Peter Schuster,
MD; Svein Faerestrand, MD, PhD
Department of Heart Disease,
Haukeland University Hospital, Institute of Medicine, University of
Bergen, Bergen, Norway.
Address for
correspondence: Peter Schuster, MD, Department of Heart Disease,
Haukeland University Hospital, N-5021 Bergen, Norway.
E-mail:
peter.schuster@med.uib.no
Abstract
The most recent treatment option of medically
refractory heart failure includes cardiac resynchronization therapy
(CRT) by biventricular pacing in selected patients in NYHA functional
class III or IV heart failure. The widely used marker to indicate left
ventricular (LV) asynchrony has been the surface ECG, but seems not to
be a sufficient marker of the mechanical events within the LV and
prediction of clinical response. This review presents an overview of
techniques for identification of left ventricular intra- and
interventricular asynchrony. Both manuscripts for electrical and
mechanical asynchrony are reviewed, partly predicting response to CRT.
In summary there is still no gold standard for assessment of LV
asynchrony for CRT, but both traditional and new echocardiographic
methods have shown asynchronous LV contraction in heart failure
patients, and resynchronized LV contraction during CRT and should be
implemented as additional methods for selecting patients to CRT.
Keywords: cardiac resynchronization pacemaker therapy;
electrical and mechanical asynchrony; echocardiography
Introduction
Cardiac Resynchronization Therapy
The most
recent treatment option of medically refractory heart failure includes
cardiac
resynchronization therapy (CRT) by biventricular pacing in selected
patients
in NYHA functional class III or IV heart failure (HF) caused by
idiopathic
dilated (DCM) or ischemic cardiomyopathy, with QRS duration
>
130
milliseconds, left ventricular (LV) end-diastolic diameter
>
55
mm, and ejection fraction
< 35%
1.
Pacemaker treatment for severe HF started at the beginning of the
1980’s,
when beneficial effects of dual chamber pacing with short
atrioventricular-delay
were claimed
2. However, a
later
study did not confirm these results
3.
Modification of ventricular mechanical activation sequence by pacing
from
the right ventricular outflow tract also demonstrated various
hemodynamic
results
4-6.
Due
to the fact that LBBB can cause asynchronous electrical activation and
deterioration
of LV pump function which can be corrected for by CRT, a new era
of
CRT by biventricular pacing of both right and left ventricle has
rapidly
developed in recent years
7-9.
There are a large number of HF patients suffering from intra- and
interventricular
asynchronous contraction and relaxation assumed by the surface
ECG
further deteriorating an already hemodynamically compromised left
ventricle
10. Biventricular
pacing
is assumed to provide a more coordinated pattern of ventricular
contraction,
and reduce intraventricular and interventricular asynchrony.
The acute improvement of LV
performance by CRT was demonstrated by reduction of capillary wedge
pressure and an improvement in peak dp/dt without increase in
myocardial oxygen consumption
11-14. Long-term clinical benefits by CRT
in terms of improvements in the 6-minutes hall walk distance, NYHA
functional class and quality of life indices and increasing maximal
and submaximal exercise capacity measured by oxygen consumption were
demonstrated in several studies, even at diminished myocardial energy
cost
15. Even
if CRT has proven to improve several hemodynamic and clinical indices
in almost 70% of the patients,
it is still difficult to define responders to CRT treatment, and most
commonly composite clinical endpoints have been used. Of major interest
is of course to decrease the number of clinical non responders, which
is described to
be at approximately 30 %
16,17.
The main focus
of this manuscript is to review LV asynchrony, and to present an
overview of techniques for identification of left ventricular
intraventricular and interventricular asynchrony.
Assessment of left ventricular asynchrony
Electrical asynchrony
Surface ECG: The widely used marker to indicate LV
asynchrony has been the surface ECG. The rational for that, is that the
electrical
delayed stimulation may lead to a mechanical delay of the respective LV
areas. In LBBB the lateral free wall is activated later than the
interventricular
septum and thus leads to a delayed contraction of LV free wall. This
surrogate
marker represented by LBBB is one of the criteria indicating
implantation
of CRT
1. It is shown that
LBBB
leads to impaired pump function which can be improved by CRT
7-9. LBBB is also a
predictor
of sudden cardiac death in DCM
18
.
