Secondary Logo

Journal Logo

Cardiovascular Anesthesiology: Core Review Article

Intraoperative Doppler Tissue Imaging Is a Valuable Addition to Cardiac Anesthesiologists’ Armamentarium: A Core Review

Skubas, Nikolaos MD, FASE

Author Information
doi: 10.1213/ane.0b013e31818a6c4c


Intraoperative transesophageal echocardiography (TEE) is commonly used for the evaluation of systolic and diastolic function of the right (RV) and left ventricle (LV) in cardiac or noncardiac surgical cases. A variety of estimations and measurements are performed with two-dimensional (2D) and Doppler echocardiography, using transgastric and mid-esophageal TEE views (Table 1).1,2 Dependence on clear and crisp visualization of both epi- and endocardium, error in measurements, calculations based on geometric assumptions that may not correspond to the true shape of the cardiac chamber, and examiner’s experience level3 may make such evaluations prone to error. Additionally, these methods cannot distinguish the effect of loading conditions on myocardial function. Doppler tissue imaging (DTI) is a novel ultrasound tool less frequently used by anesthesiologists which measures regional myocardial velocities in systole and diastole, and may be less operator-dependent than 2D or conventional Doppler.4 DTI is easy to perform and comprehend and provides objective information that can be readily used intraoperatively. (Table 2) This overview will include a description of the principles and practical aspects regarding acquisition and measurement of myocardial velocities, as well as the intraoperative clinical applications of DTI measurements.

Table 1
Table 1:
Conventional Echocardiographic Techniques for Evaluation of Cardiac Function
Table 2
Table 2:
Intraoperative Applications of Doppler Tissue Imaging (DTI)

Principles of DTI

The interaction of ultrasound with a moving target produces a reflected signal which has a different frequency than the transmitted ultrasound wave. Based on this Doppler effect, spectral (pulsed or continuous wave) and color flow Doppler is used in clinical practice to study blood flow using the equation

where Δf is the frequency difference, c is the speed of sound in biological tissues (1540 cm/s), fo is the frequency of the transmitted ultrasound wave, and cosθ is the cosine of the angle of incidence between the ultrasound plane and the direction of blood flow. Similar frequency changes occur when ultrasound is reflected off the moving myocardium. Myocardial Doppler signals have lower velocity (in the range of −20 to +20 cm/s) and higher amplitude, when compared to blood flow. DTI modifies the processing of the returned Doppler signal, thus enabling recording and displaying of Doppler signals produced by any myocardial segment.5 An example of conventional Doppler and DTI is shown in Figure 1.

Figure 1
Figure 1:
Figure 1.

Display Formats of Doppler Tissue Imaging

Newer, high-end echocardiographic systems, such as Sequoia 256 or 512 (Siemens/Acuson, Mountain View, CA), Sonos 7500 (Philips, Bothell, WA), Vivid7 (GE/Vingmed, Horten, Norway), are capable of obtaining and measuring myocardial velocities with sufficient accuracy for clinical purposes.6,7

Color DTI is obtained in the same manner as conventional color flow Doppler. A color DTI sector is positioned over the myocardial wall of interest and mean velocities are computed using autocorrelation analysis. Myocardial velocities are displayed in blue color if directed away from the transducer and in red if directed toward it. The color myocardial velocities are superimposed on a gray scale, 2D tomographic image (mid-esophageal or transgastric views).8 (Videos 1 and 2) (Please see video clip available at (Fig. 2A,B) In this way, only qualitative information (no numerical value of myocardial velocity) with high spatial, but low temporal, resolution is provided.9 This is the reason why 2D color DTI has limited intraoperative applications. Newer systems allow off-line processing of a color DTI cine loop by adding an M-mode cursor (Fig. 2C,D) or by placing one or more sample volumes (Fig. 3B) to display regional myocardial velocities in spectral format (see below).

Figure 2
Figure 2:
Figure 2.
Figure 3
Figure 3:
Figure 3.

Spectral DTI measures and displays peak myocardial velocity with pulsed wave Doppler from within a sample volume placed in the desired myocardial region. This is done in the same manner as when blood flow velocities are recorded with conventional pulsed wave Doppler (Fig. 3). Myocardial velocities are displayed below or above the zero-velocity baseline if directed away from or toward the transducer, respectively. Timed to the electrocardiogram signal, the DTI spectral display is comprised of a systolic velocity (S’) and two opposite directed velocities, in early diastole (E’) and after atrial contraction (A’).5 In the absence of disease, E’ precedes entry of blood in the LV, and appears earlier than the transmitral early (E) blood flow velocity.10 In the mid-esophageal views, DTI diastolic velocities are a mirror image of the transmitral blood flow because the myocardium moves in an opposite direction to blood flow, i.e., the cardiac base moves away from the apex as blood flows forward through the mitral annulus and toward the apex during systolic ejection (Fig. 1, compare A vs D).11 If the signal is of adequate quality, biphasic signals of low velocity are displayed during isovolumic contraction (between A’ and S’) and isovolumic relaxation (between S’ and E’) (Fig. 3A). These low velocity and short duration waves are most likely related to local shape changes as well as cardiac rotation and torsion.12 DTI velocities are also described with the subscript “a” (for annular) if recorded from the mitral annulus, or with the subscript “m” (for myocardial) if recorded anywhere in the myocardium. Practically, the DTI velocities from the basal LV segments are the same as those recorded next to the mitral annulus (Fig. 3B), unless there is extensive calcification of the mitral annulus.13 In this review, S’, E’, and A’ refer to DTI velocities recorded next to the mitral annulus, and represent longitudinal cardiac motion. The differences between the DTI display formats are summarized in Figure 4.

Figure 4
Figure 4:
Figure 4.

Techniques for Recording DTI

Longitudinal velocities are recorded in the mid-esophageal views (Fig. 5). Transverse velocities are recorded in the transgastric mid-short axis view (Fig. 6). However, excessive cardiac motion in the transverse axis can make recording of transverse spectral DTI myocardial velocities cumbersome and error-prone, and thus is not usually performed intraoperatively. Most current echocardiographic systems are equipped with a preset function that enables DTI (VTI, Velocity Tissue Imaging in GE/Vingmed; PW-TDI, pulsed-wave Tissue Doppler Imaging in Siemens/Acuson and Philips).

Figure 5
Figure 5:
Figure 5.
Figure 6
Figure 6:
Figure 6.

The technique for recording spectral DTI velocities is described in Table 3, Figure 7 and Videos 3 and 4).14 (Web Supplement Fig. 1 for a Siemens/Acuson system.) Measurements can be performed right away or the DTI loop is saved in digital format for off-line analysis.

Table 3
Table 3:
Acquisition of Myocardial Velocities with Doppler Tissue Imaging (DTI)
Figure 7
Figure 7:
Figure 7.

