Article Text


Non-invasive imaging
Two dimensional speckle tracking echocardiography: clinical applications
  1. Hermann Blessberger1,
  2. Thomas Binder2
  1. 1AKH Linz, Department of Internal Medicine I – Cardiology, Linz, Austria
  2. 2Department of Cardiology, Medical University of Vienna, Internal Medicine II, AKH, Vienna, Austria
  1. Correspondence to Professor Thomas Binder, Department of Cardiology, Medical University of Vienna, Internal Medicine II, AKH, Waehringerguertel 18-20, Vienna 1090, Austria; thomas.binder{at}

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This review is the second of two articles that focus on two dimensional speckle tracking echocardiography (STE). While the first article described the principles of STE, this review deals with its potential clinical applications. The technology of speckle tracking based strain analysis is rather new.w1 w2 However, there is considerable experience with parameters of deformation measured with tissue Doppler imaging (TDI). Since measurements of strain and strain rate (SR) correlate well with those of TDI, much of what has been shown with TDI can probably be applied to STE. Because STE has numerous advantages compared to TDI (reproducibility, complete analysis of radial and circumferential strain, twist, torsion, and rotation), it adds important information to what is already known from TDI. The number of publications which investigate STE in clinical and subclinical conditions is rapidly growing and confirms the potential of this technology. This review summarises the current experience of STE, points to potential clinical applications and future developments of STE, and describes its limitations.

STE and coronary artery disease

The echocardiographic assessment of coronary artery disease (CAD) is mainly based on the detection of regional wall motion abnormalities, lack of myocardial thickening, and visualisation of scar tissue. However, this approach is highly subjective, requires considerable operator experience, and strongly depends on image quality. Even though several different methods to quantify regional wall motion abnormalities have been proposed, none of these are robust enough to be used in clinical practice. The experience with TDI has shown that the analysis of regional tissue deformation provides important additional information and even allows quantification of ischaemic abnormalities.

Ischaemic and scarred tissue shows a reduction and delay of peak segmental strain and SR.w3 w4 This is true for longitudinal, circumferential, and radial strain/SR components.w3 w4 An important additional phenomenon—which occurs early after the onset of ischaemia and which can be detected with STE—is post-systolic thickening. Post-systolic thickening can be defined as continued myocardial thickening which is present even after aortic valve closure (figure 1).

Figure 1

Dog model of ischaemia/reperfusion. M mode tracing of the left ventricle. Myocardial ischaemia induces a reduction in contraction and causes post-systolic thickening, which are reversible after reperfusion. The dotted line represents the time of aortic valve closure. Adapted from Sutherland et al.w5

While some degree of post-systolic thickening also occurs in the normal myocardium, it is significantly more pronounced in the setting of acute ischaemia and stunning.1 w6–w8 In addition, the magnitude of post-systolic thickening is proportional to the severity of ischaemia. During the time course of acute ischaemia there is a gradual decrease of the systolic component and an increase in the post-systolic component of deformation.w9 During reperfusion, deformation returns to normal.1 w7 w9 w10 In contrast, chronic myocardial ischaemia is characterised by a reduction in peak systolic strain and SR with only mild post-systolic thickening.1 ‘Ischaemia imaging’ using the time delay of ‘thickening’/contraction could become an important future application of STE. Most systems provide display formats which allow detection of post-systolic events for all components of deformation (figure 2), some even using three dimensional STE which also allows automatic calculation of left ventricular (LV) volumes (figure 3). Further studies will now have to show if STE is able to differentiate between acute ischaemic and scarred tissue and how dyssynchrony, preload and afterload, dyskinesia, abnormal septal motion patterns, and tethering effects of adjacent segments affect ‘time to peak’ parameters.

Figure 2

This figure shows a bull's eye (polar map) display format of the time delay between the onset of aortic valve closure (AVC) and the peak of the strain curve (post-systolic index) for individual segments in a patient with acute inferior myocardial infarction. Segments which deform before AVC are assigned a time value of 0% (white or light blue). All other segments are presented in darker shades of blue depending on the delay of peak strain from aortic valve closure.

Figure 3

(A, B) Longitudinal strain in a patient with inferior lateral wall infarction. Note the delayed contraction indicated by the curves and the scar zone (blue area) in the three dimensional display. (Courtesy of Dr Peres de Isla, Madrid, Spain). (C) Reduced radial three dimensional strain values and delayed contraction in a patient with anterior infarction. Simultaneous calculation of left ventricular volumes indicates a reduced ejection fraction. (Courtesy of Dr Maunz, Kirchheim, Germany).

