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Ann Thorac Surg 1995;59:294-300
© 1995 The Society of Thoracic Surgeons

Acute Hemodynamic Effects of Atrio-Biventricular Pacing in Humans

Division of Thoracic and Cardiovascular Surgery, Department of Surgery, and Division of Cardiology, Department of Medicine, The University of Maryland School of Medicine, Baltimore, Maryland

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Standard postoperative dual-chamber pacing uses ventricular leads placed on the right ventricle that produce dysynchronous ventricular activation and contraction. The hypothesis that simultaneous stimulation of both ventricles by atrio-biventricular pacing improves hemodynamic performance compared with that observed with standard atrio-monoventricular pacing was tested in 18 patients 12 to 36 hours after elective coronary artery revascularization. Temporary epicardial pacing electrodes were placed on the right atrium and into anterior paraseptal sites on the right and left ventricle. Simultaneous biventricular activation was documented by fusion morphology of surface electrocardiograms and by isochronal epicardial activation mapping during biventricular pacing. Hemodynamic data were acquired after 10 minutes of pacing at a fixed overdrive rate during atrial pacing and during dual-chamber pacing using unipolar right ventricular, unipolar left ventricular, and bipolar biventricular (left ventricular cathode) leads. Atrio-biventricular pacing increased cardiac index and decreased systemic vascular resistance compared with atrial pacing and with atrio–right ventricular and atrio–left ventricular dual-chamber pacing (p < 0.05). These data support the use of atrio-biventricular pacing employing paraseptal electrodes to optimize hemodynamic performance.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
See also page 300.

It has become standard practice in cardiac surgical procedures to position pacing leads on the right atrial and right ventricular surface for temporary postoperative dual-chamber pacing [1]. The ventricular electrodes are customarily placed into the right ventricular muscle because this surface is easily accessible. The specific ventricular site selected is in an area free of epicardial fat and scar to ensure that the lowest pacing thresholds are obtained. However, detailed physiologic studies have shown that the single stimulation of right ventricular sites causes dysynchronous ventricular contraction due to early depolarization of the right ventricle and delayed depolarization of the left ventricle through multiple interventricular activation fronts [2]. In contrast, normal human ventricular activation, which is conducted by the Purkinje system, spreads transmurally from the endocardium to multiple paraseptal epicardial regions and results in more synchronous contraction of the ventricle [3, 4].

It is logical to propose, therefore, that producing biventricular activation by simultaneously pacing both ventricles across the septum might confer hemodynamic benefits over those of conventional atrio-monoventricular pacing, presumably by maintaining ventricular synchrony. The hypothesis that atrio-biventricular pacing achieves better acute hemodynamic performance than does conventional, dual-chamber, atrio-monoventricular pacing was tested after short-term epicardial pacing in patients who had undergone coronary revascularization. The results demonstrate that simultaneous epicardial activation of both ventricles was achieved by pacing at these sites. Increases in the cardiac index and reductions in the systemic vascular resistance were produced by atrio-biventricular pacing compared with the measurements obtained after atrial (AAI) and atrio-monoventricular pacing.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Patients undergoing elective aortocoronary bypass grafting were selected for study after informed consent was obtained in accordance with the Guidelines of the Institutional Review Board of the University of Maryland School of Medicine (approval date, November 1, 1991). Exclusion criteria were (1) age less than 25 or greater than 75 years; (2) the presence of atrial fibrillation, a conduction defect, or sinus tachycardia (>100 beats/min); (3) a postoperative cardiac index of less than 2.0 L • min^-1 • m^-2; or (4) the need for emergency operation or intraaortic balloon counterpulsation, or both. The latter two exclusion criteria were arbitrarily defined to eliminate the potentially confounding effects of pharmacologic interventions and to avoid the hemodynamic variability that can occur in patients in an unstable condition or in those with a low postoperative cardiac output.

