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Cox JL. Surgical Treatment of Supraventricular Tachyarrhythmias.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:12711286.

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Chapter 53

Surgical Treatment of Supraventricular Tachyarrhythmias

James L. Cox

EARLY SURGICAL PROCEDURES FOR ATRIAL FIBRILLATION
????The Left Atrial Isolation Procedure
????Catheter Ablation of the AV NodeHis Bundle Complex
????The Corridor Procedure
????The Atrial Transsection Procedure
THE ANATOMICAL-ELECTROPHYSIOLOGICAL BASIS OF ATRIAL FIBRILLATION
THE MAZE PROCEDURE
????Surgical Technique
????Surgical Indications
????Preoperative Electrophysiology Evaluation
????Surgical Results
????????PERIOPERATIVE RESULTS
????????LATE RESULTS
CHANGING CONCEPTS OF THE ELECTROPHYSIOLOGY OF ATRIAL FIBRILLATION
TECHNIQUES FOR ABLATING ATRIAL FIBRILLATION DURING MITRAL VALVE SURGERY
REFERENCES

?? INTRODUCTION
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Supraventricular arrhythmias due to the Wolff-Parkinson-White (WPW) syndrome, AV node reentry, automatic atrial foci, and most forms of atrial flutter have essentially disappeared from the realm of the surgeon because of the phenomenal success of less invasive radiofrequency catheter ablation techniques. Thus, the numerous surgical procedures that were once in such vogue for the treatment of those arrhythmias are now of historical interest only. The only supraventricular arrhythmia of significance to the cardiac surgeon in 2002 is atrial fibrillation.

Atrial fibrillation is present in approximately 1% of the general population15 and 6% of the population over the age of 65 years,69 making it the most common of all sustained cardiac arrhythmias. According to the Health Care Finance Administration (HFCA), atrial fibrillation results in 1.4 million outpatient visits and 227,000 hospitalizations (50% as emergencies) in the United States annually.10 The annual cost of atrial fibrillation to the federal budget is calculated by HFCA to be $6.6 billion, not including physician fees, outpatient expenses, medications, and non-Medicare patient expenses.10

Although atrial fibrillation is considered by many to be an innocuous arrhythmia, it is associated with significant morbidity and mortality due to its three detrimental sequelae: (1) an irregularly irregular heartbeat, which causes patient discomfort and anxiety; (2) loss of synchronous atrioventricular contraction, which compromises cardiac hemodynamics resulting in varying levels of congestive heart failure; and (3) stasis of blood flow in the left atrium, which increases the vulnerability to thromboembolism.

Optimal medical therapy of atrial fibrillation includes the use of drugs directed towards rhythm control, i.e., the conversion of atrial fibrillation to normal sinus rhythm. Unfortunately, these drugs frequently fail and the therapeutic goal shifts to rate control, i.e., slowing the ventricular response rate to atrial fibrillation. Although the ventricular response rate can usually be controlled medically, it is important to recognize the fact that the atria are still fibrillating and therefore all three of the detrimental sequelae associated with atrial fibrillation persist. Obviously, the hemodynamic compromise is not as great with a controlled ventricular response rate to atrial fibrillation but, just as obviously, cardiac hemodynamics are not restored to normal because of the absence of the atrial "kick." Thus pharmacologic therapy is less than optimal in a large number of patients with atrial fibrillation. Because medical therapy frequently fails to control atrial fibrillation, several surgical procedures were introduced in the 1980s to either ablate the arrhythmia or ameliorate its attendant detrimental sequelae.


?? EARLY SURGICAL PROCEDURES FOR ATRIAL FIBRILLATION
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Even though the early procedures that were developed for the surgical treatment of atrial fibrillation are no longer employed, it is virtually impossible to understand the vagaries of treating atrial fibrillation in the operating theater without understanding the lessons of those initial efforts. Indeed, most of the failures of contemporary catheter and surgical techniques in ablating atrial fibrillation result from a lack of knowledge of the problems that were identified, elucidated, and solved in the early days of development of these surgical procedures. For purposes of clarity, the schema used to describe the results of all of these procedures is shown in Figure 53-1.



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FIGURE 53-1 Schematic atrial anatomy. The atria are represented as a box with the left atrium and right atrium in the designated locations. The right atrium has two electrical "holes": the orifice of the superior vena cava (SVC) and the orifice of the inferior vena cava (IVC). It also has a right atrial appendage (RAA). The left atrium is contiguous with the pulmonary veins (PV's) and also has the left atrial appendage (LAA).

The atrial septum lies between the right and left atria. The sinoatrial node (SAN) is positioned at the top of the atrial septum, and the atrioventricular node (AVN) is at the bottom of the atrial septum, where conduction continues to the ventricles via the specialized conduction system.

