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CONTEMPORARY TOPIC
Year : 2017  |  Volume : 1  |  Issue : 2  |  Page : 126-132

Basics of tissue doppler revisited


Department of Cardiology, Mittal Hospital and Research Centre, Ajmer, Rajasthan, India

Date of Web Publication28-Aug-2017

Correspondence Address:
Sita Ram Mittal
XI/101, Brahmpuri, Ajmer - 305 001, Rajasthan
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jiae.jiae_34_17

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  Abstract 


Tissue Doppler imaging (TDI) records velocities of myocardial tissue. Routinely longitudinal velocities of medial and lateral mitral annulus and lateral tricuspid annulus are evaluated in apical four chamber view. Commonly recorded waves include isovolumic contraction wave, systolic wave, isovolumic relaxation wave, early diastolic wave, and late diastolic wave. TDI is useful in detection of subclinical systolic dysfunction and early diastolic dysfunction. It is useful in differentiating athlete's heart from hypertrophic cardiomyopathy and pericardial constriction from restrictive cardiomyopathy.

Keywords: Diastolic dysfunction, echocardiography, tissue Doppler imaging


How to cite this article:
Mittal SR. Basics of tissue doppler revisited. J Indian Acad Echocardiogr Cardiovasc Imaging 2017;1:126-32

How to cite this URL:
Mittal SR. Basics of tissue doppler revisited. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2017 [cited 2017 Nov 25];1:126-32. Available from: http://www.jiaecho.org/text.asp?2017/1/2/126/213672




  Basics of Tissue Doppler Revisited Top


In tissue Doppler imaging (TDI), Doppler echocardiography is used to record velocities of myocardial tissue. Routinely longitudinal velocities of medial and lateral mitral annulus and lateral tricuspid annulus are evaluated in apical four chamber view. Normally, during systole, the base of the ventricles descends toward the apex and moves back during diastole. The apex is relatively stationary.[1] Thus, annuli move toward transducer (apex) in systole and move away from transducer during diastole. Movement toward apex (systole) is recorded above the baseline, and movement away from apex (diastole) is recorded below baseline.

Wave forms

Normal wave form and their relation with phases of the cardiac cycle are shown in [Figure 1]. Representative normal tracing is shown in [Figure 2].
Figure 1: Correlation of various waves of tissue Doppler imaging with various phases of cardiac cycle. Ao: Aortic pressure, LV: Left ventricular pressure, LA: Left atrial pressure, MV: Mitral valve flow, TDI: Tissue Doppler imaging, IVC: Isovolumic contraction wave, Sa: Systolic wave, IVR: Isovolumic relaxation wave, Ea: Early diastolic wave, e”: Positive component of early diastolic wave, M: Mid diastolic wave, Aa: Late diastolic wave during atrial contraction

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Figure 2: Echocardiography of tissue Doppler imaging from medial mitral annulus of a normal heart. IVC: Isovolumic contraction wave, Sa: Systolic wave, IVR: Isovolumic relaxation wave, Ea: Early diastolic wave, Aa: Late diastolic wave

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Normally, following waves are seen as follows:

Isovolumic contraction

It produces a sharp but brief positive spike. In some cases, there is a small negative velocity component at the end of isovolumic contraction (IVC) which is due to slightly normal asynchrony in electromechanical contraction.[1] It correlates with the rate of contractility.

In significant systolic dysfunction, positive velocity component diminishes with relative increase in negative component. In dyskinetic myocardium, the positive velocity component is replaced by a large negative IVC wave.[1]

Rate of acceleration of the positive component of IVC wave–isovolumic acceleration is defined as the ratio of peak isovolumic velocity and time to peak isovolumic velocity.[2] It correlates with dp/dt max. Normal value has been reported to be 1.8 ± 0.5 m/s.

