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The Impact of Atrio-Biventricular Pacing on Hemodynamics and Left Ventricular Dyssynchrony Compared With Atrio–Right Ventricular Pacing Alone in the Postoperative Period After Cardiac Surgery
The Impact of Atrio-Biventricular Pacing on Hemodynamics and Left Ventricular Dyssynchrony Compared With Atrio–Right Ventricular Pacing Alone in the Postoperative Period After Cardiac Surgery Maxime Cannesson, MD,* Fadi Farhat, MD, PhD,† Maria Scarlata, MD,* Emmanuel Cassar, MD,* and Jean-Jacques Lehot, MD, PhD* Objectives: The aims of this study were to test the hypotheses that in the postoperative period after coronary artery bypass graft surgery (1) atrio–right ventricular (RA-RV) pacing induces a decrease in cardiac output compared with RA pacing alone and (2) atrio-biventricular (RA-BiV) pacing improves CO compared with RA-RV pacing. Design: A prospective observational study. Setting: A single-center university hospital. Participants: Patients referred for coronary artery bypass graft surgery. Interventions: Patients were studied during atrial, RA-RV, and RA-BiV pacing. Cardiac output (echocardiography) and left ventricular dyssynchrony were assessed at each step. Measurements and Main Results: RA-RV pacing induced a significant decrease in cardiac output (4.3 ⴞ 1.0 to 3.7 ⴞ 0.8 L/min, p < 0.01) and a significant increase in left ventricular
dyssynchrony (13 ⴞ 12 to 80 ⴞ 25 milliseconds, p < 0.01). Biventricular pacing induced a significant increase in cardiac output (3.7 ⴞ 0.8 to 4.5 ⴞ 1.0 L/min, p < 0.01) and a significant decrease in left ventricular dyssynchrony compared with right ventricular pacing (80 ⴞ 25 to 21 ⴞ 16 milliseconds, p < 0.05). Conclusions: RA-BiV pacing improves cardiac output compared with RA-RV pacing in the postoperative period after coronary artery bypass graft surgery. This improvement is related to an improvement in left ventricular synchronicity. © 2009 Elsevier Inc. All rights reserved.
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surgery (1) RA-RV pacing induces a decrease in cardiac output (CO) compared with sinus rhythm (SR) and RA pacing alone, (2) RA-BiV pacing is able to improve CO compared with RA-RV pacing alone, and (3) these changes in CO are related to changes in LV synchronicity assessed by TDI.
ARDIAC RESYNCHRONIZATION THERAPY (CRT) (also called biventricular pacing) has been shown to improve mortality and morbidity in heart failure (HF) patients with abnormal electrical activation.1-3 Twenty percent of HF patients have left bundle-branch block (LBBB).4 In these patients, left ventricular (LV) dyssynchrony consists of an asynchronous contraction between the anteroseptum and the posterior, lateral, and inferior walls, resulting in impaired LV ejection fraction (LVEF).3,5 CRT improves symptoms and survival of these patients.1,2,6,7 Many studies have shown that LV dyssynchrony assessment using Tissue Doppler Imaging (TDI) is a better predictor of response to CRT than LBBB.8-14 Little is known about CRT in acute HF or in the postoperative period after cardiac surgery.15-17 Routinely, in cardiac surgical procedures, epicardial pacing leads are placed on the right atrium (RA) and right ventricle (RV) in case of significant bradycardia or the development of atrioventricular block. It has been reported previously that atrio-RV (RA-RV) pacing may induce LV dyssynchrony and hemodynamic compromise compared with atrial pacing (RA) alone.18 On the other hand, it has recently been suggested that atrio-biventricular (RA-BiV) pacing may improve hemodynamics in post– cardiac surgery patients.18-21 However, this conclusion is not clear in the clinical setting.22 The aims of this study were to test the hypotheses that in the postoperative period after coronary artery bypass graft (CABG)
From the Departments of *Anesthesiology and Intensive Care and †Cardiac Surgery, Hospices Civils de Lyon, Louis Pradel Hospital, Claude Bernard Lyon 1 University, Lyon, France. Address reprint requests to Maxime Cannesson, MD, Service d’Anesthésie Réanimation, Hôpital Cardiologique Louis Pradel, 200 Avenue du Doyen Lépine, 69500 Bron, France. E-mail: maxime_ [email protected] © 2009 Elsevier Inc. All rights reserved. 1053-0770/09/2303-0006$36.00/0 doi:10.1053/j.jvca.2008.12.007 306
KEY WORDS: cardiac surgery, dyssynchrony, hemodynamic, cardiac output, echocardiography, biventricular pacing, cardiac resynchronization therapy
MATERIALS AND METHODS The protocol was approved by the institutional review board for human subjects of the authors’ institution (Comité Consultatif de Protection des Personnes dans la Recherche Biomédicale Lyon B). All patients gave preoperative informed and written consent. Twenty-five consecutive patients undergoing CABG surgery (9 offpump and 16 using cardiopulmonary bypass [CPB]) were studied. These patients were selected prospectively and were included from November 1, 2007, to December 22, 2007. This group consisted of 17 men and 8 women between 33 and 83 years old (mean age ⫽ 68 ⫾ 12 years, mean height ⫽ 166 ⫾ 7 cm, and mean weight ⫽ 71 ⫾ 13 kg). Patients with cardiac arrhythmias, preoperative left bundle-branch block, postoperative inotropic support, and intracardiac shunt were excluded. Preoperative LVEF was between 30% and 70% (mean LVEF ⫽ 54% ⫾ 11%). QRS duration was ⬍120 milliseconds in all patients. None of the patients had undergone pacing before inclusion in the study. Only 1 surgeon was involved in the present study (FF). Patients had an 8-cm 5F tipped catheter (Arrow International Inc, Reading, PA) inserted in the left or right radial artery and a triplelumen 16-cm 8.5F central venous catheter (Arrow International Inc) inserted in the right internal jugular vein. Pressure transducers (Medex Medical Ltd, Lancashire, UK) were placed and maintained at the midaxillary line and kept at the atrial level throughout the study protocol. All transducers were zeroed to atmospheric pressure. Over the study period, 5 patients (all were CABG patients with CPB) were excluded because of poor echocardiographic images (n ⫽ 3, patients were intubated) and accidental removal of an epicardial pacing wire (n ⫽ 2). Ventilator settings were held constant throughout the study protocol. No intravascular volume expansion was allowed during the protocol. The study was performed in the intensive care unit within 4 hours after surgery. All patients were sedated with propofol (50 mg/h) and sufentanil (10 g/h). Temporary epicardial pacing leads were placed intraoperatively by one of the authors (FF) after the end of the surgical procedure and before CPB discontinuation. One active lead (Osypka TME 67V
Journal of Cardiothoracic and Vascular Anesthesia, Vol 23, No 3 (June), 2009: pp 306-311
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Fig 1. Positions of the temporary ventricular epicardial leads for pacing. One active lead was attached to the free wall of the left ventricle near the base between the left atrial appendage and the first marginal branch (LV lead), 1 lead was attached to the free wall of the RV on the diaphragmatic side (RV lead), 1 lead was attached to the right atrial appendage, and 2 leads were attached to the pericardium as neutral. SVC, superior vena cava; IVC, inferior vena cava; RA, right atrium; Ao, aorta; PA, pulmonary artery; RV, right ventricle; LV, left ventricle.
