twist

Normal apical rotation is approximately −10° to −13° and basal rotation is around 5° in studies by MRI tagging and echocardiography. LV twist has been demonstrated to be approximately −15°.w37

RV

The assessment of TAPSE is utilised as a measure of RV function.w38 To determine TAPSE, the M mode cursor has to be oriented to the junction of the tricuspid valve plane with the RV free wall using the apical four chamber view. TAPSE is the total excursion of the tricuspid annulus from its highest position after atrial ascent to the peak descent during ventricular systole, from the apical four chamber view.w39 Myocardial strain measurements along the lateral RV wall are helpful to quantify RV longitudinal motion and provide useful information in terms of quantification and early detection of subtle myocardial abnormalities.2 RV (fractional area change) is also widely used as a measure of RV function.10

Normal RV function

Normal longitudinal velocities at the basal RV lateral wall are ≥14±2 cm/s for spectral Doppler and ≥10±2 cm/s for TDI.w40 Longitudinal strain in the free RV wall is approximately −28±4%.w41 TAPSE is normally >2.0 cm.10

Diastolic function

Up to half of all patients with symptoms of heart failure have normal or close to normal LVEF and volumes.w42 w43 These patients have traditionally been diagnosed with diastolic heart failure, but are now classified as heart failure with a normal ejection fraction (HFNEF).w44 w45

E/e′ is defined as the mitral E velocity by antegrade mitral flow corrected for the influence of relaxation e' by spectral Doppler velocity at the mitral annulus. E/e' ratio can be regarded as a preload independent index of LV relaxation and is a fairly good estimate of filling pressures.11

An E/e' ratio >15 correlates with LV end-diastolic pressure >16 mm Hg and mean pulmonary capillary wedge pressure >12 mm Hg. An E/e' ratio <8 indicates normal filling pressures. Be aware of the relatively large grey zone >8 and <15. These cut-off values are based on spectral Doppler measurements and on averaged velocities of lateral and septal mitral annulus.12 w43 The accuracy of this index is debated, at least in regards to heart failure with reduced LVEF (HFREF).w46 LV diastolic function should also be interpreted by mitral flow and pulmonary venous flow velocities in addition to left atrial volume index (LAVI).13 w47 The probability of HFNEF is strong if a patient suffers from breathlessness, has LVH and increased LAVI.

Normal LV diastolic function

E' velocity declines with increasing age.w48 As a general rule, a septal e' ≥8 cm/s and lateral e' ≥10 cm/s are usually observed in normal subjects, and will be reduced in patients with impaired LV relaxation and increased LV filling pressures.

How to assess ventricular mechanics in coronary artery disease

Longitudinal myocardial velocities from spectral Doppler have several typical changes in ischaemic myocardium and might therefore be difficult to interpret. The most reported change in ischaemia is lower velocities during the ejection period accompanied by a positive velocity in early diastole (post-systolic velocity).w49

STI is an accurate technique for the assessment of LV function in post-myocardial infarction (MI) patients7 and contributes to prognostic risk assessment,14 and is therefore the preferred method (box 6). An ischaemic myocardium will result in decreased systolic amplitudes of strain and an initial stretch followed by a shortening (figure 2). This shortening can continue during early phases of diastole commonly known as post-systolic shortening (PSS). PSS can be an active shortening or passive recoil depending on the transmural distribution of injury. Recent studies demonstrated that STI was superior to LVEF for assessment of myocardial function post-MI.7 Circumferential strains and twist mechanics remain relatively preserved in moderate myocardial ischaemia. Longitudinal strain is therefore generally the preferred method to assess reduced function in patients with coronary artery disease. In patients with larger infarcts, additional reduction in circumferential and radial strain and twist mechanics will appear.w50 w51

Box 6

Clinical use of myocardial strain

  • Ischaemic heart disease:

    • Visual assessment of wall motion

    • If apparently normal wall motion: add longitudinal strain analyses

    • Global strain may add important information about outcome

  • Stress test:

    • Visual assessment of wall motion

    • If apparently normal wall motion: add longitudinal strain analyses and ɛpssmax ratio

    • Myocardial velocities should be used with care

  • Valvular diseases:

    • Global strain might disclose reduced left ventricular (LV) function before a decline in LV ejection fraction

  • Hypertrophic cardiomyopathy:

    • Use displacement analyses to discover a reduced longitudinal LV function

  • Cardiac resynchronisation therapy:

    • The use of tissue Doppler imaging can reveal LV dyssynchrony, but currently cannot predict effect of treatment

