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Atrial fibrillation after coronary artery bypass graft surgery
Journal of Electrocardiology 39 (2006) 55 – 56 www.elsevier.com/locate/jelectrocard
Editorial
Atrial fibrillation after coronary artery bypass graft surgery Understanding disease mechanisms forms the basis for successful therapy. Such was the case with the surgical maze procedure [1] for treatment of atrial fibrillation (AF) that was based on Moe’s multi-wavelet reentry theory of AF [2]. Catheter ablation of pulmonary vein foci or pulmonary vein isolation as treatment for AF is based on the information that premature atrial contractions (PACs) trigger the onset of AF and that the predominant sites of PACs that initiate AF arise from the pulmonary veins [3]. The mechanism(s) of AF that occurs after coronary artery bypass graft surgery (CABG) is not well understood. In this issue, Jideus et al [4] documented that most episodes of AF after CABG are initiated by a PAC. They performed serial Holter recordings in 109 patients in the first few days after CABG. In 41 patients who developed AF, a PAC was the initiating event in 31 (81%). In a small pilot study, we recorded biatrial electrograms in 21 patients after CABG [5]. There were 39 episodes of atrial arrhythmias that occurred in 7 patients, all were induced by PACs. Whereas a right or left atrial PAC origin was observed in 26 episodes of atrial flutter, a left atrial PAC origin only was observed in all 13 episodes of AF. The precise site of origin of these PACs from the left atrium is unclear but may include the pulmonary veins and/or the ligament of Marshall. The latter has recently been shown to be a source of isoproterenol-sensitive atrial tachyarrhythmias [6]. That the posterior left atrial region (pulmonary veins or ligament of Marshall) is a site of origin of PACs inducing AF is supported by the observation that AF is very rare after heart transplantation because the left atrial anastomosis isolates the posterior atrium [7]. Because not all PACs induce AF, there must be a suitable anatomic or electrophysiological substrate able to maintain AF. It is well known that the incidence of AF after CABG increases with age and this likely reflects increased atrial fibrosis in the elderly [8]. Other possible factors may be inflammation of the atria due to post operative pericarditis. In a recent study in dogs [9] undergoing right atriotomy, inhomogeneity of atrial conduction and inducibility of AF after cardiac surgery were correlated with the degree of the inflammatory response. Therapy with methylprednisolone (2 mg/kg per day; 1 week preoperative and 3 days postoperative) reduced atrial conduction abnormality and inducibility of AF. The effect of steroid use for prevention 0022-0736/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2005.08.008
of postoperative AF in humans is controversial [10,11]. Recently, the human consumption of fish, resulting in an increased plasma concentration of N-3 polyunsaturated fatty acids (PUFA), has been associated with a lower incidence of AF [12]. Calo et al [13] randomized 160 patients undergoing CABG to pretreatment with PUFA or placebo. Those receiving PUFA had a significant reduction of postoperative AF (33% vs 15%), an effect that was independent of the use of b-blocker therapy. This may be due to the antiinflammatory or antiarrhythmic effects of PUFA. After bypass surgery, there is an increase in sympathetic tone. The well-established therapeutic effects of b-blocker to decrease the incidence of AF after CABG are consistent with sympathetic stimulation as a factor for postoperative AF [14]. The observation by Jideus et al [4] that they could not document a change in autonomic tone before AF onset, as assessed by lack of decrease in heart rate variability, may be due to the already high level of sympathetic tone that exists after CABG. A recent, small, well-designed randomized study (n = 55) points to the importance of the anterior epicardial fat pad in the pathogenesis of AF after CABG [15]. This fat pad is located between the aorta and pulmonary artery and frequently excised at time of surgery. It is a site of parasympathetic ganglia as confirmed by sinus node slowing during fat pad stimulation in this study. Patients randomized to preservation of the fat pad had a significantly lower incidence of AF (7%) vs those randomized to fat pad removal (33%). Thus, it appears that imbalance in sympathetic/vagal tone contributes to AF after surgery. The evidence for PACs as triggers for AF after bypass surgery is mounting; however, the exact site of origin of such PACs is not known. The latter would be a prerequisite for any targeted therapy, such as intraoperative PAC focus ablation. To sustain AF, a suitable substrate is necessary. This substrate is likely multifactorial and includes preexisting atrial fibrosis and transient electrophysiological abnormalities due to altered sympathetic/vagal tone and/or atrial myocardial inflammation. The presence or absence of a suitable substrate likely explains why some PACs induce AF whereas most PACs do not. Further knowledge of PAC origin and factors that increase the frequency of PACs may open the door to targeted perioperative therapy and reduce
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Editorial / Journal of Electrocardiology 39 (2006) 55 – 56
AF triggers, thereby reducing the common complication of AF after CABG. Peter Ott, MD Frank I. Marcus, MD Department of Internal Medicine Sarver Heart Center University of Arizona Health Sciences Center Tucson, AZ 85724, USA E-mail address: [email protected] References [1] Cox JL, Boineau JP, Schuessler RB, et al. Five year experience with the maze procedure for atrial fibrillation. Ann Thorac Surg 1993;56:814. [2] Moe GK, Abildskov JA. Atrial fibrillation as a self-sustaining arrhythmia independent of focal discharge. Am Heart J 1959;58:59. [3] Haissaguerre M, Jais P, Shah D, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med 1998;339:659. [4] Jideus L, Kesek M, Joachimson PO, et al. The role of atrial premature contractions as the main triggers of post operative atrial fibrillation. J Electrocardiol 2006;39. [5] Ott P, Massumi A, Duncan M, et al. Atrial arrhythmias after cardiac surgery: analysis of bi-atrial recordings. PACE 2000;23 part II(abst):736.
