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(Circulation. 2000;101:2703.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Predictors of Systolic Augmentation From Left Ventricular Preexcitation in Patients With Dilated Cardiomyopathy and Intraventricular Conduction Delay
From the Division of Cardiology, Department of Medicine (G.S.N., C.W.C., M.T., M.R.D., R.D.B., D.A.K.), Department of Biomedical Engineering (B.T.W., J.D., E.R.M., D.A.K.), and Department of Radiology (E.R.M.), The Johns Hopkins Medical Institutions, Baltimore, Md; and Guidant Corp, St Paul, Minn (A.K.).
Correspondence to David A. Kass, MD, Halsted 500, The Johns Hopkins Hospital, 600 N Wolfe St, Baltimore, MD 21287. E-mail dkass{at}bme.jhu.edu
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Abstract |
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Background—VDD pacing can enhance systolic function in patients with dilated cardiomyopathy and discoordinate contraction; however, identification of patients likely to benefit is unclear. We tested predictors of systolic responsiveness on the basis of global parameters as well as directly assessed mechanical dyssynchrony.
Methods and Results—Twenty-two DCM patients with conduction delay
were studied by cardiac catheterization with a
dual-sensor micromanometer to measure LV and aortic
pressures during sinus rhythm and LV free-wall pacing. Pacing enhanced
isovolumetric (dP/dtmax) and ejection-phase (pulse
pressure, PP) systolic function by 35±21% and 16.4±11%,
respectively, and these changes correlated directly
(r=0.7, P=0.001).
%
dP/dtmax was weakly predicted by baseline QRS
(r=0.6, P<0.02), more strongly by
baseline dP/dtmax (r=0.7,
P=0.001), and best by bidiscriminate analysis
combining baseline dP/dtmax 
700 mm Hg/s and QRS
155 ms to predict %dP/dtmax 25% and %PP 10%
(P<0.0005, 
2), with no false-positives.
Benefit could not be predicted by %QRS. To test whether basal
mechanical dyssynchrony predicted responsiveness to LV pacing,
circumferential strains were determined at 
80 sites throughout the
LV by tagged MRI in 8 DCM patients and 7 additional control subjects.
Strain variance at time of maximal shortening indexed dyssynchrony,
averaging 28.0±7.1% in normal subjects versus 201.4±84.3% in DCM
patients (P=0.001). Mechanical dyssynchrony also
correlated directly with %dP/dtmax
(r=0.85, P=0.008).
Conclusions—These results show that although mechanical dyssynchrony is a key predictor for pacing efficacy in DCM patients with conduction delay, combining information about QRS and basal dP/dtmax provides an excellent tool to identify maximal responders.
Key Words: heart failure • bundle-branch block • pacing • magnetic resonance imaging • mechanics
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Left ventricular (LV) or biventricular preexcitation by dual-chamber (VDD) pacing with a shortened atrioventricular interval substantially improves systolic function in some patients with dilated cardiomyopathy (DCM) and conduction delay.1 2 3 4 5 By providing early stimulation to the otherwise late-activated region, pacing probably improves contractile coordination to enhance ejection. However, the therapy involves an implantable device, making it important to identify patients most likely to benefit.6 Because the therapy targets chamber-level mechanoelectrical abnormalities, it seems plausible that easily assessed features of a failing heart may help identify responders. If so, this would contrast with current pharmacological therapy, which is broadly applied to DCM patients, usually without specific knowledge of the individual substrate that might favor one therapy over another.
To date, the principal approach for identifying pacing candidates has been QRS prolongation on a surface ECG. Recent studies have reported a weak but significant positive correlation between basal QRS width and systolic response to pacing.4 5 This was obtained by combining patients with narrow and wide QRS complexes, however, leaving unresolved whether quantitative correlations persist among subjects with conduction delay. QRS duration also correlates inversely with basal contractile function, as indexed by the maximal rate of pressure rise (dP/dtmax),7 8 suggesting that the latter may provide another predictor of pacing response. Finally, QRS duration and dP/dtmax are indirect markers of the presumed primary abnormality, mechanical dyssynchrony, so direct measures of dyssynchrony might better predict benefit.
