(Circulation. 1997;96:3273-3277.)
© 1997 American Heart Association, Inc.
Articles |
Evaluation of Different Ventricular Pacing Sites in Patients With Severe Heart Failure
Results of an Acute Hemodynamic Study
From the Department of Cardiology, Brest (France) University Hospital (J.-J.B., Y.E., M.G., J.M., S.M., J.B.) and the Cardiac Arrhythmia Center, University of Minnesota, Minneapolis (D.G.B., K.G.L.).
Correspondence to Jean-Jacques Blanc, MD, Department of Cardiology, University Hospital, Blvd Tanguy Prigent, 29609 Brest Cédex, France.
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Abstract |
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Background Multisite ventricular pacing has recently been proposed as an additional treatment for patients with severe congestive heart failure. To further assess the potential value of this technique, we compared the acute hemodynamic changes associated with pacing the right ventricular apex (RVA) or outflow tract (RVOT) alone, the left ventricle (LV) alone, or biventricular (BIV) pacing of the RVA and LV together.
Methods and Results Acute hemodynamic findings were measured in 27 patients with severe heart failure despite optimal therapy and either first-degree AV block and/or an intraventricular conduction defect. In the 23 patients with a high pulmonary capillary wedge pressure (PCWP) (>15 mm Hg), data were collected after transvenous pacing at different ventricular sites in either the VDD mode (AV delay=100 ms) or the VVI mode in patients with atrial fibrillation (n=6). The mean baseline cardiac index was 1.82 L · min-1 · m-2. Mean±SD baseline systolic blood pressure (SBP) (118.5±15.2 mm Hg), PCWP (26.4±6.6 mm Hg), and V-wave amplitude (39.1±14.6 mm Hg) were similar before and after either RVA or RVOT pacing. In contrast, LV-based pacing (either LV alone or BIV pacing) resulted in higher SBP (P<.03) and lower PCWP (P<.01) and V-wave amplitude (P<.001) than either baseline or RV pacing measurements. With LV pacing alone, SBP, PCWP, and V waves were 126.5±15.1, 20.7±5.9, and 25.5±8.1 mm Hg, respectively. The results with LV pacing alone were similar to those obtained with BIV pacing.
Conclusions In patients with severe congestive heart failure, both LV pacing alone and BIV pacing resulted in a similar and significant acute improvement in SBP, PCWP, and V-wave amplitude compared with baseline measurements and RV pacing alone. These results provide a strong basis for initiating long-term studies examining the chronic effects of LV-based pacing in patients with medically refractory congestive heart failure.
Key Words: heart failure • pacing • hemodynamics
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Introduction |
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Right apical ventricular pacing with a short AV delay has been proposed as a treatment for patients with congestive heart failure. However, the outcomes to date have been controversial.1–4 Consequently, the case of a patient in end-stage heart failure who improved dramatically after initiation of biventricular pacing helped to introduce the concept of multisite pacing.5 It was hypothesized that multisite ventricular pacing may enhance the synchronous contraction of the dysfunctional left ventricle and thereby improve overall cardiovascular function. Studies to date examining multisite ventricular pacing have been limited but suggestive of a benefit of biventricular pacing despite a high mortality rate.6 In this investigation, we evaluated the acute hemodynamic findings associated with various pacing sites and assessed whether left ventricular pacing alone rather than biventricular pacing would be of benefit in improving the acute hemodynamic status in patients with severe heart failure.