ref 45028; Osypka Medical GmbH, Berlin, Germany) was attached to the free wall of the left ventricle near the base between the left atrial appendage and the first marginal branch; 1 lead was attached to the free wall of the RV on the diaphragmatic side; 1 lead was attached to the right atrial appendage; and 2 leads were attached to the pericardium as neutral (Fig 1). The authors chose to locate the LV lead on the free wall of the left ventricle near the base between the left atrial appendage and the first marginal branch in order to have an electrical activation similar to those observed during CRT for chronic heart failure patients. A 12-lead electrocardiogram was obtained before pacing in order to measure heart rate (HR) and PR interval duration. Epicardial leads were connected to a temporary pacemaker (PACE 203H, Osypka Medical GmbH). Each patient was studied at 4 successive steps: (1) SR; (2) RA pacing using 1 atrial and 1 neutral (pericardial) lead; (3) RA-RV pacing using in addition to RA the RV lead as the active lead and the other pericardial lead as the neutral lead; and (4) RA-BiV pacing using, in addition to RA, RV and LV leads as active leads and 1 pericardial lead as the neutral lead. A 5-minute period of rest was observed between each pacing sequence. Pacing was performed at a rate between 5 and 10 beats/min faster than the intrinsic sinus rhythm. An atrioventricular delay during atrioventricular pacing was set in order to guarantee appropriate ventricular capture and in order to maximize the A wave obtained using conventional pulsed-wave Doppler from the mitral inflow on an apical 4-chamber view. The LV-to-RV delay was set at 0. At each step of the protocol the following parameters were recorded: HR; QRS duration; systolic, diastolic, and mean arterial pressures (MAP); central venous pressure; left ventricular end-diastolic volume (LVEDV)23; LVEF assessed by the biplane Simpson’s rule23; and the CO calculated by using the velocity time integral (VTI) obtained by transthoracic echocardiography (CV 70; Acuson-Siemens Corp, Mountain View, CA) from the apical 4-chamber view.23 Digital cineloops were obtained at frame rates of 30 to 90 Hz from apical 4-chamber views at a depth of 12 ⫾ 3 cm during apnea. The images were then exported to a personal computer and were analyzed offline by an observer blinded to the pacing modality. The LVEDV was measured at the onset of the QRS complex. The VTI was measured by a pulsedwave Doppler beam at the level of the LV outflow tract. The mean of 3 measurements was used. The aortic valve area was measured at
baseline and was considered constant throughout the protocol. The aortic valve area was calculated from the diameter of the aortic orifice measured at the insertion of the aortic cusp as: aortic valve area ⫽ ⫻ (aortic diameter/2)2. The stroke volume was calculated as: SV ⫽ aortic valve area ⫻ VTI of aortic blood flow. CO was calculated as: CO ⫽ stroke volume ⫻ HR. LV dyssynchrony was assessed using TDI. TDI was performed using the apical 4-chamber view for the long-axis motion of the left ventricle during apnea. A sample volume of 5 mm was positioned in the center of the analyzed segment (septal basal and lateral basal LV segments). The time resolution for tissue Doppler was 4 milliseconds. Gain setting and filters were set in order to optimize signal and reduce noise. Sweep speed was 150 mm/s. At least 5 beats were recorded, and the average value from 3 beats differing by less than 10% was used for statistical analysis. LV dyssynchrony was measured as the absolute difference in time-to-peak velocity (time delay between onset of the QRS and peak S-wave velocity) of LV opposing walls over the apical 4-chamber window8,9,13,14 (Fig 2). Echocardiographic analyses were performed by an operator blinded to the pacing protocol (EC). Data are presented as mean ⫾ standard deviation. Distribution normality was assessed by using the Kolmogorov-Smirnov test. Changes in hemodynamic and echocardiographic parameters induced by change in pacing protocol were then tested with analysis of variance for repeated measurements. If there were significant differences, post hoc testing was performed using the Tukey honest significant difference. The Pearson test was used to test linear correlation. Considering previously published results,15,19 power analysis showed that 25 patients were necessary to detect a 15% change in CO between RA-RV and RA-BiV pacing (5% type I error rate, 80% power, 2-tailed test, considering CO during RA-BiV pacing at 4.64 ⫾ 1.0 L/min). A p value ⬍0.05 was considered as statistically significant. All statistic analysis was performed by using SPSS 13.0 for Windows (SPSS Inc, Chicago, IL). RESULTS
Compared with SR, RA pacing alone induced no hemodynamic changes (Table 1). RA-RV pacing induced a significant decrease in MAP (from 89 ⫾ 11 to 78 ⫾ 9 mmHg, p ⬍ 0.001), CO (from 4.3 ⫾ 1.0 to 3.7 ⫾ 0.8 L/min, p ⬍ 0.001), LVEF
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Fig 2. A 2-dimensional gray apical 4-chamber view and LV basal septal and lateral tissue Doppler recordings. LV dyssynchrony was measured as the absolute difference in time-to-peak velocity (time delay between onset of the QRS and peak S-wave velocity) of LV opposing walls over the apical 4-chamber window.8,9,13,14 RA, right atrial; RV, right ventricular.
