| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, 6200 MD Maastricht, The Netherlands
 |
ABSTRACT |
|---|
 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The quantification of mechanical
interventricular asynchrony (IVA) was investigated. In 12 dogs left
bundle branch block (LBBB) was induced by radio frequency ablation.
Left ventricular (LV) and right ventricular (RV) pressures were
recorded before and after induction of LBBB and during LBBB + LV
apex pacing at different atrioventricular (AV) delays. Four IVA
measures were validated using computer simulations on experimentally
obtained pressure signals. The most robust measure for IVA was the time
delay between the upslope of the LV and RV pressure signals
(
Tup), estimated by cross correlation. The
induction of experimental LBBB decreased Tup
from 
6.9 ± 7.0 ms (RV before LV) to 33.9 ± 7.6 ms
(P < 0.05) in combination with a significant decrease
of LV maximal first derivative of pressure development over time
(dP/dtmax). During LV apex pacing,
Tup increased with decreasing AV delay up to
+20.9 ± 14.6 ms (P < 0.05). Interventricular
resynchronization (Tup = 0 ms)
significantly improved LV dP/dtmax by 15.1 ± 5.9%. QRS duration increased significantly after induction of LBBB
but did not change during LV apex pacing. In conclusion,
Tup is a reliable measure of mechanical IVA,
which adds valuable information concerning the nature of asynchronous
activation of the ventricles.
left bundle branch block; resynchronization
| |
INTRODUCTION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
DURING LEFT BUNDLE BRANCH BLOCK (LBBB), cardiac function is impaired most likely due to a disturbed synchrony of cardiac contraction (7). In patients with heart failure and LBBB, left ventricular (LV) or biventricular pacing therapy endeavors to improve cardiac function by restoring contractile synchrony (3, 4, 6). Indeed, in these patients, pacing therapy can produce a more synchronous pattern of contraction (9, 16) and improves cardiac function (2, 8, 9).
In general, ventricular asynchrony can be divided into intraventricular and interventricular asynchrony (IVA) (3, 9). Ventricular pacing may restore either intraventricular synchrony, interventricular synchrony, or both. Some studies (7, 9, 12) suggest the functional significance of IVA.
The duration of the QRS complex on the surface ECG is often used as a measure for total ventricular asynchrony. More detailed quantitative information about electrical asynchrony is obtained using endocardial electrical mapping techniques (17). For detailed quantification of mechanical asynchrony, MRI tagging (13) or phase imaging based on radionuclide scintography (nuclear phase imaging) (5, 7, 9, 16) has been applied. Also, echocardiography and Doppler myocardial imaging have been used to study ventricular asynchrony (7, 14). Most of these techniques provide information of intraventricular asynchrony. Only the nuclear and echocardiographic techniques have been applied to study IVA (5, 7, 9, 14, 16). More recently, assessment of IVA from LV and right ventricular (RV) pressure signals has been suggested (18, 19).
The present study was undertaken to investigate the feasibility to reliably assess IVA from simultaneously acquired LV and RV pressure signals. These pressure signals represent the combined mechanical behavior of the ventricles and expose an asynchronous time course during pacing and LBBB (11, 12). In the present study, four measures that potentially quantify mechanical IVA were derived from the pressure signals. The measures were compared and validated by computer simulations based on real pressure signals and evaluated by animal experiments during experimental LBBB and LV pacing. A reliable measure for IVA will be an important tool for future studies on elucidation of the mechanism of the influence of asynchronous activation on cardiac function.
| |
METHODS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Animal experiments. Animal handling was performed according to the Dutch Law on Animal Experimentation and The European Directive for the Protection of Vertebrate Animals used for Experimental and other Scientific Purposes (86/609/EU). The protocol was approved by the Experimental Animal Committee of the Maastricht University.
