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  •    It is possible to identify abnormal superior vena cava in superior vena cava-triggered AF
    Suman Pasupuleti M.D., Thomas Jefferson University, Philadelphia, PA

    It is well documented that ectopic beats originating in the pulmonary veins (PV) initiate atrial fibrillation (AF). Therefore, pulmonary vein isolation (PVI) is significantly effective in curing AF. However, ectopic beats initiating AF sometimes arise from non-PV foci such as the superior vena cava (SVC), left atrial posterior free wall, ligament of Marshall, crista terminalis and coronary sinus. Because the SVC accounts for the major portion of non-PV foci, SVC isolation (SVCI) in addition to PVI reduces the recurrence of AF. Higuchi et al., therefore did a study to identify differences that might exist between the SVC of patients with and without SVC-triggering of AF.

    This study was done in Japan and included 60 patients (46 men; mean age, 59 years) with drug-refractory paroxysmal (n=46) or persistent AF (n=14). Patients were assigned to one of the two groups. First group consisted of patients with premature beats from SVC triggering AF and underwent SVC isolation (SVCI) along with pulmonary vein isolation (PVI). Second group had no premature beats from SVC triggering AF and therefore only underwent PVI. All patients in this study received only circumferential antral PVI and/or SVCI.

    Rapid activity in the SVC that triggered AF was recognized in 12 patients, and they were assigned to the SVC group. The remaining 48 patients, in whom such activity was not documented, were assigned to the control group. SVC potential amplitude, SVC sleeve diameter and length were measured after PVI. Patients with SVC triggers of AF had larger SVC potential amplitude than did patients without SVC triggers. SVC sleeve length in the SVC group was significantly longer than that in the control group. There were no significant differences between the two groups with regard to SVC diameter.

    All patients were followed at 1, 3, 6, and 12 months post-ablation. The ECG was checked periodically, and 24-hour Holter monitoring was used during the first 3 months post-ablation to assess the recurrence of AF. After conclusion of the study, 15 of the 48 control group patients had a recurrence of AF and underwent repeat PVI. Eight of the 15 continued to have recurrence of AF and were put on antiarrhythmic medication. In the 12 patients in the SVC group, two had a recurrence of AF, and were put on antiarrhythmic medication. All 60 patients in this study were in sinus rhythm at their last follow up at 12 months post ablation.

    Conclusion: The present study suggests that in patients with AF, a long SVC sleeve of >30 mm and large SVC potential of >1.0 mV strongly indicate that the AF was triggered from the SVC. Future studies should be done to evaluate the role of prophylactic SVCI in patients with the above SVC variables with or without SVC triggers.

    References: Higuchi K, Yamauchi Y, Hirao K, Sasaki T, Hachiya H, Sekiguchi Y, Nitta J, Isobe M. Superior vena cava as initiator of atrial fibrillation: Factors related to its arrhythmogenicity. Heart Rhythm. 2010 Sep;7(9):1186-1191. Epub 2010 May 12.

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