Accordingly, the goal of this study was to evaluate the utility of several easily obtained measures of global baseline chamber function for predicting systolic response to optimal-site VDD pacing. We also developed a novel metric to directly quantify mechanical dyssynchrony from tagged MRI (TMRI) analysis9 10 to directly test the relation between wall dyssynchrony and systolic improvement induced by LV pacing.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Study Group
Twenty-two patients with DCM (NYHA class III to IV) provided informed consent and underwent cardiac catheterization to determine systolic influences from optimal single-site ventricular pacing. Mechanical data from a subset of these patients (n=9) were reported previously.4 Subjects were studied in normal sinus rhythm, and none had standard pacing indications. All had a QRS duration
140 ms, PR interval 160 ms, and
ejection fraction <35%. Most were in NYHA functional class III (a few
were class IV), and none had >1+ mitral regurgitation
at time of study (assessed by contrast ventriculography). Chronic
medications were unchanged (digoxin, ACE inhibitor,
diuretics). Fifteen of the patients underwent TMRI
analysis to assess dyssynchrony. Eight studies were successful,
with failure in the other cases stemming from loss of image gating due
to ECG distortion after patients were placed within the magnetic field.
Comparison TMRI data were also obtained in a normal control group with
a narrow-complex QRS (n=7). Protocols were approved by the Johns
Hopkins Medical Institutions Joint Committee on Clinical
Investigation.
Table 1
provides baseline clinical
characteristics of the patient study group. The majority had
nonischemic DCM and left bundle-branch block (LBBB). Data from
all subjects except DCM21 and DCM22 were used to analyze
predictors of mechanical response to LV free-wall pacing. Patient DCM21
was excluded from this analysis because he had a right
bundle-branch block (RBBB), and DCM22 because of a large anterolateral
infarction with akinesis.
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Catheterization Protocol
Patients were mildly sedated (midazolam 1 to 3 mg, fentanyl 50
to 100 mg). Catheters included a dual-sensor
micromanometer (Millar 550-768) to measure
simultaneous proximal aortic and LV pressures, an atrial
sensing electrode, and a quadripolar pacing electrode (Cardima, model
01-043013) advanced through a flexible sheath (Arrow, CL07680/CL07665)
placed within the coronary sinus. In patients with LBBB,
optimal response was achieved by pacing in a midlateral or
anterolateral coronary vein. In the patient with RBBB, optimal
effects were achieved by pacing the mid–right ventricular
(RV) septum.4
MR Tagging Protocol
The methods of noninvasive myocardial motion and circumferential
strain analysis by TMRI have been described
previously.9 10 Images were acquired on a GE Signa 1.5-T
scanner, with tags placed on the myocardium by saturating
the proton spins in evenly spaced planes, taking images perpendicular
to the tag planes. Two orthogonal short-axis views and a single
long-axis view were obtained, with 11 slices in each short-axis view
and tags oriented in a cartesian grid. The first long-axis slice
bisected the septum and lateral wall, with each subsequent slice being
rotated around the long axis by 20°.
Data Analysis
Invasive LV and aortic pressures were measured at rest and after
2 minutes of sustained VDD-mode pacing. LV pressure was digitally
differentiated with a moving 5-point weighted slope, from which
dP/dtmax was determined. Previous studies have
found minimal change in LV loading with acute VDD pacing, so
dP/dtmax provided an accurate measure of
systolic response.
Pulse pressure (PP) was determined as a surrogate for changes in
cardiac output. PP is more stable, with an excellent signal-to-noise
ratio compared with flow assessments. Although PP does not always
directly reflect mean flow, it did so in the present study because
VDD pacing did not alter heart rate, ventricular preload,
or arterial load.4 We have previously reported
a strong direct correlation between PP and output in this setting, with
a 1%PP corresponding to 4% to 5% change in cardiac
output.4
TMRI tags and contours were delineated with custom-made semiautomated software.11 12 Tagged points from the images yielded 3D strain tensors during systole, from which local strain and global strain maps were derived. The displacements were field-fitted in prolate spheroidal coordinates to calculate 3D Lagrangian strain tensors by the method of O’Dell et al.10 Circumferential strain (Ecc) was calculated on a mesh grid of 3 radial, 8 longitudinal, and 24 circumferential sampling points. Because midwall fibers are predominantly circumferential, Ecc represented fiber shortening or lengthening. Strain maps for the whole heart were generated first and then synthesized into a dyssynchrony index. The time of maximal negative Ecc (shortening) was determined for the whole ventricle. Strains at all sites were then assessed at this time (yielding Ecc*), and the coefficient of variation of these strains (CVEcc*) indexed dyssynchrony: CVEcc*=100%x(SDEcc*/mean ECC*).
