A 64-year-old non-smoking man with no hypertension or diabetes was admitted to the emergency department complaining of oppressive chest pain accompanied by profuse sweating lasting for four hours upon admission. His temperature was 36.1 °C, respiratory rate: 22 breaths/minute, pulse rate: 81 beats/minute, blood pressure: 114/68 mmHg, and finger oxygen saturation was 100% on ambient air. His rapid troponin I levels were 4.83 ng/ml.
An electrocardiogram revealed normal sinus rhythm and ST-segment elevations in leads II, III, and aVF(Fig. 1a).A bedside echocardiography revealed abnormal movement in the left inferior ventricular wall and a mass in the left atrium, speculated to be a myxoma. A bedside posteroanterior chest X-ray showed suspected pneumonia in the upper left lung(Fig. 1b). The patient was diagnosed with AMI. An emergency coronary angiography showed no evidence of atherosclerosis, but did reveal that the middle-to-distal right coronary artery was completely occluded (Fig. 1d), indicating an embolism without an acute manifestation of atherosclerosis.
Despite intracoronary injection of tirofiban, aspiration, and balloon dilation, blood flow was not recovered at the distal end of the right coronary artery, and no thrombus was extracted. After the percutaneous coronary intervention, antiplatelet, lipid regulation and anticoagulant therapy were provided for the patient.
On the second day of admission, the patient began to suffer from pain in both lower limbs, which was accompanied by low skin temperature and hemoptysis. Bedside Color Doppler ultrasound of the lower extremities showed incomplete embolization of the popliteal and anterior tibial arteries of the lower right extremities. Emergency angiography of lower limb arteries revealed that the onset of the right profunda artery and the popliteal artery were completely occluded, as were the distal left posterior tibial and peroneal arteries(Fig. 2a–c).
To prevent ischemic necrosis of the lower extremities, a lower extremity arteriotomy was performed under general anesthesia, and a large amount of tissue and thrombus were removed. Due to hemoptysis, afiberoptic bronchoscopy was performed under general anesthesia, and the results showed the presence of a large blood clot in the left bronchus and its subsequent airways. To discern the growth location of the left atrial mass, we also performed a transesophageal echocardiography, which showed that the mass in the left atrium grew from the entrance of the left superior pulmonary vein(Fig. 3d).
Subsequent pathological examination of the tissue and thrombususing H&E staining revealed coagulation necrosis with atypia cells (Fig. 2e). Immunohistochemical staining was positive for CD163(Fig. 4a) and negative for SMA, CD31, ERG, CK7, TTF, NapsinA, CK5/6, P63, and P40. The proliferation index (Ki-67) was approximately 2% (Fig. 4b).
A chest computed tomography (CT) scan revealed a solid lesion of the upper left lobe of the lung with irregular borders, speculated to be a lung tumor (Stage IVA). The tumor seemed to enter into the left atrium via the upper left pulmonary vein, which appeared completely occluded due to the presence of solid material in its lumen(Fig. 3a–c). Based on the patient’s medical history and examination, tumor embolism was suspected. Unfortunately, when he learned of his disease, the patient abandoned treatment and was discharged from the hospital. A week later, the patient's family was contacted by phone, and they disclosed that the patient had died three days after he was discharged.
