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(Circulation. 1999;99:2993-3001.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Effect of Pacing Chamber and Atrioventricular Delay on Acute Systolic Function of Paced Patients With Congestive Heart Failure
From the Department of Cardiology, University Hospital, Otto-von-Guericke Universität, Magdeburg, Germany (A.A., H.K.); Department of Cardiology, RWTH University Hospital, Aachen, Germany (C.S.); Department of Cardiology, University Hospital, Münster, Germany (M.B.); Department of Cardiology, University Hospital, Essen, Germany (S.S.); Department of Cardiology, Herz- und Diabeteszentrum NRW, Bad Oeynhausen, Germany (J.V.); Heart Lung Institute, University Hospital Utrecht, The Netherlands (P.B.); Guidant Corporation, St. Paul, Minn (A.K., J.D., R.S., B.T., J.S.); and Guidant Corporation, Brussels, Belgium (T.P.).
Correspondence to Angelo Auricchio, MD, PhD, Department of Cardiology, University Hospital, Leipzigerstraße 44, D-39120 Magdeburg, Germany. E-mail angelo.auricchio{at}medizin.uni-magdeburg.de
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionReferences |
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Background—Previous studies of pacing therapy for dilated congestive heart failure (CHF) have not established the relative importance of pacing site, AV delay, and patient heterogeneity on outcome. These variables were compared by a novel technique that evaluated immediate changes in hemodynamic function during brief periods of atrial-synchronous ventricular pacing.
Methods and Results—Twenty-seven CHF patients with severe left ventricular (LV) systolic dysfunction and LV conduction disorder were implanted with endocardial pacing leads in the right atrium and right ventricle (RV) and an epicardial lead on the LV and instrumented with micromanometer catheters in the LV, aorta, and RV. Patients in normal sinus rhythm were stimulated in the RV, LV, or both ventricles simultaneously (BV) at preselected AV delays in a repeating 5-paced/15-nonpaced beat sequence. Maximum LV pressure derivative (LV+dP/dt) and aortic pulse pressure (PP) changed immediately at pacing onset, increasing at a patient-specific optimal AV delay in 20 patients with wide surface QRS (180±22 ms) and decreasing at short AV delays in 5 patients with narrower QRS (128±12 ms) (P<0.0001). Overall, BV and LV pacing increased LV+dP/dt and PP more than RV pacing (P<0.01), whereas LV pacing increased LV+dP/dt more than BV pacing (P<0.01).
Conclusions—In this population, CHF patients with sufficiently wide surface QRS benefit from atrial-synchronous ventricular pacing, LV stimulation is required for maximum acute benefit, and the maximum benefit at any site occurs with a patient-specific AV delay.
Key Words: pacing • heart failure • systole • hemodynamics
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Treatment of congestive heart failure (CHF) with electrical stimulation has been proposed as additional therapy to be used in conjunction with pharmacological treatment.1 Although early studies reported short-term2 or long-term3 4 improvement with right ventricular (RV) pacing, subsequent studies did not reproduce these improvements with similar CHF patients.5 6 In contrast, a more uniform, beneficial result of pacing has been reported when the left ventricle (LV) has also been stimulated.7 8 The acute hemodynamic effect of atrial-triggered LV and simultaneous RV and LV (biventricular) pacing at a fixed AV delay of 100 ms has also been reported.9 In addition to issues about the pacing chamber, there is wide speculation regarding the need and method for optimizing the AV delay.2 4 5
The study objective was to investigate the effect of pacing chamber and
AV delay with atrial-synchronous ventricular pacing on
hemodynamic function in a specific CHF population
consisting of patients in stable New York Heart Association (NYHA)
class III or IV with severe LV systolic dysfunction, wide QRS
complex (
120 ms), normal sinus rhythm, and no history of
arrhythmia.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patients
Twenty-seven patients with NYHA class III or IV heart failure were enrolled in a multicenter prospective, randomized, single-blinded crossover study (Pacing Therapies for Congestive Heart Failure [PATH-CHF]). The complete PATH-CHF study inclusion and exclusion criteria, study design, and end points have been presented elsewhere.10 Main inclusion criteria were dilated cardiomyopathy of any origin; stable NYHA class III or IV with optimal medical therapy, including ACE inhibitors, nitrates, vasodilators, diuretics, digitalis, and ß-blockers; a surface ECG QRS duration
120 ms; and a
PR interval 150 ms. Main exclusion criteria were recent history of
atrial or ventricular tachyarrhythmia;
recent myocardial infarction; recent or pending coronary artery
revascularization; severe valve disease; dependence
on intravenous inotropes; and conventional indications for
pacemaker implantation. The protocol was approved by the ethical committees at all participating centers, as well as by the competent authorities of their respective countries. The study is monitored by a Patient Data/Safety Committee of independent reviewers. All patients provided written informed consent before participating in the study.