The experiments were performed on 12 adult mongrel dogs (28 ± 4 kg wt) of either gender. The dogs were premedicated with acepromazine (0.2 mg/kg), atropine (0.1 mg/kg), and oxycodone (2 mg/kg im). Anesthesia was induced with thiopental sodium (15 mg/kg iv) and maintained by ventilation with halothane (0.8 to 1.0%) in a 1:2 mixture of O2 and N2O. A thermal mattress was used to maintain adequate body temperature. Surface ECG was derived from limb leads. LV and RV pressures were recorded simultaneously with two catheter tip manometers (Sentron) introduced through the carotid artery and jugular vein, respectively. Pressure and ECG signals were digitized at a 200-Hz sampling rate and stored on a disk for offline analysis. After the thorax was opened, temporary myocardial pacing leads (model 6500, Medtronic) were implanted at the epicardium of the LV apex and the right atrium. These leads were connected with an external pacemaker (model 5311B AV pacing System Analyzer, Medtronic). LBBB was induced by radio frequency ablation with the use of an ablation catheter (MarinR, Medtronic) and a radio frequency power generator (Atakr, Medtronic). LBBB was characterized by a broad (±100 ms) QRS complex, which, in the dogs, was positive in lead II. Measurements were performed during sinus rhythm before induction of LBBB, after induction of LBBB, and during LBBB in combination with pacing of the LV apex. Pacing was performed in the VDD mode (atrial sensing and ventricular pacing) with AV intervals increasing from 30 ms to a maximum of 140 ms, with 10-ms steps (n = 6). Pacing at each AV delay was maintained for two to four respiratory cycles, followed by at least four respiration cycles without pacing.Signal processing and analysis. Before offline analysis of the pressure signals, a second-order Butterworth low-pass filter with a 40-Hz cut-off frequency was used to remove high-frequency artefacts/noise. To avoid phase shifts in each of the signals, the low-pass filter was applied once in forward and once in a backward direction.
Signal processing theory states that a signal is described unambiguously when the sample frequency is at least twice the maximum signal frequency. This demand is fulfilled at the 200-Hz frequency and allows for measurement of time differences more accurately than the duration of the sampling interval (1). QRS durations and PQ times were acquired by manual offline analysis of the ECG recorded in lead II. The effective paced AV delay (AVe delay) was determined as the time between the onset of the P wave and the pace spike. The AVe delay was used instead of the paced AV delay to correct for differences in position of the atrial sensing lead between the animals. Parameters were calculated for all heart beats within one complete ventilation cycle, of which mean values and standard deviations are reported. The first five beats after the onset of pacing or return to baseline were excluded from the analysis. The relative timing between the onset of electrical activation of the ventricles was calculated as the difference between the PQ time during LBBB and the AVe delay. During LBBB the PQ time represents the time between the onset of atrial activation to onset of electrical activation of the RV, whereas during LV pacing the AVe delay represents the time between the onset of atrial activation and onset of LV activation. Consequently, the difference between these parameters (PQ timeLBBB AVe delay) provides the RV-LV excitation time difference.
Quantification of IVA.
In Fig. 1, typical examples of LV and RV
pressure curves, acquired before induction of LBBB, during LBBB and
during LBBB + LV apex pacing with a short AV delay, are presented.
The curves were normalized to their full amplitude range to accentuate
timing differences. By visual inspection, it is recognized that before induction of LBBB both ventricles contracted approximately
synchronously (Fig. 1A), whereas during LBBB, the entire
systole of the LV is delayed with respect to that of the RV (Fig.
1B). In contrast, during LV pacing with short AV delay (Fig.
1C), an earlier LV than RV contraction is observed.
|
Tfull) by shifting
them in time until the cross-correlation coefficient (xcc) between the
signals reaches its maximal value
|
(1) |
Tup). By definition the timing difference
Tup is positive for an earlier LV than RV
upslope. Figure 2A shows the
cross-correlation function for the examples of LV and RV pressure
signals presented in Fig. 1. In this example, cross-correlation
analysis was restricted to the upslopes. The estimated time delay
between the signals upslopes, determined by the peak of the
cross-correlation function, was close to zero before LBBB, negative
during LBBB, and positive during pacing. In all cases, the maximal
cross-correlation coefficient was close to 1 (>0.99), indicating a
high shape similarity of the pressure wave upslopes.
|
|
(2) |
Simulations/validation of measures of IVA.
