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Asian Cardiovasc Thorac Ann 2007;15:427-431
© 2007 Asia Publishing EXchange Ltd


ORIGINAL CONTRIBUTIONS

Best Site on Right Ventricle for Open-Chest Biventricular Pacing

Giampaolo Luzi, MD, Andrea Montalto, MD, Vincenzo Polizzi, MD, Cesare C D’Alessandro, MD, Mariano Vicchio, MD, Francesco Musumeci, MD

Department of Cardiac Surgery, San Camillo Hospital, Rome, Italy

For reprint information contact: Giampaolo Luzi, MD, Tel: 39 33 5658 2510, Fax: 39 06 5235 5820, Email: luzi.g{at}libero.it, Via Boccea 170, 00167 Rome, Italy.


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Cardiac resynchronization therapy is effective in patients with a low ejection fraction and left bundle branch block, but 20%–30% do not respond despite selection of the optimal site for pacing on the left ventricle. We investigated whether optimizing the site for placement of the pacing lead on the right ventricle could further improve left ventricular function during cardiac resynchronization in 19 patients (mean age, 63 ± 5 years) undergoing coronary artery bypass with post-ischemic dilated myocardiopathy (ejection fraction, 25.8% ± 2%) and left bundle branch block. The hemodynamic response to pacing was tested with the right ventricular lead positioned at the interventricular septum, atrioventricular junction, acute margin, and the pulmonary trunk. Biventricular stimulation improved left ventricular function. When the right ventricular lead was sited at the interventricular septum, a significant improvement in all hemodynamic parameters compared to the other sites was obtained. Biventricular pacing is important to optimize cardiac resynchronization. Although further studies are needed to confirm these findings, accurate lead placement is recommended for cardiac resynchronization therapy in patients with poor cardiac function and left bundle branch block.


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Temporary atrioventricular (AV) pacing during cardiac surgery is usually achieved by placing leads on the epicardium of the right atrium and right ventricle (RV). The anterior wall of the RV is chosen because this surface is easily accessed. However, previous studies highlighted single RV stimulation as a cause of dyssynchronous ventricular contraction due to early activation of the RV and delayed activation of the left ventricle (LV) compared to the physiological mode of human ventricular activation.1 Based on these observations, cardiac resynchronization therapy was introduced in the early 1990s to treat patients with drug-resistant idiopathic dilated cardiomyopathy.2 Cardiac resynchronization therapy was approved by the Food and Drug Administration in 2001, and the American Heart Association/American College of Cardiology/North American Society for Pacing and Electrophysiology provided the major inclusion criteria for selection of patients.3 Several large studies have emphasized choosing the optimal LV pacing site as the major factor in device placement. Despite adhering to the inclusion criteria and optimal LV siting, 20% to 30% of patients do not respond to treatment.46 Thus we investigated whether different pacing sites on the RV could improve cardiac performance.


    PATIENTS AND METHODS
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Between September 2003 and February 2006, and after giving written informed consent, 19 patients (14 men and 5 women; mean age, 63 ± 5 years) undergoing elective on-pump coronary artery bypass grafting for post-ischemic dilated cardiomyopathy with low ejection fraction (< 30%), left bundle brunch block (QRS duration > 120 ms), and ventricular end-diastolic dimension ≥55 mm, underwent cardiac resynchronization therapy. They were all in sinus rhythm. In 2 patients, severe mitral valve regurgitation was corrected by mitral annuloplasty. Patient characteristics are listed in Table 1Go.


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Table 1. Profile of Patients Undergoing Cardiac Resynchronization Therapy
 
