The relationship between a hypercoagulable state and intracardiac thrombus formation is reviewed, with reference to the pathophysiology of intracardiac thrombus in patients with acute cardioembolic stroke, and those with mitral stenosis. When the development or enlargement of intracardiac thrombus is followed serially by echocardiography, the diameter of the inferior vena cava is seen to decrease as the hematocrit increases, particularly in patients with negative water balance taking diuretics. These findings strongly suggest that dehydration could play an important role in the formation of thrombus. A hypercoagulable and secondarily enhanced fibrinolytic state exists in the cardiac chamber of patients with acute cardioembolic stroke or with intracardiac thrombus. This can be evaluated by plasma levels of fibrinopeptide A, fibrinopeptide B beta 15-42, thrombin-antithrombin III complex and D-dimer. Anticoagulant treatment suppresses thrombin activity in the cardiac chamber, allowing plasma fibrinolytic activity to predominate and reduce the size of the intracardiac thrombus.

How to cite: Yasaka, M., & Beppu, S. (1993). Hypercoagulability in the left atrium: Part II: Coagulation factors. The Journal of heart valve disease, 2(1), 25–36.