A group of surgical research fellows were once challenged to ablate normal sinus rhythm in a normal dog within 5 minutes using a 2-cm diameter cryoprobe. None could do it. This was an experiment to demonstrate how difficult it is to damage a normal SA node enough to require a PPM. This is largely because normal sinus rhythm can originate from anywhere within a large area of the right atrium (RA) (the atrial pacemaker complex) distant from the anatomic SA node. Thus, if a patient has an SA node that is entirely normal preoperatively, it is virtually impossible to traumatize it enough surgically to cause permanent dysfunction. Most cases of documented postoperative SA node dysfunction were in patients whose preoperative SA node function was never evaluated, and in addition, most dysfunction was also temporary. Nevertheless, it is prudent to avoid traumatic injury of the anatomic SA node by creating lesions as far away from it as possible and by avoiding excessive retraction during surgery.

The atrial pacemaker complex, including the SA node, can be traumatized temporarily by surgical retraction that is applied to gain exposure of the inside of the left atrium (LA), especially when a mitral valve procedure or a Maze procedure is performed through a median sternotomy. This can occur regardless of whether LA exposure is gained through Waterston’s groove or by an anterior transseptal incision. Surgical approaches that require less traction for exposure, such as minimally invasive, thoracoscopic, and robotic Maze procedures, are associated with lower postoperative pacemaker requirements than are Maze procedures performed through a median sternotomy. Another potential reason for fewer pacemakers being required after these minimally invasive approaches may be surgeon selection bias, as surgeons who perform the Maze procedure by these techniques usually have had more experience with the procedure.

Surgical traction injury of the SA node is manifest early as a slower postoperative sinus rate, but the effect is temporary. ^, Simultaneously, vagal innervation of the AV node is often suppressed by the LA lesions of the Maze procedure, ^, resulting in faster spontaneous AV node rates in the immediate postoperative period. The combination of a slower SA rate and a faster AV node rate immediately after a Maze procedure often results in a temporary junctional rhythm postoperatively. Because it can take several days for the SA node and AV node rates to return to normal with restoration of sinus rhythm, surgeons often implant PPMs for temporary junctional rhythm during this recovery phase to hasten hospital discharge. This scenario can also be seen after other LA procedures such as mitral valve surgery in patients who do not have a concomitant Maze procedure.

Some surgeons are reluctant to perform the superior vena cava (SVC) lesion of a Maze procedure because they are concerned that it is too close to the anatomic SA node and therefore may injure it. Although this concern is unwarranted, again, it is prudent to place all of the RA lesions in locations that are least likely to cause any damage to the SA node or the AV node. Thus, we always place the SVC lesion in the lateral portion of the SVC orifice, which keeps it well away from the anatomic SA node and avoids all other areas of the atrial pacemaker complex ( Fig. 21.1 ). To our knowledge, there has never been a report documenting traumatic injury of the SA node caused by the SVC lesion, regardless of the energy source used and despite tens of thousands of Maze procedures having been performed.

Right atrial (RA) lesions and atrial pacemaker complex. The RA lesions of the Maze procedure are purposely positioned to create minimal damage to the atrial pacemaker complex. This includes the right atriotomy that creates the free-wall portion of the “T” lesion and provides exposure to the inside of the right atrium RA for the endocardial cryoablation extension of the lesion down to the tricuspid valve annulus.

In summary, it is virtually impossible to cause permanent SA node dysfunction by traumatic injury during surgery. Temporary SA node dysfunction caused by traction for surgical exposure invariably recovers if the SA node was normal preoperatively. However, one of the most common reasons that post-Maze patients receive a PPM is for the treatment of temporary postoperative junctional rhythm.

There is a coronary artery branch that is designated the “SA node artery” because it passes directly through the anatomic SA node. Thus it is reasonable to assume that if this SA node artery were injured, it would result in SA node dysfunction, perhaps even severe enough to require a PPM implantation. However, the relationship between the SA node artery and the anatomic SA node is not that of an end-artery, so interruption of the SA node artery has little or no effect on SA node function or dysfunction.

