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A superior septal approach to the mitral valve involves an incision of the right atrium between the tricuspid valve annulus and the high septum.
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Atriotomy flutter can result from slow conduction through this area of scar. The importance of this slow conduction in sustaining atrial flutter may only be apparent once cavotricuspid isthmus (CTI) ablation is performed.
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Knowledge of the local surgical practice with respect to the operative approaches to the atria, as well as careful attention to mapping with attention to change in cycle length and/or failure to terminate flutter after CTI ablation, is critical to making the correct diagnosis.
Introduction
Macroreentrant right atrial (RA) tachycardias have been reported following surgical incision of the atrium to treat acquired and congenital heart disease.
Ablation of atrial tachycardia after surgery for congenital and acquired heart disease using an electroanatomic mapping system: which circuits to expect in which substrate?.
Ablation of atrial tachycardia after surgery for congenital and acquired heart disease using an electroanatomic mapping system: which circuits to expect in which substrate?.
The surgeon makes a vertical incision in the RA starting near the atrioventricular groove and carried cephalad around or through the RA appendage to the superior portion of the atrial septum. Then, the surgeon incises the fossa ovalis and extends this to join the RA incision at the superior septum, where the incision is continued into the dome of the left atrium to expose the mitral valve (Supplemental Figure 1). In contrast to atriotomy flutter following a lateral RA incision, macroreentry RA flutter from a superior septal incision is less well-described in the literature. We report the mapping and ablation of 8 patients with macroreentrant atrial flutters that were dependent on slow conduction through an area of scar on the superior RA in the setting of prior surgical mitral valve repair or replacement.
Case report
Original operative reports were available in 7 of the patients, and all these patients had a superior septal approach to the mitral valve for acquired valve disease. One patient also had a tricuspid valve repair through the same right atriotomy incision. The original operative report was not available for 1 case. An electrophysiology (EP) study and ablation were performed from 1 month to 14 years after surgery. Patient ages ranged from 55 to 78 years and pre-ablation left ventricular ejection fraction from 35% to 65%. The surface electrocardiogram P-wave morphology and tachycardia cycle length (260-490 ms) of the flutter were variable. Some patients presented in atrial flutter and in other cases, arrhythmias were induced with atrial pacing. Catheter mapping and ablation were performed using the Biosense Webster (Irvine, CA) CARTO 3-dimensional electroanatomical mapping system and an irrigated, force-sensing catheter. Local activation was timed relative to a stable coronary sinus reference. An example case is detailed in Figure 1. In 7 of 8 cases, a CTI ablation had been performed either in a prior procedure (3 cases) or during the present procedure (4 cases). In the latter, the flutter was initially assessed to be CTI-dependent, but CTI ablation caused a change in flutter cycle length without termination (Figure 2), leading to remapping and diagnosis of macroreentrant flutter dependent on slow conduction through scar on the superior RA. Ablation was performed at 25–50 W for 10–30 seconds per lesion. The flutters terminated with radiofrequency ablation at the area of slow conduction between the superior vena cava (SVC) and the tricuspid annulus (TA). A linear ablation set was completed, anchored to electrically inert regions. The line was tested by pacing on each side of the line to show bidirectional block, and atrial burst and extrastimulus pacing was performed after termination to assess for inducibility. Representative electroanatomical maps are shown in Supplemental Figures 2–6. Recurrent arrhythmias postprocedure were common. Two of the patients recurred with atrial fibrillation. One patient recurred with superior septal atriotomy flutter. One patient recurred with atypical flutter and was referred for repeat EP study, where only atrial fibrillation could be induced.
Figure 1A: An activation map (early activation denoted by red and late by blue) on the left and voltage map (healthy tissue: purple and scar: red) on the right. The entire tachycardia cycle length of 260 ms was found in the right atrium, with activation rotating around an area of scar on the anterior/superior right atrium. Ablation at the blue dot terminated the tachycardia and a linear ablation was completed to eliminate channels of conduction through the scar area. B: A 12-lead electrocardiogram of the tachycardia showing positive flutter waves in the inferior leads and negative flutter waves in lead V1. C: A PentaRay (Biosense Webster) mapping catheter (TV) in the right atrium near 12 o’clock on the tricuspid annulus. D: Termination of arrhythmia with radiofrequency ablation.
Figure 2Intracardiac electrograms with coronary sinus (CS) catheter, 20-pole catheter in typical halo position about the tricuspid annulus (1,2 low lateral right atrium [RA] and 19,20 low septal RA). The left panel shows atrial flutter with tachycardia cycle length of 400 ms with proximal-to-distal CS activation. The activation about the halo is counterclockwise about the tricuspid valve annulus. Note the split signal on 13,14, which is positioned in the high anteroseptal RA. The ablation catheter is positioned at the cavotricuspid isthmus (CTI). Entrainment pacing from this location had postpacing interval of 410 ms. With radiofrequency ablation at the CTI, the tachycardia slowed to 430 ms and changed activation pattern about the halo (right panel) with TV distal poles now earlier than TV 5,6, indicating a change from typical counterclockwise RA flutter. The ablation catheter is now positioned in the anteroseptal RA near the tricuspid annulus.
We report a series of cases with macroreentrant RA flutter circuits dependent on slow conduction through an area of scar on the superior RA between the SVC and the TA. All patients had a prior history of surgical mitral valve replacement or repair, and 7 of 8 cases had a documented previous superior septal incision for surgical approach to the mitral valve. Traditional vertical left atriotomy approach to the mitral valve would not produce this flutter circuit. Coexistent CTI-dependent RA flutter was common, as has also been noted in other atriotomy flutter series. Close attention to tachycardia cycle length and TA activation pattern is critical when a suspected CTI-dependent flutter fails to terminate with ablation in the usual anatomic location.
In our series, there was 1 confirmed recurrence of the superior right atriotomy flutter. Another patient had suspected recurrent atriotomy flutter and was referred to the EP lab but presented in sinus rhythm, and only atrial fibrillation could be induced. High arrhythmia recurrence rates have been noted by others.
Lack of validated conduction time across the SVC-TA line to predict a durable result, difficult catheter stability in this location relative to a typical CTI ablation, and high burden of arrhythmic substrate in this population may explain the relatively high recurrence rate. Knowledge of the operative approaches to the atria, as well as careful attention to mapping with attention to change in cycle length and/or failure to terminate flutter after CTI ablation, is critical to making the correct diagnosis. This series highlights the importance of EP operators’ familiarity with local surgical practice and obtaining operative reports before EP study and ablation.
Ablation of atrial tachycardia after surgery for congenital and acquired heart disease using an electroanatomic mapping system: which circuits to expect in which substrate?.