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Aims To prospectively evaluate the incidence of myocardial injury after the administration of the fourth dose BNT162b2 mRNA vaccine (Pfizer‐BioNTech) against COVID‐19. Methods and results Health care workers who received the BNT162b2 vaccine during the fourth dose campaign had blood samples collected for high‐sensitivity cardiac troponin (hs‐cTn) during vaccine administration and 2–4 days afterward. Vaccine‐related myocardial injury was defined as hs‐cTn elevation above the 99th percentile upper reference limit and >50% increase from baseline measurement. Participants with evidence of myocardial injury underwent assessment for possible myocarditis. Of 324 participants, 192 (59.2%) were female and the mean age was 51.8 ± 15.0 years. Twenty‐one (6.5%) participants had prior COVID‐19 infection, the mean number of prior vaccine doses was 2.9 ± 0.4, and the median time from the last dose was 147 (142–157) days. Reported vaccine‐related adverse reactions included local pain at injection site in 57 (17.59%), fatigue in 39 (12.04%), myalgia in 32 (9.88%), sore throat in 21 (6.48%), headache in 18 (5.5%), fever ≥38°C in 16 (4.94%), chest pain in 12 (3.7%), palpitations in 7 (2.16%), and shortness of breath in one (0.3%) participant. Vaccine‐related myocardial injury was demonstrated in two (0.62%) participants, one had mild symptoms and one was asymptomatic; both had a normal electrocardiogram and echocardiography. Conclusion In a prospective investigation, an increase in serum troponin levels was documented among 0.62% of healthy health care workers receiving the fourth dose BNT162b2 vaccine. The two cases had mild or no symptoms and no clinical sequela. Clinical Trial Registration: ClinicalTrials.gov Identifier: NCT05308680.

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Sirs:Myocarditis resolves in about 50 % of cases during 2-4 weeks, but 25 % develop persistent cardiac dysfunction and 12-25 % may deteriorate leading to death or endstage dilated cardiomyopathy [1]. Presentation with heart failure and ventricular dysfunction are strong predictors of adverse outcome [2]. Viral infection is the most commonly identified cause of myocarditis. Mechanisms of injury include direct viral damage or inappropriate immune response. While the initial immune response limits the degree of viral cellular invasion and myocardial damage, non-replicating viral genomic fragments and cardiac epitopes such as myosin and beta-1 receptors might drive an ongoing adverse autoimmune response leading to inflammation through ''anti-heart auto-antibodies'' [3,4].Treatment of myocarditis includes supportive measures, heart failure therapy and treatment of arrhythmias according to current position statements [1]. Immunosuppression is advised with specific rare etiologies such as giant cell and eosinophilic myocarditis, but controversial in the prevalent lymphocytic subtype.A 28-year-old woman was admitted with weakness, dyspnea and nausea for a few days and gastroenteritis 2 weeks earlier. Otherwise, she had no history pertinent to the current illness. On admission, she was pale and nauseous, blood pressure was 90/60, pulse was 130 and ECG showed sinus tachycardia with small complexes. Troponin I was 0.22 mcg/L (normal range \ 0.04), Leukocytes were 10,600 (75 % neutrophils) and hemoglobin was 13 g/dL. She had moderate hepatic transaminase elevation (in the hundreds) and normal renal function; BNP was 2760 pgr/ ml, lactate was 1.29 mmol/L and CRP was 3.5 mg%. Chest X-ray demonstrated mild bilateral congestion. Echocardiogram showed mildly enlarged left ventricle with severe biventricular failure, left ventricular ejection fraction 23 %, normal wall thickness and severe mitral and tricuspid regurgitation. Cardiac MRI showed marked lateral wall edema without late gadolinium enhancement. On catheterization, right atrial pressure was 16 mmHg, pulmonary pressure was 45/25, mean was 30 mmHg, wedge pressure was 20 mmHg and cardiac index was 1.55 l/min/ m 2 . Right ventricular endomyocardial biopsy revealed active lymphocytic myocarditis (CD3? T lymphocyte predominant with CD68? histiocytes and without eosinophils or giant cells) associated with ongoing and wellestablished perivascular and interstitial replacing fibrosis. Electron microscopy showed no viral capsids, no evidence of myofilament loss or mitochondrial pathology.She continued to suffer from persistent weakness and nausea needing continued hospitalization with ongoing tachycardia and low blood pressures, tolerating only low doses of heart failure treatment (Losartan 12.5 mg BID, Bisoprolol 1.25 mg BID, Spironolactone 25 mg and Furosemide). The patient occasionally missed heart failure medication due to low blood pressure, but did not need inotropic support. Repeat echocardiography showed no improvement in ventricular function with a new apical thrombus (tre...