Most of what is known about atrial fibrillation (AF) has come from basic electrophysiologists and clinical electrophysiologists, and this knowledge has accrued primarily from the study of what we clinically call stand-alone AF . This refers to AF that is not associated with other heart problems that are severe enough to warrant cardiac surgery. AF that develops as a result of left-heart problems that are severe enough to warrant surgery (e.g., coronary artery disease, mitral or aortic valve disease, or other left-heart abnormalities) is called concomitant AF and is in the domain of surgeons.
There are several differences between stand-alone AF and concomitant AF. For example, patients with concomitant AF tend to have more atrial scarring and larger, thicker left atria. Early in the stage of left-heart disease, only the left atrium (LA) may be affected, and the right atrium (RA) can be entirely normal. The longer left-heart disease remains untreated, the greater the likelihood of the RA’s becoming involved in the adaptive response, especially in mitral and aortic valve disease. When both atria are adversely affected by the left-heart problem, the patient is more likely to develop AF. Thus, if the primary left-heart structural problem is not surgically corrected early in the course of coronary artery or valve disease, the RA is more likely to be involved in sustaining the AF, and the patient is more likely to need a biatrial AF ablation procedure.
Another difference between stand-alone AF and concomitant AF is that approximately 90% of the atrial triggers that induce stand-alone AF are located in and around the pulmonary veins. However, only approximately 70% of the atrial triggers are located in the pulmonary vein area in patients with concomitant paroxysmal AF (PAF) ( Fig. 25.1 ). These differences in both the anatomy and the electrophysiology of stand-alone AF and concomitant AF dictate that the outcomes for the same interventional procedure will be different in the two groups. Thus, a perfect box lesion that isolates all four pulmonary veins and the posterior left atrial wall can reach a maximum success rate of 90% for stand-alone AF but a maximum success rate of only 70% for concomitant AF.
(A) In stand-alone atrial fibrillation (AF), approximately 90% of AF triggers are located in and around the pulmonary veins. (B) In concomitant AF, approximately 70% of atrial triggers are located in and around the pulmonary veins.
Because surgeons rarely treat stand-alone AF, the most important decisions we have to make regarding the treatment of AF in patients undergoing coronary artery or valve surgery relate to concomitant AF only. The first, and by far the most important, thing that surgeons must determine in these patients is whether they have PAF (repeatedly induced by atrial triggers) or non-paroxysmal AF (non-PAF sustained by atrial macro-reentrant drivers).
Paroxysmal Atrial Fibrillation
Patients with PAF usually spend most of their time in normal sinus rhythm (NSR). They then have the spontaneous discharge of an automatic or micro-reentrant focus (trigger), usually located in or around the pulmonary veins, that induces macro-reentrant drivers in the atria resulting in AF (see Chapter 5 , Fig. 5.34 ). In patients with PAF, the resultant episode of AF may last from several minutes up to 7 days before it self-terminates or is terminated with drugs, and NSR resumes ( Fig. 25.2 ). For another episode of AF to occur, it must again be induced by an atrial trigger, which may or may not be the same one that induced the previous AF episode. This is the repetitive cycle of NSR–PAF–NSR that patients with PAF experience.
Paroxysmal atrial fibrillation (PAF): self-limiting episode of AF. Patients with PAF are usually in normal sinus rhythm (NSR). When an AF trigger suddenly fires (lower panel), it induces an episode of AF (right panel) that is either self-limited or can be terminated by antiarrhythmic drugs or electrical cardioversion in less than 1 week from its onset. The objective of interventional therapy (catheter ablation or surgical ablation) for PAF is to isolate as many triggers in and around the pulmonary veins and intervening posterior left atrial wall as possible to decrease the likelihood of the induction of an episode of AF.
