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COVID-19 pandemic and troponin: indirect myocardial injury, myocardial inflammation or myocarditis?
  1. Massimo Imazio1,2,
  2. Karin Klingel3,
  3. Ingrid Kindermann4,
  4. Antonio Brucato5,
  5. Francesco Giuseppe De Rosa6,
  6. Yehuda Adler7,
  7. Gaetano Maria De Ferrari8
  1. 1 University Cardiology, AOU Città della Salute e della Scienza di Torino, Torino, Italy
  2. 2 Department of Public Health and Pediatrics, University of Torino, Torino, Italy
  3. 3 Cardiopathology, University Hospital Tuebingen, Tuebingen, Germany
  4. 4 Department of Internal Medicine III (Cardiology, Angiology and Intensive Care), Saarland University Medical Center, Saarland University, Homburg/Saar, Germany
  5. 5 Department of biomedical and clinical sciences, Fatebenefratelli Hospital and University of Milano, Milano, Italy
  6. 6 University Infectious Diseases, University of Turin, Torino, Piemonte, Italy
  7. 7 College of Law and Business, Ramat Gan, and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
  8. 8 University Cardiology, AOU Città della Salute e della Scienza di Torino and Department of Medical Sciences, University of Torino, Torino, Italy
  1. Correspondence to Professor Massimo Imazio, University Cardiology, A.O.U. Città della Salute e della Scienza di Torino, Torino 10126, Italy; massimo_imazio{at}yahoo.it

Abstract

The initial mechanism for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection is the binding of the virus to the membrane-bound form of ACE2, which is mainly expressed in the lung. Since the heart and the vessels also express ACE2, they both could become targets of the virus. However, at present the extent and importance of this potential involvement are unknown. Cardiac troponin levels are significantly higher in patients with more severe infections, patients admitted to intensive care units or in those who have died. In the setting of COVID-19, myocardial injury, defined by an increased troponin level, occurs especially due to non-ischaemic myocardial processes, including severe respiratory infection with hypoxia, sepsis, systemic inflammation, pulmonary thrombosis and embolism, cardiac adrenergic hyperstimulation during cytokine storm syndrome, and myocarditis. At present, there are limited reports on definite diagnosis of myocarditis caused by SARS-CoV-2 in humans and limited demonstration of the virus in the myocardium. In conclusion, although the heart and the vessels are potential targets in COVID-19, there is currently limited evidence on the direct infection of the myocardium by SARS-CoV-2. Additional pathological studies and autopsy series will be very helpful to clarify the potentiality of COVID-19 to directly infect the myocardium and cause myocarditis.

  • myocarditis
  • acute coronary syndromes
  • pericardial effusion
  • thromboembolic pulmonary vascular disease

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Footnotes

  • FGDR, YA and GMDF are joint senior authors.

  • Twitter @ImazioMassimo

  • Contributors All authors have contributed and gave final approval for the submitted manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests MI and AB have been advisory board members for SOBI and Kiniksa. YA has been an advisory board member for Kiniksa.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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