Ann Thorac Surg 2005;79:517-520
© 2005 The Society of Thoracic Surgeons
Original article: Cardiovascular
Evaluation of Ventral Cardiac Denervation As a Prophylaxis Against Atrial Fibrillation After Coronary Artery Bypass Grafting
Joseph Alex, MD, MRCS*,
Levent Guvendik, MD, FRCS, FETCS
Department of Cardiothoracic Surgery, Castle Hill Hospital, Hull, United Kingdom
Accepted for publication August 4, 2004.
* Address reprint requests to Dr Alex, The Cottage, Main Road, Covenham, St Bartholomew, Louth, LN11 0PF, UK (E-mail: mrjosephalex{at}yahoo.co.uk).
 |
Abstract
|
|---|
BACKGROUND: To evaluate the efficacy of ventral cardiac denervation as a prophylaxis against post-coronary artery bypass grafting (CABG) atrial fibrillation (AF).
METHODS: Seventy consecutive patients who underwent CABG (group A) were compared to 70 consecutive subsequent patients who underwent CABG + ventral cardiac denervation (group B). Both groups were well-matched for age, gender, disease severity, LV function, Euro scores, Parsonnet scores, preoperative ß-blockers, Ca-channel blockers, digoxin, and angiotensin converting enzyme inhibitors. The same cardioplegia, bypass, and operation techniques were used in all cases. Denervation before initiating bypass increased operation time by approximately 5 minutes. Heart rate and rhythm were monitored by continuous telemetry until postoperative day 5 and then 4- hourly until discharge.
RESULTS: The cross-clamp time (p = 0.6), bypass time (p = 0.1), number of grafts (p = 0.9), inotrope usage (p = 0.4), reexploration rate (p = 1), postoperative myocardial infarction (none in either group), blood loss (p = 0.7), and length of stay (p = 0.8) were comparable in both groups. There was no significant difference in the incidence of AF; 34% in group A versus 29% in group B (p = 0.3).
CONCLUSIONS: Ventral cardiac denervation failed to significantly reduce the incidence of AF following coronary revascularization in our study.
|
Introduction
|
|---|
With an incidence ranging from 5% to 40%, atrial fibrillation (AF) after coronary artery bypass grafting (CABG) continues to remain one of its most common complications. Atrial fibrillation can significantly increase postoperative morbidity, prolong hospital stay, and resource utilization [1–11]. Furthermore, the risk of hemodynamic instability and thromboembolic complications necessitate the initiation of antiarrhythmic and anticoagulant therapy. Despite this, the precise mechanism of postbypass AF is still not completely understood and pharmacologic and surgical methods of prophylaxis continues to be evaluated. Recently Melo and colleagues [12, 13] published the results of their multicenter randomized trial in which they found ventral cardiac denervation to be an effective prophylaxis against post-CABG AF. We present the results of our study to assess the efficacy of this technique.
|
Material and Methods
|
|---|
The study was approved by the local regional ethics committee and informed consent was obtained from the patients. Prospectively collected data of 70 consecutive, elective, first-time CABG patients (group A) was compared to a subsequent group of 70 consecutive, elective, first-time CABG patients who also underwent ventral cardiac denervation (VCD) (group B). Emergency, urgent, expedited, redo cases and patients with a history of AF, were not included. Categorical data were analyzed using the 
2 test and Fisher's test while the Student's t test was used for numerical data. Statistical significance was set at p less than or equal to 0.05. The SPSS version 11.0 for windows program (SPSS Inc, Chicago, IL) was used for statistical analysis.
All operations were performed by the same surgeon using antegrade-retrograde cold St Thomas blood cardioplegia. The anesthetic technique including premedication, induction, maintenance, and reversal of anesthesia were essentially similar in both groups. Ventral cardiac denervation before initiating bypass increased operation time by about 5 minutes. The VCD was achieved by excising the adventitia and periadventitial fat using normal surgical scissors and forceps without diathermy cauterization. The excision was performed in a circumferential manner starting from around the superior vena cava, then around the ascending aorta, and finally around the pulmonary artery (Fig 1). The minimum width of the excision was 0.5 cm.
Following this, standard cardiopulmonary bypass was established between the right atrium and ascending aorta using a Stockert SIII roller pump bypass machine (Stockert Instrumente GmbH, Munchen, Germany). Moderate systemic hypothermia 32 to 33°C was maintained during bypass in all cases. Antegrade-retrograde cold St Thomas blood cardioplegia was used for myocardial protection in all cases. Systemic rewarming was commenced during the final distal anastomosis and weaning from the bypass machine was attempted when the nasopharyngeal temperature reached 36°C.