Time between end of late diastolic wave (Ea) and beginning of ejection wave (Sa) is IVC time. Normal value is <70 ms.[3]

Ejection wave (systolic wave - Sa or S')

Peak velocity of systolic wave correlates with regional systolic function. Normal systolic velocity of mitral annulus is >6 cm/s.[4] Velocity of tricuspid annulus is higher (range 9.1 ± 2.5 cm/s).[2] Myocardial velocity reaches its peak during the early phase of ejection and then gradually declines. In some cases, a smaller second peak occurs during later part of ejection [Figure 3] and [Figure 4]. If there are multiple peaks in the ejection phase, highest peak should be considered [Figure 5]. Magnitude of ejection wave progressively decreases with worsening systolic function.
Figure 3: Echocardiogram of tissue Doppler imaging from lateral mitral annulus from a normal heart showing smaller second systolic peak (s”). IVC: Isovolumic contraction, Sa and s”: Systolic waves, Ea: Early diastolic wave, Aa: Late diastolic wave, IVR: Isovolumic relaxation

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Figure 4: Another example of smaller second systolic peak (s”) recorded from lateral mitral annulus of a normal heart. IVC: Isovolumic contraction, Sa and s”: Systolic waves, IVR: Isovolumic relaxation, Ea: Early diastolic wave, Aa: Late diastolic wave

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Figure 5: Echocardiogram of tissue Doppler imaging from lateral mitral annulus of a normal heart showing taller second systolic peak s”. IVC: Isovolumic contraction, Sa and s”: Systolic waves, Ea: Early diastolic wave, Aa: Late diastolic wave

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Isovolumic relaxation

It produces a negative velocity spike after systolic waves. Normal range for isovolumic relaxation time is 70–90 m/s. Normally, there is a small positive velocity component toward the end of isovolumic relaxation. This represents slight postsystolic shortening.[1] In normal heart, postsystolic velocity is of low amplitude and occurs before mitral valve opening. In the diseased ventricle specially with dyskinetic myocardium, postsystolic shortening may be marked [Figure 6] and may extend into diastolic filling phase [Figure 7].
Figure 6: Echocardiogram of tissue Doppler imaging from medial mitral annulus of a patient with akinetic interventricular septum showing prominent postsystolic shortening. IVC: Isovolumic contraction, Sa: Systolic wave, IVR: Isovolumic relaxation, Ea: Early diastolic wave, Aa: Late diastolic wave

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Figure 7: Echocardiogram of tissue Doppler imaging from medial mitral annulus of a patient with diffuse hypokinesia showing prominent postsystolic shortening extending in diastole. Sa: Systolic wave, Ea: Early diastolic wave, Aa: Late diastolic wave

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Diastole

  1. Early diastolic filling wave (Ea or e') - If Ea shows two peaks [Figure 8], the higher one should be considered. Magnitude of Ea is closely related to myocardial relaxation. In the failing ventricle, e' is much less dependent on filling pressure than E wave velocity of transmitral flow. Therefore, when left ventricular (LV) filling pressure becomes elevated due to impaired relaxation. Magnitude of E wave increases but that of Ea decreases resulting in an increase in E/Ea ratio. This forms the basis of using E/Ea ratio as a marker of elevated LV filling pressure. With increasing diastolic dysfunction (restrictive pathology), magnitude of Ea wave progressively declines. Normal values are >12 cm/s and >8 cm/s for lateral and medial mitral annulus, respectively[5]
  2. Early diastases - Ea may be followed by an oppositely directed wave of low amplitude (e'') during early diastases [Figure 9]
  3. Mid diastolic flow velocity - In some normal persons, the significant flow may continue across mitral valve during mid diastole. It can produce a low amplitude negative wave in mid diastole [Figure 10] and [Figure 11]
  4. Late diastolic wave during atrial contraction (Aa or a') - Myocardial lengthening due to filling during atrial contraction produces a negative wave (Aa) during late diastole. Magnitude of Aa depends on the amount of ventricular filling during atrial contraction. In impaired relaxation, early ventricular filling (Ea) is diminished. It is compensated by increased filling during atrial contraction. Amplitude of Aa wave is, therefore, increased [Figure 12]. In advanced stage with restrictive pathophysiology, filling during atrial contraction is diminished with progressive reduction in Aa amplitude. Amplitude of Aa wave is also dependent on force of atrial contraction. It, therefore, also decreases with progressive atrial failure and is absent in atrial fibrillation.
Figure 8: Echocardiogram of tissue Doppler imaging from lateral tricuspid annulus showing two peaks of Ea wave (arrow). Sa: Systolic wave, Aa: Late diastolic wave

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Figure 9: Echocardiogram of tissue Doppler imaging from a normal heart showing early diastases wave (e”). Sa: Systolic wave, Ea: Early diastolic wave, Aa: Late diastolic wave