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The Left Atrial Isolation Procedure

In 1980, we described the left atrial isolation procedure (Fig. 53-2), 11 which was capable of confining atrial fibrillation to the left atrium while leaving the remainder of the heart in normal sinus rhythm (Fig. 53-3). This procedure was successful in restoring a regular ventricular rhythm without the need for a permanent pacemaker, and, unexpectedly, it also restored normal cardiac hemodynamics. The reason for the latter is that the right atrium and right ventricle beat in synchrony following the procedure. This provides a normal right-sided cardiac output that is then delivered to the left side of the heart. Despite the fact that the left atrium is isolated, and therefore cannot beat in synchrony with the left ventricle, the left ventricle adapts instantaneously to the normal right-sided output and delivers a normal forward cardiac output (Fig. 53-4). Thus, the left atrial isolation procedure alleviates two of the three detrimental sequelae of atrial fibrillation, namely irregular heartbeat and compromised hemodynamics. Unfortunately, since the left atrium may continue to fibrillate, the vulnerability to systemic thromboembolism is unchanged following this procedure.



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FIGURE 53-2 The left atrial isolation procedure confines all electrical activity in the left atrium, whether normal or abnormal, to the left atrium. This allows the normal cardiac impulse to originate in the sinoatrial node (SAN), conduct across the right atrium, and into the ventricles via the atrioventricular node (AVN). (Same schema as in Figure 53-1.)

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FIGURE 53-3 Following the left atrial isolation procedure, the left atrium may still fibrillate, but the atrial fibrillation is confined to the left atrium due to its electrical isolation from surgery. The remainder of the heart beats in a normal sinus rhythm. However, this may be difficult to discern on a standard ECG (for example, in lead II) because the size and morphology of the P wave is determined primarily by the electrical activity in the left atrium, not the right atrium. (Reproduced with permission from Williams JM, Ungerleider RM, Lofland GK, Cox JL: Left atrial isolation: new technique for the treatment of supraventricular arrhythmias. J Thorac Cardiovasc Surg 1980; 80:373.)

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FIGURE 53-4 This example of one of several experiments documenting that as long as the right atrium is beating in synchrony with the right ventricle, the contractile function of the left atrium is irrelevant to forward cardiac output.

In the control panel, the right atrium is being paced first followed by pacing of the left atrium only 40 msec later, thus mimicking the normal activation sequence between the two atria during normal sinus rhythm. Both atria were contracting normally to visual inspection. Note the hemodynamic measurements at that time. The cardiac output (minus coronary artery blood flow) was being measured continuously by means of an electromagnetic flow probe positioned around the ascending aorta. The systemic blood pressure (B.P.), the left ventricular end-diastolic pressure (LVEDP), and the pulmonary artery (P.A.) pressure were all being measured simultaneously with three separate Millar high-fidelity catheters in appropriate positions.

Once the control measurements were recorded, the LA pacing wire was suddenly disconnected without changing anything else, resulting in an electrically silent LA (middle panel) and immediate loss of all LA contraction. Note that this caused no change in any of the measured pressures or in the forward cardiac output of the heart.

The left atrial wire was then connected to a rapid atrial pacemaker to mimick a left atrial tachycardia confined to the left atrium by the left atrial isolation procedure. Again, there were no changes in any of the measured pressures or in the forward cardiac output. (Reproduced with permission from Williams JM, Ungerleider RM, Lofland GK, Cox JL: Left atrial isolation: new technique for the treatment of supraventricular arrhythmias. J Thorac Cardiovasc Surg 1980; 80:373.)

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Catheter Ablation of the AV NodeHis Bundle Complex

In 1982, Scheinman introduced catheter fulguration of the His bundle (Fig. 53-5) as a means of controlling the irregular cardiac rhythm associated with atrial fibrillation and other refractory supraventricular arrhythmias.12 This procedure was also a type of isolation procedure in that it isolated the supraventricular arrhythmia to the atria and away from the ventricles. Catheter fulguration was eventually abandoned in favor of the less traumatic radiofrequency ablative techniques that are still in use today. Elective His bundle ablation necessitates the implantation of a permanent ventricular pacemaker, which restores a normal ventricular rhythm. However, the atria continue to fibrillate following His bundle ablation, and thus this technique alleviates only one of the detrimental sequelae of atrial fibrillation, the irregular heartbeat. The hemodynamic compromise due to loss of atrioventricular synchrony and the vulnerability to thromboembolism are unaffected by His bundle ablation.



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FIGURE 53-5 Catheter ablation of the AV nodeHis bundle complex for the treatment of atrial fibrillation simply confines the arrhythmia to the atria while dictating that a permanent ventricular pacemaker be inserted afterwards. The physiology of this procedure is the same whether the ablation is via the old fulguration technique introduced in 1981 or via the radiofrequency ablation catheters that are used today. (Same schema as in Figure 53-1.)