All patients had high resolution continuous recordable telemetry (Fukuda Denshi HR500 DS5800N, Tokyo, Japan) electrocardiographic monitoring starting from the operating room until the fifth postoperative day. Following day 5, patients were monitored every 4 hours until discharge. Patients who had been on ß-blockers, calcium (Ca2+) channel blockers, angiotensin converting enzyme (ACE) inhibitors, or digoxin preoperatively were commenced on half the dose 48 hours after the operation and the dosage increased to preoperative levels when clinically indicated. None of the patients were given pharmacoprophylaxis to prevent AF. As per the protocol followed in our unit, we try to maintain serum potassium (K+) level between 4.5 to 5 meq/Lt, serum magnesium (Mg2+) level between 1.5 to 2 meq/Lt, partial pressure of arterial oxygen (PaO2) greater than 80 mm Hg, and partial pressure of arterial carbon dioxide (PaCO2) less than 40 mm Hg in all patients. Intraoperatively, AF was treated by correcting serum K+, Mg2+, PaO2, and PaCO2 followed by synchronized direct current (DC) cardioversion. Postoperatively, serum K+, Mg2+, PaO2, and PaCO2 were checked during each episode of AF and corrected before initiating further treatment. Patients who were hemodynamically stable were treated with intravenous amiodarone or sotalol, and warfarin. In addition, digoxin, ß-blockers or synchronized DC cardioversion was used if ventricular rate control was not achieved within 48 hours of initiating therapy. Immediate DC cardioversion was performed in patients who were hemodynamically unstable. Rate-controlled stable patients who failed to respond to 6 weeks of pharmacotherapy, underwent elective DC cardioversion with transesophageal echocardiograpy, to rule out intraatrial thrombus, before the procedure.
|
Results
|
|---|
Both groups were well-matched preoperatively (Table 1) in terms of, age, gender, Canadian Cardiovascular Society angina class, New York Heart Association heart failure class, angiographic coronary disease severity, left ventricular function, previous myocardial infarction, diabetes mellitus, hypertension, chronic obstructive pulmonary disease, renal dysfunction, Parsonnet score, Euro scores, preoperative ß-blockers, calcium-channel-blockers, ACE inhibitors, and digoxin. The cross-clamp time, bypass time, number of grafts, inotrope usage, reexploration rate, blood loss, and length of stay were comparable in both groups (Table 2). There was no operative mortality in either group. We found no statistically significant difference in the incidence of AF between the two groups; 34% in group A and 29% in group B (p = 0.3), respectively.
|
Comment
|
|---|
Though the majority of the cardiac autonomic nerves traverse the periadventitial connective tissue and fat pad surrounding the aortic root, superior vena cava, and the pulmonary artery to reach the heart, a lesser but significant amount of autonomic nerves reach the heart along the pulmonary veins and inferior vena cava, as branches from the tracheoesophageal autonomic supply and direct branches from thoracic segments [14, 15]. The electrophysiological characteristics of atrial cells, action potential duration, refractoriness, and conduction speed, are all modulated differently by sympathetic and parasympathetic influences. Sympathetic stimulation increases the heart rate, while the parasympathetic (vagus) slows the rate. Both innervate the sinoatrial node, atrioventricular node, and atrium. Normally there is a higher vagal tone at rest with the sympathetic tone and adrenal medullary output increasing in response to stress. Thus the clinical pattern of vagus mediated paroxysmal AF is more commonly observed in the absence of detectable heart disease, while sympathetic mediated sustained AF is more commonly observed in the presence of underlying heart disease. The vagus, due to its patchy innervation of the atria, favors macro re-entry. Fluctuating autonomic tone, with a primary increase in adrenergic tone followed by an abrupt shift towards vagal predominance, has been noted during paroxysms of AF [16–20]. Similarly a loss of vagal tone and an increase in sympathetic tone is observed before the onset of AF after bypass surgery [21].
In the predominantly elderly group of patients who undergo coronary bypass surgery, age-related structural changes such as dilatation, hypertrophy, fibrosis, and senile amyloidosis occur in varying severity within the atrium. This heterogenous myocardium, on being subjected to the operative trauma and subsequent inflammatory infiltration, becomes a mosaic of refractory periods and conduction velocities. Fluctuating autonomic tone further predisposes this susceptible myocardium to ectopic activity, reentry circuits, and AF. The aim of performing VCD is to reduce locally this fluctuation in autonomic tone, which facilitates the generation and maintenance of AF. The objective of surgical and catheter ablation techniques to treat AF is to achieve a blockade of aberrant and reentry circuits by what is essentially, partial autotransplantation and partial autonomic denervation [22–27].
