Tissue Doppler echocardiography

Tissue Doppler echocardiography
Purposemeasures the velocity of heart muscle

Tissue Doppler echocardiography (TDE) is a medical ultrasound technology, specifically a form of echocardiography that measures the velocity of the heart muscle (myocardium) through the phases of one or more heartbeats by the Doppler effect (frequency shift) of the reflected ultrasound. The technique is the same as for flow Doppler echocardiography measuring flow velocities. Tissue signals, however, have higher amplitude and lower velocities, and the signals are extracted by using different filter and gain settings. The terms tissue Doppler imaging (TDI) and tissue velocity imaging (TVI) are usually synonymous with TDE because echocardiography is the main use of tissue Doppler.

Like Doppler flow, tissue Doppler can be acquired both by spectral analysis (spectral density estimation) as pulsed Doppler[1] and by the autocorrelation technique as colour tissue Doppler[2] (duplex ultrasonography). While pulsed Doppler only acquires the velocity at one point at a time, colour Doppler can acquire simultaneous pixel velocity values across the whole imaging field. Pulsed Doppler on the other hand, is more robust against noise, as peak values are measured on top of the spectrum, and are unaffected of the presence of clutter (stationary reverberation noise).

Pulsed tissue Doppler echocardiography

This has become a major echocardiographic tool for assessment of both systolic and diastolic ventricular function. However, as this is a spectral technique, it is important to realise that measurement of peak values is dependent on the width of the spectrum, which again is a function of gain setting.

Clinical use

Spectral tissue velocity curves from the mitral annulus at the septal (left) and lateral (right) points. The curves show multiple heartbeats.

Pulsed wave spectral tissue Doppler has become a universal tool that is part of the general echocardiographic examination. Like any other echocardiographic measurement, measures by tissue Doppler should be interpreted in the context of the whole examination. The velocity curves are in general taken from the base of the mitral annulus at the insertion of the mitral leaflets, in the septal and lateral points of the four chamber view, and eventually the anterior and inferior points of the two-chamber views. For the right ventricle it is customary to use the lateral point of the tricuspid annulus only. Averaging peak velocities from the septal and lateral point has become common, although it has been shown that averaging all four points mentioned above, gives significantly less variability[3]

The method measures annular velocities to and from the probe during the heart cycle.

Single spectral tissue velocity curve from the mitral annulus. The curve shows velocities towards the probe (positive velocity) in systole, and away from the probe (negative velocities) in diastole. The most useful measures are the peak velocities, in systole S' and in early diastole (e') and late diastole during atrial contraction (a').

Annular velocities summarize the longitudinal contraction of the ventricle during systole, and elongation during diastole. Peak velocities are commonly used.

Systolic function

Peak systolic annular velocity (S') of the left ventricle is as close to a contractility measure as you can get by imaging[4] (bearing in mind that any imaging method only measures the result of fibre shortening, without measuring myocyte tension). S' has become a reliable measure of global function[5][6][7][8] It shares the advantage of annular displacement, that it is reduced also in hypertrophic hearts with small ventricles and normal ejection fraction (HFNEF), which is often seen in Hypertensive heart disease, Hypertrophic cardiomyopathy and Aortic stenosis.[9]

Likewise, peak ticuspid annular systolic velocity has become a measure of the right ventricular systolic function[10][11]

Diastolic function

As the ventricle relaxes, the annulus moves towards the base of the heart, signifying the volume expansion of the ventricle. The peak mitral annular velocity during early filling, e' is a measure of left ventricular diastolic function, and has been shown to be relatively independent of left ventricular filling pressure.[12][13][14] If there is impaired relaxation (Diastolic dysfunction), the e' velocity decreases. After the early relaxation, the ventricular myocardium is passive, the late velocity peak a' is a function of atrial contraction. The ratio between e' and a' is also a measure of diastolic function, in addition to the absolute values.

During the two filling phases, there is early (E) and late (A) blood flow from the atrium to the ventricle, corresponding to the annular velocity phases. The flow, is driven by the pressure difference between atrium and ventricle, this pressure difference is both a function of the pressure drop during early relaxation and the initial atrial pressure. In light diastolic dysfunction, the peak early mitral flow velocity E is reduced in proportion to the e', but if relaxation is so reduced that it causes increase in atrial pressure, E will increase again, while e', being less load dependent, remains low. Thus, the ratio E/e' is related to the atrial pressure, and can show increased filling pressure[15][16] although with several reservations.[17][18] In the right ventricle this is not an important principle, as the right atrial pressure is the same as central venous pressure which can easily be assessed from venous congestion.[19][20]

relation between mitral flow and mitral annulus velocity. Left: Normal person with good diastolic function; high E and e', normal E/e'. Middle, patient with diastolic dysfunction without increased filling pressure; low E and e', normal E/e' ratio. Left, patient with diastolic dysfunction and increased filling pressure; high E, low e' and high E/e'. The S' is reduced in proportion to the e'