  • Heart failure with a normal ejection fraction (diastolic heart failure)

    • Calculate E/e'. Use average e' obtained from septal and lateral mitral annulus

    • If E/e' is >8 and <15, use other echocardiographic parameters for diastolic function

    • E/e' should not be used in: normal subjects, patients with significant annular calcification, surgical rings, mitral stenosis, prosthetic mitral valves, and severe primary mitral regurgitation

  • Restrictive cardiomyopathy:

    • Assess LV longitudinal function by global strain. Longitudinal function is decreased while circumferential strain is preserved

  • Chemotherapy induced cardiomyopathy:

    • Longitudinal and radial strain analyses can reveal subclinical LV dysfunction before a decline in ejection fraction

Longitudinal strain values greater than −15%7 and −11% for circumferential strain15 in each LV segment reflect decreased function in coronary artery disease.

Territorial strain is calculated based on the theoretical perfusion territories of the three major coronary arteries in a 16 segment LV model, by averaging all segmental peak systolic strain values within each territory.w16 w52

Patients with non-ST elevation MI (NSTEMI) and occluded coronary arteries can best be detected by circumferential strain.16 w53 A territorial circumferential strain value greater than −10.0% has excellent sensitivity and specificity for identification of acute occlusions.

Myocardial viability

The use of the contrast enhanced MRI technique in combination with visual assessment of LV function has in many ways revolutionised the interpretation of viable myocardium.17 A bedside method to assess myocardial viability of an ischaemic segment will be by myocardial strain. Longitudinal strain worse than −10% immediately after primary reperfusion therapy could predict non-viable myocardium with reasonable accuracy.w54 Another study showed that a global longitudinal LV strain value of −13.7% was able to predict global LV functional recovery at 1 year follow-up after myocardial infarct.w55

Radial strain has also been used to distinguish between transmural and non-transmural infarcts with a cut-off value of approximately 17%. A corresponding cut-off value for circumferential strain is −11%.w56 w57

Stress test

The value of detecting ischaemic heart disease by nuclear imaging, MRI and echocardiographic techniques is equivalent. The current method of choice by stress echocardiography is wall motion score index. The incremental value of using strain is presently not established, but may be helpful when visual assessment of LV function is difficult.18 w58 The ratio of post-systolic shortening (ɛpss) to maximal strain (ɛmax) may be used as an objective marker of ischaemia during dobutamine stress echocardiography if ɛpssmax >35%.

A segmental systolic strain rate value greater than −1.2/s at peak dose dobutamine was an independent predictor of death in a large trial.w58

Currently, TDI based longitudinal strain and strain rate seems to best predict functional recovery during low dose dobutamine stress.w59 A peak systolic longitudinal strain of −7.0±7.3% and peak systolic longitudinal strain rate of −0.52±0.49/s showed no signs of recovery at low dose dobutamine.

Interpretation of myocardial velocities in dobutamine stress echocardiography should be used with caution due to passive motion caused by the tethering effect from the adjacent normal LV.1

Valvular disease

Significant valvular diseases result in haemo-dynamic consequences and cardiac remodelling, although patients can remain asymptomatic for long periods of time. In patients with valvular disease the timing of surgery is a major question and the role of deformation imaging is not defined. In patients with aortic valve stenoses, LV hypertrophy and reduced ejection fraction are markers of remodelling. Reduced longitudinal strain occurs at an earlier stage and LV twist is significantly increased.w60 61 Strain analyses, therefore, may help the clinician to detect myocardial remodelling before ejection fraction decreases. This is also supported by recent studies in patients with valvular regurgitations, but currently there is no clinical application of these techniques.w62

LV hypertrophy

Physiologic hypertrophy occurring with exercise is associated with complex changes in LV mechanics. To what extent cardiac contractility can increase by training is the subject of much discussion. Many studies have shown increased myocardial strain induced by training, but strain findings in athletes are disputed.w63 w64

Hypertensive heart disease is characterised by cardiac hypertrophy in response to increased cardiac afterload, followed by progressive myocardial fibrosis. These changes mainly lead to subendocardial dysfunction resulting in reduced systolic longitudinal strain due to a relative subendocardial ischaemia, whereas systolic circumferential, radial strains and torsion mechanics remain preserved.w65 w66 Changes in fibre angle orientation in hypertrophy may contribute to these changes.w67

Cardiomyopathies

Hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is defined as septum hypertrophy >1.5 cm in patients without a history of hypertension or other obvious causes.w68 Typically, longitudinal function is reduced, while circumferential function is elevatedw69 (figure 3). The specific pattern of reduced and delayed longitudinal shortening and paradoxical systolic lengthening has been proposed as being specific for HCM.w70 Torsion in HCM patients is higher at rest than in healthy individuals, but does not increase with exercise in contrast to those who are healthy.w34 The regional heterogeneity, usually with basal or mid septal longitudinal strain being most affected, appears to be unique to HCM and is not usually seen in ventricular hypertrophy related to longstanding hypertension.w71 Diastolic dysfunction appears early in disease development.