Following general anesthesia and orotracheal intubation, the operation was performed using a standard midline sternotomy, cardiopulmonary bypass (CPB), and cardioplegic arrest. No patient required vasoconstrictor administration while on CPB. A heating/cooling mattress was used in all cases. Transesophageal echocardiography (TEE) was performed by the same skilled cardiologist in all patients to test early hemodynamic performance during pacemaker implantation. Left ventricular ejection fraction was measured with the probe at the mid esophageal level, using the biplane method of discs (modified Simpson’s rule).7 Intraventricular asynchrony was evaluated in transgastric short-axis M-mode view at the basal level at an angle of approximately 0–30 degrees.8,9 By means of a Swan-Ganz catheter, mean pulmonary artery pressure, capillary wedge pressure, cardiac output, and systemic vascular resistance (by thermodilution) were measured (Oximetric 3 system; Abbott, France). Biventricular stimulation was obtained with an external temporary dual-chamber pacemaker (model 5330; Medtronic, Inc., Minneapolis, MN, USA). At the end of the surgical procedure, all pacing leads were positioned before data recording. Two temporary myocardial leads (anode and cathode) were positioned on the midlateral surface of the right atrium, one unipolar definitive lead (cathode) on the laterobasal surface of the LV, and one temporary lead (anode, indifferent lead) on the diaphragmatic surface of the RV. For the purpose of documentation, the anterior wall of the RV was oriented as a compass rose: north being the interventricular septum, south the AV junction, east the acute margin, and west the pulmonary trunk (Figure 1Go).


Figure 1
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Figure 1. Orientation of the pacing sites tested on the right ventricle.

 
After weaning from CPB, adequate volume loading, administration of protamine, normalization of vascular and pulmonary resistance, and stabilization of cardiac output and cardiac index (mean, 10 ± 1.5 min after discontinuing CPB), the pacing sites on the RV were checked in a random sequence. A univocal numeric code was assigned to each site (1 = basal condition, 2 = north, 3 = south, 4 = east, 5 = west). Using software available online, all possible permutations were calculated.10 Each numeric permutation was assigned to only one patient through randomized extraction, and the order of the pacing sites was casually varied in each patient. All temporary myocardial leads were positioned on the RV at predefined sites before taking the measurements. Each RV lead (cathode) was connected to a corresponding lead positioned on the LV (cathode) to obtain biventricular stimulation. Measurements at each site were matched with data obtained without stimulation, defined as basal.

The temporary myocardial pacemaker was programmed in DDD mode, with an AV delay of 130 msec, at a fixed rate of 5 to 10 beats per minute more than the intrinsic sinus rate (range, 75–102 beats per minute). The temporary atrial leads (cathode and anode) were connected to the atrial output, the temporary lead (indifferent) on the diaphragmatic surface of the RV was connected to the (+) ventricular output, while the (–) ventricular output was connected to a Y-connector for the definitive LV lead and the corresponding lead positioned on the RV to check the pacing sites. If inotropics were necessary, they were started before assessing the sites and not modified during the study (dopamine 4 µg·kg–1·min–1 in 5 patients, adrenaline 0.07 µg·kg–1·min–1 in 3). Measurements of cardiac index, systemic vascular resistance, aortic pressure, central venous pressure, and evaluation of LV function by TEE were obtained after 2 min stimulation at each site, and after 2 min without ventricular pacing (AAI mode with the same rate as other sites) for the basal value.

Data were analyzed using SPSS statistical software version 13.0 (SPSS, Chicago, IL, USA). Continuous data were expressed as mean ± standard deviation. One-way analysis of variance was used to evaluate the significance of the differences among the 5 groups of variables (basal, north, south, east, and west). A value of p < 0.05 was considered significant.


    RESULTS
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Before the operation, all patients were in New York Heart Association functional class III or IV, mean ejection fraction was 25.8% ± 2%, and mean LV end-diastolic diameter was 63 ± 8 mm. There were 3 ± 1.8 grafts per patient, and the cross clamp and CPB times were 45 ± 14 and 55 ± 8 min, respectively. There were no hospital deaths. As shown in Table 2Go, during biventricular pacing, all hemodynamic parameters measured at the different pacing sites showed a significant improvement compared to basal values (i.e., stimulation off). In particular, when the pacing lead on the RV was near the interventricular septum (north), we recorded the maximum hemodynamic improvement in terms of ejection fraction, cardiac index, systemic vascular resistance, and central venous pressure (Figures 2Go, 3Go, 4Go). Intraoperative TEE confirmed these findings by showing more coordinated ventricular contraction with better lateral septal wall synchronization compared to the other stimulation sites.