Heart failure with preserved ejection fraction (HFPEF)

One of the main advantages of tissue Doppler is that diastolic and systolic function can be measured by the same tool. Before the advent of tissue Doppler, systolic function was usually assessed with ejection fraction (EF), and diastolic function by mitral flow. This led to the concept of pure "diastolic heart failure". However, In hypertrophic left ventricles with small cavity size, the systolic function is reduced although EF is not, as the EF is dependent on the relative wall thickness.[21] This has led to the concept of "pure diastolic heart failure" being discarded.[9] The preferred term is now heart failure with normal ejection fraction (HFNEF) or heart failure with preserved ejection fraction (HFPEF). This is common and is often seen in hypertensive heart disease, hypertrophic cardiomyopathy and aortic stenosis, and may comprise as much as 50% of the total heart failure population.[22] The prognosis of HFPEF is the same as for heart failure with dilated hearts.[23]

Mitral valve prolapse (MVP)

Pulsed-wave tissue Doppler can be used as a way to evaluate the severeness of arrhythmic mitral valve prolapse, by looking at the peak in the middle of the systole, which looks similar to Prussian Pickelhaube helmet, hence the name Pickelhaube spike.[24] This is one of the risk markers for malignant arrhythmias in patients with myxomatous mitral valve disease (MMVD) and bileaflet mitral valve prolapse (BMVP). It's significant when exceeds 16 cm/s. The sudden systolic overload of which Pickelhaube spike is an expression can act as a trigger for the onset of ventricular arrhythmias.[25]

Normal values and physiology

Normal gender and age related reference values For both S', e' and a' have been established in the large HUNT study, comprising 1266 subjects free of heart disease, hypertension and diabetes.[26]

This study also shows that both S' and e' values decline with age, while a' increases (fig). There is also a significant correlation between S' and e', also in healthy subjects, showing the connection between systolic and diastolic function.

Age dependent normal values for S', e' and a'.

The e'/a' ratio becomes <1 about 60 years of age, which is similar to the E/A ratio of mitral flow. Women has slightly higher S' and e' velocities than men, although the difference disappears with age. The study also did show that velocities were highest in the lateral wall, and lowest in the septum. The E/e' was thus dependent on the site of e' measurement. The ratio was also age dependent.

Colour tissue Doppler

Colour tissue Doppler traces from a normal subject Left: traces from the septum and mitral ring. The similarities of the curve shape to spectral Doppler is evident. Right: multiple traces from sites along the septum. The decreasing velocities from base to apex is evident.

Unlike spectral Doppler, colour tissue Doppler samples velocities from all points of the sector, by shooting two pulses successively, and calculating the velocity from the phase shift between them by autocorrelation. The calculation is slightly different from the true Doppler effect, but the result becomes identical. This results in a single velocity value per sample volume. The result is a velocity field of (nearly) simultaneous velocity vectors towards the probe. The advantage of colour Doppler over spectral Doppler is that all velocities can be sampled simultaneously. The disadvantage is that if there is clutter noise (stationary reverberations), the stationary echoes will be integrated in the velocity calculation, resulting in an under estimate. As pulsed wave Doppler are displayed as a spectrum, the colour Doppler values will correspond to the mean of the spectrum (in the absence of clutter), giving slightly lower values. In the HUNT study, the difference in peak systolic values were about 1.5 cm/s.[26]

The local velocities are not the result of the local function, as segments are moved by the action of neighbouring segments. Thus the velocity differences velocity gradient are the main measure of regional contraction, and has become the most important employment of colour tissue Doppler, in the method of strain rate imaging.[27]

