hospitalized with chest pain who were diagnosed with myocarditis; This is a literature report from the Circulation, DOI: 10.1161/CIRCULATIONAHA.121.055913 entitled Myocarditis after BNT162b2 and mRNA-1273 Vaccination. This author reported same events for 5 patients. This is the 5th of 5 reports, refer to patient 3 in table 1.  Myocarditis occurring after the BNT162b2 mRNA and mRNA-1273 vaccines has not been reported in trials. Here, we describe 8 patients hospitalized with chest pain who were diagnosed with myocarditis by laboratory and cardiac magnetic resonance imaging (MRI) within 2-4 days of receiving either the BNT162b2 or mRNA-1273 vaccine (Table 1). Patients provided written informed consent, and the collection of clinical cases followed local Institutional Review Boards. The data that support the findings of this study are available from the corresponding author upon reasonable request.   The patient in this case refer to patient 3 in table 1, who is a 40-year-old male in US. The patient received bnt162b2 (PFIZER-BIONTECH COVID-19 VACCINE), dose 1 via an unspecified route of administration on an unspecified date (Batch/Lot number was not reported) as single dose for covid-19 immunization. The patient's medical history included had a previous infection to SARS-COV-2/previously been infected by SARS-CoV-2 without need for hospitalization. Concomitant medications were not reported. On an unspecified date, the patient experienced myocarditis, which required hospitalization. The outcome of the event was unknown. Additional patient demographics identified in table 1 was as follows: Day of presentation was 2 days after 1st dose; Presenting symptom(s) was Chest pain; The baseline troponin was 102, and the peak troponin was 520, the C-reactive protein (CRP) was 9.5 (the values of baseline troponin, peak troponin and CRP are expressed as the multiple of the upper limit of normal for each laboratory's reference range); ECG showed Diffuse ST-Segment elevation with depression in aVR, V1; Lowest left ventricular ejection fraction was 47 percent, generalized hypokinesis; The cardiac magnetic resonance imaging (MRI) findings was "Edema, delayed enhancement, pericardial effusion"; anti-inflammatory treatment included Prednisone, Colchicine for this patient; Clinical course was "Hemodynamically stable, Endomyocardial biopsy found no active myocarditis.".   Additional information on article was as follows: Chest pain was most commonly described as constant, non-positional, and non-pleuritic (only patient 7 reported pericardial pain), consistent with acute myocarditis mainly without pericardial involvement. Troponin values were elevated in all individuals and appeared to peak the day after admission, whereas none had eosinophilia. All patients were tested for and were negative for SARS-CoV-2. Left ventricular ejection fraction (LVEF) was reduced (less than 50 percent) in 2 of 8 (25 percent) patients with a median LVEF of 51.5 percent (first to third quartile: 48 to 59 percent). All but three patients (1, 2, and 5) underwent coronary imaging by computed tomography or catheter-based angiography to rule out coronary artery disease. Cardiac MRI revealed patchy delayed gadolinium enhancement consistent with myocarditis in all patients, and most patients also demonstrated findings consistent with myocardial edema. Cardiac biopsy, performed in one of the patients before initiation of steroid, did not demonstrate myocardial infiltrate.  With regard to therapy, 3 patients received nonsteroidal anti-inflammatory drugs, 2 colchicine, 2prednisone, and 3 received no medications. We would consider the use of corticosteroids in fulminant myocarditis due to the likely immune-mediated post-vaccination mechanism. However, corticosteroids could reduce the specific immune response against SARS-COV-2 triggered by the vaccine. Thus, the duration of corticosteroid administration should be limited to the resolution of the symptoms or ventricular arrhythmias or the recovery of the LVEF. All patients had resolution of their chest pain, were discharged from the hospital in stable condition, and were alive with preserved left ventricular ejection fraction (LVEF) at last contact. Pending publication of long-term outcome data after SARS-CoV-2 vaccine-related myocarditis, we suggest adherence to the current consensus recommendation to abstain from competitive sports for a period of 3-6 months with re-evaluation prior to sports participation.  The patients presented here demonstrated typical signs, symptoms, and diagnostic features of acute myocarditis. The temporal association between receiving an mRNA-based COVID-19 vaccine and the development of myocarditis is notable. Trials that tested the BNT162b2 and mRNA-1273 vaccines showed that systemic reactogenicity more often occurred after dose 2 and generally within 48 hours after vaccination. On average, our patients presented with symptoms of acute myocarditis 3 days after the second injection, and in 5 out of 8 patients fever appeared a day before, supporting the hypothesis that myocarditis could be an mRNA-vaccine related adverse reaction. The only patient who experienced myocarditis after the first vaccination had a previous infection to SARS-COV-2. No eosinophilia was noted in our patients, unlike myocarditis associated with Smallpox vaccination. Potential mechanisms for myocarditis post-mRNA-based vaccination include a non-specific innate inflammatory response or a molecular mimicry mechanism between viral spike protein and an unknown cardiac protein. As a case report collection, the current research letter emphasizes the real incidence of acute myocarditis after mRNA COVID-19 vaccine, which appears to be extremely rare. In fact, the Centers for Disease Control Vaccine Adverse Event Reporting System received reports of chest pain in 5166 and myocarditis in 399 recipients of the BNT162b2 or mRNA1273 vaccine, whereas more than 129 million individuals have been fully vaccinated with these two vaccines. In conclusion, providers should be vigilant for myocarditis after COVID-19 mRNA vaccination; further research is required to understand the long-term cardiovascular risks.  No follow-up attempts are needed; information about lot/batch number cannot be obtained.; Sender's Comments: A possibly contributory role of BNT162B2 in triggering the onset of myocarditis cannot be fully excluded, considering the temporal relationship.  More immunological and biomolecular evidences would be needed to explore the plausible physiopathologic mechanism between the vaccination and the event occurrence.  The impact of this report on the benefit/risk profile of the Pfizer product is evaluated as part of Pfizer procedures for safety evaluation, including the review and analysis of aggregate data for adverse events. Any safety concern identified as part of this review, as well as any appropriate action in response, will be promptly notified to Regulatory Authorities, Ethics Committees and Investigators, as appropriate,Linked Report(s) : US-PFIZER INC-2021768972 Same reporter/drug/event and different patients.