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. 2024 Sep 11;8(7):102568.
doi: 10.1016/j.rpth.2024.102568. eCollection 2024 Oct.

Hyperfibrinolysis: a crucial phenotypic abnormality of posttraumatic fibrinolytic dysfunction

Affiliations

Hyperfibrinolysis: a crucial phenotypic abnormality of posttraumatic fibrinolytic dysfunction

Kyosuke Takahashi et al. Res Pract Thromb Haemost. .

Abstract

Background: Traumatic fibrinolytic dysfunction is often categorized into 3 phenotypes based on the result of thromboelastography (TEG) lysis at 30 minutes (LY30): fibrinolysis shutdown, physiologic fibrinolysis, and hyperfibrinolysis. However, the molecular pathophysiology of fibrinolytic dysfunction and the association with clinical outcomes have not been fully evaluated.

Objectives: To assess whether posttraumatic fibrinolysis phenotypes identified by TEG correlate with levels of key fibrinolysis-related serum markers and with risk of mortality and hospital complications.

Methods: This is a secondary analysis of the Pragmatic, Randomized Optimal Platelet and Plasma Ratios trial. Patients were stratified according to the degree of fibrinolysis upon arrival using TEG LY30 values: low LY30, <0.8%; normal LY30, 0.81% to 0.9%; and high LY30, ≥3%. Serial values of molecular markers (0-72 hours after admission) and clinical outcomes were compared between fibrinolysis groups.

Results: A total of 547 patients were included (low LY30, 320; normal LY30, 108; high LY30, 119). The high LY30 group had higher tissue plasminogen activator and plasmin-antiplasmin values upon hospital arrival than the low LY30 or normal LY30 groups (P < .001, respectively). There was no significant difference in levels of tissue plasminogen activator, plasmin-antiplasmin, and plasminogen activator inhibitor 1 between the low LY30 and normal LY30 groups. The high LY30 group was associated with an increased risk of 24-hour and 30-day mortality, while there was no significant difference in mortality between the low LY30 and normal LY30 groups.

Conclusion: Our results suggest that hyperfibrinolysis is the most common form of traumatic fibrinolytic dysfunction and is associated with worse outcome.

Keywords: blood transfusion; hyperfibrinolysis; outcome; thromboelastography; trauma-induced coagulopathy.

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Figures

Figure 1
Figure 1
Flowchart describing study population. LY30, lysis at 30 minutes; PROPPR, Pragmatic, Randomized Optimal Platelet and Plasma Ratios; TEG, thromboelastography.
Figure 2
Figure 2
The level of fibrinolysis-related markers. (A) Tissue plasminogen activator (tPA; ×1000 ng/mL). (B) Plasmin-antiplasmin (PAP; ×1000 ng/mL). (C) Plasminogen activator inhibitor (PAI-1; ×1000 ng/mL). ∗P < .05, compared between the low lysis at 30 minutes (LY30) and normal LY30 groups. P < .05, compared between the high LY30 and low LY30 groups. P < .05, compared between the high LY30 and normal LY30 groups.
Figure 3
Figure 3
Kaplan–Meier survival curve. LY30, lysis at 30 minutes.

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