(from 47 ⫾ 5 to 39% ⫾ 5%, p ⬍ 0.001), and a significant increase in QRS duration (from 105 ⫾ 13 to 171 ⫾ 38 milliseconds, p ⬍ 0.001) compared with RA pacing alone (Table 1). RA-BiV pacing induced a significant increase in MAP (from 78 ⫾ 9 to 86 ⫾ 8 mmHg, p ⬍ 0.001) and CO (from 3.7 ⫾ 0.8 to 4.5 ⫾ 1.0 L/min), LVEF (from 39 ⫾ 5 to 49% ⫾ 5%) and a significant decrease in QRS duration (from 171 ⫾ 38 to 121 ⫾ 26 milliseconds, p ⬍ 0.001) compared with RA-RV pacing (Table 1). When RA-BiV pacing was compared with RA pacing alone, weak but significant differences in MAP (86 ⫾ 8 v 89 ⫾ 11 mmHg, respectively; p ⫽ 0.04), CO (4.5 ⫾ 1.0 v 4.3 ⫾ 1.0 L/min, respectively; p ⫽ 0.03), and QRS duration (121 ⫾ 26 v 105 ⫾ 13 milliseconds, respectively; p ⫽ 0.01) were observed (Table 1 and Figs 3 and 4). A change in pacing modality induced no changes in LVEDV and central venous pressure (Table 1).
Table 1. Changes in Hemodynamic Data Induced by Changes in Pacing Modality Sinus Rhythm
RA Pacing Alone
RA-RV Pacing
RA-BiV Pacing
Heart rate (beats/min) 81 ⫾ 12 85 ⫾ 14 86 ⫾ 13 86 ⫾ 13 MAP (mmHg) 91 ⫾ 13 89 ⫾ 11 78 ⫾ 9* 86 ⫾ 8†‡ CVP (mmHg) 10 ⫾ 4 9⫾4 10 ⫾ 4 10 ⫾ 4 LVEDV (mL) 92 ⫾ 21 98 ⫾ 29 98 ⫾ 40 104 ⫾ 31 CO (L/min) 4.3 ⫾ 0.9 4.3 ⫾ 1.0 3.7 ⫾ 0.8* 4.5 ⫾ 1.0†‡ QRS duration (ms) 104 ⫾ 15 105 ⫾ 13 171 ⫾ 38* 121 ⫾ 26†‡ LVEF (%) 48 ⫾ 4 47 ⫾ 5 39 ⫾ 5* 49 ⫾ 5† NOTE. Data are mean ⫾ standard deviation. Abbreviations: RA, right atrial; RV, right ventricular; BiV, biventricular; SAP, systolic arterial pressure; DAP, diastolic arterial pressure; MAP, mean arterial pressure; CVP, central venous pressure. *p ⬍ 0.05 RA-RV compared with RA pacing alone. †p ⬍ 0.05 RA-BiV compared with RA-RV pacing. ‡p ⬍ 0.05 RA-BiV compared with RA pacing alone.
Fig 3. Conventional aortic pulsed-wave Doppler recordings from an apical 4-chamber view obtained during RA-RV and RA-BiV pacing in an illustrative patient. A significant increase in velocity time integral in the RA-BiV pacing mode was observed. RA, right atrial; RV, right ventricular; BiV, biventricular.
Compared with SR, RA pacing alone induced no changes in LV dyssynchrony (Table 2). RA-RV pacing induced a significant increase in LV dyssynchrony compared with RA pacing alone (78 ⫾ 25 v 13 ⫾ 12 milliseconds, p ⬍ 0.001). RA-BiV pacing induced a significant decrease in LV dyssynchrony compared with RA-RV pacing (21 ⫾ 16 v 78 ⫾ 25 milliseconds, p ⬍ 0.001). When RA-BiV pacing was compared with RA pacing alone, the authors observed no significant difference in LV dyssynchrony (21 ⫾ 16 v 13 ⫾ 12 milliseconds, p ⫽ 0.19) (Fig. 4). DISCUSSION
This study shows that RA-RV pacing induces a decrease in CO compared with RA pacing and that RA-BiV pacing significantly improves CO compared with RA-RV pacing in the postoperative period after CABG surgery. This improvement is related to a restoration of LV synchronicity. The benefits of CRT are secondary to acute resynchronization of regional LV mechanics, a decrease in mitral regurgitation, and reverse remodeling that is a long-term effect of CRT.1,2,6,7,24,25 Moreover, CRT is able to improve contractility while decreasing myocardial oxygen consumption.26 Recently, TDI has been shown to be able to quantify LV dyssynchrony and to be a better predictor of response to CRT than LBBB.8-11,14,27,28 Although CRT has unambiguous indications in chronic HF patients, little is known about its efficiency in acute HF. Weisse et al16 have shown that atrio-biventricular pacing improves hemodynamics after CABG surgery compared with RA-RV pacing but did not assess LV dyssynchrony. Fox et al17 reported a successful CRT implantation in a patient with acute HF after CABG surgery. In this report, the authors had no echocardiography or Doppler analysis, and the decision to use CRT was based on QRS duration alone. The authors recently described a successful case of CRT after cardiac surgery in a patient with demonstrated LV dyssynchrony.15 In this case, the decision on CRT was based on echocardiographic LV dyssynchrony and the impossibility to wean the patient from dobutamine and mechanical ventilation.
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Fig 4. A 12-lead electrocardiogram of an illustrative patient during sinus rhythm, RA pacing, RA-RV pacing, and RA-BiV pacing. A narrow QRS during sinus rhythm and RA pacing and widened QRS during RA-RV pacing with an aspect of a left bundle-branch block were observed. QRS duration decreased during RA-BiV pacing compared with RA-RV pacing. RA, right atrial; RV, right ventricular; BiV, biventricular.
