Abstract
There has been strong evidence of myocardial injury in coronavirus disease 2019 (COVID-19) patients with significantly elevated serum cardiac troponin (cTn). While the exact mechanism of injury is unclear, possible suggested pathological mechanisms of injury are discussed. These include increased susceptibility of the myocardium and endothelium to viral invasion, underlying hyperinflammatory state and subsequent cytokine storm, a hypercoagulable and prothrombotic state, and indirect myocardial injury due to hypoxemia. As a result of these pathological mechanisms in COVID-19 patients, cTn may be elevated largely due to myocarditis, microangiopathy or myocardial infarction. The utility of cTn as a biomarker for measuring myocardial injury in these patients and assessing its ability as a prognostic factor for clinical outcome is also discussed.
Highlights
Increased levels of cardiac troponin have been correlated with higher rates of Cardiovascular diseases (CVD) complications and mortality in COVID-19 patients
Risk of severe COVID-19 illness is increased for patients with pre-existing CVD
Primary pathological mechanism of injury to myocardium is through direct viral invasion into the myocardium and endothelium or damage to the myocardium due to the underlying hyperinflammatory, hypercoagulable and prothrombotic state
Summary
COVID-19 pandemic and troponin: indirect myocardial injury, myocardial inflammation or [40]. The relevance of cTnI is further highlighted when considering that after adjusting for relevant clinical factors, even small amounts of myocardial injury were associated with a significantly increased risk of patient mortality, and that elevated levels of cTnI remain an independent predictor of death regardless of other elevated acute phase proteins and inflammatory markers in patients with CVD [67]. On patient admissions, one can measure a variety of biomarkers such as cTnT, N-terminal-pro brain natriuretic peptide, alanine transaminase, D-dimer or CRP, as determiners of inflammatory status; cTnI has been reported with the greatest prognostic value for patient risk and is the most promising agent for the hopeful identification of patients who would develop the most severe systemic inflammatory response to SARS-CoV-2 infection and subsequent cardiac complications, which can be fatal
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