I (JLC) was once honored to share a long train ride from Kiruna, Sweden, to Narvik, Norway, with the legendary cardiologist and pathologist Dr. Thomas N. James, who was universally regarded as one of medicine’s greatest experts on coronary artery anatomy and the specialized conduction system. During that trip, Dr. James made a most enlightening comment regarding the blood supply of the SA node. He stated: “The SA node artery reminds me of an interstate highway passing through a small town but with no off-ramps to that town because even though the SA node artery passes through the anatomic SA node, it has no identifiable branches to its specialized cells” (see Chapter 3 , Fig. 3.10 ). Dr. James’ point was that yes, there is a coronary artery branch that passes through the anatomic SA node, and therefore we call it the “SA node artery,” but there is no indication that it actually supplies blood to the SA node!

With this in mind, the fear that some clinicians have about interrupting the SA node artery with the SVC lesion of a Maze procedure is clearly unwarranted. Engle et al. documented that no patients in their series with disease or total obstruction of the SA node artery had dysfunctional SA nodes. Therefore, the SA node artery does not serve as an end artery to the anatomic SA node and its occlusion does not cause SA node dysfunction. The clinical results of the Maze procedure further support the concept that the SA node is not dependent on a single end artery for its blood supply. Tens of thousands of patients have undergone properly performed Maze procedures in which the superior end of the intercaval lesion was placed into the orifice of the SVC. Undoubtedly, the SA node artery was either divided or frozen in many of these cases. However, no direct relationship has ever been demonstrated between the SVC lesion of a Maze procedure and the need for new postoperative pacemakers. SA node artery injury by the RA lesions of the Maze procedure is not a cause of increased postoperative pacemaker requirements.

The AV node and the proximal portion of the His bundle are located entirely within the atrial septum (see Chapter 3 , Fig. 3.17 ). From the surgeon’s view, they are located in the triangle of Koch (see Chapter 3 , Fig. 3.18 ). This triangular anatomic space is bordered by the tendon of Todaro superiorly and the tricuspid valve annulus inferiorly with the os of the coronary sinus at its base and the membranous atrial septum at its apex. The AV node–His bundle complex is located near the apex of the triangle of Koch with the His bundle passing to the ventricles immediately posterior to the membranous septum. It is anatomically impossible for the lesions of the Maze procedure to injure the AV node–His bundle complex without crossing the tendon of Todaro and entering the triangle of Koch with an atrial septal lesion. The atrial septal lesions in the historical Maze-I and Maze-II procedures were surgical incisions that did not cross the tendon of Todaro and therefore were incapable of causing heart block. Likewise, the atrial septal lesion in the cut-and-sew Maze-III procedure, which is positioned more posteriorly in the atrial septum, also ends above the level of the tendon of Todaro. Neither the CryoMaze-III nor the Maze-IV procedure has an atrial septal lesion at all, so it is obviously impossible to injure the AV node–His bundle complex with either of these contemporary Maze procedures ( Fig. 21.2 ).

The primary differences in the Maze-I, Maze-II, and cut-and-sew Maze-III lesion patterns was a progressive repositioning of the atrial lesion from anterior to posterior. (A) In the original Maze-I procedure, the superior end of the atrial septal lesion was anterior to the superior vena cava (SVC) orifice. (B) In the Maze-II procedure, the superior end of the septal lesion was in the medial portion of the SVC orifice. (C) In the cut-and-sew Maze-III procedure, the superior end of the septal lesion was posterior to the SVC orifice. (D) There is no atrial septal lesion in either the CryoMaze-III procedure or the Maze-IV procedure. Regardless of where the superior ends of the septal lesions were positioned in the first three iterations of the Maze procedure, the lower end of the septal lesion always terminated at the tendon of Todaro (yellow dashed line) just above the os of the coronary sinus and well away from the atrioventricular node–His bundle complex, which is located at the apex of the triangle of Koch.

