**Surgery for Atrial Fibrillation**

Hunaid A. Vohra, Zaheer A. Tahir and Sunil K. Ohri *Wessex Cardiothoracic Centre, Southampton UK* 

### **1. Introduction**

256 Special Topics in Cardiac Surgery

[60] Baerman JM, Kirsh MM, de Buitleir M, Hyatt L, Juni JE, Pitt B, Morady F. Natural

[61] Chu A, Califf RM, Pryor DB, McKinnis RA, Harrell FE Jr, Lee KL, Curtis SE, Oldham

[62] Emlein G, Huang SK, Pires LA, Rofino K, Okike ON, Vander Salm TJ. Prolonged

[63] Wexelman W, Lichstein E, Cunningham JN, Hollander G, Greengart A, Shani J.

[64] Brodell GK, Cosgrove D, Schiavone W, Underwood DA, Loop FD. Cardiac rhythm and

[65] Jaeger FJ, Trohman RG, Brener S, Loop F. Permanent pacing following repeat cardiac

[66] Haught WH, Bertolet BD, Conti JB, Curtis AB, Mills RM Jr. Theophylline reverses high-

[67] Heinz G, Kratochwill C, Buxbaum P, Laufer G, Kreiner G, Siostrzonek P, Gasic S, Derfler

[69] Walsh SR, Tang T, Wijewardena C, Yarham SI, Boyle JR, Gaunt ME. Postoperative arrhythmias in general surgical patients. Ann R Coll Surg Engl. 2007 Mar; 89(2):91-5 [70] Amar D, Zhang H, Roistacher N. The incidence and outcome of ventricular arrhythmias after noncardiac thoracic surgery. Anesth Analg. 2002 Sep; 95(3):537-43 [71] Polanczyk CA, Goldman L, Marcantonio ER, Orav EJ, Lee TH. Supraventricular

[72] Christians KK, Wu B, Quebbeman EJ, Brasel KJ. Postoperative atrial fibrillation in oncardiothoracic surgical patients. Am J Surg. 2001 Dec; 182(6):713-5 [73] Bender JS. Supraventricular tachyarrhythmias in the surgical intensive care Unit: an

[74] Brathwaite D, Weissman C. The new onset of atrial arrhythmias following major

[76] American Society of Anaesthesiologists Task Force on Perioperative Management of

artery bypass grafting. Am J Cardiol. 1987 Apr 1; 59(8):798-803

coronary bypass surgery. Am Heart J. 1986 May; 111(5):923-7

valve surgery. Am J Cardiol. 1994 Sep 1; 74(5):505-7

devices. Circulation. 2002 Oct 15; 106(16):2145-61

length of stay. Ann Intern Med. 1998 Aug 15; 129(4):279-85

under-recognized event. Am Surg. 1996 Jan; 62(1):73-5.

[75] Neumar, R. W. et al. Circulation 2010; 122: S729-S767

Am Surg. 1973 Jul;39(7):380-2

surgery. Ann Thorac Surg. 1987 Aug; 44(2):150-3

1993 Nov; 126(5):1084-90

Med. 1991 Sep-Oct; 58(5):397-9

J. 1994 Dec; 128(6 Pt 1):1255-7.

114(2):462-8.

history and determinants of conduction defects following coronary artery bypass

HN Jr, Wagner GS. Prognostic effect of bundle branch block related to coronary

bradyarrhythmias after isolated coronary artery bypass graft surgery. Am Heart J.

Etiology and clinical significance of new fascicular conduction defects following

conduction disturbances in patients undergoing mitral valve surgery. Cleve Clin J

grade atrioventricular block resulting from cardiac transplant rejection. Am Heart

K, Gössinger H. Immediate normalization of profound sinus node dysfunction by aminophylline after cardiac transplantation. Am J Cardiol. 1993 Feb 1; 71(4):346-9 [68] Gregoratos G, Abrams J, Epstein AE, Freedman RA, et al. ACC/AHA/NASPE 2002

guideline update for implantation of cardiac pacemakers and antiarrhythmia

arrhythmia in patients having noncardiac surgery: clinical correlates and effect on

noncardiothoracic surgery is associated with increased mortality. Chest. 1998 Aug;

