Fig. 3.

Potential mechanisms of HF deterioration induced by COVID-19. SARS-CoV-2 entry into host cells via ACE2 induces myocardial injury by not only attacking the heart directly to cause myocarditis, but also triggering systemic inflammation and excess immune cell activation to cause a cytokine storm. With the increased release of cytokines, including IL-6 and TNF-α, endothelial cell dysfunction induced by the cytokine storm plays an important role in both plaque instability and circulatory hypercoagulability, promoting thrombosis and ACS. The occurrence of PTE caused by thrombosis worsens the hypoxia induced by lung injury, while pulmonary vasoconstriction under hypoxia increases pulmonary vascular resistance. The loss of ACE2 promoted by COVID-19 triggers both vasoconstriction by increasing the expression of Ang II and a loss of the protective effects on the heart by decreasing the expression of Ang 1–7. In patients with a pre-existing cardiac disease, these mechanisms will work together to promote the progression of HF