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Anterior Left Atrial Flutter Utilizing the Left Atrial Appendage
Case Description
The patient is a 69-year-old male with a history of coronary artery disease, bradycardia, congestive heart failure, hypertension, obesity, diabetes, and long-standing persistent atrial fibrillation for three years s/p pulmonary vein antral isolation and cavotricuspid isthmus ablation. Prior to his first ablation, his left atrial size was 49 mm by transthoracic echocardiogram from the parasternal long axis view. Three years of long-standing persistent atrial fibrillation preceded his first ablation, during which time he developed progressive worsening symptoms of dyspnea on exertion and fatigue. He did well post procedure, yet had recurrence three years later. His left atrial size after recurrence had increased to 51 mm by transthoracic echocardiogram.
During repeat ablation, voltage mapping confirmed that the pulmonary veins remained isolated, so left atrial ablation targets included mitral valve isthmus linear ablation, linear ablation of the roof, posterior wall and coronary sinus ablation. The patient did well for another six years, then redeveloped arrhythmia symptoms. He presented with worsening symptoms of palpitations, shortness of breath, and fatigue. Device interrogation revealed atrial flutter with a tachycardia cycle length (TCL) of approximately 300 ms. The left atrium was progressively more dilated, measuring 53 mm by transthoracic echocardiogram from the parasternal long axis view. As he had undergone prior ablations with extensive posterior wall ablation, it was expected that there was potentially anterior wall and left atrial appendage (LAA) involvement.
The patient was brought back to the electrophysiology lab for treatment of the latest arrhythmia. CARTO (Biosense Webster, Inc., a Johnson & Johnson company) was used with the CONFIDENSE Mapping Module via a PENTARAY catheter, with the THERMOCOOL SMARTTOUCH SF ablation catheter (F-J; Biosense Webster, Inc., a Johnson & Johnson company) via the right groin. A 10 Fr intracardiac ultrasound catheter with a decapolar coronary sinus reference catheter were placed via the left groin. No fluoroscopy was used in this case beyond collection of baseline CARTOUNIVU (Biosense Webster, Inc., a Johnson & Johnson company) images.
We perform fluoroless transseptal catheterization as follows. The SL1 wire was advanced into the superior vena cava, with subsequent advancement of the SL1 visualized under intracardiac ultrasound. The wire was then exchanged for a Brockenbrough extra sharp transseptal needle. The SL1 with Brockenbrough needle inside was pulled down to the septum under intracardiac ultrasound visualization. The transseptal puncture with the SL1 was performed under intracardiac ultrasound visualization with saline injected via the Brockenbrough needle to note bubbles in the left atrium. The Brockenbrough needle was then exchanged back for the SL1 wire, which was placed into the left superior pulmonary vein with the SL1 sheath pushed back and forth across the transseptal site several times for dilation of the septum. The intracardiac ultrasound image of the wire across the septum was used to draw the transseptal location on CARTO. Next, the SL1 was pulled back into the right atrium, and the ablation catheter was pushed across the transseptal site on CARTO into the left atrium and placed in the right superior pulmonary vein. The SL1 was then advanced back across the septum into the left atrium and the wire was exchanged for the PENTARAY catheter.
Mapping revealed isolation of the pulmonary veins. There were a few areas of low voltage on the posterior wall that were ablated with 6-second lesions at 48 watts to achieve posterior wall isolation, which did not affect the tachycardia. Activation on the coronary sinus (CS) was earliest distally. There were patchy areas of scar adjacent to normal signal on the anterior left atrium (Figure 1) as well as normal signal within the LAA by voltage mapping. Furthermore, signal along the superior mid anterior left atrium was early and fractionated. Early signal was noted in the LAA as well, although not quite as early as the left atrial anterior wall. Activation and propagation mapping (Figure 2, Video 1) along with Ripple mapping (Video 2) revealed left atrial flutter utilizing the anterior left atrial wall at the level of the anterior right superior pulmonary vein and LAA. The propagation map revealed an early meets late activation pattern anterior to the base of the LAA and a zone of slow conduction at the anterior roof near the base of the LAA (Video 1). Entrainment on the superior aspect of the mid anterior left atrium was 10 ms greater than the TCL. We could not entrain from the posterior wall.
Pulmonary antral vein isolation lesion extent was defined by voltage mapping. Ablation was performed with 5-second lesions at 50 watts. This linear lesion set was performed horizontally on the anterior wall, from the anterior aspect of the former right superior pulmonary vein isolation lesion set to the base of the LAA, which slowed the TCL by 15 ms, from 310 ms to 325 ms (Figure 3). Early activation was still noted within and around the base of the LAA. Therefore, ablation was performed around the base of the LAA with 6-second lesions at 48 watts, with slowing of the TCL to 345 ms, and after which a delay was noted in the left atrial appendage. The tachycardia terminated during isolation of the LAA (Figure 4). Additional 6-second lesions at 43 watts within the LAA were applied to achieve complete left atrial appendage isolation after termination of the tachycardia (Figure 5). The target for all lesions was 10 grams of contact force.
The patient’s CHA2DS2-VASc score was 5, necessitating the need for lifelong anticoagulation. Plans to implant a LAA closure device at a later date were also devised as an adjunct for the treatment strategy of this patient.
Discussion
Although the left atrial flutter TCL increased with anterior wall ablation, the LAA was a critical part of the circuit, so it did not terminate until LAA isolation was performed. This suggests an epicardial portion of the tachycardia circuit. Extensive scarring occurring during long-standing persistent atrial fibrillation likely promotes epicardial circuits, facilitating the perpetuation of arrhythmias exclusive from the pulmonary veins. It is also likely that these epicardial circuits are partially responsible for the greater difficulty and lower success rates seen in long-standing persistent atrial fibrillation ablation. One would expect the advent of contact force and the use of high-power short-duration lesions could help achieve higher success rates in these more difficult atrial fibrillation cases, which has been the experience of this lab.
Summary
The left atrial appendage can be very problematic, both as a major source of strokes and arrhythmogenesis. Much has been discussed regarding the pitfalls of anterior wall ablation, especially when involving the left atrial appendage. Concern over left atrial flutter and the risk of stroke with left atrial appendage isolation can be a deterrent. However, in patients with long-standing persistent atrial fibrillation and significant left atrial enlargement in which pulmonary vein antral isolation and posterior wall ablation fail, ablation of anterior wall arrhythmias, including those involving the left atrial appendage, is beneficial. Allowing patients to remain in lifelong atrial fibrillation creates higher rates of morbidity and mortality. Anticoagulation should be continued per CHA2DS2-VASc score regardless of ablation success. LAA closure or ligation may be considered in patients for whom anticoagulation is problematic or contraindicated.
In this case, the patient has now been arrhythmia free for 6 months by device interrogation, and is status-post LAA closure device implant.
Disclosure: Dr. Smith has no conflicts of interest to report regarding the content herein.
Editor’s Note: This article underwent peer review by one or more members of EP Lab Digest’s editorial board.
