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Echo parameters in CRT patients selection
Cardiac 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 Tissuevelocity imaging
o 3.3 Deformation imaging
o 3.4 Apical rocking and septalflash
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 Cutoff
Septal 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
Anteroseptalto 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, DicksteinK, Falk V, et al. ESC Guidelines for
the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force forthe Diagnosis and Treatment of Acuteand Chronic
Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of theESC. Eur
Heart J. 2012 Jun26. [Epub aheadof 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, AlonsoC, Vandrell MC, MugicaJ, Ritter P. Echocardiographic modeling of cardiac
dy ssynchrony before and duringmultisite 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
Inv estigators. 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, DeBruyne B, Vanderheyden M, Goethals M, DeZutterM, Brugada P, Geelen P. Improvement of left ventricular
f unctionafter 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, MerlinoJ, Abraham WT, Ghio S, Leclercq C, Bax JJ, Yu CM, GorcsanJ
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
resy nchronization 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
dy ssynchrony 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 ventriculardyssynchrony predicts
response and prognosis after cardiac resynchronization therapy. J Am Coll Cardiol. 2004;44(9):1834-40.
10. ↑ Van de Veire NR, Bleeker GB, YpenburgC, De Sutter J, AjmoneMarsan N, Holman ER et al. Usefulness of triplane tissue Doppler imaging
to predict acute responseto cardiac resynchronization therapy. Am J Cardiol. 2007;100:476–482.
11. ↑ Notabartolo D, MerlinoJD, SmithAL, DeLurgio DB, Vera FV, Easley KA, Martin RP, Leon AR. Usefulness of the peak velocity difference by
tissue Dopplerimaging technique as an effective predictor of responseto 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 forheart failure secondary to idiopathic dilated or ischemic cardiomyopathy. Am J Cardiol. 2003;91(6):684-8.
13. ↑ Suf folettoM, Dohi K, Cannesson M, Saba S, Gorcsan J. Novel speckle-tracking radial strain from routineblack-and-whiteechocardiographic
images to quantify dyssynchrony and predict response to cardiac resynchronization therapy. Circulation. 2006;113:960–968.
14. ↑ Mele D, Pasanisi G, Capasso F, De SimoneA, Morales MA, PoggioD, Capucci A, Tabacchi G, SallustiL, Ferrari R. Left intraventricular
my ocardial deformation dyssynchrony identifies responders to cardiac resynchronizationtherapy in patients withheart failure. Eur Heart J.
2006;27(9):1070-8.
15. ↑ Marsan NA, Bleeker GB, Ypenburg C, GhioS, Van de Veire NR, Holman ER et al. Real-timethreedimensional echocardiography permits
quantif ication 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, AlonsoC, Vandrell MC, MugicaJ, Ritter P. Echocardiographic modeling of cardiac
dy ssynchrony before and duringmultisite stimulation: a prospective study; Pacing Clin Electrophysiol. 2003;26(pt II):137–143.
17. ↑ Marcus GM, Rose E, Viloria EM, Schafer J, DeMarco T, Saxon LA, FosterE; VENTAK CHF/CONTAK-CD BiventricularPacingStudy
Inv estigators. Septal to posterior wall motion delay fails to predict reverseremodeling or clinical improvement in patients undergoing cardiac
resy nchronization therapy. J Am Coll Cardiol. 2005;46(12):2208-14.
18. ↑ Yu CM, Gorcsan J III, BleekerGB, Zhang Q, Schalij MJ, Suffoletto MS et al. Usefulness of tissueDoppler velocity and strain dyssynchrony
f or 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. Apicaltransversemotion as surrogate
parameter to determine regional left ventricular function inhomogeneities: a new, integrative approachto left ventricularasynchrony
assessment. Eur Heart J. 2009;30(8):959-68.
20. ↑ Szulik M, Tillekaerts M, Vangeel V, GanameJ, Willems R, Lenarczyk R, Rademakers F, Kalarus Z, Kukulski T, Voigt JU. . Assessment of
apical rocking: a new, integrative approachfor selection of candidates for cardiac resynchronization therapy. EurJ 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 resynchronizationtherapy: left ventricular dyssynchrony is only one of multiple mechanisms. Eur Heart J.
2009;30(8):940-9.

