Right Atrial Mass in a Patient With T-Cell Chronic Lymphocytic Leukemia

A 71-year-old woman with refractory T-cell (CD4)\udchronic lymphocytic leukemia who had been treated\udwith chemotherapy and leukapheresis with poor control of\udleucocytosis was admitted because of fever, cough, and chest\udpain. A chest x-ray showed a right basal pneumonia, and the\udcytological examination of sputum showed Aspergillus fumigatus\ud(Figure 1). The ECG at admission showed a firstdegree\udatrioventricular block (Figure 2A). The patient was\udstarted on broad-spectrum antibiotics and liposomal amphotericin\udB. Shortly before admission, because of sinus\udtachycardia, an ECG with Holter monitoring was performed;\udit showed a run of supraventricular tachycardia (Figure 2B).\udTherefore, while in the hospital, the patient underwent cardiac\udevaluation. Two-dimensional echocardiography showed\uda round (2016 mm) floating mass in the right atrium, close\udto the superior caval vein (Figure 3A, Movie). A thrombus\udnear the distal tip of the central venous catheter was suspected,\udand the patient was started on nadroparin 6000 U\udinjected subcutaneously twice daily. At the time of echocardiography,\udblood counts showed severe leucocytosis (white\udblood cell count, 396.100/L; lymphocytes, 384.940/L).\udAfter 2 weeks of therapy with low-molecular-weight heparin,\udthe patient underwent transesophageal echocardiography,\udwhich did not show any reduction of the atrial mass and\udexcluded any relation to the central venous catheter (Figure\ud3B). A cardiac computed tomography scan was performed,\udwhich showed an 8-mm defect in the right atrium with\udirregular shape and contrast enhancement (Figure 3C). The\udpatient died of multiorgan failure 52 days after admission. At\udautopsy, a multiorgan extensive leukemic infiltration was\uddetected. The atrial mass, located at the junction of the\udinferior caval vein with the atrium and attached to the crista\uddividens, measured 201815 mm (figure 3D). Histologically,\udwe found an infiltration of the atrial wall by clusters of\udcells that reached and disrupted the endocardial atrial surface,\udproviding a likely cause for the stratified thrombotic apposition\ud(Figure 4A through 4D). The clustered cells were\udCD45-positive (Figure 4C) and CD3-positive (Figure 4D)\udT-lymphocytes and were confined to the peduncle