Echo parameters in CRT patients selectionCardiac resynchronization therapy (CRT) is recommended for patients with chronic heart failure who remain

symptomatic (NYHA class II-IV) despite optimal medical treatment, with severe systolic dysfunction (left

ventricular ejection fraction (LVEF) ≤35%) and widened QRS complex.[1]

Echocardiographic assessment of CRT candidates comprises:

evaluation of left ventricular global function (ejection fraction and volumes)

evaluation of left ventricular regional function (extent and localization of infarct scar) and

evaluation of cardiac dyssynchrony.

The measurement of LVEF determines the candidacy for CRT, whereas the end-systolic volume reduction

of ≥ 10-15% after 3-6 months of device implantation usually defines echocardiographic response to CRT.

Since patients with high scar burden (especially those with posterolateral scar) are less likely to respond to

CRT, regional function assessment should also be included in the echocardiographic report.

The definition and evaluation of cardiac dyssynchrony are still subject to debate. An electrical criterion,

QRS duration >120 ms on surface electrocardiogram (ECG), is currently the only guideline-recommended

dyssynchrony parameter for patient selection for cardiac resynchronization therapy (CRT), but allows

identification of only 60-70% of responders.[1] In order to improve CRT success rate, a plethora

echocardiographic parameters to identify true mechanical dyssynchrony, i.e. uncoordinated contraction in

different myocardial regions, has been proposed, with no consensus on the incremental value of any of

these parameters.[2]

Various echocardiographic modalities have been used for dyssynchrony assessment - from conventional

M-mode and pulsed-wave Doppler techniques to myocardial deformation imaging and three-dimensional

echocardiography.

Echocardiographic evaluation of dyssynchrony involves assessment of atrioventricular, inter- and

intraventricular dyssynchrony.

Contents

 [hide] 

1 Atrioventricular dyssynchrony

2 Interventricular dyssynchrony

3 Intraventricular dyssynchrony

o 3.1 Conventional echocardiography

o 3.2 Tissue velocity imaging

o 3.3 Deformation imaging

o 3.4 Apical rocking and septal flash

o 3.5 Three-dimensional echocardiography

4 References

Atrioventricular dyssynchrony

Atrioventricular dyssynchrony can be assessed by using pulsed-wave Doppler recording of transmitral

flow. Diastolic filling time (LVFT), defined as the sum of E-wave and A-wave duration, is divided by the RR

interval duration (Figure 1) to obtain a diastolic filling ratio (LVFT/RR).

Figure 1

 

Figure 2

Significant atrioventricular dyssynchrony is assumed if LVFT/RR is <40%.[3] Short- and long-AV delays can

also be visually identified from the transmitral flow patterns (Figure 2), which is frequently used strategy for

atrioventricular delay optimization after CRT pacemaker implantation.

Atrioventricular dyssynchrony has limited predictive value for CRT response.

Interventricular dyssynchrony

Interventricular dyssynchrony refers to dyssynchrony between the left and the right ventricle and can be

measured using conventional pulsed-wave Doppler or Tissue Doppler imaging (Figures 3 and 4,

respectively).

Figure 3

 

Figure 4

The presence of inter-ventricular dyssynchrony is indicated by the difference of >40 ms between left

ventricular and right ventricular pre-ejection time (measured by pulsed-wave Doppler) [4]or by a delay of >56

ms between the onset of systolic motion in the basal right ventricular free wall versus the most delayed

basal LV segment (measured by tissue Doppler).[5]

Recent studies have reported a limited value of inter-ventricular dyssynchrony for predicting CRT response.[6]

Intraventricular dyssynchrony

Intraventricular dyssynchrony can be evaluated by conventional echocardiography, tissue velocity

measurements and deformation imaging (Table 1).

