COVID-19 pandemic and troponin: indirect myocardial injury, myocardial inflammation or myocarditis?

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.

Redefining the Prognostic Value of High-Sensitivity Troponin in COVID-19 Patients: The Importance of Concomitant Coronary Artery Disease

“…In patients with a preexisting CCS, myocardial injury may be due predominantly to a worsening of the preexisting CCS condition due to an increased mismatch of the supply/delivery of oxygen, while in patients without a preexisting diagnosis of CCS, a direct myocardial damage (myocarditis-like) may have a relevant role. However, at present, there are no findings providing evidence of direct infection and replication of SARS-CoV-2 in cardiomyocytes [ 14 ].…”

“…It is well accepted that respiratory infections—e.g., influenza A/B and previous severe acute respiratory syndrome (SARS) infections—are associated with CV events, cardiac arrhythmias [ 11 ], and especially acute coronary syndromes (ACS) [ 12 , 13 ]. A pro-inflammatory state leading to plaque instability and prothrombotic state (type 1 myocardial infarction (MI)) or a mismatch between oxygen supply and/or demand related with respiratory failure (predominantly hypoxemia) and infectious diseases (type 2 MI) have been proposed to explain those links [ 14 , 15 , 16 ]. Similar mechanisms have been postulated to explain the onset of myocardial injury in relationship with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, although a direct myocardial “myocarditis-like” effect, potentially associated with clinically relevant cardiac arrhythmias [ 17 ], has not been completely ruled out.…”

High sensitivity Troponin-T for prediction of adverse events in patients with COVID-19

“…[3][4][5] However, given the non-specific nature of troponin elevations, some have argued against its routine use unless there is clinical concern for an acute coronary plaque rupture. 6,7 The objective of this study is to determine the predictive value of high sensitivity troponin-T (hs-TnT) as compared to traditional inflammatory markers for adverse outcomes that include the need for critical care, respiratory failure requiring intubation, cardiac arrest, and in-hospital mortality.…”

COVID-19 – eine vaskuläre Systemerkrankung

“…Schwere klinische Verläufe werden bei bis zu 20 % der Infektionen beobachtet [4], sind durch die Lungenbeteiligung geprägt und gehen in der Regel mit einem "acute respiratory distress syndrome" (ARDS) einher; ein Krankheitsbild, welches über klinischradiologische und laborchemische Parameter zum Beispiel nach der BerlinKlassifikation definiert wird. Parallel zur Entwicklung der klinischen Symptomatik findet sich nach einer vorübergehend hohen Viruslast im oberen Respirationstrakt wenige Tage nach Symptombeginn insbesondere bei schweren Verläufen ein Anstieg der Viruslast in der Lunge [5,6] [11]. In der Niere finden sich bei COVID19 die typischen histologischen Veränderungen eines virusinduzierten akuten Nierenversagens mit einer Glomerulopathie und einem akuten Tubulusschaden [12], wohingegen der hämorrhagischen Colitis bei COVID19 wahrscheinlich eine Mikroangiopathieassoziierte Äthiogenese zugrunde liegt [13].…”