Statistical correlations between variables were tested by least-squares linear regression. Comparisons between normal sinus rhythm and pacing results were performed with a paired t test, and comparisons of TMRI data between DCM patients and normal volunteers were made by unpaired t test. Other tests are identified in the text where appropriate. Data are reported as mean±SD.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Hemodynamic Response to Pacing
Hemodynamic and contractile responses to LV free-wall pacing are provided in Table 2
.
dP/dtmax increased +35.5±20.8% (n=20,
P<0.0005), PP +16.4±11.2% (n=18, P<0.0005),
and systolic pressure +6.4±4.4% (n=19, P<0.0005).
Percent changes in isovolumic (dP/dtmax) and
ejection (PP) indexes of systolic function were significantly
correlated (%PP=0.36x%dP/dtmax+3.5,
n=18, r=0.71, P=0.001). This correlation is not
predicted purely from arterial pressure changes, because
dP/dtmax occurs before aortic valve opening.
Heart rate, LV end-diastolic pressure, and isovolumic
relaxation were not significantly altered by pacing.
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QRS as a Predictor of Pacing Response
Despite restriction of the present analysis to
patients with basal QRS prolongation, a modest correlation persisted
between %dP/dtmax and QRS duration (Figure 1A):
%dP/dtmax=0.61xQRS(BASE)-70.2
(r=0.55, P=0.012). Baseline QRS did not
significantly correlate with %PP (P=0.2). The extent of
QRS narrowing from pacing has been proposed to correlate with optimal
responses.13 However, we found only a weak trend
(P=0.16) between %QRS and
%dP/dtmax (Figure 1B) and no relation
between %QRS and %PP (Figure 1C, P=0.88).
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Baseline dP/dtmax as a Predictor of Pacing
Response
Baseline systolic function indexed by
dP/dtmax was more strongly and inversely
correlated with subsequent changes during LV pacing (Figure 2A):
%dP/dtmax=-0.08xdP/dtmax(BASE)+91.3
(r=0.69, P=0.001). Because these variables
have inherent correlations, we also examined absolute changes in
dP/dtmax (Figure 2B) and found it
also to be inversely correlated with baseline
dP/dtmax=-1.4xdP/dtmax(BASE)+484.7
(r=0.59, P=0.007). Baseline
dP/dtmax also correlated with %PP
(r=0.51, P=0.03). EF was a much weaker predictor
of both changes (P=0.07 and P=0.016,
respectively), although the trend was similar.
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Predictive Value of Combining Baseline QRS and Baseline
dP/dtmax
Combining basal QRS and dP/dtmax enhanced
the predictive accuracy for identifying responsive patients. Patients
with a basal QRS duration of 155 ms and baseline
dP/dtmax 700 mm Hg/s consistently
yielded the greatest improvements with pacing
(%dP/dtmax 25%). Both baseline
dP/dtmax 700 mm Hg/s and basal QRS 155
ms were significantly associated with a
%dP/dtmax 25% (n=20, P<0.0005
and P=0.004, respectively, by 2),
with similar association with %PP 10% (n=18, P=0.001
and P=0.04, respectively). Combining both criteria (Figure 3) yielded no false-positives or
false-negatives for predicting a 25% rise in
dP/dtmax (P<0.0005 by
2) and 2 false-negatives for predicting a
10% rise in PP (P=0.001 by 2).