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Figure 10: Echocardiogram of tissue Doppler imaging showing early diastases wave (e”) and mid diastolic flow wave (M). Sa: Systolic wave, Ea: Early diastolic wave, Aa: Late diastolic wave

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Figure 11: Another example of tissue Doppler imaging showing early diastases (e”) and mid diastolic wave (M). Sa: Systolic wave, Ea: Early diastolic wave, Aa: Late diastolic wave

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Figure 12: Echocardiogram of tissue Doppler imaging showing late diastolic wave velocity (Aa) more than early diastolic wave (Ea) velocity. Sa-systolic wave

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Ea/Aa ratio

Normal reference range is 1 ± 0.7 and 1.5 ± 0.6 for medial and lateral annulus, respectively.[5]

Effect of aging

There is a decrease in Sa and Ea velocities with aging with a corresponding increase in Aa velocity.[6]

Clinical application

Detection of systolic dysfunction

Ejection velocity is helpful in detecting:

  1. Patients with known genetic mutation of hypertrophic cardiomyopathy in the absence of clinically apparent disease or manifest LV hypertrophy[7]
  2. Early heart transplant rejection[8]
  3. Early Fabry cardiomyopathy[9]
  4. Subclinical chemotherapy-associated cardiomyopathy
  5. Subclinical myocardial dysfunction in aortic regurgitation and mitral regurgitation.[5]


Stress tissue Doppler imaging

Sa velocity can be used for improved identification of ischemia and viability.[5] Exercise E/Ea correlates with exercise LV filling pressure and is helpful in detecting latent diastolic dysfunction.

Determination of left ventricular dyssynchrony

It is done by determining the time from onset of QRS to peak tissue Doppler systolic velocity at the lateral wall and septal wall. A septal to lateral delay >65 ms is considered statistically significant.

Assessment of right ventricular function

Depressed Sa at the lateral tricuspid annulus supports possibility of

  • Right ventricular involvement in acute LV inferior infarction[10]
  • Right ventricular involvement in LV cardiomyopathy[11]
  • Depressed right ventricular systolic function.[12]


Regional systolic dysfunction

In cases with regional systolic dysfunction, Sa velocity of corresponding annulus is decreased [Figure 13] and [Figure 14].
Figure 13: Tissue Doppler images from a case of diffuse hypokinesia of left ventricle. (a) Lateral mitral annulus showing decreased systolic velocity (Sa). (b) Medial mitral annulus showing decreased systolic velocity (Sa). (c) Lateral tricuspid annulus showing normal systolic velocity (Sa) suggesting normal right ventricular systolic function

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Figure 14: Tissue Doppler images from a case of diffuse hypokinesia of interventricular septum and anterior wall. (a) Lateral mitral annulus showing normal systolic velocity (Sa). (b) Medial mitral annulus showing decreased systolic velocity (Sa)

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Assessment of diffuse diastolic dysfunction

Progressive impairment of ventricular relaxation increases LV filling pressure. It increases velocity of E wave of mitral flow as it is dependent on preload. Ea decreases as it is independent of relaxation and is not affected by preload. E/Ea ratio, therefore, progressively increases. Using medial mitral annulus Ea, E/Ea ratio <8 suggests normal LV filling pressure. Ratio of >15 suggests increased LV filling pressure.[13] For lateral mitral annulus, a ratio of >12 is considered as suggestive of elevated LV filling pressure.

E/Ea is not helpful in assessing filling pressure in patients with mitral valve disease (mitral annulus calcification, mitral stenosis, mitral regurgitation, mitral annuloplasty, or mitral valve replacement).

Ea velocity <8.5 cm/s with Ea/Aa ratio <1 suggests pseudonormal mitral flow pattern.[14] TDI is helpful in evaluation of ventricular relaxation in sinus tachycardia, atrial fibrillation, and hypertrophic cardiomyopathy.

Aa increases during early diastolic dysfunction but decreases as atrial function deteriorates.