In 29 patients
Alonso et al showed that reducing the QRS duration by CRT correlated to
a positive clinical response suggesting a hemodynamic improvement
associated with narrowing of QRS indicating reduction of the mechanical
asynchrony of LV contraction. The study concluded even that the optimal
placement for hemodynamic LV improvement of the right and LV leads
would be those sites that could induce
the greatest shortening of QRS duration
19.
However, still there is no evidence for prediction of clinical response
based on baseline QRS width or by the reduction of the QRS width
effected
by CRT in the individual patient.
Electrophysiological mapping: An additional method to
elucidate the intraventricular activation pattern in HF patients
eligible for CRT
is electroanatomical activation mapping. In 26 patients Peichl et
al. showed that the surface ECG is of limited value to describe the
complex
conduction disturbance of the LV
20 . They
found
differences in electroanatomical LV activation between ischemic
cardiomyopathy
and DCM with similar QRS morphology on the surface ECG.
Also Yu et al.
showed that endocardial electrical LV activation sequences was variable
among 7 HF patients with LBBB
21.
Lambiase et al. showed hemodynamic improvements in 10 HF patients
by CRT in
terms of increased cardiac output and dP/dt(max) when the LV was paced
by
placing the pacing lead away from areas with demonstrated slow
conduction
22. They
concluded that clinical non response may reflect LV lead placement in
regions with slow conduction which can
be avoided by pacing in more normally activated LV regions.
Mechanical asynchrony
3D-tagged magnetic resonance imaging (MRI): Asynchronous
contraction of LV was demonstrated in patients with DCM with
intraventricular conduction delay by Curry et al. , who used MRI
23. MRI is a time consuming method and
can so far not be employed in patients with implanted pacemakers.
Scintigraphic blood pool and phase image analysis: By using
gated equilibrium radionuclide angiography and Fourier phase analyses
Fauchier
et al. demonstrated in 103 patients with DCM that QRS duration
was
related to both interventricular and intraventricular asynchrony
24. Further, intraventricular
asynchrony was an independent predictor of cardiac event (cardiac
death, worsening
of HF and heart transplantation) in DCM and the prognosis was related
to
intraventricular rather than to interventricular asynchrony.
Another
radionuclide angioscintigraphy study by Toussaint JF et al. in 21
patients showed that resynchronization by CRT between LV apex and base
which persisted up to 12 months was also associated with a persisting
improvement in LV systolic function
25.
The same group showed in 34 patients that basal asynchrony and
early resynchronization
demonstrated by radionuclide angioscintigraphy might predict
long-term
evolution of ventricular function after CRT in patients with very broad
QRS (179
+ 18)
26
.
Kerwin et al.
used gated blood pool scintigraphy in 13 patients to demonstrate
asynchronous contraction
of LV and to show the resynchronizing effect of CRT
27. DCM with intraventricular conduction
delay was also associated with significant interventricular asynchrony.
Improvements in interventricular synchrony during CRT correlated with
acute improvements in LV ejection fraction. One limitation of the
scintigraphic methods is the relatively poor time resolution of 30 fps.
Echocardiographic methods: Echocardiography is an essential
method to diagnose HF and is also used to evaluate the effect of
treatment
to improve cardiac performance. The echocardiographic measurement of LV
fractional
shortening by M-mode and EF measured from two-dimensional images by
using
Simpsons method in accordance with the recommendations of the American
Society
of Echocardiography Committee, are widely used parameters for cardiac
evaluation
28. An additional
method is the use of the Doppler
principle to measure and quantify blood flow velocity. The method is
based
on the fact that the frequency of reflected ultrasound from a moving
target
towards the transducer is higher than the transmitted frequency.
When
the reflecting target is moving away from the transducer, the frequency
is
lower than the original transmitted ultrasound frequency. The Doppler
signals
from the moving red blood cells have low amplitude and high velocity,
and
the echocardiographic methods used are continuous wave Doppler, pulsed
Doppler
and color flow imaging. A recently developed ultrasonographic method is
tissue
velocity imaging (TVI). This method uses frequency shifts of ultrasound
waves
to calculate myocardial tissue velocity at lower velocities, but higher
intensity
compared to blood flow velocity measurement. TVI can be used to measure
movements
of cardiac structures and to assess regional LV contractility, which
has
been shown in both animal experiments and human studies
29,30. The TVI method
is used
in a wide range of cardiac diseases to characterize systolic ejection
velocities.
