ABSTRACT
Introduction: The etiology of myocarditis often remains undetermined. A large variety of infectious agents, systemic diseases, drugs, and toxins can cause the disease. We report the case of a 19-year-old man who developed myocarditis three days after Pfizer-BioNTech COVID-19 booster vaccination. Case report: A 19-year-old man, presenting with troponin-positive acute chest pain, was referred to our department. He had received the Pfizer-BioNTech COVID-19 vaccine three days prior to his admission. The diagnosis of acute myocarditis was confirmed by cardiovascular magnetic resonance imaging. Patient hemodynamic status remained stable during hospitalization. The left ventricular ejection fraction was preserved during hospital stay and at one-month follow-up. We found no evidence for another infectious or autoimmune etiology. Conclusion: Although imputability of the vaccine cannot be formally established, the findings raise the possibility of an association between mRNA COVID-19 vaccination and acute myocarditis.
ABSTRACT
INTRODUCTION: Preliminary reports indicated that smokers could be less susceptible to coronavirus SARS-CoV-2, which causes Covid-19. However, once infected an increased risk of severe disease is reported. We investigated the association between smoking and COVID-19 during an outbreak of the disease on a naval vessel. METHODS: We conducted a cross-sectional, observational study on the 1769 sailors of the same navy aircraft carrier at sea exposed at the same time to SARS-CoV2 to investigate the link between tobacco consumption and Covid-19. RESULTS: Among the 1688 crewmembers (87% men; median age = 28 [interquartile range 23-35]) included, 1279 (76%) developed Covid-19 (1038 [62%] reverse-transcriptase- polymerase chain reaction testing-positive and 241 [14%] with only clinical signs). One hundred and seven patients were hospitalized. The univariable analysis odds ratio (OR) for Covid-19 infection was 0.59 (95% confidence interval [CI], 0.45-0.78; p < .001) for current smokers versus former and nonsmokers; sex, body mass index or blood group had no significant impact. Crewmembers >50 years old had an increased risk of contracting Covid-19 (OR, 2.84 [95% CI, 1.30-7.5]; p = .01). Multivariable analysis retained the lower risk of current smokers becoming infected (OR, 0.64 [0.49-0.84]; p < .001) and age >50 years was significatively associated with Covid-19 (OR, 2.6 [1.17-6.9]; p = .03). CONCLUSIONS: Current smoking status was associated with a lower risk of developing Covid-19 but cannot be considered as efficient protection against infection. The mechanism of the lower susceptibility of smokers to SARS-CoV-2 requires further research. TRIAL REGISTRATION: IRB no.: 0011873-2020-09. IMPLICATIONS: (1) Recent epidemiologic data suggest a paradoxical link between smoking and COVID-19. (2) Among the 1688 crewmembers (with an attack rate of 76% and exposed at the same time in the same place to SARS-CoV2), we found a significantly lower risk for developing COVID-19 in current smokers (71%) versus former and nonsmokers (80%). This finding strongly supports the need for further research on nicotine physiological pathway and its impact on COVID-19 infection whilst emphasizing that tobacco smoking should not be considered as efficient protection against COVID-19.