# Hyperfibrinolysis during intra-aortic balloon pump support: a case report on targeted tranexamic acid therapy

**Authors:** Shanshan Dong, Xinshuang Chen, Qi Peng, Jun Yang, Qimei Wei

PMC · DOI: 10.3389/fcvm.2025.1746269 · Frontiers in Cardiovascular Medicine · 2026-01-02

## TL;DR

A patient on heart support developed excessive blood clot breakdown, which was successfully treated with a specific medication.

## Contribution

This case report highlights targeted tranexamic acid therapy for managing hyperfibrinolysis in intra-aortic balloon pump-supported patients.

## Key findings

- The patient showed elevated D-dimer and plasmin-α2-plasmin inhibitor complex levels, indicating hyperfibrinolysis.
- Tranexamic acid therapy effectively controlled bleeding and corrected fibrinolysis without causing thrombosis.
- The case emphasizes the need to consider secondary hyperfibrinolysis in IABP patients with infection or instability.

## Abstract

Coagulation disturbances in patients with end-stage heart failure receiving intra-aortic balloon pump (IABP) support present significant management challenges. We describe a 49-year-old male with dilated cardiomyopathy awaiting transplantation who developed secondary hyperfibrinolysis following IABP-associated infection and hemodynamic instability. The patient exhibited pronounced D-dimer elevation (peak: 55.84 μg/mL) and persistent oozing at the puncture site. At the onset of hyperfibrinolysis, laboratory tests demonstrated a markedly increased plasmin-α2-plasmin inhibitor complex (PIC: 26.56 μg/mL) and a mildly elevated thrombin-antithrombin III complex (TAT: 7.89 ng/mL), accompanied by a rise in platelet count (351 × 10⁹/L, up from 318 × 10⁹/L previously) and a decrease in fibrinogen (4.85 g/L, down from 7.98 g/L). Targeted intravenous tranexamic acid (TXA) therapy effectively controlled bleeding and corrected fibrinolysis, without inducing thrombotic complications, thereby allowing successful bridging to heart transplantation. This case underscores the importance of considering secondary hyperfibrinolysis in IABP-supported patients with infection or hemodynamic instability.

## Linked entities

- **Chemicals:** tranexamic acid (PubChem CID 5526)
- **Diseases:** dilated cardiomyopathy (MONDO:0005021)

## Full-text entities

- **Genes:** FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, F2 (coagulation factor II, thrombin) [NCBI Gene 2147] {aka PT, RPRGL2, THPH1}, PLG (plasminogen) [NCBI Gene 5340] {aka HAE4}, SERPINC1 (serpin family C member 1) [NCBI Gene 462] {aka AT3, AT3D, ATIII, ATIII-R2, ATIII-T1, ATIII-T2}
- **Diseases:** infection (MESH:D007239), thrombotic (MESH:D013927), dilated cardiomyopathy (MESH:D002311), Coagulation disturbances (MESH:D001778), bleeding (MESH:D006470), heart failure (MESH:D006333), Hyperfibrinolysis (MESH:C567640)
- **Chemicals:** TXA (MESH:D014148)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12808376/full.md

## References

21 references — full list in the complete paper: https://tomesphere.com/paper/PMC12808376/full.md

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Source: https://tomesphere.com/paper/PMC12808376