To validate the four proposed measures, computer simulations were
performed with the use of pressure signals obtained from the
experiments. To study how each measure responds to a timing difference,
the LV and RV pressure curves were shifted in time with respect to each
other approximating gradual changes in timing, similar to those
presented in Fig. 1. To enable shifting the pressure curves with
respect to each other with 1-ms steps during simulations, the signals
were reinterpolated at 1 KHz. For each temporal lag Tfull, Tup,
APP, and SI were determined. For the loop area
method, the APP as a function of the temporal
lag was also calculated without taking into account the directional
information. Simulations were performed using pressure curves acquired
during sinus rhythm before induction of LBBB, after induction of LBBB,
and during LBBB + LV apex pacing at short AV delay, to demonstrate
the effect of different initial pressure curve shapes.
20 to 20 ms. To ensure that the curve upslope
(dP/dtmax) was not affected, only the part of
the curve after instance of the peak pressure was reinterpolated.
| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Simulation results.
Figure 3 depicts how the simulated
temporal lag between in vivo recorded LV and RV pressure signals
influences the four proposed measures of IVA. A linear relation was
found between the applied temporal lag and estimated
Tfull and Tup (Fig.
3, A and B). The offset in T
between the pre-LBBB, LBBB, and LBBB + pacing results can, among
others, be attributed to timing differences in LV and RV pressure
signals between the different experimental conditions.
|
Tup (Fig. 4B) but as large as 7 ms
for Tfull (Fig. 4A) whereas errors
introduced in APP and SI were significantly larger (Fig. 4, C and D). Figure
5 shows that changing FWHM introduced significant errors in Tfull (Fig.
5A), APP, and SI (Fig. 5,
C and D), whereas Tup
is not affected by the FWHM (Fig. 5B).
|
|
Experimental results.
Table 1 presents the values of
Tfull, Tup,
APP, SI, and hemodynamic values measured before
and directly after induction of LBBB. After the induction of LBBB,
Tfull, Tup, and
APP decreased significantly compared with
pre-LBBB values. Induction of LBBB significantly increased QRS duration
and decreased LV dP/dtmax but did not change
heart rate and RV and LV systolic and end-diastolic pressures.
|
Tup and the paced AV delay is presented,
showing a large variation between the animals. This variation
completely disappeared when the AV delay was standardized with the use
of the RV-LV excitation time difference (Fig.
7B).
|
|
AVe delay, see METHODS). For
Tfull, Tup, and
APP, a sigmoid relation was found with the
lowest values during pacing with the longest AV delays and the highest
values during pacing with the shortest AV interval (25-30 ms). For
Tup, an excellent match of the results from
the various dogs was found. Tup increased in
an almost linear fashion from approximately 35 to 35 ms when the
RV-LV excitation time difference increased from 0 to 80 ms. Linear
regression provided an r2 = 0.95, a
slope = 0.7, and an intercept with the horizontal axis of 29 ms. A
similar sigmoid shape for Tfull and
APP was found, but with more variation between
animals. The data for SI were very noisy, caused by both beat-to-beat
and interanimal differences (Fig. 5D).
In Fig. 8 the relation between QRS
duration and Tup is presented for
measurements before and after induction of LBBB and during LBBB + LV apex pacing for all AV delays. A good correlation was found for the
combined before and after LBBB measurements (r = 0.81)
but a poor and completely different correlation was present during
LBBB + LV apex pacing (r = 0.63).
|
FWHMLR = FWHMLV FWHMRV) as a function of the
RV-LV excitation time difference. In most cases, the LV curve was
clearly wider than the RV curve but pacing significantly affected
FWHMLR. Moreover, RV-LV curve width differences and its
changes during pacing varied considerably between experiments.
|
Tup = 0. LV
dP/dtmax increased significantly by 15.1 ± 5.9%. There was a good correlation between Tup and improvement in LV
dP/dtmax (r = 0.86 ± 0.10). QRS duration, heart rate, and other hemodynamic parameters
showed no significant changes, except for a slight decrease of RV
systolic pressure.
|
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
The present study shows that IVA can be reliably assessed from
simultaneously acquired LV and RV pressure signals. The time difference
between the upslope of the pressure signals estimated by cross
correlation proves to be the most reliable measure because it is
virtually insensitive to changes in the shape of the curves, the
experimental results show an excellent reproducibility of Tup changes between the animals, there is a
linear relation between Tup and the applied
RV-LV excitation time difference, and it provides a beat-to-beat
measure for asynchrony in milliseconds, which can be easily interpreted.
