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Two Cases of Radiofrequency Ablation of Persistent Atrial Fibrillation: A Tailored Approach
Optimal ablative strategies for the treatment of persistent and long-standing persistent atrial fibrillation (AF) have remained the “holy grail” for the interventional electrophysiologist. There have been myriad strategies proposed as the key additional lesion sets added to the foundation of pulmonary vein isolation (PVI).1 Though durable PVI alone was touted in the past as being clinically equivalent to ablation that included additional lesion sets,2 we often find persistent AF cases with isolated PVs, presuming that abnormal substrate exists in either the left atrium (LA) or right (RA) atrium that act as drivers or non-PV triggers of recurrent AF. Additional lesion sets are thus required for rhythm control. Ablation of the LA roof, mitral isthmus, and posterior wall are common adjunctive lesions delivered in the LA after PVI is confirmed and achieved.3-5 Posterior wall isolation has been shown to be beneficial in the management of persistent AF over PVI alone.6
A tailored approach to identifying the underlying mechanism of each particular case, if possible, remains the optimal strategy. Presented below are 2 interesting cases of persistent AF and the ablative strategies used for successful ablation.
Case Presentations
Case #1:
An 80-year-old female presented with symptomatic persistent AF despite sotalol. She had prior catheter ablation with PVI and LA roof line ablation in 2014 and cryo-maze in 2017 during coronary artery bypass grafting/mitral valve repair with surgical left atrial appendage (LAA) exclusion. She maintained sinus rhythm for over 4 years, then developed recurrent AF. She underwent cardioversion with early recurrence of AF (ERAF), and then sotalol was added with repeat cardioversion and ERAF noted. Repeat catheter ablation was recommended. Preprocedural transesophageal echocardiogram (TEE) showed some residual flow and smoke within the LAA but no large communication/flow into the LA and no thrombus present.
Other past medical history included heart failure with preserved ejection fraction (EF), essential hypertension (HTN), severe pulmonary HTN, mixed hyperlipidemia, obstructive sleep apnea (OSA) on continuous positive airway pressure (CPAP), and obesity.
Echocardiogram revealed the left ventricle (LV) cavity was small and hyperdynamic, a LVEF of 70%, and mild concentric hypertrophy. The right ventricular (RV) cavity was mildly enlarged and the RV systolic function was normal. Septal flattening was consistent with RV pressure overload. There was severely elevated RV systolic pressure (RVSP). The estimated RVSP was 69 mm Hg. Estimated RA pressure was 8 mm Hg.
At baseline, despite the surface electrocardiogram (ECG) suggesting AF (Figure 1A), coronary sinus (CS) activation was regular with proximal to distal CS activation and a cycle length (CL) of 350 ms (Figure 1B).
The LA was addressed first, and there was evidence of PVI as well as complete isolation of the LA posterior wall (Figure 1C) from the prior PVI in 2014 and cryomaze in 2017.
The anterior LA was the only region that had residual voltage, and the activation was earliest at the inferior septum near the proximal CS, which suggested breakthrough conduction from the RA with passive activation of the LA.
The RA was then mapped. There was evidence of low posterolateral scar, consistent with surgical incisional scar from the patient’s prior mitral valve replacement surgery. Activation mapping showed a macroreentrant tachycardia going around the scar and a critical isthmus between the scar and inferior vena cava (IVC) (Figure 1D and Video).
Video 1. Activation mapping and animated propagation map showing a macroreentrant tachycardia going around the scar and a critical isthmus between the scar and IVC.
Ablation between the incisional scar to the IVC terminated the tachycardia. Post radiofrequency ablation (RFA), there was no further conduction noted at the ablation line and no inducible atrial flutter with burst pacing and double prematures from the CS, with and without isoproterenol (Figure 1E). The patient has since maintained sinus rhythm without any evidence of recurrent AF or atypical atrial flutter off of sotalol.
Case #2:
A 75-year-old female presented with a history of initially successful catheter ablation with PVI and LA roof line in 2013 and an 8-year period free of any clinical AF recurrence. She developed recurrent persistent AF (Figure 2A) despite sotalol and underwent elective ablation. She was experiencing symptoms of rapid palpitations, lightheadedness, presyncope, and dyspnea. She had a CHA2DS2-VASc score of 6 (HTN=1, age 75=2, transient ischemic attack [TIA]=2, female=1) on apixaban. She experienced TIA, including a sudden transient visual loss in her right eye, on July 20, 2020.
Other past medical history included essential HTN, mixed hyperlipidemia, severe OSA intolerant of CPAP (sleep study on February 20, 2018), and obesity.
An echocardiogram on July 19, 2020, revealed a LVEF of 55%-60%, grade 1 diastolic dysfunction, and no significant valvular disease. The bubble study was negative for interatrial shunt. An adenosine sestamibi study performed on May 24, 2011, showed no ischemia and normal LV function.
LA mapping showed distal PVI with residual electrical activity noted in the antral regions, particularly near the right inferior PV and carina regions. The LA roof line from the prior ablation was intact. Wide antral ablation was performed with the addition of an inferior line to achieve LA posterior wall isolation. The patient was cardioverted to sinus rhythm and repeat voltage mapping was performed during CS pacing. Figures 2B-2D show the preablation and postablation voltage maps. Figure 2E shows the postprocedural ECG.
Postprocedure, the patient has done well, without any further AF recurrence off of sotalol.
Discussion
These cases illustrate 2 patients with persistent AF following prior ablations, each requiring different ablation strategies required for rhythm control. Case 1 shows a RA mechanism for the patient’s atrial arrhythmia, despite complete PV and posterior wall isolation. Case 2 demonstrates successful rhythm control after PV and posterior wall isolation.
Current mapping technologies are particularly useful in localizing focal tachycardias and macroreentrant atrial flutters that may exist following prior ablation. However, mapping and identifying critical regions for persistent AF such as “drivers” remains elusive, and preliminary technologies to map these regions have fallen short of initial expectations.7,8 The LA posterior wall is an embryologic extension of the PVs, contain ganglionic plexi, and demonstrate tissue supporting shortest atrial CLs during AF. Heterogenous fiber orientation and variable conduction between epicardial and endocardial layers can lead to local reentry caused by anisotropic conduction.9 The posterior wall has been an attractive ablation target, albeit with the conspicuous absence of a pivotal randomized controlled trial to support widespread use of this ablation strategy. Difficulties with achieving durable posterior wall ablation and avoiding collateral damage such as esophageal injury are important considerations.
Conclusion
Persistent and long-standing persistent AF patients often have an electrophysiologic substrate that exists beyond the PVs. Ideally, a tailored approach is taken in cases where a focal trigger or macroreentrant circuit can be identified. Atypical atrial flutters are amenable to current technology mapping and provide more specific targets for tailored treatment. The role of empiric lesion sets such as isolation of the LA posterior wall for persistent AF remains controversial, without randomized controlled trial evidence.10 We look forward to the results of the prospective randomized international CAPLA trial in persistent AF patients, which should shed further light on the strategy of posterior wall isolation.11
Disclosures: Dr Phang has completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. He has no conflicts of interest to report regarding the content herein.
References
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