Acute effects of His bundle pacing versus left ventricular and right ventricular pacing on left ventricular function.
ABSTRACT Dual-chamber pacing with His bundle pacing has theoretical advantages over conventional right ventricular (RV) apical pacing. We compared indexes of left ventricular (LV) function during acute dual-chamber pacing from the His bundle and other RV and LV pacing sites. Twelve patients (6 men; 63 +/- 11 years) with a standard indication for electrophysiologic study were included. Average QRS duration was 100 +/- 19 ms. Ejection fraction was 48 +/- 15%. A pressure-volume catheter was positioned in the left ventricle through the femoral arterial access. Pressure-volume loops were collected during atrial (AAI) and dual-chamber overdrive pacing at 82 +/- 15 beats/min after 2 minutes of hemodynamic stabilization. Ventricular pacing catheter position was randomized between the RV apex, RV septal, and free wall portions of the outflow tract, LV free wall, and His bundle. His bundle capture was verified from surface electrocardiographic morphometry using standard criteria. Atrioventricular delay was set to the P wave-His duration -10 ms to minimize the effects of fusion (96 +/- 22 ms). LV only pacing, but not His pacing, resulted in improved stroke work and stroke volume compared with alternate site RV pacing. No changes in +dP/dt, LV end-systolic pressure. LV end-diastolic pressure, or cycle efficiency, were observed between RV pacing sites. In conclusion, acute His bundle pacing did not improve LV function compared with alternate site RV pacing and may be inferior to LV pacing.
- SourceAvailable from: circ.ahajournals.org[show abstract] [hide abstract]
ABSTRACT: Biventricular (BiV) and left ventricular (LV) pacing similarly augment systolic function in left bundle-branch block (LBBB)-failing hearts despite different electrical activation. We tested whether electrical synchrony is required to achieve mechanical synchronization and functional benefit from pacing. Epicardial mapping, tagged MRI, and hemodynamics were obtained in dogs with LBBB-failing hearts during right atrial, LV, and BiV stimulation. BiV and LV both significantly improved chamber hemodynamics (eg, 25% increase in dP/dt(max) and aortic pulse pressure) compared with atrial pacing-LBBB, and this improvement correlated with mechanical resynchronization. Electrical dispersion, however, decreased 13% with BiV but increased 23% with LV pacing (P<0.01). Improved mechanical synchrony and function do not require electrical synchrony. Mechanical coordination plays the dominant role in global systolic improvement with either pacing approach.Circulation 11/2002; 106(14):1760-3. · 15.20 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: BACKGROUND: Direct His-bundle pacing (DHBP) produces synchronous ventricular depolarization and improved cardiac function relative to apical pacing. Although it has been performed transiently in the electrophysiology laboratory and persistently in open-chested canines, permanent DHBP in humans has not been achieved. METHODS AND RESULTS: A total of 18 patients aged 69+/-10 years who had a history of chronic atrial fibrillation, dilated cardiomyopathy, and normal activation (ie, QRS< or =120 ms) were screened for permanent DHBP using an electrophysiology catheter. In 14 patients, the His bundle could be reliably stimulated. Of these 14, permanent DHBP using a fixed screw-in lead was successful in 12 patients. Radiofrequency atrioventricular node ablation was performed in patients exhibiting a fast ventricular response. All patients received single-chamber rate-responsive pacemakers. Acute pacing thresholds were 2.4+/-1.0 V at a pulse duration of 0.5 ms. Lead complications included exit block requiring reoperative adjustment and gross lead dislodgment. Echocardiographic improvement in heart function was shown by reductions in the left ventricular end-diastolic dimension from 59+/-8 to 52+/-6 mm (P</=0.01) and in the end-systolic dimension from 51+/-10 to 43+/-8 mm (P<0.01), with an accompanying increase in fractional shortening from 14+/-7% to 20+/-10% (P=0.05). The left ventricular ejection fraction improved from 20+/-9% to 31+/-11% (P<0. 01), and the cardiothoracic ratio decreased from 0.61+/-0.06 to 0. 