Myocardial Damage by SARS-CoV-2: Emerging Mechanisms and Therapies

Abstract

Evidence is emerging that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can infect various organs of the body, including cardiomyocytes and cardiac endothelial cells in the heart. This review focuses on the effects of SARS-CoV-2 in the heart after direct infection that can lead to myocarditis and an outline of potential treatment options. The main points are: (1) Viral entry: SARS-CoV-2 uses specific receptors and proteases for docking and priming in cardiac cells. Thus, different receptors or protease inhibitors might be effective in SARS-CoV-2-infected cardiac cells. (2) Viral replication: SARS-CoV-2 uses RNA-dependent RNA polymerase for replication. Drugs acting against ssRNA(+) viral replication for cardiac cells can be effective. (3) Autophagy and double-membrane vesicles: SARS-CoV-2 manipulates autophagy to inhibit viral clearance and promote SARS-CoV-2 replication by creating double-membrane vesicles as replication sites. (4) Immune response: Host immune response is manipulated to evade host cell attacks against SARS-CoV-2 and increased inflammation by dysregulating immune cells. Efficiency of immunosuppressive therapy must be elucidated. (5) Programmed cell death: SARS-CoV-2 inhibits programmed cell death in early stages and induces apoptosis, necroptosis, and pyroptosis in later stages. (6) Energy metabolism: SARS-CoV-2 infection leads to disturbed energy metabolism that in turn leads to a decrease in ATP production and ROS production. (7) Viroporins: SARS-CoV-2 creates viroporins that lead to an imbalance of ion homeostasis. This causes apoptosis, altered action potential, and arrhythmia.

Geriatric risk and protective factors for serious COVID-19 outcomes among older adults in Shanghai Omicron wave

“…ACE2 (angiotensin-converting enzyme 2) receptor attaches to cell surfaces in the lung, blood vessels, heart, kidney, and intestines [ 28 ]. SRA-CoV-2 can infect cardiomyocytes and cardiac endothelial cells in the heart [ 29 , 30 ]. This study found that cardiac index (D-dimer, LDH, TNT, and BNP) in severe/critical patients was significantly higher than that of mild/moderate patients, and cardiovascular was a significant risk factor for progressing to severe infection in univariate analysis.…”

Myocardial performance index increases at long‐term follow‐up in patients with mild to moderate COVID‐19

“…Evidence of cardiac damage in COVID‐19 patients has been reported in several previous studies 19–21 . Myocardial inflammation has been reported in 60% of patients with recent (<3 months) COVID‐19 infection, regardless of pre‐existing conditions 22 .…”

“…Evidence of cardiac damage in COVID‐19 patients has been reported in several previous studies. 19 , 20 , 21 Myocardial inflammation has been reported in 60% of patients with recent (<3 months) COVID‐19 infection, regardless of pre‐existing conditions. 22 Myocardial inflammation triggers a progressive fibrotic remodeling of the heart, which will lead to hardening of the cardiac tissue and altered cardiac relaxation.…”

COVID-19 and the cardiovascular system-current knowledge and future perspectives

“…However, it was proven to be a multiple organ disease also affecting the heart[ 2 , 3 ]. Studies revealed that cases of critically ill COVID-19 patients had cardiovascular complications such as myocardial damage, venous thromboembolic events, and acute coronary syndromes[ 4 ]. The presence of underlying cardiovascular comorbidities in COVID-19 patients is associated with severe disease and poor prognosis including increased risk of onset of cardiovascular complications, increased progression of underlying cardiovascular disease and risk of increased mortality both in general population as well as in diagnosed patients[ 5 ].…”