Successful superior vena cava isolation using point-by-point cryothermal ablation after failed radiofrequency ablation

Abstract

Pulmonary vein isolation is the cornerstone of catheter ablation for atrial fibrillation (AF), but non–pulmonary vein (non-PV) triggers such as the superior vena cava (SVC) also play an important role. Electrical isolation of the SVC (SVCI) can be limited by anatomical complexity and the risk of phrenic nerve or sinus node injury, particularly with radiofrequency or cryoballoon techniques. We report a 76-year-old woman with recurrent paroxysmal AF after cryoballoon pulmonary vein isolation. During repeat ablation, AF was initially induced from the left atrial posterior wall and successfully treated with radiofrequency ablation. Subsequent provocation revealed AF triggers from the SVC. Despite careful radiofrequency ablation under phrenic nerve pacing, complete SVCI could not be achieved. Point-by-point cryothermal ablation was then performed under continuous phrenic nerve monitoring, resulting in successful SVCI without complications. This case suggests that focal cryothermal ablation may be a practical and safer alternative when SVCI cannot be achieved with radiofrequency energy.

Learning objective

To understand that superior vena cava isolation (SVCI) may be challenging with radiofrequency ablation due to anatomical complexity and safety limitations related to phrenic nerve injury. This case highlights point-by-point cryothermal ablation as a feasible alternative strategy, enabling stable catheter contact, precise lesion delivery, and continuous phrenic nerve monitoring, particularly in regions where point-by-point pulsed-field ablation is not yet available.

Introduction

Pulmonary vein isolation (PVI) has become the cornerstone of catheter ablation for atrial fibrillation (AF). However, non–pulmonary vein (non-PV) triggers also contribute to the initiation and maintenance of AF, and their identification and elimination are important for durable rhythm control. Among non-PV sources, the superior vena cava (SVC) is a well-recognized site of ectopic activity. Electrical isolation of the SVC (SVCI) is therefore widely used as an adjunctive ablation strategy in selected patients [1]. Radiofrequency (RF) catheter ablation is the most common energy source for SVCI, but it carries procedural challenges and specific risks, particularly phrenic nerve (PN) and sinus node (SN) injury [2], [3]. Cryoballoon-based SVCI has also been reported, yet similar concerns about PN and SN injury persist [4]. To date, the use of point-by-point focal cryothermal ablation for SVCI has not been well described. We report a case in which SVCI could not be achieved with conventional RF ablation but was successfully accomplished using point-by-point cryothermal ablation under continuous PN monitoring.

Case presentation

A 76-year-old woman with drug-refractory paroxysmal AF was referred for repeat catheter ablation. Four years earlier, she had undergone implantation of a dual-chamber pacemaker programmed to AAI+ mode for sick sinus syndrome. Eight months before the current admission, she underwent cryoballoon ablation with successful bilateral PVI; however, AF recurred within two months despite antiarrhythmic therapy.

At the time of repeat ablation, voltage mapping of the left atrium confirmed durable isolation of all pulmonary veins, with no evidence of residual conduction. Intravenous adenosine triphosphate (ATP, 20 mg) provocation induced AF initiated by premature atrial contractions from the posterior left atrial wall. Linear RF ablation of the left atrial roof and inferior line was performed to isolate the posterior wall. Subsequent ATP administration no longer induced posterior wall triggers; however, the earliest activation was recorded on the MAP catheter (MAP 1–2), consistent with an SVC origin (Fig. 1). The patient then developed immediate recurrent atrial fibrillation (IRAF), and placement of an Advisor™ HD Grid multipolar mapping catheter in the SVC captured ectopy initiating AF from within the SVC (Fig. 2). Pacing from a multipolar catheter positioned in the SVC was performed to identify phrenic nerve capture sites. Given the presence of permanent pacemaker leads within the SVC, all ablation was performed with careful attention to avoid direct catheter–lead contact under continuous fluoroscopic guidance and 3D electroanatomic mapping. To minimize the risk of sinus node injury, we created a sinus activation map during sinus rhythm to tag the earliest right atrial activation site (sinus node region) on the 3D electroanatomic map. In addition, a catheter was positioned in the right superior pulmonary vein (RSPV) as an anatomic landmark, and the planned SVC isolation line was set cranial to the RSPV roof to avoid the sinus node region.