57+/-0.07 (P<0.01). Despite DHBP, 2 patients died at 8 and 36 months. Conclusions-Permanent DHBP is feasible in select patients who have chronic atrial fibrillation and dilated cardiomyopathy. Long-term, DHBP results in a reduction of left ventricular dimensions and improved cardiac function.Circulation 02/2000; 101(8):869-77. · 15.20 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: His-bundle electrograms recorded from intracardiac electrode catheters have been a mainstay of basic and clinical electrophysiology. However, consistent His-bundle pacing has not been as readily achieved. In 13 dogs anesthetized with sodium pentobarbital (30 mg/kg), we recorded leads II and aVR as well as the His-bundle electrogram from the aortic root. A deflectable tip multipolar catheter (4 rings, 5 mm apart) was introduced via the right jugular vein into the right ventricle (RV). In 7 dogs, using fluoroscopy, the tip was placed under the tricuspid septal leaflet. In the other 6, after thoracotomy, the same placement was made by palpation through the right atrial wall. Stable His-bundle and right bundle (Rb) branch recordings were made from distal and proximal electrode pairs, respectively. H-V intervals measured 35 +/- 6 ms from the aortic root and 33 +/- 5 ms from under the tricuspid leaflet (P = NS). Rb-V measured 25 +/- 4 ms. Consistent His-bundle pacing was accomplished from the aortic root with an average stimulus intensity of 6 +/- 10 mA and from the tricuspid leaflet at 16 +/- 8 mA (P < 0.05). In 7 anesthetized dogs we compared the hemodynamic effects of A-V sequential pacing at the same heart rates using the His-bundle recording site under the septal leaflet of the tricuspid valve (A-H pacing) or pacing from the RV apex (A-RV pacing). Under normal conditions there was a significant depression of mean blood pressure when A-RV pacing was compared with atrial pacing (AOO); but no difference was found between AOO and A-H pacing.(ABSTRACT TRUNCATED AT 250 WORDS)Pacing and Clinical Electrophysiology 10/1995; 18(10):1894-901. · 1.75 Impact Factor
Acute Effects of His Bundle Pacing Versus Left Ventricular
and Right Ventricular Pacing on Left Ventricular Function
Luigi Padeletti, MDa, Randy Lieberman, MDb, Jan Schreuder, MDc, Antonio Michelucci, MDa,
Andrea Collella, MDa, Paolo Pieragnoli, MDa, Giuseppe Ricciardi, MDa, William Eastman, MSd,
Sergio Valsecchi, PhDd, and Douglas A. Hettrick, PhDd,*
Dual-chamber pacing with His bundle pacing has theoretical advantages over conventional
right ventricular (RV) apical pacing. We compared indexes of left ventricular (LV) function
during acute dual-chamber pacing from the His bundle and other RV and LV pacing sites.
Twelve patients (6 men; 63 ? 11 years) with a standard indication for electrophysiologic
study were included. Average QRS duration was 100 ? 19 ms. Ejection fraction was 48 ?
15%. A pressure–volume catheter was positioned in the left ventricle through the femoral
arterial access. Pressure–volume loops were collected during atrial (AAI) and dual-cham-
ber overdrive pacing at 82 ? 15 beats/min after 2 minutes of hemodynamic stabilization.
Ventricular pacing catheter position was randomized between the RV apex, RV septal, and
free wall portions of the outflow tract, LV free wall, and His bundle. His bundle capture was
verified from surface electrocardiographic morphometry using standard criteria. Atrioven-
tricular delay was set to the P wave–His duration ?10 ms to minimize the effects of fusion
(96 ? 22 ms). LV only pacing, but not His pacing, resulted in improved stroke work and
stroke volume compared with alternate site RV pacing. No changes in ?dP/dt, LV
end-systolic pressure. LV end-diastolic pressure, or cycle efficiency, were observed between
RV pacing sites. In conclusion, acute His bundle pacing did not improve LV function
compared with alternate site RV pacing and may be inferior to LV pacing.
Elsevier Inc. All rights reserved. (Am J Cardiol 2007;100:1556–1560)
Right ventricular (RV) apical pacing has been shown to
acutely reduce left ventricular (LV) function.1–3These re-
ductions may be associated with less than optimal outcomes
as reported in patients with RV apical pacing in several
notable clinical trials.4–8In contrast to RV apical pacing,
His bundle pacing takes advantage of the intrinsic conduc-
tion system and may offer an attractive alternative because
contractile dyssynchrony may be avoided.9–12Recent inves-
tigations have reported improved acute LV function and
long-term benefits with His pacing using commercially
available pacing systems.13,14RV septal, LV, and biven-
tricular pacing have also been proposed as alternatives to
RV apical pacing. In this investigation, we compared in-
dexes of LV function during acute dual-chamber pacing
from the His bundle and other RV and LV pacing sites to
quantify the relative changes in LV function associated with
alternatives to RV apical pacing using pressure–volume
The experimental design was approved by the Institutional
Review Boards at the Careggi Hospital and Detroit Medical
Center, and all subjects provided written informed consent.
