Related Experiment Video
Updated: May 10, 2026
The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well
Published on: February 27, 2026
Thrombin generation in the Glasgow Myocardial Infarction Study
Machiel Smid1, Arne W J H Dielis, Henri M H Spronk
1Laboratory of Clinical Thrombosis and Haemostasis, Department of Internal Medicine, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
Insights
Patients with prior myocardial infarction (MI) showed increased thrombin generation. This suggests a potential link between enhanced thrombin activity and MI, warranting further investigation into the underlying mechanisms.
Area of Science:
- Cardiovascular Medicine
- Hemostasis and Thrombosis
- Biochemistry
Background:
- Thrombin is a critical coagulation protease implicated in atherosclerosis and myocardial infarction (MI).
- Investigating thrombin generation in MI patients is crucial for understanding disease pathology.
Purpose of the Study:
- To analyze thrombin generation in plasma from myocardial infarction (MI) patients and matched controls.
- To explore the role of thrombin in the context of MI using the Glasgow MI Study (GLAMIS) cohort.
Main Methods:
- Thrombin generation assays were performed on plasma from 356 subjects (171 cases, 185 controls) from the GLAMIS study.
- Assays were conducted at 1 and 2 pM Tissue Factor (TF) trigger concentrations, with and without thrombomodulin (TM).
- Samples were collected 3 to 9 months post-MI event.
Main Results:
- MI patients exhibited increased thrombin generation potential (ETP and peak height) at a 1 pM TF trigger compared to controls.
- An increased thrombin generation was significantly associated with MI, with odds ratios ranging from 2.0 to 2.6.
- No significant differences were observed in TM-mediated thrombin generation reduction between cases and controls.
Conclusions:
- Patients with a history of MI demonstrate elevated thrombin generation compared to controls.
- The findings suggest unaltered anticoagulant activity in MI patients, as indicated by similar TM reduction.
- Further research is necessary to elucidate the mechanisms driving enhanced thrombin generation post-MI.
Background:
Thrombin is a key protease in coagulation also implicated in complex pathology including atherosclerosis. To address the role of thrombin in relation to myocardial infarction (MI) we explored thrombin generation analysis in plasma from patients and controls that had participated in the Glasgow MI Study (GLAMIS).
Methods:
Thrombin generation at 1 and 2 pM TF and with and without thrombomodulin (TM) was performed on plasmas from 356 subjects (171 cases, 185 age and sex matched controls) from GLAMIS collected between 3 and 9 months after the MI event.
Results:
Although thrombin generation was slightly delayed in cases (lag time increased from 3.3 to 3.6 min) at the highest trigger, the overall potential to generate thrombin was increased by 7% for the ETP and by 15% for the peak height (both at the 1 pM TF trigger) in cases. Addition of TM did not reveal differences. Furthermore, an increased thrombin generation was associated with MI [normalized ETP: adjusted OR for the highest percentile = 2.4 (95% CI 1.3-4.5) and normalized peak height: adjusted OR = 2.6 (1.3-5.0)] at the lowest trigger; normalized ETP and peak height being 2.1 (1.1-3.8) and 2.0 (1.0-4.1) at the higher 2 pM trigger.
Conclusion:
In GLAMIS, patients with a previous MI had an increased thrombin generation compared to controls. The absence of a clear difference in TM reduction suggests an unaltered anticoagulant activity in these patients. Further research is needed in order to unravel the underlying mechanisms of enhanced thrombin generation after MI.
Related Concept Videos
01:30Acute Coronary Syndrome III: Diagnostic Studies
01:20Blood Studies for Cardiovascular System I: Cardiac Biomarkers
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...