Recently published studies suggest that postoperative RABiV pacing is able to improve hemodynamics compared with RA-RV pacing.18-20 However, a recent study from Vogel et al22 found that pacing modality (RA-RV, RA-BiV, RA alone, and SR) had no impact on CO and LV contractility in patients undergoing cardiac surgery. In this study, patients presented with a baseline LVEF ⬍35% and a QRS duration ⬎120 milliseconds. The authors observed no changes in QRS duration between SR, RA alone, and RA-BiV pacing modalities, suggesting that resynchronization objectives may not have been reached. Moreover, these data should be compared with previously published results showing that LV dyssynchrony induced by RV pacing is augmented in case of impaired ventricular function.29 It would have been interesting to study mechanical dyssynchrony in this study in order
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to further explore the relationship between dyssynchrony, CO, and LV contractility. RV pacing is able to induce LV dyssynchrony and decrease CO and LVEF.30,31 In chronic HF patients, RV pacing has even been shown to increase the risk of death or acute HF hospitalization. Several studies suggest that biventricular pacing has the ability to reverse the abnormal activation pattern induced by RV pacing and to restore hemodynamics.32 The present results support this hypothesis by describing the acute deleterious effect of RV pacing on CO. This effect seems to be related only to LV dyssynchrony induced by this pacing mode. By performing RA-BiV pacing, the authors were able to restore LV synchronicity and significantly increase CO. The authors found that RA-BiV pacing was able to weakly but significantly increase CO compared with RA pacing alone. This observation may be related only to the slight increase in HR necessary to guarantee atrial capture. However, this could be important because this pacing mode could be used in order to increase CO by increasing HR in patients presenting with circulatory failure. A recent study by Dzemali et al20 found similar results in patients with a dilated left ventricle but also in some patients with normal LV function. This hypothesis requires further exploration. In the present study, the authors chose to exclude patients requiring postoperative inotropic support in order to focus on the physiology of RA-BiV pacing in this setting. Further studies should assess the ability of RA-BiV pacing to decrease the need for inotropic support in the postoperative period after cardiac surgery. This alternative seems very attractive because RA-BiV13 pacing is able to increase contractility while decreasing myocardial oxygen consumption.26 The present data are supported by a recent study by Dzemali et al20 showing that RA-BiV pacing is able to improve cardiac output and decrease myocardial oxygen consumption after cardiopulmonary bypass. Consequently, it may have significant clinical impact in patients undergoing CABG surgery. STUDY LIMITATIONS
The authors did not perform RA-LV pacing. However, recent studies suggest that RA-LV pacing can increase CO.33 This pacing modality may be interesting because it requires fewer epicardial leads than RA-BiV pacing and thus may decrease the rate of potential mechanical complications re-
Table 2. Changes in LV Dyssynchrony Analysis Induced by Changes in Pacing Modality Sinus Rhythm
RA Pacing Alone
RA-RV Pacing
RA-BiV Pacing
Time-to-peak velocity Basal septal (ms) 180 ⫾ 27 182 ⫾ 27 184 ⫾ 58 224 ⫾ 44†‡ Basal lateral (ms) 186 ⫾ 27 188 ⫾ 25 229 ⫾ 52* 230 ⫾ 55‡ LV dyssynchrony (ms) 12 ⫾ 10 13 ⫾ 12 78 ⫾ 25* 21 ⫾ 16† NOTE. Data are mean ⫾ standard deviation. Abbreviations: RA, right atrial; RV, right ventricular; BiV, biventricular. *p ⬍ 0.05 RA-RV compared with RA pacing alone. †p ⬍ 0.05 RA-BiV compared with RA-RV pacing. ‡p ⬍ 0.05 RA-BiV compared with RA pacing alone.
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lated to lead application or removal. Further studies are required to test and confirm this hypothesis. Moreover, further studies should randomize the pacing protocol. In the present study, the authors used conventional tissue Doppler imaging and only assessed longitudinal dyssynchrony. Recent studies suggest that newer technologies such as velocity vector imaging,34 tissue synchronization imaging,9 and radial dyssynchrony assessment using speckle-tracking radial strain14 may be useful to predict response to CRT. However, conventional TDI has been described as accurate for LV dyssynchrony analysis,13 and recent data suggest that no approach is better than the others.35 Because the present study was performed in the postoperative period after cardiac surgery, the authors cannot exclude that tethering of the interventricular septum wall occurred in some patients and that this may have interfered with the dyssynchrony analysis. However, the authors observed an increase in LV dyssynchrony during RA-RV pacing compared with RA pacing and a decrease in LV dyssynchrony during RA-BiV pacing
compared with RA-RV pacing in every patient. Thus, it is more likely that tethering did not impact the final results. All pacing modes were set at a rate higher than the sinus rhythm. Theoretically, this higher rate could have induced reduced filling and thus could explain differences between right atrial pacing and sinus rhythm. Finally, the authors did not investigate the effects of RV-to-LV timing on hemodynamics. In the present study, this interval was set at 0. Further studies should focus on this parameter. In conclusion, the authors found that RA-BiV pacing significantly improved hemodynamics compared with RA-RV pacing in the postoperative period after CABG surgery. This improvement is related to a restoration of LV synchronicity. This observation has potential clinical applications. Further studies are planned to test the ability of postoperative biventricular pacing to decrease the need for postoperative inotrope support that has been shown to be related to increased morbidity.36
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13. Penicka M, Bartunek J, De Bruyne B, et al: Improvement of left ventricular function after cardiac resynchronization therapy is predicted by tissue Doppler imaging echocardiography. Circulation 109:978-983, 2004 14. Suffoletto MS, Dohi K, Cannesson M, et al: Novel speckletracking radial strain from routine black-and-white echocardiographic images to quantify dyssynchrony and predict response to cardiac resynchronization therapy. Circulation 113:960-968, 2006 15. Cannesson M, Gostoli B, Rosamel P, et al: Successful cardiac resynchronization therapy after cardiac surgery. Anesth Analg 104:7174, 2007 16. Weisse U, Isgro F, Werling C, et al: Impact of atrio-biventricular pacing to poor left-ventricular function after CABG. Thorac Cardiovasc Surg 50:131-135, 2002 17. Fox DJ, Petkar S, Davidson NC, et al: Biventricular pacing in a patient with ventilatory and inotropic dependant heart failure following coronary artery bypass surgery. Europace 7:490-491, 2005 18. Pham PP, Balaji S, Shen I, et al: Impact of conventional versus biventricular pacing on hemodynamics and tissue Doppler imaging indexes of resynchronization postoperatively in children with congenital heart disease. J Am Coll Cardiol 46:2284-2289, 2005 19. Berberian G, Quinn TA, Kanter JP, et al: Optimized biventricular pacing in atrioventricular block after cardiac surgery. Ann Thorac Surg 80:870-875, 2005 20. Dzemali O, Bakhtiary F, Israel CW, et al: Impact of different pacing modes on left ventricular function following cardiopulmonary bypass. Thorac Cardiovasc Surg 56:87-92, 2008 21. Gaudiani VA, Castro LJ, Fisher AL: Biventricular pacing during cardiac operations. Heart Surg Forum 6:E126-E128, 2003 22. Vogel M, Schmidt MR, Kristiansen SB, et al: Validation of myocardial acceleration during isovolumic contraction as a novel noninvasive index of right ventricular contractility: Comparison with ventricular pressure-volume relations in an animal model. Circulation 105:1693-1699, 2002 23. Schiller NB, Shah PM, Crawford M, 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 2:358-367, 1989 24. Kanzaki H, Bazaz R, Schwartzman D, et al: A mechanism for immediate reduction in mitral regurgitation following cardiac resyn-