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Methods |
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After giving informed consent, NYHA class III or IV patients with stable congestive heart failure despite optimal medical management were enrolled in this prospective study if they had first-degree AV block and/or a bundle-branch block. Patients were studied in the nonsedated, fasting state. They were treated on the day of the evaluation with their usual heart failure medical therapies, which typically included digoxin, diuretics, and an ACE inhibitor. A fluid-filled pulmonary artery catheter was used for measurement of pulmonary artery capillary wedge pressure and cardiac output (thermodilution technique), and a femoral artery catheter was used for recording blood pressure. For patients in sinus rhythm, a 7F bipolar catheter was positioned transvenously via the femoral vein into the high right atrium. A second bipolar catheter was positioned in the right ventricular apex and subsequently moved to the outflow tract, and a third catheter was advanced across the aortic valve in a retrograde fashion to pace the lateral wall of the left ventricle. Pacing was performed with an AV delay of 100 ms, as described below, with a pacing output of 3 V at 0.5 ms with an external pacing device (model 5346, Medtronic Inc).
Baseline data recorded in all patients included measurement of systolic, diastolic, and mean arterial and pulmonary artery pressures, mean capillary wedge pressure (PCWP), and V-wave pressures (all mm Hg) and cardiac index (L · min-1 · m-2). These measurements were repeated 5 minutes later. Patients with a PCWP <15 mm Hg despite the presence of congestive failure clinically were excluded from the study. Cardiac index was measured only once during the baseline evaluation and not with each pacing protocol because of concerns regarding the effects of multiple fluid boluses on subsequent hemodynamic measurements. Pacing in the VDD mode was then performed by pacing either the right ventricular apex alone, the right ventricular outflow tract alone, the left lateral free wall alone, or both the left lateral free wall (anode) and the right ventricular apical (cathode) sites simultaneously. The pacing order was randomized. Pacing was performed for 3 minutes before data acquisition at each pacing site. For patients in atrial fibrillation, the VVI pacing rate was programmed 10 bpm above the spontaneous rate. Another series of baseline measurements was obtained 3 minutes after the final pacing protocol. The prepacing and postpacing baseline measurement data were averaged and were reported as the baseline data. A change in hemodynamic parameters of >20% was considered significant. Statistical analysis was performed with the Wilcoxon paired test with a Bonferroni correction. A value of P<.01 was considered statistically significant.
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Results |
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A total of 27 patients were screened, and 23 of 27 patients with a baseline PCWP
15 mm Hg were included in the pacing portion of
the study. The clinical profile of these 23 patients is summarized in
Table 1
. The ventricular rate
of the 6 patients in atrial fibrillation was 
70 bpm, because most
were treated with digoxin and amiodarone. Baseline
hemodynamic measurements were recorded in 14
patients (Table 2). Data could not be
obtained in 7 patients with permanent right ventricular
pacing and in 2 others for technical reasons. In the baseline state,
the mean systolic arterial pressure, PCWP, and
V-wave amplitude pressure were 118±15, 26±7, and 39±15 mm Hg,
respectively. The mean cardiac index was 1.82±0.35 L ·
min-1 · m-2.
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Comparison Between Baseline and Right Ventricular Pacing
A comparison of hemodynamic parameters
after pacing with each of the pacing sites is summarized in Table 2
and
Fig 1. When mean
hemodynamic values under baseline conditions and after
right ventricular apical pacing were compared, there were
no significant differences in any parameters examined.
Although some individual patients appeared to benefit from pacing of
the right ventricular outflow tract, others showed some
element of hemodynamic deterioration. There were
consequently no significant changes in the mean values of the
parameters examined.
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Comparison Between Baseline and Left Ventricular Pacing
Pacing of either the left ventricle alone or in combination with
right ventricular pacing resulted in a significant
improvement in a number of hemodynamic variables
compared with those observed under basal conditions (Table 2, Fig 1).
With left ventricle–based pacing, there was a significant increase in
systolic blood pressure (7%, P<.01) and a decrease
in both PCWP (22%, P<.01) and the mean V-wave amplitude
(35%, P<.001). In 3 patients, pacing of the left ventricle
alone resulted in the disappearance of the V wave (Fig 2).
