Key result
NOACs are linked to a ~25% higher absolute rate of early breakthrough stroke or TIA versus VKAs.
Why the study?
Do NOACs compared to VKAs affect the clinical severity and timing of onset of acute ischemic stroke/TIA in patients with NVAF?
Cohort (n=381)
No
Do NOACs compared to VKAs affect the clinical severity and timing of onset of acute ischemic stroke/TIA in patients with NVAF?
Absolute Event Rate: 32% vs 7%
p-value: p=<0.001
Patients on NOACs who develop ischemic stroke/TIA tend to have milder neurological deficits at discharge but are more likely to experience these events within the first 3 months of treatment initiation compared to those on VKAs.
Early post-NOAC ischemic events in NVAF may warrant closer monitoring; leaves open causality versus confounding in observational data.
Background and Purpose: In Japan, four non-vitamin K antagonist oral anticoagulants (NOACs) became available in clinical use for prevention of stroke in patients with non-valvular atrial fibrillation (NVAF) between 2011 through 2014. The aim of this study is to determine underlying characteristics and ischemic stroke/TIA features of patients taking NOACs or warfarin, a vitamin K antagonist (VKA) prior to stroke/TIA. Methods: We enrolled oral anticoagulant (OAC) users for NVAF, who were admitted to our stroke center for acute ischemic stroke/TIA between March 2011 and June 2015 (ClinicalTrials.gov Identifier: NCT02251665). Results: 381 OAC users who developed stroke/TIA were studied. Of these, 63 patients took NOACs [23 women, 77±9 years, dabigatran in 33 (7 taking higher dosage between two official ones), rivaroxaban in 22 (5), apixaban in 8 (3), edoxaban in none] and 318 took VKA (143 women, 79±8 years). There were no significant differences between NOACs users and VKA users in sex, age, CHADS2 score (median 3[IQR 2-4] vs. 3 [2-4]), history of ischemic stroke/TIA (57% vs. 51%) and prior antiplatelet use (25% vs. 24%). Admission NIHSS score tended to be lower (3 [1-15] vs. 7 [2-20], p=0.076) and discharge NIHSS score was lower (1[0-5] vs 3[1-13], p=0.032) in NOACs users. Discharge mRS (2 [1-4] vs. 3 [1-4]) and mortality during hospitalization (5% vs. 4%) were similar between two groups. A different point was timing of stroke/TIA after initiating OAC ; 6% of NOAC users developed events within 14 days and 32% within 3 months, whereas 4% and 7% of VKA users did, respectively (p<0.001). Congestive heart failure tended to be more common in NOACs users developing events within 3 months than those developing events later (43% vs. 19%, p=0.070). Conclusions: NOACs users tended to show milder neurological deficits than VKA users during acute hospitalization of ischemic stroke/TIA, although discharge mRS was similar. NOACs users often developed stroke/TIA within the initial 3 months after initiating OAC, particularly between 14 days and 3 months. One would take special care of ischemic events during early months after initiating NOACs.
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Seki et al. (2016) conducted a cohort in Acute ischemic stroke or TIA with non-valvular atrial fibrillation (n=381). Non-vitamin K antagonist oral anticoagulants (NOACs) vs. Warfarin (VKA) was evaluated on Stroke or TIA within 3 months of initiating oral anticoagulation (p=<0.001). NOAC users admitted for ischemic stroke or TIA more frequently developed events within 3 months of initiation compared to VKA users (32% vs 7%, p<0.001), despite lower discharge NIHSS scores.
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