One of the most frequently referenced surgical papers in the AF literature is the 2015 Cardiothoracic Surgery Network (CTSN) Clinical Trials article published in The New England Journal of Medicine documenting that patients with persistent AF who require mitral valve surgery have superior outcomes if the AF is ablated concomitantly during the mitral surgery than if the AF is ignored. However, one of the major so-called “complications” in that trial was a dramatic increase in the need for postoperative pacemakers in patients who received biatrial Maze procedures rather than left-sided-only lesions. This observation was interpreted as confirmation that the RA lesions in the biatrial Maze group were responsible for the increased postoperative pacemaker requirements.

The problem with that interpretation is that according to their own data, the differences in postoperative pacemaker requirements were not due to SA node injury but to AV node–His bundle injury that caused postoperative heart block. Yet none of the biatrial Maze procedures in that study included an atrial septal lesion! The absence of an atrial septal lesion in these patients makes it anatomically impossible for the RA lesions to have created heart block necessitating a postoperative pacemaker. Other possible explanations for the increased need for pacemakers in the biatrial Maze group include the following: (1) more AF was successfully ablated with the biatrial Maze than with the LA-only lesions ; (2) more patients who received the biatrial Maze also underwent double valve replacement; (3) because of the more extensive valve surgery, the aortic cross-clamp times had to be longer in the biatrial Maze group; and (4) there was no documentation of preoperative SA node function in either group of patients. However, what can be stated with absolute certainty is that the RA lesions in the biatrial Maze group did not cause the increased incidence of heart block and subsequent pacemaker implantations because none of the RA lesions were anywhere near the AV node–His bundle complex.

Finally, it is worth recalling that for nearly 20 years before the first Maze procedure, elective His bundle ablation was a common surgical procedure to treat supraventricular tachyarrhythmias, including AF, that could not be controlled medically (see Chapter 11 , Fig. 11.3 ). It seems that with the RA open on cardiopulmonary bypass and the ability to localize the site of the His bundle under direct vision using a handheld electrode, surgical division of the His bundle would be a simple operation. However, even after hours of blunt and sharp surgical dissection in the posterior septal space and triangle of Koch after map-guided localization of the His bundle, it was sometimes virtually impossible to create heart block on purpose. In fact, it was so difficult that in the mid-1970s, cryosurgery was introduced by our group at Duke University specifically to replace surgical dissection in the effort to create elective heart block more reliably. This personal experience over 2 decades is why we are confident in stating that a single, carefully placed atrial septal lesion in the Maze procedure will not inadvertently create heart block, and it renders comical any suggestion that a surgical procedure that has no septal lesion at all can inadvertently create heart block. The RA lesions of the Maze procedure do not cause heart block.

The AV node artery penetrates the posterior interventricular septum through the posterior septal space to reach the AV node located in the lower anterior interatrial septum ( Fig. 21.3 ). In the early years of Wolff-Parkinson-White syndrome surgery, patients with posterior–septal accessory pathways represented the greatest challenge to arrhythmia surgeons because of intense efforts to avoid surgical injury of the AV node artery. At that time, the AV node artery was assumed to be an end artery whose interruption would automatically lead to heart block. In the late 1970s, I (JLC) became suspicious that posterior–septal accessory pathways were intimately associated with the AV node artery and that its meticulous preservation was the primary reason why surgery for these accessory pathways failed so often. Therefore, a new surgical approach was developed in which the AV node artery was purposely divided in patients with posterior–septal accessory pathways. During the ensuing 15 years, I purposely divided the AV node artery surgically in 115 consecutive patients with posterior–septal pathways, and not one patient developed heart block. This observation confirmed that like the SA node artery, the AV node artery is not an end artery, and its division will not cause heart block.

The atrioventricular (AV) node artery typically penetrates the posterior ventricular septum to exit from the floor of the posterior septal space before entering the atrial septum to reach the AV node.