Fig. 1.

During ATP provocation, the earliest atrial activation was recorded on the MAP catheter (electrodes 1–2) positioned at the SVC–right atrial junction, and the ectopy reproducibly initiated atrial fibrillation.

Abbreviations: ATP, adenosine triphosphate; MAP, multipolar mapping catheter; AP, anteroposterior; SVC, superior vena cava. LA, left atrium; RA, right atrium.

Fig. 2.

(A) Anteroposterior fluoroscopic view showing an Advisor™ HD Grid multipolar mapping catheter positioned within the SVC. (B) Intracardiac electrograms during immediate recurrent atrial fibrillation (IRAF) demonstrating SVC ectopy that initiates AF (arrow), confirming an SVC origin of the triggers.

Abbreviations: AF, atrial fibrillation; IRAF, immediate recurrent atrial fibrillation; SVC, superior vena cava; AP, anteroposterior; HD Grid, high-density grid mapping catheter (Advisor™ HD Grid);RSPV, right superior pulmonary vein; RA, right atrium; CS, coronary sinus.

Circumferential RF ablation was delivered at SVC sites without PN capture (30 W for up to 30 s). At sites where PN capture was present, RF energy was limited to 20 W while maintaining continuous PN pacing to monitor diaphragmatic contraction. Despite careful titration of power and lesion delivery, complete SVCI could not be achieved, and conduction between the SVC and right atrium persisted.

Given the concern for further RF delivery near PN capture sites, we elected to perform point-by-point cryothermal ablation as an alternative strategy using a focal cryoablation catheter (Freezor Xtra, 6-mm tip; Medtronic) connected to a CryoConsole system. Continuous phrenic nerve (PN) pacing to capture the diaphragm was maintained from a catheter positioned in the superior vena cava (SVC) throughout cryoablation (output 5 V at cycle length 1000 ms [60 bpm]), and diaphragmatic motion was closely monitored. Based on activation mapping, focal cryothermal applications (240 s per lesion) were delivered to the dominant residual conduction gap along the SVC–right atrial junction, targeting a catheter tip temperature of −80 °C. During the first cryoapplication, AF terminated and complete electrical isolation of the SVC was achieved. A second, consolidative freeze was subsequently applied at an adjacent site along the SVC–right atrial junction to reinforce lesion durability. After confirming complete SVC isolation, ATP was administered and burst atrial pacing from the right atrium was performed using the same provocation protocol as before ablation; however, no atrial premature contractions or AF triggers originating from the SVC were observed, and AF was no longer inducible.

This approach resulted in complete electrical isolation of the SVC. Post-ablation electroanatomic mapping confirmed the lesion set: red tags represented prior RF lesions, yellow tags indicated PN capture sites, and blue tags marked the cryothermal lesions placed under PN monitoring (Fig. 3). No change in diaphragmatic excursion was observed during or after cryoablation. Pacemaker interrogation immediately after the procedure showed no change in pacing threshold, sensing, or lead impedance compared with baseline, and the atrial sensing percentage was also unchanged.

Fig. 3.

Post-ablation electroanatomic maps in the right anterior oblique (RAO) view showing the lesion sets at the SVC–right atrial junction. (A) After RF ablation, conduction persisted across the SVC–right atrial junction. (B) After adjunctive focal cryothermal ablation, complete SVC isolation was achieved. Yellow tags indicate phrenic nerve (PN) capture sites, red tags indicate RF ablation sites without PN capture, and blue tags indicate cryothermal ablation sites delivered under continuous PN pacing.

Abbreviations: PN, phrenic nerve; RAO, right anterior oblique; RF, radiofrequency; SVC, superior vena cava.

The patient had an uneventful post-procedural course and was discharged the following day. Pacemaker parameters (threshold, sensing, and lead impedance) remained unchanged compared with baseline on post-procedural and subsequent follow-up interrogations, and Holter monitoring over more than one year of follow-up showed no recurrence of AF. Serial chest radiographs demonstrated normal diaphragmatic motion without evidence of PN palsy.