DTI Myocardial Velocities, Myocardial Function, and Limitations of DTI

Myocardial velocities, recorded with DTI from the basal segments next to the mitral annulus, allow quantification of regional longitudinal cardiac motion in a manner not previously possible. From a clinical point of view, such recordings of the longitudinal cardiac motion provide important data about subendocardial function, the region most vulnerable to ischemia.15

The appreciation of clinical applications and limitations of DTI requires comprehension of myocardial anatomy. Myocytes are organized in sheets that lie in planes parallel to the cardiac long axis. Myocyte orientation varies within these planes: it is circumferential in the mid-wall and longitudinal in the endocardial region (forming a right-handed helix) and epicardial surface (forming a left-handed helix).16 During systole, the endo- and epicardial myocyte sheets take a more perpendicular angle toward the mid-wall. As a result, a 14% shortening of the long axis is accompanied by a 40% thickening of the LV wall in the radial axis.17 (Fig. 8) This is seen with TEE in the mid-esophageal views as systolic descent and diastolic ascent of the mitral annulus, and in the transgastric views as systolic thickening and diastolic thinning of the LV wall segments.

Figure 8
Figure 8:
Figure 8.

The limitations of DTI are related to Doppler. DTI measures only the component of motion which is parallel to the ultrasound beam, and DTI velocities decrease by about 20% if the Doppler angle is approximately 30°.18 In addition, the immobile spectral DTI sample volume records velocity produced by both longitudinal and transverse cardiac motion. This complex motion cannot be further analyzed with DTI because of poor spatial resolution. In order to optimize Doppler measurements, it is important to note that, i) in the mid-esophageal views, the mid and apical segments have an inward curvature as the broad LV base tapers towards the apex, and ii) in the transgastric views, the septal and lateral segments are curved. Therefore, ideal “matching” between the Doppler beam and the direction of myocardial motion occurs (a) in the basal segments in the mid-esophageal views and (b) in the middle of the inferior and the anterior segment in the transgastric views. If these prerequisites are met, DTI recordings will approximate the motion of longitudinal and circumferential fibers, respectively.

Factors Affecting DTI Velocities

  1. Myocardial DTI velocities are directly related to the number of contracting myocytes and myocardial β-adrenergic receptors density.19 Normal myocardial segments have higher S’ and E’ and myocardial β-adrenergic receptor density and lower amount of interstitial fibrosis when compared with dysfunctional segments.19
  2. Location: more fibers are found towards the LV base than apex and in lateral and inferior than septal segments.20 This results to heterogeneity: DTI velocities are lowest in the septum, and all velocities decrease from the basal to the mid-apical segments (Fig. 9).21–24 Therefore, velocities from different walls (i.e., septal and lateral in the mid-esophageal four chamber view) or segments cannot be used interchangeably.
  3. Figure 9
    Figure 9:
    Figure 9.
  4. Heart rate: S’ velocity is positively correlated with heart rate.25 Activation of the sympathetic nervous system increases both heart rate and contractility (and thus, mitral annular excursion and S’).25
  5. Age: advancing age increases A’ and decreases S’ and E’ velocities25–29 as fibrous tissue replaces myocardial fibers.
  6. Preload: S’ and E’ velocities are directly dependent on preload,30,31 if cardiac function is normal. The effect of preload on A’ is less pronounced. In diastolic dysfunction, E’ becomes relatively preload-independent and remains low even if the LV filling pressures are increased.32
  7. Afterload: In healthy subjects, acute increases in afterload decrease E’ velocity,33 whereas in patients with chronically increased afterload, both S’ and E’ are decreased.34
  8. Tethering: DTI velocities are recorded from an immobile sample volume, and presence of a DTI velocity cannot exclude passive motion of the segment due to tethering to adjacent segments. This may account for conflicting results regarding the effect of load alterations on basal versus other myocardial segments.30
  9. Pericardiotomy and mechanical ventilation: although theoretically both may affect DTI recordings because of cardiac motion (e.g., during cardiac surgery and opening of the pericardium), this has not been observed35* intraoperatively. The effect of respiration can be further minimized if DTI is used to record longitudinal velocities during end-expiration.

The clinical implications of the above is that S’ should not be used as a substitute for contractility36 and that underlying hemodynamics should be considered when repeated measurements are performed at different times. However, repeated DTI measurements from a single site may reveal the effect of various loading conditions on LV wall motion dynamics. This was seen in mechanically ventilated, postcoronary revascularization patients when administration of 500 mL colloid IV, caused a significant increase in S’ (8.4 ± 2.6 – 9.6 ± 2.5 cm/s, P < 0.001).31 It would also be prudent to regard the mitral annulus or basal myocardial velocity as reflecting the velocity of the entire wall (basal, mid, and apical segments).

DTI Measurements

Possible measurements using DTI include peak velocity (cm/s), acceleration or deceleration (cm/s2) and time intervals (ms). From the clinician’s point of view, peak velocity and the E’/A’ ratio provide the most information. DTI velocities are generally lower when recorded with TEE than with transthoracic echocardiography (TTE).37 In TTE, the different acoustic windows used place the basal segments in the far field and allow for more parallel alignment with the Doppler beam. Even under controlled, experimental conditions,38 DTI recordings between TTE and TEE are not comparable. Few studies have reported DTI in anesthetized, mechanically ventilated patients (Table 4).31,35,37,39–41

Table 4
Table 4:
Doppler Tissue Imaging (DTI) Measurements in Anesthetized, Mechanically Ventilated Patients

Normal DTI values recorded with TTE are shown in Table 5.5,42 Postbypass, DTI velocities change, probably reflecting the effects of cardiopulmonary bypass or vasoactive medications.37,40,41

Table 5
Table 5:
Doppler Tissue Imaging (DTI) Velocities: Normal Values Recorded with Transthoracic Echocardiography

Clinical Applications of DTI

The clinical applications of DTI in the nonsurgical patient have been extensively studied. Data of clinical interest to the anesthesiologist or intensive care physician are summarized in Table 6.

Table 6
Table 6:
Intraoperative Applications of Doppler Tissue Imaging (DTI)

Ventricular Contractility

DTI velocities can detect alterations in regional and global LV contractility that compare favorably with sonomicrometry and pressure-volume measurements.43 The clinical utility of S’ to track changes in LV systolic function was demonstrated in a rapid pacing-induced heart failure model, where S’ was closely related to LV ejection fraction (EF) at all levels of function.44 Longitudinal S’ correlates better than EF45 with LV +dP/dt in healthy and diseased subjects without regional wall motion abnormalities (RWMA).46

Estimation of Ejection Fraction

S’ velocity is a quick and easy means of estimating LV EF. TTE S’ measurements from a single,47 or average S’ from two or more, usually opposite, basal segments have been found to correlate well with LV EF.48–51 Cutoff values or calculation formulae are shown in Table 7.49,50 If RWMA are present, the estimation or calculation of LV EF should be done using the average S’ of as many segments as possible.48 The association between S’ and clinical performance has not been extensively evaluated in patients undergoing a general anesthetic. S’ from the mid-anterior LV segment (transgastric mid-LV short axis using TEE) correlated well with fractional area change before and after coronary artery surgery.40