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The Corridor Procedure

In 1985, Guiraudon described the corridor procedure (Fig. 53-6) for the treatment of atrial fibrillation,13 an open heart technique that isolated a strip of atrial septum (the "corridor") harboring both the SA node and the AV node, thereby allowing the SA node to drive the ventricles. This procedure corrected the irregular heartbeat associated with atrial fibrillation, but both atria either continued to fibrillate postoperatively or developed their own asynchronous intrinsic rhythm because they were both totally isolated from the septal "corridor." In addition, both atria were also isolated from their respective ventricles, thereby precluding the possibility of atrioventricular synchrony on either side of the heart. Therefore, neither the hemodynamic compromise nor the vulnerability to thromboembolism associated with atrial fibrillation was alleviated by the corridor procedure and it was soon abandoned.



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FIGURE 53-6 Guiraudon's corridor procedure resulted in the surgical isolation of both the right and left atria from their respective ventricles and allowed both to continue to fibrillate postoperatively. Since synchronous atrioventricular contraction was thereby precluded, the resultant physiology of this procedure was the same as that following catheter ablation of the His bundle and insertion of a rate-responsive pacemaker. The only potential advantage of the corridor procedure over catheter His bundle ablation was the lack of need for a permanent pacemaker. Unfortunately, a large number of these patients did in fact require permanent pacemakers postoperatively, probably because of devascularization of the sinoatrial node resulting in an iatrogenic sick sinus syndrome. Of course, the major disadvantage of the corridor procedure when comparing the two was that it was an open heart procedure. (Same schema as in Figure 53-1.)

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The Atrial Transsection Procedure

All three of the surgical and/or catheter techniques developed up to that time had attempted to isolate and confine atrial fibrillation to a certain region of the atria so that its effects on the ventricles could be minimized. It was obvious that a much better approach would be to try to ablate the atrial fibrillation itself and thus restore the heart's normal sinus rhythm. Using our best canine model for atrial fibrillation,14 the first ablative surgical procedure tried was a simple incision encompassing all of the orifices of the pulmonary veins to totally isolate them from the remainder of the heart (Fig. 53-7A).15 Unfortunately, this incision had no effect whatsoever on the ability of the atria to fibrillate in any animal. This is particularly interesting in view of the subsequent demonstration of the importance of the pulmonary vein orifices in serving as the "initiating site" for paroxysmal atrial fibrillation.



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FIGURE 53-7 Various surgical procedures initially attempted in the experimental laboratory to ablate atrial fibrillation. See text for discussion. (Reproduced with permission from Cox JL, Schuessler RB, D'Agostino HJ Jr, et al: The surgical treatment of atrial fibrillation, III: development of a definite surgical procedure. J Thorac Cardiovasc Surg 1991; 101:569.)

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The second series of experiments incorporated pulmonary vein isolation plus a lateral incision to the level of the mitral valve annulus and a medial incision to the interatrial septum (Fig. 53-7B). These incisions prevented the atria from fibrillating in every animal. However, once these left atrial and septal incisions were completed, the animals immediately converted from atrial fibrillation to stable atrial flutter. Since we suspected that the atrial "flutter wave" was occurring in the right atrium, we simply extended the medial left atriotomy across the body of the left atrium between the superior vena cava (SVC) and inferior vena cava (IVC) posteriorly and down to the level of the right free-wall tricuspid valve annulus (Fig. 53-7C). We then worked backwards to see if we could eliminate a portion of the procedure and still cure atrial fibrillation in the animal model. We learned that, at least in this model, it was not necessary to encircle the pulmonary veins and therefore we were left with a single long incision across both atria and down into the septum (Fig. 53-7D). In the animal model we were employing, this so-called atrial transsection procedure invariably prevented the induction and maintenance of atrial fibrillation or atrial flutter in every animal.15 Unfortunately, the procedure was effective but not curative in its clinical application and it became apparent that the surgical cure of atrial fibrillation would require a more complete understanding of the underlying electrophysiology of atrial fibrillation.


?? THE ANATOMICAL-ELECTROPHYSIOLOGICAL BASIS OF ATRIAL FIBRILLATION
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Our experimental and clinical studies during the mid-1980s documented that there are three interacting components in atrial flutter and atrial fibrillation that determine the findings on the peripheral ECG and thus dictate the clinical diagnosis. These three components include: (1) macro-reentrant circuit(s), (2) passive atrial conduction in that portion of the atrium not involved in the macro-reentrant circuit, and (3) atrioventricular conduction (Figs. 53-8 and 53-9). The electrophysiological characteristics of these three components define a spectrum of atrial arrhythmias, extending from simple atrial flutter, through several types of transitional arrhythmias, to complex atrial fibrillation.16



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FIGURE 53-8 The three components of atrial flutter are the macro-reentrant circuit that is usually, but not always, located in the right atrium (the "flutter wave"); passive conduction to the rest of the atrial muscle; and conduction through the AV node where a 2:1 block occurs en route to the ventricles. The flutter wave drives all of the electrical activity in the heart, including both atria and both ventricles. In humans, it takes 200 msec for the electrical activity to complete one cycle around the flutter wave. This corresponds to 300 cycles per minute, which means that as long as the cycle length is stable and the passive atrial conduction is stable, both atria will beat regularly 300 times per minute. This gives rise to the "sawtooth" appearance of the P wave on the peripheral ECG during classic atrial flutter.