STE is also able to detect regional abnormalities of peak systolic strain in ischaemic myocardium (figure 4). For example, LV global longitudinal strain at a cut-off of −15% was superior to LV ejection fraction (EF) in revealing myocardial infarctions larger than 20%, with a sensitivity of 90% and a specificity of 86%, as compared to contrast enhanced cardiac MRI in patients with ST elevation myocardial infarction (STEMI).w11

Figure 4

Bull's eye display of longitudinal peak systolic strain (LPSS) in a patient with anterior myocardial infarction (AMI). Left = before AMI, right = 1 month after AMI. The per cent values of longitudinal strain for the individual segments are presented and colour coded. Different shades of red represent negative strain (contraction) while blue denotes positive strain (relaxation). The image on the left shows a normal pattern with values ranging from −16% to −28%. (Segments denoted with an x could not be assessed for technical reasons.) Global longitudinal peak systolic strain (GLPSS) is −20.1%. The image on the right shows significantly reduced LPSS in the left anterior descending (LAD) territory. GLPSS has now dropped to −14.3%. GLPSS is averaged from the individual strain values of all left ventricle segments.

A reduction in peak systolic strain is not only present in acute ischaemic and scarred myocardium but interestingly also in patients with severe CAD (three vessel or left main CAD) at rest and in the absence of manifest ischaemia or regional wall motion abnormalities (sensitivity and specificity of STE were both 79%).2 This suggests that STE is more sensitive than the ‘eye’ in detecting contraction abnormalities. If these findings can be confirmed in larger series, STE could not only be used to detect segments with regional wall motion abnormalities but also to detect subclinical contraction abnormalities caused by CAD. It might be possible that STE could be used to screen patients for ‘significant’ CAD.

Stress tests (ie, dobutamine) in combination with tissue deformation imaging allows even better identification of ischaemic segments and further discrimination of ischaemic syndromes.1 w12 w13 Several authors suggest that SR is more sensitive than strain in identifying ischaemic segments during dobutamine stress echocardiography.w14 However, it is currently still unclear which deformation parameter or component of strain/SR (longitudinal, circumferential or radial) best reflects ischaemia. It is also unclear if STE is equally reliable in all segments since studies have shown that STE is more reliable in the anterior territories (supplied by the left anterior descending artery, and the ramus circumflexus) than in the right coronary artery territory.w15 Possibly it will be necessary to normalise individual segments with respect to resting and stress values for strain.

Finally, STE can also be used to detect abnormalities of myocardial mechanics caused by CAD. Scarred myocardium impairs the twisting and untwisting of the LV. Patients with anterior myocardial infarction and impaired systolic function (EF <45%) show a reduction in apical rotation, peak LV twist, as well as peak positive and negative twist velocity.w16 After revascularisation, LV torsion improves.w17 These changes can be studied with STE and help us to understand the haemodynamic sequelae of myocardial infarction.


In summary, STE could be an extremely powerful tool for the detection and differentiation of ischaemic coronary syndromes. Deformation parameters are more sensitive than our eye in detecting contractile abnormalities. Thus, STE could be used as a ‘screening technique’ for ischaemia and CAD. Furthermore, it could be possible to quantify directly the extent of contractile impairment and provide valuable information on the potential of the myocardium to recover after reperfusion. STE could be integrated into dobutamine stress protocols and help detect exercise induced ischaemia, hibernating myocardium, and stunned and scarred tissue. It will now be necessary to determine which other factors influence deformation and post-systolic thickening. Nevertheless, deformation imaging with STE could help ‘highlight’ abnormal segments which then need further evaluation using other modalities.

Valvular heart disease

Aortic stenosis

Monitoring of left ventricular function (LVF) in aortic stenosis (AS) is crucial since a reduction in LVF indicates a poor outcome in the unoperated patient. In the early stages of disease, concentric LV hypertrophy (LVH) is able to compensate for increased LV afterload caused by valve obstruction. However, as stenosis progresses LVF deteriorates.w18 In the early stages of this process LV impairment may be subtle and undetectable by calculations of EF. Thus, early detection of LV dysfunction could play an important role in the timing of aortic valve replacement and in the management of patients with AS.w19

