CLINICAL RESEARCH
Ventricular Pacing Lead Location Alters Systemic Hemodynamics and Left Ventricular Function in Patients With and Without Reduced Ejection Fraction
Randy Lieberman, MD*,*,
Luigi Padeletti, MD ,
Jan Schreuder, MD ,
Kenneth Jackson, PA*,
Antonio Michelucci, MD,
Andrea Colella, MD,
William Eastman, MS ,
Sergio Valsecchi, BS and
Douglas A. Hettrick, PhD
* Harper Hospital, Detroit, Michigan
University of Florence, Florence, Italy
San Raffaele University Hospital, Milan, Italy
Medtronic, Inc., Minneapolis, Minnesota
Manuscript received December 26, 2005;
revised manuscript received April 17, 2006,
accepted April 25, 2006.
* Reprint requests and correspondence: Dr. Randy Lieberman, Department of Cardiology, Harper University Hospital, 3990 John R, Detroit, Michigan 48201 (Email: rlieberm{at}dmc.org).
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Abstract
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OBJECTIVES: We compared left ventricular (LV) systolic and diastolic function during right ventricular (RV), LV, and biventricular (BiV) pacing in patients with narrow QRS duration with and without LV dysfunction.
BACKGROUND: The optimal RV pacing lead location for patients with a standard indication for ventricular pacing remains controversial.
METHODS: Left ventricular pressure and volume data were determined via conductance catheter during electrophysiology study in 31 patients divided into groups with ejection fraction (EF)  40% (n = 17) or EF <40% (n = 14). QRS duration was 91 ± 18 versus 106 ± 25 ms, respectively (p = NS). Hemodynamic data were recorded during atrial and dual chamber pacing from the RV apex, RV free wall, RV septum, LV free wall, and BiV.
RESULTS: In patients with EF 40%, RV pacing at 1 or more sites, but not LV free wall or BiV pacing, significantly (p < 0.05) impaired cardiac output (CO), stroke work (SW), EF, and LV relaxation compared with atrial overdrive pacing. Right ventricular pacing also impaired hemodynamics and LV function in patients with EF <40%. However, LV and BiV pacing increased CO, SW, EF, and LV +dP/dtMAX in patients with LV dysfunction. Left ventricular and BiV pacing enhanced an index of global LV cycle efficiency in patients with depressed EF. The detrimental hemodynamic effects of RV pacing were attenuated by selecting the optimal RV pacing site.
CONCLUSIONS: Right ventricular pacing worsens LV function in patients with and without LV dysfunction unless the RV pacing site is optimized. Left ventricular and BiV pacing preserve LV function in patients with EF >40% and improve function in patients with EF <40% despite no clinical indication for BiV pacing.
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Abbreviations and Acronyms
| | AAI = atrial overdrive pacing | | AV = atrioventricular | | BiV = biventricular | | CE = cycle efficiency | | DYS = dyssynchrony index | | EF = ejection fraction | | LV = left ventricular | | LVEDP = left ventricular end-diastolic pressure | | LVF = left ventricular free wall | | LVSP = left ventricular systolic pressure | | RCE = regional cycle efficiency | | RV = right ventricular | | RVA = right ventricular apex | | RVF = right ventricular outflow tract free wall | | RVOT = right ventricular outflow tract | | RVS = right ventricular outflow tract septum | | SV = stroke volume | | SW = stroke work |
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The optimal right ventricular (RV) pacing lead location for patients with a standard indication for ventricular pacing remains controversial. Clinical studies comparing atrial and ventricular-based pacing have demonstrated that atrial pacing modes delay the development of atrial tachyarrhythmias and reduce hospitalization for congestive heart failure compared to ventricular pacing modes (1–3). These results suggested that right ventricular apex (RVA) pacing might be detrimental to left ventricular (LV) function, presumably because bypass of the His-Purkinje system produces dysynchronous LV contraction. Indeed, several clinical and experimental studies examining the consequences of RVA pacing observed that this technique caused prolonged QRS duration, LV asymmetrical hypertrophy, dilatation, remodeling, mitral valve regurgitation, altered myocyte histology, reduced exercise capacity, and coronary perfusion abnormalities (4–7). The DAVID (Dual Chamber with VVI Implantable Defibrillator) Trial also suggested that RVA pacing was associated with an increased risk of death and hospitalization for heart failure in patients with an implantable defibrillator (8). The RV outflow tract (RVOT) was initially suggested as a potentially favorable alternative to RVA pacing. However, most investigations that compared RVOT to RVA pacing yielded equivocal results. This may be due to the heterogeneous populations and methodology of the trials as well as the short follow-up durations (9–12). Other recent clinical trials examined the utility of LV or biventricular (BiV) pacing to avoid the adverse hemodynamic consequences associated with RVA pacing (13–15). The results of these studies were encouraging and emphasized an important relationship among ventricular pacing site(s), hemodynamics, and LV dyssynchrony. However, many patients indicated for RV pacing do not meet clinical requirements for BiV pacing. Thus, proper ventricular lead positioning may have important clinical ramifications for this broad device population. We compared systemic hemodynamics and LV systolic and diastolic function during acute RV, LV, and BiV pacing in patients with and without preexisting LV dysfunction who did not meet current clinical indications for cardiac resynchronization therapy.