In contrast to the findings of Melo and colleagues [14, 15], despite the younger age of our patients, VCD failed to significantly reduce the incidence of AF. Unlike the single myocardial protection technique (antegrade-retrograde cold blood cardioplegia) we used, different techniques (crystalloid or blood cardioplegia, with or without hypothermia and off-pump cases) were used in their study. This in effect reduced the benefit of the greater number of patients they analyzed. Post-CABG AF is paroxysmal in a large proportion of patients and does not always give rise to clinical symptoms. All patients in our study had continuous telemetry monitoring until the fifth postoperative day compared to the 34% in their study who were again only monitored until the fourth postoperative day. The higher overall incidence of AF in our study was a manifestation of the higher detection rate. As previously mentioned [14, 15], anatomically the route taken by autonomic nerves to the heart is highly variable. The actual denervation achieved in each patient is neither quantitatively nor qualitatively comparable, unless the innervation is mapped out before denervation and a histologic analysis carried out on the excised tissue. The main limitation of our study is the comparatively smaller number of patients in each group and the potential risk of type-II error. However, this risk is offset to an extent by two factors. First, we standardized variable factors such as surgeon, surgical technique, method of myocardial protection, and AF detection technique. Second, our AF detection rate was much higher. Another limitation, applicable to both studies, is that though the autonomic neuronal pathway to the heart has been anatomically delineated and described, we did not perform histologic analysis of the excised fat pad. Thus we may have included a proportion of patients with anatomic variations in their autonomic innervation in our studies. Given these limitations, the result of our study fails to support the observation by Melo and colleagues [14, 15] on the effectiveness of ventral cardiac denervation in reducing the incidence of post-CABG AF.
|
References
|
|---|
- Cox JL. A perspective of postoperative atrial fibrillation in cardiac operations Ann Thorac Surg 1993;56:405-409.[Medline]
- Willems S, Weiss C, Meinertz T. Tachyarrhythmias following coronary artery bypass graft surgery: epidemiology, mechanisms, and current therapeutic strategies J Thorac Cardiovasc Surg 1997;45:232-237.
- Alamassi GH, Showalter T, Nicolosi AC, et al. Atrial fibrillation after cardiac surgery Ann Surg 1997;226:501-513.[Medline]
- Aranki SF, Shaw DP, Adams DH, et al. Predictors of atrial fibrillation after coronary artery surgeryCurrent trends and impact on hospital resources. Circulation 1996;94:390-397.[Abstract/Free Full Text]
- Creswell LL, Schuessler RB, Rosenbloom M, Cox JL. Hazards of postoperative atrial arrhythmias Ann Thorac Surg 1993;56:539-549.[Abstract]
- Frost L, Molgaard H, Christiansen EH, et al. Atrial fibrillation and flutter after coronary artery bypass surgery: epidemiology, risk factors and preventive trials Int J Cardiol 1992;36:253-261.[Medline]
- Matthew JP, Parks R, Savino JS, et al. Atrial fibrillation following coronary artery bypass graft surgery: predictors, outcomes, and resource utilization Multicenter study of perioperative ischemia research group. JAMA 1996;276:300-306.
- Reddy S, Young B, Xue Q, et al. Review of methods to predict and detect atrial fibrillation in post-cardiac surgery patients J Electrocardiol 1999;32(suppl):23-28.
- Ducceschi V, D'Andrea A, Liccardo B, et al. Perioperative clinical predictors of atrial fibrillation occurrence following coronary artery surgery Eur J Cardiothorac Surg 1999;16:435-439.[Abstract/Free Full Text]
- Hravanak M, Hoffman LA, Saul MI, Zullo TG, Whitman GR. Resource utilization related to atrial fibrillation after coronary artery bypass grafting Am J Crit Care 2002;11:228-238.[Abstract/Free Full Text]
- Veledar E, Thompson T, Mahoney E, et al. Predictors of atrial fibrillation following open heart surgery: implications for cost-effective targeted, preventive therapy J Am Coll Cardiol 2001;37(suppl A):493A.
