Periprocedural anticoagulation for atrial fibrillation ablation is a critical issue in the era of the widespread use of direct oral anticoagulants（DOAC）. Uninterrupted warfarin is now established as a standard care of periprocedural anticoagulation. However, there is still a debate with regard to the management of DOAC because of a lack of evidence or experience. “Uninterrupted DOAC”might be feasible though bleeding complications can be fatal without specific antidotes. Thus, we investigated the feasiblity of“minimally-interrupted DOAC ; MID”protocol as a periprocedural oral anticoagulation management for atrial fibrillation ablation. Under the MID protocol, DOAC was discontinued just one dose before the procedure. We investigated the effects of MID on anticoagulation during procedures by measuring given unfractionated heparin doses and time to target ACT（activated clotting time）>300seconds among a total of consecutive 135 patients undergone atrial fibrillation ablation in our institute. Time to target ACT（TTA）was significantly delayed in the rivaroxaban group（RG）and apixaban group（AG）as compared to dabigatran group（DG）, though DG was comparable to warfarin group（WG）. Required total heparin dose was significantly larger in patients of factor Xa inhibitors than those of WG or DG. Based on our results, the response to unfractionated heparin might be different in factor-Xa inhibitors as compared to dabigatran under MID protocol. Our results suggest that optimal periprocedural anticoagulation protocol should be discussed specifically for each of DOAC besides warfarin.
A 45-year-old male with a history of prior ablation procedure for atrioventricular reentrant tachycardia（AVRT）via a left accessory pathway（AP）at another hospital in 2002 was referred to our institution for recurrent supraventricular tachycardia（SVT）in 2016. The earliest atrial activation during right ventricular（RV）pacing was located at posterior left atrium without decrement property. The clinical SVT with a tachycardia cycle length（TCL）of 344 ms with ventricular-atrial（VA）interval of 142 ms was easily induced by catheter manipulation. The retrograde atrial activation sequence during the SVT was identical to that of RV pacing. RV entrainment pacing revealed the “VAV” response with post-pacing interval - TCL of 108 ms and stimulus-atrial - VA interval of 82 ms, and captured the His potential in a antegrade fashion, indicating orthodromic AVRT with the left posterior AP. Although the VA interval was slightly prolonged after radiofrequency application to the site with earliest atrial activation via transseptal access, the retrograde atrial activation sequence remained unchanged. The findings of VA block with the adenosine triphosphate injection and atrioventricular nodal（AVN）pattern during para-Hisian pacing suggested the successful elimination of AP. The fact that the eccentric atrial sequence remained after ablation might be due to the residual conduction of the leftward extension of the slow pathway located close to the AP. In cases like this, electrophysiologists should be aware of the presence of the AVN leftward extension when the eccentric atrial sequence persists after the elimination of left posterior AP.
A sixty-nine year old male with structurally normal heart suffered from a syncope and facial trauma during walking after alcohol intake. He had undergone catheter ablation for paroxysmal atrial fibrillation associated with chest compression ten months before. Holter electrocardiogram showed a number of “asymptomatic” atrial tachycardia（AT）and no episode of bradycardia. In the second session of catheter ablation for the AT, multiple ATs originating from the right atrium were induced. At the end of the session, we confirmed that no tachycardias could be induced despite isoproterenol infusion after the radiofrequency ablation at the earliest sites of all of the ATs. Head-up tilt test（HUT）was preformed to investigate the cause of the syncope three days after the second session. At three minutes from the onset of head-up with isoproterenol infusion, frequent premature atrial contractions（PAC）accompanied by chest compression were observed following the systolic blood pressure drop to 80mmHg. A fast AT（cycle length : 250bpm）spontaneously occurred and a syncope was concurrently reproduced at seven minutes. After his lying supine, the AT was immediately terminated and no PAC occurred. Although we could not induce any tachycardias by any maneuver in the catheterization laboratory, the AT was surprisingly provoked from non-pulmonary vein origin only by HUT. This is an interesting case that the syncope was initiated only when the fast AT and the vasodepressor vagal response co-instantaneously occurred.