Recent research showed the usefulness of TVI for assessing the severity
of
LV and interventricular asynchrony in patients with HF receiving CRT
because
of the excellent time resolution which can be achieved by TVI providing
frame
rates of 100 frames per second (fps) or more, i.e. a time resolution of
10
ms. Another assessment of regional LV function is the calculation of
the
myocardial velocity gradient or strain rate imaging, reflecting
deformation and thereby a more direct measurement of contraction and
relaxation using data set from color-coded TVI
31-33. Postprocessing the color coded TVI
(c-TVI) data set can as well be used to evaluate the time related
contraction pattern of the LV, which is less angle dependent than
strain itself. Major interest of the regional time aspect of LV
contraction measured bt TVI has increased because of the promising
results of CRT in HF patients.
Conventional echocardiography
M-Mode: Using the septal-to-posterior wall motion delay in
M-mode recordings from the parasternal short axis view Pitzalis et al.
demonstrated in 20 patients that a septal-to-posterior wall motion
delay of
> 130 ms and QRS duration
>
150 ms predicted response to CRT in terms of > 15 % reduction
of left ventricular end-systolic volume index in 79% of the patients.
The authors demonstrated the prediction of reverse
remodelling by septal-to-posterior wall motion delay to be more precise
than
the QRS duration ( accuracy 85% vs. 65%)
34.
The same group demonstrated using this method in 60 patients that
ischemic cardiomyopathy, changes in the QRS duration after
implantation, and SPWMD significantly correlated with progression
toward HF (defined as a worsening clinical condition leading to a
sustained increase in conventional therapies, hospitalization, cardiac
transplantation, and death). A long SPWMD remained significantly
associated with a reduced risk of HF progression. An improvement in
LVEF was observed in 79% of the patients with a baseline SPWMD of
>
130 ms and in 9% of those with an SPWMD of <130 ms (p <0.0001).
35
The
septal-to-posterior wall motion delay in M-mode recordings can also be
examined in the parastrenal long axis view and a decrease of the
posterior delay during CRT can be shown (
Figure 1).
Prior to CRT
3 Months of CRT
Figure
1: The septal-to-posterior wall motion delay in M-mode
recordings can be examined in the parastrenal long axis view and a
decrease of the posterior delay during CRT can be shown
Doppler echocardiography: The measurement of
interventricular electromechanical delay using pulsed Doppler imaging
was examined by Rouleau et al in 35 patients with DCM
36. A QRS width of more than 150 ms was
correlated with a delayed aortic flow compared to the pulmonary flow as
well as a delayed mitral annulus systolic wave compared to tricuspid
annulus systolic wave. The authors concluded that QRS of
more than 150 ms is a good marker of interventricular mechanical
asynchrony.
Various
echocardiographic parameters of ventricular asynchrony were examined by
Bordachar et. al in 41 patients undergoing CRT. Changes in
interventricular asynchrony, defined as the difference between the
aortic and pulmonary pre-ejection delays and determined as the time
from the onset of the QRS complex to the beginning of each respective
systolic ejection by pulsed wave Doppler imaging were not
correlated with changes in cardiac output, whereas several TVI
modalities could confirm high correlation with hemodynamic changes
37.
The use of
pulsed tissue velocity Doppler imaging by Ansalone et al in 21 non
ischemic patients receiving CRT demonstrated a reduction of
asynchronous contraction of LV basal
segments. After CRT, LV performance improved significantly in patients
with
better LV resynchronization evaluated by TVI, whereas the QRS narrowing
was
not predictive of this functional improvement
38.
The effect of
inflow based AV optimization adopted from use in DDD pacing
39 showed in CRT responders, that changes
in preload only partly could explain the improved LV performance in
terms of pulse pressure. The authors emphasize the importance of LV
resynchronization for improved LV performance
40.