There is increasing evidence that a reduction of LV strain and SR precedes haemodynamic effects of LV impairment.3 Consistently, TDI and STE based studies show that the reduction in longitudinal strain correlates well with the severity of AS.3 4 w20 STE assessed global longitudinal LV strain is significantly lower in asymptomatic AS patients (effective orifice area <1 cm2, EF >55%) compared to healthy EF matched controls.5 The reduction of longitudinal strain appears to be most prominent in the basal segments (figure 5). Conversely, radial and circumferential strain values do not reflect early impairment of LV function.4 A basal longitudinal strain below −13% was associated with a more severe degree of AS in terms of effective orifice area. In addition, performance in exercise stress testing was poorer in subjects with a global longitudinal strain below a cut-off of −18%. A basal longitudinal strain under −13% even predicted a higher cardiac event rate during a 12 month follow-up period.5 It is possible that this impairment of longitudinal functional reserve also reflects irreversible subendocardial fibrosis. However, there is evidence that the deterioration in deformation is at least partially reversible: an increase of all three orthogonal strain and SR components could be observed after aortic valve replacement in patients with severe AS and an EF >55%.w21

Figure 5

Patient with asymptomatic severe aortic stenosis (aortic valve area (AVA) 0.8 cm2, mean gradient 64 mmHg), normal systolic left ventricular function (ejection fraction 65%), and significantly reduced global longitudinal peak systolic strain values (GLPSS −8.3%). Note that especially the basal segments (with the exception of basal lateral) are significantly reduced.

It remains to be shown whether asymptomatic patients with normal EF but with reduced longitudinal strain and/or impairment in the functional reserve of longitudinal contraction will benefit from earlier aortic valve surgery, or whether these patients will soon develop overt LV dysfunction (measured by EF). From a practical point of view, AS patients are ideal candidates for STE. The presence of a thick myocardium, which is usually also very echogenic, allows good border delineation and reliable calculations of strain/SR.

STE and AS

In summary, STE is more sensitive than EF in detecting systolic dysfunction in AS. Early deterioration of systolic function in AS is predominantly reflected by a reduction in (basal) longitudinal strain. This effect appears to be at least partially reversible. Future studies will have to determine if deformation parameters will play a role in the timing of aortic valve surgery.

Aortic and mitral regurgitation (LV volume overload)

Volume overload of the LV in aortic regurgitation (AR) and mitral regurgitation (MR) is compensated by progressive enlargement and hypercontractility of the LV. Elevated wall stress and increased oxygen demand eventually result in deterioration of LVF. Early detection of systolic dysfunction could be useful for the timing of mitral and aortic valve surgery. Thus, it is appealing to use STE for the assessment of contractile function in volume overload.

However, early experience using TDI to measure strain and SR showed that deformation is not only related to contractility but is also influenced by the size and geometry of the ventricle (Hooke's law).1 w22 To keep the stroke volume constant and to adapt for regurgitant flow, the ventricle can either dilate or increase its contractility. To detect subclinical dysfunction in a volume overloaded ventricle, it might thus be necessary to correct deformation parameters for LV volume or loading conditions (index).

Patients with severe and moderate AR show a reduction in both longitudinal and radial SR and strain values when compared to age matched healthy controls.w23 It has also been demonstrated that LV function improves after aortic valve replacement performed for AR with or without AS.w22

Early LV dysfunction in patients with MR and normal LVEF is characterised by a reduction of global longitudinal strain as well as longitudinal, circumferential, and radial SR.6 7 w24 Longitudinal strain and SR were shown to be the first affected in the remodelling process, while circumferential and radial SR deteriorate as disease progresses.6

Measurement of deformation parameters during exercise testing helps to identify patients with MR who already display a reduction in functional reserve. These patients fail to show an increase of global longitudinal strain during physical stress. Lancellotti et al found that an increase of global longitudinal strain below 1.9% during bicycle stress test was associated with a worse outcome after mitral valve surgery.7 In patients with chronic severe MR, preoperative measurement of longitudinal strain in an interventricular sentinel segment predicted postoperative LV contractile function. Furthermore, longitudinal SR below −0.80/s in the mid septal segment predicted a reduction in EF of >10% after mitral valve replacement.w25

Chronic MR also results in impaired myocardial mechanics during diastole. Borg et al demonstrated that the untwisting motion of the LV is delayed and slowed during early diastolic relaxation. Since the severity of MR as well as the progression of LV remodelling correlate with these torsion parameters, they may be an indicator for LV dysfunction in such patients.w24

STE and volume overload

In summary, early experience with TDI and STE suggests that deterioration of strain/SR (radial, circumferential, and longitudinal components) precedes overt LV dysfunction in patients with volume overload. Exercise testing to detect impaired deformation response is helpful to unmask decreased contractile reserve. Which values best reflect dysfunction, which cut-off values denote irreversible myocardial damage, and whether these values must be corrected for other factors that influence deformation (LV loading conditions, LV volume) remain under investigation.