[6] Doshi RN, Wu TJ, Yashima M, et al. Relation between ligament of Marshall and adrenergic atrial tachyarrhythmia. Circulation 1999; 100:876. [7] Landolina M, Petracci B, Gaetano MF, et al. Atrial arrhythmias: prevalence in heart transplant patients. Heart Rhythm 2005;2(abstr):S2. [8] Mathew JP, Fontes ML, Tudor IC, et al. A multicenter risk index for atrial fibrillation after cardiac surgery. JAMA 2004;291:1720. [9] Ishii Y, Schuessler RB, Gaynor LG, et al. Inflammation of atrium after cardiac surgery is associated with inhomogeneity of atrial conduction and atrial fibrillation. Circulation 2005;111:2881. [10] Yared JP, Starr NJ, Torres FK, et al. Effects of single dose postinduction dexamethasone on recovery after surgery. Ann Thorac Surg 2000;69:1420. [11] Halvorsen P, Raeder J, White PF, et al. The effect of dexamethasone on side effects after coronary revascularization procedures. Anesth Analg 2003;189:153. [12] Mozaffarian D, Psaty BM, Rimm EB, et al. Fish intake and risk of incident of atrial fibrillation. Circulation 2004;110:368. [13] Calo L, Bianconi L, Colivicchi F, et al. N-3 fatty acids for the prevention of atrial fibrillation after coronary artery bypass surgery. J Am Coll Cardiol 2005;45:1723. [14] Crystal E, Connolly SJ, Sleik K, et al. Interventions on prevention of post operative atrial fibrillation in patients undergoing heart surgery. A meta-analysis. Circulation 2002;106:75. [15] Cummings JE, Gill J, Akhras R, et al. Preservation of the anterior fat pad paradoxically decreases the incidence of post operative atrial fibrillation in humans. J Am Coll Cardiol 2004;43:994.
Editorial
Atrial fibrillation after coronary artery bypass graft surgery Understanding disease mechanisms forms the basis for successful therapy. Such was the case with the surgical maze procedure [1] for treatment of atrial fibrillation (AF) that was based on Moe’s multi-wavelet reentry theory of AF [2]. Catheter ablation of pulmonary vein foci or pulmonary vein isolation as treatment for AF is based on the information that premature atrial contractions (PACs) trigger the onset of AF and that the predominant sites of PACs that initiate AF arise from the pulmonary veins [3]. The mechanism(s) of AF that occurs after coronary artery bypass graft surgery (CABG) is not well understood. In this issue, Jideus et al [4] documented that most episodes of AF after CABG are initiated by a PAC. They performed serial Holter recordings in 109 patients in the first few days after CABG. In 41 patients who developed AF, a PAC was the initiating event in 31 (81%). In a small pilot study, we recorded biatrial electrograms in 21 patients after CABG [5]. There were 39 episodes of atrial arrhythmias that occurred in 7 patients, all were induced by PACs. Whereas a right or left atrial PAC origin was observed in 26 episodes of atrial flutter, a left atrial PAC origin only was observed in all 13 episodes of AF. The precise site of origin of these PACs from the left atrium is unclear but may include the pulmonary veins and/or the ligament of Marshall. The latter has recently been shown to be a source of isoproterenol-sensitive atrial tachyarrhythmias [6]. That the posterior left atrial region (pulmonary veins or ligament of Marshall) is a site of origin of PACs inducing AF is supported by the observation that AF is very rare after heart transplantation because the left atrial anastomosis isolates the posterior atrium [7]. Because not all PACs induce AF, there must be a suitable anatomic or electrophysiological substrate able to maintain AF. It is well known that the incidence of AF after CABG increases with age and this likely reflects increased atrial fibrosis in the elderly [8]. Other possible factors may be inflammation of the atria due to post operative pericarditis. In a recent study in dogs [9] undergoing right atriotomy, inhomogeneity of atrial conduction and inducibility of AF after cardiac surgery were correlated with the degree of the inflammatory response. Therapy with methylprednisolone (2 mg/kg per day; 1 week preoperative and 3 days postoperative) reduced atrial conduction abnormality and inducibility of AF. The effect of steroid use for prevention 0022-0736/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2005.08.008