PP was not recorded in 2 patients with
%dP/dtmax 25%; however, on the basis of
the regression relating %PP and %dP/dtmax
(see above), the predicted %PP was 16% in each case.
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Mechanical Dyssynchrony as a Predictor of Pacing Response
Figure 4 displays TMRI strain maps
for a control subject (A) and a DCM patient (B) from base to apex (top
to bottom) and septum to lateral wall (left to right). The time of
maximal negative Ecc is denoted by an asterisk on each plot.
Contraction was synchronous in the normal heart, with nearly all
strains negative (shortening), with similar amplitude and phase. In
contrast, the DCM heart with LBBB displayed
heterogeneity of strain magnitude and temporal pattern.
There was marked phase delay between early septal and late lateral
shortening, with reciprocal stretch of the anteroseptal territory
(positive strain) during the latter. Near-akinetic transition regions
(posterior wall) were observed in this patient with normal
coronary arteries and idiopathic disease.
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Table 3 summarizes these results. Ecc*
was -18.6±2.9% in normal subjects, versus -5.3±2.1% in DCM hearts
(P=0.001), consistent with DCM cardiodepression.
Strain variance was low in normal subjects:
CVEcc*=28.0±7.1%, versus 201.4±84.3% in the
DCM with LBBB (P=0.001). Thus, dyssynchrony in DCM subjects
was nearly an order of magnitude greater than in control subjects. As
displayed in Figure 5, mechanical
dyssynchrony was well correlated with
%dP/dtmax:
%dP/dtmax=0.18xCVEcc*-8.8
(n=8, r=0.85, P=0.008).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In normal14 15 or hypertrophied16 hearts, ventricular preexcitation induces discoordination, and the extent of dyssynchrony correlates with depression of ejection- and isovolumic-phase systolic indexes. This dysfunction can be offset by concomitant stimulation of the opposing wall to restore synchrony, and improvement depends on the extent of dyssynchrony generated by the first lead.17 18 Such observations have suggested that patients with DCM and basal discoordination might benefit from LV or biventricular VDD pacing, and this was recently confirmed.2 3 4 5 However, the response magnitude varies, highlighting the importance of identifying responsive individuals.6
The present study is the first to systematically test potential
markers of clinical response to pacing. We demonstrated that mechanical
dyssynchrony is a good predictor of systolic improvement, but
recognizing that MRI analysis is not widely available and is
also labor-intensive, global surrogate markers were sought. Here we
found that a bidiscriminate approach that uses both basal QRS duration
(155 ms) and dP/dtmax (700 mm Hg/s)
provides a fairly robust prediction of patients likely to display at
least a 25% rise in dP/dtmax and 10% rise in
arterial PP. The latter correlates directly with cardiac
output in this setting and would be associated with a 40% to 50% rise
in output.4 Although we measured baseline
dP/dtmax invasively, this parameter
can be assessed with Doppler cardiography, as validated by several
previous studies.19 20
Baseline dP/dtmax values in the present study
group were remarkably low despite the absence of bradycardia or
systolic hypotension. Many previous studies of DCM in which
patients with conduction delay were not targeted8 21 22 23
have reported consistent values for
dP/dtmax of 900 mm/s, 30% higher than in
the present study but similar to values during pacing. Yet, the
functional status, ejection fraction, etc, of the present patient
group was indistinguishable from those in these previous studies. It is
unlikely that the presence of only minor mitral
regurgitation in the present study explained this
difference, because MR would be expected to exacerbate dilation and
basal depression. Thus, the major difference appears to lie in the
discoordination, suggesting that dP/dtmax is
particularly sensitive to this behavior.
The TMRI method uniquely provides detailed quantitative 3D analysis of regional myocardial dyssynchrony with adequate sensitivity even in DCM hearts. However, the analysis is complex and unlikely to be implemented in the general clinical arena. Alternative imaging methods, such as contrast echocardiography,24 3D echo imaging,25 or cine modes on standard MRI systems, may prove useful in this regard. On the basis of the present data, such evaluations may further improve targeting of pacing therapy. However, our results already demonstrate that the basal QRS and dP/dtmax criteria provide sufficient discrimination to define robust responders with virtually no false-positives.
