Heart failure secondary to myocarditis after SARS-CoV-2 reinfection: a case report

• Published in: International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases Vol. 113; pp. 175 - 177
• Main Authors: Riedel, Patrícia Gabriela, Sakai, Vitoria Fedrizzi, Toniasso, Sheila de Castro Cardoso, Brum, Maria Carlota Borba, Fernandes, Fernando Schmidt, Pereira, Robson Martins, Baldin, Camila Pereira, Baldin, Cícero de Campos, Takahasi, Anderson Yudi, Shiki, Hugo, Krepsky, Ana Maria Rocha, Macedo, Damasio Trindade, Merlo, Álvaro Roberto Crespo, Rohde, Luis Eduardo Paim, Joveleviths, Dvora
• Format: Report
• Language: English
• Published: 01-12-2021
• DOI: 10.1016/j.ijid.2021.10.031
• EISSN: 1878-3511

INTRODUCTIONCardiac involvement in COVID-19 can range from mild damage to severe myocarditis. The precise mechanism by which COVID-19 causes myocardial injury is still unknown. Myocarditis following administration of COVID-19 vaccines, especially those based on mRNA, has also been described. However, no reports of heart failure following reinfection with SARS-CoV-2 in patients immunized with an inactivated vaccine have been identified. CASE DESCRIPTIONThe patient was a 47-year-old male construction worker of African descent, with type II diabetes and a history of infection by SARS-CoV-2 in December 2020 and May 2021, confirmed by RT-PCR. He received two doses of an inactivated vaccine against COVID-19. Between the two COVID-19 episodes with positive RT-PCR, he had two episodes of bacterial lung infection. After the second episode of SARS-CoV-2 infection, he was diagnosed with severe heart failure as a sequela of myocarditis. CONCLUSIONIt is essential to perform a thorough follow-up after infection with SARS-CoV-2 since, even with proper immunization, it is possible that the patient was reinfected and suffered severe cardiac sequelae as a consequence. The hypothesis of an etiology associated with the use of an inactivated vaccine against COVID-19, with a potential immune enhancement mechanism following reinfection with SARS-CoV-2, cannot be rejected.