Electrocardiogram Changes in an Athlete Recovering from COVID-19 Infection: Pericarditis or Not?
An 18-year-old African American male with recent SARS-CoV-2 infection (COVID-19) presented to our clinic for abnormal electrocardiogram (ECG) changes. He is a college football player and plays every day without any limitations. Two months ago, he developed fever of 100.9°F and headache. COVID-19 test was positive which was treated conservatively for 2 weeks at home. After recovery, he followed up with his primary care physician. He was asymptomatic with no complain of chest pain, shortness of breath, palpitations, dizziness, syncope, or lower extremity edema. He has no known family history of premature coronary artery disease or sudden cardiac death. ECG revealed ST segment elevation in leads V1-V3 (Figure 1) raising concern for COVID-19 pericarditis. He was prescribed indomethacin 50 mg three times a day and colchicine 0.6 mg twice a day. He was advised against return to play and referred to our pericardial clinic.
During evaluation at clinic, he appeared comfortable at rest without any acute complaints. Blood pressure was 110/68 mm Hg, heart rate 80 beats per minute, respiratory rate 12 breaths/minute with 100% oxygen saturation on room air and temperature 97.9°F. Physical examination revealed regular heart sounds with no audible murmurs or friction rub. Laboratory investigation revealed serum creatinine of 1.49 mg/dL (reference range: 0.73-1.22 mg/dL), troponin <0.01 ng/mL test results (reference range: 0.000-0.029 ng/mL), C-reactive protein (CRP) 0.5 mg/dL (reference range: <0.9 mg/dL) and erythrocyte sedimentation rate (ESR) 5 mm/hour (reference range: 0-15 mm/hour). Chest x-ray showed no pulmonary consolidation, pleural effusion, or cardiomegaly. Repeat ECG revealed persistent ST segment elevation in leads V1-V3. He underwent a transthoracic echocardiogram (TTE) showing normal biventricular function with an approximate ejection fraction of 60%. There was no pericardial effusion. Cardiac magnetic resonance imaging (CMR) revealed no thickening of pericardium, delayed enhancement, or pericardial edema. There was no evidence of constrictive physiology or myocardial inflammation to suggest myocarditis (Figure 2A-D).
What is the most appropriate next step in management?