(Circulation. 1999;99:1567-1573.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Improved Left Ventricular Mechanics From Acute VDD Pacing in Patients With Dilated Cardiomyopathy and Ventricular Conduction Delay
From the Division of Cardiology, Department of Medicine, the Johns Hopkins Medical Institutions, Baltimore, Md. Dr Chen was a Clinical Research Fellow from the Division of Cardiology, Department of Medicine, Veterans General Hospital Taipei, and National Yang-Ming University, Taiwan, ROC.
Correspondence to David A. Kass, MD, Halsted 500, the Johns Hopkins Hospital, 600 N Wolfe St, Baltimore, MD 21287. E-mail dkass{at}eureka.wbme.jhu.edu
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Abstract |
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Background—Ventricular pacing can improve hemodynamics in heart failure patients, but direct effects on left ventricular (LV) function from varying pacing site and atrioventricular (AV) delay remain unknown. We hypothesized that the magnitude and location of basal intraventricular conduction delay critically influences pacing responses and that single-site pacing in the delay-activated region yields similar or better responses to biventricular pacing.
Methods and Results—Aortic and LV pressures were measured in 18
heart failure patients (mean±SD: LV ejection fraction, 19±7%; LV
end-diastolic pressure, 25±8 mm Hg; QRS duration,
157±36 ms). Data under normal sinus rhythm were compared with
ventricular pacing (VDD) at varying sites and AV delays
(randomized order). Right ventricular (RV) apical or
midseptal pacing had negligible contractile/systolic effects.
However, LV free-wall pacing raised dP/dtmax by
23.7±19.0% and pulse-pressure by 18.0±18.4%
(P<0.01). Biventricular pacing yielded less
change (+12.8±9.3% in dP/dtmax, P<0.05
versus LV). Pressure-volume analysis performed in 11 patients
consistently revealed minimal changes with RV pacing but
increased stroke work and lower end-systolic volumes with LV
pacing. Optimal AV intervals averaged 125±49 ms, and within this
range, AV delay had less influence on LV function than pacing site.
Basal QRS duration positively correlated with %
dP/dtmax
(P<0.005), but pacing efficacy was not associated with
QRS narrowing. Conduction delay pattern generally predicted pacing
sites with most effect.
Conclusions—VDD pacing acutely enhances contractile function in heart failure patients with intraventricular conduction delay. Single-site pacing at the site of greatest delay achieves similar or greater benefits to biventricular pacing in such patients. These data clarify pacing-effect mechanisms and should help in candidate identification for future studies.
Key Words: mechanics • ventricles • pacing • conduction • heart failure
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Dual-chamber (VDD) pacing with ventricular preexcitation is a novel therapy for patients with dilated cardiomyopathy (DCM) currently undergoing clinical trials throughout the United States and Europe. Initial research focused on the utility of shortening atrioventricular (AV) conduction to optimize chamber filling and limit mitral regurgitation and used standard right ventricular apical (RVA) pacing.1 2 3 4 5 However, subsequent clinical trials raised doubts about the general efficacy of this approach.6 7 8 Attention then shifted to RV septal (RVS) pacing9 and multisite pacing as methods to restore contractile synchrony in subjects with baseline intraventricular conduction delay.10 11 Recently, Blanc and colleagues12 compared RV, left ventricular (LV), and biventricular (BiV) pacing modes in DCM patients and reported that LV free-wall (LVFW) pacing acutely enhanced femoral systolic pressure while lowering pulmonary wedge pressure. Interestingly, responses from single LV sites were similar to BiV pacing (LVFW+RVA). The mechanisms for these results remain unclear, because improved chamber loading, reduced mitral regurgitation,3 5 and enhanced contractile function each could explain the observations. To date, no study has directly assessed effects of varying VDD pacing site on LV systolic and diastolic function or the added influence of varying AV delay. Furthermore, the dependence of RV or LV pacing efficacy on basal QRS morphology is unknown.
To address these issues, we conducted an acute catheterization study of VDD pacing effects in patients with DCM, varying both site and AV interval and evaluating their effects on LV mechanics. The following hypotheses were tested: (1) single-site pacing in the region of delayed activation in DCM patients with underlying conduction delay achieves a response as good as or better than BiV pacing; (2) baseline QRS-interval prolongation correlates with the magnitude of systolic mechanical response; and (3) pacing site has a greater impact on the response than AV delay unless this delay is unusually short.