Regional diastolic dysfunction

Lateral myocardial infarction affects movement of lateral mitral annulus. Septal myocardial infarction affects movement of medial mitral annulus. Valve surgery affects medial mitral annulus velocity [Figure 15] and [Figure 16].
Figure 15: Tissue Doppler images showing regional diastolic dysfunction. (a) Lateral mitral annulus showing Ea velocity taller than Aa velocity suggesting normal diastolic function. (b) Lateral tricuspid annulus showing Aa velocity much more than Ea velocity suggesting impaired relaxation

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Figure 16: Tissue Doppler images showing regional diastolic dysfunction. (a) Lateral mitral annulus showing Ea wave velocity more than Aa velocity suggesting normal diastolic function. Sa: Systolic wave. (b) Medial mitral annulus showing Aa velocity more than Ea velocity suggesting impaired relaxation of interventricular septum. Sa-systolic wave

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Evaluation of systolic and diastolic function

Myocardial performance index is calculated as follows:



[Figure 17] it is a measure of overall systolic and diastolic dysfunction. Normal value is <0.49. Value >0.55 suggests bad prognosis.[16] Normal value for right ventricle is 0.28 ± 0.04.
Figure 17: Tissue Doppler imaging of medial mitral annulus showing prolongation of isovolumic contraction time and isovolumic relaxation time with reduced systolic wave duration (Sa). Myocardial performance index is significantly increased suggesting impaired systolic and diastolic dysfunction of left ventricle

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Differentiation between physiologic and pathologic hypertrophy

Ventricular relaxation (Ea) is normal in physiologic hypertrophy as in athletes. On the other hand, it is impaired (Decreased Ea) in pathologic hypertrophy of hypertension and hypertrophic cardiomyopathy.[17] Other conditions with thick ventricular walls, for example, infiltrative cardiomyopathy and restrictive cardiomyopathy also have reduced Ea.[4]

Differentiation of constrictive pericarditis from restrictive cardiomyopathy

In constrictive pericarditis, myocardial relaxation is normal. Ea is, therefore, not affected. Ea of 8 cm/s or greater suggests pericardial constriction.[18] Ea increases as constriction gets worse. As a result, E/Ea decreases as diastolic filling pressure increases.[18] On the other hand, Ea decreases in restrictive cardiomyopathy. As a result, E/Ea increases as diastolic filling pressure increases.[19]

Prognostic maker of survival

In hypertensive patients, patients of acute myocardial infarction and heart failure, patients with Ea <5 cm/s or E/Ea >15 have a poor prognosis.[4],[20],[21],[22]

Assessment of myocardial viability

The presence of postsystolic shortening during acute myocardial ischemia predicts possibility of functional recovery after reperfusion therapy.[4]

Limitations

  • Angle dependency[23]
  • Influence of overall heart motion.[23]


Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Smiseth OA, Edvardsen T. Myocardial mechanics, velocity, strain, strain rate, cardiac synchrony and twist. In: Otto CM, editor. The Practice of Clinical Echocardiography. Philadelphia: Elsevier; 2012. p. 177-96.  Back to cited text no. 1
    
2.
Kjærgaard J. Assessment of right ventricular systolic function by tissue Doppler echocardiography. Dan Med J 2012;59:B4409.  Back to cited text no. 2
    
3.
Lind B, Nowak J, Cain P, Quintana M, Brodin LA. Left ventricular isovolumic velocity and duration variables calculated from colour-coded myocardial velocity images in normal individuals. Eur J Echocardiogr 2004;5:284-93.  Back to cited text no. 3
    
4.
Powell BD, Espinosa RE, Cheuk-Man YU, Oh JK. Tissue Doppler imaging and dyssynchrony assessment. In: Oh JK, Seward JB, Tajik AJ, editors. The Echo Manual. New Delhi: Lippincott William and Wilkins; 2006. p. 80-96.  Back to cited text no. 4
    
5.
Kadappu KK, Thomas L. Tissue Doppler imaging in echocardiography: Value and limitations. Heart Lung Circ 2015;24:224-33.  Back to cited text no. 5
    
6.
Nagueh SF, Appleton CP, Gillebert TC, Marino PN, Oh JK, Smiseth OA, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. Eur J Echocardiogr 2009;10:165-93.  Back to cited text no. 6
    
7.
Nagueh SF, Bachinski LL, Meyer D, Hill R, Zoghbi WA, Tam JW, et al. Tissue Doppler imaging consistently detects myocardial abnormalities in patients with hypertrophic cardiomyopathy and provides a novel means for an early diagnosis before and independently of hypertrophy. Circulation 2001;104:128-30.  Back to cited text no. 7
    
