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| TECHNOLOGY |
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| Year : 2002 | Volume
: 3
| Issue : 1 | Page : 3 |
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Technology-A: Tissue doppler imaging in coronary artery disease
Gabriel W Yip, Steve R Ommen
Division of Cardiovascular Diseases and, Internal Medicine, Mayo Clinic, Rochester, Minnesota, USA
| Date of Web Publication | 22-Jun-2010 |
Correspondence Address:
Steve R Ommen
Mayo Clinic, 200 First Street SW, Rochester, MN 55905
USA
 Source of Support: None, Conflict of Interest: None  | Check |
 Abstract | | |
Tissue Doppler imaging (TDI) has rapidly evolved over the last decade as a sensitive clinical tool of measuring both global and regional myocardial velocities and their relationship to the cardiac cycle with high spatial and temporal resolution.
Measurement of mitral annular velocities reflects global left ventricular LV function at rest or during stress echocardiography.
Regional analysis of peak segmental systolic myocardial velocities during stress improves accuracy of novice readers, of interpreting basal segments, and concordance between observers.
Moreover, it has higher sensitivity and comparable specificity to standard dobutamine stress echocardiography in detecting myocardial viability.
Myocardial velocity gradient, being independent of cardiac translational movement, has also shown promise for detecting resting and induced ischemia and viable myocardium. Strain rate imaging (SRI), based on tissue Doppler technology, has clinical potential of quantitative assessment of regional contractility and function during stress echocardiography. Abnormal wall motion during isovolumic contraction and relaxation periods and their clinical implications of correlating myocardial viability has been discussed. Improved data acquisition and rapid post-processing of TDI will facilitate its incorporation into standard regional myocardial assessment.
How to cite this article:
Yip GW, Ommen SR. Technology-A: Tissue doppler imaging in coronary artery disease. Heart Views 2002;3:3 |
| 1.Background | |  |
1.1 Detection and assessment of coronary artery disease
Coronary artery disease (CAD) remains the leading cause of death in the USA, causing one in every 4.9 deaths and over 12 million people report a history of angina, previous heart attack or both [1].
Accurate early identification of CAD is critical in reducing morbidity and mortality. Stress echocardiography is widely used to diagnose flow-limiting CAD. In general, exercise and pharmacologic stress echocardiography are more sensitive in detection of myocardial ischemia than electrocardiographic variables and have evolved as cost-effective alternatives to nuclear methods [2],[3],[4].
Traditional diagnostic criteria of regional dysfunction are based on detection of: 1) regional delay in myocardial motion, 2) differences in amplitude and direction of regional wall motion and 3) regional wall thickening and thinning characteristics. Unfortunately, most stress-echo interpretations are still based on subjective visual recognition of abnormalities of wall motion or thickening with segments scored in a semi-quantitative manner.
Furthermore, issues of reproducibility [5] and requirement for adequate training [6] are also important limitations of the technique.
An objective and quantitative assessment of regional wall motion should enhance concordance between interpreters and improve accuracy of the novice readers.
In this regard, tissue Doppler echocardiography (TDI) and strain rate imaging (SRI) - an evolving technology of the former, may herald an improvement in the noninvasive assessment of regional myocardial function.
1.2 Evolution of tissue imaging
Tissue Doppler imaging (TDI) is an extension of conventional Doppler flow echocardiography and has been proven to be a useful and feasible clinical tool for assessing global as well as regional ventricular function since its introduction in the early 90s. Isaaz et al [8] pioneered pulsed-wave Doppler measurements of myocardial wall velocity and mitral annular motion in the late 1980s. In 1994, Sutherland et al [9] and Yamazaki et al [10] introduced color-coded Doppler myocardial imaging which recently became a standard built-in technology in many commercially available equipment packages.
TDI has been validated both in vitro [11],[12] and in vivo [13],[14],[15],[16],[17] . It has been clinically applied in assessing regional and global left ventricular (LV) systolic [18],[19] and diastolic function [20],[21],[22],[23],[24] ; estimating the LV filling pressure in various clinical states [25],[26],[27],[28],[29] and detecting allograft rejection in cardiac transplant recipients [30],[31],[32],[33].
It helps in differentiating constrictive pericarditis from restrictive cardiomyopathy [34],[35] , differentiating athletic heart from hypertrophic cardiomyopathy [36] , and detecting hypertrophic cardiomyopathy (HCM) gene carriers even in the absence of fulminant phenotypic expression [37].
