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Atrial fibrillation arising from a silent superior vena cava

Open AccessPublished:December 06, 2022DOI:https://doi.org/10.1016/j.hrcr.2022.12.002

      Keywords

      Introduction

      Atrial fibrillations (AF) can originate from the pulmonary veins (PVs), and globally, PV isolation has been established as a treatment method of choice for AF.
      • Haïssaguerre M.
      • Jaïs P.
      • Shah D.C.
      • et al.
      Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins.
      However, approximately 20% of AF cases are triggered by non-PV origins,
      • Lin W.S.
      • Tai C.T.
      • Hsieh M.H.
      • et al.
      Catheter ablation of paroxysmal atrial fibrillation initiated by non-pulmonary vein ectopy.
      ,
      • Shah D.
      • Haissaguerre M.
      • Jais P.
      • Hocini M.
      Nonpulmonary vein foci: do they exist?.
      including those in the superior vena cava (SVC). However, the inducibility of non-PV triggers is unpredictable, and AF triggers are difficult to identify. Adenosine triphosphate (ATP) can unmask dormant conduction between the SVC and the right atrium (RA) after ablation and between the PVs and the left atrium (LA).
      • Esato M.
      • Nishina N.
      • Kida Y.
      • Chun Y.
      A case of paroxysmal atrial fibrillation with a non-pulmonary vein trigger identified by intravenous adenosine triphosphate infusion.
      Furthermore, ATP has been used to induce PV and non-PV AF triggers.
      • Kuroi A.
      • Miyazaki S.
      • Usui E.
      • et al.
      Adenosine-provoked atrial fibrillation originating from non-pulmonary vein foci: the clinical significance and outcome after catheter ablation.
      Notably, the induction of AF by ATP injection and accurate identification of triggers is clinically useful. We observed the effects of ATP, including dormant SVC-RA conduction and firing from the nonablated SVC.

