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Hypercoagulability in the left atrium: Part II: Coagulation factors
The Journal of Heart Valve Disease
|January 1, 1993
Summary
Dehydration may promote intracardiac thrombus formation, contributing to cardioembolic stroke. Anticoagulant therapy can reduce thrombus size by suppressing thrombin activity and enhancing fibrinolysis.
Area of Science:
- Cardiology
- Hematology
- Pathophysiology
Background:
- Intracardiac thrombus formation is linked to hypercoagulable states.
- Conditions like acute cardioembolic stroke and mitral stenosis are associated with intracardiac thrombus.
- Pathophysiology involves complex interactions between coagulation and fibrinolysis.
Purpose of the Study:
- To review the relationship between hypercoagulable states and intracardiac thrombus.
- To explore the role of dehydration in thrombus formation.
- To evaluate the impact of anticoagulant treatment on intracardiac thrombus.
Main Methods:
- Serial echocardiography to monitor thrombus and inferior vena cava diameter.
- Hematocrit and water balance assessment, especially in patients on diuretics.
- Measurement of plasma markers: fibrinopeptide A, fibrinopeptide B beta 15-42, thrombin-antithrombin III complex, and D-dimer.
Main Results:
- Decreased inferior vena cava diameter correlated with increased hematocrit, suggesting dehydration's role.
- A hypercoagulable and secondarily enhanced fibrinolytic state was identified in cardiac chambers.
- Plasma levels of specific markers indicated this prothrombotic and fibrinolytic state.
Conclusions:
- Dehydration appears to be a significant factor in intracardiac thrombus development.
- Anticoagulant therapy effectively reduces intracardiac thrombus by modulating thrombin activity and promoting fibrinolysis.