This review will examine the role of tissue Doppler techniques (myocardial velocity assessment and strain rate imaging) in the detection of coronary artery disease.
| 2.Physical Basis and Technical Aspects | | |
2.1 Tissue Doppler Imaging
The pulsed and color Doppler echocardiography can detect motion and velocity of both moving blood and myocardial tissue.
We have traditionally processed blood flow signals in the conventional Doppler flow imaging, so that the high velocity and low amplitude Doppler signals reflected by the moving blood are measured whereas the myocardial Doppler signals with high amplitude but low velocity are suppressed.
To better analyze myocardial signals, the high-pass filter used to optimize blood flow signals is minimized. In addition, a signal intensity threshold filter has to be altered with lower gain amplification to eliminate the weak intensity of blood flow signals.
These improve the ability to measure low velocity myocardial signals that are typically in the range of 0.6 - 24 cm/s. TDI analysis, with generally favorable signal to noise ratio, is relatively independent of 2-dimensional image quality. Another important aspect of the TDI is high frame rate image acquisition, which is crucial for temporal resolution. With digital parallel processing techniques, frame rate of >150 frames per second can be achieved with increased pulse-repetition frequency (PRF) and narrow sector angle of region of interest (ROI).
As in the blood flow Doppler, the myocardial velocity can be assessed using pulsed-wave or color-encoded for both speed and direction. Color Doppler allows for visual semiquantitation of myocardial motion, superimposed on conventional M-mode and two-dimensional images. However, the color-encoded TDI signal processing gives mean velocities whereas real-time pulse-Doppler analysis represents the highest peak velocity from the sample volume selected. With narrow sector angle, the color TDI has now achieved a temporal resolution comparable to the pulsed-wave Doppler but requires off-line analysis that can be time-consuming and the facility may not be widely available. Using specific software, the color Doppler data can also be processed to display in-color M-mode, by drawing a straight or curve line anywhere within the color available. Such anatomically curved TDI M-modes display direction, timing and synchronicity of motion with high frame rates (5-20msec) within the selected segments.
In order to optimize the TDI signals, the color gain should be set to level just below the color-noise artifact. The upper velocity range for the myocardial velocities should also be maximized to a level just below the highest velocity recorded at rest or during stress echocardiography so as to enhance sensitivity of velocity measurement. The usual setting of the upper limit of the velocity scale is around 14 to 20cm/sec for both resting and stress TDI. The myocardial velocity data can then be analyzed real-time or off-line by computer workstation.
As mentioned, pulse-waved TDI as opposed to color-coded TDI measures peak, rather than mean myocardial velocities. It does not require off-line analysis and provides instantaneous temporal display of Doppler spectral velocity data [Figure 1]. The sampling, however, cannot be localized to the endocardial or epicardial layers. While requiring off-line analysis, color Doppler has the advantage of simultaneously acquiring multiple segments in one view and this is particularly useful within a limited acquisition window of stress echocardiography [Figure 2].
2.2 Strain rate imaging
First introduced in 1973 by Mirsky and Parmley [40] , strain (e) and strain rate (SR) are measures of regional myocardial thickening and thinning of the heart muscle. Myocardial strain is a dimensionless index of change in myocardial length in response to an applied force. Strain rate is the time derivative of strain with unit of change per second (sec -1) and represents the differential velocity of two points adjusted for the distance between them [Figure 3]. Strain rate imaging (SRI) is therefore an extension of technology derived from the tissue Doppler imaging (TDI).
Previously, intrinsic myocardial deformation or strain was invasively measured by tracking movement of implanted radio-opaque markers (eg., metallic beads) by biplane cineangiography [41],[42] or video technique [43] , measuring mutual motion and angulation of three needles pierced into the myocardial wall, using an electromagnetic inductive technique [44] , or by sonomicrometry in the myocardium [45].
Now both parameters (strain and strain rate) can be derived non-invasively from either magnetic resonance imaging (MRI) tagging techniques [46],[47],[48] or echocardiography using M-mode [49],[50] or more commonly high frame rate (>150 frames/sec) tissue Doppler velocity data after post-processing [51],[52] [Figure 4],[Figure 5]. These non-invasive techniques overcome the inherent limitations of overall cardiac translation and motion influence by adjacent segments in assessment of local intrinsic LV function [53].