The simulations on in vivo recorded pressure signals revealed a linear
relation between the applied temporal lag and the estimated time delay
both for Tfull as for
Tup, but this finding is trivial based on
pure mathematical considerations. However, experimentally a similar
relation was found between Tup and a major
part of the range of RV-LV excitation time differences (Fig.
7B). The intercept of the estimated mechanical IVA with the
horizontal axis is probably due to the electromechanical delay. The
observed intercept value of 29 ms is within the range of values of the interval between the Q wave and LV pressure rise in intact dog hearts
(21 ± 5 to 33 ± 14 ms) (10). The slope between
Tup and the RV-LV excitation time difference
was <1. This may be explained by different fusion patterns and timing
of the merging wave fronts coming from the LV (pacing) and RV (right
bundle branch). With decreasing or increasing RV-LV excitation time
difference during LBBB + pacing, one ventricle will eventually be
completely activated via the other one through transseptal conduction.
Therefore, more extreme values of the RV-LV excitation time difference
will cause no further change in IVA, which explains the sigmoid shape
of the relation between applied RV-LV excitation time difference and
mechanical IVA. Variations in Tup values
during LBBB between the animals can be attributed to differences in
trans septal conduction time.
The results from Figs. 6 and 7 indicate the importance of standardizing the AV delay by introduction of the RV-LV excitation time difference. An alternative method for standardizing the AV delay was introduced by Auricchio et al. (2), who normalized AV delay on PR interval. For the present study, where absolute differences in timing between the LV and RV are relevant, the RV-LV excitation time difference is preferred.
The two IVA measures, which are based on analysis of the pressure
curves during the full cycle (Tfull and
APP), performed less that
Tup. The simulations show that both measures
are sensitive to shape changes in the pressure curves. Shape changes
similar to those produced by simulations also occur during experimental variation of the mode of activation and are therefore a plausible explanation the lower reproducibility of
Tfull and APP. The
experiments reveal that changes in shape occur gradually with
increasing AV delay (Fig. 9), thus explaining the still smooth, instead
of noisy, behavior of the experimental results for
Tfull and APP for each separate animal (Fig. 7, A and C).
An additional problem of APP, exposed by the
simulations, is the nonlinear relation with the imposed timing
differences between the LV and RV pressure waves. Within the range of
timing differences in the present study, however, the relation with
APP is approximately linear. The similarity
between the experimental results for APP and
Tfull illustrates that the reliability of an
IVA estimate is not determined by the method of assessing it (RV-LV
pressure loop vs. cross correlation) but rather by restricting the
analysis to the upslope of the pressure curves. Time domain restriction to the contraction phase is not possible for the loop method because the loop method is essentially a frequency domain measurement. The SI
is clearly the worst-performing measure of IVA, due to a high
sensitivity to curve shape. Also, the range of the SI values in the
experiments is small and the SI does not contain directional information.
The good correlation between QRS duration and IVA in the canine hearts before and during LBBB is in agreement with the data presented by Rouleau et al. (14) for patients with dilated cardiomyopathy and a large range of QRS durations. However, the present study shows that during LBBB + LV apex pacing the correlation between QRS duration and IVA is lower and completely different. This is in agreement with a nuclear phase imaging study in LBBB patients during biventricular pacing therapy (9). Moreover, it indicates that IVA adds valuable information concerning the nature of asynchronous activation of the ventricles.
In patients with dilated cardiomyopathy and QRS durations >150 ms, IVA
values determined with echocardiography ranged between 77 ± 15 and 88 ± 26 ms (14). Similar values (85 ± 31 ms) were found with nuclear phase imaging for patients with isolated LBBB (7). The smaller IVA values for dogs found in the
present study (33.9 ± 7.6 ms) are not surprising because the
QRS duration is also smaller in dogs (123.7 ± 20.2 ms) than in patients.