Because there is a 2:1 conduction block in the AV node, the ventricles are activated only 150 times per minute, but they activate in a very regular fashion in response to the consistent block of the stable atrial flutter wave. The combination of a regular P wave of 300 beats per minute and a regular ventricular response of 150 beats per minute on the standard ECG results in the clinical diagnosis of "atrial flutter." (Same schema as in Figure 53-1.) (Reproduced with permission from Cox JL, Canavan TE, Schuessler RB, et al: The surgical treatment of atrial fibrillation, II: intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg 1991; 101:406.)

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FIGURE 53-9 Atrial fibrillation may be induced by electrical stimuli in the pulmonary veins or elsewhere in the atria, or it may result from deterioration of a large atrial flutter wave. Regardless of its origin, once atrial fibrillation is established, it is characterized electrically by the presence of multiple macro-reentrant circuits in the atria. These reentrant circuits are usually smaller than the large single flutter wave that causes atrial flutter but they are still classified as macro-reentrant. Once atrial fibrillation is established, the electrical events are identical in paroxysmal (intermittent) atrial fibrillation and chronic (continuous) atrial fibrillation. (Same schema as in Figure 53-1.) (Reproduced with permission from Cox JL, Canavan TE, Schuessler RB, et al: The surgical treatment of atrial fibrillation, II: intraoperative electrophysiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg 1991; 101:406.)

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In addition to elucidating the mechanism of atrial flutter and atrial fibrillation, these experimental and clinical electrophysiologic studies also documented that our initial hopes of obtaining computerized electrophysiological maps of atrial fibrillation and using them to guide the specific surgical technique, as we had done in other arrhythmias, was not feasible. Since the macro-reentrant circuits responsible for atrial flutter and atrial fibrillation are so fleeting in nature, it would be impossible to use activation maps to guide surgery even with on-line maps. As a result, we sought to develop a surgical technique that would be capable of interrupting any and all macro-reentrant circuits that might potentially develop in the atria, thereby precluding the ability of the atrium to flutter or fibrillate. In addition, it was recognized that the surgical incisions would have to be placed so that the SA node could resume activity postoperatively and "direct" the propagation of the sinus impulse throughout both atria. This would allow all of the atrial myocardium to be activated postoperatively, resulting in preservation of atrial transport function, a prerequisite for the restoration of normal cardiac hemodynamics and the prevention of stasis of blood flow in the left atrium with the resultant potential for thromboembolism. The surgical procedure that was conceived to accomplish these goals is based on the concept of a maze17 and, as a result, was named the "Maze procedure" (Fig. 53-10).



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FIGURE 53-10 The Maze procedure is designed to preclude the ability of the atria to harbor any macro-reentrant circuits and therefore to preclude the ability of the atria to fibrillate. This could be accomplished by "bread-loafing" the heart, but the atria could not be activated by the SA node thereafter. Thus, the Maze procedure not only abolishes atrial fibrillation but is also designed to allow the SA node to take over atrial activation postoperatively and to allow the impulse generated in the SA node to activate all of the myocardium of both atria and then be conducted via the AV node into the ventricles. One way of accomplishing these goals is to create a set of lesions based on the concept of a maze with one site of entrance (the SA node) into the box (the atria) and one site of exit (the AV node) from the box, with one true route between the entrance and exit and multiple blind alleys along the way to provide activation to all areas of the atria. (Same schema as in Figure 53-1.) (Reproduced with permission from Cox JL, Schuessler RB, D'Agostino HJ Jr, et al: The surgical treatment of atrial fibrillation, III: development of a definite surgical procedure. J Thorac Cardiovasc Surg 1991; 101:569.)

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?? THE MAZE PROCEDURE
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Surgical Technique

The original surgical technique, the Maze-I procedure (Fig. 53-11), 18 was modified to become the Maze-II procedure (Fig. 53-12) because of late chronotropic problems with the sinoatrial node and intra-atrial conduction delays that resulted in decreased left atrial contraction. However, the Maze-II procedure proved to be exceedingly difficult technically and as a result, it was modified again to become the Maze-III procedure (Fig. 53-13).19,20 The Maze-III procedure soon became the surgical technique of choice for the treatment of medically refractory atrial flutter and atrial fibrillation. Most of the incisions originally performed as a part of the Maze-III procedure have been replaced by cryolesions so that the procedure can be performed by minimally invasive techniques.21 In addition, the new minimally invasive technique avoids removal of the left atrial appendage. The orifice of the appendage is now cryoablated circumferentially and then closed from inside the left atrium.