Study Protocol
Temporary myocardial pacemaker leads (model TPW42, 2-0 braided steel; Ethicon, Somerville, NJ) were placed against the midlateral surface of the right atrium 1 to 2 cm apart and into the superficial myocardium 2 to 4 cm apart on either side of the septum at the anterior distal third of the right and left ventricles (Fig 1). Atrio-monoventricular pacing was performed, making each paraseptal electrode unipolar. Biventricular pacing was performed by using the left ventricular electrode as the cathode (negative polarity) and the right ventricular electrode as the anode. An external, constant-current, dual-chamber demand pacemaker (model 5330; Medtronic Inc, Minneapolis, MN) was paced at a fixed rate that was 5 to 10 beats/min greater than the intrinsic sinus rate (range, 85 to 105 beats/min) for 10 minutes in each of the four pacing modes: (1) AAI, (2) atrio–right ventricular, (3) atrio–left ventricular, and (4) atrio–biventricular. Once the overdrive rate was established, the rate was held constant for each patient and for each pacing mode for the entire study period. Each of the four pacing modes was instituted in a predetermined sequence that corresponded to the last digit of the hospital registration number. Surface electrocardiograms were obtained at the beginning and end of each 10-minute study period to document stable pacing capture and the absence of competition from intrinsic beats. Before dual-chamber pacing, the surface electrocardiogram was used to confirm the presence of bipolar atrial capture and to document the presence of a corresponding right atrial a pressure wave through the proximal port of the pulmonary artery catheter. The standard atrioventricular delay interval of 150 ms was used for all pacing modes at twice the pacing threshold current [1].

View larger version (22K): [in this window] [in a new window]   Fig 1. . Electrode location and pacing configuration. The atrioventricular delay was 150 ms; the rate was fixed at 5 to 10 beats/min greater than the sinus rate and held constant for all pacing modes in each patient. Ventricular leads were positioned 1 to 2 cm lateral to the interventricular septum (approximately 4 to 5 cm apart) on the lower third of the anterior ventricular surface. (AAI = atrial pacing from lateral right atrial surface [bipolar]; A-BiV = atrioventricular pacing using bipolar electrodes in paraseptal right ventricle [anode] and left ventricle [cathode]; A-LV = atrioventricular pacing using electrode in paraseptal low anterior left ventricle [unipolar]; A-RV = atrioventricular pacing using electrode in paraseptal low anterior right ventricle [unipolar]; LV = left ventricle; RA = right atrium; RV = right ventricle.)

Hemodynamic studies were performed in 18 additional patients in the fasting state 12 to 36 hours after operation. Pacing was performed after the patients had remained hemodynamically stable for at least 2 hours. Baseline blood pressures were measured from the radial artery, pulmonary artery, pulmonary capillary (wedge), and right atrium. The midchest position was used for the zero reference level. Cardiac output was measured at end-expiration by the thermodilution method using balloon-tipped catheters (BOC Healthcare, Oxnard, CA) and bedside computers (Abbot Critical Care Systems, Chicago, IL). Cardiac output was measured in triplicate by research nurses who were blinded to the specific pacing therapy that had been used. When the measurement varied by more than 10%, additional output determinations were made to establish reproducibility. Corresponding hemodynamic data derived from the median cardiac output value were used for calculation of the cardiac index and systemic vascular resistance.

Hemodynamic data were acquired after 10 minutes in each pacing mode. Surface electrocardiograms were recorded during each pacing mode to confirm the presence of altered ventricular activation indicating dual-chamber (atrioventricular), biventricular, and monoventricular capture. Simultaneous electrocardiograms and arterial blood pressure waveforms were recorded using a multichannel strip chart recorder (Marquette Electronics, Milwaukee, WI). Baseline sinus rhythm and AAI measurements were repeated at the conclusion of the study to exclude hemodynamic drift over the 90-minute to 100-minute study period. No patient showed a drift of more than 10% (cardiac output or blood pressure) nor did the condition of any patient become unstable during the study period.

Statistical Analysis
Data are summarized as the mean ± standard error of the mean. The null hypothesis that the four experimental conditions (AAI pacing, atrio–right ventricular pacing, atrio–left ventricular pacing, and atrio-biventricular pacing) had no effect was tested using single-factor, repeated-measures analysis of variance. When the analysis of variance revealed a significant effect, significant subgroups were isolated using Scheffé's F procedure, Fisher's PLSD test ( = 0.05), and a post hoc, two-tailed, paired t test [6].