Although the decrease in LV dP/dtmax after
induction of LBBB is associated with an increase in IVA (more negative
Tup) and QRS duration (Table 1), the increase
in LV dP/dtmax due to interventricular resynchronization (Table 2) leaves the QRS duration unaltered. This
finding, together with the good correlation between IVA and improvement
in LV dP/dtmax, supports the idea that IVA
contains important information. Further studies, including indexes of
intraventricular asynchrony and IVA and the use of other pacing sites,
are required to fully elucidate the importance of the various aspects
of asynchronous activation for ventricular function.
A disadvantage of the currently presented method is its invasive nature requiring biventricular catheterization. Noninvasive alternatives may be provided by echocardiography or tissue Doppler imaging. MRI tagging can only provide IVA if the RV tags can also be analyzed. This has not been reported yet. In the echocardiography and tissue Doppler imaging study (14) mentioned earler, IVA was assessed as the timing difference between the opening of the pulmonary and aortic valves and the timing difference between onset of the positive waves recorded at the lateral corners of the tricuspid and mitral annulus. In nuclear phase imaging studies, timing differences are derived from a user defined region of interest in a cross section of the ventricles excluding the septum (7, 9).
An important advantage of the cross-correlation method, however, is that it incorporates the full contraction phase of the ventricles and that the pressure curves represent the true average of the contraction of the entire ventricles. Consequently, this method is more sensitive to timing differences and less sensitive to noise than a single point measurement in time, such as the opening of valves. Other advantages of the currently presented technique to assess IVA from LV and RV pressure curves are the accuracy and the relatively plain techniques. Moreover, this IVA measure provides beat-to-beat values and does not require the injection of radioisotopes.
In conclusion, mechanical IVA can be quantified reliably as the
Tup of the LV and RV pressure waves with the
use of cross correlation. Induction of LBBB increases both QRS duration
and Tup significantly, but LV pacing during
LBBB increases Tup at unchanged QRS duration.
Tup relates linearly with the applied electrical delay between the ventricles during LV apex pacing at
different AV delays. Interventricular resynchronization is associated
with an improvement of LV dP/dtmax. Therefore,
Tup provides important information about the
asynchronous contraction between the LV and RV during LBBB with our
without ventricular pacing.
| |
FOOTNOTES |
|---|
Address for reprint requests and other correspondence: X. A. A. M. Verbeek, Dept. of Physiology, Cardiovascular Research Institute Maastricht, Maastricht Univ., PO Box 616, 6200 MD Maastricht, The Netherlands (E-mail: x.verbeek{at}fys.unimaas.nl).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
May 23, 2002;10.1152/ajpheart.00051.2002
Received 25 February 2002; accepted in final form 16 May 2002.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Augustijn, CH,
Arts T,
Prinzen FW,
and
Reneman RS.
Mapping the sequence of contraction of the canine left ventricle.
Pflügers Arch
419:
529-533,
1991[Web of Science][Medline].
2.
Auricchio, A,
Stellbrink C,
Block M,
Sack S,
Vogt J,
Bakker P,
Klein H,
Kramer A,
Ding J,
Salo R,
Tockman B,
Pochet T,
and
Spinelli J.
Effect of pacing chamber and atrioventricular delay on acute systolic function of paced patients with congestive heart failure. The Pacing Therapies for Congestive Heart Failure Study Group. The Guidant Congestive Heart Failure Research Group.
Circulation
99:
2993-3001,
1999
3.
Bakker, PF,
Meijburg HW,
de Vries JW,
Mower MM,
Thomas AC,
Hull ML,
Robles De Medina EO,
and
Bredee JJ.
Biventricular pacing in end-stage heart failure improves functional capacity and left ventricular function.
J Interv Card Electrophysiol
4:
395-404,
2000[Web of Science][Medline].
4.
Blanc, JJ,
Etienne Y,
Gilard M,
Mansourati J,
Munier S,
Boschat J,
Benditt DG,
and
Lurie KG.
Evaluation of different ventricular pacing sites in patients with severe heart failure: results of an acute hemodynamic study.