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Comparison Between Left and Right Apical Ventricular
Pacing (Table 2)
Left ventricular pacing, compared with right
ventricular apical pacing (available in 23 patients),
induced a significant increase in mean systolic blood pressure
(P=.0001) and a significant decrease in capillary wedge
pressure (P=.0001). At least one parameter
improved significantly (>20%) in 16 of 23 patients in left
ventricular pacing and deteriorated in 1.
Comparison Between Left and Biventricular Pacing
The mean hemodynamic data were not significantly
modified between these two pacing sites. One parameter
improved by >20% in biventricular pacing compared with
left ventricular pacing in 3 patients but deteriorated in
5. Biventricular pacing shortened significantly
(P<.01) QRS duration (from 163±28 ms during left
ventricular pacing to 142±21 ms).
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Discussion |
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The results of this prospective randomized study support the hypothesis that direct left ventricular activation with a temporary pacing system results in a significant improvement in cardiovascular function in patients with congestive heart failure and conduction system disease. Compared with either baseline measurements or those obtained with right ventricular pacing of the apex or outflow tract alone, PCWP, V-wave amplitude, and systolic blood pressure were significantly improved with acute left-ventricle–based stimulation, either alone or together with right ventricular pacing. Acute hemodynamic results comparing left ventricular pacing alone with biventricular pacing were similar. These data support the hypothesis that activation of the left ventricle, rather than activation of both ventricles simultaneously, may be the most important factor in achieving benefit from pacing therapy in such patients. The potential benefits associated with pacing the left ventricle alone in such patients have not been reported previously.
Despite optimal medical management, the results from this study demonstrate that pacing of the left ventricular free wall in patients with end-stage cardiac failure (mean ejection fraction, 27±6%) has the potential for further improving the acute hemodynamic status. We selected patients with intraventricular and/or AV conduction defects on the hypothesis that AV conduction delay may lead to dysynchronous left ventricular contraction. Patients with these conduction system abnormalities and congestive heart failure have previously been the subject of similar studies evaluating the potential benefit of right ventricle–based pacing therapies for congestive heart failure.7–9 The present study used a well-accepted pacing study design to evaluate the potential benefit of a new kind of pacing therapy.4,10 We evaluated pacing of the lateral free wall of the left ventricle on the basis of the case report of a patient who demonstrated a marked acute and long-term improvement from this approach.5 The hemodynamic data argue in support of the hypothesis that in patients with severe heart failure and conduction system disease, left ventricle–based pacing improves the efficiency of pump function. However, an important caveat needs to be made: the acute hemodynamic changes that we observed do not necessarily guarantee that either long-term hemodynamic improvement or a clinically apparent benefit will be sustained. Nevertheless, our findings provide a solid rationale for long-term prospective studies. In brief, although chronic pacing of the left ventricle continues to present technical challenges, the data from the present study and from other recent publications suggest that chronic left ventricle–based pacing therapy may offer new hope for some patients with severe end-stage congestive heart failure.
Received August 14, 1997; revision received September 23, 1997; accepted September 23, 1997.
