Key result
Symptomatic intracranial hemorrhage occurred early in NOAC therapy with small, non-expanding hematomas, even in patients with acceptable mean systolic blood pressure control (137.8 mmHg) prior to onset.
Observational (n=6)
No
Symptomatic intracranial hemorrhage during NOAC therapy may present with small, non-expanding hematomas even without reversal agents, but stricter blood pressure control may be needed to prevent onset.
Supports heightened early vigilance for ICH on NOACs; leaves open whether stricter BP targets prevent onset in prospective studies.
OBJECTIVES: The first non-vitamin K antagonist oral anticoagulant (NOAC) introduced to the market in Japan was dabigatran in March 2011, and three more NOACs, rivaroxaban, apixaban, and edoxaban, have since become available. Randomized controlled trials of NOACs have revealed that intracranial hemorrhage (ICH) occurs less frequently with NOACs compared with warfarin. However, the absolute incidence of ICH associated with NOACs has increased with greater use of these anticoagulants, and we wanted to explore the incidence, clinical characteristics, and treatment course of patients with NOACs-associated ICH. METHODS: We retrospectively analyzed the characteristics of symptomatic ICH patients receiving NOACs between March 2011 and September 2014. RESULTS: ICH occurred in 6 patients (5 men, 1 woman; mean ± SD age, 72.8 ± 3.2 years). Mean time to onset was 146.2 ± 111.5 days after starting NOACs. Five patients received rivaroxaban and 1 patient received apixaban. None received dabigatran or edoxaban. Notably, no hematoma expansion was observed within 24 h of onset in the absence of infusion of fresh frozen plasma, activated prothrombin complex concentrate, recombinant activated factor VIIa or hemodialysis. When NOAC therapy was initiated, mean HAS-BLED and PANWARDS scores were 1.5 ± 0.5 and 39.5 ± 7.7, respectively. Mean systolic blood pressure was 137.8 ± 15.9 mmHg within 1 month before spontaneous ICH onset. CONCLUSION: Six symptomatic ICHs occurred early in NOAC therapy but hematoma volume was small and did not expand in the absence of infusion of reversal agents or hemodialysis. The occurrence of ICH during NOAC therapy is possible even when there is acceptable mean systolic blood pressure control (137.8 ± 15.9 mmHg) and HAS-BLED score ≤ 2. Even stricter blood pressure lowering and control within the acceptable range may be advisable to prevent ICH during NOAC therapy.
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Akiyama et al. (2015) conducted an observational in Symptomatic intracranial hemorrhage during NOAC therapy (n=6). Non-vitamin K antagonist oral anticoagulants (NOACs) was evaluated on Clinical characteristics, hematoma volume, and hematoma expansion of NOAC-associated symptomatic intracranial hemorrhage. Symptomatic intracranial hemorrhage occurred early in NOAC therapy with small, non-expanding hematomas, even in patients with acceptable mean systolic blood pressure control (137.8 mmHg) prior to onset.
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