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Methods |
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Study Group
Eighteen patients with DCM (NYHA class III to IV) provided informed consent and underwent cardiac catheterization. The protocol was approved by the Joint Committee on Clinical Investigation of the Johns Hopkins Medical Institutions. Patients were in normal sinus rhythm (NSR), all but 1 with an AV interval >150 ms, and none with prior indications or need for pacing. Most had minimal or mild (+1) mitral regurgitation. Patients maintained chronic medications to the time of study (generally digoxin, an ACE inhibitor, and diuretics, with carvedilol in 1 patient, patient 18). They were studied under mild sedation (midazolam 1 to 3 mg, fentanyl 50 to 100 mg).
Table 1
provides clinical
characteristics. Most patients (13 of 18) had nonischemic DCM
with an LBBB conduction delay pattern (11 of 18). Two had right
bundle-branch block (RBBB), 1 bifascicular block (RBBB+left anterior
hemiblock), 1 an indeterminate pattern, and the remaining no delay.
Mean ejection fraction was 19±7%, with an average heart rate of
84±14 bpm, AV interval of 204.1±69.2 ms, and QRS width (mean of
12-lead measurements) of 156.8±35.8 ms.
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Catheterization Protocol
A combined 6F dual pressure-volume (PV) catheter (Millar
550-768) was advanced through a 90-cm flexible long sheath (Arrow
CL-07690) and placed so that the pigtail tip lay at the distal LV apex.
The sheath was continuously flushed with heparin/saline. The catheter
provided simultaneous proximal aortic and
ventricular cavity micromanometer
pressures and chamber volume. Pressure offset was calibrated to an
external zero pressure at study conclusion. Time-varying cavity volumes
were derived from the conductance catheter as previously
described.13 14
A steerable electrode catheter was positioned at the RVA or mid to upper RVS and a second catheter in the right atrium for atrial sensing. A flexible sheath fitted with a steerable electrode catheter was positioned in the coronary sinus. The steerable catheter was removed and replaced with a 1.4F high-torque guidewire which was then advanced to a lateral marginal vein or anterior cardiac vein, and a 3F quadripolar catheter (Elecath 204-12723) was advanced over the wire to this site for LV epicardial pacing. Pacing was generally achieved in a position midway between the base and apex.
Pacing in VDD mode was initiated at the RVA (n=17), RVS (n=15), LVFW (n=11), or combined RVS (or RVA) and LVFW (BiV; n=10). Not every site was studied in all 19 patients. At each site, 3 or 4 different AV intervals were studied. Each AV interval differed by 25 to 30 ms, with the longest delay being 20 to 70 ms shorter than the intrinsic AV interval, ensuring inclusion of an interval near 120 ms in each patient. Data were recorded after 2 minutes at steady state for each condition, and the order of pacing site and AV interval was randomized. Pacing was then suspended for 1 to 2 minutes, and repeat NSR data were obtained before the pacing intervention was changed. Multiple NSR data provided assessment of physiological variance for each parameter (expressed by coefficient of variation=SD/meanx100). Hemodynamic changes with pacing were assessed relative to the immediately preceding NSR data.
Data Analysis
In 7 studies, the volume catheter signal was uninterpretable
(ie, isovolumic) because of low signal-to-noise ratios. Thus, the
primary analysis in all patients was based on the
micromanometer data. In addition to aortic
systolic pressure, pulse pressure (PP) was used as a surrogate
for changes in cardiac output. At a constant heart rate and vascular
load, PP directly correlates with cardiac output.15 To
directly test the validity of this assumption, data from all subjects
in whom both PP and PV-loop data were obtained at 
2 VDD pacing sites
with varying responses (5 patients, n=15 observations) were subjected
to multiple regression, including terms for between-subject
differences. The result was highly significant, with an overall
regression of r=0.88 (P=0.008) and mean slope of
5.1±1.6 (ie, 
5% change in cardiac output for each 1% change in
PP).
Ventricular micromanometer pressures
yielded peak-systolic and end-diastolic pressure
(EDP). EDP equaled the pressure when dP/dt exceeded 10% of
dP/dtmax. Pressure was digitally differentiated
by use of a running 5-point weighted slope, and peak and minimal values
were determined. These values were also normalized to instantaneous
pressure (eg, dP/dtmax/IP) to minimize load
effects. Two relaxation time constants were determined from pressure
data between dP/dtmin and the point at which
pressure was <EDP+5 mm Hg: 
F based on a
monoexponential decay and L
based on a logistic decay.16 Neither fit forced pressure
decay to zero. In patients with interpretable conductance-volume data,
LV PV loops were derived and used to assess loop area (stroke work) and
steady-state end-diastolic and systolic
volumes.
Statistical analysis was performed with commercial software using repeated-measures ANOVA with posthypothesis testing of pacing-site differences by Tukey's test. Other tests are identified in the text where appropriate. All data are presented as mean±SD.