Patients with indications for electrophysiologic examination
were studied as part of a broader trial of alternate site
ventricular pacing.3Subjects were excluded from analysis if
they had a previously implanted device, valvular insuffi-
ciency or stenosis, or measured QRS duration ?125 ms. A
7Fr, 12-electrode combination high fidelity micromanome-
ter-conductance catheter (CD Leycom, Zoetermeer, The
Netherlands) was positioned in the LV apex through the
femoral arterial access.15Pressure–volume loops were col-
lected after 2 minutes of right atrial appendage (AAI pacing
mode) and dual-chamber overdrive pacing. A Swan-Ganz
catheter was placed in the proximal pulmonary artery from
the femoral vein for the determination of pulmonary artery
pressure and stroke volume. Parallel conductance volume
for conductance volume calibration was assessed by injec-
tion of 10 ml of hypertonic saline (6%) into the pulmonary
artery as previously described.15Absolute LV volumes were
calculated by matching effective conductance stroke vol-
ume with simultaneously measured thermodilution stroke
volume and by subtracting parallel conductance from total
volume. Temporary or permanent pacing electrodes were
positioned in the RV apex, RV outflow tract free wall, RV
outflow tract septum, LV free wall, and His bundle. The LV
lead was positioned transvenously in the epicardial lateral or
posterolateral LV wall through the coronary sinus using
standard resynchronization therapy techniques. Lead loca-
tion was confirmed from fluoroscopic inspection and elec-
trocardiographic morphometry using previously published
criteria.12,13,16His bundle capture was verified by paced
QRS duration and morphometry identical to intrinsic QRS
aUniversity of Florence, Florence, Italy;
Michigan;cSan Raffaele Hospital Milan, Italy; anddMedtronic, Inc. Min-
neapolis, Minnesota. Manuscript received April 23, 2007; revised manu-
script received and accepted June 19, 2007.
*Corresponding author: Tel: 763-526-0293; fax: 763-514-2701.
E-mail address: firstname.lastname@example.org (D. Hettrick).
bHarper Hospital, Detroit,
0002-9149/07/$ – see front matter © 2007 Elsevier Inc. All rights reserved.
Figure 1. Raw hemodynamic data including electrocardiogram (ECG), LV
volume, LV pressure, LV dP/dt, and LV pressure volume loops for 1
patient during control (AAI) pacing (left) and during His pacing (right).
The electrocardiographic waveforms were recorded directly from the con-
ductance catheter. No changes in the QRS morphology were observed.
However, changes in dP/dt, LV pressure morphometry, global LV volume
signal, and the combined LV pressure–volume signal are apparent. Note
that preload (LV end-diastolic volume) is lower during His pacing. This
may be due in part to relatively shorter AV delays that limit total LV filling.
Figure 2. Example pressure volume data from 1 patient during alternate site
pacing. In this patient, His pacing compared well with other RV pacing
sites but not as well with LV pacing. Note the decreased end-systolic
volume combined with increased end-diastolic volume during LV pacing.
Figure 3. QRS duration for various pacing modalities. QRS duration was
longer during RV and LV pacing compared with His and atrial pacing.
QRS duration was similar between His and atrial pacing.ap ?0.05 versus
AAI;bp ?0.05 versus His.
Patient demographics and history
PatientAge (yrs)/Sex QRS (ms)EF (%) Cardio-
Totals 63 ? 11 6 (men) 100 ? 1948 ? 15
Arrhythmias and Conduction Disturbances/LV Function During His Pacing
duration and morphometry (Figure 1).17No leads were
permanently placed in the His. Atrioventricular (AV) delay
was set to the P wave–His duration ?10 ms to minimize the
possible effects of fusion.
QRS duration was calculated using standard electrocar-
diographic leads. LV pressure, volume, and function were
averaged during 8 to 10 beats at end expiration from the raw
LV pressure and conductance volume data using commer-
cially available software (Conduct NT, Leycom). LV stroke
work was calculated as the area of the steady-state pressure–
volume diagram. The time constant (?) of isovolumic relax-
ation was determined assuming a non-zero asymptote.
