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Review
. 2020 Aug:178:114114.
doi: 10.1016/j.bcp.2020.114114. Epub 2020 Jun 21.

SARS-CoV-2 and cardiovascular complications: From molecular mechanisms to pharmaceutical management

Lin Wu  1 , Aislinn M O'Kane  2 , Hu Peng  3 , Yaguang Bi  1 , Dagmara Motriuk-Smith  4 , Jun Ren  5
Affiliations
Review

SARS-CoV-2 and cardiovascular complications: From molecular mechanisms to pharmaceutical management

Lin Wu et al. Biochem Pharmacol. 2020 Aug.

Abstract

The coronavirus disease 2019 (COVID-19), elicited by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, is a pandemic public health emergency of global concern. Other than the profound severe pulmonary damage, SARS-CoV-2 infection also leads to a series of cardiovascular abnormalities, including myocardial injury, myocarditis and pericarditis, arrhythmia and cardiac arrest, cardiomyopathy, heart failure, cardiogenic shock, and coagulation abnormalities. Meanwhile, COVID-19 patients with preexisting cardiovascular diseases are often at a much higher risk of increased morbidity and mortality. Up-to-date, a number of mechanisms have been postulated for COVID-19-associated cardiovascular damage including SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2) activation, cytokine storm, hypoxemia, stress and cardiotoxicity of antiviral drugs. In this context, special attention should be given towards COVID-19 patients with concurrent cardiovascular diseases, and special cardiovascular attention is warranted for treatment of COVID-19.

Keywords: ACE2; COVID-19; Cardiovascular; Cytokine storm; SARS-CoV-2.

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Conflict of interest statement

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

None
Graphical abstract
Fig. 1
Fig. 1
Relationship between ACE2 and SARS-CoV-2-related cardiovascular injury. (A) Organ distribution of ACE2 may be associated with clinical symptoms of COVID-19 patients. (B) Potential mechanism of cardiovascular injury induced by ACE2-mediated SARS-CoV-2 infection. SARS-CoV-2 uses ACE2 receptor for viral entry and replication. ACE2, but not ACE, is downregulated through binding of the spike protein of SARS-CoV-2 and ACE2. This leads to an increased level of Ang II and subsequent cardiovascular injury. (C) Impact of RAAS Blockers (ACEI and ARB) on cardiovascular system of COVID-19 patients. On the one hand, RAAS blockers upregulate the expression of ACE2, thereby leading to increased viral entry and replication and cardiovascular injury. On the other hand, RAAS blockers contribute to Ang II inhibition directly or indirectly (caused by upregulated ACE2), which may attenuate cardiovascular injury. AT1R, Ang II type 1 receptor; MasR, mitochondrial assembly receptor.
Fig. 2
Fig. 2
Resemblance in lung injury between paraquat poisoning and COVID-19 infection. In both cases, there is gradual ground glass opacity slowly progressed into the advanced stages of lung tissue consolidation (solidifying process). Imaged taken from a COVID-19 patient in Wuhan, courtesy of Dr. Hu Peng, ICU physician in Wuhan. The COVID-19 patient received written consent and was recovered from COVID-19 later. Classical paraquat image was from China-Radiology https://mp.weixin.qq.com/s/MMSq1ufNkWIUyAKEPcvxQQ.
See this image and copyright information in PMC

References

    1. Wu J.T., Leung K., Leung G.M. Nowcasting and forecasting the potential domestic and international spread of the 2019-nCoV outbreak originating in Wuhan, China: a modelling study. Lancet. 2020;395(10225):689–697. - PMC - PubMed
    1. Lu R., Zhao X., Li J., Niu P., Yang B., Wu H., Wang W., Song H., Huang B., Zhu N., Bi Y., Ma X., Zhan F., Wang L., Hu T., Zhou H., Hu Z., Zhou W., Zhao L., Chen J., Meng Y., Wang J., Lin Y., Yuan J., Xie Z., Ma J., Liu W.J., Wang D., Xu W., Holmes E.C., Gao G.F., Wu G., Chen W., Shi W., Tan W. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet. 2020;395(10224):565–574. - PMC - PubMed
    1. Yin Y., Wunderink R.G. MERS, SARS and other coronaviruses as causes of pneumonia. Respirology. 2018;23(2):130–137. - PMC - PubMed
    1. Zhang S., Diao M., Yu W., Pei L., Lin Z., Chen D. Estimation of the reproductive number of novel coronavirus (COVID-19) and the probable outbreak size on the Diamond Princess cruise ship: a data-driven analysis. Int. J. Infect. Dis. 2020;93:201–204. - PMC - PubMed
    1. Russell C.D., Millar J.E., Baillie J.K. Clinical evidence does not support corticosteroid treatment for 2019-nCoV lung injury. Lancet. 2020;395(10223):473–475. - PMC - PubMed

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