It is important to note that the MR and echo techniques assess different strains that are not interchangeable. There are inherent strengths and weaknesses to each that are beyond the scope of this review.
2.3 Myocardial velocity gradient
The MVG is simply a measure of regional radial strain rate of a small area of myocardium. Unfortunately, based on processed color-encoded velocity data, it lacks spatial resolution and, therefore, may not detect lower strain rate. Technical development of on-line, high speed and large quantity image acquisition and storage system together with an automated myocardial edge detection technique should facilitate such application in future. Normally, the endocardium moves faster than the epicardium except during isovolumic relaxation when the reverse is seen. Thus, there is a gradient of increasing velocity from the epicardium to the endocardium as myocardial wall thickens in systole, which can be served as a marker of regional contractility. The myocardial velocity gradient (MVG) can be obtained from color M-mode recording of anteroseptal or posterior wall from parasternal position using either high frame rate M-mode data [38] or lower frame rate (up to 59 frames/sec) two-dimensional data [39].
Several other methods, including centerline methods [54] , color kinesis [55] , and automatic boundary detection [56] have been proposed to aid qualitative interpretation of wall motion scoring and to give some semi-quantitative measure of regional contractility. In general, these methods require reasonable endocardial border definition and /or lengthy time for post-acquisition data analysis.
| 3. Clinical Application of Tissue Doppler Techniques | | |
3.1 Myocardial Velocity Assessment (Standard TDI)
3.1a Global assessment of LV function to detect CAD
The global LV systolic function can be assessed by peak mitral annular (MA) velocity in apical views.
Although myocardial synchronous contraction and relaxation depends critically on coordination of circumferential and longitudinal fibers, the longitudinal fibers are particularly vulnerable to myocardial ischemia and activation disturbance likely related to their subendocardial position [57].
Because the epicardial apex is relatively fixed [58] , the longitudinal fiber shortening draws the atrioventricular ring towards the apex of the ventricle. Not only does this contribute to the fall in the left ventricular cavity volume with ejection, but at the same time increases the volume of the left atrium.
Similarly, during diastole, the backward movement of the atrioventricular ring aids the LV filling. Dumesnil et al.
showed that with a 40% decrease of LVEF (M-mode) in disease, there might be only 15-20% corresponding decrease in the circumferential fiber (short-axis) shortening [59] , highlighting the significant contribution of longitudinal fibers in overall LV function.
Since the introduction of the concept of mitral annular descent by echocardiography in 1967, it has been shown that the peak systolic mitral annular amplitude and total excursion correlate well with LV stroke volume [60],[61],[62],[63] . Its amplitude and velocity have been used as an index of ejection fraction (EF) and been shown to correlate with the LVEF obtained by radionuclide ventriculography in humans [64],[65],[66].
The systolic MA amplitude also predicts mortality in patients with chronic heart failure [67] . Decreased MA excursion was demonstrated during balloon angioplasty [68] and was normalized within 48 hours of a successful procedure [69] . The asynchrony of a particular annular site correlates with reversible defects on thallium myocardial perfusion [70] , and with distribution of coronary stenosis by angiography [71] . Additionally, the MA motion shown to be abnormal just before vein grafting in coronary artery disease normalized within four hours of operation [72] . The regional asynchrony as reflected by the timing, amplitude and velocity of the MA motion is further aggravated by dobutamine stress [73] . The asynchrony can occur in the absence of symptoms and ECG changes and thus provides sensitive, non-invasive and highly reproducible evidence of ischemia.
Tissue Doppler not only defines and measures the mitral annular movement, but also gives high temporal relationship. Decrease in peak systolic descent velocity at a mitral annular site with corresponding longer time to peak correlates with LV asynergy and infarct regions in patients with previous myocardial infarction [74] . Henein et al demonstrated that a combination of systolic and diastolic long axis disturbances at rest in patients with peripheral vascular disease can be used to predict peri-operative surgical risk as assessed by adenosine thallium emission tomography [75] . They proposed a long axis score that could stratify these patients into two categories of high or moderate/ low risks. However, general application of this score in other population groups with different pre-test likelihood of coronary disease is still unknown. The sensitivity and specificity of the scoring and whether it could further stratify lower risk group require further study.