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Methods
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The Institutional Review Boards at the Detroit Medical Center and Carregi Hospital approved the experimental design, and all subjects provided written informed consent. Patients with indications for electrophysiologic study or device implantation were prospectively stratified into 2 groups based on LV ejection fraction (EF) 40% or <40%. Ejection fraction was determined before electrophysiologic study using standard echocardiographic techniques. Patients with a previously implanted device, valvular insufficiency or stenosis, or QRS duration >120 ms were excluded from participation.
LV pressure and volume measurements.
Left ventricular pressure and volume were measured using a 7-F 12-electrode combination high-fidelity micromanometer-conductance catheter (CD Leycom, Zoetermeer, the Netherlands) inserted through a femoral artery and advanced into the LV apex over an 0.025 flexible guidewire using fluoroscopic guidance. The catheter was connected to a cardiac function analyzer (CFL 512, CD Leycom) that automatically recorded and displayed pressure and 7 segmental volumes delineated by the electrodes. This method is based on measuring time-varying electrical conductance of ventricular blood segments perpendicular to the LV long axis. A fluid-filled Swan-Ganz catheter (Edwards Life Science, Irving, California) was placed via a femoral vein and advanced into the proximal pulmonary artery for the determination of pulmonary artery pressure and stroke volume (thermodilution) and parallel conductance for conductance volume calibration. Parallel conductance was assessed by injection of 10 ml hypertonic saline (6%) into the pulmonary artery (16). Effective conductance stroke volume (SV) was defined as the difference between conductance volumes at the times of +dP/dtMAX and –dP/dtMIN. Absolute LV volumes were calculated by matching effective conductance SV with simultaneously measured thermodilution SV and by subtracting parallel conductance from total volume. The pigtail of the conductance catheter was accurately positioned in the apex, and the interelectrode spacing was adjusted to the long heart axis. Segmental volumes originating from the proximal ascending aorta were discarded. Pulsatile arterial pressure was measured continuously via the side port of the arterial introducer in a subset of patients. Temporary pacing electrodes were positioned in the RVA, RVOT free wall (RVF), RVOT septum (RVS), and LV free wall (LVF). Lead location was confirmed using standard criteria (17). High septal position was determined using a right anterior oblique fluoroscopic view. Right ventricular outflow tract septum position was confirmed by negative QRS morphology in lead I. Right ventricular outflow tract free wall was confirmed by positive morphology in lead I.
Experimental protocol.
Experimental interventions were performed after electrophysiologic study and before device implant. Constant atrial overdrive pacing (AAI) was maintained throughout the protocol at a rate of 10 beats/min greater than the sinus rate. Baseline data were recorded during AAI pacing. Each patient was randomly assigned to receive dual chamber pacing from the RVA, RVS, RVF, LVF, and BiV (LV-RVS) using a Latin square design. Atrioventricular (AV) delay was programmed to the measured p to His interval minus 10 ms in order to limit the potential effects of atrial contraction and partial intrinsic conduction through the AV node. Data were collected and digitized at 250 Hz under steady-state hemodynamic conditions after a minimum of 2 min of stabilization at each pacing configuration.
