Elevated troponin in patients with Coronavirus Disease 2019
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Myocarditis is defined as an inflammatory disease of the myocardium diagnosed by established histological, immunological and immunohistochemical criteria. Many viruses are cardiotropic, meaning they bind directly on molecular targets in the myocardium. Myocardial damage may be due to different mechanisms. In the initial phase of viral myocarditis, direct virus-mediated lysis of cardiomyocytes occurs.

This is usually followed by a robust T-cell response that can lead to further heart injury and ventricular dysfunction. In COVID-19, particular attention has been given to the role of Angiotensin Converting Enzyme 2 (ACE2), the binding receptor for SARS-CoV-2 cellular entry. ACE2 is highly expressed in pericytes of adult human hearts, which indicates an intrinsic susceptibility of heart to SARS-CoV-2 infection. SARS-CoV-2 appears to not only gain initial entry through ACE2 but also to subsequently downregulate ACE2 expression, resulting in reduced conversion of Angiotensin II (Ang-II) to Angiotensin 1-7 (Ang-1-7). The latter physiologically mediates protective cardiovascular effects in target organs.

In autopsies of patients who died from the SARS outbreak in 2002, 35% of heart samples showed the presence of viral RNA in the myocardium, which in turn was associated with reduced ACE2 protein expression. SARS-CoV-2 may share the same mechanism with the first SARS-coronavirus because the two viruses are highly homologous in genome.

Conclusively, Elevated troponin levels are frequent in patients with COVID-19 and significantly associated with fatal outcomes. Several mechanisms may explain this phenomenon: viral myocarditis, cytokine-driven myocardial damage, microangiopathy, and unmasked CAD.

At present, none of these mechanisms have been definitely proven to be the main driver of troponin elevation and/or myocardial damage in patients with COVID-19. However, we posit that, although COVID-19 initially presents as a primarily respiratory condition, it quickly involves the cardiovascular system through an imbalance of the renin-angiotensin-aldosterone system mediated by ACE2 depletion. This mechanism may complicate the clinical course mediated through the inflammatory response, endothelial dysfunction and microvascular damage.

Source: https://www.onlinejcf.com/article/S1071-9164(20)30357-2/fulltext
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