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FIGURE 53-11 The Maze-I procedure. The lower left panel shows a posterior view of both atria. The left upper panel is drawn as if the atria had been cut in half with the front half flipped upwards. The incisions of the Maze-I procedure are shown and the heavy dark arrows represent the direction of propagation of a sinus beat away from the SA node following the procedure. The two atrial appendages are excised and the pulmonary veins are completely encircled.

The right panel is a cut-away view of the right atrium to show the position of the atrial septotomy and the direction of impulse propagation through the atrial septum in an anterior-to-posterior direction. Note that the septotomy is anterior to the orifice of the superior vena cava (SVC) and that there is a small atriotomy connecting the septotomy incision to the orifice of the SVC. (Reproduced with permission from Cox JL, Jaquiss RD, Schuessler RB, Boineau JP: Modification of the Maze procedure for atrial flutter and atrial fibrillation, II: surgical technique of the Maze III procedure. J Thorac Cardiovasc Surg 1995; 110:485.)

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FIGURE 53-12 The Maze-II procedure. The small atriotomy located just anterior to the orifice of the SVC in the Maze-I procedure was later discovered to be traversing directly through the so-called "sinus tachycardia" region of the atrial pacemaker complex and as a result was responsible for the inability of patients to generate a normal chronotropic response to exercise or excitement following the Maze-I procedure. Moreover, the anterior location of the septotomy frequently interrupted or severely impeded interatrial conduction across the rapidly conducting Bachmann's bundle. This caused the left atrium to activate up to 150 msec after activation of the right atrium rather than the normal 40 msec. This delay in interatrial conduction resulted in the left atrium being activated nearly simultaneously with the left ventricle (AV interval of 150 msec.), i.e., when the mitral valve was closed. Thus, when this abnormal interatrial conduction delay occurred, it actually prevented the left atrium from contracting postoperatively.

For these two reasons, the culprit lesions of the Maze-I procedure were eliminated and the resultant modification is shown in this diagram. Unfortunately, the atrial septotomy in the Maze-II procedure was in the middle of the medial portion of the orifice of the SVC (right panel) and thus the left-sided exposure was limited, making the procedure extremely difficult to perform technically. As a result, it was further modified to become the Maze-III procedure. (Reproduced with permission from Cox JL, Jaquiss RD, Schuessler RB, Boineau JP: Modification of the Maze procedure for atrial flutter and atrial fibrillation, II: surgical technique of the Maze III procedure. J Thorac Cardiovasc Surg 1995; 110:485.)

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FIGURE 53-13 The Maze-III procedure. The atrial septotomy was moved to a position posterior to the orifice of the SVC without altering the concept of the Maze-II procedure. However, the Maze-III procedure is far easier to perform technically than the previous two iterations. This pattern of lesions has been used exclusively since April 1992. (Reproduced with permission from Cox JL, Jaquiss RD, Schuessler RB, Boineau JP: Modification of the Maze procedure for atrial flutter and atrial fibrillation, II: surgical technique of the Maze III procedure. J Thorac Cardiovasc Surg 1995; 110:485.)

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Surgical Indications

The major indication for surgery is intolerance of the arrhythmia. In many respects, patients with paroxysmal atrial flutter/fibrillation are more symptomatic than those with chronic atrial fibrillation. Major symptoms in the paroxysmal group include dyspnea on exertion, easy fatigability, lethargy, malaise, and a general sense of impending doom during the periods of atrial flutter/fibrillation. The patients with chronic atrial fibrillation are usually better adapted to the sensation of an irregular heartbeat, but the majority of them complain of exercise limitations, dypsnea on exertion, and easy fatigability. In addition, they frequently express concern over the possibility of having a stroke. In fact, 19.5% of the patients in our series had experienced at least one episode of cerebral thromboembolism that resulted in significant temporary or permanent neurologic deficit. Finally, all patients who are considered for surgery must have failed the maximal drug therapy preoperatively.

Preoperative Electrophysiology Evaluation

For several years, a preoperative endocardial catheter electrophysiology study was required in all patients with atrial flutter and in patients with paroxysmal atrial fibrillation. The primary purpose of this study was to: (1) determine SA node function; (2) localize the site of the reentrant circuit in patients with atrial flutter; and (3) try to detect any underlying electrophysiological abnormality that might be triggering the atrial fibrillation, such as an automatic atrial focus, an accessory atrioventricular connection, or AV node reentry. These electrophysiological studies have proven to be a bit superfluous in today's environment and as a result we no longer require that a patient undergo a formal study prior to surgery. We have never thought it wise to try to perform electrophysiology studies in patients with chronic atrial fibrillation because the SA node cannot be evaluated without electrical cardioversion, which would introduce the risk of thromboembolism. We require all males over the age of 40 years to undergo an elective cardiac catheterization prior to surgery to rule out coronary artery disease.