Parameter Echo modality CutoffSeptal to posterior wall motion delay[7] M-mode ≥ 130

ms

Septal to lateral Ts delay[8] Tissue velocity imaging ≥ 60 ms

Max delay in Ts in 4 basal LV segments[9] Tissue velocity imaging > 65 ms

SD of Ts of 6 basal LV segments[10] Tissue velocity imaging ≥ 36.5 ms

Max delay in Ts in 12 basal and mid LV segments[11] Tissue velocity imaging ≥ 100 ms

SD of Ts in 12 basal and mid LV segments (Dyssynchrony Index)[12]

Tissue velocity imaging ≥ 32.6 ms

Anteroseptal to posterior time to peak strain difference (radial strain)[13]

2D speckle tracking ≥ 130 ms

SD of time-to peak longitudinal strain in 12 basal and mid LV segments[14]

Colour –Tissue Doppler imaging

> 60 ms

SD of time to minimum systolic volume of 16 LV segments (systolic dyssynchrony index)[15]

3D echocardiography > 5.6 %

Conventional echocardiography

Conventional echocardiographic markers of dyssynchrony comprise:

- septal to posterior wall motion delay (cut-off >130 ms)[7] and

- left ventricular electromechanical delay (cut-off >140 ms)[16]

Septal to posterior wall motion delay is assessed by M-mode echocardiography from parasternal short-

axis view at the papillary muscle level. It is calculated as the interval between the maximal posterior

displacement of the septum and the maximal displacement of the left posterior wall (Figure 5). This

method is not applicable in patients with previous septal or posterior wall myocardial infarction.

Figure 5

Left ventricular electromechanical delay (pre-ejection time) is determined as the time from QRS onset to

aortic flow onset (Figure 3B). Predictive value of both methods is disputed.[17]

Tissue velocity imaging

With tissue velocity imaging, longitudinal velocities of basal (or basal and mid) myocardial segments are

measured from standard apical views.

Tissue velocity- derived dyssynchrony parameters can be broadly divided into:

time delays between opposing walls and

standard deviations of time-to-peak systolic velocities.

Methods involving measurements of longitudinal velocities from 2, 4, 6 and 12 myocardial segments have

been described (Table 1). Regional myocardial velocity curves can be created online using spectral pulsed

tissue Doppler imaging or offline from digitally stored color tissue Doppler cine-loops. The latter method

reduces the time for both online image acquisition and offline image analysis. Since systolic velocity

usually refers to the ejection phase, the first step in dyssynchrony measurements is to define the ejection

period by indicating the aortic valve opening and closure in the pulsed-wave Doppler recording in the left

ventricular outflow tract. Second step is to identify the highest systolic peak between aortic valve opening

and closure, which is not necessarily the first peak. If there are several peaks in the ejection phase with

the same amplitude, the earliest peak should be selected. Although tissue velocity imaging-based

parameters appeared promising in several single-center studies, recent multicenter trial raised doubts

regarding the reproducibility and predictive value of these parameters.[6]

Deformation imaging

In contrast to the timing of myocardial velocity peaks, myocardial deformation parameters (strain, strain

rate) have the potential of distinguishing active contraction from passive motion caused by tethering of

adjacent myocardial regions. Deformation data can be obtained from color Tissue Doppler or two-

dimensional speckle tracking images.

Standard deviation of time-to-peak longitudinal strain is a Doppler-derived parameter which can be

calculated after the extraction of regional longitudinal strain curves from 12 basal and mid segments in

standard apical views. The standard deviation of time from ECG onset to peak negative strain > 60 ms has

been proposed as a strain dyssynchrony index. The data on superiority of this parameter over longitudinal

velocity-based indices are contradictory.[18]

At present, the difference ≥130 ms in peak radial strain between the basal anteroseptal and basal posterior

wall segments is one of most commonly used speckle tracking-based dyssynchrony parameter (Figure 6).