Global cycle efficiency was calculated as previously de-
scribed3,18using the formula: cycle efficiency ? stroke
work/[(?LV pressure) ? (?LV volume)]. This index quan-
tifies distortions in the pressure–volume diagram, presum-
ably due to asynchronous LV contraction. The calculation
assumes that ideal synchronous contraction produces a cy-
cle efficiency value of 1.0.
All hemodynamic data obtained during dual-chamber
pacing with a different ventricular pacing site were com-
pared using 1-way analysis of variance for repeated mea-
sures. A Student’s Neuman-Keuls test was used for post hoc
Figure 4. Changes in parameters of LV systolic function during various
pacing modalities. His and RV free wall pacing resulted in decreased stroke
work (A) and stroke volume (B) compared with AAI. Strike volume was
lower for His and all RV sites compared with LV pacing. RV apical and
RV septal pacing resulted in decreased LV dP/dt (C) compared with AAI
pacing.ap ?0.05 versus AAI;bp ?0.05 versus LV free wall.
Figure 5. Changes in LV hemodynamics and efficiency during various
pacing modalities. No changes in LV end-systolic pressure (A) were ob-
served between groups. LV free wall pacing resulted in a significant
increase in LV end-diastolic pressure (B). Cycle efficiency (C) was also
similar between pacing sites.ap ?0.05 versus AAI.
The American Journal of Cardiology (www.AJConline.org)
comparisons. A p value ?0.05 was considered significant.
Data are presented a mean ? SD.
Demographic data are listed in Table 1. The average pacing
rate was 82 ? 15 beats/min. Average QRS duration was
100 ? 19 ms. The programmed paced AV delay was
96 ? 22 ms. Figures 1 and 2 show raw data from individual
patients. QRS duration (Figure 3) was similar between AAI
(85 ? 12 ms) and His (92 ? 11 ms) pacing, but significantly
(p ?0.05) longer during RV and LV pacing. LV only
pacing, but not His pacing, resulted in improved stroke
work and stroke volume compared with alternate site RV
pacing (Figure 4). LV pacing resulted in a significant in-
crease in LV end-diastolic pressure. No changes in ?dP/dt,
LV end-systolic pressure, LV end-diastolic pressure, or
global cycle efficiency were observed between RV pacing
sites (Figure 5). Additional hemodynamic parameters are
listed in Table 2. His pacing resulted in lower cardiac
output, compared with AAI and LV, and lower magnitude
?dP/dtmincompared with AAI.
The results of this study suggest that, despite retaining
intrinsic QRS duration, direct His pacing with a short AV
delay resulted in decreased LV function compared with AAI
and LV pacing and LV function similar to RV pacing. LV
pacing was equivalent to AAI. His pacing and all RV pacing
sites resulted in decreased stroke work and stroke volume
compared with AAI and LV pacing.
Several studies have confirmed the feasibility of long-
term His bundle pacing with conventional pacing systems in
both animals9,10,19and humans.11,13Deshmukh and col-
leagues12observed a reduction in LV dimensions and im-
proved cardiac function with His bundle pacing in patients
with chronic atrial fibrillation and dilated cardiomyopathy.
Occhetta et al14also observed that permanent para-Hisian
pacing is feasible and allows an improvement in functional
status and mitral regurgitation during long-term follow-up
compared with conventional RV apical pacing. However,
these studies primarily compared His with RV pacing but
not to LV pacing or to intrinsic conduction. We recently
reported that RV pacing worsens LV function in patients
with and without LV dysfunction unless the RV pacing site
is optimized. Furthermore, LV and biventricular pacing
preserved LV function in patients with normal ejection
fraction and improved LV function in patients with ejection
fraction ?40%.3The present results further indicate that His
pacing may not necessarily produce acute beneficial hemo-
dynamic effects. Optimization of His pacing may depend on
loading conditions and appropriate AV delay. Although LV
end-diastolic volume was not significantly different be-
tween LV and His pacing in this small population (Table 2),
LV end-diastolic pressure was higher (Figure 5). Further-
more, individual patient data (Figures 1 and 2) also suggest
slightly improved preload during LV pacing. Whether acute
improvements in LV function lead to long-term improve-
ments remains uncertain, but recent investigations into
biventricular pacing suggest that they may.20
The present results also provide additional evidence dis-
puting the contention that a QRS duration ?120 ms is a
surrogate for LV dyssynchrony.21QRS duration is currently
a prerequisite for cardiac resynchronization therapy, and
narrowing the QRS is often considered a surrogate marker
for optimal RV pacing site.7However, our results indicate
that reduced LV function during His pacing was associated
with a narrow QRS duration. In addition, a wide QRS
duration occurred with reduced LV function during RV
pacing, and a wide QRS was observed with improved LV
function during LV pacing. Therefore, QRS duration may
be of little value in predicting both ventricular synchrony
and LV function.
