REVIEW

Possible effects of coronavurus infection (COVID-19) on the cardiovascular system

Larina VN, Golovko MG, Larin VG
About authors

Pirogov Russian National Research Medical University, Moscow, Russia

Correspondence should be addressed: Larina Vera Nikolaevna
Ostrovityanova, 1, Moscow, 117997; ur.liam@vaniral

About paper

Acknowledgements: the authors thank Gennady V. Poryadin, Professor at the Department of Pathophysiology and Clinical Pathophysiology (the Faculty of General Medicine, Pirogov Russian National Research Medical University), DMSc and the correspondent member of RAS, for his invaluable critical comments on this paper.

Author contribution: Larina VN conceived and planned the study, analyzed the literature, interpreted the literature data, and revised the manuscript; Golovko MG and Larin VG planned the study, analyzed the literature, interpreted the literature data, and wrote the draft of the manuscript.

Received: 2020-04-03 Accepted: 2020-04-17 Published online: 2020-04-18
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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
Table 1. Characteristics of coronaviruses
Note: * — overall rates; ** — in hospitalized patients; *** — depending on time, geographical area and medical help available.
Table 2. A non-exhaustive list of clinical trials of drugs for the prevention and treatment of COVID-19