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Regression of intracardiac thrombus after embolic stroke
M Yasaka1, T Yamaguchi, T Miyashita
1Department of Medicine, National Cardiovascular Center, Osaka, Japan.
Insights
Anticoagulant therapy can lead to intracardiac thrombus regression in patients with cardiogenic cerebral embolism. Fibrinolytic activity appears key to this thrombus resolution process.
Area of Science:
- Cardiology
- Hematology
- Vascular Medicine
Background:
- Intracardiac thrombi pose a risk for embolic events, particularly in patients with acute cardiogenic cerebral embolism.
- Understanding the mechanisms of thrombus regression during anticoagulant therapy is crucial for optimizing patient management.
Purpose of the Study:
- To investigate the pathophysiology of intracardiac thrombus regression under anticoagulant therapy.
- To correlate changes in specific plasma markers with thrombus size reduction.
Main Methods:
- Two-dimensional echocardiography was used to assess intracardiac thrombi in 82 patients with acute cardiogenic cerebral embolism.
- Nine patients with intracardiac thrombi received warfarin potassium for anticoagulation, with serial echocardiograms and plasma marker measurements (fibrinopeptide A, fibrinopeptide B beta 15-42, D-dimer).
Main Results:
- Eight of nine patients showed gradual intracardiac thrombus size reduction.
- Reduced plasma fibrinopeptide A levels correlated with thrombus regression, while fibrinopeptide B beta 15-42 and D-dimer remained elevated.
- One patient experienced thrombus disappearance with immediate embolization.
- Mobile and smaller thrombi regressed more rapidly than nonmobile and larger ones.
Conclusions:
- Intracardiac thrombus regression during anticoagulation may be driven by a predominance of plasma fibrinolytic activity over inhibited thrombin activity.
- The findings suggest a dynamic interplay between coagulation and fibrinolysis in thrombus resolution.
Abstract:
Using two-dimensional echocardiography, we studied the pathophysiology of intracardiac thrombus regression accompanied by anticoagulant therapy in 82 consecutive patients with acute cardiogenic cerebral embolism. We noted intracardiac thrombus in 15 patients; nine of the 15 were started on anticoagulant therapy with warfarin potassium to maintain the prothrombin time between 2.5 and 3.5 (international normalized ratio). Serial two-dimensional echocardiograms were obtained for these nine patients before and after anticoagulation, with the plasma levels of fibrinopeptide A, fibrinopeptide B beta 15-42, and D-dimer measured at the same time. In eight of the nine patients the intracardiac thrombi gradually decreased in size while the plasma level of fibrinopeptide A fell to within the normal range and the plasma levels of fibrinopeptide B beta 15-42 and D-dimer remained above the normal ranges. In the other patient the thrombus disappeared, with embolization to the right arm immediately after starting anticoagulant therapy. Mobile or small thrombi regressed earlier than nonmobile or large ones. We conclude that regression of intracardiac thrombi after anticoagulation may be based on the relative predominance of plasma fibrinolytic activity over anticoagulation-inhibited thrombin activity.