Functional
mitral regurgitation is reduced by CRT in patients with HF and LBBB
shown in 24 patients
by Breithardt et al, explained by a more coordinated LV contraction and
due
to the increased closing force (left ventricular systolic pressure rise)
41 .
Newer echocardiographic methods
Contrast echocardiography: A new echocardiographic method
based on contrast variability imaging was used in 10 patients by
Kawaguchi et al. to quantify asynchrony and magnitude of
resynchronization achieved by CRT
42.
The method showed that lateral wall motion occurred earlier during CRT
and that both spatial and temporal asynchrony in the LV contraction
declined with LV pacing and CRT correlated with increasing ejection
fraction.
Borderline detection: A semiautomatic border detection
method based on the fact that each region of the ventricular
endocardial wall undergoes a periodic cycle of inward and outward
displacement was performed in 34 patients by Breithardt et al. The
authors showed a septal-lateral resynchronization during CRT by using
this echocardiographic phase analysis of radial endocardial wall motion
predicting an acute hemodynamic response (dp/dt)
43 .
Three dimensional echocardiography: Three dimensional (3 D)
echocardiography has been used by Kim et al. to document hemodynamic
improvement
by CRT and additionally to identify LV segments with asynchrony
44. The latter 3D echocardiographic
method uses
semi-automated contour analysis by a fast-rotating second harmonic
transducer and was used in 16 patients by Krenning et al. to
demonstrate a reduction of the LV contraction delay during CRT. The
authors claim that this new 3D echocardiographic method might also be
used to select the optimal pacing site
during CRT
45.
Tissue Color Doppler Velocity Imaging (c-TVI): The
excellent time resolution of c-TVI by using a postprocessing procedure
is used in several studies to demonstrate the regional time aspect of
LV contraction. In addition to the high time resolution another main
advantage of c-TVI method is the possibility of comparing the
contraction pattern of different LV regions simultaneously
from the recording. Synchronicity of LV contraction pattern in the
structurally
normal heart is demonstrated and compared to HF patients with
bundle
brunch block showing a significant asynchrony within the LV in
the
HF patients
46,47.
(
Figure 2)
A
B
Figure
2: c-TVI curves at basal sites of interventricular septum (IS)
and lateral free wall (LFW). A Control
person: normal peak velocity and synchronous peaks at IS (yellow line)
and LFW (red line). B Heart
failure patient with LBBB: reduced peak velocities and asynchronous
peaks at IS (yellow line) and LFW (green line).
Comparing
surface ECG with the mechanical contraction pattern in HF patients
showed that neither QRS duration nor QRS pattern predicts the
mechanical asynchrony. Even HF patients
with normal QRS width can have significant LV asynchronous contraction
48,49. The reduction of
post systolic LV contraction was demonstrated during CRT by Soegard et
al. and is assumed to be an indirect marker of LV resynchronization
50. Based on data from 25 patients
receiving CRT the same group did also show by tissue Doppler imaging
that occurrence of postsystolic contraction prior to CRT may
predicts improved systolic performance and reversed LV remodelling
during CRT whereas QRS duration failed to
predict resynchronization efficacy
51
.
Using c-TVI
has shown resynchronization during CRT, both as measurement of regional
contraction timed to the QRS complex by Yu et al. and measured as
an absolute resynchronization of the contraction of LV septum and the
lateral free wall by Schuster et al.
and by Bax et al.
52-53,54. One study by Bax et al in 25 patients
showed a possible predictive value of c-TVI asynchrony prior to
implantation which points in the same direction as Yu et al
in 30 patients
55,56.
Strain and strain rate imaging: The measurement of LV
segment shortening or lengthening (strain) is also used to demonstrate
resynchronization during CRT, but the more angle dependency of strain
compared to TVI allows only the measurement of relative
resynchronization because of the fact that the different regions have
to be examined in separate recordings. However a resynchronization
effect by CRT is shown using the strain method by Breithardt et al.
57
Summary
The above
mentioned manuscripts deal partly with concordance or disconcordance of
electrical and
mechanical markers of asynchrony. Despite the findings of
angioscintigraphic asynchrony related to the QRS complex
58, in summary surface ECG seems not to
be a sufficient marker of the mechanical events within the LV. However,
the invasive endocardial activation mapping correlated well with tissue
Doppler imaging to locate the latest segment of activation in the
7 patients with HF and LBBB published by Yu et al.
