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
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
15-19Informations 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