Myocarditis and Pericarditis After COVID-19 mRNA Vaccination: Practical Considerations for Care Providers.

The mRNA vaccines against COVID-19 infection have been effective in reducing the number of symptomatic cases worldwide. With widespread uptake, case series of vaccine-related myocarditis/pericarditis have been reported, particularly in adolescents and young adults. Men tend to be affected with greater frequency, and symptom onset is usually within 1 week after vaccination. Clinical course appears to be mild in most cases. On the basis of the available evidence, we highlight a clinical framework to guide providers on how to assess, investigate, diagnose, and report suspected and confirmed cases. In any patient with highly suggestive symptoms temporally related to COVID-19 mRNA vaccination, standardized workup includes serum troponin measurement and polymerase chain reaction testing for COVID-19 infection, routine additional lab work, and a 12-lead electrocardiogram. Echocardiography is recommended as the imaging modality of choice for patients with unexplained troponin elevation and/or pathologic electrocardiogram changes. Cardiovascular specialist consultation and hospitalization should be considered on the basis of the results of standard investigations. Treatment is largely supportive, and myocarditis/pericarditis that is diagnosed according to defined clinical criteria should be reported to public health authorities in every jurisdiction. Finally, we recommend COVID-19 vaccination in all individuals in accordance with the Health Canada and National Advisory Committee on Immunization guidelines. In patients with suspected myocarditis/pericarditis after the first dose of an mRNA vaccine, deferral of a second dose is recommended until additional reports become available.

Late cardiac assessment in children diagnosed with post-streptococcal reactive arthritis: a long term study.

OBJECTIVES: Unlike rheumatic fever (RF), the association of post-streptococcal reactive arthritis (PSRA) and carditis is controversial. The American Heart Association recommends anti-streptococcal prophylaxis for PSRA for one year, repeating echocardiogram and discontinuation of prophylaxis if normal. In this study the possibility of late cardiac involvement was investigated in a cohort of children with PSRA. METHODS: Children diagnosed with PSRA and followed at the Paediatric Rheumatology Units at two medical centres in Israel had echocardiography carried out by a paediatric cardiologist, at least 1 year following diagnosis. RESULTS: 146 patients with PSRA met the study criteria. Of these, 69 had undergone echocardiography 1-6.9 years (mean 3.6 years ± 1.5 years) after diagnosis. All had normal major parameters. Twenty (29.0%) patients had minimal cardiac findings, including 5 (7.2%) mild mitral insufficiency, 12 (17.4%) minimal mitral insufficiency, 2 (2.9%) mild tricuspid insufficiency and one patient (1.4%) had very mild, aortic insufficiency. Of the 77 patients who did not have echocardiography, 31 were randomly excluded from the initial study list, 26 refused to undergo echocardiography, and 20 were lost to follow-up. All were asymptomatic according to their medical record or telephone questionnaire. There were no significant differences in clinical or demographic data between those with or without echocardiography. CONCLUSIONS: No late cardiac involvement was found in our paediatric PSRA patients. Therefore, different approaches to antibiotic prophylaxis for PSRA and ARF are probably suggested. A prospective, controlled study is needed to definitively assess the necessity of prophylaxis in PSRA.

Acute myocarditis. Role of histological and virological examination in the diagnosis and assessment of immunosuppressive treatment.

Twelve patients, who presented with congestive cardiac failure after a recent influenza like illness, had a clinical diagnosis of acute myocarditis confirmed histologically after endomyocardial biopsy. Eight were under 30 years of age. Serological testing suggested a viral aetiology in six patients. Nine patients were treated with immunosuppressive drugs (prednisolone and azathioprine in seven, prednisolone alone in two). At two months, seven patients showed clinical and haemodynamic improvement (ejection fraction rose from 26.8 to 49% and left ventricular end diastolic pressure fell from 26.4 to 16.2 mm Hg) with biopsy evidence of healed myocarditis. In two, activity persisted. At six months' follow up only four of these patients had maintained their improvement. One patient relapsed after stopping treatment, subsequently improving on its reinstatement. Two patients developed severe interstitial myocardial fibrosis with gradual deterioration. Virology and myocardial histology were complementary in the diagnosis of acute myocarditis in these young patients, whose response to immunosuppressive treatment was variable. An apparent early response could not be clearly separated from variables in the natural history of the condition. Serial endomyocardial biopsies showed a progression to congestive cardiomyopathy in two patients. Multicentre controlled trials will be necessary to assess fully the role of immunosuppressive treatment in this condition.