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Published on: September 9, 2012
Factor XI as a risk factor for persistent left ventricular thrombus following acute myocardial infarction
Krystian Mróz1, Elżbieta Paszek2,3, Grzegorz Józef Nowicki4
1Clinical Department of Interventional Cardiology, St. John Paul II Hospital, Kraków, Poland. k10mroz@gmail.com.
Insights
Elevated Factor XI (FXI) levels may increase the risk of unresolved left ventricular thrombus (LVT) after myocardial infarction (MI), even with standard treatment. Assessing FXI could identify high-risk patients for future targeted therapies.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Thrombosis Research
Background:
- Mechanisms of persistent left ventricular thrombus (LVT) after acute myocardial infarction (MI) remain poorly understood.
- Left ventricular thrombus (LVT) is a significant complication following acute myocardial infarction (MI).
Purpose of the Study:
- To investigate the association between elevated Factor XI (FXI) levels and persistent LVT after acute MI.
- To explore FXI's role in LVT development and resolution in post-MI patients.
Main Methods:
- 148 patients with LVT post-MI received standard anticoagulation and dual antiplatelet therapy.
- Factor XI (FXI) levels, fibrin clot permeability (Ks), clot lysis time, and plasminogen activator inhibitor-1 were assessed 3 months post-MI.
- LVT resolution was evaluated at 3 and 6 months post-MI.
Main Results:
- Higher FXI levels were observed in patients with persistent LVT at 3 and 6 months post-MI.
- Elevated FXI (>120%) and low Ks independently predicted LVT persistence at 6 months.
- FXI showed weak inverse correlation with Ks and positive correlation with clot lysis time and PAI-1.
Conclusions:
- Elevated FXI may predispose individuals to unresolved LVT post-MI, even during anticoagulation.
- FXI assessment could identify high-risk patients for LVT persistence.
- Future FXI inhibition therapies may benefit patients prone to unresolved LVT.
Background:
Mechanisms underlying unresolved left ventricular thrombus (LVT) developed afteracute myocardial infarction (MI) are unclear.
Aims:
To investigate whether elevated factor (F) XI is associated with persistent LVT followingacute MI.
Methods:
In consecutive 148 patients (aged 63.9 [6.9] years) with LVT detected during hospitalization for acute MI, all of whom received oral anticoagulation with dual antiplatelet therapy, we assessedFXI levels 3 months post-MI, while off anticoagulation, along with plasma fibrin clot permeability(Ks), clot lysis time, and plasminogen activator inhibitor-1. LVT resolution was evaluated 3 and6 months post MI.
Results:
Plasma FXI (median 111.5%, first-third quartile 101.5%-121.0%) weakly correlated inverselywith Ks and positively with both clot lysis time and plasminogen activator inhibitor-1 (all P <0.05),without any other associations. Compared with patients who achieved thrombus resolution, patientswith persistent LVT at 3 and 6 months (75 [50.7%] and 44 [29.7%], respectively), had higher FXI by8.3% and 12.1%, respectively (both P <0.05). Elevated FXI (>120%), detected in 42 (28.4%) patients,along with low Ks, predicted LVT persistence solely at 6 months following MI, independently of age,sex, and previous MI/percutaneous coronary intervention (odds ratio, 6.73; 95% confidence interval,1.92-23.54; P = 0.003).
Conclusions:
To our knowledge, this study is the first to demonstrate that elevated FXI may predisposeto unresolved LVT post MI while on anticoagulation, which suggests that FXI assessment might helpidentify patients prone to this complication who could possibly benefit from FXI inhibition in the future.
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