A 66-year-old man without any known comorbidities or allergies presented to our emergency department with ten-day progressive shortness of breath without chest pain, abdominal distension, decreased effort tolerance, and 12 kg weight gain within the last ten days. The first assessment showed an afebrile patient (36.5 C) with sinus tachycardia (108 bpm), hypertension (153/110 mmHg), respiratory rate 15/min, SpO2 87% on room air, signs of low voltage in ECG (Figures 1(a) and 1(b)), anasarca, ascites, pleura effusion, and a massive pericardial effusion on ultrasound evaluation.
39 days prior, the unvaccinated patient was tested positive for SARS-CoV-2 (by RT-PCR) as part of a health care workers' screening. Prior to the infection, the patient was healthy and fit, doing cycling regularly. During the infection, the patient remained asymptomatic. On admission, the patient was tested negative for influenza, respiratory syncytial virus, and SARS-CoV-2 by RT-PCR. SARS-CoV-2-IgG was positive. Laboratory assessment (Table 1) showed leucocytosis with absolute lymphopenia, elevated C-reactive protein, and IL-6 indicating an inflammatory process. Furthermore, biomarkers of myocardial damage were elevated while NT-pro-BNP was within normal limits. We suspected concomitant shock physiology as serum lactate was elevated (3.3 mmol/l).
A CT-thorax scan showed bilateral lower lobe collapse consolidations, large bilateral pleural effusion, pericardial effusion, and ground-glass opacification in the left upper lobe. Dedicated echocardiography (supplemental files, video 1) revealed reduced left and right ventricular function, collapse of the left and right atrium, and a massive circumferential pericardial effusion (48.9 mm apical) suggesting echocardiographic tamponade (Figure 2). We suspected new-onset heart failure and echocardiographic pericardial tamponade. The patient was admitted to our medical intensive care unit for noninvasive ventilation and high-flow nasal cannula oxygen therapy for one day.
Due to pericardial tamponade, a step-by-step approach was initiated with pericardiocentesis first for symptomatic therapy and assessing the most common etiologies of pericardial effusion. An ultrasound-guided pericardial drainage was placed, and 850 ml of serosanguinous fluid was removed. Fluid analysis tested negative by RT-PCR for SARS-CoV-2, revealing high-level LDH and protein indicating an exudative process; microbiology (including mycobacterial and fungal culture) remained negative as well as serology for cardiotropic pathogens. Interferon-y (QuantiFERON) testing was positive. After pericardiocentesis, symptoms improved. Cytologic evaluation of the pericardial fluid was suspicious for high malignant lymphoma. Further flow cytometry and immunophenotyping excluded a monoclonal cell population as well as PET-CT showed no pathologic extracardiac FDG uptake, which could have indicated a highly proliferative tumor mass or active tuberculosis. Pleurocentesis was performed for diagnostic purpose and symptomatic treatment. The exudative fluid showed no evidence of malignancy or infection but indicating polyserositis. After removal of at least 1850 ml in total over 9 days, echocardiography showed minimal residual effusion and the drainage was removed. Left ventricular function recovered, but the right ventricular global function was still impaired. Echocardiography revealed hypertrophy of the free right ventricular wall. Cross-sectional studies (Figure 3) confirmed myocardial inflammation indicating myocarditis with diffuse biventricular fibrosis. Cardiac catheterization excluded occlusive coronary artery disease.
A duplex and compression sonography of the upper extremities was performed due to new-onset pain in both arms. It confirmed thrombosis of the left subclavian vein and symmetrical thrombophlebitis of the cephalic vein. An extensive vasculitis and collagenosis screening revealed elevated ANA titer (1 : 100) with high positivity for Ro52, borderline positivity for nRNP/Sm, negative anti-ds-DNA, anti-Sm-antibodies, and normal complement C3/C4. Direct Coombs test (anti-Fy(b)) was positive without evidence of hemolysis. An antiphospholipid syndrome evaluation revealed a slight elevated anti-cardiolipin-IgM titer. Serology for hepatitis A, B, C, and E and HIV was negative. Urine analysis and sediment showed no evidence of concomitant nephropathy. Past medical history was negative for joint pain, skin rash or mucosal lesions, alopecia, and neuropsychiatric abnormalities. Although ACR/EULAR criteria for SLE were negative, 100 mg oral prednisolone was administered for seven days in the set of acute myopericarditis and suspected autoimmune etiology. Within the next three weeks, the patient recovered slowly with loss of about 15 kg along with diuretics and guideline-directed medical heart failure therapy. Left and right ventricular function improved. The elevated liver enzymes had normalized along the improvement of cardiac function suggesting congestive hepatopathy. The patient was discharged after 23 days and followed in our outpatient clinic.
Two weeks later, the patient reported an improvement of his physical performance without any complaints. The laboratory assessment revealed a rise in the ANA titer up to 1 : 320 with persisting high positivity for Ro52 and a positive RT-PCR for SARS-CoV-2 in a nasopharyngeal swab with a cycle threshold of 35.5 indicating low viral shedding. Echocardiography showed a persisting moderate reduced right ventricular function and a pericardial effusion of 8 mm around the right ventricle. A rheumatologic examination was intended but is still pending due to patient's concerns. At a six-month telephone follow-up, the patient was asymptomatic and again at his prior exercise capacity but refused any further medical consultation.