Circulation
96:
3273-3277,
1997
5.
Bramlet, DA,
Morris KG,
Coleman RE,
Albert D,
and
Cobb FR.
Effect of rate-dependent left bundle branch block on global and regional left ventricular function.
Circulation
67:
1059-1065,
1983
6.
Cazeau, S,
Ritter P,
Bakdach S,
Lazarus A,
Limousin M,
Henao L,
Mundler O,
Daubert JC,
and
Mugica J.
Four chamber pacing in dilated cardiomyopathy.
Pacing Clin Electrophysiol
17:
1974-1979,
1994[Medline].
7.
Grines, CL,
Bashore TM,
Boudoulas H,
Olson S,
Shafer P,
and
Wooley CF.
Functional abnormalities in isolated left bundle branch block. The effect of interventricular asynchrony.
Circulation
79:
845-853,
1989
8.
Kass, DA,
Chen CH,
Curry C,
Talbot M,
Berger R,
Fetics B,
and
Nevo E.
Improved left ventricular mechanics from acute VDD pacing in patients with dilated cardiomyopathy and ventricular conduction delay.
Circulation
99:
1567-1573,
1999
9.
Kerwin, WF,
Botvinick EH,
O'Connell JW,
Merrick SH,
DeMarco T,
Chatterjee K,
Scheibly K,
and
Saxon LA.
Ventricular contraction abnormalities in dilated cardiomyopathy: effect of biventricular pacing to correct interventricular dyssynchrony.
J Am Coll Cardiol
35:
1221-1227,
2000
10.
Kettunen, R,
Timisjarvi J,
Kouvalainen E,
Anttila P,
and
Hirvonen L.
Electromechanical delay in the intact dog heart.
Int J Cardiol
9:
161-171,
1985[Web of Science][Medline].
11.
Kingma, I,
Tyberg JV,
and
Smith ER.
Effects of diastolic transseptal pressure gradient on ventricular septal position and motion.
Circulation
68:
1304-1314,
1983
12.
Little, WC,
Reeves RC,
Arciniegas J,
Katholi RE,
and
Rogers EW.
Mechanism of abnormal interventricular septal motion during delayed left ventricular activation.
Circulation
65:
1486-1491,
1982
13.
McVeigh, ER,
Prinzen FW,
Wyman BT,
Tsitlik JE,
Halperin HR,
and
Hunter WC.
Imaging asynchronous mechanical activation of the paced heart with tagged MRI.
Magn Reson Med
39:
507-513,
1998[Web of Science][Medline].
14.
Rouleau, F,
Merheb M,
Geffroy S,
Berthelot J,
Chaleil D,
Dupuis JM,
Victor J,
and
Geslin P.
Echocardiographic assessment of the interventricular delay of activation and correlation to the QRS width in dilated cardiomyopathy.
Pacing Clin Electrophysiol
24:
1500-1506,
2001[Medline].
15.
Schreuder, JJ,
Steendijk P,
van der Veen FH,
Alfieri O,
van der Nagel T,
Lorusso R,
van Dantzig JM,
Prenger KB,
Baan J,
Wellens HJ,
and
Batista RJ.
Acute and short-term effects of partial left ventriculectomy in dilated cardiomyopathy: assessment by pressure-volume loops.
J Am Coll Cardiol
36:
2104-2114,
2000
16.
Toussaint, JF,
Lavergne T,
Ollitraut J,
Hignette C,
Darondel JM,
De Dieuleveult B,
Froissart M,
Le Heuzey JY,
Guize L,
and
Paillard M.
Biventricular pacing in severe heart failure patients reverses electromechanical dyssynchronization from apex to base.
Pacing Clin Electrophysiol
23:
1731-1734,
2000[Medline].
17.
Vassallo, JA,
Cassidy DM,
Marchlinski FE,
Buxton AE,
Waxman HL,
Doherty JU,
and
Josephson ME.
Endocardial activation of left bundle branch block.
Circulation
69:
914-923,
1984
18.
Yu, Y,
Auricchio A,
Ding J,
Kramer A,
Hoersch W,
Huvelle E,
and
Spinelli J.