Figure 6

Apical rocking and septal flash

The direct mechanical consequences of dyssynchronous contraction induced by left bundle branch block

can be described by apical rocking and septal flash. A short initial septal contraction within the isovolumic

contraction period results of a short inward motion of the septum (septal flash) and causes the apex to

move septally. The delayed activation of the lateral wall pulls then the apex laterally during the ejection

time while stretching the septum. This typical motion pattern of the apex is described “apical rocking”. The

presence of septal flash can be visualized in parasternal (short- and long-axis) and apical (4-chamber)

views. It can also be identified on gray scale images or colour M-mode, and quantified by the amplitude of

early radial septal velocities (Figure 7).

Figure 7

Apical rocking motion can be easily visualized in apical 4-chamber view and quantified by measuring

apical transverse motion (Video 1).

Video 1: Typical apical rocking in a patient with left bundle branch block

Both apical rocking and septal flash have been shown to have predictive value for a CRT response which

is superior to velocity-based dyssynchrony parameters.[19][20][21]

Three-dimensional echocardiography

Although the feasibility of three-dimensional echocardiography to determine the timing of regional

volumetric changes has been demonstrated, at present, there is no sufficient evidence to recommend

three-dimensional echocardiography for dyssynchrony assessment.

References

1. ↑ 1.0 1.1 Task Force Members, McMurray JJ, Adamopoulos S, Anker SD, Auricchio A, Böhm M, Dickstein K, Falk V, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of the ESC. Eur Heart J. 2012 Jun 26. [Epub ahead of print] www.escardio.org/guidelines.

2. ↑  Yu CM, Sanderson JE, Gorcsan J 3rd. Echocardiography, dyssynchrony, and the response to cardiac resynchronization therapy. Eur Heart J. 2010;31(19):2326-37.

3. ↑  Cazeau S, Bordachar P, Jauvert G, Lazarus A, Alonso C, Vandrell MC, Mugica J, Ritter P. Echocardiographic modeling of cardiac dyssynchrony before and during multisite stimulation: a prospective study. Pacing Clin Electrophysiol 2003; 26:137–143.

4. ↑  Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger L, Klein W, Tavazzi L; CARE-HF study Steering Committee and Investigators. The CARE-HF study (CArdiac REsynchronisation in Heart Failure study): rationale, design and end-points. Eur J Heart Fail. 2001;3(4):481-9.

5. ↑  Penicka M, Bartunek J, De Bruyne B, Vanderheyden M, Goethals M, De Zutter M, Brugada P, Geelen P. Improvement of left ventricular function after cardiac resynchronization therapy is predicted by tissue Doppler imaging echocardiography. Circulation. 2004;109(8):978-83.

6. ↑ 6.0 6.1 Chung ES, Leon AR, Tavazzi L, Sun JP, Nihoyannopoulos P, Merlino J, Abraham WT, Ghio S, Leclercq C, Bax JJ, Yu CM, Gorcsan J 3rd, St John Sutton M, De Sutter J, Murillo J. Results of the Predictors of Response to CRT (PROSPECT) trial. Circulation. 2008;117(20):2608-16.

7. ↑ 7.0 7.1 Pitzalis MV, Iacoviello M, Romito R, Massari F, Rizzon B, Luzzi G, Guida P, Andriani A, Mastropasqua F, Rizzon P. Cardiac resynchronization therapy tailored by echocardiographic evaluation of ventricular asynchrony. J Am Coll Cardiol. 2002;40(9):1615-22.

8. ↑  Bax JJ, Marwick TH, Molhoek SG, Bleeker GB, van Erven L, Boersma E, Steendijk P, van der Wall EE, Schalij MJ. Left ventricular dyssynchrony predicts benefit of cardiac resynchronization therapy in patients with end-stage heart failure before pacemaker implantation. Am J Cardiol. 2003;92:1238–1240.

9. ↑  Bax JJ, Bleeker GB, Marwick TH, Molhoek SG, Boersma E, Steendijk P, van der Wall EE, Schalij MJ. Left ventricular dyssynchrony predicts response and prognosis after cardiac resynchronization therapy. J Am Coll Cardiol. 2004;44(9):1834-40.

