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Uninterrupted use of direct oral anticoagulants versus vitamin K antagonists for catheter ablation of atrial fibrillation with PVAC gold: incidence of silent cerebral microembolic events.
Journal of Interventional Cardiac Electrophysiology : An International Journal of Arrhythmias and Pacing 2020 September 20
BACKGROUND: Silent cerebral microembolic events (SCE) after duty-cycled ablation of atrial fibrillation using PVAC have been detected by cerebral magnet resonance imaging (MRI) in a substantial number of patients. The purpose of this study was to investigate if uninterrupted oral anticoagulation with non-vitamin K antagonists (NOACs) compared with vitamin K antagonists (VKA) affects the incidence of SCE after pulmonary vein isolation (PVI) using PVAC Gold.
METHODS: Eighty-four consecutive patients (62 ± 15 years, 58% male) undergoing a first PVI were prospectively enrolled. Of these, 42 were on VKA and 42 on uninterrupted NOAC treatment. An activated clotting time (ACT) ≥ 350 s was targeted for ablation.
RESULTS: Cerebral MRI the day after PVI revealed acute diffusion-weighted positive lesions in 11/42 (26%) VKA compared with 14/42 (33%) in NOAC patients (p = 0.634). No differences were found for lesion size, number of lesions/patient, and number of lesions indicating cerebral infarction (2.4% for VKA and 4.8% for NOAC patients). Seventy-five percent of NOAC patients with sporadic ACT levels < 300 s during PVI developed SCE compared with 22% of corresponding VKA patients (p = 0.030). VKA and NOAC subgroups with ACT ≥ 350 s had no reduced incidence of SCE compared with ACT 300-350 s.
CONCLUSIONS: A significant, but comparable, number of patients under uninterrupted anticoagulation with VKA or NOACs still experience SCE after PVAC Gold PVI. NOAC patients with sporadic subtherapeutic ACT levels during PVI are at the highest risk for SCE while permanent ACT levels ≥ 350 s did not further reduce the incidence of SCE in both groups.
METHODS: Eighty-four consecutive patients (62 ± 15 years, 58% male) undergoing a first PVI were prospectively enrolled. Of these, 42 were on VKA and 42 on uninterrupted NOAC treatment. An activated clotting time (ACT) ≥ 350 s was targeted for ablation.
RESULTS: Cerebral MRI the day after PVI revealed acute diffusion-weighted positive lesions in 11/42 (26%) VKA compared with 14/42 (33%) in NOAC patients (p = 0.634). No differences were found for lesion size, number of lesions/patient, and number of lesions indicating cerebral infarction (2.4% for VKA and 4.8% for NOAC patients). Seventy-five percent of NOAC patients with sporadic ACT levels < 300 s during PVI developed SCE compared with 22% of corresponding VKA patients (p = 0.030). VKA and NOAC subgroups with ACT ≥ 350 s had no reduced incidence of SCE compared with ACT 300-350 s.
CONCLUSIONS: A significant, but comparable, number of patients under uninterrupted anticoagulation with VKA or NOACs still experience SCE after PVAC Gold PVI. NOAC patients with sporadic subtherapeutic ACT levels during PVI are at the highest risk for SCE while permanent ACT levels ≥ 350 s did not further reduce the incidence of SCE in both groups.
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