References

  1. ↑ Isaaz K, Thompson A, Ethevenot G, Cloez JL, Brembilla B, Pernot C (July 1989). "Doppler echocardiographic measurement of low velocity motion of the left ventricular posterior wall". The American Journal of Cardiology. 64 (1): 66–75. doi:10.1016/0002-9149(89)90655-3. PMID 2741815.
  2. ↑ McDicken WN, Sutherland GR, Moran CM, Gordon LN (1992). "Colour Doppler velocity imaging of the myocardium". Ultrasound in Medicine & Biology. 18 (6–7): 651–4. doi:10.1016/0301-5629(92)90080-t. PMID 1413277.
  3. ↑ Thorstensen A, Dalen H, Amundsen BH, Aase SA, Stoylen A (March 2010). "Reproducibility in echocardiographic assessment of the left ventricular global and regional function, the HUNT study". European Journal of Echocardiography. 11 (2): 149–56. doi:10.1093/ejechocard/jep188. PMID 19959533.
  4. ↑ Thorstensen A, Dalen H, Amundsen BH, Støylen A (December 2011). "Peak systolic velocity indices are more sensitive than end-systolic indices in detecting contraction changes assessed by echocardiography in young healthy humans". European Journal of Echocardiography. 12 (12): 924–30. doi:10.1093/ejechocard/jer178. PMID 21940728.
  5. ↑ Gulati VK, Katz WE, Follansbee WP, Gorcsan J (May 1996). "Mitral annular descent velocity by tissue Doppler echocardiography as an index of global left ventricular function". The American Journal of Cardiology. 77 (11): 979–84. doi:10.1016/s0002-9149(96)00033-1. PMID 8644649.
  6. ↑ Vinereanu D, Ionescu AA, Fraser AG (January 2001). "Assessment of left ventricular long axis contraction can detect early myocardial dysfunction in asymptomatic patients with severe aortic regurgitation". Heart (British Cardiac Society). 85 (1): 30–6. doi:10.1136/heart.85.1.30. PMC 1729596. PMID 11119457.
  7. ↑ Vinereanu D, Florescu N, Sculthorpe N, Tweddel AC, Stephens MR, Fraser AG (July 2001). "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". The American Journal of Cardiology. 88 (1): 53–8. doi:10.1016/s0002-9149(01)01585-5. PMID 11423058.
  8. ↑ Støylen A, Skjaerpe T (September 2003). "Systolic long axis function of the left ventricle. Global and regional information". Scandinavian Cardiovascular Journal : SCJ. 37 (5): 253–8. doi:10.1080/14017430310015000. PMID 14534065. S2CID 13007825.
  9. 1 2 Yip G, Wang M, Zhang Y, Fung JW, Ho PY, Sanderson JE (February 2002). "Left ventricular long axis function in diastolic heart failure is reduced in both diastole and systole: time for a redefinition?". Heart (British Cardiac Society). 87 (2): 121–5. doi:10.1136/heart.87.2.121. PMC 1766981. PMID 11796546.
  10. ↑ Alam M, Wardell J, Andersson E, Samad BA, Nordlander R (August 1999). "Characteristics of mitral and tricuspid annular velocities determined by pulsed wave Doppler tissue imaging in healthy subjects". Journal of the American Society of Echocardiography. 12 (8): 618–28. doi:10.1053/je.1999.v12.a99246. PMID 10441217.
  11. ↑ Meluzín J, Spinarová L, Bakala J, Toman J, Krejcí J, Hude P, Kára T, Soucek M (February 2001). "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". European Heart Journal. 22 (4): 340–8. doi:10.1053/euhj.2000.2296. PMID 11161953.
  12. ↑ Rodriguez L, Garcia M, Ares M, Griffin BP, Nakatani S, Thomas JD (May 1996). "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". American Heart Journal. 131 (5): 982–7. doi:10.1016/s0002-8703(96)90183-0. PMID 8615320.
  13. ↑ Sohn DW, Chai IH, Lee DJ, Kim HC, Kim HS, Oh BH, Lee MM, Park YB, Choi YS, Seo JD, Lee YW (August 1997). "Assessment of mitral annulus velocity by Doppler tissue imaging in the evaluation of left ventricular diastolic function". Journal of the American College of Cardiology. 30 (2): 474–80. doi:10.1016/s0735-1097(97)88335-0. PMID 9247521.
  14. ↑ Pelà G, Regolisti G, Coghi P, Cabassi A, Basile A, Cavatorta A, Manca C, Borghetti A (August 2004). "Effects of the reduction of preload on left and right ventricular myocardial velocities analyzed by Doppler tissue echocardiography in healthy subjects". European Journal of Echocardiography. 5 (4): 262–71. doi:10.1016/j.euje.2003.10.001. PMID 15219541.
