As described in Chapter 9 , a number of lessons were learned from surgery for other arrhythmias that were critical to the development of surgery for atrial fibrillation (AF). The treatment of patients with the Wolff-Parkinson-White (WPW) syndrome and ischemic ventricular tachycardia dominated clinical arrhythmia surgery in the 1970s, but by the early 1980s, surgical procedures had been developed for essentially all clinically important arrhythmias except AF (see Chapter 9 ). Arrhythmia surgery reached its peak during the decade of the 1980s with frequent operations being performed in some centers for the WPW syndrome, ischemic and non ischemic ventricular tachycardia, automatic atrial arrhythmias, and atrioventricular node reentry tachycardia (AVNRT). The most active period in the development of surgery for AF was also in that decade, especially from 1980 to 1987.
Surgical Isolation Procedures for Atrial Fibrillation
His Bundle Ablation
The first interventional procedure used clinically for the treatment of patients with AF was surgical His bundle ablation, though it was not developed specifically for the treatment of those with AF. Obviously, successful His bundle ablation necessitated the implantation of a permanent ventricular pacemaker ( Fig. 11.1 ) Elective His bundle ablation was first performed for patients with WPW syndrome whose accessory pathways could not be divided successfully ( Fig. 11.2A ). Although the primary objective of WPW surgery was always to divide the accessory atrioventricular (AV) connection responsible for the arrhythmia (see Chapter 9 ), it was sometimes impossible to do so, especially in the earliest days of arrhythmia surgery. Because the macro-reentrant circuit responsible for the reciprocating tachycardia of the WPW syndrome includes antegrade conduction through the AV node and retrograde conduction across the accessory pathway ( Fig. 11.2B ), the reentrant circuit can be interrupted by ablating the His bundle but only as a last resort if the accessory pathway cannot be successfully divided ( Fig. 11.2C ). His bundle ablation in patients with the WPW syndrome ablates the reciprocating tachycardia but leaves the patient with an abnormal ventricular activation pattern postoperatively because the ventricles are activated across the accessory pathway, not through the AV node ( Fig. 11.2D ). However, there is no need for a postoperative ventricular pacemaker.
(A) Diagram of the four chambers of the heart and propagation of a normal sinus rhythm impulse (red arrows) through the heart. (B) Ablation of the His bundle confines the sinus-generated impulse to the two atria, which continue to be activated in a normal manner. However, ventricular activation must be maintained by a permanent ventricular pacemaker after His bundle ablation. PM, pacemaker.
(A) In patients with the Wolff-Parkinson-White (WPW) syndrome, antegrade conduction across the accessory atrioventricular connection (yellow area) causes ventricular preexcitation, resulting in a “delta wave” on the standard electrocardiogram.
(B) If antegrade conduction across the accessory pathway is blocked, the following beat will conduct retrograde and result in the reciprocating tachycardia characteristic of WPW syndrome.
(C) The primary objective in WPW surgery is to divide the accessory pathway, but when this cannot be accomplished, the reciprocating tachycardia can be terminated permanently by ablating the His bundle as a last resort.
(D) Ablation of the His bundle in patients with WPW syndrome results in abnormal, but effective, ventricular conduction postoperatively and does not require a permanent ventricular pacemaker.
Fortunately, it was rarely necessary to ablate the His bundle as a last resort in patients with WPW syndrome. More commonly, His bundle ablation was used to treat patients with other medically refractory supraventricular tachycardias that could not be adequately localized by intraoperative mapping to allow for focal ablation. These arrhythmias included automatic atrial tachycardias in either atrium and occasionally poorly defined refractory atrial reentrant tachycardias. The intraoperative localization of automatic atrial tachycardias was especially problematic because the general anesthesia required for surgery usually suppressed the automatic focus, making it impossible to localize. Because automatic foci do not respond to programmed electrical stimulation, the automatic atrial arrhythmias could not be induced intraoperatively. In these cases, the surgeon frequently had no choice but to resort to His bundle ablation for both automatic right atrial tachycardia, which was usually multifocal in origin ( Fig. 11.3A ), and automatic left atrial tachycardia, which was usually unifocal in origin ( Fig. 11.3B ). At that time, atrial flutter and AF were poorly understood, and if either could not be controlled by medical therapy and was sufficiently symptomatic, His bundle ablation with pacemaker implantation was performed to confine the arrhythmia to the atria, thus protecting the ventricles ( Fig. 11.3C and 11.3D ).
