COVID-19 pandemic and troponin: indirect myocardial injury, myocardial inflammation or myocarditis?
Heart
; 106(15): 1127-1131, 2020 08.
Article
in English
| MEDLINE | ID: covidwho-536149
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.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Pneumonia, Viral
/
Troponin
/
Coronavirus Infections
/
Inflammation
/
Myocarditis
Type of study:
Observational study
/
Prognostic study
Limits:
Humans
Language:
English
Journal:
Heart
Journal subject:
Cardiology
Year:
2020
Document Type:
Article
Affiliation country:
Heartjnl-2020-317186
Similar
MEDLINE
...
LILACS
LIS