Table 7
Table 7:
Estimation of Ejection Fraction (EF) by Doppler Tissue Imaging (DTI) Systolic (S’) Velocity Using Trans-Thoracic Echocardiography

Detection of Ischemia

DTI is a promising tool for the real-time detection and quantification of ischemia-induced regional myocardial dysfunction. DTI of the longitudinal axis is able to detect ischemia-induced changes earlier52 and more consistently than epicardial electrocardiogram, myocardial lactate extraction or global hemodynamics changes,53 even in the presence of normal LV EF and unchanged transmitral flow patterns.54 In an animal model of regional ischemia, S’, E’, and E’/A’ decreased within 5 s of ischemia onset, in proportion to the reduction in regional myocardial blood flow (as quantified with microspheres). These changes correlated closely to the myocardial shortening decline (recorded with sonomicrometry) and appeared in advance of 2D echocardiographic changes (such as reduction of systolic excursion and passive paradoxic motion).55,56 The reduction of S’ and E’ during ischemia was accompanied by increased isovolumic relaxation velocity, whereas reperfusion was associated with a transient increase of S’ to a value higher than at baseline, followed by a decrease, identifying myocardial stunning55 (Fig. 10). Consequently, while DTI may be more sensitive than visual evaluation of RWMA in detecting regional ischemia, it is unable to distinguish active ischemia from reperfusion-induced contractile dysfunction. The isovolumic contraction velocity decreases during milder degrees of myocardial ischemia (reduction of coronary artery flow by 50%)57 and precedes the development of infarction. Because it disappeared in those segments that eventually developed more than 20% infarcted tissue, it remained unchanged in smaller infarcts.58

Figure 10
Figure 10:
Figure 10.

After a first myocardial infarction, S’ is significantly reduced in all basal LV segments, even when 2D echocardiographic function is normal.59 The infarcted segments demonstrate the largest reduction in velocity, prolongation of the Q-to-peak-S’ time interval and reduction in E’ without A’ changes, resulting in E’/A’ <1.48,50,60 In myocardial segments remote from ischemia, DTI velocities will remain the same or even decrease, depending upon the presence or absence of functional reserve.56 Prolongation of intervals or velocities ratios are easy to measure, are not influenced by the Doppler angle of incidence, and offer additional information in identifying ischemic LV segments. A longer Q-to-peak-S’ interval in the ischemic area delays regional relaxation and leads to systolic tension persisting in diastole. This manifests as systolic velocity during isovolumic relaxation (appearing in the same direction with S’). This represents postsystolic shortening of the ischemic area61 (Fig. 10) and is associated with adverse effects on overall systolic and diastolic LV function.62 Postsystolic shortening is a marker of myocardial viability, as it predicts the recovery of function after coronary reperfusion.63 An isovolumic relaxation period (S’end-to-E’onset) >85 ms,64,65 or an earlier onset of transmitral flow early velocity, compared to DTI E’,65 also aid in identifying LV ischemic segments. The E’/A’ ratio is easy to recognize visually, and a ratio E’/A’ <1 is found in the majority of akinetic and hypokinetic segments.64 Regional DTI diastolic abnormalities relate to global LV diastolic filling pattern, since patients with an abnormal transmitral E/A ratio <1 have more LV segments with DTI E’/A’ <1 than patients with normal transmitral E/A >1.64

Stress Echocardiography

Recognition of wall motion abnormalities on 2D echocardiography during stress echocardiography remains difficult and uncertain, especially if endocardial definition is suboptimal. There is a need for an objective method to quantify myocardial function. DTI S’ velocities recorded from the mitral annulus are more sensitive than 2D observation in detecting the myocardial response to dobutamine stress echocardiography. Coronary artery disease can be diagnosed accurately and objectively from off-line measurements of S’ velocities during dobutamine stress. S’ increased at a dose of 1 μg · kg−1 · min−1, while 2D changes did not become apparent until 3 μg · kg−1 · min−1.66 The characteristic features of the ischemic myocardial response to dobutamine stress are diminished (≤50%–75% increase from baseline)67 or show a lack of increase68 of S’, development of prominent postsystolic shortening63,69 and unchanged or slightly decreased E’.69 At peak stress, S’ increases ≥100% in normal subjects.70 The utility of DTI in unmasking coronary artery disease in the anesthetized, mechanically ventilated cardiac patient is worth studying, since S’ changes occur at relatively low dose infusion of dobutamine.

Diastolic Function and Estimation of Filling Pressures

The Doppler patterns of transmitral and pulmonary venous flow are influenced by loading conditions and do not always represent actual LV diastolic properties, such as relaxation.71 E’ is related to LV diastolic properties, such as elastic recoil and relaxation, regardless of filling pressures or systolic function.72 E’ changes in the same direction with preload when diastolic function is normal. This effect is less pronounced in ventricles with impaired relaxation, where E’ decreases and remains low even when ventricular filling pressure is high, as in patients with advanced diastolic dysfunction (pseudonormal and restrictive filling pattern) (Fig. 11).32 This disassociation between preload and E’ is used to diagnose the different stages of diastolic dysfunction and estimate filling pressures by evaluating the transmitral E/A and DTI E’/A’ ratios together.73

Figure 11
Figure 11:
Figure 11.
  1. The best evidence of normal diastolic function is a ratio E’/A’ >1 during a Valsalva maneuver (which decreases preload and minimizes its effect on E’).74 Abnormal relaxation is the first stage of diastolic dysfunction, and the ratio E’/A’ inverts (E’/A’ <1) (Fig. 11). This occurs at an early age (5th decade), even in the presence of a normal transmitral flow pattern.75,76 As diastolic dysfunction progresses, E’ decreases and E’/A’ remains <1, despite any normalization of transmitral flow E/A due to augmented preload (E/A ≥1.5).75 In the last stage of diastolic dysfunction (restrictive transmitral flow pattern E/A >2), an A’ >5 cm/s may predict a favorable response to afterload reduction.77
  2. The combination of transmitral flow E (affected by both volume and relaxation) and DTI E’ (expressing relaxation but not volume) can be used to assess LV filling pressures (Fig. 12). The ratio E/E’ (measured in the same units) was associated with pulmonary capillary wedge pressure (PCWP) independent of the underlying pathology47,72 or LV systolic function.78 The mean PCWP can be calculated as
  3. Figure 12
    Figure 12:
    Figure 12.

