Introduction: Intracerebral hemorrhage (ICH) is a severe stroke subtype associated with high mortality and disability. Hematoma expansion (HE) is a major determinant of poor outcomes in ICH, yet effective treatments to limit HE remain elusive. Tranexamic acid, an antifibrinolytic agent, has been proposed to reduce ongoing bleeding in ICH, based on its success in trauma and surgical settings. The STOP-MSU trial tested whether tranexamic acid within 2 hours of symptom onset could reduce HE in spontaneous ICH. However, no effect was found. We hypothesized that fibrinolysis would explain the results. Methods: We conducted a prospective, multicenter observational study across six medical centers in the United States. Eligible patients were adults aged 21 or older who presented with a radiologically confirmed spontaneous ICH within 12 hours of symptom onset. Whole blood samples were collected within 12 hours of ICH symptom onset and analyzed with thromboelastography (TEG). TEG is a non-invasive, point-of-care assay that assesses coagulation factors, fibrinogen, platelets, and fibrinolysis in a single waveform. Fibrinolysis is measured as the percentage of accelerated fibrinolysis within 30 minutes (LY30), with hyperfibrinolysis defined as >8%. Results: A total of 110 patients with spontaneous ICH had readable TEG results. The median time from symptom onset to first blood draw was 6.3 hours IQR 4.6–9.4 hours, and from hospital admission to first blood draw was 2.6 hours 1.6–4.3 hours. The TEG results showed inactive fibrinolysis with a median LY30 value of 0.1% IQR 0.0%–0.6% at first blood draw for this cohort. Only one patient exhibited hyperfibrinolysis with a LY30 of 16%. Most patients (n = 87, 79.1%) had LY30 values less than 1%. Using a more liberal threshold of >3% for hyperfibrinolysis, only 3 patients (2.7%) in our cohort would have met the requirements for tranexamic acid treatment. Conclusion: There is little fibrinolysis to correct in patients with acute spontaneous ICH. Thus, tranexamic acid seems unlikely to have a biologically plausible mechanism to reduce hematoma expansion and improve patient outcomes. These results suggest that alternative therapeutic mechanisms, such as agents promoting coagulation cascade activation, may be more effective in preventing hematoma expansion in ICH patients.
Nascimento et al. (Thu,) studied this question.