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chronization therapy: Insights from mechanical activation strain mapping. J Am Coll Cardiol 44:1619-1625, 2004 25. Linde C, Leclercq C, Rex S, et al: Long-term benefits of biventricular pacing in congestive heart failure: Results from the MUltisite STimulation in Cardiomyopathy (MUSTIC) study. J Am Coll Cardiol 40:111-118, 2002 26. Nelson GS, Berger RD, Fetics BJ, et al: Left ventricular or biventricular pacing improves cardiac function at diminished energy cost in patients with dilated cardiomyopathy and left bundle-branch block. Circulation 102:3053-3059, 2000 27. Pitzalis MV, Iacoviello M, Romito R, et al: Cardiac resynchronization therapy tailored by echocardiographic evaluation of ventricular asynchrony. J Am Coll Cardiol 40:1615-1622, 2002 28. Kanzaki H, Jacques D, Sade LE, et al: Regional correlation by color-coded tissue Doppler to quantify improvements in mechanical left ventricular synchrony after biventricular pacing therapy. Am J Cardiol 92:752-755, 2003 29. Dohi K, Pinsky MR, Kanzaki H, et al: Effects of radial left ventricular dyssynchrony on cardiac performance using quantitative tissue Doppler radial strain imaging. J Am Soc Echocardiogr 19:475482, 2006 30. Tops LF, Schalij MJ, Holman ER, et al: Right ventricular pacing can induce ventricular dyssynchrony in patients with atrial fibrillation
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after atrioventricular node ablation. J Am Coll Cardiol 48:1642-1648, 2006 31. Tops LF, Suffoletto MS, Bleeker GB, et al: Speckle-tracking radial strain reveals left ventricular dyssynchrony in patients with permanent right ventricular paing. J Am Coll Cardiol 50:1180-1188, 2007 32. Kindermann M, Hennen B, Jung J, et al: Biventricular versus conventional right ventricular stimulation for patients with standard pacing indication and left ventricular dysfunction: The Homburg Biventricular Pacing Evaluation (HOBIPACE). J Am Coll Cardiol 47:1927-1937, 2006 33. Flynn MJ, McComb JM, Dark JH: Temporary left ventricular pacing improves haemodynamic performance in patients requiring epicardial pacing postcardiac surgery. Eur J Cardiothorac Surg 28:250253, 2005 34. Cannesson M, Tanabe M, Suffoletto MS, et al: Velocity vector imaging to quantify ventricular dyssynchrony and predict response to cardiac resynchronization therapy. Am J Cardiol 98:949-953, 2006 35. Chung ES, Leon AR, Tavazzi L, et al: Results of the Predictors of Response to CRT (PROSPECT) trial. Circulation 117:2608-2616, 2008 36. Fellahi JL, Parienti JJ, Hanouz JL, et al: Perioperative use of dobutamine in cardiac surgery and adverse cardiac outcome: Propensity-adjusted analyses. Anesthesiology 108:979-987, 2008
dyssynchrony (13 ⴞ 12 to 80 ⴞ 25 milliseconds, p < 0.01). Biventricular pacing induced a significant increase in cardiac output (3.7 ⴞ 0.8 to 4.5 ⴞ 1.0 L/min, p < 0.01) and a significant decrease in left ventricular dyssynchrony compared with right ventricular pacing (80 ⴞ 25 to 21 ⴞ 16 milliseconds, p < 0.05). Conclusions: RA-BiV pacing improves cardiac output compared with RA-RV pacing in the postoperative period after coronary artery bypass graft surgery. This improvement is related to an improvement in left ventricular synchronicity. © 2009 Elsevier Inc. All rights reserved.
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surgery (1) RA-RV pacing induces a decrease in cardiac output (CO) compared with sinus rhythm (SR) and RA pacing alone, (2) RA-BiV pacing is able to improve CO compared with RA-RV pacing alone, and (3) these changes in CO are related to changes in LV synchronicity assessed by TDI.
ARDIAC RESYNCHRONIZATION THERAPY (CRT) (also called biventricular pacing) has been shown to improve mortality and morbidity in heart failure (HF) patients with abnormal electrical activation.1-3 Twenty percent of HF patients have left bundle-branch block (LBBB).4 In these patients, left ventricular (LV) dyssynchrony consists of an asynchronous contraction between the anteroseptum and the posterior, lateral, and inferior walls, resulting in impaired LV ejection fraction (LVEF).3,5 CRT improves symptoms and survival of these patients.1,2,6,7 Many studies have shown that LV dyssynchrony assessment using Tissue Doppler Imaging (TDI) is a better predictor of response to CRT than LBBB.8-14 Little is known about CRT in acute HF or in the postoperative period after cardiac surgery.15-17 Routinely, in cardiac surgical procedures, epicardial pacing leads are placed on the right atrium (RA) and right ventricle (RV) in case of significant bradycardia or the development of atrioventricular block. It has been reported previously that atrio-RV (RA-RV) pacing may induce LV dyssynchrony and hemodynamic compromise compared with atrial pacing (RA) alone.18 On the other hand, it has recently been suggested that atrio-biventricular (RA-BiV) pacing may improve hemodynamics in post– cardiac surgery patients.18-21 However, this conclusion is not clear in the clinical setting.22 The aims of this study were to test the hypotheses that in the postoperative period after coronary artery bypass graft (CABG)
From the Departments of *Anesthesiology and Intensive Care and †Cardiac Surgery, Hospices Civils de Lyon, Louis Pradel Hospital, Claude Bernard Lyon 1 University, Lyon, France. Address reprint requests to Maxime Cannesson, MD, Service d’Anesthésie Réanimation, Hôpital Cardiologique Louis Pradel, 200 Avenue du Doyen Lépine, 69500 Bron, France. E-mail: maxime_ [email protected] © 2009 Elsevier Inc. All rights reserved. 1053-0770/09/2303-0006$36.00/0 doi:10.1053/j.jvca.2008.12.007 306
KEY WORDS: cardiac surgery, dyssynchrony, hemodynamic, cardiac output, echocardiography, biventricular pacing, cardiac resynchronization therapy