8.
Stengel SM, Allemann Y, Zimmerli M, Lipp E, Kucher N, Mohacsi P, et al. Doppler tissue imaging for assessing left ventricular diastolic dysfunction in heart transplant rejection. Heart 2001;86:432-7.  Back to cited text no. 8
    
9.
Pieroni M, Chimenti C, Ricci R, Sale P, Russo MA, Frustaci A, et al. Early detection of fabry cardiomyopathy by tissue Doppler imaging. Circulation 2003;107:1978-84.  Back to cited text no. 9
    
10.
Dokainish H, Abbey H, Gin K, Ramanathan K, Lee PK, Jue J, et al. 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.  Back to cited text no. 10
    
11.
Dokainish H, Sengupta R, Patel R, Lakkis N. Usefulness of right ventricular tissue Doppler imaging to predict outcome in left ventricular heart failure independent of left ventricular diastolic function. Am J Cardiol 2007;99:961-5.  Back to cited text no. 11
    
12.
Meluzín J, Spinarová L, Bakala J, Toman J, Krejcí J, Hude P, et al. 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.  Back to cited text no. 12
    
13.
Ommen SR, Nishimura RA, Appleton CP, Miller FA, Oh JK, Redfield MM, et al. 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.  Back to cited text no. 13
    
14.
Plana JC, Desai MY, Klein AL. Assessment of diastolic function by echocardiography. In: Otto CM, editor. The Practice of Clinical Echocardiography. Philadelphia: Elsevier; 2012. p. 197-217.  Back to cited text no. 14
    
15.
Tei C, Ling LH, Hodge DO, Bailey KR, Oh JK, Rodeheffer RJ, et al. New index of combined systolic and diastolic myocardial performance: A simple and reproducible measure of cardiac function – A study in normals and dilated cardiomyopathy. J Cardiol 1995;26:357-66.  Back to cited text no. 15
    
16.
Colonna P, Hoffmann R. Evaluation of systolic and diastolic LV function. In: Zamorano JL, Bax JJ, Rademakers FE, Knuuti J, editors. The ESC Textbook of Cardiovascular Imaging. London: Springer; 2010. p. 307-22.  Back to cited text no. 16
    
17.
Vinereanu D, Florescu N, Sculthorpe N, Tweddel AC, Stephens MR, Fraser AG, et al. 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.  Back to cited text no. 17
    
18.
Rajagopalan N, Garcia MJ, Rodriguez L, Murray RD, Apperson-Hansen C, Stugaard M, et al. Comparison of new Doppler echocardiographic methods to differentiate constrictive pericardial heart disease and restrictive cardiomyopathy. Am J Cardiol 2001;87:86-94.  Back to cited text no. 18
    
19.
Koyama J, Ray-Sequin PA, Davidoff R, Falk RH. Usefulness of pulsed tissue doppler imaging for evaluating systolic and diastolic left ventricular function in patients with AL (primary) amyloidosis. Am J Cardiol 2002;89:1067-71.  Back to cited text no. 19
    
20.
Wang M, Yip GW, Wang AY, Zhang Y, Ho PY, Tse MK, et al. Peak early diastolic mitral annulus velocity by tissue Doppler imaging adds independent and incremental prognostic value. J Am Coll Cardiol 2003;41:820-6.  Back to cited text no. 20
    
21.
Hillis GS, Møller JE, Pellikka PA, Gersh BJ, Wright RS, Ommen SR, et al. Noninvasive estimation of left ventricular filling pressure by E/e' is a powerful predictor of survival after acute myocardial infarction. J Am Coll Cardiol 2004;43:360-7.  Back to cited text no. 21
    
22.
Lee CH, Hsieh MJ, Chu CM, Chen CC, Hsieh IC, Hung KC, et al. Prognostic significance of diastolic dysfunction by tissue Doppler imaging in patients with chronic heart failure. Am J Med Sci 2009;337:415-20.  Back to cited text no. 22
    
23.
Mararu D, Badano LP. Myocardial deformation imaging from tissue Doppler to 2D speckle tracking. In: Zamorano JL, Bax JJ, Rademakers FE, Knutti J, editors. The ESC Textbook of Cardiovascular Imaging. London: Springer; 2010. p. 55-76.  Back to cited text no. 23
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17]



 

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