Data Collection
Acute data were collected while the patients were under general
anesthesia, including fentanyl, propofol, and
O2 during pacemaker implantation. Chronic pacing
leads were implanted with screw-in leads (Sweet-Tip, Guidant Corp) in
the right atrial appendage and RV, and an epicardial lead (model 4316,
Guidant Corp, or model 4965, Medtronic) was attached to the
surface of the LV via a limited thoracotomy. The LV pacing site was
most commonly on the apex but could also be on midlateral segments. Two
8F dual-transducer pressure catheters (model SPC-780c, Millar
Instruments) were placed to measure right atrial, RV, aortic, and LV
pressures. Pressure catheters and pacing leads were connected to a
custom external pacing computer (FlexStim, Guidant Corp) to acquire
hemodynamic signals and execute a transient pacing
protocol (FlexStim protocol) as previously described.10
The FlexStim protocol is designed to measure the immediate effects of
pacing, account for local baseline shifts, and allow statistical
comparison of multiple pacing combinations within individuals. Briefly,
the RV, LV, or both ventricles (BV) were stimulated in a VDD mode
(atrial sense followed by ventricular pacing at a
predetermined AV delay) at 1 of 5 AV delays preset to percentages of
the patient's intrinsic PR interval measured with the pacing leads.
Each combination of pacing chamber and AV delay was randomly repeated 5
times by pacing for 5 beats separated by 15 nonpaced beats.
Raw data were recorded on a digital tape recorder with 16-bit resolution at a 12 000-Hz sampling rate and then downsampled to 500 Hz for offline analysis. The following measurements were made automatically with custom software: aortic diastolic pressure, aortic systolic pressure (ASP), pulse pressure (PP=ASP-aortic diastolic pressure), LV pressure-derivative maximum (LV+dP/dt) and minimum (LV-dP/dt) by the method of Kass et al,11 LV end-diastolic pressure (LV EDP), RV maximum pressure derivative (RV +dP/dt), and RV systolic pressure. LV EDP was measured at the time when dP/dt reached 10% of the maximum. Reported QRS durations are the maximum of leads II, V1, and V6 measured automatically and validated manually by 2 independent observers.
Statistics
Parameters were calculated for each beat of a
pacing sequence as a percentage change from their average value during
the immediately preceding 6 nonpaced beats (ie, local baseline). The
first paced beat was always discarded, because its
hemodynamic effects were systematically biased by the
diastolic behavior of a preceding nonpaced beat and a
transitory cycle length decrease caused by the switch to a short AV
delay. In addition, beats altered by a premature
ventricular complex were discarded. A 3-way ANOVA
was applied to individual results to analyze differences
between AV delays and pacing chambers while accounting for the ordered
pacing beat number and interaction between the main effects. The AV
delay and pacing chamber were considered the treatment variables
and the beat number was considered a blocking factor when ANOVA results
were reported. A similar 2-way ANOVA was applied to individual
results at a selected optimal AV delay for each pacing chamber. We used
corresponding 4-way and 3-way ANOVA tests to analyze group
results by adding individuals as a treatment variable. Tukey
methodology was used to evaluate multiple comparisons of the main
effects in the full ANOVA models. A paired t test was used
to evaluate the effects of pacing compared with no pacing. A
P value of 0.0001 was considered statistically significant
for ANOVA tests. A P value of 0.05 was considered
statistically significant before Tukey corrections for individual
results, whereas a more stringent P value of 0.01 was
selected for group results owing to the larger number of sample points.