MATERIALS AND METHODS The protocol was approved by the institutional review board for human subjects of the authors’ institution (Comité Consultatif de Protection des Personnes dans la Recherche Biomédicale Lyon B). All patients gave preoperative informed and written consent. Twenty-five consecutive patients undergoing CABG surgery (9 offpump and 16 using cardiopulmonary bypass [CPB]) were studied. These patients were selected prospectively and were included from November 1, 2007, to December 22, 2007. This group consisted of 17 men and 8 women between 33 and 83 years old (mean age ⫽ 68 ⫾ 12 years, mean height ⫽ 166 ⫾ 7 cm, and mean weight ⫽ 71 ⫾ 13 kg). Patients with cardiac arrhythmias, preoperative left bundle-branch block, postoperative inotropic support, and intracardiac shunt were excluded. Preoperative LVEF was between 30% and 70% (mean LVEF ⫽ 54% ⫾ 11%). QRS duration was ⬍120 milliseconds in all patients. None of the patients had undergone pacing before inclusion in the study. Only 1 surgeon was involved in the present study (FF). Patients had an 8-cm 5F tipped catheter (Arrow International Inc, Reading, PA) inserted in the left or right radial artery and a triplelumen 16-cm 8.5F central venous catheter (Arrow International Inc) inserted in the right internal jugular vein. Pressure transducers (Medex Medical Ltd, Lancashire, UK) were placed and maintained at the midaxillary line and kept at the atrial level throughout the study protocol. All transducers were zeroed to atmospheric pressure. Over the study period, 5 patients (all were CABG patients with CPB) were excluded because of poor echocardiographic images (n ⫽ 3, patients were intubated) and accidental removal of an epicardial pacing wire (n ⫽ 2). Ventilator settings were held constant throughout the study protocol. No intravascular volume expansion was allowed during the protocol. The study was performed in the intensive care unit within 4 hours after surgery. All patients were sedated with propofol (50 mg/h) and sufentanil (10 g/h). Temporary epicardial pacing leads were placed intraoperatively by one of the authors (FF) after the end of the surgical procedure and before CPB discontinuation. One active lead (Osypka TME 67V
Journal of Cardiothoracic and Vascular Anesthesia, Vol 23, No 3 (June), 2009: pp 306-311
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Fig 1. Positions of the temporary ventricular epicardial leads for pacing. One active lead was attached to the free wall of the left ventricle near the base between the left atrial appendage and the first marginal branch (LV lead), 1 lead was attached to the free wall of the RV on the diaphragmatic side (RV lead), 1 lead was attached to the right atrial appendage, and 2 leads were attached to the pericardium as neutral. SVC, superior vena cava; IVC, inferior vena cava; RA, right atrium; Ao, aorta; PA, pulmonary artery; RV, right ventricle; LV, left ventricle.
ref 45028; Osypka Medical GmbH, Berlin, Germany) was attached to the free wall of the left ventricle near the base between the left atrial appendage and the first marginal branch; 1 lead was attached to the free wall of the RV on the diaphragmatic side; 1 lead was attached to the right atrial appendage; and 2 leads were attached to the pericardium as neutral (Fig 1). The authors chose to locate the LV lead on the free wall of the left ventricle near the base between the left atrial appendage and the first marginal branch in order to have an electrical activation similar to those observed during CRT for chronic heart failure patients. A 12-lead electrocardiogram was obtained before pacing in order to measure heart rate (HR) and PR interval duration. Epicardial leads were connected to a temporary pacemaker (PACE 203H, Osypka Medical GmbH). Each patient was studied at 4 successive steps: (1) SR; (2) RA pacing using 1 atrial and 1 neutral (pericardial) lead; (3) RA-RV pacing using in addition to RA the RV lead as the active lead and the other pericardial lead as the neutral lead; and (4) RA-BiV pacing using, in addition to RA, RV and LV leads as active leads and 1 pericardial lead as the neutral lead. A 5-minute period of rest was observed between each pacing sequence. Pacing was performed at a rate between 5 and 10 beats/min faster than the intrinsic sinus rhythm. An atrioventricular delay during atrioventricular pacing was set in order to guarantee appropriate ventricular capture and in order to maximize the A wave obtained using conventional pulsed-wave Doppler from the mitral inflow on an apical 4-chamber view. The LV-to-RV delay was set at 0. At each step of the protocol the following parameters were recorded: HR; QRS duration; systolic, diastolic, and mean arterial pressures (MAP); central venous pressure; left ventricular end-diastolic volume (LVEDV)23; LVEF assessed by the biplane Simpson’s rule23; and the CO calculated by using the velocity time integral (VTI) obtained by transthoracic echocardiography (CV 70; Acuson-Siemens Corp, Mountain View, CA) from the apical 4-chamber view.23 Digital cineloops were obtained at frame rates of 30 to 90 Hz from apical 4-chamber views at a depth of 12 ⫾ 3 cm during apnea. The images were then exported to a personal computer and were analyzed offline by an observer blinded to the pacing modality. The LVEDV was measured at the onset of the QRS complex. The VTI was measured by a pulsedwave Doppler beam at the level of the LV outflow tract. The mean of 3 measurements was used. The aortic valve area was measured at
baseline and was considered constant throughout the protocol. The aortic valve area was calculated from the diameter of the aortic orifice measured at the insertion of the aortic cusp as: aortic valve area ⫽ ⫻ (aortic diameter/2)2. The stroke volume was calculated as: SV ⫽ aortic valve area ⫻ VTI of aortic blood flow. CO was calculated as: CO ⫽ stroke volume ⫻ HR. LV dyssynchrony was assessed using TDI. TDI was performed using the apical 4-chamber view for the long-axis motion of the left ventricle during apnea. A sample volume of 5 mm was positioned in the center of the analyzed segment (septal basal and lateral basal LV segments). The time resolution for tissue Doppler was 4 milliseconds. Gain setting and filters were set in order to optimize signal and reduce noise. Sweep speed was 150 mm/s. At least 5 beats were recorded, and the average value from 3 beats differing by less than 10% was used for statistical analysis. LV dyssynchrony was measured as the absolute difference in time-to-peak velocity (time delay between onset of the QRS and peak S-wave velocity) of LV opposing walls over the apical 4-chamber window8,9,13,14 (Fig 2). Echocardiographic analyses were performed by an operator blinded to the pacing protocol (EC). Data are presented as mean ⫾ standard deviation. Distribution normality was assessed by using the Kolmogorov-Smirnov test. Changes in hemodynamic and echocardiographic parameters induced by change in pacing protocol were then tested with analysis of variance for repeated measurements. If there were significant differences, post hoc testing was performed using the Tukey honest significant difference. The Pearson test was used to test linear correlation. Considering previously published results,15,19 power analysis showed that 25 patients were necessary to detect a 15% change in CO between RA-RV and RA-BiV pacing (5% type I error rate, 80% power, 2-tailed test, considering CO during RA-BiV pacing at 4.64 ⫾ 1.0 L/min). A p value ⬍0.05 was considered as statistically significant. All statistic analysis was performed by using SPSS 13.0 for Windows (SPSS Inc, Chicago, IL). RESULTS
Compared with SR, RA pacing alone induced no hemodynamic changes (Table 1). RA-RV pacing induced a significant decrease in MAP (from 89 ⫾ 11 to 78 ⫾ 9 mmHg, p ⬍ 0.001), CO (from 4.3 ⫾ 1.0 to 3.7 ⫾ 0.8 L/min, p ⬍ 0.001), LVEF
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Fig 2. A 2-dimensional gray apical 4-chamber view and LV basal septal and lateral tissue Doppler recordings. LV dyssynchrony was measured as the absolute difference in time-to-peak velocity (time delay between onset of the QRS and peak S-wave velocity) of LV opposing walls over the apical 4-chamber window.8,9,13,14 RA, right atrial; RV, right ventricular.