      Case report

      A 62-year-old male patient with paroxysmal AF underwent ablation for the second time at our hospital after providing his consent. He had no structural heart disease, and the left ventricular ejection fraction was normal. The PVs were successfully isolated using a cryoballoon during the first ablation, which was conducted 5 years before the second ablation. The patient did not undergo the empiric linear ablation, defragmentation, SVC isolation, or non-PV trigger provocation test during the initial ablation. Two years after the first ablation, paroxysmal AF recurred. During the second ablation, the patient’s atria were electroanatomically mapped using a 20-pole multielectrode catheter (Pentaray; Biosense Webster, Diamond Bar, CA) during coronary sinus pacing. The mapping showed that all PVs remained isolated and no low-voltage areas were detected in either atrium. The absence of reconduction between all PVs and the LA was verified using ATP (20 mg; 0.3 mg/kg). Notably, no SVC potential was recorded above the upper border of the sinus node (Figure 1). To assess the presence of non-PV AF foci, a 5–10 mcg bolus of isoproterenol was intravenously administered; however, it failed to provoke AF. Further, ATP (20 mg) was administered after moving the PentaRay catheter from the LA to the SVC. Thus, SVC potential was immediately induced, followed by ectopic firing within the SVC, resulting in AF (Figure 2). At our hospital, atrioventricular sequential pacing was performed during the blockage of atrioventricular conduction by intravenous ATP administration. It helped us confirm the dormant SVC-RA conduction easily and prevent worsening of circulatory dynamics. ATP elicited 2 pharmacological effects: (1) dormant conduction between the RA and SVC, and (2) AF firing arising from the SVC, which degenerated to AF and ceased spontaneously within 10 seconds. The pharmacological effects of ATP in this patient were not uniform. At certain times, ATP induced only the SVC-RA dormant conduction (no SVC ectopy, Figure 3A ), whereas at other times, firing occurred within the SVC, but the absence of SVC-RA dormant conduction prevented degeneration into AF (Figure 3B). Therefore, we isolated the SVC with an open-irrigation 3.5-mm-tip catheter (ThermoCool SmartTouch SF; Biosense Webster, Diamond Bar, CA). Given that the dormant conduction tended to quickly disappear, ATP was repeatedly administered while monitoring the SVC potential using a decapolar ring catheter (Lasso NAV 2515; Biosense Webster, Diamond Bar, CA). Furthermore, SVC was isolated anatomically above the SVC-RA junction by targeting the electrical breakdown point where the earliest SVC activation occurred during dormant conduction by repeated ATP injection. We confirmed SVC isolation and noninducibility of AF using ATP after waiting for 30 minutes. The patient remained free of AF recurrences for 1 year.
      Figure thumbnail gr1
      Figure 1Three-dimensional electroanatomical right atrial voltage map (CARTO3) during a sinus rhythm prior to the patient’s second ablation. No superior vena cava (SVC) potential was recorded above the upper border of the sinus node. LAO = left anterior oblique view; RA = right atrium; RAO = right anterior oblique view; SN = sinus node.
      Figure thumbnail gr2
      Figure 2Superior vena cava (SVC) potential was observed using a multielectrode mapping catheter (PentaRay; Biosense Webster). This figure shows that atrial fibrillation (AF) was provoked from SVC by intravenous adenosine triphosphate (ATP). A: SVC potential prior to ATP injection progressed starting from the intravenous injection of ATP. No SVC potential was recorded prior to ATP injection; however, a firing from the SVC was observed during atrial and ventricular sequential pacing, ie, after blockage of atrioventricular conduction by intravenous ATP (asterisk) (sweep speed 13 mm/s). B: Enlarged view of the black square in A. Electrically dissociated pulmonary vein potential was detected (orange arrow). The site of earliest activation initiating AF was in the SVC (black arrow), soon followed by AF resulting from SVC-right atrium (RA) conduction (asterisk) (sweep speed 67 mm/s). C: Fluoroscopic view of RA (anterior-posterior view). PentaRay was located in the SVC. AP = atrial pacing; CS = coronary sinus; RV = right ventricle; VP = ventricular pacing.
      Figure thumbnail gr3
      Figure 3Effects of adenosine triphosphate (ATP), including atrial fibrillation (AF) induction and dormant superior vena cava (SVC) conduction. A: Conduction blockage by an intravenous injection of ATP. During atrial and ventricular sequential pacing, dormant SVC-right atrium (RA) conduction was induced, but did not provoke AF (red arrows) (sweep speed 33 mm/s). SVC potential was observed using a multielectrode mapping catheter (PentaRay; Biosense Webster). B: At other times, intravenous injection of ATP resulted in rapid firing within the SVC; however, AF was not provoked because of the absence of SVC-RA conduction (black arrowhead). This phenomenon was observed when RV pacing failed owing to atrioventricular reconduction upon attenuation of ATP (sweep speed 67 mm/s). AP = atrial pacing; CS = coronary sinus; RA = right atrium; RV = right ventricle; VP = ventricular pacing.