This ratio has been validated in awake patients in either atrial fibrillation80 or sinus tachycardia.79 The ratio E/E’ may be less predictive of LV filling pressures in the presence of normal LV function,81 when both transmitral flow-E and E’ are preload dependent. In older patients with normal LV function, age and hypovolemia may jointly decrease E’ and increase the ratio E/E’ disproportionately to the filling pressures.27 The site of DTI recording will have an impact on the ratio E/E’ as well. In a small number of cardiac surgical patients, the septal DTI velocities were decreased postoperatively, while the lateral mitral annulus velocities did not.82 Since DTI measures regional velocity, any particular E’ should not be considered a direct measurement of global myocardial relaxation, especially in patients with coronary artery disease where LV relaxation is not uniform at baseline. However, the lateral mitral annulus site is rarely involved in ischemic heart disease,47 and E’ recording at this location usually will represent LV relaxation. Therefore, to estimate LV filling pressures using the E/E’ ratio, the mid-esophageal four chamber view should probably be used to record the lateral mitral annulus site E’. The application of the E/E’ ratio in the anesthetized patient in the operating room merits further investigation.

Valvular Heart Disease

DTI can be useful in detecting LV dysfunction in patients with regurgitant valvular lesions, who may be asymptomatic despite the presence of LV dilation and increased wall stress. Among asymptomatic patients with variable severity of aortic83,84 or mitral85 regurgitation, myocardial contractile reserve (diagnosed as an increase of LVEF >5% during exercise) was present if longitudinal S’ (measured from the lateral or septal mitral annulus) was normal at rest. Among patients with stenotic valvular lesions, there is a significant inverse relationship between S’, E’, and E’/A’ ratio and severity of aortic86 and mitral stenosis.87

Heart Failure Prognosis

Significantly decreased DTI velocities (S’ ≤3 cm/s, E’ ≤3 cm/s, A’ ≤4 cm/s) and E/E’ >20 independently identified those heart failure patients at risk of cardiac death.88,89

Cardiomyopathies and Constrictive Pericarditis

DTI may be the diagnostic tool of choice when conventional echocardiography cannot differentiate physiologic (the result of exercise in healthy individuals) from pathologic hypertrophy, or constrictive pericarditis from restrictive cardiomyopathy. In hypertensive patients, LV hypertrophy is pathologic if DTI demonstrates asynchronous regional systolic contraction and relaxation, and abnormal diastolic function,10,90,91 postsystolic shortening suggestive of subendocardial ischemia,92 or decreased velocities.93 Both constrictive pericarditis and restrictive cardiomyopathy have similar clinical (heart failure) and echocardiographic presentation (restrictive transmitral flow pattern). In constrictive pericarditis, E’ velocity is normal, indicating preserved elastic recoil, even when the respiratory variation in transmitral E wave is blunted or absent. However, E’ is reduced in restrictive cardiomyopathy as a result of intrinsic myocardial disease.94

RV Function

The echocardiographic assessment of RV function is cumbersome, and measurement of volumes and calculation of EF is inaccurate because of anatomic (irregular shape, presence of trabeculations, different embryologic origin of the inflow and outflow tracts) and physiologic (load dependency and pericardial influence) factors. DTI velocities from the free RV wall (Fig. 13 and Video 5), lateral to the tricuspid annulus, have been used to evaluate RV function.95 Although easy to perform, DTI of the tricuspid annulus represents only the longitudinal myocardial fiber function and is affected by translational motion and rotation of the whole heart.95 The excursion of the tricuspid annulus is greater when compared to the mitral annulus because of the shape of the ventricle and the DTI velocities are significantly higher in the RV.96 In contrast to the LV, only the RV E’ tissue velocities correlate with age.97 A tricuspid annulus S’ <10–11.5 cm/s is associated with RVEF <45%.95,98 As is the case with LV velocities, TTE- and TEE-recorded tricuspid annulus velocities may not be comparable because of different views, DTI modality (color vs spectral) and/or potential effect of general anesthesia. The RV free wall tricuspid annulus velocities of precoronary artery bypass graft patients were higher with TTE of the apical four chamber view than with TEE of the modified deep transgastric LV view99 and were not related to hemodynamics. Attempts to correlate the mean right atrial pressure with the E/E’ ratio derived from the transtricuspid flow and the lateral tricuspid annulus in anesthetized patients are not always successful.100,101 DTI can have diagnostic value in RV infarction. A low S’ identified those patients with RV myocardial infarction102–104 or proximal right coronary artery involvement,104 while an S’ <8 cm/s was predictive of cardiac death or rehospitalization at 1 yr.103

Figure 13
Figure 13:
Figure 13.

Mechanical Dyssynchrony

In normal synchronous hearts, segmental S’ peak almost simultaneously, whereas in dyssynchronous hearts, the lateral segments peak considerably later than the septal which results in insufficient ejection. Pacing of the affected region allows synchronized mechanical activity and improves ejection.105 Mechanical dyssynchrony as determined by longitudinal DTI velocities may be superior to electrocardiography in predicting response to cardiac resynchronization therapy. The most recent guidelines suggest the use of color DTI for recognition of mechanical dyssynchrony.


Currently, DTI with pulsed wave Doppler is a rapid method to obtain direction, timing, and velocity of regional longitudinal myocardial motion and quantify systolic and diastolic function. While extensively investigated in awake patients, the potential intraoperative applications need to be verified. Although DTI provides regional measurements, sampling from different sites will help compensate for any differences, facilitating the evaluation of global EF and diastolic function and calculation of filling pressures. Repeated DTI observations in the same patient enable the detection of regional ischemia (decrease in S’ and E’ and E’/A’ <1), and appearance or detection of postsystolic shortening is a sensitive index of ischemic but viable myocardium. DTI has also been used to detect subclinical ventricular dysfunction in asymptomatic patients with valvular disease and differentiate physiologic from pathologic hypertrophy and distinguish constrictive pericarditis from cardiomyopathy. DTI is based on Doppler, and its major limitations are due to mismatch between the imaging plane and the direction of myocardial motion and to tethering of neighboring segments. Doppler strain and speckle tracking are newer techniques that may overcome some of those limitations. Doppler strain measures local myocardial deformation from the velocity gradient between two sample points along the myocardial wall. Although not limited by tethering, since measurements are in reference to myocardium and not to an immobile transducer, it is still subject to the Doppler angle limitation.17,106 Speckle tracking derives myocardial velocity in two dimensions from tracking of acoustic markers, produced by the interaction of ultrasound with tissue. Speckle tracking is not based on Doppler and measurements are independent from insonation angle and tethering.17 In addition, it is automated and provides regional as well as global measurements. Both Doppler strain and speckle tracking are considered research techniques and have not found wide-spread acceptance in everyday clinical practice. Currently, if the limitations are taken into consideration, DTI can be a helpful diagnostic modality, offering quick, real time insights into clinical diagnostic challenges.