10. ↑  Van de Veire NR, Bleeker GB, Ypenburg C, De Sutter J, Ajmone Marsan N, Holman ER et al. Usefulness of triplane tissue Doppler imaging to predict acute response to cardiac resynchronization therapy. Am J Cardiol. 2007;100:476–482.

11. ↑  Notabartolo D, Merlino JD, Smith AL, DeLurgio DB, Vera FV, Easley KA, Martin RP, Leon AR. Usefulness of the peak velocity difference by tissue Doppler imaging technique as an effective predictor of response to cardiac resynchronization therapy. Am J Cardiol. 2004;94:817– 820.

12. ↑  Yu CM, Fung WH, Lin H, Zhang Q, Sanderson JE, Lau CP. Predictors of left ventricular reverse remodeling after cardiac resynchronization therapy for heart failure secondary to idiopathic dilated or ischemic cardiomyopathy. Am J Cardiol. 2003;91(6):684-8.

13. ↑  Suffoletto M, Dohi K, Cannesson M, Saba S, Gorcsan J. Novel speckle-tracking radial strain from routineblack-and-white echocardiographic images to quantify dyssynchrony and predict response to cardiac resynchronization therapy. Circulation. 2006;113:960–968.

14. ↑  Mele D, Pasanisi G, Capasso F, De Simone A, Morales MA, Poggio D, Capucci A, Tabacchi G, Sallusti L, Ferrari R. Left intraventricular myocardial deformation dyssynchrony identifies responders to cardiac resynchronization therapy in patients with heart failure. Eur Heart J. 2006;27(9):1070-8.

15. ↑  Marsan NA, Bleeker GB, Ypenburg C, Ghio S, Van de Veire NR, Holman ER et al. Real-time threedimensional echocardiography permits quantification of left ventricular mechanical dyssynchrony and predicts acute response to cardiac resynchronization therapy. J Cardiovasc Electrophysiol. 2008;4:392–399.

16. ↑  Cazeau S, Bordachar P, Jauvert G, Lazarus A, Alonso C, Vandrell MC, Mugica J, Ritter P. Echocardiographic modeling of cardiac dyssynchrony before and during multisite stimulation: a prospective study; Pacing Clin Electrophysiol. 2003;26(pt II):137–143.

17. ↑  Marcus GM, Rose E, Viloria EM, Schafer J, De Marco T, Saxon LA, Foster E; VENTAK CHF/CONTAK-CD Biventricular Pacing Study Investigators. Septal to posterior wall motion delay fails to predict reverse remodeling or clinical improvement in patients undergoing cardiac resynchronization therapy. J Am Coll Cardiol. 2005;46(12):2208-14.

18. ↑  Yu CM, Gorcsan J III, Bleeker GB, Zhang Q, Schalij MJ, Suffoletto MS et al. Usefulness of tissue Doppler velocity and strain dyssynchrony for predicting left ventricular reverse remodeling response after cardiac resynchronization therapy. Am J Cardiol. 2007;8:1263–70.

19. ↑  Voigt JU, Schneider TM, Korder S, Szulik M, Gürel E, Daniel WG, Rademakers F, Flachskampf FA. Apical transverse motion as surrogate parameter to determine regional left ventricular function inhomogeneities: a new, integrative approach to left ventricular asynchrony assessment. Eur Heart J. 2009;30(8):959-68.

20. ↑  Szulik M, Tillekaerts M, Vangeel V, Ganame J, Willems R, Lenarczyk R, Rademakers F, Kalarus Z, Kukulski T, Voigt JU. . Assessment of apical rocking: a new, integrative approach for selection of candidates for cardiac resynchronization therapy. Eur J Echocardiogr. 2010;11(10):863-9.

21. ↑  Parsai C, Bijnens B, Sutherland GR, Baltabaeva A, Claus P, Marciniak M, Paul V, Scheffer M, Donal E, Derumeaux G, Anderson L. Toward understanding response to cardiac resynchronization therapy: left ventricular dyssynchrony is only one of multiple mechanisms. Eur Heart J. 2009;30(8):940-9.