Nifekalant unmasked residual gap of superior vena cava isolation by suppressing immediate recurrence of intra‐superior vena cava fibrillation

Abstract

Nifekalant successfully suppressed intra‐superior vena cava fibrillation, which complicated the evaluation of the gap of superior vena cava isolation.

A 78‐year‐old female was referred to our hospital for radiofrequency (RF) catheter ablation of symptomatic paroxysmal atrial fibrillation (AF). The ablation was performed using Rhythmia HDx™ (Boston Scientific). Because the patient was in AF at the start of the session, we performed direct current cardioversion (DCC). After that, immediate recurrence of AF (IRAF) repeatedly occurred from the superior vena cava (SVC) (Figure 1A,B). Because it was difficult to maintain sinus rhythm (SR), we performed SVC isolation during AF. With an encircling SVC ablation, the AF in the atria gradually organized and was terminated during the 21st RF application, while the fibrillatory activity inside the SVC (intra‐SVC fibrillation) persisted (Figure 1C). At that point, we diagnosed an SVC exit block. However, the SVC entrance block could not be evaluated because a subsequent DCC resulted in immediate recurrences of intra‐SVC fibrillation.

FIGURE 1.

(A) Immediate recurrence of atrial fibrillation (IRAF) from the superior vena cava (SVC) after initial cardioversion. (B) A magnified view of the timing of IRAF initiation (corresponds to the dotted box in A). (C) AF termination in the atria after the 21st RF application, while the fibrillatory activity was sustained inside the SVC. Asterisks indicate pacing spikes from the ablation catheter to check phrenic nerve capture. CS, coronary sinus; d, distal; DCC, direct current cardioversion; HRA, high right atrium; p, proximal.

The atria remained in SR during subsequent pulmonary vein isolation (PVI). On the other hand, intra‐SVC fibrillation continued even after PVI. We administered 4 μg (0.07 μg/kg) of isoproterenol (ISP) to test the durability of the SVC exit block and the inducibility of extra‐PV foci. After that, atrial depolarization became rapid and irregular, with similar atrial sequence and P‐wave polarity as SR (Figure 2A and Figure S1). The intra‐SVC fibrillation still immediately recurred after multiple DCCs. Once the effect of ISP disappeared, the atria regained almost regular SR whereas the intra‐SVC fibrillation persisted. The differential diagnoses were (i) ISP‐induced SVC reconnection with the irregular conduction of intra‐SVC fibrillation to the atria, and (ii) ISP‐induced premature atrial contractions (PACs) originating near the high right atrium under a complete SVC exit block.

FIGURE 2.

(A) Transiently irregular atrial rhythm observed after isoproterenol infusion at 4 μg (0.07 μg/kg). The corresponding body surface electrocardiogram is presented in Figure S1B. Comparison of body surface electrocardiogram before and after 7 mg of nifekalant infusion. The infusion prolonged the QT interval by 60 ms (400 to 460 ms). (C) Comparison of the interatrial conduction time from high right atrium to distal coronary sinus electrodes before and after nifekalant infusion. Abbreviations as in Figure 1.

To suppress the immediate recurrences of intra‐SVC fibrillation, we considered ablation of the focal source of intra‐SVC fibrillation (e.g., the area with high‐frequency depolarization during intra‐SVC fibrillation or the earliest site at the onset). However, the risk of SVC stenosis and phrenic nerve injury could be increased if multiple RF applications inside the SVC were required.

Finally, to suppress intra‐SVC fibrillation, we administered a low dose (7 mg, 0.13 mg/kg) of nifekalant. The QT interval was prolonged from 400 ms to 460 ms (Figure 2B), whereas the interatrial conduction time from the high right atrium to the distal coronary sinus remained almost the same (Figure 2C). At that point, intra‐SVC fibrillation was successfully suppressed even under continuous ISP infusion at 80–160 μg/h (0.025–0.05 γ). Two gaps were detected and ablated sequentially by high‐resolution gap mapping: one in the posterior wall (Figure 3A) and the other in the lateral wall with 2:1 right atrium‐SVC conduction (Figure 3B). After additional RF applications and a 60‐min nifekalant washout, a bidirectional SVC conduction block was confirmed despite the recurrence of intra‐SVC fibrillation under ISP infusion at 80 μg/h (Figure 4).

FIGURE 3.

Intracardiac electrocardiograms and gap maps of the superior vena cava (SVC) acquired after nifekalant infusion. (A). A gap on the posterior side of the SVC, (B). Another gap with 2:1 right atrium‐SVC conduction on the lateral side of the SVC. Left panels indicate the activation sequences inside the SVC. The middle and right panels are the activation maps for each gap. The catheter (Orion™) positions correspond to the beats presented in the left panels and are superimposed on the activation maps. Curved arrows represent the gap conduction directions, and the red tags indicate the SVC ablation points performed before the gap mapping. PA, posteroanterior; RA, right atrium; RL, right lateral. Other abbreviations as in Figure 1.

FIGURE 4.

(A) Intracardiac electrocardiogram after touch‐up ablation under isoproterenol infusion at 80 μg/h. the atria presented an almost regular rhythm with sporadic premature atrial contractions under intra‐superior vena cava (SVC) fibrillation and its recurrence after direct current cardioversion. Abbreviations as in Figure 1.

SVC is one of the major AF triggers besides pulmonary veins. Sometimes, intra‐SVC fibrillation persists after circumferential isolation is completed. Suppressing the immediate recurrence of intra‐SVC fibrillation is essential for the definitive diagnosis of SVC exit and entrance block.

This case illustrates the usefulness of nifekalant when intra‐SVC fibrillation complicates the evaluation of gap conduction after ablation. Nifekalant is a selective antagonist of the rapidly activated delayed rectifier potassium channel (IKr) and prolongs the effective refractory period of the myocardium. It does not inhibit inward sodium or calcium currents and thus has minimal negative inotropic and dromotropic effects. Nifekalant is mainly used for hemodynamically unstable ventricular arrhythmia. However, it has also been shown to reduce the defibrillation threshold of AF and terminate AF. ¹ , ² Recently, Masuda et al. reported that nifekalant could also facilitate the identification of extra‐PV foci by suppressing IRAF. ³ , ⁴ Using nifekalant, we aimed to suppress the immediate recurrence of intra‐SVC fibrillation to evaluate SVC gap conduction. Because the interatrial conduction time from the high right atrium to the distal coronary sinus was not prolonged after nifekalant infusion, the drug probably did not affect depolarization and the conduction velocity of the atrial muscle, confirming a previous report. ⁵ Na channel blockers (class I drugs) constitute another possible means of suppressing intra‐SVC fibrillation. However, using these agents might suppress gap conduction as well as intra‐SVC fibrillation because they have a negative dromotropic effect.

In conclusion, low‐dose nifekalant suppressed the immediate recurrence of intra‐SVC fibrillation during the evaluation of gap conduction and successfully unmasked ISP‐induced gap conductions. When SVC isolation is complexed by intra‐SVC fibrillation, this pharmacological method may be an effective alternative to terminating it by the ablation inside SVC.

FUNDING INFORMATION

None.

CONFLICT OF INTEREST

None.

ETHICS APPROVAL

N/A.

Supporting information

Figure 1

Sekihara T, Oka T, Nakano T, Ozu K, Sakata Y. Nifekalant unmasked residual gap of superior vena cava isolation by suppressing immediate recurrence of intra‐superior vena cava fibrillation. J Arrhythmia. 2022;38:1094–1098. 10.1002/joa3.12788

DATA AVAILABILITY STATEMENT

Available upon reasonable request.