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Results |
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Baseline Data
Resting cardiac index was 2.0±0.41 L · min-1 · m-2 at a mean heart rate of 82.1±12.3 bpm. Contractile function indexed by dP/dtmax was depressed, at 760.1±241.2 mm Hg/s (typical value in normal individuals is 1700±300 mm Hg/s), and diastolic function was abnormal, as evidenced by an elevated LVEDP: 24.8±7.8 mm Hg and prolonged isovolumic relaxation:
F, 171±118 ms (versus
46±3 in normals) and L, 46.3±17.3 ms (versus
21±1 in normals).
Ventricular Responses to VDD Pacing
Individual results for dP/dtmax,
arterial PP, and peak-systolic pressure for each
pacing site are shown in Figure 1, and percent changes for these and other parameters are given in
Table 2. Data are at optimized AV
interval for each site in each patient, which on average was 125±48.7
ms.
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Although RVA and RVS pacing had negligible effects on these parameters, all 3 rose significantly and consistently with LVFW and BiV pacing. For LVFW pacing, dP/dtmax increased 23.7±19% (an absolute change of 147.2±109.5 mm Hg/s), peak-systolic pressure rose 5.7±4.4%, and PP increased 18±18.4%. These changes were significantly greater than with RVA pacing (P<0.005) and generally higher than RVS pacing. BiV pacing induced quantitatively smaller responses than LVFW pacing (P<0.05 for dP/dtmax by paired t test). Heart rate was not directly altered by VDD-mode pacing, with heart rate for NSR and VDD pacing being similar regardless of pacing site (85.2±14 versus 85.1±13 bpm for RVA; 80.2±11.3 versus 79.6±11.6 bpm for RVS; 81.1±11.9 versus 80.1±12.1 bpm for LVFW; and 81.1±12.7 versus 80.9±12.1 bpm for BiV).
In contrast to systole, VDD pacing had little effect on diastolic function (EDP, peak negative dP/dt, and relaxation time constants). If anything, relaxation was slightly faster with right heart pacing (P<0.01 combining both RVA and RVS data), whereas it tended to prolong with LVFW pacing (P<0.0001 versus right heart responses by Mann-Whitney U test).
Figure 2 displays steady-state PV loops
from a patient with a baseline LBBB. Neither RVA nor RVS pacing induced
changes in the resting PV loop, consistent with the
hemodynamics shown in Table 2
. However, LVFW
pacing reduced end-systolic volume and increased loop width
(stroke volume) and area (stroke work). BiV pacing also enhanced stroke
work and stroke volume but less so than LVFW pacing. As previously
noted, percent changes in cardiac output (or stroke volume) correlated
with simultaneous changes in PP. For the subject in Figure 2, the correlation r value was 0.98
(P=0.005). Loop data with RVA (n=11) or RVS (n=9) pacing
revealed enhanced stroke work or stroke volume in only 4 instances. In
contrast, systolic improvement was observed in 8 of 10 PV-loop
cases (5 studies) with LV or BiV pacing (P=0.002,
2). In patients with resting QRS prolongation,
LVFW+BiV pacing increased stroke work by 45±43% (P=0.04)
and stroke volume by 40±40% (P=0.02), whereas RVA+RVS
pacing yielded minimal changes in both variables.
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Influence of Basal QRS Duration and Changes in QRS Duration
With Pacing
To test whether LV systolic response to VDD pacing
depended on underlying conduction delay, basal QRS duration was plotted
against the %dP/dtmax induced by VDD pacing
in each patient. Because RVA pacing yielded minimal or negative changes
in dP/dtmax in most patients, we first performed
the analysis excluding this site. Data were fit by multiple
regression with pacing site as a categorical variable and QRS
duration as a continuous variable and revealed dependence of
contractile response on QRS duration (P<0.005, multiple
regression r=0.65) even accounting for pacing site (Figure 3). This was also significant
(P<0.05) if RVA pacing was included.
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Mechanical improvement with pacing was not associated with QRS
narrowing. Rather, QRS duration tended to widen with pacing overall
(+11.2±27%, combined data, n=50, P<0.005), although
variability for each site (Table 2) was too high to reach
significance.
Influence of AV Interval
Figure 4 shows influences of AV
interval with VDD pacing on chamber filling (LVEDP) and
systolic function (dP/dtmax). RVA and RVS
pacing site data are combined and contrasted to combined data with LVFW
and BiV pacing. LVEDP and dP/dtmax declined very
slightly as AV interval shortened to near 120 ms and fell more at
shorter delays with greater preload decline (P<0.05 and
P<0.01, respectively). Enhancement of
dP/dtmax from LVFW or BiV over RV pacing was
observed at AV intervals between 100 and 160 ms, with a maximum at 125
ms.