The mitral annular velocity has also been shown to be a sensitive marker of alteration of LV contractility induced by inotropic stimulation. In studying 12 normal volunteers, Gorcsan et al. showed that peak mitral annular velocity increased significantly with corresponding decrease in time to peak velocity at very low dose (1mcg/kg/min) dobutamine. A further linear dose-dependent incremental increase of the velocity was observed up to the target infusion of 5mcg/kg/min [76] . In contrast, regional peak velocities did not change until the 2mcg/kg/min dose and no change of myocardial wall thickening and ejection fraction was observed until 3mcg/kg/min. These data support the mitral annular velocity as a sensitive marker of global systolic function, even when the endocardial definition is suboptimal for estimation of LV volumes and ejection fractions. The MA velocity provides important insight in terms of amplitude, velocity and timing in relation to the cardiac cycle.
3.1b Regional assessment of LV function for detection of CAD
For detection of induced myocardial ischemia, assessing abnormal regional function within each vascular territory may be more important than the global function. Measurement of the annular displacement reflects abnormality in each wall and does not allow a segmental evaluation pertaining to a vascular territory.
Segmental TDI can quantitate the extent of abnormal myocardium and also detect regional delays in the onset of motion, which has been shown to precede changes in regional myocardial systolic amplitude of motion [77] . TDI assessment is more accurate and objective than human visual assessment, which can, at best, detect motion delays of 89 ms (or about 70 ms if abnormal image is viewed side-by -side with the normal) [78] . By comparison, Derumeaux et al. demonstrated that TDI can detect a 30 msec prolongation of isovolumic relaxation time during acute animal ischemia which correlates with >70% stenosis of the culprit artery [79] . Regional delay in myocardial motion is, therefore, an important early marker of ischemia. The accurate identification and quantification of delays, amplitude and velocity of regional wall motion during both rest and stress echocardiographic studies should improve both the sensitivity and specificity of ischemia detection.
Both pulsed-wave and color tissue Doppler velocity have been used to quantify regional wall motion changes with dobutamine stress echocardiography and exercise echocardiography. However, it has been shown that dobutamine results in greater regional systolic myocardial velocities than maximal exercise, and enhances the differences between ischemia and normal zones [80].
In experimental settings, myocardial velocity has been shown to accurately reflect changes in regional and global LV function induced with dobutamine, esmolol, and ischemia [81],[83] . In humans, differential changes of the systolic velocity during stress have correlated with normal, ischemia, and scar responses interpreted by standard wall motion scoring. The ischemic segments have lower resting systolic velocity than the normal segments while scarred segments are even slower than ischemic segments. Both scar and ischemic segments have lower peak systolic velocity with blunted incremental response to stress than the normal segments. Furthermore, these velocity changes correlate well with abnormalities on myocardial perfusion imaging. Heart rate, functional capacity and regional dysfunction (scar or coronary ischemia) are independent determinants of peak exercise myocardial velocities [86],[87].
It is recognized that there is a gradual decrease of the longitudinal myocardial velocities from the base to the apex. This results from a relatively stationary apex and differences in myofiber orientation. Having established good correlation between regional LV dysfunction and peak systolic myocardial velocity, the next step toward clinical application is to identify normal ranges for different myocardial segments and then apply these as diagnostic criteria for the identification of significant coronary artery disease.
Katz et al. studied 60 patients, aged 56 ±10 years to determine the normal and abnormal segmental velocity response to dobutamine stress and the sensitivity, specificity and accuracy of TDI in detecting abnormal wall motion at peak stress [83] . Two groups of patients receiving comparable dobutamine and atropine dosages were identified: 21 patients had normal stress echocardiography and reached target heart rate at peak stress and serve as control, whereas 19 had abnormal wall motion at peak stress. Apical segments in the long axis were excluded because of significantly lower myocardial velocities and unfavorable wide angle of incidence with respect to the transducer. A peak of systolic velocity of 5.5cm/sec or less with the peak stress was found to have an average sensitivity of 96%, specificity of 81% and accuracy of 86% for identifying abnormal segments at peak stress as defined by routine 2-dimensional criteria.