Similarly, P values of 0.001 for individual results and
0.0001 for group results were considered statistically significant for
the t tests. Average data are shown as mean±SD unless
otherwise noted.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Table 1
summarizes
demographic and baseline hemodynamic data for the 27
patients enrolled in the study. Two patients (patients 1 and 22) were
excluded from further analysis because LV and aortic pressure
could not be recorded. All patients were able to tolerate the acute
procedure without major complications.
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Hemodynamic Impulse Response
Hemodynamic parameter changes during
the brief pacing periods of the FlexStim protocol appeared immediately
at pacing onset and diminished rapidly during the subsequent nonpacing
period (Figure 1). This was quantified
with impulse response plots, which showed the average
parameter measurement over all repetitions of a pacing
combination in a patient on 5 paced beats and during the 15 nonpaced
beats that followed pacing (Figure 2).
Typically for LV+dP/dt and PP parameters, changes from
baseline occurred on the first paced beat, reached a maximum change
during the next 4 paced beats, and then returned to baseline levels
within 5 nonpaced beats. For all patients, recovery occurred within 10
nonpaced beats for every pacing chamber and AV delay combination. The
paced-beat number had a statistical effect on parameter
variation for most patients even when the first pace was discarded
(ANOVA, P<0.0001).
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Effects of Pacing Chamber
The statistical significance of the change in LV systolic
parameters averaged over all AV delays for each pacing
chamber is shown in Table 2 for each
patient. For the population average, pacing in any chamber
significantly increased LV+dP/dt (P<0.0001), whereas BV and
LV pacing significantly increased ASP and PP (P<0.0001).
The selection of pacing chamber was a significant determinant of
changes in all 3 LV systolic parameters (ANOVA,
P<0.0001). LV+dP/dt, ASP, and PP changes with BV and LV
pacing were significantly greater than the effects of RV pacing for the
population; and LV pacing effects on LV+dP/dt were greater than the
effects of BV pacing (P<0.01).
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Population changes in other hemodynamic
parameters averaged over all AV delays for each pacing
chamber are shown in Table 3. Changes to
parameters that partially reflect LV diastolic
performance were statistically significant but small and
inconsistent. The LV EDP decreased, indicating lowered filling
pressures, but the absolute value of LV–dP/dt also decreased,
indicating slower relaxation. Average changes in RV systolic
parameters were also relatively small and
inconsistent.
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Interpatient Variability of Pacing Chamber Effects
With the FlexStim protocol, the effects of pacing were
statistically established for each individual (Table 2
). Most
but not all patients had statistical improvement in short-term
hemodynamic function with pacing at some site
(P<0.001): RV, LV, or BV pacing significantly increased
both LV+dP/dt and PP in 15 patients (60%), increased only LV+dP/dt in
5 patients (20%), and did not increase LV+dP/dt or PP in 5 patients
(20%). Patients in this last group had significantly shorter QRS
widths from surface ECG compared with other patients (180±22 versus
128±12 ms; t test, P<0.0001) and had less
incidence of left bundle-branch block (20 of 20 patients versus 1 of 5
patients; 
2, P<0.0001) but were
not statistically different for other demographic measures. Patients in
this last group were retrospectively classified as type II, whereas all
other patients were classified as type I. As shown in Figure 3, all type I patients had significant
improvement in LV+dP/dt or PP with pacing in the optimal chamber, and
all but 2 of them had a surface QRS width >150 ms, whereas none of the
type II patients had improvement in LV+dP/dt or PP, and all of them had
a QRS width <150 ms. When patients were divided into type I and type
II subgroups, RV-paced changes in ASP and PP reached significant levels
for each subgroup (Table 2). The statistical differences among
pacing chambers were similar for the type I and type II subgroups,
although parameter responses were in opposite
directions.