The correlation between short-term responsiveness to pacing and long-term clinical outcome remains unknown. Although it may turn out that having an excellent immediate hemodynamic response is ultimately counterproductive or that no response does not preclude long-term benefit, both seem unlikely. PP and dP/dtmax provide direct evidence of the magnitude by which resynchronization assists systolic function in a given patient; therefore, as with a pharmacological agent, one would expect at least a binary discrimination between having some response and long-term benefit. Alonso et al26 recently reported that QRS narrowing with pacing was more often observed in patients displaying long-term benefit, yet the present data found no immediate relation between such narrowing and mechanical response. This intriguing disparity remains to be resolved by more data and prospective analyses.
Study Design Limitations
We did not perform invasive catheterization in
normal volunteers to test whether LV or biventricular
pacing improves or worsens systolic function in individuals
with narrow-complex QRS. Studying normal patients invasively poses
potential risks and no possible benefit and thus was not feasible.
However, analogous data have been reported in animal studies, and these
consistently demonstrate that single-site (LV or RV) pacing of
a heart with normal conduction (narrow QRS) produces a significant
decline in dP/dtmax and other markers of
systolic function.14 15 17 18 27
We also limited our analysis to DCM patients with widened QRS
complexes, and it remains possible that some individuals with more
narrow complexes might also benefit. Previous studies have reported
regional wall motion abnormalities, heterogeneous wall
stress, and myocardial perfusion in DCM patients with normal-appearing
epicardial vessels,28 29 although none reported QRS
durations to test correlations with these phenomena. Certainly, surface
ECG–based estimates may underestimate the temporal spread of
depolarization if early and late portions have relatively low voltages.
However, there is evidence that the pacing-responsive population with a
narrow QRS duration is small. Auricchio et al5 reported
correlations between QRS and mechanical response to pacing and found
little effect in individuals with a duration <155 ms. These data have
been further extended to 74 patients (A. Auricchio and C. Stellbrink,
personal communication), and only 3% of patients with a QRS
<155 ms had a positive pacing response as defined in our study (ie,
both %dP/dtmax 25% and %PP 10%).
Even after the threshold for a positive response had been lowered to a
5% rise in each variable, the false-negative rate was only 12%.
This indicates that although some patients have substantial enough
mechanical dyssynchrony to benefit from pacing therapy yet have a
narrow QRS complex, this population is small.
Patients with normal hearts and conduction delay were not studied either; although such data would be interesting, it fell outside the focus of our study. Basal function in this group would most likely be similar to a normal heart into which an RV pacemaker was inserted to produce an LBBB pattern. Adding an LV free-wall pacemaker (ie, biventricular pacing) improves function, as reported experimentally.17 We speculate that the major difference in this regard between DCM and normal hearts is that any improvement with recoordination becomes more significant in the former as other functional mechanisms fail.
Conclusions
The concept of targeting heart failure therapy individually by
prospectively identifying factors to predict clinical responsiveness is
an attractive one. This is currently elusive for pharmacological
therapy, although differences in patient response to treatment are
common. Our growing understanding of molecular and biochemical
signaling changes in heart failure may ultimately provide the needed
insight. Device therapies by their nature generally demand targeting to
specific patient groups. The present data demonstrate the ability
to identify an optimal candidate group who display substantial acute
functional responses to pacing, and such pretreatment predictions are
relatively unique among heart failure therapies. These issues should
become increasingly important as 3 major multicenter trials commence
this year to study the effects of chronic pacing on exercise capacity,
hospitalization, and mortality.
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Acknowledgments |
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This study was supported by grants from CPI/Guidant, including a fellowship award (C.W. Curry); National Institutes of Health grant HL-45683 (Dr McVeigh); and SBIR grant HL-62028 (Dr Nelson). Dr McVeigh is an Established Investigator of the AHA. Dr Kass is a consultant for CPI/Guidant.
Received October 26, 1999; revision received January 14, 2000; accepted January 28, 2000.