Surgical Results

Between September 25, 1987, and April 16, 1992, 32 patients had the Maze-I procedure and 15 patients had the Maze-II procedure. For the reasons mentioned earlier, the Maze-III became the standard thereafter and by July 1, 2000, 308 patients had undergone the Maze-III procedure for the treatment of atrial flutter and/or atrial fibrillation.

PERIOPERATIVE RESULTS

The perioperative mortality rate (within 3 months following surgery) was 2.9% with the independent determinants of operative death being (1) preoperative congestive heart failure, (2) preoperative hypertension, and (3) performance of the Maze procedure concomitantly with a double valve replacement. The most common perioperative complication following the Maze procedure was postoperative arrhythmias, usually atrial flutter or atrial fibrillation, which occurred in 37% of patients. As described earlier, the Maze procedure was designed to interrupt the macro-reentrant circuits that must be able to form for the atria to fibrillate. The actual physical size of these circuits is determined by the duration of the refractory period at any given site in the atria (Figs. 53-14 and 53-15). Normally, atrial refractory periods are relatively long and as a result the macro-reentrant circuits are relatively large, i.e., over 6 to 7 cm in diameter. In this situation, the macro-reentrant circuits cannot form between the suture lines of the Maze procedure (Fig. 53-16A) and therefore the atrium cannot fibrillate. During the immediate postoperative period and until the atria heal from surgery, local refractory periods may be much shorter and thus the macro-reentrant circuits can be much smaller (Fig. 53-16B). As a result, it is possible to form macro-reentrant circuits between the suture lines of the Maze procedure and have postoperative atrial fibrillation even following the performance of a technically perfect operation.



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FIGURE 53-14 When atrial myocardium is activated by a propagating wavefront (from left to right in this diagram), the leading edge of the wavefront is caused by the simultaneous depolarization of the millions of myocardial cells lying along the edge of that wavefront. The cells are briefly incapable of being excited again (refractory) because they are already depolarized. A trailing edge of repolarization soon follows and the cells again become excitable. The distance between the depolarization wavefront and the trailing repolarization "wave" (sometimes referred to as the "wavelength") is illustrated as an arrow in this figure and represents the duration of the local refractory period in this region of the atrium. (Reproduced with permission from Cox JL, Schuessler RB, Lappas DG, Boineau JP: An 8 1/2 year clinical experience with surgery for atrial fibrillation. Ann Surg 1996; 224:267.)

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FIGURE 53-15 The length of the arrow in Figure 53-14 will determine the minimum size that a macro-reentrant circuit can be in that region of the atria. In other words, the duration of the local refractory period determines the lower limits of the size of the macro-reentrant circuit. In this illustrative diagram, if the arrow representing the duration of the local refractory period is bent so that its point almost, but not quite, touches its tail, this would represent the smallest size that a reentrant circuit can be in that region of the atrium. If the arrow is long, the reentrant circuit is large (left panel). If the arrow is shorter, the reentrant circuit can be smaller (right panel). (Reproduced with permission from Cox JL, Schuessler RB, Lappas DG, Boineau JP: An 8 1/2 year clinical experience with surgery for atrial fibrillation. Ann Surg 1996; 224:267.)

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FIGURE 53-16 There is a critical relationship between the size of a local macro-reentrant circuit and the distance between the incisions (or other type of blocking lesions) of the Maze procedure. Under normal circumstances, even in diseased atria, the local refractory periods of the atria are relatively long and they are longer in the right atrium than in the left atrium. It is most fortuitous that the proximity of the incisions of the Maze procedure is such that they will prevent macro-reentry in the atrium in virtually all cases if the lesion pattern is placed correctly and if each and every lesion is transmural (A). There are two exceptions to this rule. Immediately postoperatively the refractory periods are shorter than normal for a few weeks, probably because of increased circulating catecholamines, atrial irritability, pericarditis, and other conditions associated with the surgery itself. As a result, smaller macro-reentrant circuits can form between the Maze incisions (B), a temporary phenomenon responsible for perioperative atrial fibrillation in over one third of patients having the Maze procedure. Fortunately, when the atria heal, the susceptiblility of the atria to fibrillation disappears because of the return of the refractory periods to their normal preoperative durations.

In the case of perioperative atrial fibrillation following the Maze procedure, the problem is that the reentrant circuits are too small. In extremely large atria, the Maze incisions may be too far apart to interrupt the normal-sized macro-reentrant circuits. Thus, it is absolutely essential to resect a portion of the atria when performing the Maze procedure in extremely large atria so that at the end of the procedure the size of both the right and left atria approaches normal. (Reproduced with permission from Cox JL, Schuessler RB, Lappas DG, Boineau JP: An 8 1/2 year clinical experience with surgery for atrial fibrillation. Ann Surg 1996; 224:267.)