Cain et al. studied 242 patients undergoing standard dobutamine stress echocardiography and recording myocardial velocities using TDI at rest and peak stress and establishing site-specific normal ranges for basal and mid-ventricular segments [88] . 114 consecutive patients underwent coronary angiography within 2 months of the stress echocardiography. 128 patients had a normal dobutamine stress without angiography, including 57 patients with a low (18 ±15 %) pretest probability of coronary artery disease. The 2-dimensional stress echo was interpreted by an expert reader blinded to patient's clinical, angiographic, and the myocardial velocity data. Sensitivity and specificity of wall motion scoring and myocardial peak systolic velocities were obtained by comparison with angiographic evidence of coronary artery disease (>50% diameter stenosis). The wall motion scoring and peak systolic myocardial velocity yielded comparable sensitivity (88% vs 83%) and specificity (81% vs 72%) and similar overall accuracy (86% vs 80%) (all p-values not significant). Interestingly, inexperienced users measuring the myocardial velocities obtained high intraobserver as well as interobserver concordance with an expert. Similar to previous reports of interobserver variation of 10% or less [84] , this study confirmed high reproducibility of TDI measurements. This is an important advantage if integrated into stress echocardiographic interpretation. In a subsequent study, these same authors have suggested a hybrid approach of combining wall motion scoring in the apical segments and myocardial velocity assessment in other segments for eventual clinical application of this technique [89] . The multicenter, crossover study of 77 patients who underwent harmonic dobutamine stress echocardiography and subsequent coronary angiography, showed that integration of regional myocardial velocity data into stress echocardiographic interpretation would improve accuracy of novice readers, of interpreting basal segments, and in interobserver variability.
Early attention focused on measurement of peak systolic velocity as the parameter likely to be most useful in assessing regional LV systolic function with stress, but more recently other parameters such as the time to peak systolic velocity and the velocity time integral (i.e., total systolic displacement) have been proposed as equally important measures [90] . The multicenter, multinational MYDISE study (MYocardial Doppler In Stress Echocardiography) is an ongoing study assessing the feasibility and reproducibility of these TDI methods. Early results indicate that TDI does enhance both objectivity and reproducibility of stress echocardiography [91].
3.1c Use of TDI velocity assessment in myocardial viability
There are many reports on clinical feasibility of TDI in the setting of induced ischemia during stress echocardiography, but fewer reports on the clinical potential of tissue Doppler imaging in detecting myocardial viability. Rambaldi et al. reported detection of hibernating myocardium in 40 patients with chronic ischemic heart disease and LV dysfunction (mean EF 3311%) using regional peak systolic myocardial velocity during dobutamine stress echocardiography. F18-fluorodeoxyglucose single photon emission computer tomography (FDG-SPECT) served as the reference [92] . The baseline regional peak systolic myocardial velocity did not differ between viable and non-viable segments. However, viable myocardium showed higher systolic velocities at low and peak-dose dobutamine than non-viable segments. An increase in regional systolic velocity low-dose of >10·5 cm/s predicted viability. For the prediction of viability, the sensitivity (95%CI) of pulsed-wave Doppler was significantly better than standard dobutamine stress echocardiography {87%(82-92) versus 75% (67-81)}, while the specificity {52%(44-59) versus 51% (45-59)} was comparable.
3.1d Limitations of TDI
Like many other regional quantitative myocardial indices, tissue myocardial velocity is affected by cardiac translation. Moreover, adjacent ischemic or scarred segments may affect normal segments through "tethering" of their motion, thus lowering the measured velocity, and conversely, normal segments may augment the velocity in abnormal segments. Because of a relatively fixed epicardial apex and a longitudinal velocity gradient from base to apex, apical velocities are close to zero and differentiating normal from abnormal apical segments based on their myocardial velocity is difficult.
To partially circumvent this problem, the imaging window is narrowed to a sector angle of 20-30 for imaging individual ventricular wall with tilting in an apical view so that the whole wall is parallel to sampling cursor. In this way, the frame rate is enhanced, and the proximal one-third of the apical segments can be measured for myocardial velocities within acceptable angle of insonation.
3.2 Myocardial strain rate imaging
Because strain and strain rate are derived from the motion of segments relative to each other, tethering and translation will affect both velocity vectors equally and are therefore minimized. Measurement of strain at one site reflects function at that site and therefore might be expected to have greater spatial resolution than tissue Doppler velocity data alone. Normally, the longitudinal strain rates in the anterior and septal walls are comparable but higher than those in the antero-lateral and infero-lateral walls [93].
Myocardial strain derived from color tissue Doppler data promises to improve the quantitation of regional myocardial contractile function in the future.
