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

https://doi.org/10.1016/j.bcp.2020.114114Get rights and content

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

SARS-CoV-2
COVID-19
Cardiovascular
ACE2
Cytokine storm

Abbreviations

ACE
Angiotensin-converting enzyme
Ang
Angiotensin
ARB
Angiotensin receptor blocker
ARDS
Acute respiratory distress syndrome
CAD
Coronary artery disease
COVID-19
Coronavirus disease 2019
CVD
Cardiovascular diseases
DIC
Disseminated intravascular coagulation
ECMO
Extracorporeal membranous oxygenation
HFpEF
Heart failure with preserved ejection fraction
ICU
Intensive care unit
IFN
Interferon
IL
Interleukin
IP-10
Interferon -γ inducible protein 10
MCP-1
monocyte chemoattractant protein 1
MERS
Middle East respiratory syndrome
MOF
Multiple organ failure
NT-proBNP
N-terminal pro-brain natriuretic peptide
RAAS
Renin-angiotensin-aldosteron system
RDRP
RNA-dependent RNA polymerase proteins
ROS
reactive oxygen species
SARS-CoV-2
Severe acute respiratory syndrome coronavirus 2
TNF
Tumor necrosis factor

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1

Equal contribution.

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