      Discussion

      The remarkable point in this study is the confirmation of the characteristic effect of ATP and its occurrence in the SVC that was not ablated. SVC is an important source of non-PV AF trigger factors. The SVC frequently manifests as an origin of AF because of an ATP bolus injection.
      • Lin W.S.
      • Tai C.T.
      • Hsieh M.H.
      • et al.
      Catheter ablation of paroxysmal atrial fibrillation initiated by non-pulmonary vein ectopy.
      ,
      • Tsai C.F.
      • Tai C.T.
      • Hsieh M.H.
      • et al.
      Initiation of atrial fibrillation by ectopic beats originating from the superior vena cava: electrophysiological characteristics and results of radiofrequency ablation.
      ,
      • Santangeli P.
      • Marchlinski F.E.
      Techniques for the provocation, localization, and ablation of non-pulmonary vein triggers for atrial fibrillation.
      ATP and acetylcholine are parasympathetic neurotransmitters that stimulate cardiac tissue and generate autonomic activation. ATP and acetylcholine share similar G-protein receptor–effector coupling systems, and activation of these systems can induce AF via stimulation of the ganglionated plexi.
      • Po S.S.
      • Scherlag B.J.
      • Yamanashi W.S.
      • et al.
      Experimental model for paroxysmal atrial fibrillation arising at the pulmonary vein-atrial junctions.
      ,
      • Cheung J.W.
      • Ip J.E.
      • Chung J.H.
      • et al.
      Differential effects of adenosine on pulmonary vein ectopy after pulmonary vein isolation: implications for arrhythmogenesis.
      Thus, the injection of ATP to search for non-PV triggers of AF after PV isolation is a routine practice.
      • Esato M.
      • Nishina N.
      • Kida Y.
      • Chun Y.
      A case of paroxysmal atrial fibrillation with a non-pulmonary vein trigger identified by intravenous adenosine triphosphate infusion.
      ATP also restores PV-LA conduction by hyperpolarizing PV cells via Na+ current availability. The effects of ATP on SVC-RA dormant conduction after isolation are similar to the effects on isolated PVs. These effects are not uncommon, considering the similarities between the SVC and PVs.
      • Nath S.
      • Lynch 3rd, C.
      • Whayne J.G.
      • Haines D.E.
      Cellular electrophysiological effects of hyperthermia on isolated guinea pig papillary muscle. Implications for catheter ablation.
      • Datino T.
      • Macle L.
      • Qi X.Y.
      • et al.
      Mechanisms by which adenosine restores conduction in dormant canine pulmonary veins.
      • Miyazaki S.
      • Taniguchi H.
      • Komatsu Y.
      • et al.
      Clinical impact of adenosine triphosphate injection on arrhythmogenic superior vena cava in the context of atrial fibrillation ablation.
      Therefore, we often administer ATP to confirm the absence of reconnection between the SVC and RA after SVC or PV isolation. ATP-induced hyperpolarization was more clearly observed in ablated cells than in nonablated cells because ablation causes substantial depolarization of the cells.
      • Datino T.
      • Macle L.
      • Qi X.Y.
      • et al.
      Mechanisms by which adenosine restores conduction in dormant canine pulmonary veins.
      Pascale and colleagues
      • Pascale P.
      • Shah A.J.
      • Knecht S.
      Adenosine reveals dormant conduction of an arrhythmogenic thoracic vein despite the absence of previous ablation.
      reported a case of ATP-induced SVC-RA dormant conduction during a repeat ATP injection in a patient with recurrent AF after PV isolation. They reported that ATP can possibly provoke conduction in electrically silent SVC despite no previous ablation and hypothesized that alternation between electrical quiescence and recovery of excitability in venous muscular sleeve leads to AF. Although the non-PV trigger of AF was suspected to be present in the SVC, this was not electrophysiologically proven. In the present case, ATP provoked venoatrial conduction in electrically silent SVC, thereby supporting their hypothesis that AF is spontaneously provoked from the silent SVC by ATP administration. To the best of our knowledge, this is the first case to be reported on the induction of AF from the silent SVC by ATP injection, as well as SVC-RA dormant conduction.

      Conclusion

      ATP induced SVC firing and SVC-RA dormant conduction, developing AF from the SVC that was not ablated. Non-PV origins are often challenging to identify, because they are difficult to reproducibly induce. It is necessary to carefully examine the inducibility of AF from SVC to reduce recurrence in patients after PV isolation. Thus, even if potential is absent in the SVC, the possibility that SVC is the origin of AF can be excluded using ATP.
      Key Teaching Points
      • Superior vena cava (SVC) is one of the non–pulmonary vein origins of atrial fibrillation (AF).
      • The effects of adenosine triphosphate (ATP) included AF firing from SVC and dormant conduction between SVC and right atrium.
      • Both of the ATP effects were observed and AF revealed from SVC, on which ablation had not been performed.

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