1.Lang RM, Bierig M, Devereux R, Flachskampf FA, Foster E, Pellikka PA, Picard MH, Roman MJ, Seward JB, Shanewise JS, Solomon SD, Spencer KT, Sutton MS, Stewart WJ; Chamber Quantification Writing Group; American Society of Echocardiography’s Guidelines and Standards Committee; European Association of Echocardiography. Recommendations for chamber quantification: a report from the American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr 2005;18:1440–63
2.Quinones MA, Otto CM, Stoddard M, Waggoner AD, Zoghbi WA. Recommendations for quantification of Doppler echocardiography: a report from the Doppler quantification task force of the nomenclature and standards committee of the Am Society of Echocardiography. J Am Soc Echocardiogr 2002;15: 167–84
3.Bergquist BD, Leung JM, Bellows WH. Transesophageal echocardiography in myocardial revascularization: I. Accuracy of intraoperative real-time interpretation. Anesth Analg 1996;82: 1132–8
4.Isaaz K, Thompson A, Ethevenot G, Cloez JL, Brembilla B, Pernot C. Doppler echocardiographic measurement of low velocity motion of the left ventricular posterior wall. Am J Cardiol 1989;64:66–75
5.Waggoner AD, Bierig SM. Tissue Doppler imaging: a useful echocardiographic method for the cardiac sonographer to assess systolic and diastolic ventricular function. J Am Soc Echocardiogr 2001;14:1143–52
6.Walker A, Olsson E, Wranne B, Ringqvist I, Ask P. Accuracy of spectral Doppler flow and tissue velocity measurements in ultrasound systems. Ultrasound Med Biol 2004;30:127–32
7.Kjaergaard J, Korinek J, Belohlavek M, Oh JK, Sogaard P, Hassager C. Accuracy, reproducibility, and comparability of Doppler tissue imaging by two high-end ultrasound systems. J Am Soc Echocardiogr 2006;19:322–8
8.Wilkenshoff UM, Sovany A, Wigström L, Olstad B, Lindström L, Englvall J, Janerot-Sjöberg B, Wranne B, Hatle L, Sutherland GR. Regional mean systolic myocardial velocity estimation by real-time color Doppler myocardial imaging: a new technique for quantifying regional systolic function. J Am Soc Echocardiogr 1998;11:684–92
9.Garcia MJ, Thomas JD, Klein AL. New Doppler echocardiographic applications for the study of diastolic function. J Am Coll Cardiol 1998;32:865–75
10.Rodriguez L, Garcia M, Ares M, Griffin BP, Nakatani S, Thomas JD. Assessment of mitral annular dynamics during diastole by Doppler tissue imaging: comparison with mitral Doppler inflow in subjects without heart disease and in patients with left ventricular hypertrophy. Am Heart J 1996;131:982–7
11.Isaaz K. Tissue Doppler imaging for the assessment of left ventricular systolic and diastolic functions. Curr Opin Cardiol 2002;17:431–42
12.Garcia MJ, Rodriguez L, Ares M, Griffin BP, Klein AL, Stewart WJ, Thomas JD. Myocardial wall velocity assessment by pulsed Doppler tissue imaging: characteristic findings in normal subjects. Am Heart J 1996;132:648–56
13.Soeki T, Fukuda N, Shinohara H, Sakabe K, Onose Y, Sawasa Y, Tamura Y. Mitral inflow and mitral annular motion velocities in patients with mitral annular calcification: evaluation by pulsed Doppler echocardiography and pulsed Doppler tissue imaging. Eur J Echocardiography 2002;3:128–34
14.Hill JC, Palma RA. Doppler tissue imaging for the assessment of left ventricular function: a systematic approach for the sonographer. J Am Soc Echocardiogr 2005;18:80–90
15.Gallagher KP, Matsuzaki M, Koziol JA, Kemper WS, Ross J Jr. Regional myocardial perfusion and wall thickening during ischemia in conscious dogs. Am J Physiol 1984;247:H727–H738
16.Sengupta PP, Krishnamoorthy VK, Korinek J, Narula J, Vannan MA, Lester SJ, Tajik AJ, Seward JB, Khanderia BK, Belohlavek M. Left ventricular form and function revisited: applied translational science to cardiovascular ultrasound imaging. J Am Soc Echocardiogr 2007;20:539–51
17.Thomas JD, Popovic ZB. Assessment of left ventricular function by cardiac ultrasound. J Am Coll Cardiol 2006;48:2012–5
18.Skulstad H, Urheim S, Edvardsen T, Andersen K, Lyseggen E, Vartdal H, Ihlen H, Smiseth OA. Grading of myocardial dysfunction by tissue Doppler echocardiography. A comparison between velocity, displacement, and strain imaging in acute ischemia. J Am Coll Cardiol 2006;47:1672–82
19.Shan K, Bick RJ, Poindexter BJ, Shimoni S, Letsou GV, Reardon MJ, Howell JF, Zoghbi WA, Nagueh SF. Relation of tissue Doppler derived myocardial velocities to myocardial structure and beta-adrenergic receptor density in humans. J Am Coll Cardiol. 2000;36:891–6
20.Greenbaum RA, Ho SY, Gibson DG, Becker AE, Anderson RH. Left ventricular fibre architecture in man. Br Heart J 1981;45:248–63
21.Donovan CL, Armstrong WF, Bach DS. Quantitative Doppler tissue imaging of the left ventricular myocardium: validation in normal subjects. Am Heart J 1995;130:100–4
22.Galiuto L, Ignone G, DeMaria AN. Contraction and relaxation velocities of the normal left ventricle using pused-wave tissue Doppler echocardiography. Am J Cardiol 1998;81:609–14
23.Haendchen RV, Wyatt HL, Maurer G, Zwehl W, Bear M, Meerbaum S, Corday E. Quantification of regional cardiac function by two-dimensional echocardiography. I. Patterns of contraction in the normal left ventricle. Circulation 1983;67:1234–45
24.Hatle L, Sutherland GR. Regional myocardial function-a new approach. Eur Heart J 2000;21:1337–57
25.Peverill RE, Gelman JS, Mottram PM, Moir S, Jankelowitz C, Bain JL, Donelan L. Factors associated with mitral annular systolic and diastolic velocities in healthy adults. J Am Soc Echocardiogr 2004;17:1146–54
26.Onose Y, Oki T, Mishiro Y, Yamada H, Abe M, Manabe K, Kageji Y, Tabata T, Wakatsuki T, Ito S. Influence of aging on systolic left ventricular wall motion velocities along the long and short axes in clinically normal patients determined by pulsed tissue Doppler imaging. J Am Soc Echocardiogr 1999; 12:921–6
27.Tighe DA, Vinch CS, Hill JC, Meyer TE, Goldberg RJ, Aurigemma GP. Influence of age on assessment of diastolic function by Doppler tissue imaging. Am J Cardiol 2003;91:254–7
28.Yamada H, Oki T, Mishiro Y, Tabata T, Abe M, Onose Y, Wakatsuki T, Ito S. Effect of aging on diastolic left ventricular myocardial velocities measured by pulsed tissue Doppler imaging on healthy subjects. J Am Soc Echocardiogr 1999;12:574–81