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Conduction Delay Pattern and Long AV Intervals
Although mean data (Table 2) indicated that LVFW or BiV
pacing was beneficial, RV pacing was not always ineffective. In both
subjects with RBBB (patients 15 and 16), RVS pacing yielded changes
greater than those from LVFW pacing and similar to BiV pacing. For
example, dP/dtmax rose 18.3% and 15.9% with RVS
pacing, versus 7.7% and 7.3% with LVFW. Interestingly, RVA pacing
still lowered dP/dtmax in both patients (-10.8%
and -5.7%). Similar patterns occurred with PP and systolic
blood pressure. RVS pacing was also effective in 2 patients with very
long AV intervals (ie, >300 ms, patients 12 and 13) despite an LBBB
morphology. For example, in these patients,
dP/dtmax rose by 19% with RVS pacing, although
it still increased more with LVFW pacing (27.2%).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The present data support recent findings showing that LVFW or BiV pacing in patients with DCM and underlying ventricular conduction delay enhances systolic pressures.10 12 We provide the first demonstration that these changes relate primarily to direct improvement of LV systolic function, with minimal changes in diastolic filling pressures or relaxation. We further clarify the value of selecting an appropriate AV delay near 120 ms, although within this range, small differences in delay have far less influence than pacing site. Although a wider baseline QRS was associated with greater mechanical improvement by pacing, changes in the QRS with pacing did not predict efficacy. If anything, BiV pacing induced the smallest change in QRS width yet did not have the largest mechanical benefit. Last, and admittedly based on a small sample, patients with RBBB and those with very long AV delays may benefit from RVS pacing.
Mechanisms of VDD Pacing Effects
VDD pacing has 2 primary effects on the heart. The first relates
to the AV interval, which influences the timing of atrial contraction
relative to the preceding and subsequent QRS complexes. Shortening the
interval can diminish mitral regurgitation, lengthen
the time available for diastolic filling,1 3 5
and alter the filling pattern from one characterized principally by an
early-filling wave to one with more
physiologically balanced early and late
(atrial) filling components.1 4 The latter pattern should
also lower mean atrial pressures even if net filling is
similar,17 18 possibly explaining declines in
pulmonary wedge pressure.12
The second mechanism relates to changing contraction coordination. Acute single-site pacing in normal hearts induces discoordinate wall motion, reducing contractile function.19 20 The prematurely activated region shortens against little load with little net contribution to systole. The late-activated region encounters a more compliant early-stimulated wall and stretches this region during its systole, further reducing ejection efficiency. This results in higher end-systolic volume and rightward shift of the ventricular end-systolic pressure-volume relation.19 21
Patients with underlying RV or LV conduction delays are analogous to those having single-site pacing in the opposing ventricle. One may therefore predict that pacing the region with delayed activation with an appropriate AV delay might improve contractile synchrony and systolic function and lower end-systolic volumes. The present data support this hypothesis, because pacing the LVFW in patients with LBBB (or RVS in those with RBBB) significantly improved systolic function. In patients with PV-loop data, this was accompanied by an increase in stroke volume and stroke work, reduced end-systolic volume, and minimal change in end-diastolic volume. There was also a direct relation between the magnitude of conduction delay (QRS duration) and systolic contractile response to VDD, supporting the notion that the more dissynchronous the heart at baseline, the more likely it is that pacing benefits function.
VDD pacing had no significant beneficial or detrimental effects on
diastolic relaxation or the diastolic PV
relation. The latter is not surprising, because pacing-induced
discoordination or varying AV delay does not directly alter chamber
compliance.19 However, discoordination prolongs
relaxation,22 so it might seem paradoxical that LVFW
pacing tended to lengthen relaxation despite systolic
improvement, whereas relaxation shortened with RV pacing despite
negligible systolic changes. However, abnormalities such as
altered calcium cycling linked to reduced sarcoplasmic reticular
proteins and function23 24 and ß-adrenergic
signaling25 also contribute potently to relaxation delay
and are not directly altered by improved contractile synchrony. It is
unlikely that altered systolic loading was important, in that
the systolic pressure change with pacing was small and imposed
throughout ejection (ie, Figure 2).
BiV Versus Single-Site Pacing
This is only the second study to directly compare BiV with
single-site pacing in patients with DCM, and consistent with
the report by Blanc et al,12 single-site pacing was equal
or superior to BiV pacing in patients with underlying LBBB-type
conduction delay. One might expect that LV pacing would shift early
activation to the left heart and not necessarily achieve mechanical
asynchrony. However, it is likely that myocardial conduction emanating
from LV epicardial pacing is slow compared with intrinsic conduction
via the conducting fascicle, so mechanical forces remain synchronized
even with early excitation. Some RV-LV stimulation delay may be
important, given the often disproportionate rise in LV mass in DCM
patients, and may help explain similar if not diminished mechanical
responses with BiV pacing.