The regional strain values have been validated to correlate with those obtained from sonomicrometry in an acute ischemic canine model [53] . The real-time color SRI was shown to have moderately good correlation (weighted k of 0.55) with the wall motion score of standard echocardiography in 15 patients with acute myocardial infarction [94] and also in identifying infarct related artery of 20 similar patients (weighted k of 0.64) undergoing coronary angiography [95].
Voigt et al. compared 12 patients with history of transmural myocardial infarction with 10 normal controls and found that longitudinal peak segmental systolic strain and strain rate decreased with increasing wall motion score [96] . Edvardsen et al showed that longitudinal segmental systolic strain and strain rate are more sensitive in detecting regional myocardial ischemia than tissue Doppler velocity measurements in patients undergoing percutaneous coronary intervention [97].
In the canine model, reduced systolic strain appears earlier than tissue Doppler velocity abnormality and semi-quantitative visual wall motion abnormalities in acute ischemia [98] . Using closed chest animals, the strain rate has been shown to correlate linearly with maximal value of the first LV pressure time derivative (dP/dtmax) and peak elastance(Emax), both global measures of LV systolic function or contractility [99],[100] . In both normal human and stunned porcine myocardium, the dobutamine-induced increase in systolic strain rate (SR) preceded the increase in strain itself (e) and the increase in LV systolic wall thickening [76],[99].
An increase of peak systolic strain rate of more than -0.23 per sec from rest during low-dose dobutamine discriminates viable from non-viable myocardium, as determined by 18F-fluorodeoxyglucose positron emission tomography (FDG PET). The regional SRI compares favorably with TDI with better sensitivity (83% vs 69%) and specificity (84% vs 64%) in the detection of myocardial viability [101].
All these indicate that segmental strain rate analysis has a promising and potentially superior role than tissue Doppler imaging in quantitative assessment of regional contractility and function during stress echocardiography.
3.2a Myocardial velocity gradient in detection of induced ischemia and viability
The MVG has an advantage of being independent of translational movement of the heart [102] . Secondly, it is more sensitive in differentiating ischemic from non-ischemic segments in submaximal dobutamine challenge than either endocardial velocity measurements or wall motion abnormality [103].
It detects resting regional myocardial dysfunction in post-MI patients with single vessel coronary disease [11],[103] and induced ischemia during submaximal dobutamine stress echocardiography in patients with single vessel coronary disease, prior MI and preserved LV function [104] . It has been used in distinguishing viable from non-viable segments during low-dose dobutamine in patients with significant chronic triple coronary disease (>70% diameter narrowing) and LV dysfunction (LV ejection fraction <50%) [105].
3.2b Abnormal left ventricular wall movement during isovolumic periods
Recently, there has been a renewed research interest in clinical significance of inward wall movement during the isovolumic contraction (IVCT) and relaxation (IVRT) period detected either by TDI or SRI in ischemic and post-ischemic myocardium. During coronary occlusion in dogs, most of the systolic lengthening occurs during IVCT and most of the subsequent shortening during the IVRT with more rapid change of LV pressure during these phases than during ejection [106] . Thus, the abnormal wall motion during these periods may serve as better measures of regional LV function than peak wall motion during systole.
3.2c Post-ejection wall motion
The delay of segmental longitudinal or radial LV contraction until after the aortic valve closure is termed as post-systolic shortening (PSS) or thickening (PST) respectively. PSS (or PST) represents LV asynchronous wall motion during IVRT period [Figure 6] and has major effects on subsequent ventricular filling [107] . However, it is uncertain whether it directly causes or indirectly worsens global LV diastolic dysfunction. It has been reported in clinical conditions other than myocardial ischemia or stunning, e.g., activation abnormalities as in left bundle branch block [108] , syndrome X [109] , hypertrophic cardiomyopathy [110] and aortic stenosis [111] . Possible mechanisms have been postulated. It may be due to delayed active contraction after reduction of regional wall stress and relaxation of other adjacent LV segments, or to delayed passive inward movement caused by adjacent normal contracting LV segments as the LV pressure rapidly falls and the regional wall stress decreases.
