Determinants of Endogenous Fibrinolysis in Whole Blood Under High Shear in Patients With Myocardial Infarction

Rahim Kanji, Ying X. Gue, Mohamed F. Farag, Neil H. Spencer, Nicola J. Mutch, Diana A. Gorog*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)
4 Downloads (Pure)


Hypofibrinolysis is a recently-recognized risk factor for recurrent cardiovascular events in patients with ST-segment elevation myocardial infarction (STEMI), but the mechanistic determinants of this are not well understood. In patients with STEMI, we show that the effectiveness of endogenous fibrinolysis in whole blood is determined in part by fibrinogen level, high sensitivity C-reactive protein, and shear-induced platelet reactivity, the latter directly related to the speed of thrombin generation. Our findings strengthen the evidence for the role of cellular components and bidirectional crosstalk between coagulatory and inflammatory pathways as determinants of hypofibrinolysis.

Original languageEnglish
Pages (from-to)1069-1082
Number of pages14
JournalJACC: Basic to Translational Science
Issue number11
Early online date14 Nov 2022
Publication statusPublished - Nov 2022

Bibliographical note

This work was supported in part by a grant from Alpha MD, London, United Kingdom. Dr Mutch was supported by the British Heart Foundation PG/15/82/31721 and Friends of Anchor. Dr Gorog has received institutional research grants from Bayer, Medtronic, Alpha MD, and Boehringer Ingelheim; has received speaker’s fees from AstraZeneca and Boehringer Ingelheim; and is related through family to a company director in Thromboquest Ltd, but neither she, nor her spouse or children, have financial involvement or equity interest in and they have received no financial assistance, support, or grants from the aforementioned. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.


  • fibrinolysis
  • Myocardial infarction
  • platelet function
  • thrombosis


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