(from 47 ⫾ 5 to 39% ⫾ 5%, p ⬍ 0.001), and a significant increase in QRS duration (from 105 ⫾ 13 to 171 ⫾ 38 milliseconds, p ⬍ 0.001) compared with RA pacing alone (Table 1). RA-BiV pacing induced a significant increase in MAP (from 78 ⫾ 9 to 86 ⫾ 8 mmHg, p ⬍ 0.001) and CO (from 3.7 ⫾ 0.8 to 4.5 ⫾ 1.0 L/min), LVEF (from 39 ⫾ 5 to 49% ⫾ 5%) and a significant decrease in QRS duration (from 171 ⫾ 38 to 121 ⫾ 26 milliseconds, p ⬍ 0.001) compared with RA-RV pacing (Table 1). When RA-BiV pacing was compared with RA pacing alone, weak but significant differences in MAP (86 ⫾ 8 v 89 ⫾ 11 mmHg, respectively; p ⫽ 0.04), CO (4.5 ⫾ 1.0 v 4.3 ⫾ 1.0 L/min, respectively; p ⫽ 0.03), and QRS duration (121 ⫾ 26 v 105 ⫾ 13 milliseconds, respectively; p ⫽ 0.01) were observed (Table 1 and Figs 3 and 4). A change in pacing modality induced no changes in LVEDV and central venous pressure (Table 1).
Table 1. Changes in Hemodynamic Data Induced by Changes in Pacing Modality Sinus Rhythm
RA Pacing Alone
RA-RV Pacing
RA-BiV Pacing
Heart rate (beats/min) 81 ⫾ 12 85 ⫾ 14 86 ⫾ 13 86 ⫾ 13 MAP (mmHg) 91 ⫾ 13 89 ⫾ 11 78 ⫾ 9* 86 ⫾ 8†‡ CVP (mmHg) 10 ⫾ 4 9⫾4 10 ⫾ 4 10 ⫾ 4 LVEDV (mL) 92 ⫾ 21 98 ⫾ 29 98 ⫾ 40 104 ⫾ 31 CO (L/min) 4.3 ⫾ 0.9 4.3 ⫾ 1.0 3.7 ⫾ 0.8* 4.5 ⫾ 1.0†‡ QRS duration (ms) 104 ⫾ 15 105 ⫾ 13 171 ⫾ 38* 121 ⫾ 26†‡ LVEF (%) 48 ⫾ 4 47 ⫾ 5 39 ⫾ 5* 49 ⫾ 5† NOTE. Data are mean ⫾ standard deviation. Abbreviations: RA, right atrial; RV, right ventricular; BiV, biventricular; SAP, systolic arterial pressure; DAP, diastolic arterial pressure; MAP, mean arterial pressure; CVP, central venous pressure. *p ⬍ 0.05 RA-RV compared with RA pacing alone. †p ⬍ 0.05 RA-BiV compared with RA-RV pacing. ‡p ⬍ 0.05 RA-BiV compared with RA pacing alone.
Fig 3. Conventional aortic pulsed-wave Doppler recordings from an apical 4-chamber view obtained during RA-RV and RA-BiV pacing in an illustrative patient. A significant increase in velocity time integral in the RA-BiV pacing mode was observed. RA, right atrial; RV, right ventricular; BiV, biventricular.
Compared with SR, RA pacing alone induced no changes in LV dyssynchrony (Table 2). RA-RV pacing induced a significant increase in LV dyssynchrony compared with RA pacing alone (78 ⫾ 25 v 13 ⫾ 12 milliseconds, p ⬍ 0.001). RA-BiV pacing induced a significant decrease in LV dyssynchrony compared with RA-RV pacing (21 ⫾ 16 v 78 ⫾ 25 milliseconds, p ⬍ 0.001). When RA-BiV pacing was compared with RA pacing alone, the authors observed no significant difference in LV dyssynchrony (21 ⫾ 16 v 13 ⫾ 12 milliseconds, p ⫽ 0.19) (Fig. 4). DISCUSSION
This study shows that RA-RV pacing induces a decrease in CO compared with RA pacing and that RA-BiV pacing significantly improves CO compared with RA-RV pacing in the postoperative period after CABG surgery. This improvement is related to a restoration of LV synchronicity. The benefits of CRT are secondary to acute resynchronization of regional LV mechanics, a decrease in mitral regurgitation, and reverse remodeling that is a long-term effect of CRT.1,2,6,7,24,25 Moreover, CRT is able to improve contractility while decreasing myocardial oxygen consumption.26 Recently, TDI has been shown to be able to quantify LV dyssynchrony and to be a better predictor of response to CRT than LBBB.8-11,14,27,28 Although CRT has unambiguous indications in chronic HF patients, little is known about its efficiency in acute HF. Weisse et al16 have shown that atrio-biventricular pacing improves hemodynamics after CABG surgery compared with RA-RV pacing but did not assess LV dyssynchrony. Fox et al17 reported a successful CRT implantation in a patient with acute HF after CABG surgery. In this report, the authors had no echocardiography or Doppler analysis, and the decision to use CRT was based on QRS duration alone. The authors recently described a successful case of CRT after cardiac surgery in a patient with demonstrated LV dyssynchrony.15 In this case, the decision on CRT was based on echocardiographic LV dyssynchrony and the impossibility to wean the patient from dobutamine and mechanical ventilation.