21. The possibility of improving the LV
function deteriorated by asynchrony using CRT, calls for a method of
selecting patients with mechanical LV asynchrony prior to implantation
of CRT. The published material so far demands in our opinion at least
one additional method to surface
ECG to reveal LV asynchrony. Several non invasive methods have been
used
and in small studies even predicted clinical or hemodynamic improvement
by
CRT. There is still no gold standard for assessment of LV asynchrony
for CRT,
but both traditional and new echocardiographic methods have shown both
asynchronous
LV contraction in HF patients, and resynchronized LV contraction during
CRT
and should be implemented as additional methods for selecting patients
to
CRT.
References
1. Gregoratos G, Abrams J, Epstein AE,
Freedman RA, Hayes DL, Hlatky MA et al. ACC/AHA/NASPE 2002 guideline
update for implantation of cardiac pacemakers and antiarrhythmia
devices: summary article: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines
(ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines).
Circulation 2002;106:2145-61.
2. Hochleitner M, Hortnagl
H, Ng CK, Gschnitzer F, Zechmann W. Usefullness of Physiological
Dual-chamber Pacing in Drug Resistant Idiopathic Dilated
Cardiomyopathy. Am J Cardiol 1990;66:198-202.
3.
Gold MR, Feliciano Z, Gottlieb SS, Fisher ML. Dual-Chamber Pacing With
a Short
Atrioventricular Delay in Congestive Heart Failure: A Randomized Study.
J
Am Coll Cardiol 1995;26:967-73.
4. Cowell
R, Morris-Thurgood J, Ilsley C, Paul V. Septal short atrioventricular
delay pacing: additional hemodynamic improvements in heart failure.
PACE. 1994;17:1980-3.
5. Gold MDP, Shorofsky MDP,
Metcalf BA, Feliciano MD, Fisher MD, Gottlieb MD. The Acute Hemodynamic
Effects of Right Ventricular Septal Pacing in Patients With Congestive
Heart Failure Secondary to Ischemic or Idiopathic Dilated
Cardiomyopathy. Am J Cardiol 1997;79:679-81.
6. Victor F, Leclercq C,
Mabo P,
Pavin D, Deviller A, de Place C et al. Optimal right ventricular pacing
site
in chronically implanted patients; A prospective randomized crossover
comparison
of apical and outflow tract pacing. J Am Coll Cardiol 1999;33:311-6.
7. Grines
CL, Bashore TM, Boudoulas H, Olson S, Shafer P, Wooley CF. Functional
abnormalities in isolated left bundle branch block. The effect of
interventricular asynchrony. Circulation 1989;79:845-53.
8. Prinzen FW, Cheriex EC,
Delhaas T,
van Oosterhout MF, Arts T, Wellens HJ et al. Asymmetric thickness of
the left
ventricular wall resulting from asynchronous electric activation: a
study
in dogs with ventricular pacing and in patients with left bundle branch
block.
Am Heart J 1995;130:1045-53.
9.
Verbeek XA, Vernooy K, Peschar M, Cornelussen RN, Prinzen FW.
Intra-ventricular resynchronization for optimal left ventricular
function during pacing in experimental
left bundle branch block. J Am Coll.Cardiol. 2003;42:558-67.
10. Xiao
HB, Brecker SJD, Gibson DG. Effects of Abnormal Activation on the Time
Course of the Left-Ventricular Pressure Pulse in Dilated
Cardiomyopathy. Brit Heart Journal 1992;68:403-7.
11. Blanc JJ,
Etienne Y, Gilard M, Mansourati J, Munier S, Boschat J et al.
Evaluation of different ventricular pacing sites in patients with
severe heart failure: Results of an acute hemodynamic study.
Circulation 1997;96:3273-7.
12. Leclercq C, LeBreton H,
Pavin
D, Victor F, Mabo P, Daubert C. Acute hemodynamic response to
biventricular
DDD pacing in patients with severe congestive heart failure and without
conventional
indication for permanent pacemaker. Circulation 1997;96:520.
