Mapping and Ablation of an Atypical Left Atrial Flutter Using the EnSite Precision Cardiac Mapping System

Electroanatomic mapping technology has evolved dramatically over the past 20 years. Computer processing/engineering advances have led to iterative evolutions in software programs that increasingly permit electrophysiologists to map arrhythmias with enhanced rapidity and accuracy. The EnSite Precision Cardiac Mapping System (Abbott), first approved in Europe in January 2016, represents one of the latest such evolutions in electroanatomic navigation.

 

In the following case report, an atypical left atrial flutter was mapped and successfully ablated using the EnSite Precision Cardiac Mapping System.

The patient is a 72-year-old female with a past medical history notable for paroxysmal atrial fibrillation and typical, cavotricuspid isthmus-dependent atrial flutter. She underwent an uneventful catheter-based ablation of both of these arrhythmias in spring 2014. 

 

The patient’s atrial arrhythmias remained quiescent from the time of her ablation, without the need for antiarrhythmic drug therapy, until spring 2017. At this time (and in the absence of either the development of an arrhythmia-predisposing medical condition or the need for a proarrhythmic medication), the patient began to experience recurrent palpitations. A 12-lead ECG (Figure 1) and ambulatory ECG monitoring revealed the presence of persistent, atypical-appearing atrial flutter. The decision was made to perform a repeat EP study and catheter ablation of the clinically manifest atrial flutter and, if necessary, reisolation of the pulmonary veins.

 

Pre-procedural CT imaging showed four pulmonary veins without evidence of stenosis. The left atrium was noted to be mildly dilated. A pre-electrophysiology study transesophageal echocardiogram showed a dilated left atrium, an intact interatrial septum, and no left atrial appendage thrombus.

 

The ablation procedure was performed under general anesthesia with an INR of 2.4. Prior to transseptal puncture, an electroanatomic map of the right atrium was created. The atrial flutter circuit was then studied from the right atrium using entrainment mapping and activation/propagation mapping. Entrainment with the ablation catheter positioned at both the cavotricuspid isthmus and the interatrial septum, respectively, revealed long post-pacing intervals. Neither alteration in the atrial flutter cycle length nor devolution of atrial flutter to atrial fibrillation was seen during entrainment exercises. Using the aforementioned mapping techniques, in conjunction with assessment of the coronary sinus decapolar catheter atrial electrogram sequence, it was determined that the atrial flutter circuit arose from the left atrium.

 

Transseptal puncture was performed using fluoroscopic and intracardiac ultrasound imaging. Once left atrial access was obtained, an electroanatomic map of the left atrium and pulmonary vein geometry was created by sweeping an Advisor FL Circular Mapping Catheter, Sensor Enabled (Abbott) within the left atrial endocardial cavity. Voltage and activation/propagation maps were simultaneously collected. The EnSite Precision Cardiac Mapping System’s SparkleMap feature was then utilized to create a video representation of the atrial flutter activation pattern superimposed upon the anatomic and voltage map — permitting direct visualization of the atrial flutter propagation sequence (Figures 2-3). A fractionation map was also created, whereby fractionated endocardial electrograms were automatically tagged by the EnSite Precision software, thus allowing further overlay of potentially relevant data onto a single map.

 

Coalescing the various electroanatomic mapping data described above with standard entrainment mapping, the patient’s atrial flutter circuit was identified as involving the left atrial roof. The pulmonary veins were noted to be electrically silent with a cuff of antral scar (voltage <0.15 mV) identified around each vein orifice.

 

Ablation of the left atrial flutter was then performed using a 3.5 mm tip TactiCath Quartz Contact Force Ablation Catheter (Abbott), with a power setting of 20W and a goal of 10-20 g of force. Catheter stability was monitored via proximal electrogram assessments, intermittent fluoroscopy, and EnSite Precision navigation. Esophageal temperature monitoring was performed continually during ablation with an indwelling esophageal temperature probe. 

 

Ablation proceeded along the length of the left atrial roof dome, beginning at the scar tissue border along the superior margin of the right superior pulmonary vein, and continuing leftward to the left superior pulmonary vein. Care was taken to create as superior/cranial a line as possible so as to avoid esophageal temperature rises posteriorly and thermal damage to Bachmann’s bundle anteriorly. Point-by-point tags were created during the ablation catheter drag as local potential electrograms were either eliminated or split into double potentials.

 

As the ablation line was created, the atrial flutter circuit gradually slowed from 260 msec to approximately 400 msec. Atrial flutter terminated abruptly with ablation lesion application to the anterior-superior ridge, between the left superior pulmonary vein and the left atrial appendage (Figure 4). After completion of the left atrial roof line and termination of atrial flutter, bidirectional block was confirmed via differential pacing from both the Advisor catheter (positioned in the left atrial appendage) and the ablation catheter (positioned on the posterior left atrial wall). Double potentials or an absence of electrical signals was observed at each point ablated along the roof line.

 

After ablation of the left atrial flutter line, isoproterenol was infused and burst pacing was performed. No atrial fibrillation or atrial flutter was induced. Bidirectional block was again confirmed along the left atrial roof. Cavotricuspid isthmus block was also confirmed to be durable from the patient’s initial ablation.

One month post ablation, the patient remains arrhythmia free, on no antiarrhythmic drug therapy.

The left atrial roof is suspected to harbor substrate that can support macroreentry around the pulmonary veins. Ablation of the left atrial roof can transect directly (and thus terminate) an atrial flutter circuit traversing the left atrial roof.

 

In addition, the left atrial roof can be the site of fractionated electrograms that can foster localized electrical activity capable of engendering atrial fibrillation. Ablation of the left atrial roof can prolong the atrial fibrillatory cycle length and be effective in rendering atrial fibrillation non-inducible post ablation.^1,2

 

Left atrial roof ablation carries with it the risk of atrial-esophageal fistula formation and altered left atrial hemodynamics (per disruption of Bachmann’s bundle). Furthermore, gaps within a left atrial roof line can be proarrhythmic.

 

The clinical benefit of an empiric left atrial roof line has been found to be similar to the benefit of an empiric mitral isthmus line, though it usually requires less time to create and is associated with higher rates of bidirectional block. It remains unanswered as to whether creation of an empiric left atrial roof line at the time of atrial fibrillation ablation (without an antecedent history of roof-dependent atrial flutter) merits the associated risk of proarrhythmia or damage to contiguous structures.^3,4