However, whether postsystolic shortening and thickening might represent an active, or passive process, its clinical implications are still in debate. Gibson et al. noted delayed inward motion during isovolumic relaxation as a common finding in patients with acute myocardial infarction using digitalized ventriculography at a data acquisition rate of 50 frames/sec but that invariably resolved after successful reperfusion [112] . Using sonomicrometry in an acute ischemic canine model, the degree of PSS correlates with regional systolic function immediately after reperfusion and also late functional recovery 2-3 weeks after the reperfusion [113],[114].
Based on centerline method of analyzing endocardial wall motion in 35 patients with acute myocardial infarction undergoing ventriculography before and after angioplasty, PSS in the infarct region predicts recovery after reperfusion [115] . In 23 patients with angiographically proven significant coronary artery disease, 98% of all hypo- and akinetic regions with PST and only 6% of those without PST improved at low dose dobutamine stress-echo. Furthermore, 92% of segments with PST and 38% without PST improved after revascularization [116] . All these indicate that PSS (PST) is related to myocardial viability. Larger clinical trials are needed for defining its role in myocardial viability.
One of the potential clinical applications using SRI in detecting PST is differentiation of ischemic from reperfused yet stunned myocardium during dobutamine stress echocardiography. In closed chest porcine model, total and graded ischemia results in delayed onset and decrease in regional systolic strain and strain rate but increased post-systolic thickening [117],[118] . Dobutamine infusion causes a further decrease in maximal regional strain and concomitant increase in postsystolic thickening in persistent ischemic segments, whereas it normalizes regional PST gradually with further increase in systolic strain and strain rate at higher stimulation in the stunned myocardium [99].
SRI can also depict segmental PSS as a prolonged transition from myocardial compression to expansion i.e., prolonged time from peak R wave on ECG to compression/expansion crossover (TCEC) [Figure 7]. Using this new parameter, prolonged TCEC correlates with and spatially quantifies ischemic myocardium measured from both stained porcine myocardium [119] and perfusion defects from myocardial contrast echocardiography [120] . An initial study of 40 patients suggests that this new parameter is feasible with additional 5 minutes of SRI to standard dobutamine stress-echo time. In normal myocardial segments, TCEC at peak stress decreases significantly from baseline but this response is attenuated in ischemic segments. Using a 20% reduction of TCEC as cut-off based on receiver operator characteristic curves, sensitivity and specificity for detection of ischemic segments were 77% and 55% respectively with corresponding values of 62% and 88% for standard dobutamine stress-echo [121].
3.2d Pre-ejection velocities
ntraction represent asynchronous and rapid myocardial contraction after ventricular activation but before aortic valve opening, resulting in minor changes in the LV volume and wall thickness. Similar to postsystolic thickening in the IVRT period, they are also sensitive to acute myocardial ischemia and correlates with transmural myocardial infarct[Figure 8]. It has been shown in acute ischemic animal models that segmental IVCT velocities decreased to zero when >20% transmural necrosis was involved in the corresponding segment after staining. The IVCT velocities also correlated better with extent of transmural infarct after reperfusion than segmental peak systolic and early diastolic velocities [122] . Thus, the resting segmental IVCT velocity potentially provides a rapid clinical, non-invasive bedside technique of quantifying transmural extent of viable myocardium after reperfusion in acute myocardial infarction.
Strain and strain rate measurements have their technical limitations. Similar to any Doppler techniques, they are highly dependent on angle of insonation. Every effort is made to ensure the tissue direction is less than 30o from the beam direction but this is technically challenging in the apical segments as the angle becomes wider. The narrow sector angle approach on individual wall obviates some of the above problem. But it lacks of concurrent comparison of regional wall motion with contralateral segments. Like myocardial Doppler velocities, strain is markedly load-dependent [53].
| 4. Future Directions | | |
Further clinical trials will be needed for determining sensitivity, specificity and accuracy of using individual segmental strain and SR parameters or in combination, for detecting induced ischemia by either exercise or pharmacological stress, and also their clinical role in assessing myocardial viability either at rest or with low-dose dobutamine. Furthermore, whether delayed onset of regional asynchrony is better than strain and SR indices in detection of induced ischemia will require further clinical validation.
Current TDI and SRI have the advantage of high temporal and spatial resolution but depend heavily on data postprocessing of these images, which will likely increase computative demands in future. With future advance in image acquisition and postprocessing, it is hoped that the imaging techniques could become easier to use and apply clinically. The rapid assessment of regional myocardial velocities and strain could play a useful role in standard stress echocardiography and in detection of regional ischemia and viability at rest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]
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