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Hemodynamic studies were performed in 18 patients (7 female) after they had undergone elective coronary revascularization. The mean age was 64 ± 3 years (range, 41 to 72 years). Preoperative left ventricular function was greater than 40% in 14 of 18 patients (78%), as assessed by left ventriculography.

Electrocardiographic verification of altered ventricular depolarization during each pacing mode was documented by differences in the QRS duration and morphology (Fig 2). Electrocardiograms obtained during each monoventricular pacing mode demonstrated the bundle-branch morphologic pattern previously described for monoventricular pacing: right ventricular pacing caused a left bundle-branch pattern and left ventricular pacing caused a right bundle-branch pattern. Biventricular pacing produced a QRS morphology that was distinct from that observed with single-chamber stimulation of either ventricle. The direction of the QRS complex in limb lead I was invariably negative, as is the case for left ventricular pacing. The QRS duration did not differ significantly between biventricular and monoventricular pacing. The postoperative intrinsic conduction patterns and sinus rhythm PR interval duration obtained both immediately after operation and at the time of study (153 ± 3 ms; range, 130 to 180 ms) were not significantly altered from the preoperative measurements. There was no correlation between the postoperative duration of the PR interval in sinus rhythm and the hemodynamic effects of pacing.

View larger version (13K): [in this window] [in a new window]   Fig 2. . Representative simultaneous limb and precordial surface electrocardiograms obtained from 1 patient during atrio–right ventricular (A-RV), atrio–left ventricular (A-LV), and atrio–biventricular (A-BiV) pacing showing a differing QRS duration and morphology for each mode. Note that the pacing artifact for the 0.5-ms rectangular pacing pulse for each atrial and ventricular stimulus is not visible on each tracing, as commonly occurs with the limited sampling rate and digitization of standard electrocardiographic recorders.

View larger version (2K): [in this window] [in a new window]   Fig 3. . Representative epicardial activation maps constructed for 1 patient during atrio–right ventricular pacing (A-RV), atrio–left ventricular pacing (A-LV), and atrio-biventricular pacing (A-BiV). The corresponding total ventricular activation times were 121, 127, and 121 ms, respectively. Colors are isochrons in 18-ms increments (0.125 total ventricular activation time per hue). (L = left; LAD = left anterior descending artery; PDA = posterior descending artery; R = right.)

View larger version (23K): [in this window] [in a new window]   Fig 4. . Cardiac index for each patient by pacing mode. (AAI = atrial pacing; A-BiV = atrio-biventricular pacing; A-LV = atrio–left ventricular pacing; A-RV = atrio–right ventricular pacing.)

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

The idea that the pacing site affects hemodynamic function is not contemporary. Early attempts to find a relationship between the ventricular pacing site and hemodynamic function in human subjects yielded inconclusive findings because of the small numbers of patients studied and the unspecified or mixed locations of the pacing electrodes [7–10]. Even under more controlled experimental conditions, the optimal monoventricular pacing site remained controversial, in that either right ventricular [11, 12] or left ventricular [13–15] stimulation was favored, or no significant difference was found between either ventricular site [16–20].

The relationship between the myocardial activation front and the force of ventricular contraction has also been examined. Although Wiggers [21] believed that the activation and contraction of the stimulated ventricle was abnormal, he concluded that the contralateral ventricle was stimulated over the normal conduction pathway. Lister and co-workers [2] constructed epicardial activation maps to demonstrate that the paced depolarization of the contralateral ventricle did not occur through the normal conduction system but through multiple aberrant pathways. Less atrioventricular valve regurgitation resulted when (as in the normal conduction sequence) the papillary muscles were stimulated early. The myocardium activated the earliest manifested the fastest conduction, the earliest contraction, and the greatest degree of asynchronous movement. As a consequence, pacing sites over areas of large myocardial mass, such as the left ventricular free wall, yielded the greatest reduction in force, because this area contracted by means of paced depolarization. The sequence of ventricular activation and the amount of muscle activated by paced conduction were specific for each pacemaker site. The epicardial activation maps obtained during paraseptal biventricular stimulation in the present study confirm the fact that activation spreads along the epicardium from the paraseptal pacing sites to basal ventricular segments. This study cannot address whether ischemia, cardioplegia, or reperfusion alters impulse propagation from the epicardium to the endocardium. One of the most effective experimental pacemaker sites identified by Lister and co-workers [2] was the anteroinferior paraseptal region, which was the cathodal stimulation site used for epicardial biventricular pacing in the present study.

