To elucidate the pathophysiology of intracardiac thrombus formation, serial two-dimensional echocardiographic examinations were performed on 30 consecutive patients with acute cardiogenic cerebral embolism in parallel with measurement of hematocrit and plasma levels of antithrombin III. The data from groups of patients with and without newly formed or enlarged thrombi were compared. Intracardiac thrombi were detected in eight of the 30 patients (27%), four at admission and four after admission. Enlargement of the thrombus was observed in four, and systemic embolization recurred in three of the eight. Antithrombin III levels already were low at admission in patients who later developed thrombi or had enlarged thrombi on serial examinations. When the development or enlargement of an intracardiac thrombus was detected by echocardiography, the diameter of the inferior vena cava was found to be reduced. At the same time, a decrease in antithrombin III and an increase in hematocrit were demonstrated. Intracardiac thrombi are frequently detected by repeated echocardiographic examination in patients with cerebral embolism. Dehydration seems to accelerate thrombus formation that is reflected by a decrease in antithrombin III. A low antithrombin III level at admission and/or a decrease in antithrombin III after admission may indicate the possible recurrence of embolism.