13. Kass
DA, Chen CH, Curry C, Talbot M, Berger R, Fetics B et al. Improved left
ventricular
mechanics from acute VDD pacing in patients with dilated cardiomyopathy
and
ventricular conduction delay. Circulation1999;99:1567-73.
14. Nelson GS, Berger RD,
Fetics
BJ, Talbot M, Spinelli JC, Hare JM et al. Left ventricular or
biventricular
pacing improves cardiac function at diminished energy cost in patients
with
dilated cardiomyopathy and left bundle-branch block. Circulation
2000;102:3053-9.
15. Auricchio A, Stellbrink C,
Sack
S et al. Long-term clinical effect of hemodynamically optimized cardiac
resynchronization
therapy in patients with heart failure and ventricular conduction
delay.
J Am Coll Cardiol. 2002 ;39 :2026-33.
16.
Abraham
WT, Fisher WG, Smith AL, DeLurgio DB, Leon AR, Loh E et al. Cardiac
resynchronization
in chronic heart failure. N Eng J Med 2002;346:1845-53.
17.
Young JB, Abraham WT, Smith AL, Leon AR, Lieberman R, Wilkoff B et al.
Combined
cardiac resynchronization and implantable cardioversion defibrillation
in
advanced chronic heart failure: the MIRACLE ICD Trial. JAMA 2003;
289:2685-94.
18. Baldasseroni
S, Opasich C, Gorini M, Lucci D, Marchionni N, Marini M et al. Left
bundle-branch
block is associated with increased 1-year sudden and total mortality
rate
in 5517 outpatients with congestive heart failure: A report from the
Italian
network on congestive heart failure. Am Heart l 2002;143:398-405.
19. Alonso
C, Leclercq C, Victor F, Mansour H, dePlace C, Pavin D et al.
Electrocardiographic
predictive factors of long-term clinical improvement with multisite
biventricular
pacing in advanced heart failure. Am J Cardiol 1999;84:1417-21.
20.
Peichl
P, Kautzner J, Cihak R, Bytesnik J. The spectrum of inter- and
intraventricular
conduction abnormalities in patients eligible for cardiac
resynchronization
therapy. PACE. 2004;27:1105-12.
21.
Fung JWH, Yu CM, Yip G,
Zhang
Y, Chan H, Kum CC et al. Variable left ventricular activation pattern
in
patients with heart failure and left bundle branch block. HEART
2004;90:17-9.
22. Lambiase
PD, Rinaldi A, Hauck J, Mobb M, Elliott D, Mohammad S et al.
Non-contact
left ventricular endocardial mapping in cardiac resynchronisation
therapy.
HEART 2004;90:44-51.
23. Curry
CW, Nelson GS, Wyman BT, Declerck J, Talbot M, Berger RD et al.
Mechanical
dyssynchrony in dilated cardiomyopathy with intraventricular conduction
delay
as depicted by 3D tagged magnetic resonance imaging. Circulation
2000;101:E2.
24. Fauchier
L, Marie O, Casset-Senon D, Babuty D, Cosnay P, Fauchier JP.
Reliability
of QRS duration and morphology on surface electrocardiogram to identify
ventricular
dyssynchrony in patients with idiopathic dilated cardiomyopathy.
Am
J Cardiol 2003;92:341-4.
25. Toussaint
JF, Lavergne T, Ollitraut J, Hignette C, Darondel JM, de Dieuleveult B
et
al. Biventricular pacing in severe heart failure patients reverses
electromechanical
dyssynchronization from apex to base. PACE 2000; 23:1731-4.
26. Toussaint JF, Lavergne T,
Kerrou
K, Froissart M, Ollitrault J, Darondel JM et al. Basal asynchrony and
resynchronization
with biventricular pacing predict long-term improvement of LV function
in
heart failure patients. PACE. 2003;26:1815-23.
27.
Kerwin WF, Botvinick EH, O'Connell JW,
Merrick
SH, DeMarco T, Chatterjee K et al. Ventricular contraction
abnormalities
in dilated cardiomyopathy: effect of biventricular pacing to correct
interventricular
dyssynchrony. J Am Coll Cardiol 2000;35:1221-7.
28. Schiller
NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H et al.