More recent laboratory investigations using sophisticated experimental techniques have demonstrated the existence of abnormal contraction patterns and reductions in the contractile force and the maximum rate of increase of left ventricular pressure during ventricular epicardial pacing [22–25]. The observed rightward shift of the pressure–volume loops and accompanying reductions in the end-diastolic volume and stroke volume are least for pacing sites closest to the native conduction system, such as those near the septal region [26]. Additional studies have demonstrated that ventricular pacing has adverse effects on the end-systolic pressure–volume relationship [27] and causes reductions in mechanically effective muscle mass [24, 28]. The latter effects are thought to be predominantly related to decreased synchrony and not to fundamental differences in the force–interval relationship or to beat-to-beat alterations in the myofibrillar calcium supply during excitation–contraction coupling [29]. The experimentally observed abnormalities in systolic wall motion that accompany the early activation and contraction of paced myocardium with corresponding late activation of distant areas and late systolic relaxation of paced areas [23, 30] may act in combination with known effects of ventricular pacing on transseptal gradients [25], septal movement [23], and biventricular volume interactions [26]. In the setting of biventricular pacing, leads placed on each side of the septum may correct the paradoxic septal movement that has been observed frequently after revascularization [31, 32]. The improvement in the cardiac index observed for atrio-biventricular pacing versus atrio-monoventricular pacing may be related to the more effective contraction of the septum during biventricular pacing. Preliminary studies in which intraoperative transesophageal echocardiography was performed during biventricular pacing have yielded findings to support this explanation.

The beneficial effect of atrio-biventricular pacing also may be related to underlying arteriosclerotic coronary artery disease or to the operation that was performed 18 to 36 hours before the study. In the only investigation to evaluate the effects of pacing sites in patients with coronary artery disease, Raichlen and colleagues [33] examined the hemodynamic effects of atrioventricular pacing using sites on the left and right ventricles in patients before (but not after) revascularization. They noted left ventricular pacing sites to be inferior to right apical sites in those patients with high-grade left anterior descending coronary artery lesions. Regional ischemia may have been a confounding factor in this analysis, as left ventricular pacing sites proved to produce optimal results in those patients who did not have left anterior coronary artery lesions. In the present study, few patients had significant preoperative anterior wall segment abnormalities (4 of 18) and all patients with significant left anterior descending coronary artery lesions (17 of 18) had undergone complete revascularization with internal mammary artery or saphenous vein grafts. The negative effect of ventricular pacing on the maximum rate of increase of left ventricular pressure–end-diastolic volume relationship in the presence of regional ischemia has been well identified by laboratory investigations [25].

The factors just cited may help to explain why atrio-biventricular pacing is superior to atrio-monoventricular pacing, but they do not fully explain the unexpected finding that this pacing mode was superior to AAI. One additional explanation involves the fixed 150-ms atrioventricular delay interval that was used during pacing in this study. It is known that alteration of this interval has an effect on ventricular filling. However, the literature on long-term dual-chamber pacing is divided on the optimal atrioventricular interval delay (shorter versus longer), because multiple variables, which include diastolic compliance, presystolic valve regurgitation, and intraventricular conduction defects, are involved [34, 35]. In the present study, the fixed 150-ms atrioventricular delay may have played a role in causing atrio-biventricular pacing to be superior to AAI, but a statistically significant relationship between the preoperative or postoperative PR intervals and the hemodynamic effects of pacing was not observed. The preoperative PR intervals were not significantly altered after operation. The atrio-monoventricular pacing modes would also have been superior to AAI pacing, if the hemodynamic effects were due solely to the fixed atrioventricular delay.

Neurohumoral or reflex mechanisms may also account for the observed increase in the cardiac index produced by atrio-biventricular pacing, without alterations in the right or left heart pressures. The increased cardiac index and reduced vascular resistance resulting from biventricular stimulation may be related to known consequences of dual-chamber pacing, which include the systemic or intramyocardial release of catecholamines [36], reflex-mediated baroreceptor and autonomic nervous system activation [37], or the release of vasodilatory substances, such as atrial natriuretic peptides [38, 39].