In principle, patients with pathological hypertrophy display subendocardial dysfunction.w26 This dysfunction is most likely caused by fibrosis related to the increased wall stress and microvascular disturbances. Subendocardial dysfunction subsequently causes impairments in longitudinal contractile function.w27 Interestingly, the reduction in longitudinal function is initially compensated by an increase in radial function.w28 w29 Thus, ventricles often appear to be hypercontractile when EF of the Simpson method is used.w27 w30

Discrimination between different causes of LVH such as physiological adaptation in professional athletes, hypertensive heart disease, and hypertrophic cardiomyopathy (HCM) is often challenging. Conventional findings such as abnormal diastolic function, detection of ‘inadequate’ LVH (relative wall thickness), integrated myocardial backscatter, and cut-off values for LV mass are technically difficult and often fail to distinguish clearly between the different causes of hypertrophy.

Measurements of longitudinal function using TDI and M mode to quantify mitral annular velocities have shown that tissue velocities are less in hypertensives with hypertrophy and patients with HCM compared to normal individuals. Measurement of mitral annular velocity by STE proved to be feasible and well reproducible. However, values might be lower compared to TDI.8 w31 The reduction in longitudinal function involves not only the hypertrophied but also the non-hypertrophied segments.w32 This was confirmed by studies using STE. These studies also showed that strain/SR imaging is more specific than tissue velocities.9 w29

Patients with HCM and hypertensive heart disease display a specific regional and directional strain/SR pattern and a prolonged time to peak systolic strain (strain index). Moreover, patients with HCM and hypertensive heart disease show disturbed myocardial mechanics. LV systolic torsion is increased due to increased rotation of the basal segments. In contrast, untwisting of the LV during early diastole is significantly delayed and reduced.10 w33 w34 This effect seems to be related to the degree of LVH.

Athletes with hypertrophy appear to have a specific contraction pattern at rest which is predominantly driven by radial and circumferential contraction, whereas longitudinal strain is lower in comparison to healthy controls.w29 However, during exercise athletes are able to recruit longitudinal contraction to a greater extent than healthy individuals and HCM patients.11 w29 This suggests that exercise echocardiography might help to distinguish physiological from pathological forms of hypertrophy.


In summary, subclinical LV dysfunction, which can be seen with STE, is common in LVH. Studies using STE have clearly demonstrated that the different causes for hypertrophy show specific ‘deformation’ and myocardial motion patterns. In particular, longitudinal deformation is impaired in pathological states. STE could help to differentiate between physiological and pathological causes of hypertrophy.

STE in dilated cardiomyopathy

Dilatation of the LV in dilated cardiomyopathy (DCM) is a compensatory mechanism that ensures an adequate stroke volume in the presence of impaired LVF. LV remodelling eventually leads to a spherical LV which further reduces systolic LV function due to inefficient myocardial fibre interplay. While stroke volume is still normal in the early stages of disease, fibre shortening can already be reduced. As the disease progresses, EF eventually drops.

Global longitudinal, circumferential, and radial strain and corresponding systolic, early and late diastolic SRs are all reduced in patients with idiopathic DCM.12 The degree of impairment also correlates well with EF. A subset of patients with DCM displays an abnormal apical and basal rotation pattern (opposite basal or apical rotation).12 w35 Additionally, a ‘longitudinal rotation’ has been described which refers to a ‘swinging motion’ of the LV apex during systole if imaged in a horizontal long axis plane.13

Other aspects of DCM have also been studied. An interesting finding is that of a reduction in peak atrial systolic strain in the setting of idiopathic DCM. This suggests that the atrial myocardium is also affected in the disease process.14


In conclusion, STE could be an important tool to assess patients with DCM. It allows early detection of LV contractile dysfunction and provides information on segmental and global contractile function on top of LVEF. STE could, thus, be a more subtle modality to monitor LV dysfunction and even permit us to assess the effects of treatment (ie, pharmacotherapy). Furthermore, the analysis of myocardial mechanics and regional deformation abnormalities in these patients could aid in the differential diagnosis between ischaemic and dilated cardiomyopathy. The potential of STE in the setting of dyssynchrony will be described in the following section.