Patients with Cardiac Rhythm Management Devices. Practice advisory for the perioperative management of patients with cardiac rhythm management devices, pacemakers and implantable cardioverter-defibrillators: a report by the American Society of Anaesthesiologists Task Force on Perioperative Management of Patients with Cardiac Rhythm Management Devices. Anaesthesiology. 2005 Jul;103(1):186-98 [77] Kirkpatrick JR, Heilbrunn A, Sankaran S. Cardiac arrhythmias: an early sign of sepsis. Atrial Fibrillation (AF) is characterised by rapid and disorganised depolarisation of the atria resulting in uncoordinated atrial contraction. It is the most common cardiac arrhythmia encountered in clinical practice increasing in prevalence with age and the presence of heart disease1 It is estimated that it affects 2.5 million people in the United States and 4.5 million in the European Union.2,3 The actual incidence of the arrhythmia may be much higher owing to undetected or asymptomatic patients within the population. Since it is an age-associated arrhythmia its incidence has steadily risen over the past decade and will continue to increase due to a growing population of the elderly in the western world. Contributing risk factors include hypertension, diabetes, coronary artery disease, valvular disease, electrolyte imbalance.4 Patients with atrial fibrillation have a higher risk for stroke, heart failure and death.5Given the significant morbidity and mortality associated with AF and its associated economic burden, it is not surprising that there has been great interest in developing effective treatments for it.

Atrial fibrillation is a supraventricular arrhythmia where uncoordinated rapid atrial contractions produce an irregular ventricular response. The atria may discharge between 300-600 beats per minute but not all these impulses are conducted by the AV node. Ventricular response can be between 100-160 beats per minute in untreated patients with normal AV conduction. This chaotic rhythm disrupts normal movement of blood through the heart reducing cardiac output and increasing the risk for thromboembolism such as stroke as a consequence of stasis of blood in the atria.6

The serious morbidity and mortality associated with AF are attributed to three detrimental consequences:


Medical therapy remains the most common and first line treatment for patients with AF but frequently ineffective at restoring sinus rhythm leaving the patient susceptible to cardiovascular morbidity and mortality. Therefore, the goal of pharmacological therapy is often shifted from rhythm control (maintenance of sinus rhythm) to rate control (slowing the ventricular response to AF).7

The Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) trial demonstrated no survival benefit of rhythm control strategy over a rate control strategy.

Surgery for Atrial Fibrillation 259

In recent years there has been considerable progress in understanding the pathophysiology of AF. It was initially thought that AF was caused by random, multiple wavelets generated throughout the atria that propagated new wavelets to cause re-entry mechanism. In the 1980s, several procedures were developed aimed at curing atrial fibrillation. However, most of these were abandoned due to their inability to address all three detrimental sequelae of atrial fibrillation. It was discovered that electrical impulses were incapable of crossing areas

This fostered the development of the Maze procedure, designed and first reported by Cox and colleagues in which multiple incisions were made and sutured in a manner that blocked the aberrant impulses within the atrium (figure 2). These incisions directed the SA node impulse to initiate and propagate throughout the atria to the AV node along a specified route created by the Maze incisional lesions18. However, recently studies have demonstrated that the initiation of paroxysmal but not necessarily persistent or permanent AF are generated by electrical waves from focal sources, particularly near the pulmonary veins. Haissaguerre et al.19 mapped the triggers of paroxysmal AF to originate around the orifices of the pulmonary veins in 94% of patients with atrial diameters of less than 5cm. These findings have directed the development of more precisely targeted procedures that can be

Fig. 2. The pathway taken in the atria by the aberrant impulses in atrialfibrillation (arrows). The thick lines are the ablation lesions used in the Maze procedure. Key- SAN: sino-atrial

node, AVN: atrio-ventricular node, RAA: right atrial appendage, LAA: left atrial appendage, SVC: superior vena cava, IVC: inferior vena cava, PVs: pulmonary veins.

**3. Electrophysiology of AF** 

of the heart that had been incised and sutured.16,17

performed less invasively with less destruction of normal tissue.

Although rate control slows the ventricular response to AF, preventing tachycardia induced cardiomyopathy, it does not reduce the rates of thromboembolism or congestive heart failure. The atria are still in fibrillation and there is loss of the atrial "kick" resulting in worsening of congestive heart failure and requires indefinite anticoagulation with warfarin to counter the risk for developing thromboembolism. Although warfarin reduces the annual risk of ischaemic stroke and systemic thromboembolism to approximately 2%, its use is associated with significant morbidity with a 2% annual risk of drug associated haemorrhage.8,9,10 Anticoagulation may reduce lifetime relative risk of stroke by 60% but does not eliminate it11

Although the results of the AFFIRM trial demonstrated no long-term benefit of rhythm versus rate control, some patients may still have advantages of being in sinus rhythm. These include freedom from palpitations, increased exercise tolerance and prevention of atrial remodelling. 12,13

Ineffective results with rate and rhythm control strategies have helped to encourage the development of new interventional catheter and surgical treatments. Although catheter ablation is an established therapeutic option, the highest success rates are typically seen in patients with paroxysmal AF and minimal structural heart disease.14

Therefore it is limited to a small number of patients treated by highly skilled electrophysiologists. On the other hand, almost all cardiac surgeons are capable of performing surgical ablation of AF.