The present results should be interpreted within the con-
straints of the trial limitations. We studied a population of
patients with and without a history of congestive heart
failure and with variable ejection fraction (Table 1). There-
fore, our data were underpowered to perform comparisons
of patients with or without preexisting LV dysfunction. We
did not evaluate the effect of increased or decreased heart
rate on His pacing. However, we maintained a constant
heart rate for all pacing sites, including control atrial pacing.
We did not optimize AV delay at any pacing site, but paced
with AV delay ?10 ms than the atrial pace to His interval.
However, this definition may still allow relative amounts of
intrinsic AV conduction to occur between sites, especially
between the left ventricle and His bundle. Although, QRS
duration during His pacing was similar in both morphometry
(Figure 1) and duration (Figures 1 and 3) to atrial pacing, it is
possible that some RV capture occurred in some patients.
Acknowledgment: We thank Paola Cardano, Sara Over-
gaard, Katie Reichardt, and Amy Skaleski for their excellent
assistance in data collection and analysis.
1. Kass DA, Chen CH, Curry C, Talbot M, Berger R, Fetics B, Nevo E.
Improved left ventricular mechanics from acute VDD pacing in pa-
Hemodynamic effects of ventricular pacing
AAI HIS RV Apical RV Free Wall RV SeptalLV
Cardiac output (L/min)
Relaxation time constant (ms)
Peak negative LV dP/dt (mm Hg/s)
LV end-diastolic volume (ml)
4.9 ? 2.2
40 ? 12
?1,265 ? 507
163 ? 63
3.6 ? 1.5*,†
46 ? 18
?1,123 ? 453*
151 ? 57
4.5 ? 2.3‡
45 ? 13
?1,149 ? 440*
158 ? 62
3.9 ? 1.8*,†
44 ? 12
?1,117 ? 395*
160 ? 65
4.1 ? 2.2†
46 ? 18
?1,141 ? 419*
162 ? 61
5.0 ? 2.2
42 ? 11
?1,116 ? 414*
160 ? 66
Data are presented as mean ? SD; n ? 12.
* p ?0.05 versus AAI;†p ?0.05 versus LV;‡p?0.05 versus His.
Arrhythmias and Conduction Disturbances/LV Function During His Pacing
tients with dilated cardiomyopathy and ventricular conduction delay.
2. Auricchio A, Stellbrink C, Block M, Sack S, Vogt J, Bakker P, Klein
H, Kramer A, Ding J, Salo R, et al. Effect of pacing chamber and
atrioventricular delay on acute systolic function of paced patients with
congestive heart failure. The Pacing Therapies for Congestive Heart
Failure Study Group. The Guidant Congestive Heart Failure Research
Group. Circulation 1999;99:2993–3001.
3. Lieberman R, Padeletti L, Schreuder J, Jackson K, Michelucci A,
Colella A, Eastman W, Valsecchi S, Hettrick DA. Ventricular pacing
lead location alters systemic hemodynamics and left ventricular func-
tion in patients with and without reduced ejection fraction. J Am Coll
4. Andersen HR, Nielsen JC, Thomsen PE, Thuesen L, Mortensen PT,
Vesterlund T, Pedersen AK. Long-term follow-up of patients from a
randomized trial of atrial versus ventricular pacing for sick-sinus
syndrome. Lancet 1997;350:1210–1216.
5. Connolly SJ, Kerr CR, Gent M, Roberts RS, Yusuf S, Gillis AM, Sami
MH, Talajic M, Tang AS, Klein GJ, Lau C, Newman DM. Effects of
physiologic pacing versus ventricular pacing on the risk of stroke and
death due to cardiovascular causes. Canadian Trial of Physiologic
Pacing Investigators. N Engl J Med 2000;342:1385–1391.