Data analysis.
Multiple indexes of LV pressure, volume, and function were calculated and averaged over 8 to10 beats at end expiration from the raw LV pressure and conductance volume data using commercially available software (Conduct NT, Leycom) including LV systolic (LVSP) and end-diastolic (LVEDP) pressure, +dP/dtMAX and –dP/dtMIN, LV end-systolic (LVESV) and end-diastolic volume (LVEDV), LV SV, stroke work (SW), cardiac output, EF, and the time constant of isovolumic relaxation ( , assuming a non-zero asymptote). End-diastole was identified immediately before the isovolumic increase in LV dP/dt, and end-systole was defined as the maximum ratio of LV pressure to volume. Effective arterial elastance (EA), an index of LV afterload, was calculated by (LVESP)/SV (18).
Systolic and diastolic dyssynchrony index (DYSD and DYSS, respectively) were determined as previously described (19). These indexes quantify LV contractile dyssynchrony based on the relative changes in the volume signals derived from individual pairs of electrodes on the conductance catheter. Global cycle efficiency (CE) was calculated as previously described (20) by the formula CE = SW/( LV pressure · LV volume). This index quantifies distortions in the shape of the pressure-volume diagram (Fig. 1). The calculation assumes that the optimal contraction would have CE value near 1.0, corresponding to a rectangular pressure volume diagram. Decreases in cycle efficiency may be caused by multiple factors, including isovolumic volume shifts as well as changes in afterload and ventricular stiffness. Regional cycle efficiency (RCE) was similarly calculated from the most basal and most apical segmental volume signal plotted against LV pressure. Differences in regional cycle efficiency during isovolumic filling or emptying may indicate inefficient pattern contraction or relaxation due to dyssynchrony. In order to evaluate whether the optimal RV pacing site varied between patients, the RV pacing sites resulting in the maximum or minimum SW and +dP/dtMAX were compared to AAI. QRS duration was determined from the 12-lead electrocardiogram.
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Figure 1 Representative steady-state pressure-volume diagrams from 1 patient with an ejection fraction (EF) 40% (A) and EF <40% (B). Groups during atrial overdrive pacing and during dual-chamber pacing and dual chamber biventricular (BiV) pacing. (C) Comparison of basal atrial overdrive (AAI) data from A and B. Rectangle in part A illustrates calculation of global cycle efficiency. Cycle efficiency is equal to the percentage of area occupied by the actual pressure volume loop within a rectangle determined by left ventricular (LV) pulse pressure and LV pulse volume. LVF = left ventricular free wall; RAA = right atrial; RVA = right ventricular apex; RVF = right ventricular outflow tract free wall; RVS = right ventricular outflow tract septum.
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Statistical analysis.
Hemodynamic data collected during dual-chamber pacing were compared based on ventricular pacing site and normal and depressed EF groups using 2-way ANOVA for repeated measures. A Student-Neuman-Keuls test was used for post hoc comparisons. Dual-chamber pacing interventions were compared to AAI pacing using one-way repeated-measure ANOVA with Dunnet's test. Demographic data between groups were compared using t test or Fischer exact test. A probability (p) value <0.05 was considered significant. All data are reported as mean values ± SD unless indicated.
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Results
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A total of 31 patients were enrolled (n = 17 EF 40%; n = 14 EF <40%). Age, gender, and QRS duration were similar between groups (Table 1). Patients with reduced EF had a greater incidence of cardiomyopathy, congestive heart failure, coronary artery disease, myocardial infarction, and previous coronary bypass surgery than patients with normal EF. No differences in the incidence of bradycardia and atrial and ventricular tachyarrhythmias were observed between groups.
