In a substantial proportion of patients with recent systemic embolization, no evident source of embolism or predisposing factors can be verified. As yet unidentified cardiac abnormalities may play a role in the pathogenesis of the peripheral embolic events. The authors report the case of a 72-year-old man who presented with atrial fibrillation and recurrent in situ thrombus formation in the territory of the fossa ovalis. A deviated and malattached atrial septum primum without a patent foramen ovale may predispose to local thrombus formation in patients with atrial fibrillation. Further studies are required to establish the clinical importance of such an atrial septal malformation in specific subgroups of patients with ischemic stroke.
In a substantial proportion of patients with recent systemic embolization, no evident source of embolism or predisposing factors can be identified. As yet unidentified abnormalities presumably may play a role in the pathogenesis of the peripheral embolic events. In patients with atrial fibrillation, the left atrial appendage is by far the most frequent localization for intracardiac thrombus formation. We report the case of a patient who presented with atrial fibrillation and recurrent thrombus formation in an unusual left atrial location.
Case Presentation
A 72-year-old man with a history of hypertension was admitted because of palpitation and mildly reduced exercise tolerance. Electrocardiography demonstrated atrial fibrillation. The laboratory findings were within normal limits. Transthoracic echocardiography revealed an enlarged left atrium, moderate left ventricular hypertrophy, normal left ventricular function, and the absence of organic valve disease. Before the planned cardioversion, transesophageal echocardiography (TEE) was performed to exclude intracardiac thrombus formation. In the midtransesophageal longitudinal atrial view, the overlapping part of the atrial septum primum (ASP) was deviated from the atrial septum secundum (ASS) over a length of 25 mm, separating a tent-shaped area from the left atrium. A short segment of the central part of the ASP was closely attached to the limbus of the ASS. The free space between the ASP and ASS was filled with a nonmobile thrombus (35 × 15 mm) that partially protruded into the body of the left atrium ( Figure 1 , Video 1 ). The other parts of the cardiac chambers and great vessels were free of thrombus formation. Dense spontaneous echo contrast representing a low-flow state in the dilated left atrium was also present, which might have contributed to the development of the thrombus. The left atrial appendage was free from thrombus formation despite demonstrating a low emptying flow velocity profile (19 cm/sec). Duplex ultrasonography of the lower extremities excluded deep venous thrombosis. Lung scintigraphy demonstrated no perfusion or ventilation defect. Ultrasound Doppler of the neck showed normal flow in the carotid and vertebral arteries, with no signs of thrombi or significant atherosclerosis. The planned cardioversion was canceled, and enoxaparin was administered subcutaneously in a therapeutic dose twice a day. The patient remained free of symptoms during the treatment period. After 12 days of heparin treatment, repeat TEE demonstrated the absence of the thrombus in the territory of the foramen ovale, while the dense spontaneous echo contrast persisted in the dilated left atrium ( Figure 2 , Video 2 ). Contrast TEE combined with the Valsalva and cough maneuver excluded the presence of a patent foramen ovale (PFO). Heparin was transitioned to warfarin as oral anticoagulant therapy.
The patient was followed up regularly after hospital discharge, and international normalized ratio values were strictly controlled in an outpatient clinic. Eighteen months after the previous hospital admission, the patient arbitrarily omitted his oral anticoagulant therapy and some days later developed a sudden onset of flaccid right hemiplegia and global aphasia. On readmission, his signs and symptoms were compatible with a severe left hemispheric cerebrovascular insult. Urgent TEE showed a slightly mobile thrombus (26 × 18 mm) arising from the area between the ASP and the ASS and protruding into the left atrium ( Figure 3 , Video 3 ). Brain computed tomography indicated a subcortical cerebral infarction (72 × 43 mm) in the left temporoparietal lobe ( Figure 4 ). Supportive care and treatment with subcutaneously given enoxaparin were initiated. The patient’s neurologic condition and mental status did not improve significantly, and he died on the 23rd day of hospitalization from complications of bilateral pneumonia.
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