Perimyocarditis After COVID-19 mRNA Vaccine: The Role of Cardiac Magnetic Resonance Imaging
A 22-year-old male with past medical history of Coxsackie myocarditis in 2019 presented to the emergency department with acute chest pressure and diaphoresis. He described his chest pain as squeezing with radiation to the back. The patient denied dyspnea, edema, and lightheadedness. Physical examination and vital signs were within normal limits. Cardiovascular exam showed regular rate, normal rhythm, S1, S2 sounds, and no pericardial rub. He was taking no medications and had received his second dose of the Pfizer (BNT162b2) mRNA Coronavirus-19 disease (COVID-19) vaccine 3 days prior to symptoms onset.
Laboratory examination showed high sensitivity C-reactive protein (hs-CRP) (3.15 mg/L), high-sensitivity troponin T (126 ng/mL) and brain natriuretic peptide (105 pg/mL) levels were all elevated. Severe acute respiratory syndrome-Coronavirus-2 (SARS-CoV-2) IgG test was positive indicative of prior infection or prior vaccination status. Electrocardiogram (ECG) showed diffuse ST-segment elevation suggestive of pericarditis. Chest x-ray (CXR) was negative. Bedside echocardiography (echo) demonstrated mildly reduced ejection fraction (EF) (45%). In our patient, cardiac magnetic resonance imaging (CMR) identified a small pericardial effusion, and profound basal inferolateral and lateral myocardial involvement (Figure 1A).
Figure 1A: Timeline of Disease Course
BNP: Brain Natriuretic Peptide; CMR: Cardiac Magnetic Resonance Imaging; DHE: Delayed Enhancement; Hs-CRP: High Sensitivity C - reactive protein; LV: Left Ventricle; RV: Right Ventricle; RV: Right Ventricle Outflow Tract
Given his clinical and imaging findings, he was diagnosed with perimyocarditis secondary to COVID-19 vaccination. He was prescribed aspirin 650 mg TID and colchicine 0.6 mg BID. Unfortunately, he discontinued aspirin therapy due to gastrointestinal distress. He was then given a 1-month prednisone taper (30 mg). At 6-week follow-up, the patient noted his pain was significantly improved. The patient had completed his steroid taper and laboratory markers and ECG were normal. Echo showed EF recovery without the presence of a pericardial effusion.
What is the best step in management to assess for improvement in perimyocardial inflammation?