Representative pressure-volume diagrams for 1 patient from each group are shown in Figure 1. Patients with preexisting LV dysfunction demonstrated reduced EF and LV +dP/dtMAX, –dP/dtMIN, decreased basal cycle efficiency, elevated LVEDV, and impaired diastolic relaxation compared to patients with EF 40%. Pacing rate for experimental interventions was higher in patients with normal as compared to reduced EF. Programmed AV delay was similar during dual-chamber pacing (103 ± 31 vs. 110 ± 23 ms) between groups. All pacing locations resulted in increased QRS duration relative to control. However, QRS duration was typically shorter during BiV pacing compared to the other pacing sites (Tables 2 and 3).
In patients with EF 40%, 1 or more RV pacing sites, but not LVF or BiV pacing, reduced SW, cardiac output, stroke volume, EF, and impaired diastolic relaxation (Table 2, Figs. 2 and 3). Right ventricular pacing sites also resulted in reduced LV systolic pressure, stroke volume, and +dP/dtMAX, –dP/dtMIN and pulse pressure in patients with EF <40%. Left ventricular and BiV pacing increased SW, cardiac output, SV, EF, and +dP/dtMAX in patients with EF <40% compared to RV pacing (Table 3). Furthermore, LVF and BiV pacing also enhanced CE compared to RV pacing and AAI pacing in patients with depressed EF (Fig. 3). Diastolic dyssynchrony index (DYSD) also decreased with RV pacing (Table 3). Preload (LVEDV), afterload (EA), and mean pulmonary wedge pressure were unchanged in both groups.
Figure 4 shows an example of the 6 segmental pressure-volume diagrams ranging from apex (segment 1) to base (segment 6) during atrial overdrive and dual-chamber pacing from different ventricular sites in 1 patient with LV dysfunction. These data are summarized over the population in Figures 5A and 5B using RCE of the most apical and basal volume segment. Regional cycle efficiency depended on pacing site and varied between the apex and base within pacing site in patients with EF <40%, but not the group with EF 40%. In general, RVA pacing attenuated the apical RCE, and RVF and RVS pacing attenuated the basal RCE in the EF <40% group. Right ventricular minimum stroke work and +dP/dtMAX were significantly lower compared to AAI, whereas the RV maximum values were similar to AAI (Fig. 6).
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Figure 4 Regional and global LV pressure volume loops during atrial overdrive and dual chamber pacing from different ventricular sites in a representative patient with EF <40%. Regions are numbered from apex (1) to base (6), corresponding to the sequential volume channels along the axis of the conductance catheter. These individual signals form the global pressure-volume loop when summed. Note that RV pacing from different sites changes the regional contributions to the global pressure volume loop. Right ventricular apex pacing has a greater impact on the apical segments. Conversely, RVS and RVF pacing primarily distort the basal segment. Left ventricular and biventricular pacing result in more homogenous distribution of regional work. Abbreviations as in Figures 1 and 2.
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Figure 6 Stroke work (SW) (top) and +dP/dtMAX (bottom) at the RV pacing site (RVA, RVS, or RVF), resulting in maximum (MAX RV) and minimum (MIN RV) stroke work or +dP/dtMAX compared with stroke work measured during control (AAI). The site of maximal stroke work or +dP/dtMAX was not different from AAI. Thus, RV pacing does not necessitate attenuated hemodynamics. However, the optimal RV site varied between patients. *p < 0.05 versus AAI, (RM ANOVA with Student-Neuman-Keuls post-hoc comparison). Other abbreviations as in Figures 1 and 2.
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Discussion
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General.
The majority of patients indicated for ventricular pacing do not meet current clinical indications for cardiac resynchronization therapy pacing. Furthermore, the optimal ventricular pacing site for patients with conventional indications for ventricular pacing remains controversial. The present results, comparing the impact of several ventricular pacing sites on indices of LV systolic and diastolic function using pressure-volume analysis, demonstrate that ventricular pacing lead location has a significant impact on LV function. In particular, acute RV pacing caused potentially deleterious reductions in cardiac output and SW concomitant with impaired diastolic relaxation and increased LV end-diastolic pressure in patients with and without impaired LV function. The results further indicate that LV and BiV pacing significantly improved hemodynamics and function compared to RV pacing at 3 different sites in patients with preexisting LV dysfunction.
Patient population.