The goal of AF surgery in patients with PAF is to isolate as many of the AF triggers as possible from the rest of the heart. Because we know that roughly 70% of these triggers are located in and around the pulmonary veins, it is logical to isolate this area of the heart with a box lesion around the pulmonary veins and intervening posterior left atrial wall (the “pulmonary vein cuff”), which should result in a 70% success rate. Over the years, we have learned the approximate distribution of the other non-pulmonary vein atrial triggers ( Fig. 25.3 ), so we can now predict the success of any AF isolation or ablation procedure that one might use for concomitant PAF. Of the triggers within the pulmonary vein cuff, 20% or more are located in the posterior left atrial wall ( Fig. 25.4 ). The remaining 50% within the pulmonary vein cuff are in the right and left pulmonary veins, and we assume that they are equally distributed between the two pairs of veins. Thus, simple isolation of the pulmonary veins in pairs with a bipolar clamp can be expected to produce a success rate of approximately 50% in patients with concomitant PAF ( Fig. 25.5 ). Adding a roof and floor lesion to the pulmonary vein isolation (PVI) to isolate the additional 20% of triggers in the posterior left atrial wall creates a box lesion around the entire pulmonary vein cuff and therefore increases the expected success rate in PAF to 70% ( Fig. 25.6 ). At least 10% of the atrial triggers in patients with PAF reside in the left atrial appendage (LAA). Thus, if LAA occlusion (LAAO), which includes LAA electrical isolation or LAA amputation, is added to a box lesion in patients with PAF, the success rate can be expected to reach approximately 80% ( Fig. 25.7 ). It is important to understand that catheter-based devices that are used to close the LAA endocardially do not electrically isolate the LAA from the LA even though the LAA may be successfully occluded. Likewise, neither endocardial nor epicardial suture closure of the LAA electrically isolates the LAA; therefore, neither of them improves the success rate of adding LAAO to a box lesion for patients with PAF. The only currently available LAA occluding devices that electrically isolate the LAA are epicardial devices that devascularize the musculature of the LAA itself, such as the surgical AtriClip and the catheter-based LARIAT device. Of course, surgical amputation of the LAA serves the same purpose.
Distribution of atrial triggers in concomitant paroxysmal atrial fibrillation (PAF). AF triggers can be located anywhere in either atrium, but approximately 70% of them are located in and around the pulmonary veins and in the posterior left atrial wall between the two pairs of pulmonary veins. We refer to this area encompassing all four pulmonary veins and the intervening posterior left atrial wall as the “pulmonary vein cuff.”
Proportional distribution of “pulmonary vein cuff” triggers in concomitant paroxysmal atrial fibrillation (PAF). Approximately 20% of the atrial triggers are located in the posterior left atrial wall between the two pairs of pulmonary veins (shadowed area). This means that the remaining 50% of triggers within the pulmonary vein cuff are located within or in the immediate vicinity of the pulmonary veins. If they are distributed evenly between the two pairs of pulmonary veins, then each pair of pulmonary veins harbors approximately 25% of the atrial triggers present in patients with concomitant PAF.
Pulmonary vein isolation (PVI) for concomitant paroxysmal atrial fibrillation (PAF). On the basis of the distribution of potential atrial triggers, PVI alone would be expected to have a success rate of approximately 50% in patients with concomitant PAF.
Box lesion for concomitant paroxysmal atrial fibrillation (PAF). A box lesion encompassing all four pulmonary veins and the posterior left atrial wall would be expected to have a success rate of approximately 70% in patients with concomitant PAF.
Box lesion plus left atrial appendage occlusion (LAAO) for concomitant paroxysmal atrial fibrillation (PAF). The combination of a box lesion with LAAO would be expected to have a success rate of approximately 80% in patients with concomitant PAF. Because this combination of lesions can be performed without opening the left atrium, it is a reasonable alternative to the Maze procedure in patients undergoing coronary bypass graft (CABG), aortic valve replacement (AVR), or CABG plus AVR by surgeons less experienced in arrhythmia surgery.
One disadvantage of performing only a box lesion plus LAAO for concomitant PAF in patients undergoing coronary artery bypass graft (CABG) and/or aortic valve replacement (AVR) is that these lesions do not render the atria incapable of fibrillating. It only decreases the likelihood of having recurrent episodes of AF by isolating most of the potential triggers that induce each episode. Thus, nonpulmonary vein triggers, arrhythmia triggers, and nonarrhythmia triggers can still induce AF (see Chapter 5 ). The only way the atria can become incapable of fibrillating is by performing a Maze procedure, but this requires opening the atrium. Most experienced arrhythmia surgeons perform Maze procedures routinely in patients with any type of AF who require cardiac surgery. However, a box lesion plus LAAO is a reasonable alternative for the treatment of concomitant PAF, especially for surgeons who are less experienced in arrhythmia surgery.
Non-paroxysmal Atrial Fibrillation
The current classification of AF is not always helpful in deciding which interventional approach is best in a given patient with AF because it is based solely on the duration of the episodes of AF (see Chapter 52 ). PAF episodes last less than 1 week, persistent AF episodes last between 1 week and 1 year, and long-standing persistent AF (LSpAF) lasts more than 1 year. After AF has been initiated, macro-reentrant drivers sustain the AF until it spontaneously terminates or is terminated by drug therapy or electrical cardioversion. After AF has been induced, the electrophysiologic events in the atria during AF are the same regardless of the duration of the episode. Thus, the primary physiologic difference in PAF, persistent AF, and LSpAF is the electrical stability of the macro-reentrant AF drivers ( Fig. 25.8 ).