Dilated cardiomyopathy

Dilated cardiomyopathy is typically associated with reduction of strains in all three directions. Rotation is reduced at the apex and the base resulting in a decreased LV twist.w72 Currently LVEF is regarded as the measurement of choice in dilated cardiomyopathy.

Strain and TDI measurements have contributed to improved understanding of LV dyssynchrony(figure 4). LV dyssynchrony has usually been determined by tissue Doppler velocities as the maximal time difference in peak systolic velocities between several LV walls. A difference of 130 ms by radial velocities has shown a response to cardiac resynchronisation therapy (CRT).w73 A number of longitudinal and radial dyssynchrony indices have been proposed for selection of patients for CRT.19

Figure 4

Dyssynchrony demonstrated by speckle tracking echocardiography in a patient with left bundle branch block. White arrow indicates delayed contraction in the lateral segments (red, blue, and pink strain curves).

Patients with idiopathic dilated cardiomyopathy often display a cardiac swinging motion, with the apex appearing to move in a clockwise rotation during systole as viewed from the apical four chamber view (apical rocking or longitudinal rotation).w74 Longitudinal rotation has been proposed to predict success of CRT in dilated cardiomyo-pathy subjects, even in patients with a narrow QRS (<130 ms).

Strain delay index has been defined as the sum of the difference between peak and end-systolic strain across 16 segments as a measure of wasted energy in heart failure patients. The strain delay index could predict a response to CRT.w75

Despite a large number of different techniques and dyssynchrony indices, there is currently a lack of consensus on which indices should be used to predict CRT response.20 w76

Restrictive cardiomyopathy and constrictive pericarditis

Restrictive cardiomyopathies are associated with reduced longitudinal strain, while circumferential strain and LV torsion remain relatively preserved. Ejection fraction therefore may remain unchanged before disease progression impairs circumferential strain.w77 Constrictive pericarditis, on the other hand, is typically characterised by reduced circumferential strain and twist with preserved longitudinal function.w78 w79

Chemotherapy induced cardiomyopathy

Myocardial deformation has been shown to be more sensitive than conventional echocardiographic measures in detecting early cardio-toxicity.w80–w82 As an example, strain rate was reduced in patients receiving trastuzumab for breast cancer without any changes in LVEF.w83 Furthermore, impaired LV myocardial deformation and mechanical dyssynchrony was shown in children following anthracycline treatment despite having normal LV shortening fractions.w84 Therefore, subclinical reduction in longitudinal and radial strain and strain rate despite unchanged LVEF is useful when evaluating dosages and frequency of chemotherapy.w83

Conclusion

Echocardiography is the preferred method for assessment of ventricular function in most cases. Novel deformation techniques have increased our understanding of cardiac mechanics. These methods can currently be used as a diagnostic support to traditional echocardiographic methods.

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References

  1. A detailed review on the technical and clinical aspects of strain techniques.
  2. A comprehensive comparison between different TDI techniques, documenting that myocardial strain is more accurate than the other techniques.
  3. An all inclusive paper about the different echocardiographic velocity and deformation techniques.
  4. The first study to document the use of E/e' to estimate LV filling pressures.
  5. Guideline paper about echocardiographic evaluation of diastolic function.
  6. A comprehensive paper on assessment of cardiovascular and cardiac haemodynamics by echocardiography.
  7. A new approach by STI to identify coronary occlusions in patients with non-ST elevation acute coronary syndrome.
  8. An important paper on how to use contrast enhanced MRI to identify viable myocardium.
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Supplementary materials

  • Web only appendix hrt.2009.184390

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Footnotes

  • Competing interests In compliance with EBAC/EACCME guidelines, all authors participating in Education in Heart have disclosed potential conflicts of interest that might cause a bias in the article. Thor Edvardsen has received honoraria from GE Vingmed.

  • Provenance and peer review Commissioned; internally peer reviewed.