Myocarditis in an Adolescent Patient After mRNA COVID-19 Vaccine
A 17-year-old boy
- Starting 1 day after the 2nd dose of the #CovidVaccine (Pfizer-BioNTech): progressively worsening substernal chest pain and exertional dyspnea ⇒ Myocarditis https://www.jem-journal.com/article/S0736-4679(21)00733-2/fulltextFocal Myocarditis in an Adolescent Patient After mRNA COVID-19 Vaccine
Published:September 26, 2021DOI:https://doi.org/10.1016/j.jemermed.2021.09.017
Abstract
Background: In May 2021, the U.S. Food and Drug Administration expanded the Emergency Use Authorization for the Pfizer-BioNTech mRNA Coronavirus disease 2019 (COVID-19) Vaccine (BNT162b2) to include adolescents 12–15 years of age. As vaccine administration continues to increase, potential adverse outcomes, to include myocarditis, are being reported to the Vaccine Adverse Event Reporting System.
Case Report: This case report describes a 17-year-old male patient who developed focal myocarditis mimicking an ST-segment elevation myocardial infarction (STEMI) 3 days after administration of an mRNA COVID-19 vaccine.
Why Should an Emergency Physician Be Aware of This? Myocarditis is a rare complication in adolescents receiving mRNA COVID-19 vaccines. Focal myocarditis may demonstrate localizing electrocardiographic changes consistent with a STEMI. Overall, complications of the mRNA COVID-19 vaccines are extremely rare. The vaccine continues to be recommended by public health experts, as the benefits of vaccinations greatly outweigh the rare side effects.
Case Presentation
In June of 2021, a thin, otherwise healthy 17-year-old male presented to the Emergency Department with 3 days of progressively worsening substernal chest pain and exertional dyspnea that began 1 day after his second BNT162b2 vaccination. He had no family history of premature coronary artery disease. Upon presentation, the patient's vitals were within normal limits; blood pressure 119/79 mm Hg, heart rate 90 beats/min, respiration rate 16 breaths/min, and pulse oximetry 97% on room air. His physical examination was benign, including lungs clear to auscultation, no murmurs/rubs/gallops on cardiac examination, and non-reproducible chest pain. The patient's chest x-ray study showed no acute cardiopulmonary abnormalities. The initial electrocardiogram (ECG) showed sub-1-mm lateral ST elevations with sub-1-mm depression in lead III (Figure 1). Bedside ultrasound showed a trace pericardial effusion without wall motion abnormalities. Initial troponin was elevated, at 0.08 ng/mL (normal [nl] < 0.03 ng/mL). Repeat ECG (Figure 2) demonstrated 1-mm elevations in leads I and aVL, with reciprocal depression in lead III. At this time, Cardiology was consulted and a code STEMI was called, given localizing ECG changes meeting STEMI criteria. The patient was given 324 mg of aspirin and sublingual nitroglycerin without improvement in the patient's chest pain. Intravenous diltiazem was then administered for concerns of possible coronary vasospasm, without improvement in the patient's chest pain or normalization of the patient's ECG. Cardiology elected to obtain a coronary computed tomography angiogram (CCTA), as there was high suspicion for myocarditis and low suspicion for acute coronary syndrome given the patient's age and lack of risk factors. The CCTA showed normal coronary origins with a coronary artery calcium score of 0. Repeat troponin returned at 0.22 ng/mL. The patient was then admitted to the Cardiology service for suspected myocarditis. C-reactive protein was noted to be elevated at 1.9 mg/dL (nl ≤ 0.5 mg/dL), whereas the erythrocyte sedimentation rate was normal at 14 mm/h (nl 0–20 mm/h). Trended troponins continued to rise, with a peak value of 0.39 ng/mL. Cardiac magnetic resonance imaging was performed and showed diffuse, subepicardial delayed gadolinium enhancement of the anterior and lateral wall of the left ventricle, with corresponding heterogeneous T1 signal prolongation and increased short tau inversion recovery signal consistent with a high-risk pattern for myocarditis as depicted in Figure 3; left ventricular ejection fraction was preserved at 55%. The patient was monitored on the Cardiology service for 1 day and was discharged after subsequent troponins downtrended, with plans for close follow-up with the Cardiology Department. The patient followed up in the Pediatric Cardiology clinic 1 month after discharge and endorsed complete resolution of symptoms. No additional laboratory tests or imaging were completed at this time. He was placed on a 6-month activity restriction.
Discussion
Although the BNT162b2 was the first mRNA vaccine approved for Emergency Use Authorization by the U.S. Food and Drug Administration (FDA), the vaccine strategy is not new. In 1990, mRNA was injected into mouse skeletal muscle in vivo, resulting in transcription of proteins (). The mRNA COVID-19 vaccine contains nucleoside-modified messenger RNA that encodes immunogens derived from the spike glycoprotein (S) of SARS-CoV-2 (). The body's immune response to these immunogens is believed to cause a suspected hypersensitivity myocarditis, although the mechanism is not yet known. Antibody-mediated responses to the spike proteins have also been theorized. New research suggests that elevated levels of anti-spike immunoglobulin G may be linked to more severe systemic infection (). Biologic agents such as fostamatinib, a therapeutic small-molecule inhibitor of Syk kinase approved by the FDA, are currently being studied to decrease said response ().
Myocarditis is defined as inflammation of the cardiac myocardium, and it is caused by immune-mediated, toxic, and infectious, most commonly viral, etiologies (). With the exception of the smallpox vaccination, post-vaccination myocarditis is thought to be a relatively rare occurrence (,). Recent reports of myocarditis after novel Emergency Use-Authorized vaccines raise concern for a possible trend of adverse effects (). According to the Centers for Disease Control and Prevention reports and Vaccine Adverse Event Reporting System (VAERS) data, there were 573 reports of myocarditis and pericarditis after two doses of an mRNA, with a predilection for affecting young adolescent males (data through May 31, 2021) (). In the 16–39-year age group, a rate of 16.1 per 1 million vaccine doses, or 0.00161%, is reported to VAERS (). It is unknown what the true rate of myocardial involvement is in SARS-CoV-2 infection, but estimates range from 7–23% (). Most patients recover with minimal sequelae, though ventricular dysrhythmias are more common in those with healed myocarditis (,,).
Clinical presentations of myocarditis can vary widely, from nonspecific symptoms like chest tightness and shortness of breath to fulminant heart failure. The differential for myocarditis includes acute coronary syndrome, septic myocardial malfunction, and cardiac myopathy (). Laboratory diagnostic modalities typically include metabolic panel, cardiac troponin T, brain natriuretic peptide, and ECG (). ECG changes are often diffuse and nonspecific, although focal myocarditis may result in ECG changes that can mimic an acute coronary syndrome, such as in this case (). For patients with findings concerning for myocarditis, American Heart Association guidelines recommend one or more cardiac imaging modalities, which may include echocardiogram or magnetic resonance imaging (). Cardiac catheterization is performed at the discretion of the cardiologist, however, some argue there should be a consideration for endomyocardial biopsy at the time of the procedure (). Management of myocarditis from any cause is largely supportive (,,).
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