Does tranexamic acid affect intraventricular hemorrhage growth in acute ICH? An analysis of the STOP-AUST trial.

CT scan cerebral hemorrhage hematoma expansion hemorrhage intracerebral hemorrhage intraventricular hemorrhage spot sign

Journal

European stroke journal
ISSN: 2396-9881
Titre abrégé: Eur Stroke J
Pays: England
ID NLM: 101688446

Informations de publication

Date de publication:
Mar 2022
Historique:
received: 01 09 2021
accepted: 19 12 2021
entrez: 18 3 2022
pubmed: 19 3 2022
medline: 19 3 2022
Statut: ppublish

Résumé

Trials of tranexamic acid (TXA) in acute intracerebral hemorrhage (ICH) have focused on the imaging outcomes of intraparenchymal hematoma growth. However, intraventricular hemorrhage (IVH) growth is also strongly associated with outcome after ICH. Revised definitions of hematoma expansion incorporating IVH growth have been proposed. We sought to evaluate the effect of TXA on IVH growth. We analyzed data from the STOP-AUST trial, a prospective randomized trial comparing TXA to placebo in ICH patients presenting ≤ 4.5 h from symptom onset with a CT-angiography spot sign. New IVH development at follow-up, any interval IVH growth, and IVH growth ≥ 1 mL were compared between the treatment groups using logistic regression. The treatment effect of TXA against placebo using conventional (> 6 mL or 33%), and revised definitions of hematoma expansion (> 6 mL or 33% or IVH expansion ≥ 1 mL, > 6 mL or 33%, or any IVH expansion, and > 6 mL or 33% or new IVH development) were also assessed. Treatment effects were adjusted for baseline ICH volume. The analysis population consisted of 99 patients (50 placebo, 49 TXA). New IVH development at follow-up was observed in 6/49 (12%) who received TXA and 13/50 (26%) who received placebo (aOR: 0.38 [95% CI: 0.13-1.13]). Any interval IVH growth was observed in 12/49 (25%) who received TXA versus 26/50 (32%) receiving placebo (aOR: 0.69 [95% CI: 0.28-1.66]). IVH growth ≥ 1 mL did not differ between the two groups. Using revised definitions of hematoma expansion, no significant difference in treatment effect was observed between TXA and placebo. IVH may be attenuated by TXA following ICH; however, studies with larger cohorts are required to investigate this further. http://www.clinicaltrials.gov; Unique identifier: NCT01702636.

Sections du résumé

Background UNASSIGNED
Trials of tranexamic acid (TXA) in acute intracerebral hemorrhage (ICH) have focused on the imaging outcomes of intraparenchymal hematoma growth. However, intraventricular hemorrhage (IVH) growth is also strongly associated with outcome after ICH. Revised definitions of hematoma expansion incorporating IVH growth have been proposed.
Aims UNASSIGNED
We sought to evaluate the effect of TXA on IVH growth.
Methods UNASSIGNED
We analyzed data from the STOP-AUST trial, a prospective randomized trial comparing TXA to placebo in ICH patients presenting ≤ 4.5 h from symptom onset with a CT-angiography spot sign. New IVH development at follow-up, any interval IVH growth, and IVH growth ≥ 1 mL were compared between the treatment groups using logistic regression. The treatment effect of TXA against placebo using conventional (> 6 mL or 33%), and revised definitions of hematoma expansion (> 6 mL or 33% or IVH expansion ≥ 1 mL, > 6 mL or 33%, or any IVH expansion, and > 6 mL or 33% or new IVH development) were also assessed. Treatment effects were adjusted for baseline ICH volume.
Results UNASSIGNED
The analysis population consisted of 99 patients (50 placebo, 49 TXA). New IVH development at follow-up was observed in 6/49 (12%) who received TXA and 13/50 (26%) who received placebo (aOR: 0.38 [95% CI: 0.13-1.13]). Any interval IVH growth was observed in 12/49 (25%) who received TXA versus 26/50 (32%) receiving placebo (aOR: 0.69 [95% CI: 0.28-1.66]). IVH growth ≥ 1 mL did not differ between the two groups. Using revised definitions of hematoma expansion, no significant difference in treatment effect was observed between TXA and placebo.
Conclusions UNASSIGNED
IVH may be attenuated by TXA following ICH; however, studies with larger cohorts are required to investigate this further.
Registration UNASSIGNED
http://www.clinicaltrials.gov; Unique identifier: NCT01702636.