  15. ↑ Nagueh SF, Middleton KJ, Kopelen HA, Zoghbi WA, Quiñones MA (November 1997). "Doppler tissue imaging: a noninvasive technique for evaluation of left ventricular relaxation and estimation of filling pressures". Journal of the American College of Cardiology. 30 (6): 1527–33. doi:10.1016/s0735-1097(97)00344-6. PMID 9362412.
  16. ↑ Farias CA, Rodriguez L, Garcia MJ, Sun JP, Klein AL, Thomas JD (August 1999). "Assessment of diastolic function by tissue Doppler echocardiography: comparison with standard transmitral and pulmonary venous flow". Journal of the American Society of Echocardiography. 12 (8): 609–17. doi:10.1053/je.1999.v12.a99249. PMID 10441216.
  17. ↑ Mullens W, Borowski AG, Curtin RJ, Thomas JD, Tang WH (January 2009). "Tissue Doppler imaging in the estimation of intracardiac filling pressure in decompensated patients with advanced systolic heart failure". Circulation. 119 (1): 62–70. doi:10.1161/CIRCULATIONAHA.108.779223. PMC 3169300. PMID 19075104.
  18. ↑ Park JH, Marwick TH (December 2011). "Use and Limitations of E/e' to Assess Left Ventricular Filling Pressure by Echocardiography". Journal of Cardiovascular Ultrasound. 19 (4): 169–73. doi:10.4250/jcu.2011.19.4.169. PMC 3259539. PMID 22259658.
  19. ↑ Skjaerpe T, Hatle L (August 1986). "Noninvasive estimation of systolic pressure in the right ventricle in patients with tricuspid regurgitation". European Heart Journal. 7 (8): 704–10. doi:10.1093/oxfordjournals.eurheartj.a062126. PMID 2945720.
  20. ↑ Ommen SR, Nishimura RA, Hurrell DG, Klarich KW (January 2000). "Assessment of right atrial pressure with 2-dimensional and Doppler echocardiography: a simultaneous catheterization and echocardiographic study". Mayo Clinic Proceedings. 75 (1): 24–9. doi:10.4065/75.1.24. PMID 10630753.
  21. ↑ Maciver DH (March 2011). "A new method for quantification of left ventricular systolic function using a corrected ejection fraction". European Journal of Echocardiography. 12 (3): 228–34. doi:10.1093/ejechocard/jeq185. PMID 21216767.
  22. ↑ Hogg K, Swedberg K, McMurray J (February 2004). "Heart failure with preserved left ventricular systolic function; epidemiology, clinical characteristics, and prognosis". Journal of the American College of Cardiology. 43 (3): 317–27. doi:10.1016/j.jacc.2003.07.046. PMID 15013109.
  23. ↑ Muntwyler J, Abetel G, Gruner C, Follath F (December 2002). "One-year mortality among unselected outpatients with heart failure". European Heart Journal. 23 (23): 1861–6. doi:10.1053/euhj.2002.3282. PMID 12445535.
  24. ↑ Ignatowski D, Schweitzer M, Pesek K, Jain R, Muthukumar L, Khandheria BK, Tajik AJ (May 2020). "Pickelhaube Spike, a High-Risk Marker for Bileaflet Myxomatous Mitral Valve Prolapse: Sonographer's Quest for the Highest Spike". Journal of the American Society of Echocardiography. 33 (5): 639–640. doi:10.1016/j.echo.2020.02.004. PMID 32199779. S2CID 214617051.
  25. ↑ Coutsoumbas GV, Di Pasquale G (October 2021). "Mitral valve prolapse with ventricular arrhythmias: does it carries a worse prognosis?". European Heart Journal Supplements. 23 (Suppl E): E77–E82. doi:10.1093/eurheartj/suab096. PMC 8503385. PMID 34650360.
  26. 1 2 Dalen H, Thorstensen A, Vatten LJ, Aase SA, Stoylen A (September 2010). "Reference values and distribution of conventional echocardiographic Doppler measures and longitudinal tissue Doppler velocities in a population free from cardiovascular disease". Circulation: Cardiovascular Imaging. 3 (5): 614–22. doi:10.1161/CIRCIMAGING.109.926022. PMID 20581050. S2CID 20030498.
  27. ↑ Heimdal A, Støylen A, Torp H, Skjaerpe T (November 1998). "Real-time strain rate imaging of the left ventricle by ultrasound". Journal of the American Society of Echocardiography. 11 (11): 1013–9. doi:10.1016/s0894-7317(98)70151-8. PMID 9812093.

Further reading

  • Sutherland GR, Hatle L, Claus P, D'hooge J, Bijnens BH (2006). Doppler Myocardial Imaging: A Textbook (1st ed.). Hasselt, Belgium: BSWK. ISBN 978-90-810592-1-3.
  • Marwick TH, Yu CM, Sun JP, eds. (2007). Myocardial Imaging: Tissue Doppler and Speckle Tracking. Malden, Mass.: Wiley-Blackwell. ISBN 978-1-4051-6113-8.
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