STE and dyssynchrony

Cardiac resynchronisation therapy (CRT) has become an important pillar in heart failure treatment. Numerous echo parameters have been tested to aid in the selection of candidates. However, no single parameter is currently able to predict the response to CRT accurately.w36 This is also true for TDI which has several limitations and lacks reproducibility and robustness. STE could overcome some of the shortcomings of TDI. Quantification of dyssynchrony requires the assessment of temporal and regional changes of strain/SR. It is as yet unclear which component of strain/SR and which timing interval best describes dyssynchrony. Suffoletto and Delgado proposed the radial strain component (interval defined by time difference of peak systolic septal wall to peak systolic posterior wall strain of 130 ms and above) (figures 6 and 7).15 16 w35 w37

Figure 6

Systolic frame of speckle tracking echocardiography derived radial tissue velocities in a patient with cardiomyopathy and dyssynchrony. Note that movement of septum is opposed to that of the remaining left ventricular wall.

Figure 7

Right: Radial strain curves and curved M mode in the same patient as in figure 6. Asynchronous contraction is reflected by temporal dispersion of positive strain peaks between different segments. The occurrence of negative radial strain indicates thinning/stretching of myocardium. Left: normal strain distribution and timing in a patient with synchronous contraction. AVC, aortic valve closure.

Since STE can distinguish between actively and passively stretched LV segments, it could allow quantification of scar burden in potential CRT candidates with ischaemic cardiomyopathy. This is important since the magnitude of scar burden is inversely correlated to CRT response. The absence of passively stretched LV segments in apical four chamber view during systole (two dimensional STE longitudinal strain +5% or above) seems highly sensitive for CRT response.17 Furthermore, STE assessed global longitudinal LV strain proved to be a good parameter reflecting overall LV scar burden compared to MRI in patients suffering from ischaemic dilated cardiomyopathy.w38

Because STE is the more sensitive parameter for LV dysfunction, and since it also allows assessment of regional function, STE derived strain could be a valuable parameter for defining CRT response. This is a relevant issue, since it could help explain why many patients exhibit a clinical response to CRT but no measureable increase in EF.

Different display formats of regional STE strain (ie, bull's eye approach) can help to document regional improvements of contractile function. In addition, temporal curves of strain/SR also show the magnitude of resynchronisation with CRT. This could also be of value in the selection of optimal pacing site and in pacing (VV) optimisation of CRT.15 w39 w40

STE and dyssynchrony

In conclusion, STE appears particularly attractive for the selection and follow-up of candidates for CRT. STE has many advantages compared to TDI and is more practical. The extent of dyssynchrony can be quantified with STE. STE permits assessment of ‘scar burden’ and is a more subtle tool for determining regional and global function. STE might also be useful for the optimisation of CRT and for determining the optimal pacing site during implantation.

STE in other conditions

STE can be used to monitor LV systolic function in several disease entities. For example, longitudinal peak systolic strain is reduced in patients with type 2 diabetes.w41 Other conditions in which STE has been studied include: patients with heart failure and normal EF, catheter ablation for atrial fibrillation, tako-tsubo cardiomyopathy, Cushing syndrome, rheumatoid arthritis, atrial septum defect or Fabry disease (figure 8).w42–w50 Abnormal patterns of contraction which denote subclinical disease could be found in all of these disease states. Furthermore, these studies underline the superiority of STE to LVEF in detecting LV dysfunction.

Figure 8

Patient with Fabry disease with normal ejection fraction (68%). Speckle tracking analysis of longitudinal (A–C) and radial function (D). (A) Post-systolic index; (B) longitudinal peak systolic strain; (C) peak systolic strain rate; (D) radial function. Note that longitudinal function is significantly reduced (global longitudinal peak systolic strain (GLPSS) −6.5%). The apical segments in particular show a reduction in longitudinal strain. There is also delayed contraction in the apical and mid posterior segments (A). Peak strain rate is also reduced (C); radial function (D) is nearly normal.

In addition, STE is able to detect the immediate and long term effects of drug treatment on the heart. For example, STE and TDI based strain/SR imaging has been used to study the cardiotoxic effects of chemotherapies and monoclonal antibody therapy.w51 w52 Subtle cardiac abnormalities could be observed shortly after administration of anthracyclines or trastuzumab, even at low doses.18 w51 These findings suggest that LV systolic impairment—and not diastolic dysfunction—is the predominant effect of chemotherapy.

An interesting further application of STE is the assessment of atrial function, which is still in its early stages but which could open an entirely new array of indications.19 w53–w55

STE and other conditions

In summary, STE is able to detect ‘subclinical’ systolic dysfunction in numerous disease entities. STE provides new insights into the role of the heart in non-cardiac diseases. It allows earlier detection of systolic dysfunction, provides prognostic information, and could possibly also be used to monitor treatment effects.