Identifiants

pubmed: 35300248
doi: 10.1177/23969873211072402
pii: 10.1177_23969873211072402
pmc: PMC8921778
doi:

Banques de données

ClinicalTrials.gov
['NCT01702636']

Types de publication

Journal Article

Langues

eng

Pagination

15-19

Informations de copyright

© European Stroke Organisation 2022.

Déclaration de conflit d'intérêts

Declaration of conflicting interests: The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: AM reports honoraria paid for advisory board, speaker fees, and travel from Stryker and Boehringer Ingelheim. SMD reports lectures and advisory boards activities for Medtronic, Amgen, and Boehringer Ingelheim. All other authors declare no competing interests.

Références

Neurology. 2013 Apr 2;80(14):1295-9
pubmed: 23516315
Neurosurgery. 2006 Oct;59(4):767-73; discussion 773-4
pubmed: 17038942
Neuroradiology. 2016 Sep;58(9):867-76
pubmed: 27380041
Int J Stroke. 2021 Aug;16(6):640-647
pubmed: 33131467
Neurocrit Care. 2020 Dec;33(3):732-739
pubmed: 32219678
Stroke Vasc Neurol. 2021 Nov 30;:
pubmed: 34848566
Lancet. 2018 May 26;391(10135):2107-2115
pubmed: 29778325
Neurology. 2019 Aug 27;93(9):e879-e888
pubmed: 31371565
Stroke. 2020 Apr;51(4):1120-1127
pubmed: 32078498
N Engl J Med. 2005 Feb 24;352(8):777-85
pubmed: 15728810
Lancet Neurol. 2020 Dec;19(12):980-987
pubmed: 33128912
Lancet Neurol. 2018 Oct;17(10):885-894
pubmed: 30120039
Int J Stroke. 2014 Jun;9(4):519-24
pubmed: 23981692

Auteurs

Vignan Yogendrakumar (V)

Department of Neurology, Melbourne Brain Centre at the Royal Melbourne Hospital, University of Melbourne, Parkville, VIC, Australia.

Teddy Y Wu (TY)

Department of Neurology, Christchurch Hospital, Christchurch, New Zealand.

Leonid Churilov (L)

Department of Neurology, Melbourne Brain Centre at the Royal Melbourne Hospital, University of Melbourne, Parkville, VIC, Australia.
Melbourne Medical School, University of Melbourne, Heidelberg, VIC, Australia.

Turgut Tatlisumak (T)

Department of Neurology, Helsinki University Hospital, Helsinki, Finland.

Daniel Strbian (D)

Department of Neurology, Helsinki University Hospital, Helsinki, Finland.

Jiann-Shing Jeng (JS)

Department of Neurology, National Taiwan University Hospital, Taipei, Taiwan.

Timothy J Kleinig (TJ)

Department of Neurology, Royal Adelaide Hospital, Adelaide, SA, Australia.

Gagan Sharma (G)

Department of Neurology, Melbourne Brain Centre at the Royal Melbourne Hospital, University of Melbourne, Parkville, VIC, Australia.

Bruce Cv Campbell (BC)

Department of Neurology, Melbourne Brain Centre at the Royal Melbourne Hospital, University of Melbourne, Parkville, VIC, Australia.

Henry Zhao (H)

Department of Neurology, Melbourne Brain Centre at the Royal Melbourne Hospital, University of Melbourne, Parkville, VIC, Australia.

Chung Y Hsu (CY)

Department of Neurology, China Medical University Hospital, Taichung, Taiwan.

Atte Meretoja (A)

Department of Neurology, Helsinki University Hospital, Helsinki, Finland.

Geoffrey A Donnan (GA)

Department of Neurology, Melbourne Brain Centre at the Royal Melbourne Hospital, University of Melbourne, Parkville, VIC, Australia.

Stephen M Davis (SM)

Department of Neurology, Melbourne Brain Centre at the Royal Melbourne Hospital, University of Melbourne, Parkville, VIC, Australia.

Nawaf Yassi (N)

Department of Neurology, Melbourne Brain Centre at the Royal Melbourne Hospital, University of Melbourne, Parkville, VIC, Australia.
Population Health and Immunity Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia.

Classifications MeSH