Evidence of contact activation in patients suffering from ST-elevation myocardial infarction
Kjeld Christensen1, Huda Kozarcanin2, Kristina N Ekdahl2
1Department of Cardiology, Örebro University Hospital, Sweden; Linnæus Center for Biomaterials Chemistry, Linnæus University, SE-391 82 Kalmar, Sweden.
Insights
Factor XIIa activation is elevated in ST-elevation myocardial infarction (STEMI) patients, suggesting its potential as an anticoagulation target. Contact system activation, particularly FXIIa/AT, plays a significant role in cardiac infarction.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Thrombosis Research
Background:
- Factor XIIa (FXIIa) is a potential target for anticoagulation therapy in arterial thrombosis.
- The contact system's role in cardiac infarction requires further investigation.
Purpose of the Study:
- To investigate the involvement of the contact system in ST-elevation myocardial infarction (STEMI).
- To quantify Factor XII (FXII) activation in STEMI patients.
Main Methods:
- 165 STEMI patients and 100 healthy controls were enrolled.
- FXIIa/AT and FXIIa/C1INH complex levels were measured using ELISA at different time points (admission, 1-3 days post-PCI, 3 months post-PCI).
Main Results:
- FXIIa/AT levels were significantly higher in STEMI patients at admission compared to controls, normalizing by 1-3 days post-PCI.
- FXIIa/C1INH levels were significantly elevated in STEMI patients at admission and 1-3 days post-PCI compared to controls.
- Both complex levels showed significant differences between admission/1-3 days post-PCI and 3 months post-PCI.
Conclusions:
- Elevated FXIIa/AT and FXIIa/C1INH complexes indicate FXII activation in STEMI patients.
- FXIIa/AT elevation suggests clot propagation-mediated FXII activation, a potential anticoagulation target.
- FXIIa/C1INH elevation may reflect endothelial cell activation in STEMI.
Introduction:
Factor (F) XIIa is an attractive target for anticoagulation in arterial thrombosis. The aim of this study is to investigate the degree of involvement of the contact system in cardiac infarctions.
Methods And Patients:
165 patients suffering from ST-elevation myocardial infarction (STEMI) and 100 healthy controls were included in the study. Samples were drawn at admission before percutaneous intervention (PCI), 1-3days post-percutaneous intervention (PCI) and, in one-third of the patients, 3months after PCI. In order to investigate the degree of Factor XII (FXII) activation, changes in FXIIa/AT and FXIIa/C1INH complex levels were quantified by ELISA.
Results:
FXIIa/AT levels at admission (0.89±0.50; p<0.01) were significantly higher than those in normal individuals (0.39±0.28), but the levels after 1-3days (0.33±0.33; p<0.05) were essentially normalized. In contrast, the FXII/C1INH levels at admission (1.40±0.72; p<0.001) and after 1-3days (0.83±0.59; p<0.001) were both significantly higher than those in normal individuals (0.40±0.30). FXIIa/AT and FXIIa/C1INH complexes at admission (p<0.001; p<0.001) and after 1-3days (p<0.02; p<0.001) were significantly different from those at 3months. No significant differences were observed when the data were stratified for patency (open/closed culprit lesions).
Conclusion:
Both FXIIa/AT and FXIIa/C1INH complexes were significantly increased and reflected the activation of FXII in STEMI patients at admission. In particular, FXIIa/AT complex elevations support the hypothesis that clot propagation-mediated FXII activation had occurred, and this activation may be a target for anticoagulation in patients with cardiac infarction. Based on previous studies, the FXIIa/C1INH complex levels were primarily interpreted to reflex endothelial cell activation.
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