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Echo parameters in crt patients selection

  • 1. Echo parameters in CRT patients selection Cardiac 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
  • 2.  3 Intraventricular dyssynchrony o 3.1 Conventional echocardiography o 3.2 Tissuevelocity imaging o 3.3 Deformation imaging o 3.4 Apical rocking and septalflash 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
  • 3. 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).
  • 5. 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 Cutoff Septal 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 Anteroseptalto 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]
  • 6. 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
  • 7. 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
  • 8. 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
  • 9. 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, DicksteinK, Falk V, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: The Task Force forthe Diagnosis and Treatment of Acuteand Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association (HFA) of theESC. Eur Heart J. 2012 Jun26. [Epub aheadof 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, AlonsoC, Vandrell MC, MugicaJ, Ritter P. Echocardiographic modeling of cardiac dy ssynchrony before and duringmultisite 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 Inv estigators. 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, DeBruyne B, Vanderheyden M, Goethals M, DeZutterM, Brugada P, Geelen P. Improvement of left ventricular f unctionafter 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, MerlinoJ, Abraham WT, Ghio S, Leclercq C, Bax JJ, Yu CM, GorcsanJ 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 resy nchronization 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 dy ssynchrony 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 ventriculardyssynchrony predicts response and prognosis after cardiac resynchronization therapy. J Am Coll Cardiol. 2004;44(9):1834-40. 10. ↑ Van de Veire NR, Bleeker GB, YpenburgC, De Sutter J, AjmoneMarsan N, Holman ER et al. Usefulness of triplane tissue Doppler imaging to predict acute responseto cardiac resynchronization therapy. Am J Cardiol. 2007;100:476–482. 11. ↑ Notabartolo D, MerlinoJD, SmithAL, DeLurgio DB, Vera FV, Easley KA, Martin RP, Leon AR. Usefulness of the peak velocity difference by tissue Dopplerimaging technique as an effective predictor of responseto 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 forheart failure secondary to idiopathic dilated or ischemic cardiomyopathy. Am J Cardiol. 2003;91(6):684-8. 13. ↑ Suf folettoM, Dohi K, Cannesson M, Saba S, Gorcsan J. Novel speckle-tracking radial strain from routineblack-and-whiteechocardiographic images to quantify dyssynchrony and predict response to cardiac resynchronization therapy. Circulation. 2006;113:960–968. 14. ↑ Mele D, Pasanisi G, Capasso F, De SimoneA, Morales MA, PoggioD, Capucci A, Tabacchi G, SallustiL, Ferrari R. Left intraventricular my ocardial deformation dyssynchrony identifies responders to cardiac resynchronizationtherapy in patients withheart failure. Eur Heart J. 2006;27(9):1070-8. 15. ↑ Marsan NA, Bleeker GB, Ypenburg C, GhioS, Van de Veire NR, Holman ER et al. Real-timethreedimensional echocardiography permits quantif ication 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, AlonsoC, Vandrell MC, MugicaJ, Ritter P. Echocardiographic modeling of cardiac dy ssynchrony before and duringmultisite stimulation: a prospective study; Pacing Clin Electrophysiol. 2003;26(pt II):137–143. 17. ↑ Marcus GM, Rose E, Viloria EM, Schafer J, DeMarco T, Saxon LA, FosterE; VENTAK CHF/CONTAK-CD BiventricularPacingStudy Inv estigators. Septal to posterior wall motion delay fails to predict reverseremodeling or clinical improvement in patients undergoing cardiac resy nchronization therapy. J Am Coll Cardiol. 2005;46(12):2208-14. 18. ↑ Yu CM, Gorcsan J III, BleekerGB, Zhang Q, Schalij MJ, Suffoletto MS et al. Usefulness of tissueDoppler velocity and strain dyssynchrony f or 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. Apicaltransversemotion as surrogate parameter to determine regional left ventricular function inhomogeneities: a new, integrative approachto left ventricularasynchrony assessment. Eur Heart J. 2009;30(8):959-68. 20. ↑ Szulik M, Tillekaerts M, Vangeel V, GanameJ, Willems R, Lenarczyk R, Rademakers F, Kalarus Z, Kukulski T, Voigt JU. . Assessment of apical rocking: a new, integrative approachfor selection of candidates for cardiac resynchronization therapy. EurJ 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 resynchronizationtherapy: left ventricular dyssynchrony is only one of multiple mechanisms. Eur Heart J. 2009;30(8):940-9.