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D. J. Bradley, E. A. Bradley, K. L. Baughman, R. D. Berger, H. Calkins, S. N. Goodman, D. A. Kass, and N. R. Powe Cardiac Resynchronization and Death From Progressive Heart Failure: A Meta-analysis of Randomized Controlled Trials JAMA, February 12, 2003; 289(6): 730 - 740. [Abstract] [Full Text] [PDF]
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C-M Yu, H Lin, Q Zhang, and J E Sanderson High prevalence of left ventricular systolic and diastolic asynchrony in patients with congestive heart failure and normal QRS duration Heart, January 1, 2003; 89(1): 54 - 60. [Abstract] [Full Text] [PDF]
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S. Cazeau, C. Alonso, G. Jauvert, A. Lazarus, and P. Ritter Cardiac resynchronization therapy Europace, January 1, 2003; 5(s1): S42 - S48. [Abstract] [Full Text] [PDF]
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C. Stellbrink and B. Nowak The importance of being synchronous: on the prognostic value of ventricular conduction delay in heart failure J. Am. Coll. Cardiol., December 4, 2002; 40(11): 2031 - 2033. [Full Text] [PDF]
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M. V. Pitzalis, M. Iacoviello, R. Romito, F. Massari, B. Rizzon, G. Luzzi, P. Guida, A. Andriani, F. Mastropasqua, and P. Rizzon Cardiac resynchronization therapy tailored by echocardiographic evaluation of ventricular asynchrony J. Am. Coll. Cardiol., November 6, 2002; 40(9): 1615 - 1622. [Abstract] [Full Text] [PDF]
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C. Leclercq, S. Walker, C. Linde, J. Clementy, A.J. Marshall, P. Ritter, P. Djiane, P. Mabo, T. Levy, F. Gadler, et al. Comparative effects of permanent biventricular and right-univentricular pacing in heart failure patients with chronic atrial fibrillation Eur. Heart J., November 2, 2002; 23(22): 1780 - 1787. [Abstract] [Full Text] [PDF]
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O. A. Breithardt, C. Stellbrink, A. P. Kramer, A. M. Sinha, A. Franke, R. Salo, B. Schiffgens, E. Huvelle, A. Auricchio, and PATH-CHF Study Group Echocardiographic quantification of left ventricular asynchrony predicts an acute hemodynamic benefit of cardiac resynchronization therapy J. Am. Coll. Cardiol., August 7, 2002; 40(3): 536 - 545. [Abstract] [Full Text] [PDF]
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M. Kawaguchi, T. Murabayashi, B. J. Fetics, G. S. Nelson, H. Samejima, E. Nevo, and D. A. Kass Quantitation of basal dyssynchrony and acute resynchronization from left or biventricular pacing by novel echo-contrast variability imaging J. Am. Coll. Cardiol., June 19, 2002; 39(12): 2052 - 2058. [Abstract] [Full Text] [PDF]
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M. Santini and R. Ricci Biventricular pacing in patients with heart failure and intraventricular conduction delay: state of the art and perspectives. The European view Eur. Heart J., May 1, 2002; 23(9): 682 - 686. [Full Text] [PDF]
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A. Auricchio, J. Ding, J. C. Spinelli, A. P. Kramer, R. W. Salo, W. Hoersch, B. H. KenKnight, H. U. Klein, and for the PATH-CHF Study Group Cardiac resynchronization therapy restores optimal atrioventricular mechanical timing in heart failure patients with ventricular conduction delay J. Am. Coll. Cardiol., April 3, 2002; 39(7): 1163 - 1169. [Abstract] [Full Text] [PDF]
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D.A Kass Ventricular dyssynchrony and mechanisms of resynchronization therapy Eur. Heart J. Suppl., April 1, 2002; 4(suppl_D): D23 - D30. [Abstract] [PDF]
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A Auricchio and H.U Klein Beyond expectations: a decade of positive results with cardiac resynchronization therapy for heart failure Eur. Heart J. Suppl., April 1, 2002; 4(suppl_D): D95 - D101. [Abstract] [PDF]
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R.G Charles Cardiac resynchronization therapy: when and for whom? Eur. Heart J. Suppl., April 1, 2002; 4(suppl_D): D117 - D121. [Abstract] [PDF]
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