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Table 2. Hemodynamics During Intraoperative Biventricular Pacing at Sites on Right Ventricle
 

Figure 2
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Figure 2. Ejection fraction (EF) without cardiac resynchronization therapy (basal) and with pacing at sites on the right ventricle (north = interventricular septum, south = atrioventricular junction, east = acute margin, west = pulmonary trunk).

 

Figure 3
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Figure 3. Aortic pressure (AP) without cardiac resynchronization therapy (basal) and with pacing at sites on the right ventricle (north = interventricular septum, south = atrioventricular junction, east = acute margin, west = pulmonary trunk).

 

Figure 4
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Figure 4. Central venous pressure (CVP) without cardiac resynchronization therapy (basal) and with pacing at sites on the right ventricle (north = interventricular septum, south = atrioventricular junction, east = acute margin, west = pulmonary trunk).

 

    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Cardiac resynchronization therapy has been validated by 2 large controlled trials: MUSTIC, with a crossover design; and MIRACLE, a parallel placebo-controlled trial. The inclusion criteria were: severe heart failure despite optimal medical therapy, depressed LV ejection fraction, and wide QRS complex (> 120 ms) with left bundle branch block. Compared to medical therapy, cardiac resynchronization resulted in significantly better functional class, exercise tolerance, and quality of life, with a reduction in hospitalization.11,12 The CARE-HF study demonstrated a clear survival benefit of cardiac resynchronization compared to medical treatment alone.13 Recent investigations have focused on the optimal LV pacing site to obtain better lateral septal wall synchronization; however, some patients still do not respond to resynchronization.14,15 Thus we investigated the optimal pacing site on the RV and found the best LV performance with the lead placed near the interventricular septum. A significant improvement in all hemodynamic parameters and more coordinated ventricular contraction compared with other sites was obtained in all patients.

The sequence of stimulation on the RV was randomized to overcome any time-related differences due to post-CPB changes. Atrial pacing was employed as for biventricular stimulation (DDD mode) in basal conditions, with biventricular stimulation off (AAI mode) to overcome the interference that sinus rate variation might have had on measurements. A fixed AV delay was employed to overcome the possibility that a change in ventricular filling might affect the results. The position of the LV lead was chosen according to previous studies showing that the posterior basal wall is the best site for cardiac resynchronization therapy. It should be noted that stimulation at the AV junction (south) showed the least improvement in LV function, aortic pressure, and lateral septal wall synchronization, probably due to being the most distant from the Purkinje fibers. This may explain why the paraseptal region (north) is better than other pacing sites on the RV for resynchronization therapy, as well as producing more synchronous ventricular contraction as revealed by intraoperative TEE. This was previously demonstrated by Foster and colleagues1 who underlined the importance of AV pacing using paraseptal electrodes to optimize hemodynamic performance, and by Lister and colleagues16 who found less AV valve regurgitation when the papillary muscles are stimulated earlier, as in the normal conduction sequence.

Pitzalis and colleagues9 suggested that a long delay between displacement of the septum and the posterior wall is useful for selecting patients who will benefit from early postoperative resynchronization therapy and long-term reverse remodeling; and that the presence of echocardiographic LV asynchrony predicts an improvement in LV ejection fraction of > 5% with a sensitivity of 92% and specificity of 78%. Therefore, simultaneous activation of the septal and posterior basal regions obtained with biventricular cathodal stimulation could explain the best performance recorded in the setting of cardiac resynchronization therapy in our series of patients. Our data indicate that the choice of pacing site on the RV is important to optimize the effect of cardiac resynchronization, but longer follow-up with more patients is needed to confirm these preliminary findings.

This study was performed on a limited number of patients and not randomized because of strict inclusion criteria. The hemodynamic measurements were intraoperative only, because the leads on the RV were subsequently removed. Furthermore, data recording might have been affected by general anesthesia and the short time after discontinuing CPB. Nevertheless, the results indicate that biventricular pacing provides significant early improvement in the hemodynamic parameters of patients undergoing coronary artery bypass grafting for post-ischemic dilated cardiomyopathy and left bundle branch block. Choosing a pacing site near the interventricular septum enhanced LV performance compared to other sites on the RV.