Recommendations
for quantitation of the left ventricle by two-dimensional
echocardiography.
American Society of Echocardiography Committee on Standards,
Subcommittee
on Quantitation of Two-Dimensional Echocardiograms.
J.Am.Soc.Echocardiogr.
1989;2:358-67.
29.
Gorcsan J, 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.
30.
Zamorano J, Wallbridge DR, Ge J, Drozd J, Nesser J, Erbel R.
Non-invasive
assessment of cardiac physiology by tissue Doppler echocardiography - A
comparison
with invasive haemodynamics. Eur Heart J 1997;18:330-9.
31.
Heimdal A, Stoylen A, Torp H, Skjaerpe T. Real-time strain rate imaging
of
the left ventricle by ultrasound. J.Am.Soc.Echocardiogr. 1998;11:1013-9.
32.
Urheim S, Edvardsen T, Torp H, Angelsen B, Smiseth OA. Myocardial
strain
by Doppler echocardiography. Validation of a new method to quantify
regional
myocardial function Circulation 2000;102:1158-64.
33. Edvardsen T, Gerber BL, Garot J,
Bluemke
DA, Lima JA, Smiseth OA. Quantitative assessment of intrinsic regional
myocardial
deformation by Doppler strain rate echocardiography in humans:
validation
against three-dimensional tagged magnetic resonance imaging.
Circulation
2002;106:50-6.
34. Pitzalis MV, Iacoviello M, Romito R,
Massari
F, Rizzon B, Luzzi G et al. Cardiac resynchronization therapy tailored
by
echocardiographic evaluation of ventricular asynchrony. J Am Coll
Cardiol
2002;40:1615-22.
35. Pitzalis MV, Iacoviello M, Romito R,
Guida
P, De Tommasi E, Luzzi G et al. Ventricular asynchrony predicts a
better
outcome in patients with chronic heart failure receiving cardiac
resynchronization
therapy. J Am Coll.Cardiol. 2005;45:65-9.
36.
Rouleau FDR, Merheb M, Geffroy S, Berthelot J, Chaleil D, Dupuis JM et
al.
Echocardiographic assessment of the interventricular delay of
activation
and correlation to the QRS width in dilated cardiomyopathy. PACE
2001;24:1500-6.
37. Bordachar P, Lafitte S, Reuter S,
Sanders
P, Jais P, Haissaguerre M et al. Echocardiographic parameters of
ventricular
dyssynchrony validation in patients with heart failure using sequential
biventricular
pacing. J Am Coll Cardiol 2004;44:2157-65.
38. Ansalone G, Giannantoni P, Ricci R, Trambaiolo
P, Laurenti A, Fedele F et al. Doppler myocardial imaging in patients
with heart failure receiving biventricular pacing treatment. Am Heart
J 2001;142:881-96.
39. Kindermann M, Frohlig G,
Doerr T, Schieffer H. Optimizing the AV delay in DDD pacemaker patients
with high degree AV block: mitral valve Doppler versus impedance
cardiography. Pacing Clin.Electrophysiol. 1997;20:2453-62.
40. Auricchio A,
Ding J, Spinelli JC, Kramer AP, Salo RW, Hoersch W et al. Cardiac
resynchronization therapy restores optimal atrioventricular mechanical
timing in heart failure patients with ventricular conduction delay. J
Am Coll Cardiol 2002;39:1163-9.
41. Breithardt OA, Sinha AM, Schwammenthal E,
Bidaoui N, Markus KU, Franke A et al. Acute effects of cardiac
resynchronization therapy on functional mitral regurgitation in
advanced systolic heart failure. J Am Coll Cardiol 2003;41:765-70.
42. Kawaguchi M,
Murabayashi T, Fetics BJ, Nelson GS, Samejima H, Nevo E et al.
Quantitation of basal dyssynchrony and acute resynchronization from
left or biventricular pacing by novel echo-contrast variability
imaging. J Am Coll Cardiol 2002;39:2052-8.
.
43. Breithardt OA,
Stellbrink C, Kramer AP, Sinha AM, Franke A, Salo R et al.
Echocardiographic quantification of left ventricular asynchrony
predicts an acute hemodynamic benefit of cardiac resynchronization
therapy. J Am Coll Cardiol 2002;40:536-45.