It remains possible that BiV pacing may improve on single-site pacing if there is an inability to control the timing between RV and LV activation, as with second- and third-degree heart block or atrial fibrillation. BiV pacing might also be useful in patients with profound first-degree AV block and a normal QRS complex. Single-site pacing would be anticipated to reduce systolic function and thereby offset benefits from improved chamber filling, whereas BiV would probably better maintain electrical and mechanical synchrony in such patients. Future developments in pacing technology should allow variable timing between RV and LV stimulation, so that this delay can be optimized in a given patient. Whether this will indeed enhance function beyond that from single-site pacing remains to be determined.
Methodological Considerations and Limitations
This is the first study to use LV epicardial pacing with a
catheter introduced via the coronary sinus. This differs from
the open-chest epicardial pacing used by Foster et al10 or
endocardial pacing used by Blanc et al12 but is similar to
methods currently being tested for long-term results.26 In
the study by Blanc et al, nearly 25% of patients had atrial
fibrillation, whereas we excluded these patients to facilitate
contractile function analysis, because
contractility varies with RR interval.24
We also excluded patients with preexisting pacemakers,26
because this could reflect different substrates. This does not mean
that neither group may benefit from VDD pacing.
There were several technical limitations. Continuous-cardiac-output catheters were used to circumvent the need for repeated fluid boluses, but substantial variability persisted. We therefore used PP as a surrogate, assuming a constant arterial impedance and heart rate. The high correlation between percent changes in both parameters supports this assumption. In addition, the conductance (volume) catheter method failed in 7 of 19 patients because of inadequate signal-to-noise ratio.
Finally, this short-term study may not reflect long-term responses. Long-term trials targeting optimal single-site pacing need to be performed and are under way at our and other institutions. Given the rise in dP/dtmax with pacing and the poor outcomes often reported with long-term inotropic trials for DCM, one could raise concerns over pacing benefits. However, improving contractile coordination differs from interventions elevating intracellular calcium, such as adrenergic stimulation or phosphodiesterase III inhibition, and may not have the same energetic consequences. This hypothesis is currently being tested. The present data help rationalize ongoing and future long-term trials and assist in identifying the appropriate target group.
The present data, along with results of other recent studies, support the notion that VDD pacing in DCM patients and ventricular conduction delay may be therapeutically useful. In particular, the data help clarify the mechanism for such effects and define the patient group for which right or left heart pacing is most likely to be beneficial. There have been no single-site left heart chronic pacing multicenter trials to date, but our data suggest that such approaches deserve consideration, particularly in patients with LBBB. We await the results of such randomized clinical trials to determine whether VDD pacing will indeed be a useful addition to heart failure treatment.
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Acknowledgments |
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This study was supported by a grant from Guidant/Cardiac Pacemakers, Inc; a General Clinical Research Center Grant (RR-00052) from the National Health Service; a Fogarty Foundation Grant (Dr Nevo); and fellowship grants from Colin Medical Inc (B. Fetics) and Guidant/CPI (Dr Chen).
Received October 8, 1998; revision received December 3, 1998; accepted December 18, 1998.