    ACKNOWLEDGMENTS
 
We are grateful to Dr. Giovanni Melina for his kind contribution and final review of our manuscript.


    REFERENCES
 TOP
 ABSTRACT
 INTRODUCTION
 PATIENTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Foster AH, Gold MR, McLaughlin JS. Acute hemodynamic effects of atrio-biventricular pacing in humans. Ann Thorac Surg 1995;59:294–300.[Abstract/Free Full Text]

  2. Cazeau S, Ritter P, Bakdach S, Lazarus A, Limousin M, Henao L, et al. Four chamber pacing in dilated cardiomyopathy. Pacing Clin Electrophysiol 1994;17:1974–9.[Medline]

  3. Auricchio A, Stellbrink C, Block M, Sack S, Vogt J, Bakker P, 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.[Abstract/Free Full Text]

  4. Leclercq C, Hare JM. Ventricular resynchronization: current state of the art. Circulation 2004;109:296–9.[Free Full Text]

  5. Bax JJ, Ansalone G, Breithardt OA, Derumeaux G, Leclercq C, Schalij MJ, et al. Echocardiographic evaluation of cardiac resynchronization therapy: ready for routine clinical use? A critical appraisal. J Am Coll Cardiol 2004;44:1–9.[Abstract/Free Full Text]

  6. Dekker AL, Phelps B, Dijkman B, van der Nagel T, van der Veen FH, Geskes GG, et al. Epicardial left ventricular lead placement for cardiac resynchronization therapy: Optimal pace site selection with pressure-volume loops. J Thorac Cardiovasc Surg 2004;127:1641–7.[Abstract/Free Full Text]

  7. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-Dimensional Echocardiograms. J Am Soc Echocardiogr 1989;2:358–67.[Medline]

  8. Pitzalis MV, Iacoviello M, Romito R, Massari F, Rizzon B, Luzzi G, et al. Cardiac resynchronization therapy tailored by echocardiographic evaluation of ventricular asynchrony. J Am Coll Cardiol 2002,40:1615–22.[Abstract/Free Full Text]

  9. Pitzalis MV, Iacoviello M, Romito R, Guida P, De Tommasi E, Luzzi G, et al. Ventricular asynchrony predicts a better outcome in patients with chronic heart failure receiving cardiac resynchronization therapy. J Am Coll Cardiol 2005;45:65–9.[Abstract/Free Full Text]

  10. Progetti in Visual Basic 6. Available at: http://www.flanguasco.org/VisualBasic/VisualBasic.html. Accessed 04 April 2007.

  11. Auricchio A, Abraham WT. Cardiac resynchronization therapy: current state of the art: cost versus benefit. Circulation 2004;109:300–7.[Free Full Text]

  12. Cazeau S, Leclercq C, Lavergne T, Walker S, Varma C, Linde C, et al. Effects of multisite biventricular pacing in patients with heart failure and intraventricular conduction delay. N Engl J Med 2001;344:873–80.[Abstract/Free Full Text]

  13. Abraham WT, Fisher WG, Smith AL, Delurgio DB, Leon AR, Loh E, et al. Cardiac resynchronization in chronic heart failure. N Engl J Med 2002;346:1845–53.[Abstract/Free Full Text]

  14. Hay I, Melenovsky V, Fetics BJ, Judge DP, Kramer A, Spinelli J, et al. Short-term effects of right-left heart sequential cardiac resynchronization in patients with heart failure, chronic atrial fibrillation, and atrioventricular nodal block. Circulation 2004;110:3404–10.[Abstract/Free Full Text]

  15. Sogaard P, Kim WY, Jensen HK, Mortensen P, Pedersen AK, Kristensen BO, et al. Impact of acute biventricular pacing on left ventricular performance and volumes in patients with severe heart failure. A tissue Doppler and three-dimensional echocardiographic study. Cardiology 2001;95:175–82.

  16. Lister JW, Klotz DH, Jomain SL, Stuckey JH, Hoffman BF. Effect of pacemaker site on cardiac output and ventricular activation in dogs with complete heart block. Am J Cardiol 1964;14:494–503.[Medline]





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Francesco Musumeci
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Right arrow Coronary disease
Right arrow Electrophysiology - arrhythmias


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