29.Munagala VK, Jacobsen SJ, Mahoney DW, Rodeheffer RJ, Bailey KR, Redfield MM. Association of newer diastolic function parameters with age in healthy subjects: a population-based study. J Am Soc Echocardiogr 2003;13:1049–56
30.Andersen NH, Terkelsen CJ, Sloth E, Poulsen SH. Influence of preload alterations on parameters of systolic left ventricular long-axis function: a Doppler tissue study. J Am Soc Echocardiogr 2004;17:941–7
31.Ama R, Segers P, Roosens C, Claessens T, Verdonck P, Poalaert J. The effects of load on systolic mitral annular velocity by tissue Doppler imaging. Anesth Analg 2004;99:332–8
32.Firstenberg MS, Greenberg NL, Main ML, Drinko JK, Odabashian JA, Thomas JD, Garcia MJ. Determinants of diastolic myocardial tissue Doppler velocities: influences of relaxation and preload. J Appl Physiol 2001;90:299–307
33.Oki T, Fukuda K, Tabata T, Mishiro Y, Yamada H, Abe M, Onose Y, Wakatsuki T, Iuchi A, Ito S. Effect of an acute increase in afterload on left ventricular regional wall motion velocity in healthy subjects. J Am Soc Echocardiogr 2006;1999:476–83
34.Eidem BW, McMahon CJ, Ayres NA, Kovalchin JP, Denfield SW, Altman CA, Bezold LI, Pignatelli RH. Impact of chronic left ventricular preload and afterload on Doppler tissue imaging velocities: a study in congenital heart disease. J Am Soc Echocardiogr 2005;18:830–8
35.Simmons LA, Weidemann F, Sutherland GR, D’hooge J, Bijnens B, Sergeant P, Wouters PF. Doppler tissue velocity, strain, and strain rate imaging with transesophageal echocardiography in the operating room: a feasibility study. J Am Soc Echocardiogr 2002;15:768–76
36.Carabello BA. Evolution of the study of left ventricular function. Everything old is new again. Circulation 2002;105:2701–3
37.Williams RI, Haaverstad R, Sianos G, Vourvouri E, Fraser AG. Perioperative tissue Doppler echocardiography and bypass graft flowmetry in patients undergoing coronary revascularization: predictive power for late recovery of regional myocardial function. J Am Soc Echocardiogr 2002;15:1201–10
38.Cheung MHM, Li J, White P, Smallhorn JF, Redington AN, Vogel M. Doppler tissue echocardiography: can transesophageal echocardiography be used to acquire functional data? J Am Soc Echocardiogr 2003;16:732–7
39.Norrild K, Pedersen TF, Sloth E. Transesophageal tissue Doppler echocardiography for evaluation of myocardial function during aortic valve replacement. J Cardiothorac Vasc Anesth 2007;21:367–70
40.Skarvan K, Filipovic M, Wang J, Brett W, Seeberger M. Use of myocardial tissue Doppler imaging for intraoperative monitoring of left ventricular function. Br J Anaesth 2003;91:473–80
41.Casthely PA, Bunik T, Casthely PA, Yoganathan T, Komer C, Mekhjian H Jr. Nicardipine or nitroglycerin in patients with failed percutaneous coronary angioplasty: effect on myocardial diastolic function. J Cardiothorac Vasc Anesth 2003;17:604–12
42.Sun JP, Popovic ZB, Greenberg NL, Xu XF, Asher CR, Stewart WJ, Thomas JD. Noninvasive quantification of regional myocardial function using Doppler-derived velocity, displacement, strain rate, and strain in healthy volunteers: effects of aging. J Am Soc Echocardiogr 2004;17:132–8
43.Gorcsan J, III, Strum DP, Mandarino WA, Gulati VK, Pinsky MR. Quantitative assessment of alterations in regional left ventricular contractility with color-coded tissue Doppler echocardiography. Comparison with sonomicrometry and pressure-volume relations. Circulation 1997;95:2423–33
44.Tabata T, Cardon LA, Armstrong G, Fukamach K, Takagaki M, Ochiai Y, McCarthy PM, Thomas JD. An evaluation of the use of new Doppler methods for detecting longitudinal function abnormalities in a pacing-induced heart failure model. J Am Soc Echocardiogr 2003;16:424–31
45.Bach DS. Quantitative Doppler tissue imaging as a correlate of left ventricular contractility. Int J Card Imaging 1996;12:191–5
46.Yamada H, Oki T, Tabata T, Iuchi A, Ito S. Assessment of left ventricular systolic wall motion velocity with pulsed tissue Doppler imaging: comparison with peak dP/dt of the left ventricular pressure curve. J Am Soc Echocardiogr 1998;11: 442–9
47.Nagueh SF, Middleton KJ, Kopelen HA, Zoghbi WA, Quinones MA. Doppler tissue imaging: a non-invasive technique for evaluation of left ventricular relaxation and estimation of filling pressures. J Am Coll Cardiol 1997;30:1527–33
48.Alam M, Wardell J, Anderson E, Samad BA, Nordlander R. Effects of first myocardial infarction on left ventricular systolic and diastolic function with the use of mitral annular velocity determined by pulsed wave Doppler tissue imaging. J Am Soc Echocardiogr 2000;13:343–52
49.Vinereanu D, Khokhar A, Tweddel AC, Cinteza M, Fraser AG. Estimation of global left ventricular function from the velocity of longitudinal shortening. Echocardiography 2002;19:177–85
50.Fukuda K, Takashi O, Tabata T, Iuchi A, Ito S. Regional left ventricular wall motion abnormalities in myocardial infarction and mitral annular decent velocities studied with pulsed tissue Doppler imaging. J Am Soc Echocardiogr 1998;11:841–8
51.Gulati VK, Katz WE, Follansbee WP, Gorcsan J, III. Mitral annular descent velocity by tissue Doppler echocardiography as an index of global left ventricular function. Am J Cardiol 1996;77:979–84
52.Henein MY, Anagnostopoulos C, Das SK, O’Sullivan C, Underwood SR, Gibson DG. Left ventricular long axis disturbances as predictors for thallium perfusion defects in patients with known peripheral vascular disease. Heart 1998;79: 295–300
53.Leone BJ, Norris RM, Safwat A, Foex P, Ryder WA. Effects of progressive myocardial ischaemia on systolic function, diastolic dysfunction, and load dependent relaxation. Cardiovasc Res 1992;26:422–9
54.Bolognesi R, Tsialtas D, Barilli AL, Manca C, Zeppellini R, Javernaro A, Cucchini F. Detection of early abnormalities of left ventricular function by hemodynamic, echo-tissue Doppler imaging, and mitral flow techniques in patients with coronary artery disease and normal ejection fraction. J Am Soc Echocardiogr 2001;14:764–72