(A) Elective His bundle ablation is an effective therapy for automatic right atrial tachycardia in which the specific site(s) of origin of the tachycardia cannot be identified by intraoperative mapping. Automatic right atrial tachycardia is typically multifocal in origin. A ventricular pacemaker is required after surgery.
(B) Elective His bundle ablation is also an effective therapy for automatic left atrial tachycardia in which the specific site(s) of origin of the tachycardia cannot be identified by intraoperative mapping. Automatic left atrial tachycardia is typically unifocal in origin. A ventricular pacemaker is required after surgery.
(C) Elective His bundle ablation was an effective therapy for refractory atrial flutter before learning that its macro-reentrant driver (the “atrial flutter wave”) uses the cavotricuspid isthmus as a part of its circuit. When elective His bundle ablation was used to treat patients with atrial flutter, a ventricular pacemaker was required after surgery.
(D) Before identifying the electrical events that occur during atrial fibrillation (AF), elective His bundle ablation was used to treat patients with refractory AF. A ventricular pacemaker was required after surgery.
The first lesson we learned when trying to create heart block by elective ablation of the AV node–His bundle complex was that it was surprisingly difficult to accomplish surgically. This observation seems paradoxical in view of the ease with which heart block can be caused inadvertently when performing surgery at or below the tricuspid valve annulus such as tricuspid valve repair or replacement and closure of membranous ventricular septal defects in tetralogy of Fallot. Elective His bundle ablation was performed through an incision identical to that described in Chapter 9 for dividing posterior septal accessory pathways in patients with the WPW syndrome (see Fig. 9.7 ), and the fat pad in the anterior portion of the posterior septal space was dissected free of the ventricular septum. In addition, the AV node artery was originally identified and divided in hopes of creating heart block by that maneuver alone, but as described in Chapters 3 and 9 , the AV node is not an end artery, and its division does not result in heart block (see Figs. 3.19 and 3.20 ).
Even extensive surgical dissection in this region proved to be an unreliable method for creating heart block. Therefore cryoablation of the His bundle replaced surgical dissection as the technique of choice in the mid-1970s. The right atrium (RA) was opened in the usual manner, but no incision was made inside the atrium. The only clinical cryoprobes available at the time were non disposable nitrous oxide probes of varying sizes. Nitrous oxide cooled the cryoprobes to–60°C, but the temperature of the cryoprobe could be held at any level above 0°C if so desired. We took advantage of that feature to “ice map” for the location of the His bundle just above the tricuspid valve annulus and immediately posterior to the membranous atrial septum by first cooling the cryoprobe to only 0°C. After the exact location of the His bundle was identified, conduction through it was temporarily blocked, but conduction returned a few seconds after stopping the freeze. By moving the probe to slightly different positions in the known region of the His bundle, it was possible to find a single spot where 0°C caused temporary heart block. After that position was found, we cooled to 0°C to cause temporary heart block, stopped the freeze without moving the probe tip, waited for the return of AV conduction, and then cooled down to–60°C for 2 minutes. Cryoablation of the His bundle proved to be far easier and more reliable than surgical dissection and remained the procedure of choice for elective His bundle ablation until Scheinman developed the catheter fulguration technique for His bundle ablation in 1982.
Left Atrial Isolation Procedure
A disproportionate number of the patients with automatic atrial tachycardias in whom we had to ablate the His bundle and implant permanent pacemakers were younger than 30 years of age and included several teenagers. This was stimulation enough to try to devise some better way to treat un mappable automatic atrial tachycardias that would not necessitate lifelong pacemaker dependence. Because the sinoatrial (SA) node is in the upper lateral RA and the AV node–His bundle complex is in the atrial septum, it seemed rather obvious that if we could devise a way to separate the body of the left atrium (LA) from the rest of the heart surgically, it would isolate the automatic focus to the LA and allow the rest of the heart to stay in a normal sinus rhythm ( Fig. 11.4 and Fig. 9.16 ).
(A) Automatic left atrial tachycardia could be confined to the atria by creating heart block. A ventricular pacemaker was required after surgery. (B) The left atrium (LA) is isolated from the remainder of the heart after a left atrial isolation procedure for an automatic left atrial tachycardia. Note that the sinoatrial node is capable of generating a normal sinus rhythm after isolation of the LA with normal activation of the right atrium, right ventricle, and left ventricle. PM, pacemaker.
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