Activation of the contact system in patients with a first acute myocardial infarction
Joke Konings1, José W P Govers-Riemslag, Henri M H Spronk
1Laboratory for Clinical Thrombosis and Haemostasis, Department of Internal Medicine, Cardiovascular Research Institute Maastricht, Maastricht University Medical Centre, Maastricht, The Netherlands. J.Konings@maastrichtuniversity.nl
Insights
Contact system activation, specifically factor XI (FXI), is increased during acute myocardial infarction (AMI). However, these contact system markers do not predict recurrent cardiovascular events after AMI.
Area of Science:
- Cardiovascular Research
- Hemostasis and Thrombosis
- Contact System Biology
Background:
- The role of the contact system in arterial thrombosis remains incompletely understood, with conflicting clinical findings.
- Limited data exists on the contact system's involvement in arterial thrombosis progression.
Purpose of the Study:
- To investigate contact system activation during acute myocardial infarction (AMI).
- To assess contact system activation at 3 and 6 months post-AMI.
- To determine if contact system activation predicts recurrent cardiovascular events.
Main Methods:
- Plasma samples from first-time AMI patients were collected at admission, 3, and 6 months post-event.
- Levels of activated factor XI (FXIa), FXIIa, and kallikrein complexes with C1 esterase inhibitor (C1INH) were measured.
- Levels of FXIa complexes with α1-antitrypsin (AT) were quantified; recurrent events were tracked for one year.
Main Results:
- Elevated FXIa-C1INH levels were observed during the acute AMI phase compared to later time points.
- No significant changes in FXIa-AT, FXIIa-C1INH, or kallikrein-C1INH levels were detected over time.
- Contact system enzyme-inhibitor complexes did not predict recurrent cardiovascular events within one year post-AMI.
Conclusions:
- Factor XI activation is increased during AMI, but not driven by contact activation via FXIIa.
- Elevated FXIIa-C1INH levels were not observed, suggesting FXI activation during AMI is independent of FXIIa.
- Contact system activation markers were not predictive of recurrent events one year after the initial AMI.
Introduction:
The contribution of the contact system to arterial thrombosis is unclear, results of clinical studies are conflicting. Particularly, little is known about the involvement of the contact system in the progression of arterial thrombosis. Therefore, we investigated the activation of the contact system during an acute myocardial infarction (AMI) and 3 and 6 months following the acute event.
Methods:
Plasma of patients with a first AMI was collected on admission and 3 and 6 months after the AMI. The levels of complexes of activated factor XI (FXIa), FXIIa and kallikrein with C1 esterase inhibitor (C1INH) and the levels of complexes of FXIa with α1-antitrypsin (AT) were measured in these plasmas. Recurrent cardiovascular events were recorded during a one year period after the AMI.
Results:
We observed that the levels of FXIa-C1INH were elevated during the acute phase compared to the steady-phase 3 and 6 months after the AMI. The levels of FXIa-AT, FXIIa-C1INH and kallikrein-C1INH did not change over time. The levels of FXIa-C1INH, FXIa-AT, FXIIa-C1INH and kallikrein-C1INH were not predictive for a recurrent event.
Conclusion:
We observed that during an AMI, the activation of FXI was increased. The levels of FXIIa-C1INH were not elevated, suggesting that activation of FXI during the acute phase did not result from contact activation. The levels of the enzyme inhibitor complexes were not predictive for a recurrent event one year after the first AMI.
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