- Melo J, Voigt P, Sonmez B, et al. Ventral cardiac denervation reduces the incidence of atrial fibrillation after coronary artery bypass grafting J Thorac Cardiovasc Surg 2004;127:511-515.[Abstract/Free Full Text]
- Melo J, Ferreira MM, Abecassis M, et al. Partial cardiac denervation reduces the incidence of atrial fibrillation after coronary revascularization. Paper presented at the 82nd Meeting of The American Association for Thoracic Surgery, Washington DC, May 5–8, 2002..
- Pauza D, Skripa V, Pauzienne N, Stropus R. Morphology, distribution and variability of the epicardial neural subplexus in the human heart Anat Rec 2000;259:353-382.[Medline]
- Gray H, Bannister LH, Berry MM, Williams PL. Gray's anatomy: the anatomical basis of medicine and surgeryLondon, UK: Churchill Livingstone; 1995.
- Bettoni M, Zimmermann M. Autonomic tone variations before the onset of paroxysmal atrial fibrillation Circulation 2002;105:2753-2759.[Abstract/Free Full Text]
- Schauerte P, Scherlag BJ, Patterson E, et al. Focal atrial fibrillation: experimental evidence for a pathophysiologic role of the autonomic nervous system J Cardiovasc Electrophysiol 2001;12:592-599.[Medline]
- Takei M, Tsuboi M, Usui T, et al. Vagal stimulation prior to atrial rapid pacing protects the atrium from electrical remodelling in anesthetised dogs Jpn Circ J 2001;65:1077-1081.[Medline]
- Zimmermann M, Kalusche D. Fluctuation in autonomic tone is a major determinant of sustained atrial arrhythmias in patients with focal ectopy originating from the pulmonary veins J Cardiovasc Electrophysiol 2001;12:285-291.[Medline]
- Kanoupakis EM, Manios EG, Mavrakis HE, et al. Relation of autonomic modulation to recurrence of atrial fibrillation following cardioversion Am J Cardiol 2000;86:954-958.[Medline]
- Dimmer C, Tavernier R, Gjorgov N, et al. Variations in autonomic tone preceding onset of atrial fibrillation after coronary artery bypass grafting Am J Cardiol 1998;82:22-25.[Medline]
- Cox JL, Schuesseler RB, Agostino Jr HR, et al. The surgical treatment of atrial fibrillationIII. Development of a definitive surgical procedure. J Thorac Cardiovasc Surg 1991;101:569-583.[Abstract]
- Cox JL, Jaquiss RDB, Schuessler RB, Boineau JP. Modification of the maze procedure for atrial flutter and atrial fibrillationII. Surgical technique of the maze III procedure. J Thorac Cardiovasc Surg 1995;110:485-495.
- Vogt PR, Brunner La Rocca HP, Candinas J, et al. Temporary loss of cardiac autonomic innervation after the maze procedure Eur J Cardiothorac Surg 1997;12:75-81.[Abstract]
- Pasic M, Musci M, Siniawski H, et al. The Cox-maze III procedure: parallel normalization of sinus node dysfunction, improvement of atrial function, and recovery of the cardiac autonomic nervous system J Thorac Cardiovasc Surg 1999;118:287-296.[Abstract/Free Full Text]
- Schauerte P, Scherlag BJ, Pitha J, et al. Catheter ablation of cardiac autonomic nerves for prevention of vagal atrial fibrillation Circulation 2000;102:2774-2780.[Abstract/Free Full Text]
- Douglas Jr JM, Swain ME, Slotkin TA, et al. Cryosurgical denervation of the heart: acute and chronic effects J Thorac Cardiovasc Surg 1990;100:198-209.[Abstract]
This article has been cited by other articles:
|
|
|
|
 
F. Onorati, A. Curcio, G. Santarpino, D. Torella, P. Mastroroberto, L. Tucci, C. Indolfi, and A. Renzulli
Routine ganglionic plexi ablation during Maze procedure improves hospital and early follow-up results of mitral surgery.
J. Thorac. Cardiovasc. Surg.,
August 1, 2008;
136(2):
408 - 418.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Dunning, T. Treasure, M. Versteegh, S. A.M. Nashef, and on behalf of the EACTS Audit and Guidelines Commit
Guidelines on the prevention and management of de novo atrial fibrillation after cardiac and thoracic surgery
Eur. J. Cardiothorac. Surg.,
December 1, 2006;
30(6):
852 - 872.
[Full Text]
[PDF]
|
|
|
Top
Abstract
Introduction