Few previously conducted clinical investigations have compared ventricular pacing sites in patients who do not meet current clinical requirements for resynchronization therapy. Simantirakis et al. recently observed improved LV function using both echocardiographic (13) and pressure-volume analyses (14) during acute LV and BiV pacing as compared to RVA pacing in patients with permanent atrial fibrillation and narrow-QRS duration that required rate control. Turner et al. (15) demonstrated improved contractile synchrony during LV pacing in patients with congestive heart failure in the presence of either a narrow or prolonged QRS duration. The current results confirm and extend these previous observations by quantifying the direct cardiovascular consequences of alternate site RV versus LV versus BiV pacing in normal and dysfunctional myocardium and by suggesting that the benefit of alternate-site ventricular pacing may vary between populations as well as between patients within those populations.
Role of dyssynchrony.
The present results support previous studies indicating that reduced EF is associated with basal LV contractile dyssynchrony, despite narrow QRS duration (21–23). For example, we observed lower basal global and regional cycle efficiency as well as generally increased dyssynchrony (DYSS, DYSD, Tables 2 and 3) in patients with EF <40%. Furthermore, QRS duration was greater during LV compared to BiV pacing, even though LV performance was similar during pacing from these sites. These data confirm previous reports that QRS duration alone is a reliable indicator of neither mechanical synchrony nor LV function (21–23). Right ventricular pacing also produced increased LVEDP with no change in LVEDV in patients with EF >40%, perhaps indicating the influence of ventricular interaction (24).
The shape of the LV pressure diagram, as quantified by global cycle efficiency, improved during LV and BiV pacing in patients with EF <40%. In contrast, RV pacing had minimal impact on global cycle efficiency. However, the similarities in global cycle efficiency observed during RV pacing may have resulted from dissimilar changes in regional cycle efficiency and synchrony that depended on pacing site. This caveat is illustrated in Figures 4 and 5, in which segmental pressure-volume loops are plotted during atrial overdrive and dual-chamber pacing from different ventricular sites in 1 patient with LV dysfunction. Note that RV pacing from different sites produced important alterations in the regional contributions to the global pressure-volume loop. Right ventricular apex pacing had a greater impact on apical segment loop morphology, whereas RVS and RVF pacing distorted the shape of the LV regional pressure-volume diagram in the basal segments. In contrast, LV and BiV pacing caused a more homogenous distribution of segmental work in the EF <40% group. These observations suggest that pacing site may influence overall global LV function depending on its relative effects on regional function and synchrony. The observations further suggest that avoiding the imposition of regional contractile dysfunction may be as important as the restoration of synchrony in order to improve long-term outcome.
RVA versus RVOT.
Several clinical trials have previously compared RVOT and RVA pacing (9–12,25), but many of these studies were limited by small sample size or brief trial duration. The current results suggest that LV systolic and diastolic function may vary acutely with RV pacing sites in patients with normal and depressed EF, respectively. No RV pacing site was superior, and RV pacing did not compromise stroke work or +dP/dtMAX when the optimal RV pacing site was compared to AAI (Fig. 6). Thus, acute hemodynamic optimization during lead placement may be desired to attenuate the detrimental effects of long-term remodeling associated with RV pacing (7). Interestingly, hemodynamic optimization of ventricular pacing lead location has been demonstrated to improve cardiac performance during placement of temporary ventricular pacing leads during cardiac surgery (26). Such optimization may also be possible in patients in the catheterization laboratory using minimally or non-invasive techniques such as arterial pulse pressure, pulse oximetry, or trans thoracic echocardiography.
RV versus LV and BiV.
Previous animal (27) and clinical (25,28) trials have shown that both BiV and LV pacing resulted in LV systolic function superior to RV pacing. The current findings confirm and extend these previous results in patients without preexisting LV dysfunction and with a narrow QRS duration. Hay (25) and Bordacher et al. (28) demonstrated that BiV pacing appeared to improve LV isovolumic relaxation in comparison to LV pacing in patients with congestive heart failure and a prolonged QRS duration. In contrast, our results indicated that –dP/dtMAX and were similar between BiV and LVF pacing sites in both patient groups (Table 2). The explanation for the difference in our results compared with those of the previous studies is not clear but may have been related to differences in the baseline characteristics of the study populations. However, when considered together, the current and previous results suggest that single-site LV pacing may represent a useful alternative to BiV pacing in some patients, despite potential subtle effects on diastolic function.