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References |
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1. Hochleitner M, Hörtnagl H, Ng CK, Hörtnagl H, Oschnitzer F, Zechmann W. Usefulness of physiologic dual-chamber pacing in drug-resistant idiopathic dilated cardiomyopathy. Am J Cardiol. 1990;66:198–202.[Medline] [Order article via Infotrieve]
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5. Cazeau S, Ritter P, Bakdach S, Lazarus A, Limousin M, Henao L, Mundler O, Daubert JC, Mugica J. Four chamber pacing in dilated cardiomyopathy. Pacing Clin Electrophysiol. 1994;17:1974–1979.[Medline] [Order article via Infotrieve]
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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. L. Navia, F. A. Atik, R. A. Grimm, M. Garcia, P. R. Vega, U. Myhre, R. C. Starling, B. L. Wilkoff, D. Martin, P. L. Houghtaling, et al. Minimally Invasive Left Ventricular Epicardial Lead Placement: Surgical Techniques for Heart Failure Resynchronization Therapy Ann. Thorac. Surg., May 1, 2005; 79(5): 1536 - 1544. [Abstract] [Full Text] [PDF]
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W. Y. Vanagt, X. A. Verbeek, T. Delhaas, M. Gewillig, L. Mertens, P. Wouters, B. Meyns, W. J. Daenen, and F. W. Prinzen Acute Hemodynamic Benefit of Left Ventricular Apex Pacing in Children Ann. Thorac. Surg., March 1, 2005; 79(3): 932 - 936. [Abstract] [Full Text] [PDF]
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M. Heinke, R. Surber, H. Kühnert, G. Dannberg, G. Schwarz, and H. R. Figulla Transoesophageal left ventricular pacing in heart failure patients with permanent right ventricular pacing Europace, January 1, 2005; 7(6): 617 - 620. [Abstract] [Full Text] [PDF]
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J. Vogt, J. Heintze, B. Lamp, B. Hansky, and D. Horstkotte Standard haemodynamic measurements Eur. Heart J. Suppl., August 1, 2004; 6(suppl_D): D29 - D34. [Abstract] [Full Text] [PDF]
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C. Stellbrink, O.-A. Breithardt, and P. Hanrath Technical considerations in implanting left ventricular pacing leads for cardiac resynchronisation therapy Eur. Heart J. Suppl., August 1, 2004; 6(suppl_D): D43 - D46. [Abstract] [Full Text] [PDF]
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C. Stellbrink, O.-A. Breithardt, A.-M. Sinha, and P. Hanrath How to discriminate responders from non-responders to cardiac resynchronisation therapy Eur. Heart J. Suppl., August 1, 2004; 6(suppl_D): D101 - D105. [Abstract] [Full Text] [PDF]
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H. Ashikaga, J. H. Omens, N. B. Ingels Jr., and J. W. Covell Transmural mechanics at left ventricular epicardial pacing site Am J Physiol Heart Circ Physiol, June 1, 2004; 286(6): H2401 - H2407. [Abstract] [Full Text] [PDF]
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W. G. Stevenson and M. O. Sweeney Single Site Left Ventricular Pacing for Cardiac Resynchronization Circulation, April 13, 2004; 109(14): 1694 - 1696. [Full Text] [PDF]
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P Schuster, S Faerestrand, and O-J Ohm Colour tissue velocity imaging can show resynchronisation of longitudinal left ventricular contraction pattern by biventricular pacing in patients with severe heart failure Heart, August 1, 2003; 89(8): 859 - 864. [Abstract] [Full Text] [PDF]
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G. P. Walcott, S. B. Melnick, C. R. Killingsworth, W. M. Smith, and R. E. Ideker Effects of burst stimulation during ventricular fibrillation on cardiac function after defibrillation Am J Physiol Heart Circ Physiol, July 11, 2003; 285(2): H766 - H774. [Abstract] [Full Text] [PDF]
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M. Peschar, H. de Swart, K. J. Michels, R. S. Reneman, and F. W. Prinzen Left ventricular septal and apex pacing for optimal pump function in canine hearts J. Am. Coll. Cardiol., April 2, 2003; 41(7): 1218 - 1226. [Abstract] [Full Text] [PDF]
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A. Duncan, D. Wait, D. Gibson, and J.-C. Daubert Left ventricular remodelling and haemodynamic effects of multisite biventricular pacing in patients with left ventricular systolic dysfunction and activation disturbances in sinus rhythm: sub-study of the MUSTIC (Multisite Stimulationin Cardiomyopathies) trial Eur. Heart J., March 1, 2003; 24(5): 430 - 441. [Abstract] [Full Text] [PDF]
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G. Neri, P. Zanco, F. Zanon, and R. Buchberger Effect of biventricular pacing on metabolism and perfusion in patients affected by dilated cardiomyopathy and left bundle branch block: evaluation by positron emission tomography Europace, January 1, 2003; 5(1): 111 - 115. [Abstract] [PDF]
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