STEMI Mimic: Focal Myocarditis in an Adolescent Patient After mRNA COVID-19 Vaccine

After a cluster of patients developing pneumonia and viral prodromal symptoms in Wuhan, China, a novel coronavirus, ultimately deemed severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was discovered (,). After over a year of causing unprecedented death, disease, and economic collapse, the first vaccine in America was given in New York City on December 14, 2020. Initially, this vaccine was only approved for adults ages 18 years and older, however, effective May 2021, the Emergency Use Authorization was amended to allow the BNT162b2 SARS-CoV-2 vaccination to be administered to those between the ages of 12 and 18 years old (). As of June 27, 2021, over 323,000,000 vaccines have been administered in the United States, with the majority being the mRNA subtype. Adverse outcomes of the mRNA COVID-19 vaccines are rare but do include myocarditis, anaphylaxis, and death (). Sparse evidence exists regarding the incidence of myocarditis after mRNA vaccination, however, cases are beginning to be reported (,). With the exception of the smallpox vaccination, post-vaccination myocarditis is thought to be a relatively rare occurrence (,). We present a case of focal myocarditis mimicking an ST-segment elevation myocardial infarction (STEMI) in a 17-year-old patient after BNT162b2 mRNA SARS-CoV-2 vaccination.

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.

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 (,,).

Although reported cases of myocarditis with the mRNA SARS-CoV-2 vaccine exist, the rate of myocardial involvement after vaccination seems to be significantly less than the rate of myocardial involvement from SARS-CoV-2 infection. In light of the greater public health concern surrounding SARS-CoV-2 infection, authorities still recommend vaccination, as it is likely safer than infection from the representative virus (,).

As vaccine administration continues to increase, possible adverse outcomes to include myocarditis are becoming more widely recognized. Focal myocarditis may demonstrate localizing ECG changes consistent with a STEMI. The mechanisms of myocardial inflammation, treatment, and long-term complications of suspected COVID-19 mRNA vaccination-related myocarditis are still unclear and require further investigation. At this time, rates of myocardial involvement by SARS-CoV-2 is 7–23%, and rates of myocarditis after vaccination is 0.00161% (,). In light of the greater public health concern surrounding SARS-CoV-2 infection, authorities still recommend vaccination, as it is likely safer than infection from the representative virus (,).