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Effects of AV Delay
For all patients combined and for type I and type II subgroups, AV
delay was a significant determinant of changes in all LV
systolic parameters (ANOVA, P<0.0001).
Figure 4 shows the paced change in
systolic parameters as a function of AV delay for
the patient subgroups. For type I patients, LV+dP/dt and PP AV delay
functions were positive and unimodal, with a peak at the middle AV
delay setting [0.5x(PR–30 ms)]. For type II patients, AV delay
functions were negative for all parameters. For both type I
and type II patients, there was significant interaction between AV
delay and pacing chamber (ANOVA chamber/AV delay interaction,
P<0.0001).
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Interpatient Variability of AV Delay Effects
The detailed relationship between AV delay and LV+dP/dt or PP
varied among individuals (ANOVA chamber/patient and AV delay/patient
interactions, P<0.0001). One way to measure these
differences is to compare the peaks of the AV delay functions for each
patient, defined as the optimal AV delays. The optimal AV delays for
the same pacing chamber and parameter varied widely among
patients and often differed for PP and LV+dP/dt within an individual
(examples in Figures 5 and 6). On average (Table 4), the optimal AV delays were similar
among pacing chambers for peak ASP and PP, but for the type I patients,
they were significantly shorter for RV pacing and BV pacing compared
with LV pacing for LV+dP/dt (paired t test, RV<LV
P<0.008, BV<LV P<0.04). The optimal acute
benefit attained for each patient group and pacing chamber is shown in
Table 5. Statistical results at the
optimal AV delays were similar to those over all AV delays (Table 2), except for type II patients, whose optima were near baseline
at the longest AV delays.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The major finding of this study is that the acute LV systolic function of patients with moderate to severe CHF, LV systolic dysfunction, and prolonged ventricular activation is significantly and consistently improved by ventricular pacing at an optimal combination of AV delay and site, while LV diastolic and RV systolic parameter changes are relatively small and inconsistent. Patients with QRS>150 ms exhibit large positive LV systolic changes with pacing, whereas patients with QRS<150 ms exhibit predominantly negative LV systolic changes. However, even for these latter patients, LV systolic function could be optimized by individualized selection of AV delay and pacing chamber. In this patient population, which is dominated by LV conduction disorders, LV stimulation alone or in combination with RV stimulation substantially increases LV systolic benefits compared with RV stimulation alone.
Hemodynamic Impulse Response
We found that systolic parameters changed
immediately with the onset and cessation of pacing, which confirms an
observation made by Blanc et al,9 who also showed these
changes persist after several minutes of steady-state pacing. Others
have shown similar increases in PP12 and
LV+dP/dt13 in CHF patients with steady-state VDD pacing.
Furthermore, PP and stroke volume changes were associated with
steady-state pacing in a study of CHF patients13 and have
been shown to be proportional in animal studies with the FlexStim
protocol.14 Thus, the effects of transient and
steady-state ventricular stimulation appear to be
qualitatively similar and probably arise from the same mechanism, which
we surmise is a direct change of the ventricular
electromechanical activation patterns. Under the conditions of our
study (patients under general anesthesia and only transient
pacing), the compensatory reflex response to stimulation should be
small, certainly less than for steady-state stimulation of unsedated
patients, and therefore the measured effects of ventricular
stimulation would tend to be larger and reflect mainly the direct
mechanisms.
Pacing Mechanisms
A number of potential mechanisms to explain the positive effects
of pacing in CHF patients have been discussed
previously.12 These mechanisms primarily involve
correcting abnormal electrical conduction15 that
presumably generates mechanical dysfunction. CHF patients exhibit
abnormally short or long left-side mechanical AV delays outside the
normal range of 180 to 250 ms,12 resulting in increased
mitral regurgitation and reduced effective preload.
