Pathogenesis and management of myocardial injury in coronavirus disease 2019

Abstract

The outbreak of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, has become a major health crisis and a worldwide pandemic. COVID-19 is characterized by high infectivity, long incubation period, diverse clinical presentations, and strong transmission intensity. COVID-19 can cause myocardial injury as well as other cardiovascular complications, particularly in senior patients with pre-existing medical conditions. The current review summarizes the epidemiological characteristics, potential mechanisms, clinical manifestations, and recent progress in the management of COVID-19 cardiovascular complications.

Keywords: Blood vessels; COVID-19; Heart; Inflammation; SARS-CoV-2.

Figure 1

Schematic representation of the mechanisms underlying COVID‐19‐related myocardial injury and potential treatment strategies: (1) direct infection through angiotensin‐converting enzyme 2 (ACE2); (2) myocardial oxygen supply/demand imbalance; (3) abnormal coagulation and microcirculatory disturbance; (4) cytokine storm. G‐CSF, granulocyte colony‐stimulating factor; IFN, interferon; IL, interleukin; IP‐10, interferon‐γ inducible protein 10; MCP‐1, monocyte chemoattractant protein 1; MIP‐1α, macrophage inflammatory protein 1α; SARS‐CoV‐2, severe acute respiratory syndrome coronavirus 2; TMPRSS2, type II transmembrane serine protease; TNF, tumour necrosis factor.

Figure 2

Schematic representation of molecular pathways underlying the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) cellular invasion and injury. SARS‐CoV‐2 invasion is mediated by the S protein binding to its ligand angiotensin‐converting enzyme 2 (ACE2), which is primed by type II transmembrane serine proteases (TMPRSS2) through cleaving S protein into S1 and S2 subunits to facilitate the exposure of receptor‐binding domain (RBD) on S1 subunit. The binding of RBD to ACE2 is followed by receptor‐mediated endocytosis. Activation of the renin–angiotensin system, up‐regulation of the tumour necrosis factor (TNF)‐α pathway and the Ras pathway following ACE2 attachment can injure cells/tissues that highly express ACE2. *These mechanisms are speculated based on SARS‐CoV studies and the similarity of two viruses. AP‐1, activator protein 1; CCL2, C‐C motif chemokine ligand 2; ERK, extracellular signal‐regulated kinase; TACE, tumour necrosis factor‐α‐converting enzyme.