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References |
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F. Eberhardt, M. Heringlake, M. S. Massalme, A. Dyllus, M. Misfeld, H.-H. Sievers, U. K.H. Wiegand, and T. Hanke The effect of biventricular pacing after coronary artery bypass grafting: A prospective randomized trial of different pacing modes in patients with reduced left ventricular function. J. Thorac. Cardiovasc. Surg., June 1, 2009; 137(6): 1461 - 1467. [Abstract] [Full Text] [PDF]
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P. Dilaveris, G. Giannopoulos, A. Synetos, C. Aggeli, L. Raftopoulos, P. Arsenos, K. Gatzoulis, and C. Stefanadis Effect of biventricular pacing on ventricular repolarization and functional indices in patients with heart failure: lack of association with arrhythmic events Europace, June 1, 2009; 11(6): 741 - 750. [Abstract] [Full Text] [PDF]
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S. A. Hunt, W. T. Abraham, M. H. Chin, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. Jessup, M. A. Konstam, D. M. Mancini, K. Michl, et al. 2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the International Society for Heart and Lung Transplantation J. Am. Coll. Cardiol., April 14, 2009; 53(15): e1 - e90. [Full Text] [PDF]
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M. Jessup, W. T. Abraham, D. E. Casey, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. A. Konstam, D. M. Mancini, P. S. Rahko, M. A. Silver, et al. 2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the International Society for Heart and Lung Transplantation J. Am. Coll. Cardiol., April 14, 2009; 53(15): 1343 - 1382. [Full Text] [PDF]
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2009 WRITING GROUP TO REVIEW NEW EVIDENCE AND UPDA, M. Jessup, W. T. Abraham, D. E. Casey, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. A. Konstam, D. M. Mancini, P. S. Rahko, et al. 2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the International Society for Heart and Lung Transplantation Circulation, April 14, 2009; 119(14): 1977 - 2016. [Full Text] [PDF]
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2005 WRITING COMMITTEE MEMBERS, S. A. Hunt, W. T. Abraham, M. H. Chin, A. M. Feldman, G. S. Francis, T. G. Ganiats, M. Jessup, M. A. Konstam, D. M. Mancini, et al. 2009 Focused Update Incorporated Into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the International Society for Heart and Lung Transplantation Circulation, April 14, 2009; 119(14): e391 - e479. [Full Text] [PDF]
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K. Chakir, S. K. Daya, T. Aiba, R. S. Tunin, V. L. Dimaano, T. P. Abraham, K. Jaques, E. W. Lai, K. Pacak, W.-Z. Zhu, et al. Mechanisms of Enhanced {beta}-Adrenergic Reserve From Cardiac Resynchronization Therapy Circulation, March 10, 2009; 119(9): 1231 - 1240. [Abstract] [Full Text] [PDF]
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W. Mullens, R. A. Grimm, T. Verga, T. Dresing, R. C. Starling, B. L. Wilkoff, and W.H. W. Tang Insights from a cardiac resynchronization optimization clinic as part of a heart failure disease management program. J. Am. Coll. Cardiol., March 3, 2009; 53(9): 765 - 773. [Abstract] [Full Text] [PDF]
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W. Mullens, T. Verga, R. A. Grimm, R. C. Starling, B. L. Wilkoff, and W.H. W. Tang Persistent hemodynamic benefits of cardiac resynchronization therapy with disease progression in advanced heart failure. J. Am. Coll. Cardiol., February 17, 2009; 53(7): 600 - 607. [Abstract] [Full Text] [PDF]
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U. Bildirici, A. Vural, A. Agacdiken, T. Sahin, U. Celikyurt, T. Kilic, and D. Ural Comparison of the effects of left vs. right ventricular pacing on left ventricular remodelling Europace, December 1, 2008; 10(12): 1387 - 1391. [Abstract] [Full Text] [PDF]
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S. S. Barold, A. Ilercil, and B. Herweg Echocardiographic optimization of the atrioventricular and interventricular intervals during cardiac resynchronization Europace, November 1, 2008; 10(suppl_3): iii88 - iii95. [Abstract] [Full Text] [PDF]
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J. Gorcsan III Is the magnet a better crystal ball for predicting response to cardiac resynchronization therapy? J. Am. Coll. Cardiol. Img., September 1, 2008; 1(5): 569 - 571. [Full Text] [PDF]
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A. E. Epstein, J. P. DiMarco, K. A. Ellenbogen, N.A. M. Estes III, R. A. Freedman, L. S. Gettes, A. M. Gillinov, G. Gregoratos, S. C. Hammill, D. L. Hayes, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) Developed in Collaboration With the American Association for Thoracic Surgery and Society of Thoracic Surgeons J. Am. Coll. Cardiol., May 27, 2008; 51(21): e1 - e62. [Full Text] [PDF]
