Fig. 1. Effects of viral infection on the cardiovascular system and the myocardium

Fig. 2. Interactions between SARS-CoV-2 and the renin-angiotensin-aldosterone system. Interaction between SARS-CoV-2 and the renin-angiotensin-aldosterone system. Invasion of host cells (alveolar type II cells, in particular) by SARS-CoV-2 occurs through the binding of the virus to the functional domain of ACE2. ACE2 expression changes following endocytosis of the viral complex. This results in the accumulation of a potent vasoconstrictor angiotensin II and, possibly, mitigates the vasodilator effect of angiotensin (1–7). Local activation of the renin-angiotensin-aldosterone system can mediate damage to the lungs in response to viral infection, whereas increased ACE2 expression can aggravate pulmonary damage in patients with COVID-19. ACE2 converts angiotensin I to angiotensin (1–9) (its functions are being studied) and angiotensin II to angiotensin (1–7). This process is accompanied by inactivation of angiotensin II and synthesis of angiotensin (1–7); the latter stimulates vasodilation, reduces oxidative stress and fibrosis. ACE — angiotensin-converting enzyme; ACEI — ACE inhibitors; ARB — angiotensin II receptor blockers; SMC — smooth muscle cells. ACE — angiotensin-converting enzyme; ACEIs — ACE inhibitors; ARBs — angiotensin II receptor blockers; SMCs — smooth muscle cells