Images in cardiovascular medicine. Right atrial mass in a patient with T-cell chronic lymphocytic leukemia: an unusual mechanism of thrombus formation.

A 71-year-old woman with refractory T-cell (CD4) chronic lymphocytic leukemia who had been treated with chemotherapy and leukapheresis with poor control of leucocytosis was admitted because of fever, cough, and chest pain. A chest x-ray showed a right basal pneumonia, and the cytological examination of sputum showed Aspergillus fumigatus (Figure 1). The ECG at admission showed a firstdegree atrioventricular block (Figure 2A). The patient was started on broad-spectrum antibiotics and liposomal amphotericin B. Shortly before admission, because of sinus tachycardia, an ECG with Holter monitoring was performed; it showed a run of supraventricular tachycardia (Figure 2B). Therefore, while in the hospital, the patient underwent cardiac evaluation. Two-dimensional echocardiography showed a round (2016 mm) floating mass in the right atrium, close to the superior caval vein (Figure 3A, Movie). A thrombus near the distal tip of the central venous catheter was suspected, and the patient was started on nadroparin 6000 U injected subcutaneously twice daily. At the time of echocardiography, blood counts showed severe leucocytosis (white blood cell count, 396.100/L; lymphocytes, 384.940/L). After 2 weeks of therapy with low-molecular-weight heparin, the patient underwent transesophageal echocardiography, which did not show any reduction of the atrial mass and excluded any relation to the central venous catheter (Figure 3B). A cardiac computed tomography scan was performed, which showed an 8-mm defect in the right atrium with irregular shape and contrast enhancement (Figure 3C). The patient died of multiorgan failure 52 days after admission. At autopsy, a multiorgan extensive leukemic infiltration was detected. The atrial mass, located at the junction of the inferior caval vein with the atrium and attached to the crista dividens, measured 201815 mm (figure 3D). Histologically, we found an infiltration of the atrial wall by clusters of cells that reached and disrupted the endocardial atrial surface, providing a likely cause for the stratified thrombotic apposition (Figure 4A through 4D). The clustered cells were CD45-positive (Figure 4C) and CD3-positive (Figure 4D) T-lymphocytes and were confined to the peduncle