Identification of patients suitable for ventricular resynchronization therapy based on normalized LV-RV pressure loop area (Abstract).
Pacing Clin Electrophysiol
23:
555,
2000.
19.
Yu, Y,
Auricchio A,
Ding J,
Kramer A,
Huvelle E,
Potty P,
and
Spinelli J.
Is resynchronization between left and right ventricles responsible for improving hemodynamic function of heart failure patients with LBBB? (Abstract).
Pacing Clin Electrophysiol
23:
589,
2000.
This article has been cited by other articles:
|
|
 |
|
  L. Johnson, H. K. Kim, M. Tanabe, J. Gorcsan, D. Schwartzman, S. G. Shroff, and M. R. Pinsky Differential effects of left ventricular pacing sites in an acute canine model of contraction dyssynchrony Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H3046 - H3055. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Kurita, K. Onishi, K. Dohi, M. Tanabe, N. Fujimoto, T. Tanigawa, M. Setsuda, N. Isaka, T. Nobori, and M. Ito Impact of heart rate on mechanical dyssynchrony and left ventricular contractility in patients with heart failure and normal QRS duration Eur J Heart Fail, June 1, 2007; 9(6-7): 637 - 643. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. A. Quinn, G. Berberian, S. E. Cabreriza, L. J. Maskin, A. D. Weinberg, J. W. Holmes, and H. M. Spotnitz Effects of sequential biventricular pacing during acute right ventricular pressure overload Am J Physiol Heart Circ Physiol, November 1, 2006; 291(5): H2380 - H2387. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Load dependence of cardiac output in biventricular pacing: left ventricular volume overload in pigs. J. Thorac. Cardiovasc. Surg., March 1, 2006; 131(3): 666 - 670.
|
|
|
|
|
|
X. A. A. M. Verbeek, A. Auricchio, Y. Yu, J. Ding, T. Pochet, K. Vernooy, A. Kramer, J. Spinelli, and F. W. Prinzen Tailoring cardiac resynchronization therapy using interventricular asynchrony. Validation of a simple model Am J Physiol Heart Circ Physiol, March 1, 2006; 290(3): H968 - H977. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Vernooy, X. A.A.M. Verbeek, M. Peschar, H. J.G.M. Crijns, T. Arts, R. N.M. Cornelussen, and F. W. Prinzen Left bundle branch block induces ventricular remodelling and functional septal hypoperfusion Eur. Heart J., January 1, 2005; 26(1): 91 - 98. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R A Bleasdale and M P Frenneaux Cardiac resynchronisation therapy: when the drugs don't work. Heart, December 1, 2004; 90(suppl_6): vi2 - vi4. [Full Text] [PDF]
|
|
|
|
 |
|
 R.A. Bleasdale, M.S. Turner, C.E. Mumford, P. Steendijk, V. Paul, J.V. Tyberg, J.A. Morris-Thurgood, and M.P. Frenneaux Left Ventricular Pacing Minimizes Diastolic Ventricular Interaction, Allowing Improved Preload-Dependent Systolic Performance Circulation, October 19, 2004; 110(16): 2395 - 2400. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. S. Turner, R. A. Bleasdale, D. Vinereanu, C. E. Mumford, V. Paul, A. G. Fraser, and M. P. Frenneaux Electrical and Mechanical Components of Dyssynchrony in Heart Failure Patients With Normal QRS Duration and Left Bundle-Branch Block: Impact of Left and Biventricular Pacing Circulation, June 1, 2004; 109(21): 2544 - 2549. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. A Breithardt, P. Claus, and G. R Sutherland Do we understand who benefits from resynchronisation therapy? Eur. Heart J., April 1, 2004; 25(7): 535 - 536. [Full Text] [PDF]
|
|
|
|
 |
|
 X. A. A. M. Verbeek, K. Vernooy, M. Peschar, R. N. M. Cornelussen, and F. W. Prinzen Intra-ventricular resynchronization for optimal left ventricular function during pacing in experimental left bundle branch block J. Am. Coll. Cardiol., August 6, 2003; 42(3): 558 - 567. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