Similar to our findings, Nishimura et al16 and Auricchio
and Salo12 showed that an appropriate AV delay is required
to maximize cardiac output in CHF patients. They suggest the optimal AV
delay may normalize the mechanical timing between left atrium and LV,
thus reducing regurgitation and maximizing effective
preload. Our observation that paced changes in PP are a positive
unimodal function of AV delay is consistent with this
mechanism.
CHF patients also have relatively uncoordinated contraction patterns in the LV,17 which could impair systolic function. BV pacing may improve systolic function in the short term by altering the segmental LV and interventricular septal contractile sequence in patients with depressed LV function,18 which would be expected to correlate with increased LV+dP/dt, a global measure of systolic pump performance.
There is a close relationship between abnormal contraction patterns and electrical activation disturbances, such as a wide QRS complex.19 This relationship may explain why a sufficiently wide QRS and left bundle-branch block tend to predict short-term pacing benefit. Patients may not benefit from pacing unless the conduction disorder and underlying ventricular incoordination are suitably abnormal. It may also explain why stimulation that includes the LV is far better than RV-only stimulation in a population with a high incidence of LV conduction disorders. It is our hypothesis that atrial-synchronous pacing that preexcites the ventricular wall ipsilateral to the conduction disorder restores a more normal activation pattern, thus coordinating wall motion and increasing pumping effectiveness.
Clinical Implications
Because CHF patients have heterogeneous symptoms,
etiologies, and substrates, and pacing may operate through multiple
mechanisms requiring individual optimization, it should not be
surprising that the previously reported clinical benefit of pacing is
ambiguous. Our results show that both positive and negative effects of
pacing occur, at least in the short term. The outcome depends on pacing
parameters and individual variables. The most important
pacing parameter is pacing chamber, but AV delay
significantly modulates the result. The most important variable for
predicting acute pacing benefit in the present study was QRS width.
If the distinction between type I and type II patients also applies to
long-term pacing benefit, studies including a mixture of such patients
will necessarily have mixed results. The seemingly contradictory
results regarding the benefit of RV pacing3 5 6 20 might
be explained by the weak and strongly patient-dependent
hemodynamic effects of RV pacing and fortuitous
differences in clinical patient populations.21 On the
other hand, the consistently reported positive results with LV
pacing7 8 9 12 13 can be understood as a consequence of the
large hemodynamic response to left-sided pacing in a
majority of studied patients. Thus, it would seem important to account
for these individual variations in future studies of pacing therapy for
CHF. Selection of the optimal pacing parameters for an
individual patient can minimize the negative effects of pacing on type
II patients and maximize the positive effects of pacing on type I
patients, with optimized cardiac output increase being 2 to 4 times
more than with suboptimal pacing.
Limitations
This was an acute study performed during surgery on patients under
general anesthesia, which can affect preload, afterload,
and other hemodynamic variables; results may differ
for unsedated patients with chronic pacing. Although this study focused
on LV systolic function, the chronic response to pacing may
depend also on long-term alterations of diastolic function
and RV function, although they changed minimally and
inconsistently during the acute protocol. The results may not
extrapolate to other CHF populations, particularly those with less
severe symptoms, nonsystolic dysfunction, paroxysmal or chronic
atrial fibrillation, sick sinus syndrome or complete AV block, or more
severe AV conduction blocks. A limitation of our protocol is that the
paced-beat number has a significant effect on the
hemodynamic response. The first beat in a pacing period
was excluded from analysis because of expected effects of the
initial AV delay shortening. However, the order effects of subsequent
beats were unexpected, and although they were accounted for in the
ANOVA statistical analysis, results may differ when such
systematic beat-number effects are excluded. As a check of the
sensitivity of the results to beat number, statistical analyses
were repeated with alternative combinations of paced beats. None of our
study conclusions changed for these alternative statistical
treatments.