55.Derumeaux G, Ovize M, Loufoua J, Andre-Fouet X, Minaire Y, Cribier A, Letac B. Doppler tissue imaging quantitates regional wall motion during myocardial ischemia and reperfusion. Circulation 1998;97:1970–7
56.Bach DS, Armstrong WF, Donovan CL, Muller DWM. Quantitative Doppler tissue imaging for assessment of regional myocardial velocities during transient ischemia and reperfusion. Am Heart J 1996;132:721–5
57.Shimizu M, Nii M, Konstantinov IE, Li J, Redington AN. Isovolumic but not ejection phase Doppler tissue indices detect left ventricular dysfunction caused by coronary stenosis. J Am Soc Echocardiogr 2005;18:1241–6
58.Pislaru C, Bruce CJ, Belohlavek M, Seward JB, Greenleaf JF. Intracardiac measurement of pre-ejection myocardial velocities estimates the transmural extent of viable myocardium early after reperfusion in acute myocardial infarction. J Am Coll Cardiol 2001;38:1748–56
59.Palmes PP, Masuyama T, Yamamoto K, Kondo H, Sakata Y, Takiuchi S, Kuzuya T, Hori M. Myocardial longitudinal motion by tissue velocity imaging in the evaluation of patients with myocardial infarction. J Am Soc Echocardiogr 2000;13:818–26
60.Elnoamany MF, Badran HM, Elazm THA, Abdelaziz ES. Asynchrony of left ventricular systolic performance after the first myocardial infarction in patients with narrow QRS complexes: Doppler tissue imaging study. J Am Soc Echocardiogr 2006;19:1449–57
61.Edvardsen T, Urheim S, Skulstad H, Steine K, Ihlen H, Smiseth OA. Quantification of left ventricular systolic function by tissue Doppler echocardiography. Added value of measuring pre- and postejection velocities in ischemic myocardium. Circulation 2002;105:2071–7
62.Gibson DG, Prewitt TA, Brown DJ. Analysis of left ventricular wall movement during isovolumic relaxation and its relation to coronary artery disease. Br Heart J 1976;38:1010–19
63.Takayama M, Norris RM, Brown A, Armiger LC, Rivers JT, White HD. Postsystolic shortening of acutely ischemic canine myocardium predicts early and late recovery of function after coronary artery reperfusion. Circulation 1988;78:994–1007
64.García-Fernández MA, Azevedo J, Moreno M, Bermejo J, Pérez-Castellano N, Puerta P, Desco M, Antoranz C, Serrano JA, García E, Delcán JL. Regional diastolic function in ischaemic heart disease using pulsed wave Doppler tissue imaging. Eur Heart J 1999;20:496–505
65.Guron CW, Hartford M, Persson A, Herlitz J, Thelle D, Caidahl K. Timing of regional left ventricular lengthening by pulsed tissue Doppler. J Am Soc Echocardiogr 2004;17:307–12
66.Gorcsan J, III, Deswal A, Mankad S, Mandarino WA, Mahler CM, Yamazaki N, Katz WE. Quantification of the myocardial response to low dose of dobutamine using tissue Doppler echocardiographic measures of velocity and velocity gradient. Am J Cardiol 1998;81:615–23
67.Katz WE, Gulati VK, Mahler CM, Gorcsan J, III. Quantitative evaluation of the segmental left ventricular response to dobutamine stress by tissue Doppler echocardiography. Am J Cardiol 1997;79:1036–42
68.Yamada E, Garcia M, Thomas JD, Marwick TH. Myocardial Doppler velocity imaging: a quantitative technique for interpretation of dobutamine echocardiography. Am J Cardiol 1998;82:806–9
69.Celutkiene J, Sutherland GR, Laucevicius A, Zakarlaite D, Rudys A, Grabauskiene V. Is post-systolic motion the optimal ultrasound parameter to detect induced ischemia during dobutamine stress echocardiography? Eur Heart J 2004;25:932–42
70.Maedler CF, Payne N, Wilkenshoff UM, Cohen A, Derumeaux G, Pierard LA, Englvall J, Brodin LA, Sutherland GR, Fraser AG. Non-invasive diagnosis of coronary artery disease by quantitative stress echocardiography: optimal diagnostic models using off-line tissue Doppler in the MYDISE study. Eur Heart J 2003;24:1584–94
71.Maurer MS, Spevack D, Burkhoff D, Kronzon I. Diastolic dysfunction. Can it be diagnosed by Doppler echocardiography? J Am Coll Cardiol 2004;44:1543–9
72.Ommen SR, Nishimura RA, Appleton CP, Miller FA, Oh JK, Redfield MM, Tajik AJ. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: a comparative simultaneous Doppler-catheterization study. Circulation 2000;102:1788–94
73.Farias CA, Garcia MJ, Sun JP, Klein AL, Thomas JD. Assessment of diastolic function by tissue Doppler echocardiography: comparison with standard transmitral and pulmonary venous flow. J Am Soc Echocardiogr 1999;12:609–17
74.Dumesnil JG, Paulin C, Pibarot P, Coulombe D, Arsenault M. Mitral annulus velocities by Doppler tissue imaging: practical implications with regard to preload alterations, sample position, and normal values. J Am Soc Echocardiogr 2002;15: 1226–31
75.Sohn DW, Chai IH, Lee DJ, Kim HC, Kim HS, Oh BH, Lee MM, Park YB, Choi YS, Seo JD, Lee YW. Assessment of mitral annulus velocity by Doppler tissue imaging in the evaluation of left ventricular diastolic function. J Am Coll Cardiol 1997;30:474–80
76.Oki T, Tabata T, Yamada H, Wakatsuki T, Shinohara H, Nishikado A, Iuchi A, Fukuda K, Ito S. Clinical application of pulsed Doppler tissue imaging for assessing abnormal left ventricular relaxation. Am J Cardiol 1997;79:921–8
77.Sohn DW, Kim YJ, Lee MM, Park YB, Choi YS, Lee YW. Differentiation between reversible and irreversible restrictive left ventricular filling patterns with the use of mitral annulus velocity. J Am Soc Echocardiogr 2000;13:891–5
78.Rivas-Gotz C, Manolios M, Thohan V, Nagueh SF. Impact of left ventricular ejection fraction on estimation of left ventricular filling pressures using tissue Doppler and flow propagation velocity. Am J Cardiol 2003;91:780–4
79.Nagueh SF, Mikati I, Kopelen HA, Middleton KJ, Quinones MA, Zoghbi WA. Doppler estimation of left ventricular filling pressure in sinus tachycardia. A new application of tissue Doppler imaging. Circulation 1998;98:1644–50
80.Sohn DW, Song JM, Zo JH, Chai IH, Kim HS, Chun HG, Kim HC. Mitral annulus velocity in the evaluation of left ventricular diastolic function in atrial fibrillation. J Am Soc Echocardiogr 1999;12:927–31
81.Jacques DC, Pinsky MR, Severyn D, Gorcsan J, III. Influence of alterations in loading on mitral annular velocity by tissue Doppler echocardiography and its associated ability to predict filling pressures. Chest 2004;126:1910–8
