Data Management And Sharing System of China National Clinical Research Center for Neurological Diseases

《国家中心数据管理与共享系统操作说明书 —— 研究者部分》

Tranexamic acid for acute intracerebral hemorrhage growth based on imaging assessment (TRAIGE): a multicenter; randomized; placebo-controlled trial

First author：刘婧伊

Corresponding author：刘丽萍,王拥军

cerebral hemorrhage tranexamic acid hematoma spot sign blend sign black hole sign

essential_information

2021-04-01

Published articles

Journal：Stroke and Vascular Neurology

Publication type: Original Research

IF(IF): 4.081

PMID: 33795488 Link To Pubmed Full text Download

Background And Purpose

Studies show tranexamic acid can reduce the risk of death and early neurological deterioration after intracranial hemorrhage. We aimed to assess whether tranexamic acid reduces hematoma expansion and improves outcome in intracerebral hemorrhage patients susceptible to hemorrhage expansion.

Method

We did a prospective, double-blind, randomized, placebo-controlled trial at 10 stroke centers in China. Acute supratentorial intracerebral hemorrhage patients were eligible if they had indication of hemorrhage expansion on admission imaging (e.g., spot sign, black hole sign, or blend sign), and were treatable within 8 hours of symptom onset. Patients were randomly assigned (1:1) to receive either 1 g intravenous tranexamic acid bolus followed by an 8 h infusion of 1 g tranexamic acid or a matching placebo (saline). The primary outcome was intracerebral hematoma growth (>33% relative or >6 mL absolute) at 24 h. Clinical outcomes were assessed at 90 days. This trail is registered at ClinicalTrials.gov (NCT02625948).

Conclusion

Among patients susceptible to hemorrhage expansion treated within 8 hours of stroke onset, tranexamic acid did not significantly prevent intracerebral hemorrhage growth. We found it was safe and caused less 90-day death. Larger studies are needed to assess safety and efficacy of tranexamic acid in intracerebral hemorrhage patients.

Main results

Of the 171 included patients, 124 (72.5%) were male, and the mean age was 55.9±11.6 years. Baseline mean intracranial hemorrhage volume was 23.7±18.7 ml. 89 patients received tranexamic acid and 82 received placebo. The treatment groups were well balanced at baseline. The primary outcome did not differ significantly between the groups: 36 (40.4%) patients in the tranexamic acid group and 34 (41.5%) patients in the placebo group had intracranial hemorrhage growth (odds ratio [OR] 0.96 [95% CI 0.52-1.77], p=0.89). Less proportion of death were observed in tranexamic acid treatment group than placebo group (8.1% vs 10.0%), but there were no significant differences in secondary outcomes including absolute intracranial hemorrhage growth, death, and dependency. Major thromboembolic events occurred in 2 patients, 1 in each group (P=0.96).