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C. Valzania, F. Gadler, R. Winter, F. Braunschweig, L.-A. Brodin, P. Gudmundsson, G. Boriani, and M. J. Eriksson Effects of cardiac resynchronization therapy on coronary blood flow: Evaluation by transthoracic Doppler echocardiography Eur J Heart Fail, May 1, 2008; 10(5): 514 - 520. [Abstract] [Full Text] [PDF]
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M. Brignole, D. Oddone, R. Maggi, G. Lupi, R. Bollini, S. Corallo, S. Robotti, A. Solano, P. Donateo, and F. Croci Resynchronization of the left ventricular contraction by tailored programming of right and left ventricular pacing Europace, April 1, 2008; 10(4): 489 - 495. [Abstract] [Full Text] [PDF]
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K. Chakir, S. K. Daya, R. S. Tunin, R. H. Helm, M. J. Byrne, V. L. Dimaano, A. C. Lardo, T. P. Abraham, G. F. Tomaselli, and D. A. Kass Reversal of Global Apoptosis and Regional Stress Kinase Activation by Cardiac Resynchronization Circulation, March 18, 2008; 117(11): 1369 - 1377. [Abstract] [Full Text] [PDF]
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F. Braunschweig and P. J. Hauptman Cardiac resynchronization therapy in the intensive care setting; the promise and peril of using implantable devices off label Eur J Heart Fail, March 1, 2008; 10(3): 220 - 221. [Full Text] [PDF]
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D. A. Kass An epidemic of dyssynchrony: but what does it mean? J. Am. Coll. Cardiol., January 1, 2008; 51(1): 12 - 17. [Abstract] [Full Text] [PDF]
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M. Stockburger, S. Fateh-Moghadam, A. Nitardy, O. Celebi, A. Krebs, D. Habedank, and R. Dietz Baseline Doppler parameters are useful predictors of chronic left ventricular reduction in size by cardiac resynchronization therapy Europace, January 1, 2008; 10(1): 69 - 74. [Abstract] [Full Text] [PDF]
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J. van Dijk, P. Knaapen, I.K. Russel, T. Hendriks, C.P. Allaart, C.C. de Cock, and O. Kamp Mechanical dyssynchrony by 3D echo correlates with acute haemodynamic response to biventricular pacing in heart failure patients Europace, January 1, 2008; 10(1): 63 - 68. [Abstract] [Full Text] [PDF]
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M. W. Kimmel, N. D. Skadsberg, C. L. Byrd, D. J. Wright, T. G. Laske, and P. A. Iaizzo Single-site ventricular and biventricular pacing: investigation of latest depolarization strategy Europace, December 1, 2007; 9(12): 1163 - 1170. [Abstract] [Full Text] [PDF]
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M. Biffi, M. Bertini, M. Ziacchi, and G. Boriani Left ventricular pacing by automatic capture verification Europace, December 1, 2007; 9(12): 1177 - 1181. [Abstract] [Full Text] [PDF]
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P. Ritter, S. Cazeau, D. Gras, and J.-C. Daubert Cardiac resynchronization therapy implantation: a blend of skill and technology Eur. Heart J. Suppl., December 1, 2007; 9(suppl_I): I107 - I112. [Abstract] [Full Text] [PDF]
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G. B Bleeker, C.-M. Yu, P. Nihoyannopoulos, J. de Sutter, N. Van de Veire, E. R Holman, M. J Schalij, E. E van der Wall, and J. J Bax Optimal use of echocardiography in cardiac resynchronisation therapy Heart, November 1, 2007; 93(11): 1339 - 1350. [Abstract] [Full Text] [PDF]
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R E Lane, A W C Chow, J Mayet, D P Francis, N S Peters, R J Schilling, and D W Davies The interaction of interventricular pacing intervals and left ventricular lead position during temporary biventricular pacing evaluated by tissue Doppler imaging Heart, November 1, 2007; 93(11): 1426 - 1432. [Abstract] [Full Text] [PDF]
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F. Tabrizi, A. Englund, M. Rosenqvist, L. Wallentin, and U. Stenestrand Influence of left bundle branch block on long-term mortality in a population with heart failure Eur. Heart J., October 2, 2007; 28(20): 2449 - 2455. [Abstract] [Full Text] [PDF]
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D. A. Kass Highlighting the R in CRT Circulation, September 25, 2007; 116(13): 1434 - 1436. [Full Text] [PDF]
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T. Breidthardt, M. Christ, M. Matti, D. Schrafl, K. Laule, M. Noveanu, T. Boldanova, T. Klima, W. Hochholzer, A. P Perruchoud, et al. QRS and QTc interval prolongation in the prediction of long-term mortality of patients with acute destabilised heart failure Heart, September 1, 2007; 93(9): 1093 - 1097. [Abstract] [Full Text] [PDF]
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C. Schmidt, J. Frielingsdorf, M. Debrunner, R. Tavakoli, M. Genoni, E. Straumann, O. Bertel, and B. Naegeli Acute biventricular pacing after cardiac surgery has no influence on regional and global left ventricular systolic function Europace, June 1, 2007; 9(6): 432 - 436. [Abstract] [Full Text] [PDF]