82.Malouf PJ, Madani M, Gurudevan S, Waltman TJ, Raisinghani AB, DeMaria AN, Blanchard DG. Assessment of diastolic function with Doppler tissue imaging after cardiac surgery: effect of the “postoperative septum” in on-pump and off-pump procedures. J Am Soc Echocardiogr 2006;19:464–7
83.Vinereanu D, Ionescu AA, Fraser AG. Assessment of left ventricular long axis contraction can detect early myocardial dysfunction in asymptomatic patients with severe aortic regurgitation. Heart 2001;85:30–6
84.Paraskevaidis IA, Tsiapras D, Kyrzopoulos S, Cokkinos P, Iliodromitis EK, Parissis J, Kremastinos DT. The role of left ventricular long-axis contraction in patients with asymptomatic aortic regurgitation. J Am Soc Echocardiogr 2006;19:249–54
85.Haluska BA, Short L, Marwick TH. Relationship of ventricular longitudinal function to contractile reserve in patients with mitral regurgitation. Am Heart J 2003;146:183–8
86.Giorgi D, Di Bello V, Talini E, Palagi C, Donne MGD, Nardi C, Verunelli F, Mariani MA, Di Cori A, Caravelli P, Mariani M. Myocardial function in severe aortic stenosis before and after aortic valve replacement: a Doppler tissue imaging study. J Am Soc Echocardiogr 2005;18:8–14
87.Özdemir K, Altunkeser BB, Gok H, Ýçli A, Temizhan A. Analysis of the myocardial velocities in patients with mitral stenosis. J Am Soc Echocardiogr 2002;15:472–8
88.Wang M, Yip GWK, Wang AYM, Zhang Y, Ho PY, Tse MK, Lam PKW, Sanderson JE. Peak early diastolic mitral annulus velocity by tissue Doppler imaging adds independent and incremental prognostic value. J Am Coll Cardiol 2003;41:820–6
89.Yamamoto K, Oki T, Tanaka H, Ishimoro T, Wakatsuki T, Ito S. Prognostic value of the atrial systolic mitral annular velocity in patients with left ventricular systolic dysfunction. J Am Soc Echocardiogr 2003;16:333–9
90.Severino S, Caso P, Galderisi M, De Simone M, Petrocellli A, de Divitiis O, Mininni N. Use of pulsed Doppler tissue imaging to assess regional left ventricular diastolic dysfunction in hypertrophic cardiomyopathy. Am J Cardiol 1998;82:1394–8
91.Naqvi TZ, Neyman G, Broyde A, Mustafa J, Siegel RJ. Comparison of myocardial tissue Doppler with transmitral flow Doppler in left ventricular hypertrophy. J Am Soc Echocardiogr 2001;14:1153–60
92.Pai RG, Gill KS. Amplitudes, durations, and timings of apically directed left ventricular myocardial velocities: II. Systolic and diastolic asynchrony in patients with left ventricular hypertrophy. J Am Soc Echocardiogr 1998;11:112–18
93.Vinereanu D, Florescu N, Sculthorpe N, Tweddel AC, Stephens MR, Fraser, AG. Differentiation between pathologic and physiologic left ventricular hypertrophy by tissue Doppler assessment of long-axis function in patients with hypertrophic cardiomyopathy or systemic hypertension and in athletes. Am J Cardiol 2001;88:53–8
94.Ha JW, Oh JK, Ommen SR, Ling LH, Tajik AJ. Diagnostic value of mitral annular velocity for constrictive pericarditis in the absence of respiratory variation in mitral inflow velocity. J Am Soc Echocardiogr 2002;15:1468–71
95.Meluzin J, Špinarová L, Bakala J, Toman J, Krejci J, Hude P, Kara T, Soucek M. Pulsed Doppler tissue imaging of the velocity of tricuspid annular systolic motion. A new, rapid, and non-invasive method of evaluating right ventricular systolic function. Eur Heart J 2001;22:340–8
96.Alam M, Wardell J, Anderson E, Samad BA, Nordlander R. Characteristics of mitral and tricuspid annular velocities determined by pulsed wave Doppler tissue imaging in healthy subjects. J Am Soc Echocardiogr 1999;12:618–28
97.Nikitin NP, Witte KKA, Thackray SDR, de Silva R, Clark AL, Cleland JGF. Longitudinal ventricular function: normal values of atrioventricular annular and myocardial velocities measured with quantitative two-dimensional color Doppler tissue imaging. J Am Soc Echocardiogr 2003;16:906–21
98.Miller D, Farah MG, Liner A, Fox K, Schluchter M, Hoit BD. The relation between quantitative right ventricular ejection fraction and indices of tricuspid annular motion and myocardial performance. J Am Soc Echocardiogr 2004;17:443–7
99.David JS, Tousignant CP, Bowry R. Tricuspid annular velocity in patients undergoing cardiac operation using transesophageal echocardiography. J Am Soc Echocardiogr 2006;19:329–34
100.Nageh MF, Kopelen HA, Zoghbi WA, Quinones MA, Nagueh SF. Estimation of mean right atrial pressure using tissue Doppler imaging. Am J Cardiol 1999;84:1448–51
101.Michaux I, Filipovic M, Skarvan K, Schneiter S, Seeberger M. Accuracy of tissue Doppler estimation of the right atrial pressure in anesthetized, paralyzed, and mechanically ventilated patients. Am J Cardiol 2006;97:1654–6
102.Alam M, Wardell J, Anderson E, Samad BA, Nordlander R. Right ventricular function in patients with first myocardial infarction: assessment by tricuspid annular motion and tricuspid annular velocity. Am Heart J 2000;139:710–15
103.Dokainish H, Abbey H, Gin K, Ramanathan K, Lee PK, Jue J. Usefulness of tissue Doppler imaging in the diagnosis and prognosis of acute right ventricular infarction with inferior wall acute left ventricular infarction. Am J Cardiol 2005;95:1039–42
104.Özdemir K, Altunkeser BB, Içli A, Özdil H, Gök H. New parameters in identification of right ventricular myocardial infarction and proximal right coronary artery lesion. Chest 2003;124:219–26
105.Abraham T, Dimaano VL, Liang HY. Role of tissue Doppler and strain echocardiography in current clinical practice. Circulation 2007;116:2597–609
106.Marwick TH. Measurements of strain and strain rate by echocardiography. Ready for prime time? J Am Coll Cardiol 2006;47:1313–27

*Skubas N, Ryjikov N, Slepian R, Levin S, Girardi L, Krieger K, Tunick PA, Kronzon I. The effect of pericardiotomy on left ventricular diastolic myocardial tissue velocity. J Am Soc Echocardiogr 2004;17:PI-44 (abstract).
Cited Here

†Brown NI, Slepian R, Purcell MH, Mishra R, Skubas N. Atrial contraction is influenced by ventricular systole: a tissue Doppler echocardiographic study in cardiac surgical patients. American Society of Anesthesiologists Annual Meeting, Atlanta, GA 2005;A-346 (abstract).
Cited Here

© 2009 International Anesthesia Research Society