Archives

  • 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • br Conflict of interest br Acknowledgment br Introduction

    2019-06-19


    Conflict of interest
    Acknowledgment
    Introduction Several investigators recently showed that the superior vena cava (SVC) was one of the major foci for initiating atrial tachyarrhythmias, such as atrial tachycardia (AT) and atrial fibrillation (AF) [1–4]. Conduction block between the atrium and thoracic veins has been reported and is well recognized in the pulmonary veins; however, conduction block from the SVC to the right atrium (RA) is rare [3,5]. In this case, a conduction block at the exit site of the SVC–RA connection was strongly suggested using a circular multipolar catheter (Lasso) and CARTO mapping. Because of the conduction block, 2 different forms of atrial tachyarrhythmias were observed in the SVC and atrium. We performed successful catheter ablation of this unusual arrhythmia by achieving electrical isolation of the SVC.
    Case report A 62-year-old man had frequent palpitations for 3 years, and incessant AT and paroxysmal AF were documented by surface 12-lead electrocardiogram (ECG). Because the tachyarrhythmias were drug-refractory, he was referred for catheter ablation of the atrial tachyarrhythmias. The AT (atrial adenylyl cyclase length=240ms) demonstrated an upright P wave in the inferior leads, a negative P wave in the aVR lead, and a positive P wave in the V1 lead, resembling that of sinus rhythm (Fig. 1). Echocardiography revealed normal systolic function and no structural abnormalities.
    Electrophysiological procedures Electrophysiological procedures were performed after informed consent was obtained. All local electric potentials were recorded using a computerized EP system (EP Lab, Bard, USA) under local anesthesia. A 5-Fr, 10-pole catheter was placed from the right jugular vein into the coronary sinus, and a 4-Fr, 5-pole catheter was placed in the His bundle region. A baseline electrophysiological study revealed AT with a cycle length of about 340ms, relatively regular but irregular rhythm, and 2:1 atrioventricular (AV) conduction. We inserted the catheter into the 4 pulmonary veins, but the earliest atrial activation was recorded in the upper RA. The RA was reconstructed using 3-dimensional electroanatomical mapping (CARTO XP, Biosense Webster Inc., USA) with a 3.5-mm tip steerable catheter (Navistar, Biosense Webster Inc., USA). CARTO mapping revealed that the earliest atrial activation occurred at the posteroseptal site of the SVC–RA junction. When the catheter was advanced into the SVC, local potentials in the SVC revealed fibrillation (Fig. 2A). We speculated that the AT originated from the SVC; the SVC fibrillation conducted to the RA with a conduction block at the SVC–RA junction, and the global atrium exhibited AT. To confirm this hypothesis, we administered intravenous adenosine triphosphate (ATP; 20mg), which accelerated the SVC–RA conduction and shortened the atrial cycle length (Fig. 2AII), consequently converting the AT to transient atrial fibrillation (AF; Fig. 2AIII). Complete AV block due to ATP was also observed in Fig. 2AII. After cardioversion with 150J, we recorded SVC potentials subsequent to the atrial potentials with a 20-pole circular mapping catheter (Variable Lasso, Biosense Webster Inc., USA). During sinus rhythm, the RA–SVC connection demonstrated 1:1 conduction (Fig. 2B). We recognized premature atrial beats as the earliest activation recorded by the Lasso catheter placed in the SVC. Initiation of tachycardia was observed after frequent premature atrial beats originating from the SVC (Fig. 2B). During tachycardia, activation in the SVC exhibited fibrillation; however, the potentials recorded in the atrium demonstrated AT (Fig. 2B). Subsequently, AF was terminated by cardioversion with 150J, and we placed a Lasso catheter at the SVC–RA junction to identify the SVC–RA connection. During sinus rhythm, the earliest SVC potentials were recorded by electrodes 3–4 of the Lasso catheter, and both electrodes 3–4 of the Lasso catheter and the ablation catheter exhibited fragmented potentials (Fig. 2B), suggesting that the SVC–RA connection was located at a posteroseptal site of the SVC–RA junction (Fig. 3A). Furthermore, the location of this site corresponded to the location of the earliest activation visualized by CARTO mapping (Fig. 3B).