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Fig 4. A 12-lead electrocardiogram of an illustrative patient during sinus rhythm, RA pacing, RA-RV pacing, and RA-BiV pacing. A narrow QRS during sinus rhythm and RA pacing and widened QRS during RA-RV pacing with an aspect of a left bundle-branch block were observed. QRS duration decreased during RA-BiV pacing compared with RA-RV pacing. RA, right atrial; RV, right ventricular; BiV, biventricular.
Recently published studies suggest that postoperative RABiV pacing is able to improve hemodynamics compared with RA-RV pacing.18-20 However, a recent study from Vogel et al22 found that pacing modality (RA-RV, RA-BiV, RA alone, and SR) had no impact on CO and LV contractility in patients undergoing cardiac surgery. In this study, patients presented with a baseline LVEF ⬍35% and a QRS duration ⬎120 milliseconds. The authors observed no changes in QRS duration between SR, RA alone, and RA-BiV pacing modalities, suggesting that resynchronization objectives may not have been reached. Moreover, these data should be compared with previously published results showing that LV dyssynchrony induced by RV pacing is augmented in case of impaired ventricular function.29 It would have been interesting to study mechanical dyssynchrony in this study in order
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to further explore the relationship between dyssynchrony, CO, and LV contractility. RV pacing is able to induce LV dyssynchrony and decrease CO and LVEF.30,31 In chronic HF patients, RV pacing has even been shown to increase the risk of death or acute HF hospitalization. Several studies suggest that biventricular pacing has the ability to reverse the abnormal activation pattern induced by RV pacing and to restore hemodynamics.32 The present results support this hypothesis by describing the acute deleterious effect of RV pacing on CO. This effect seems to be related only to LV dyssynchrony induced by this pacing mode. By performing RA-BiV pacing, the authors were able to restore LV synchronicity and significantly increase CO. The authors found that RA-BiV pacing was able to weakly but significantly increase CO compared with RA pacing alone. This observation may be related only to the slight increase in HR necessary to guarantee atrial capture. However, this could be important because this pacing mode could be used in order to increase CO by increasing HR in patients presenting with circulatory failure. A recent study by Dzemali et al20 found similar results in patients with a dilated left ventricle but also in some patients with normal LV function. This hypothesis requires further exploration. In the present study, the authors chose to exclude patients requiring postoperative inotropic support in order to focus on the physiology of RA-BiV pacing in this setting. Further studies should assess the ability of RA-BiV pacing to decrease the need for inotropic support in the postoperative period after cardiac surgery. This alternative seems very attractive because RA-BiV13 pacing is able to increase contractility while decreasing myocardial oxygen consumption.26 The present data are supported by a recent study by Dzemali et al20 showing that RA-BiV pacing is able to improve cardiac output and decrease myocardial oxygen consumption after cardiopulmonary bypass. Consequently, it may have significant clinical impact in patients undergoing CABG surgery. STUDY LIMITATIONS
The authors did not perform RA-LV pacing. However, recent studies suggest that RA-LV pacing can increase CO.33 This pacing modality may be interesting because it requires fewer epicardial leads than RA-BiV pacing and thus may decrease the rate of potential mechanical complications re-
Table 2. Changes in LV Dyssynchrony Analysis Induced by Changes in Pacing Modality Sinus Rhythm
RA Pacing Alone
RA-RV Pacing
RA-BiV Pacing
Time-to-peak velocity Basal septal (ms) 180 ⫾ 27 182 ⫾ 27 184 ⫾ 58 224 ⫾ 44†‡ Basal lateral (ms) 186 ⫾ 27 188 ⫾ 25 229 ⫾ 52* 230 ⫾ 55‡ LV dyssynchrony (ms) 12 ⫾ 10 13 ⫾ 12 78 ⫾ 25* 21 ⫾ 16† NOTE. Data are mean ⫾ standard deviation. Abbreviations: RA, right atrial; RV, right ventricular; BiV, biventricular. *p ⬍ 0.05 RA-RV compared with RA pacing alone. †p ⬍ 0.05 RA-BiV compared with RA-RV pacing. ‡p ⬍ 0.05 RA-BiV compared with RA pacing alone.
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lated to lead application or removal. Further studies are required to test and confirm this hypothesis. Moreover, further studies should randomize the pacing protocol. In the present study, the authors used conventional tissue Doppler imaging and only assessed longitudinal dyssynchrony. Recent studies suggest that newer technologies such as velocity vector imaging,34 tissue synchronization imaging,9 and radial dyssynchrony assessment using speckle-tracking radial strain14 may be useful to predict response to CRT. However, conventional TDI has been described as accurate for LV dyssynchrony analysis,13 and recent data suggest that no approach is better than the others.35 Because the present study was performed in the postoperative period after cardiac surgery, the authors cannot exclude that tethering of the interventricular septum wall occurred in some patients and that this may have interfered with the dyssynchrony analysis. However, the authors observed an increase in LV dyssynchrony during RA-RV pacing compared with RA pacing and a decrease in LV dyssynchrony during RA-BiV pacing
compared with RA-RV pacing in every patient. Thus, it is more likely that tethering did not impact the final results. All pacing modes were set at a rate higher than the sinus rhythm. Theoretically, this higher rate could have induced reduced filling and thus could explain differences between right atrial pacing and sinus rhythm. Finally, the authors did not investigate the effects of RV-to-LV timing on hemodynamics. In the present study, this interval was set at 0. Further studies should focus on this parameter. In conclusion, the authors found that RA-BiV pacing significantly improved hemodynamics compared with RA-RV pacing in the postoperative period after CABG surgery. This improvement is related to a restoration of LV synchronicity. This observation has potential clinical applications. Further studies are planned to test the ability of postoperative biventricular pacing to decrease the need for postoperative inotrope support that has been shown to be related to increased morbidity.36
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