A 79-year-old female patient had been complaining of chest pain for over 2 weeks. She described a tingling in the pre-cardiac area that was unrelated to breathing or activity, and could not be relieved by rest. She reported no radiating pain. Occasionally, the patient experienced night sweats, fatigue, acid reflux, and belching. Nausea, vomiting, and abdominal pain were also present. The vomiting of the gastric contents ultimately resolved itself. Before presentation, however, she had a continuous fever for 4-5 days with a peak body temperature of 38.5 C, which was occasionally accompanied by a dry cough. Self-reported use of oral antipyretics reduced her temperature to normal. The patient experiences lack of sleep, poor appetite, and a poor mental state. She had a history of cerebral infarction. No obvious change in body weight had recently occurred. The patient denied a family history of high blood pressure, diabetes, and coronary heart disease.
The patients physical examination upon admission revealed a temperature of 36.4 C, pulse rate of 103 bpm, breathing rate of 20 breaths/min, and blood pressure of 99/75 mmHg. Physical examination revealed that her superficial lymph nodes were not enlarged. There were no abnormal heaves. The apex beat was 0.5 cm inside the midline of the fifth intercostal space. No cardiac murmurs or rubs were heard and no other abnormalities were found during the rest of the examination. A blood routine examination revealed no obvious abnormality. Her white blood cell count was 5.01 x 109/L, lymphocyte percentage was 19.4%, red blood cell count was 3.77 x 1012/L, hemoglobin concentration was 109 g/L, and platelet count was 71 x 109/L. Multi-tumor marker protein chromatin immunoprecipitation (ChIP) detection (female, 12 items) showed no special abnormalities. Her ferritin concentration was 529.08 ng/ml, and the values of five key cardiac enzymes were as follows: aspartate aminotransferase, 149.6 U/L; lactate dehydrogenase, 809.0 U/L; alpha-hydroxybutyrate dehydrogenase, 602.0 U/L; phosphocreatine kinase isozyme, 27.4 U/L; and C-reactive protein, 37.26 mg/L. Her 72-h blood bacterial culture was negative. Her erythrocyte sedimentation rate was measured, and three results of the tuberculosis antibody ChIP, four results of coagulation, four results of blood transfusion, and liver and kidney functions were all normal.
Conventional ECG revealed that the patient's right atrium was enlarged, and a hypoechoic mass (40 mm x 39 mm) was found to be connected to the bottom of the lateral wall. The mass appeared to oscillate with the cardiac cycle in the tricuspid valve orifice, causing right ventricular inflow tract stenosis in diastolic periods. The right and the left ventricles were both roughly normal in size. A large amount of pericardial effusion was detected (Figures 1A-D). Subsequently, an IE33 ultrasound machine (Philips, Amsterdam, Netherlands), of which the probe frequency was 2.5 MHz, was used to obtain myocardial contrast ECG images. An ultrasound contrast agent was purchased from SonoVue (Bracco, Italy) and was reconstituted by adding 5 ml of 0.9% sodium chloride solution, then injected intravenously.
After injection, the contrast agent rapidly filled the right atrium and the right ventricle, followed by the left atrium and the left ventricle. After several cardiac cycles, a large amount of scattered ultrasound contrast agent was observed in the right atrial mass (Figures 2A,B). Contrast-enhanced computed tomography (CT) revealed a mass near the aortic arch, which was mildly enhanced in the arterial phase (Figure 3A) and reduced in the venous phase (Figure 3B). When evaluating inflammation by positron emission tomography (PET)/CT (Figure 4), masses in the right atrium, the walls of the right atrium and the right ventricle were discovered to be non-homogeneously thickened. In addition, 18F-fluorodeoxyglucose uptake was increased. The ascending aorta-para-aortic soft tissue density mass and increased 18F-fluorodeoxyglucose metabolism indicated that both the right atrial and aorta-ascending-para-aorta tumors were malignant.
Finally, a pathological examination of the cell mass in the pericardial effusion (Figure 5) diagnosed it as diffuse large B-cell non-Hodgkin's lymphoma. The immunohistochemical results were as follows: BCL-2 (+, 90%), CD19+, CD20+, CD5+, CD79a+, c-Myc (+, 30%), Ki-67 (+, 80%), and MUM-1+.
With the collection of multi-modality imaging data and histologic findings, the patient's heart mass was finally diagnosed as cardiac lymphoma which needed to be differentiated from other space-occupying cardiac lesions. Because it was a mass with a rich blood supply, while benign lesions or thrombi in the heart tend to have poor blood supply, it was considered to be a malignant mass on imaging and was confirmed as lymphoma by pathological examination.
The patient declined treatment and ultimately died 1 year later.