A 58-year-old man presented with chest tightness, cough, and asthma without fever in late October 2020. The patient took aminophylline and inhaled budesonide, but without obvious effect. His condition began to worsen gradually and he was admitted to a local hospital on 4 November, 2020. Electrocardiogram showed an elevated ST segment in leads II, III, and arteriovenous fistula (AVF). Echocardiography showed segmental wall motion abnormalities, and the LVEF was decreased (36%). Laboratory examinations showed elevated cardiac troponin I (cTnI) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels. Thus, the patient was transferred to a cardiology care unit (CCU) for acute inferior myocardial infarction and heart failure. Coronary computed tomography (CT) angiography results showed only mild stenosis in the coronary arteries. The patient's symptoms improved insignificantly after the administration of medications that improved cardiac function. During hospitalization, he had fever with temperature of 39.5 C. Blood work showed a white blood cell (WBC) count of 9.7 x 109/L, hemoglobin level of 117 g/L, platelet count of 186 x 109/L, and high levels (2.2 x 109/L) and percentage (22.8%) of eosinophils. As the patient presented with cough and asthma, he was administered anti-infective and antipyretic treatment. Four days later, the patient's body temperature decreased to normal, and the fever symptoms were relieved. He was discharged from the hospital on 19 November, 2020. Two weeks later, the symptoms including fever, cough, and asthma recurred. Upon revisiting the local hospital, the patient's chest CT showed bronchiectasis with infection. He was administered antibiotics for 7 days but with poor effect and had fever with a temperature of 38 C.
With no significant relief from symptoms, he revisited our hospital and was admitted to the respiratory department with bronchiectasis. Physical examinations revealed a body temperature of 37.6 C, pulse rate of 111 times/min, respiration rate of 20 breaths/min, and blood pressure of 130/80 mmHg. The laboratory examination showed the following test results: eosinophil count 3.36 x 109/L, percentage of eosinophils 32.10%, cTnI level of 1.032 ng/mL, and BNP level of 1,073 pg/mL. The patient had 1-year history of bronchial asthma and allergic rhinitis. He had a 30-year smoking history, smoking approximately 7 cigarettes per day and quitting smoking for 1 year. The patient did not show any history of hypertension, coronary heart disease, diabetes mellitus, food or drug allergies, infectious diseases, or parasitic infections. Echocardiography showed an enlarged heart and decreased LVEF (47%). It also showed that there were masses in both ventricular apexes with a small amount of pericardial effusion (Figure 2A). Contrast echocardiography showed no perfusion in either of the ventricular apical masses (Figure 2B). Hence, we considered the masses to be thrombi.
Eosinophilia and Loeffler endocarditis with thrombus in the RV was considered a probable diagnosis. The patient was administered low-molecular-weight heparin (subcutaneous injection, 5,000 IU (international units), twice daily) and oral prednisone (60 mg, once daily). Nine days later, a routine blood work showed that eosinophils had decreased to within the normal range (0.37 x 109/L); however, frequent syncope persisted. The patient then underwent thrombectomy and tricuspid valve replacement. Pathological results showed an RV thrombus, endocardial fibroplasia, and eosinophilic infiltration. The symptoms relieved significantly after the operation, and he was discharged with oral prednisone (60 mg, once daily) and warfarin (3.75 mg, once daily). Six months later, prednisone was gradually tapered down to 10 mg daily. The patient continued to feel well for 2 years following surgery when he stopped taking prednisone and warfarin on his own. However, 6 months later, the patient experienced edema in both legs and was readmitted. Blood work showed elevated eosinophils once again (5.13 x 109/L). Echocardiography revealed a hypoechoic mass attached to the RVIT (Figure 1C), and contrast echocardiography showed no perfusion in the mass. Thus, the patient was diagnosed to have a recurrence of thrombus . He was once again prescribed oral prednisone (60 mg, once daily) and warfarin (4.5 mg, once daily). At the 3-month follow-up, no edema was noticed in the patient's legs. The eosinophils had restored to normal conditions, and the RV thrombus had dissolved. Thus, the medication was changed to long-term low-dose prednisone (10 mg, once daily) maintenance therapy. The patient remained in good health at later follow-up visits.
A probable diagnosis of Loeffler endocarditis was considered. The patient was advised to undergo an endomyocardial biopsy but he refused invasive testing. He also refused to undergo cardiac magnetic resonance (CMR) due to noise intolerance. A bone marrow puncture showed eosinophilia. Genetic FIP1L1/PDGFRA, platelet-derived growth factor receptor-beta (PDGFRB), FGFR1/d8z2 (8p11), and parasite testing were negative. Other abnormal examination results included immunoglobulin G (IgG) 24.9 g/L , immunoglobulin E (IgE) 1,890 IU /mL , and urinary microalbumin 122.74 mg/L . Combined with clinical symptoms and examinations, the final diagnosis was eosinophilic granulomatosis polyangiitis (EGPA) involving multiple organs, including the heart (Loeffler endocarditis), lungs, kidneys, and nasal sinuses. This diagnosis was made according to the Classification Criteria of the American College of Rheumatology for eosinophilic granulomatosis polyangiitis (EGPA). The therapeutic medications included prednisone and mycophenolate mofetil for anti-immunotherapy, warfarin for anticoagulation, sacubitril valsartan, metoprolol, spironolactone, and dapagliflozin for heart failure. The patient's temperature returned to normal, and symptoms of tightness in chest, shortness of breath, and asthma alleviated substantially. During the regular outpatient follow-up visits, eosinophil count, IgG, and IgE levels returned to the normal range, electrocardiogram returned to a normal pattern, LVEF was improved to above 50%, and mural thrombi in both ventricles disappeared in echocardiography (Figure 2C). The patient's exercise tolerance improved significantly and he reported the ability to play basketball for up to an hour. Prednisone and mycophenolate mofetil were gradually tapered down to a maintenance dose. Because the patient had no uncomfortable symptoms and was in a good condition, he requested discontinuation of the medications for heart failure. A recent follow-up reported normal immunoglobulin levels, normal cardiac function, and no mural thrombus in the heart.