Article Figures & Data
Figures
- Figure 1
Conceptual representation of stratified results of secondary risks of restarting anticoagulation following a bleeding event, over time to restart. AC: anticoagulation.
- Figure 2
Overall response from survey participants on timing of oral anticoagulant re-initiation across 11 clinical scenarios.4 Reproduced with open access from Xu et al.4 2018 Public Library of Science under CC BY 4.0. DOAC, direct oral anticoagulant; HTN, hypertension; ICH, intracerebral hemorrhage; IPH, intraparenchymal hemorrhage.
- Figure 3
Bleeding risk by intracranial hemorrhage subtype. SDH. subdural hematoma; sICrH, spontaneous intracranial hemorrhage; tICrH, traumatic intracranial hemorrhage.
- Figure 4
The Parkland Protocol (modified Berne Norwood criteria) categorizes traumatic brain injury (TBI) patterns as low, moderate or high risk for hematoma expansion when considering venous thromboembolism (VTE) prophylaxis. Reproduced with conditional permission from Phelan et al.21 Copyright 2012 Wolters Kluwer Health.
- Figure 5
HRs according to the timing of warfarin initiation. (A) Thromboembolic events; (B) ischemic stroke; (C) major bleeding; (D) composite end point; (E) all-cause mortality. OAT: oral anticoagulation therapy. Reproduced with permission from Park et al.8 Copyright 2016 Elsevier.
- Figure 6
Timing of anticoagulant therapy after severe traumatic intracranial hemorrhage. Reproduced with permission from Divito et al.10 Copyright 2019 Elsevier.
- Figure 7
Timing of secondary events following intracranial hemorrhage by event type. Reproduced with permission from Hawryluk et al.3 Copyright 2010 John Wiley and Sons. CNS, central nervous system.
Tables
- Table 1
Ongoing and pending clinical trials of anticoagulation restart after intracranial hemorrhage
Sponsor Eligibility* Intervention Primary outcome measure Follow-up period Proposed sample size SoSTART NCT03153150 University of Edinburgh All sICrH (ICH, non-aneurysmal SAH, IVH, SDH) with non-valvular AF and CHA2DS2-VASc ≥2 Oral anticoagulation (DOAC or VKA antagonist) versus no anticoagulation teatment Composite event rate: acute coronary, non-fatal stroke or vascular death 1 year 800 ASPIRE NCT03907046 Yale School of Medicine and Yale New Haven Hospital; NINDS ICH (including IVH), 14–120 days prior, with non-valvular AF and CHA2DS2-VASc ≥2 Apixaban versus aspirin Composite event rate: non-fatal hemorrhagic or ischemic stroke or death 1–3 years 700 STATICH NCT03186729 Oslo University Hospital sICH with antithrombotic indication; stratified by AF (anticoagulant arm) and not (antiplatelet arm) Anticoagulant treatment versus no treatment Symptomatic ICH 2 years 500 A3ICH NCT03243175 University Hospital, Lille sICH with non-valvular AF and CHA2DS2-VASc ≥2 Apixaban versus LAAC versus neither intervention (standard care with or without antithrombotic treatment) Composite event rate: fatal and non-fatal, cardiovascular/cerebrovascular, ischemic/hemorrhagic, incracranial/extracranial 2 years 300 APACHE-AF NCT02565693 UMC Utrecht sICH (including IVH) on anticoagulant treatment Apixaban versus no antithrombotic treatment Composite event rate: non-fatal stroke or vascular death 12–72 months 100 ENRICH-AF NCT03950076 Population Health Research Institute sICrH (IPH, IVH, cSAH) or non-penetrating traumatic SDH, with non-valvular AF and CHA2DS2-VASc ≥2, >14 days ago Edoxaban versus no anticoagulant Composite stroke events: ischemic, hemorrhagic, unspecified 2 years 1200 RESTART-T NCT04229758 University of Texas at Austin Traumatic ICrH and provider intent to reinitiate DOAC therapy DOAC at 1 vs 2 vs 4 weeks Composite event rate: hemorrhagic and thromboembolic events 60 days 1100 *Broad summaries of primary eligibility criteria, excluding multiple inclusion and exclusion.
AF, atrial fibrillation; cSAH, convexal subarachnoid hemorrhage; DOAC, direct oral anticoagulant; ICrH, intracranial hemorrhage; IPH, intraparenchymal hemorrhage; IVH, intraventricular hemorrhage; LAAC, left atrial appendage closure; SDH, subdural hematoma; sICH, spontaneous intracerebral hemorrhage; VKA, vitamin K antagonist.
