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Prothrombin fragment F1 + 2 and thrombin-antithrombin III complex are useful markers of the hypercoagulable state in
Insights
Patients with atrial fibrillation (AF) and mitral stenosis show high thrombosis risk. Antithrombotic therapy, especially warfarin, effectively reduces hypercoagulable markers in AF patients.
Area of Science:
- Cardiology
- Hematology
- Thrombosis Research
Background:
- Atrial fibrillation (AF) is a significant risk factor for thrombosis.
- Identifying hypercoagulable states in AF patients is crucial for effective treatment.
- Molecular markers can indicate in vivo coagulation activation.
Purpose of the Study:
- To identify hypercoagulable patients with atrial fibrillation (AF).
- To assess the impact of antithrombotic therapy on coagulation markers in AF.
- To compare the efficacy of aspirin versus warfarin in managing hypercoagulability in AF.
Main Methods:
- Studied 83 patients with AF.
- Measured plasma levels of thrombin-antithrombin III complex (TAT) and prothrombin fragment 1 + 2 (PTF).
- Analyzed marker levels in relation to mitral stenosis and antithrombotic treatment (aspirin, warfarin).
Main Results:
- Elevated TAT and PTF levels were more common in AF patients with mitral stenosis.
- AF patients without mitral stenosis on antithrombotics had lower TAT and PTF than those untreated.
- Warfarin significantly reduced PTF levels more than aspirin.
Conclusions:
- AF patients with mitral stenosis not on warfarin are at extremely high hypercoagulable risk.
- AF patients without mitral stenosis on no antithrombotics may be moderately hypercoagulable.
- Warfarin demonstrates superior control of in vivo coagulation activation compared to aspirin in AF patients.
Abstract:
It is well known that atrial fibrillation (AF) is one of the most important diseases that predispose patients to thrombosis. We have attempted to identify patients with AF in the hypercoagulable state by measuring molecular markers such as thrombin-antithrombin III complex (TAT) and prothrombin fragment 1 + 2 (PTF) and determining the effect of antithrombotic therapy on these markers; 83 patients with AF were studied. Increased levels of plasma TAT and PTF were more frequently observed in patients with AF and associated mitral stenosis than in patients with AF alone. In cases of AF without mitral stenosis, plasma levels of TAT and PTF were significantly lower in those patients receiving antithrombotic agents (aspirin or warfarin) than in those receiving no antithrombotic agents. Furthermore, plasma levels of PTF were significantly lower in patients given warfarin than in those receiving aspirin. These results suggest that (1) patients with AF and mitral stenosis who are not given warfarin are in an extremely hypercoagulable state and (2) some patients with AF without mitral stenosis who are not given antithrombotic agents are also moderately hypercoagulable. In vivo activation of blood coagulation was more effectively controlled in patients receiving warfarin than in those taking aspirin.