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Acknowledgments |
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This study was supported entirely by Guidant Corporation, St. Paul, Minn, and by an unrestricted grant by Guidant to the Department of Cardiology, University Hospital Magdeburg, Germany. We are indebted to the patients who participated in this trial and to the physicians who referred their patients for study inclusion. The investigators gratefully acknowledge the nurses and colleagues at each institution of the ICU, Heart Failure Program, and Surgery without whose help and logistic support this study would not be possible. Dr Auricchio wishes to thank the CHF Research Group of Guidant for the outstanding technological support, with special thanks to Michael Hull, MS, for excellent statistical assistance.
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Footnotes |
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This work was supported by a grant from Guidant Corporation.
Received October 23, 1998; revision received March 18, 1999; accepted March 26, 1999.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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M. Poullis and M. Shackcloth Coronary grafts flow and cardiac pacing modalities: the importance of the cardiac resynchronisation trials Eur. J. Cardiothorac. Surg., January 1, 2005; 27(1): 177 - 178. [Full Text] [PDF]
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I. Hay, V. Melenovsky, B. J. Fetics, D. P. Judge, A. Kramer, J. Spinelli, C. Reister, D. A. Kass, and R. D. Berger Short-Term Effects of Right-Left Heart Sequential Cardiac Resynchronization in Patients With Heart Failure, Chronic Atrial Fibrillation, and Atrioventricular Nodal Block Circulation, November 30, 2004; 110(22): 3404 - 3410. [Abstract] [Full Text] [PDF]
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H. Kanzaki, R. Bazaz, D. Schwartzman, K. Dohi, L. E. Sade, and J. Gorcsan III A mechanism for immediate reduction in mitral regurgitation after cardiac resynchronization therapy: Insights from mechanical activation strain mapping J. Am. Coll. Cardiol., October 19, 2004; 44(8): 1619 - 1625. [Abstract] [Full Text] [PDF]
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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]
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J. Vogt, J. Heintze, B. Lamp, B. Hansky, and D. Horstkotte Standard haemodynamic measurements Eur. Heart J. Suppl., August 1, 2004; 6(suppl_D): D29 - D34. [Abstract] [Full Text] [PDF]
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C. Stellbrink, O.-A. Breithardt, and P. Hanrath Technical considerations in implanting left ventricular pacing leads for cardiac resynchronisation therapy Eur. Heart J. Suppl., August 1, 2004; 6(suppl_D): D43 - D46. [Abstract] [Full Text] [PDF]
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B. Pieske Reverse remodeling in heart failure - fact or fiction? Eur. Heart J. Suppl., August 1, 2004; 6(suppl_D): D66 - D78. [Abstract] [Full Text] [PDF]
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J. Vogt, B. Lamp, B. Hansky, J. Heintze, L. Faber, H. Guldner, R. Korfer, and D. Horstkotte The Bad Oeynhausen Experience Eur. Heart J. Suppl., August 1, 2004; 6(suppl_D): D122 - D127. [Abstract] [Full Text] [PDF]
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S.M. Kanhai, E.P. Viergever, and J.J. Bax Cardiogenic shock shortly after initial success of cardiac resynchronization therapy Eur J Heart Fail, June 1, 2004; 6(4): 477 - 481. [Abstract] [Full Text] [PDF]
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H. Ashikaga, J. H. Omens, N. B. Ingels Jr., and J. W. Covell Transmural mechanics at left ventricular epicardial pacing site Am J Physiol Heart Circ Physiol, June 1, 2004; 286(6): H2401 - H2407. [Abstract] [Full Text] [PDF]
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A Auricchio and C M Yu Beyond the measurement of QRS complex toward mechanical dyssynchrony: cardiac resynchronisation therapy in heart failure patients with a normal QRS duration Heart, May 1, 2004; 90(5): 479 - 481. [Abstract] [Full Text] [PDF]
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