In summary, atrio-biventricular pacing increased cardiac index and decreased systemic vascular resistance compared with atrio-monoventricular and AAI pacing. The hemodynamic improvement conferred by atrio-biventricular pacing versus the improvement that occurred with atrio-monoventricular and AAI pacing may be due to a combination of factors, including more effective wall motion of the ventricular septum, alterations in the atrioventricular interval, or neurohumoral or baroreceptor reflex effects, or combinations of these factors. Further studies are in progress to elucidate the nature of these observations, with the goal to apply site-specific pacing therapy to optimize postoperative hemodynamic performance in patient subsets with ventricular wall motion abnormalities and with impaired cardiac conduction.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
We acknowledge the intellectual contributions of Morton M. Mower, MD, and Cardiac Pacemakers, Inc, St. Paul, MN, to this study. The secretarial assistance of Susan McHugh and the services of Robert Wise, Michael Fiocco, MD, and Robert Klautz, MD, PhD, also are acknowledged. The support of Anthony L. Imbembo, MD, is appreciated.

This research was supported, in part, by a Pangborn Fund Award from The University of Maryland at Baltimore.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Presented at the Fortieth Annual Meeting of the Southern Thoracic Surgical Association, Panama City Beach, FL, Nov 4–6, 1993.

Address reprint requests to Dr Foster, Division of Thoracic and Cardiovascular Surgery, The University of Maryland School of Medicine, 22 S Greene St, Baltimore, MD 21201.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 

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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]

				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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				M. R Gold ELECTROPHYSIOLOGY: Permanent pacing: new indications Heart, September 1, 2001; 86(3): 355 - 360. [Full Text] [PDF]

				S. Cazeau, C. Leclercq, T. Lavergne, S. Walker, C. Varma, C. Linde, S. Garrigue, L. Kappenberger, G. A. Haywood, M. Santini, et al. Effects of Multisite Biventricular Pacing in Patients with Heart Failure and Intraventricular Conduction Delay N. Engl. J. Med., March 22, 2001; 344(12): 873 - 880. [Abstract] [Full Text] [PDF]

				C LECLERCQ and J-C DAUBERT Why biventricular pacing might be of value in refractory heart failure? Heart, August 1, 2000; 84(2): 125 - 126. [Full Text] [PDF]

				S. Walker, T.M. Levy, A.J.S. Coats, N.S. Peters, and V.E. Paul Bi-ventricular pacing in congestive cardiac failure. Current experience and future directions Eur. Heart J., June 1, 2000; 21(11): 884 - 889. [PDF]

				M. Debrunner, B. Naegeli, and O. Bertel The Acute Effects of Transvenous Biventricular Pacing in a Patient With Congestive Heart Failure Chest, June 1, 2000; 117(6): 1798 - 1800. [Abstract] [Full Text] [PDF]

				P. Deshmukh, D. A. Casavant, M. Romanyshyn, and K. Anderson Permanent, Direct His-Bundle Pacing : A Novel Approach to Cardiac Pacing in Patients With Normal His-Purkinje Activation Circulation, February 29, 2000; 101(8): 869 - 877. [Abstract] [Full Text] [PDF]

				P. RITTER Cardiac stimulation in heart failure: are we going too fast, are we going too far? Europace, January 1, 2000; 2(1): 1 - 3. [PDF]

				D. A. Kass, C.-H. Chen, C. Curry, M. Talbot, R. Berger, B. Fetics, and E. Nevo Improved Left Ventricular Mechanics From Acute VDD Pacing in Patients With Dilated Cardiomyopathy and Ventricular Conduction Delay Circulation, March 30, 1999; 99(12): 1567 - 1573. [Abstract] [Full Text] [PDF]

				C. Leclercq, S. Cazeau, H. Le Breton, P. Ritter, P. Mabo, D. Gras, D. Pavin, A. Lazarus, and J.-C. Daubert Acute hemodynamic effects of biventricular DDD pacing in patients with end-stage heart failure J. Am. Coll. Cardiol., December 1, 1998; 32(7): 1825 - 1831. [Abstract] [Full Text] [PDF]