Study limitations.
The role of LV lead location in patients indicated for cardiac resynchronization therapy has been studied recently using +dP/dtMAX (29) or a conductance catheter (30). Both trials reported that the optimal LV pacing lead location varied substantially between patients. We did not attempt to identify the best LV free wall lead location in the current investigation (30). Nevertheless, our results support the general hypothesis that the ideal site for RV or LV pacing should be tailored to the individual hemodynamic response of each patient. We quantified LV dyssynchrony using regional cycle efficiency (CE). This index is sensitive to volume shifts during isovolumic contraction and relaxation (20). The index may also be sensitive to afterload changes that can alter the trajectory of the PV loop during ejection. However, we observed no changes in EA, an index of LV afterload with pacing sites (Figs. 2 and 3). Recent studies (25) have emphasized the potential influence of heart rate on optimal lead position. Heart rate was held constant in the present trial by atrial pacing. Thus, paired analyses within patients should not have been affected by heart rate. Finally, BiV pacing interventions were performed with LVF and RVS. It is unknown whether other RV sites would have produced similar results during BiV pacing.
Conclusions.
Ventricular pacing lead location has an important impact on LV function in patients with a narrow QRS duration in the presence or absence of preexisting LV dysfunction. Left ventricular functioning and BiV pacing preserved and improved systemic hemodynamics, LV function, and LV cycle efficiency compared to RV sites in patients with normal and depressed EF, respectively. Our data emphasize that optimizing hemodynamics during pacemaker implantation may be important in the selection of alternate ventricular pacing sites in patients with normal and depressed LV function.
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Acknowledgments
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The authors thank Ms. Amy Skaleski and Ms. Paola Cardano for their helpful assistance.
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Footnotes
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This trial was supported by a grant from Medtronic, Inc. Mr. Eastman, Mr. Valsecchi, and Dr. Hettrick are Medtronic employees. Drs. Lieberman, Padeletti, and Schreuder are paid consultants of Medtronic.
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References
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April 28, 2009;
53(17):
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[Abstract]
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P. P. H.M. Delnoy, J. P. Ottervanger, H. O. Luttikhuis, D. H.S. Vos, A. Elvan, A. R. Ramdat Misier, W. P. Beukema, P. Steendijk, and N. M. van Hemel
Pressure-volume loop analysis during implantation of biventricular pacemaker/cardiac resynchronization therapy device to optimize right and left ventricular pacing sites
Eur. Heart J.,
April 1, 2009;
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[Abstract]
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V. Delgado, L. F. Tops, S. A. Trines, K. Zeppenfeld, N. Ajmone Marsan, M. Bertini, E. R. Holman, M. J. Schalij, and J. J. Bax
Acute Effects of Right Ventricular Apical Pacing on Left Ventricular Synchrony and Mechanics
Circ Arrhythm Electrophysiol,
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[Abstract]
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M. O. Sweeney and F. W. Prinzen
Ventricular Pump Function and Pacing: Physiological and Clinical Integration
Circ Arrhythm Electrophysiol,
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C. Butter and G. Hindricks
Cardiac resynchronization therapy: haemodynamic background and perspectives
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[Abstract]
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P. A. Gould, G. Kong, V. Kalff, S. J. Duffy, A. J. Taylor, M. J. Kelly, and D. M. Kaye
Improvement in cardiac adrenergic function post biventricular pacing for heart failure
Europace,
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[Abstract]
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Q. Shan, Y. Jin, and K. Cao
Reversible left ventricular dyssynchrony and dysfunction resulting from right ventricular pre-excitation
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[Abstract]
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M. M. Scheinman and E. Keung
The Year in Clinical Cardiac Electrophysiology
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H.-F. Tse and C.-P. Lau
Selection of Permanent Ventricular Pacing Site: How Far Should We Go?
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