of postoperative AF in humans is controversial [10,11]. Recently, the human consumption of fish, resulting in an increased plasma concentration of N-3 polyunsaturated fatty acids (PUFA), has been associated with a lower incidence of AF [12]. Calo et al [13] randomized 160 patients undergoing CABG to pretreatment with PUFA or placebo. Those receiving PUFA had a significant reduction of postoperative AF (33% vs 15%), an effect that was independent of the use of b-blocker therapy. This may be due to the antiinflammatory or antiarrhythmic effects of PUFA. After bypass surgery, there is an increase in sympathetic tone. The well-established therapeutic effects of b-blocker to decrease the incidence of AF after CABG are consistent with sympathetic stimulation as a factor for postoperative AF [14]. The observation by Jideus et al [4] that they could not document a change in autonomic tone before AF onset, as assessed by lack of decrease in heart rate variability, may be due to the already high level of sympathetic tone that exists after CABG. A recent, small, well-designed randomized study (n = 55) points to the importance of the anterior epicardial fat pad in the pathogenesis of AF after CABG [15]. This fat pad is located between the aorta and pulmonary artery and frequently excised at time of surgery. It is a site of parasympathetic ganglia as confirmed by sinus node slowing during fat pad stimulation in this study. Patients randomized to preservation of the fat pad had a significantly lower incidence of AF (7%) vs those randomized to fat pad removal (33%). Thus, it appears that imbalance in sympathetic/vagal tone contributes to AF after surgery. The evidence for PACs as triggers for AF after bypass surgery is mounting; however, the exact site of origin of such PACs is not known. The latter would be a prerequisite for any targeted therapy, such as intraoperative PAC focus ablation. To sustain AF, a suitable substrate is necessary. This substrate is likely multifactorial and includes preexisting atrial fibrosis and transient electrophysiological abnormalities due to altered sympathetic/vagal tone and/or atrial myocardial inflammation. The presence or absence of a suitable substrate likely explains why some PACs induce AF whereas most PACs do not. Further knowledge of PAC origin and factors that increase the frequency of PACs may open the door to targeted perioperative therapy and reduce
56
Editorial / Journal of Electrocardiology 39 (2006) 55 – 56
AF triggers, thereby reducing the common complication of AF after CABG. Peter Ott, MD Frank I. Marcus, MD Department of Internal Medicine Sarver Heart Center University of Arizona Health Sciences Center Tucson, AZ 85724, USA E-mail address: [email protected] References [1] Cox JL, Boineau JP, Schuessler RB, et al. Five year experience with the maze procedure for atrial fibrillation. Ann Thorac Surg 1993;56:814. [2] Moe GK, Abildskov JA. Atrial fibrillation as a self-sustaining arrhythmia independent of focal discharge. Am Heart J 1959;58:59. [3] Haissaguerre M, Jais P, Shah D, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med 1998;339:659. [4] Jideus L, Kesek M, Joachimson PO, et al. The role of atrial premature contractions as the main triggers of post operative atrial fibrillation. J Electrocardiol 2006;39. [5] Ott P, Massumi A, Duncan M, et al. Atrial arrhythmias after cardiac surgery: analysis of bi-atrial recordings. PACE 2000;23 part II(abst):736.
[6] Doshi RN, Wu TJ, Yashima M, et al. Relation between ligament of Marshall and adrenergic atrial tachyarrhythmia. Circulation 1999; 100:876. [7] Landolina M, Petracci B, Gaetano MF, et al. Atrial arrhythmias: prevalence in heart transplant patients. Heart Rhythm 2005;2(abstr):S2. [8] Mathew JP, Fontes ML, Tudor IC, et al. A multicenter risk index for atrial fibrillation after cardiac surgery. JAMA 2004;291:1720. [9] Ishii Y, Schuessler RB, Gaynor LG, et al. Inflammation of atrium after cardiac surgery is associated with inhomogeneity of atrial conduction and atrial fibrillation. Circulation 2005;111:2881. [10] Yared JP, Starr NJ, Torres FK, et al. Effects of single dose postinduction dexamethasone on recovery after surgery. Ann Thorac Surg 2000;69:1420. [11] Halvorsen P, Raeder J, White PF, et al. The effect of dexamethasone on side effects after coronary revascularization procedures. Anesth Analg 2003;189:153. [12] Mozaffarian D, Psaty BM, Rimm EB, et al. Fish intake and risk of incident of atrial fibrillation. Circulation 2004;110:368. [13] Calo L, Bianconi L, Colivicchi F, et al. N-3 fatty acids for the prevention of atrial fibrillation after coronary artery bypass surgery. J Am Coll Cardiol 2005;45:1723. [14] Crystal E, Connolly SJ, Sleik K, et al. Interventions on prevention of post operative atrial fibrillation in patients undergoing heart surgery. A meta-analysis. Circulation 2002;106:75. [15] Cummings JE, Gill J, Akhras R, et al. Preservation of the anterior fat pad paradoxically decreases the incidence of post operative atrial fibrillation in humans. J Am Coll Cardiol 2004;43:994.