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Enhanced coagulation activation in troponin T-positive unstable angina pectoris
1Department of Cardiology, Medical Clinic, University Hospital Eppendorf, Hamburg, Federal Republic of Germany.
Insights
In unstable angina, increased coagulation activation, indicated by fibrin monomers, is linked to higher troponin T levels, suggesting myocardial cell injury and potentially worse outcomes.
Area of Science:
- Cardiology
- Hematology
- Biochemistry
Background:
- Unstable angina pectoris involves intracoronary thrombus formation and systemic coagulation activation.
- Elevated circulating troponin T signifies myocardial cell injury and is linked to adverse outcomes in unstable angina.
- The relationship between coagulation activation and myocardial injury in unstable angina requires further investigation.
Purpose of the Study:
- To quantitatively assess systemic coagulation activation and myocardial cell injury in patients with unstable angina.
- To explore the interrelation between coagulation markers and troponin T levels.
Main Methods:
- Serial blood samples were collected for up to 10 days from 22 patients with coronary heart disease and unstable angina.
- Systemic coagulation activation was assessed by measuring plasma fibrin monomers and prothrombin fragment F1+2.
- Myocardial cell injury was evaluated by measuring serum troponin T levels.
Main Results:
- Patients with elevated maximal troponin T levels showed significantly higher maximal fibrin monomer concentrations within 48 hours (6.3+/-4.8 vs. 2.9+/-2.3 mg/L; p = 0.04).
- A higher proportion of troponin T-positive patients had increased plasma fibrin monomer levels (67% vs. 15%; p = 0.04).
- Plasma prothrombin fragment F1+2 levels trended higher in troponin T-positive patients, though not significantly.
Conclusions:
- Enhanced coagulation activation, particularly indicated by fibrin monomers, is associated with myocardial cell injury in unstable angina.
- This heightened coagulation activation may contribute to the adverse outcomes observed in troponin T-positive unstable angina patients.
Abstract:
Intracoronary thrombus formation and systemic activation of coagulation have been demonstrated in unstable angina pectoris. Circulating troponin T as a marker of minor myocardial cell injury is associated with adverse outcome in this condition. Little information exists about the interrelation of coagulation activation and myocardial cell injury in unstable angina. We quantitatively assessed systemic activation of coagulation and myocardial cell injury in serial blood samples obtained up to 10 days from 22 patients with angiographically documented coronary heart disease and unstable angina pectoris at rest. In the nine patients with increased maximal levels of serum troponin T, maximal concentrations of fibrin monomers during the first 48 hours were higher than those in patients with persistently normal troponin T concentrations (6.3+/-4.8 vs. 2.9+/-2.3 mg/L; p = 0.04). The proportion of patients with at least one blood sample showing an increased concentration of plasma fibrin monomer was also higher in the group with increased troponin T (67% vs. 15%; p = 0.04). Plasma prothrombin fragment F1+2 levels showed a nonsignificant trend toward higher values in troponin T-positive patients. Enhanced activation of coagulation in patients with troponin T-positive unstable angina may contribute to the adverse outcome associated with this condition.