6. Lamas GA, Lee KL, Sweeney MO, Silverman R, Leon A, Yee R,
Marinchak RA, Flaker G, Schron E, Orav EJ, Hellkamp A, et al, Mode
Selection Trial in Sinus-Node Dysfunction. Ventricular pacing or
dual-chamber pacing for sinus-node dysfunction. N Engl J Med 2002;
7. Tse HF, Yu C, Wong KK, Tsang V, Leung YL, Ho WY, Lau CP.
Functional abnormalities in patients with permanent right ventricular
pacing: the effect of sites of electrical stimulation. J Am Coll Cardiol
8. Wilkoff B, Cook JR, Epstein AE, Greene HL, Hallstrom AP, Hsia H,
Kutalek SP, Sharma A, Dual Chamber and VVI Implantable Defibril-
lator Trial Investigators. Dual-chamber pacing or ventricular backup
pacing in patients with an implantable defibrillator; The dual chamber
and VVI implantable defibrillator (DAVID) trial. JAMA 2002;288:
9. Karpawich PP, Gates J, Stokes KB. Septal His-Purkinje ventricular
pacing in canines: a new endocardial electrode approach. Pacing Clin
10. Mabo P, Scherlag BJ, Munsif A, Otomo K, Lazzara R. A technique for
stable His bundle recording and pacing: electrophysiological and
11. Amitani S, Miyahara K, Sohara H, Kakura H, Koga M, Moriyama Y,
Taira A, Nagano S, Miura N, Misumi K, Sakamoto H. Experimental
His-bundle pacing: histopathological and electrophysiological exami-
nation. Pacing Clin Electrophysiol 1999;22:562–566.
12. Deshmukh P, Casavant DA, Romanyshyn M, Anderson K. Permanent,
direct His bundle pacing: a novel approach to cardiac pacing in
patients with normal His-Purkinje activation. Circulation 2000;101:
13. Zanon F, Baracca E, Aggio S, Pastore G, Boaretto G, Cardano P,
Marotta T, Rigatelli G, Galasso M, Carraro M, Zonzin P. A feasible
approach for direct His-bundle pacing using a new steerable catheter to
facilitate precise lead placement. J Cardiovasc Electrophysiol 2006;
14. Occhetta E, Bortnik M, Magnani A, Francalacci G, Piccinino C,
Plebani L, Marino P. Prevention of ventricular desynchronization by
permanent para-Hisian pacing after atrioventricular node ablation in
chronic atrial fibrillation: a crossover, blinded, randomized study ver-
sus apical right ventricular pacing. J Am Coll Cardiol 2006;47:1938–
15. Baan, J, Van Der Velde ET, De Bruin HG, Smeenk GJ, Koops J, Van
Duk AD, Temmerman D, Senden J, Buis B. Continuous measurement
of left ventricular volume in animals and humans by conductance
catheter. Circulation 1984;70:812–823.
16. Lieberman R, Grenz D, Mond HG, Gammage MD. Selective site
pacing: defining and reaching the selected site. Pacing Clin Electro-
17. Cantu F, De Filippo P, Cardano P, De Luca A, Gavazzi A. Validation
of criteria for selective His bundle and para-hisian permanent pacing.
Pacing Clin Electrophysiol 2006;29:1326–1333.
18. Varma C, O’Callaghan P, Mahon NG, Hnatkova K, McKenna W,
Camm AJ, Rowland E, Brecker SJ; Effect of multisite pacing on
ventricular coordination. Heart 2002;87:322–328.
19. Sweeney MO, Shea JB, Fox V, Adler S, Nelson L, Mullen TJ, Belk P,
Casavant D, Sheldon T. Randomized pilot study of a new atrial-based
minimal ventricular pacing mode in dual-chamber implantable cardio-
verter-defibrillators. Heart Rhythm 2004;1:160–167.
20. Steendijk P, Tulner SA, Bax JJ, Oemrawsingh PV, Bleeker GB, van
Erven L, Putter H, Verwey HF, van der Wall EE, Schalij MJ. Hemo-
dynamic effects of long-term cardiac resynchronization therapy: anal-
ysis by pressure-volume loops. Circulation 2006;113:1295–1304.
21. Leclercq C, Faris O, Tunin R, Johnson J, Kato R, Evans F, Spinelli J,
Halperin H, McVeigh E, Kass DA. Systolic improvement and mechan-
ical resynchronization does not require electrical synchrony in the
dilated failing heart with left bundle-branch block. Circulation 2002;
The American Journal of Cardiology (www.AJConline.org)