Discussion

This case illustrates the feasibility and potential safety of point-by-point focal cryothermal ablation for SVCI in a patient in whom conventional RF ablation was unsuccessful. Although RF-based SVCI has been associated with high acute success rates, several anatomical and technical factors can limit its efficacy. The SVC–right atrial junction frequently exhibits irregular and inhomogeneous myocardial sleeves, making stable catheter contact and durable lesion formation challenging [5]. In addition, proximity to the PN and SN requires cautious power titration, which may lead to residual conduction gaps and incomplete isolation.

Cryoballoon ablation has emerged as an alternative strategy for SVCI, with reported acute success rates of approximately 80–85%. However, the balloon-based approach is still constrained by anatomical limitations and the risk of PN or SN injury, and precise lesion placement is more difficult compared with focal techniques [4]. In both RF and cryoballoon ablation, PN injury—occasionally irreversible—remains an important concern [2].

By contrast, point-by-point focal cryothermal ablation may offer a practical advantage when additional RF delivery is limited by proximity to critical structures. Freeze-mediated catheter adhesion can improve contact stability and enables anatomically tailored lesion delivery to close residual conduction gaps under continuous phrenic nerve pacing. In our case, we used a focal cryocatheter (Freezor Xtra, 6-mm tip) with a target temperature of −80 °C and a 240-second freeze per lesion—settings consistent with prior clinical use of focal cryothermal catheters—and achieved AF termination with immediate SVC isolation during the first application, followed by an additional consolidative freeze at an adjacent site to enhance lesion durability [6]. Recent studies have suggested that high-power, short-duration (HPSD) RF strategies can facilitate efficient SVC isolation, including protocols such as 50 W HPSD ablation and very-high-power short-duration delivery (e.g., 70 W for 4 s), even in anatomically challenging regions [7], [8]. However, in the present case, we elected not to pursue HPSD/vHPSD RF delivery because a transvenous pacemaker lead coursed through the SVC, and we prioritized minimizing any potential risk of lead-related injury and unpredictable interactions during high-power energy delivery in close proximity. Instead, we selected focal cryothermal ablation, which provides freeze-mediated catheter adhesion and stable, anatomically tailored lesion delivery under continuous phrenic pacing.

Another important safety consideration in the present case is the presence of transvenous pacemaker leads coursing through the SVC. Because both radiofrequency and cryothermal ablation are thermal modalities, potential lead-related concerns include insulation injury and alteration of the lead–tissue interface, particularly if direct catheter–lead contact occurs [9]. Cryothermal ablation also provides freeze-mediated catheter adhesion, which can enhance catheter stability and may help minimize unintended catheter–lead interaction; however, evidence directly comparing lead outcomes between thermal energy sources remains limited. Pulsed-field ablation (PFA), a non-thermal modality with relative myocardial selectivity, may theoretically reduce the risk of thermal collateral injury to intracardiac leads; nevertheless, clinically relevant electromagnetic interference can occur, and appropriate peri-procedural device management and post-procedure interrogation remain essential [10]. Moreover, because energy delivery in contact with intracardiac leads or metallic objects may pose unpredictable interactions, meticulous attention to avoid catheter–lead contact during PFA delivery would also be required.

In the Japanese clinical context, point-by-point PFA catheters are not yet widely available. In this setting, focal cryothermal ablation may represent a pragmatic and accessible alternative for achieving safe, anatomically tailored SVCI when RF delivery is constrained by anatomical limitations or safety concerns. Our experience suggests that this approach can be implemented using currently approved cryothermal systems, potentially serving as a bridge until point-by-point PFA technology becomes more widely accessible.

Taken together, this case highlights that point-by-point cryothermal ablation can provide an effective option for SVCI, particularly in patients at high risk of PN or SN injury and in healthcare environments where newer energy sources such as PFA are not yet available.

Conclusion

We report a case of successful SVC isolation achieved with point-by-point focal cryothermal ablation after unsuccessful RF ablation. This strategy allowed precise lesion delivery under continuous PN monitoring, resulting in durable SVCI without complications. Focal cryothermal ablation may be considered as an alternative option for SVCI in situations where RF ablation is limited by safety concerns or fails to achieve complete isolation, especially in regions where point-by-point PFA catheters are not yet available.

Informed consent

Written informed consent for publication of this case report and accompanying figures was obtained from the patient.

Declaration of competing interest

The authors declare that they have no conflicts of interest related to this work.