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

[Display omitted] •Hypofibrinolysis is a recently-recognized risk factor for recurrent cardiovascular events in patients with STEMI, but its mechanistic determinants are not well understood.•In patients with STEMI, we show that the effectiveness of endogenous fibrinolysis in whole blood is related t...

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Published inJACC. Basic to translational science Vol. 7; no. 11; pp. 1069 - 1082
Main Authors Kanji, Rahim, Gue, Ying X., Farag, Mohamed F., Spencer, Neil H., Mutch, Nicola J., Gorog, Diana A.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.11.2022
Elsevier
Subjects
fibrinolysis
myocardial infarction
Original Research - Clinical
platelet function
thrombosis
vWF
OT
myocardial infarction
LT
platelet function
fibrinolysis
ACS
thrombosis
MACE
PCI
STEMI
PAI
t-PA
PCI, percutaneous coronary intervention
MACE, major adverse cardiovascular events
OT, occlusion time
STEMI, ST-segment elevation myocardial infarction
ACS, acute coronary syndrome
LT, lysis time
vWF, von Willebrand factor
PAI, plasminogen activator inhibitor
t-PA, tissue plasminogen activator
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Abstract [Display omitted] •Hypofibrinolysis is a recently-recognized risk factor for recurrent cardiovascular events in patients with STEMI, but its mechanistic determinants are not well understood.•In patients with STEMI, we show that the effectiveness of endogenous fibrinolysis in whole blood is related to fibrinogen, hs-CRP, and shear-induced platelet reactivity, the latter related to thrombin generation.•Endogenous fibrinolysis in whole blood is only weakly related to plasma clot lysis in response to t-PA, indicating an important role for cellular components in determining fibrinolytic status.•These findings strengthen the evidence for bidirectional crosstalk between coagulation and inflammation and provide mechanistic insights that could help guide pharmacological strategies to treat hypofibrinolysis, a potentially modifiable cardiovascular risk factor. 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.
AbstractList • Hypofibrinolysis is a recently-recognized risk factor for recurrent cardiovascular events in patients with STEMI, but its mechanistic determinants are not well understood. • In patients with STEMI, we show that the effectiveness of endogenous fibrinolysis in whole blood is related to fibrinogen, hs-CRP, and shear-induced platelet reactivity, the latter related to thrombin generation. • Endogenous fibrinolysis in whole blood is only weakly related to plasma clot lysis in response to t-PA, indicating an important role for cellular components in determining fibrinolytic status. • These findings strengthen the evidence for bidirectional crosstalk between coagulation and inflammation and provide mechanistic insights that could help guide pharmacological strategies to treat hypofibrinolysis, a potentially modifiable cardiovascular risk factor. 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.
[Display omitted] •Hypofibrinolysis is a recently-recognized risk factor for recurrent cardiovascular events in patients with STEMI, but its mechanistic determinants are not well understood.•In patients with STEMI, we show that the effectiveness of endogenous fibrinolysis in whole blood is related to fibrinogen, hs-CRP, and shear-induced platelet reactivity, the latter related to thrombin generation.•Endogenous fibrinolysis in whole blood is only weakly related to plasma clot lysis in response to t-PA, indicating an important role for cellular components in determining fibrinolytic status.•These findings strengthen the evidence for bidirectional crosstalk between coagulation and inflammation and provide mechanistic insights that could help guide pharmacological strategies to treat hypofibrinolysis, a potentially modifiable cardiovascular risk factor. 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.
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.
Author Gorog, Diana A.
Kanji, Rahim
Gue, Ying X.
Mutch, Nicola J.
Spencer, Neil H.
Farag, Mohamed F.
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CitedBy_id crossref_primary_10_1177_10760296231181917
crossref_primary_10_3389_fcvm_2022_1054541
crossref_primary_10_1055_s_0043_1777794
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Issue 11
Keywords vWF
OT
myocardial infarction
LT
platelet function
fibrinolysis
ACS
thrombosis
MACE
PCI
STEMI
PAI
t-PA
PCI, percutaneous coronary intervention
MACE, major adverse cardiovascular events
OT, occlusion time
STEMI, ST-segment elevation myocardial infarction
ACS, acute coronary syndrome
LT, lysis time
vWF, von Willebrand factor
PAI, plasminogen activator inhibitor
t-PA, tissue plasminogen activator
Language English
License This is an open access article under the CC BY-NC-ND license.
2022 The Authors.
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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Drs Mutch and Gorog contributed equally to this work and are joint senior authors.
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Snippet [Display omitted] •Hypofibrinolysis is a recently-recognized risk factor for recurrent cardiovascular events in patients with STEMI, but its mechanistic...
Hypofibrinolysis is a recently-recognized risk factor for recurrent cardiovascular events in patients with ST-segment elevation myocardial infarction (STEMI),...
• Hypofibrinolysis is a recently-recognized risk factor for recurrent cardiovascular events in patients with STEMI, but its mechanistic determinants are not...
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SubjectTerms fibrinolysis
myocardial infarction
Original Research - Clinical
platelet function
thrombosis
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Title Determinants of Endogenous Fibrinolysis in Whole Blood Under High Shear in Patients With Myocardial Infarction
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