STE and the right ventricle

Several factors must be considered when assessing right ventricular (RV) function with STE. Compared to the LV, the RV is thinner, more trabeculated, and the interventricular septum contributes mainly to the contraction of the LV versus the RV (tethering effect). Studies with STE and other techniques have also demonstrated that the contraction mechanics of the RV differ significantly from that of the LV.w56 Furthermore, the pulmonary circulation is a low resistance system compared to the systemic circulation. All these factors make it more difficult to obtain and interpret speckle information from the RV.

Most experience with STE in the setting of RV function has been gathered by using regional and global peak systolic longitudinal strain. Since the RV mainly contracts in a longitudinal direction, this component of deformation probably best reflects RV function. Computation of longitudinal deformation using STE is feasible, reproducible, robust, and compares well with TDI measurements. However, the effects of preload and afterload on STE derived measured deformation parameters and the distribution of myocardial velocities, strain, and SR throughout the RV still remain unclear.w57–w60 Clinical studies have shown that STE permits assessment of RV function in many disease entities:

  • Deformation parameters are reduced in pulmonary hypertension in a graded manner (figure 9).20

  • RV segmental and global longitudinal peak systolic strain is reduced and delayed in patients with acute pulmonary thromboembolism. All these effects are reversible upon treatment.21

  • Deformation abnormalities are present in patients with systemic sclerosis even in the absence of pulmonary hypertension.w61

  • Longitudinal strain values improve after pulmonic valve replacement.w62

  • Patients with atrial septal defects have elevated global peak systolic strain values which normalise after interventional occlusion.w63

  • Patients with arrhythmogenic right ventricular cardiomyopathy show an abnormal contraction pattern.w64

Figure 9

Speckle tracking echocardiography in a healthy normal control with normal right ventricular (RV) function (global longitudinal peak systolic strain (GLPSS) −25.9%) and normal systolic pulmonary artery pressure (sPAP) (28 mmHg) (A); a patient with moderately reduced RV function (GLPSS −17.0%) and sPAP of 75 mmHg (B); and a patient with severely reduced RV function (GLPSS −14.0%) and sPAP of 70 mmHg (C). Patient B and C both have precapillary pulmonary hypertension.

STE and the RV

In summary, data on the potential clinical application of STE for the RV is rapidly evolving. Many questions, however, remain unanswered. Which parameter should be used to assess RV function? Are deformation parameters affected by changing preload and afterload conditions? What are the prognostic and clinical implications of these findings? In addition, it will be necessary to modify the analysing algorithms and quantification tools of STE to account for the many factors that distinguish the RV from the LV.


STE is an exciting new field in echocardiography. The potential to easily derive deformation parameters from two dimensional images without the limitations of TDI makes STE an appealing tool for clinical and investigational echocardiography. Much of the early findings with TDI is reproducible with STE. STE provides important information on ventricular function, and is able to detect subclinical disease. This opens a broad spectrum of new clinical applications including cardiomyopathies, hypertrophy, valvular heart disease, and systemic disorders which can affect the heart. The possibility to detect and distinguish ischaemic syndromes could have a major impact on the diagnosis and management of CAD. STE can also be used during stress testing, which further enhances its diagnostic yield both in CAD and in valvular heart disease. STE can help to refine treatment strategies such as the timing of surgery in valvular heart disease. Finally, STE could play an important role in the assessment of dyssynchrony and diastolic function, and in quantifying RV function. A major endeavour will now be to test the validity of this method on a larger scale and to relate measurements of STE to hard end points.

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  1. This review extensively outlines the alterations of LV deformation parameters in the setting of acute or chronic ischaemia (at rest and during dobutamine stress).

  2. This study shows that STE is a reliable method for identifying severe CAD at rest in patients without regional wall motion abnormalities.

  3. Cramariuc and co-workers showed that a lower longitudinal LV strain was linked to a more severe degree of aortic stenosis, to a higher LV mass, and a concentric LV geometry.

  4. This paper investigated the altered myocardial mechanics in idiopathic dilated cardiomyopathy by means of STE. Opposite basal and apical LV rotation could be observed in some patients.

  5. This study used STE technology to evaluate left atrial myocardial function and showed impairment of atrial contraction in patients with idiopathic dilated cardiomyopathy.

  6. Reference values for left atrial longitudinal strain.

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