Objectives: To describe myocarditis as an adverse event after coronavirus disease 2019 (COVID-19) vaccination, including a detailed description of clinical phenotypes and diagnostic test results and differences by age, sex, and degree of troponin level elevation.
Study design: Retrospective cross-sectional study.
Setting, participants: Cases of suspected myocarditis following the administration of a COVID-19 vaccine in Victoria during 22 February 2021 - 30 September 2022 reported to Surveillance of Adverse Events Following Vaccination In the Community (SAEFVIC), with symptom onset within 14 days of vaccination, and deemed to be confirmed myocarditis according to the Brighton Collaboration Criteria.
Main outcome measures: Demographic (sex, broad age group), vaccine, and clinical presentation characteristics; cardiac investigation results (troponin levels, electrocardiography, echocardiography, cardiac magnetic resonance imaging [cMRI]).
Results: Of 454 SAEFVIC reports of suspected COVID-19 vaccine-associated myocarditis, 206 were deemed confirmed cases. The median age of people with confirmed myocarditis was 21 years (interquartile range [IQR], 16-32 years; range, 10-76 years); 129 were aged 24 years or younger (63%), 155 were male (75%). The median time from vaccination to symptom onset was two days (IQR, 1-4 days); 201 cases (98%) followed the administration of mRNA vaccines; five cases followed vaccination with AZD122. Forty-six cases followed first vaccine doses (22%), 138 second doses (67%), and 22 cases third vaccine doses (11.0%). In 201 cases, people initially presented to emergency departments; 129 people were admitted to hospital (63%; median length of stay, two days; IQR, 1-3 days). Five people were admitted to intensive care. Echocardiographic abnormalities were identified in 26 of 200 patients (13%); electrocardiographic abnormalities were identified in 105 of 206 patients (51%; less frequently in female than male patients: adjusted odds ratio, 0.75; 95% confidence interval, 0.64-0.89). Troponin levels were elevated in 205 of 206 patients; the median increase was greater in male (95.3-fold; IQR, 5.8-273-fold) than female patients (9.9-fold; IQR, 4.7-50-fold). No cMRI abnormalities were found in patients for whom the troponin increase was threefold or less.
Conclusion: The clinical severity of COVID-19 vaccine-associated myocarditis in Victoria was generally mild. Markers of a more severe phenotype were more frequently recorded for male patients and people aged 24 years or younger. A threefold troponin increase could be used as a threshold for risk stratification of people with COVID-19 vaccine-associated myocarditis, especially in hospitals with limited access to cMRI facilities.
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