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Because there are critical relationships between the size of the macro-reentrant circuits, the distance between the Maze suture lines, and the effectiveness of the procedure in curing atrial fibrillation, the Maze procedure may fail when performed in extremely large atria. Since the pattern of incisions is always the same, even in the presence of normal long atrial refractory periods (and therefore of large macro-reentrant circuits), the distance between the incisions may be so great in large atria that the reentrant circuits can still form between them following the surgery. This is why the "cut-and-sew" technique is recommended for extremely large atria so that before the incisions are closed, atrial muscle can be resected to decrease the distance between the Maze suture lines.

A most gratifying result is the extremely low incidence (0.7%) of perioperative neurologic events that occur in association with performance of the Maze procedure (Fig. 53-17).22 As noted, 20% of patients had suffered some type of significant thromboembolic event due to the atrial fibrillation preoperatively. Since these patients have early postperative atrial fibrillation as often as do other cardiac surgery patients, we believe that careful closure of the left atrial appendage during surgery most likely explains this apparent paradox.



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FIGURE 53-17 Relative percentages of patients undergoing cardiac surgery who experience either a minor or major cerebral thromboembolic event during the perioperative period. (CABG = coronary artery bypass grafting; MVR = mitral valve replacement; AVR = aortic valve replacement.) (Data from 1998 STS National Adult Surgery Database.)

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LATE RESULTS

In reporting our own surgical results regarding the effectiveness of the Maze procedure in "curing" atrial fibrillation (and/or atrial flutter), we have adhered to the following definitions: perioperative arrhythmias are those that occur within 3 months of surgery, and arrhythmia recurrence is the documentation of a single episode of atrial flutter and/or atrial fibrillation more than 3 months after surgery.

Using these definitions, 98% of patients were cured of atrial fibrillation by the Maze procedure alone and half of the other 2% of patients were cured with a combination of surgery and postoperative drug therapy, an overall cure rate of 99%. Other groups that have adhered to the concept of the Maze procedure have attained similar results.2325 Groups that have chosen to modify the procedure by violating the basic concept of the Maze procedure have had poorer results.26

One of the major benefits of the Maze procedure is that it essentially abolishes the threat of stroke associated with atrial fibrillation.27,28 The long-term stroke rate following the Maze procedure is 0.1% per year (Fig. 53-18).



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FIGURE 53-18 Group I risk factors that increase the likelihood of having a stroke and/or TIA due to atrial fibrillation include hypertension, old age, diabetes mellitus, ischemic heart disease, and congestive heart failure. (I = patients with group I risk factors plus a prior history of either a stroke or TIA due to atrial fibrillation; II = patients with group I risk factors for stroke due to atrial fibrillation; AC = anticoagulation; lone AF = atrial fibrillation in the absence of any other demonstrable heart disease.) (Modified and reproduced with permission from Cox JL, Ad N, Palazzo T: Impact of the Maze procedure on the stroke rate in patients with atrial fibrillation. J Thorac Cardiovasc Surg 1999; 118:883.)

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Overall, 15% of our patients have required pacemakers postoperatively but virtually all of them either already had pacemakers implanted before surgery, were known to have sick sinus syndrome preoperatively, or had abnormal sinoatrial nodes "unmasked" by abolishing the patient's atrial fibrillation. Nevertheless, the need for postoperative pacemakers is higher in our own series than in most other series, probably because of the more extensive extracardiac dissection that we perform routinely in "preparing" the field for performance of the Maze procedure itself. This suspicion would seem to be confirmed by the fact that only 6% of our patients required pacemakers after undergoing the Maze procedure using minimally invasive techniques in which we perform very little extracardiac dissection.

In our series, all patients were documented to have both right atrial and left atrial transport function in the immediate postoperative period that contributed to forward cardiac output. On late follow-up evaluation, 98% of patients have continued to have right atrial transport function and 93% of patients with the Maze-III procedure have had documented left atrial function as well. Documentation of atrial transport function is difficult and for that reason we have used multiple tests in various combinations to arrive at these figures. These tests include transthoracic and transesophageal echocardiography, dynamic magnetic resonance imaging, and atrioventricular sequential pacing versus ventricular-only pacing with multiple determinations of cardiac output.

In 1996, we developed a minimally invasive Maze procedure that is performed through a 7-cm incision in the right anterior 4th intercostal space and utilizes cryosurgery rather than surgical incisions for the creation of the atrial lesions of the Maze procedure.21 This newer, less invasive surgical approach has resulted in earlier extubation, shorter ICU stays, shorter hospitalizations, quicker recuperation and return to work, a decreased need for postoperative pacemakers (6% versus 17% following median sternotomy), and a decreased incidence of perioperative atrial fibrillation (22% versus 37% with median sternotomy).


?? CHANGING CONCEPTS OF THE ELECTROPHYSIOLOGY OF ATRIAL FIBRILLATION
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The electrophysiology of atrial fibrillation described above, in which multiple macro-reentrant circuits are present in the atria, is relevant once atrial fibrillation has begun. Thus, the macro-reentrant circuits in the atria during atrial fibrillation are responsible only for the maintenance of atrial fibrillation, not for the induction of atrial fibrillation. Therefore, the real objective of the Maze procedure can best be described as creating atrial lesions that preclude the ability of the atria to fibrillate by preventing the possibility of macro-reentrant circuits from forming. The idea was that if the atria cannot harbor macro-reentrant circuits, then by definition they cannot fibrillate.