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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]
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C. Valzania, F. Gadler, M. J. Eriksson, A. Olsson, G. Boriani, and F. Braunschweig Electromechanical effects of cardiac resynchronization therapy during rest and stress in patients with heart failure Eur J Heart Fail, June 1, 2007; 9(6-7): 644 - 650. [Abstract] [Full Text] [PDF]
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J. D. Burkhardt and B. L. Wilkoff Interventional Electrophysiology and Cardiac Resynchronization Therapy: Delivering Electrical Therapies for Heart Failure Circulation, April 24, 2007; 115(16): 2208 - 2220. [Abstract] [Full Text] [PDF]
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R. H. Helm, M. Byrne, P. A. Helm, S. K. Daya, N. F. Osman, R. Tunin, H. R. Halperin, R. D. Berger, D. A. Kass, and A. C. Lardo Three-Dimensional Mapping of Optimal Left Ventricular Pacing Site for Cardiac Resynchronization Circulation, February 27, 2007; 115(8): 953 - 961. [Abstract] [Full Text] [PDF]
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W. T. Abraham Response to Abraham Circulation, December 12, 2006; 114(24): 2692 - 2698. [Full Text] [PDF]
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M. Stockburger, S. Fateh-Moghadam, A. Nitardy, H. Langreck, W. Haverkamp, and R. Dietz Optimization of cardiac resynchronization guided by Doppler echocardiography: haemodynamic improvement and intraindividual variability with different pacing configurations and atrioventricular delays Europace, October 1, 2006; 8(10): 881 - 886. [Abstract] [Full Text] [PDF]
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L. Santangelo, E. Ammendola, V. Russo, C. Cavallaro, F. Vecchione, S. Garofalo, A. D'Onofrio, and R. Calabro Influence of biventricular pacing on myocardial dispersion of repolarization in dilated cardiomyopathy patients Europace, July 1, 2006; 8(7): 502 - 505. [Abstract] [Full Text] [PDF]
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Q. Zhang, J. W.-H. Fung, A. Auricchio, J. Y.-S. Chan, L. C.C. Kum, L. W. Wu, and C.-M. Yu Differential change in left ventricular mass and regional wall thickness after cardiac resynchronization therapy for heart failure Eur. Heart J., June 2, 2006; 27(12): 1423 - 1430. [Abstract] [Full Text] [PDF]
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N. M. Hawkins, M. C. Petrie, M. R. MacDonald, K. J. Hogg, and J. J.V. McMurray Selecting patients for cardiac resynchronization therapy: electrical or mechanical dyssynchrony? Eur. Heart J., June 1, 2006; 27(11): 1270 - 1281. [Abstract] [Full Text] [PDF]
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P. Steendijk, S. A. Tulner, J. J. Bax, P. V. Oemrawsingh, G. B. Bleeker, L. van Erven, H. Putter, H. F. Verwey, E. E. van der Wall, and M. J. Schalij Hemodynamic Effects of Long-Term Cardiac Resynchronization Therapy: Analysis by Pressure-Volume Loops Circulation, March 14, 2006; 113(10): 1295 - 1304. [Abstract] [Full Text] [PDF]
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M. S. Suffoletto, K. Dohi, M. Cannesson, S. Saba, and J. Gorcsan III Novel Speckle-Tracking Radial Strain From Routine Black-and-White Echocardiographic Images to Quantify Dyssynchrony and Predict Response to Cardiac Resynchronization Therapy Circulation, February 21, 2006; 113(7): 960 - 968. [Abstract] [Full Text] [PDF]
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D. Vollmann, L. Luthje, P. Schott, G. Hasenfuss, and C. Unterberg-Buchwald Biventricular Pacing Improves the Blunted Force-Frequency Relation Present During Univentricular Pacing in Patients With Heart Failure and Conduction Delay Circulation, February 21, 2006; 113(7): 953 - 959. [Abstract] [Full Text] [PDF]
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C. Leclercq, G. Ansalone, F. Gadler, G. Boriani, N. Perez-Castellano, N. Grubb, S. Sack, and E. Boulogne Biventricular vs. left univentricular pacing in heart failure: rationale, design, and endpoints of the B-LEFT HF study. Europace, January 1, 2006; 8(1): 76 - 80. [Abstract] [Full Text] [PDF]
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Z. I. Whinnett, J. E.R. Davies, K. Willson, A. W. Chow, R. A. Foale, D. W. Davies, A. D. Hughes, D. P. Francis, and J. Mayet Determination of optimal atrioventricular delay for cardiac resynchronization therapy using acute non-invasive blood pressure. Europace, January 1, 2006; 8(5): 358 - 366. [Abstract] [Full Text] [PDF]
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J. J. Bax, T. Abraham, S. S. Barold, O. A. Breithardt, J. W.H. Fung, S. Garrigue, J. Gorcsan III, D. L. Hayes, D. A. Kass, J. Knuuti, et al. Cardiac Resynchronization Therapy: Part 2--Issues During and After Device Implantation and Unresolved Questions J. Am. Coll. Cardiol., December 20, 2005; 46(12): 2168 - 2182. [Abstract] [Full Text] [PDF]
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