44. Kim WY, Sogaard P,
Mortensen PT, Jensen HK, Pedersen AK, Kristensen BO et al. Three
dimensional echocardiography documents haemodynamic improvement by
biventricular pacing in patients with severe heart failure. Heart
2001;85:514-20.
45. Krenning
BJ, Szili-Torok T, Voormolen MM, Theuns DA, Jordaens LJ, Lancee CT et
al. Guiding and optimization of resynchronization therapy with dynamic
three-dimensional echocardiography and segmental volume--time curves: a
feasibility study. Eur J Heart Fail. 2004;6:619-25.
46.
Schuster P, Faerstrand S, Ohm O, Martens D, Torkildsen R,
Øyehaug O. Feasability of color tissue velocity imaging for
assesment of regional timing of left ventricular longitudinal movement.
Scand Cardiovasc J 2004;38:39-45.
47. Schuster P, Faerestrand S, Ohm OJ. Color
Doppler Tissue Velocity Imaging Demonstrates Significant Asynchronous
Regional Left Ventricular Contraction and Relaxation in Patients With
Bundle Branch Block and Heart Failure Compared to Control Subjects.
Cardiology 2004: 102; 220-7.
48. Yu CM, Yang H, Lau CP,
Wang Q, Wang S, Lam L et al. Regional left ventricle mechanical
asynchrony in patients with heart disease and normal QRS duration:
implication for biventricular pacing therapy. PACE. 2003;26:562-70.
49.
Schuster P, Faerestrand S, Ohm OJ. Color Doppler Tissue
Velocity Imaging Can Disclose Systolic Left Ventricular Asynchrony
Independent of the QRS Morphology in Patients with Severe Heart
Failure. PACE. 2004;27:460-7.
50. Sogaard
P, Kim WY, Jensen HK, Mortensen P, Pedersen AK, Kristensen BO et al.
Impact of acute biventricular pacing on left ventricular performance
and volumes in patients with severe heart failure - A tissue Doppler
and three-dimensional echocardiographic study. Cardiology
2001;95:173-82.
51.
Sogaard P, Egeblad H, Kim WY, Jensen HK, Pedersen AK,
Kristensen BO et al. Tissue doppler imaging predicts improved systolic
performance and reversed left ventricular remodeling during long-term
cardiac resynchronization therapy. J Am Coll Cardiol 2002;40:723-30.
52. Yu CM, Chau E, Sanderson JE, Fan K, Tang MO,
Fung WH et al. Tissue Doppler echocardiographic evidence of reverse
remodeling and improved synchronicity by simultaneously delaying
regional contraction after biventricular pacing therapy in heart
failure. Circulation 2002;105:438-45.
53. Bax JJ,
Molhoek SG, van Erven L, Voogd PJ, Somer S, Boersma E et al. Usefulness
of myocardial tissue Doppler echocardiography to evaluate left
ventricular dyssynchrony before and after biventricular pacing in
patients with idiopathic dilated cardiomyopathy. Am J Cardiol
2003;91:94-7.
54. Schuster P, Faerestrand
S, Ohm OJ. Colour tissue velocity imaging can show resynchronisation of
longitudinal left ventricular contraction pattern by biventricular
pacing in patients with severe heart failure. Heart 2003;89:859-64.
55. Bax JJ, Marwick TH, Molhoek
SG, Bleeker GB, van Erven L, Boersma E et al. Left ventricular
dyssynchrony predicts benefit of cardiac resynchronization therapy in
patients with end-stage heart failure before pacemaker implantation. Am
J Cardiol 2003;92:1238-40.
56. 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;91:684-8.
57. Breithardt OA, Stellbrink C, Herbots L, Claus
P, Sinha AM, Bijnens B et al. Cardiac resynchronization therapy can
reverse abnormal myocardial strain distribution in patients with heart
failure and left bundle branch block. J Am Coll Cardiol 2003;42:486-94.
58.
Toussaint JF, Lavergne T,
Kerrou K, de Dieuleveult B, Ponce F, Froissart M et al. Ventricular
coupling of electrical and mechanical dyssynchronization in heart
failure patients. PACE. 2002;25:178-82.