For a variety of reasons, we were never able to document the spontaneous onset of atrial fibrillation in any of our extensive experimental or clinical studies. However, in 1998, Haissaguerre et al published a seminal article documenting that atrial fibrillation is usually induced by stimulation from a site within the orifice of one or more of the pulmonary veins.29 This article is at once one of the most important and yet one of the most poorly understood articles ever published in the electrophysiology literature. The findings were completely compatible with our earlier findings and in fact they completed the picture of the electrophysiology of atrial fibrillation. The Hassaguirre article showed how atrial fibrillation is induced and our earlier work showed how atrial fibrillation is maintained. Unfortunately, the article was taken by many to mean that all that was needed to cure atrial fibrillation was to isolate the orifices of the pulmonary veins, a misconception that led to the development of our own first surgical procedure to ablate atrial fibrillation (see above). What resulted from the misinterpretation of this article was the development of a variety of surgical devices and procedures designed to encircle the pulmonary veins as the sole treatment for atrial fibrillation, an approach that has resulted in a predictable and unacceptable 30% failure rate.

This unfortunate misinterpretation of Hassaguirre's article ignores the fact that chronic (continuous) atrial fibrillation of 10 years duration or longer does not require any type of induction stimulus since the atria are always in atrial fibrillation. It also ignores the seminal work of Wijffels and Allessie, who showed that once the atria begin to fibrillate, they undergo a process of electrical "remodelling," in which the more they fibrillate, the more they will fibrillate in the future, or as those authors state, "Atrial fibrillation begets atrial fibrillation."30,31 These established facts negate any importance of the pulmonary veins in chronic atrial fibrillation, which includes roughly one half of the patients who suffer from atrial fibrillation. Therefore, simple encirclement of the pulmonary veins is not a scientifically sound surgical approach to the treatment of chronic atrial fibrillation. On the other hand, pulmonary vein isolation for the treatment of paroxysmal atrial fibrillation is a reasonable procedure and can be expected to cure about 90% of patients with that specific type of atrial fibrillation. Thus, if surgeons are to treat atrial fibrillation effectively, it is extremely important that they understand the difference between the induction of atrial fibrillation and the maintenance of atrial fibrillation and the difference between paroxysmal (intermittent) and chronic (continuous) atrial fibrillation.


?? TECHNIQUES FOR ABLATING ATRIAL FIBRILLATION DURING MITRAL VALVE SURGERY
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Following the phenomenal success of radiofrequency (RF) catheter ablation for the WPW syndrome, AV node reentry tachycardia, and other supraventricular arrhythmias in the 1990s,32 clinical electrophysiologists began to apply it for the attempted treatment of atrial fibrillation.33 Largely because of the availability of RF catheters and the initial reports of Hassaguirre's studies, surgeons began to use RF catheters intraoperatively in an effort to ablate atrial fibrillation in patients who were already undergoing surgery for mitral valve disease.34 The major objective was no longer to create a Maze procedure but rather to encircle the pulmonary veins. Unfortunately, the RF lesions were frequently not transmural, thereby offering at best only a temporary barrier to electrical conduction and, in addition, pulmonary vein isolation was used in many patients with chronic atrial fibrillation. The 30% failure rate was thus predictable. Unfortunately, without really understanding the underlying electrophysiology of atrial fibrillation, several medical device companies have now developed products designed to do nothing more than encircle the pulmonary veins despite the fact that pulmonary vein encirclement, even when accomplished by completely transmural lesions, is effective in only 90% of 50% of the patients with atrial fibrillation. In actuality, pulmonary vein encirclement alone can occasionally ablate chronic atrial fibrillation if the isolated "cuff" of left atrium surrounding the pulmonary veins is so large that it inadvertently ablates all of the surrounding macro-reentrant circuits in the left atrium. The problem with this scenario is that so much of the left atrium is excluded by the isolated cuff that there may be not effective left atrial contraction postoperatively. Nevertheless, the overall atrial fibrillation ablation cure rate of 70% to 80% that is now being accomplished in some centers is certainly an improvement over simply ignoring the atrial fibrillation in patients undergoing mitral valve surgery as has been the practice in the past.

We continue to apply the complete Maze procedure in patients with atrial fibrillation who require mitral valve surgery, utilizing the cryosurgical rather than the "cut-and-sew" technique to avoid leaving suture lines in the posterior left atrium. The technique presently advocated adds only 20 minutes to the overall procedure and is, as it has always been, just as effective in patients with mitral valve disease as it is in patients without mitral valve or other cardiac disease.


?? REFERENCES
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