Cardiovascular Manifestations and Mechanisms in Patients with COVID-19

Qingyu Dou; Xin Wei; Kehua Zhou; Shujuan Yang; Peng Jia

doi:10.1016/j.tem.2020.10.001

Cardiovascular Manifestations and Mechanisms in Patients with COVID-19

Trends Endocrinol Metab. 2020 Dec;31(12):893-904. doi: 10.1016/j.tem.2020.10.001. Epub 2020 Oct 16.

Authors

Qingyu Dou¹, Xin Wei², Kehua Zhou³, Shujuan Yang⁴, Peng Jia⁵

Affiliations

¹ National Clinical Research Center of Geriatrics, Geriatric Medicine Center, West China Hospital, Sichuan University, Chengdu, China; International Institute of Spatial Lifecourse Epidemiology (ISLE), Hong Kong, China.
² Department of Cardiology, West China Hospital, Sichuan University, Chengdu, China.
³ Department of Hospital Medicine, ThedaCare Regional Medical Center-Appleton, Appleton, WI, USA; International Institute of Spatial Lifecourse Epidemiology (ISLE), Hong Kong, China.
⁴ West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu, China; International Institute of Spatial Lifecourse Epidemiology (ISLE), Hong Kong, China. Electronic address: [email protected].
⁵ Department of Land Surveying and Geo-Informatics, The Hong Kong Polytechnic University, Hong Kong, China; International Institute of Spatial Lifecourse Epidemiology (ISLE), Hong Kong, China. Electronic address: [email protected].

Abstract

Coronavirus disease 2019 (COVID-19) patients with pre-existing cardiovascular disease (CVD) or with cardiovascular complications have a higher risk of mortality. The main cardiovascular complications of COVID-19 include acute cardiac injury, acute myocardial infarction (AMI), myocarditis, arrhythmia, heart failure, shock, and venous thromboembolism (VTE)/pulmonary embolism (PE). COVID-19 can cause cardiovascular complications or deterioration of coexisting CVD through direct or indirect mechanisms, including viral toxicity, dysregulation of the renin-angiotensin-aldosterone system (RAAS), endothelial cell damage and thromboinflammation, cytokine storm, and oxygen supply-demand mismatch. We systematically review cardiovascular manifestations, histopathology, and mechanisms of COVID-19, to help to formulate future research goals and facilitate the development of therapeutic management strategies.

Keywords: ACE2; COVID-19; cardiovascular; cytokine storm; endothelial cell damage; thromboinflammation; type 2 myocardial infarction.

Publication types

Research Support, Non-U.S. Gov't
Systematic Review

MeSH terms

Angiotensin-Converting Enzyme 2 / metabolism
Arrhythmias, Cardiac / immunology
Arrhythmias, Cardiac / metabolism
Arrhythmias, Cardiac / physiopathology
COVID-19 / immunology
COVID-19 / metabolism
COVID-19 / physiopathology*
Cardiovascular Diseases / immunology
Cardiovascular Diseases / metabolism
Cardiovascular Diseases / physiopathology*
Cytokine Release Syndrome / immunology
Cytokine Release Syndrome / physiopathology
Heart Diseases / immunology
Heart Diseases / metabolism
Heart Diseases / physiopathology
Heart Failure / immunology
Heart Failure / metabolism
Heart Failure / physiopathology
Humans
Hypoxia / immunology
Hypoxia / metabolism
Hypoxia / physiopathology
Myocardial Infarction / immunology
Myocardial Infarction / metabolism
Myocardial Infarction / physiopathology
Myocarditis / immunology
Myocarditis / metabolism
Myocarditis / physiopathology
Pulmonary Embolism / immunology
Pulmonary Embolism / metabolism
Pulmonary Embolism / physiopathology
Renin-Angiotensin System / physiology
SARS-CoV-2 / immunology
SARS-CoV-2 / metabolism
Shock / immunology
Shock / metabolism
Shock / physiopathology
Troponin / metabolism
Venous Thromboembolism / immunology
Venous Thromboembolism / metabolism
Venous Thromboembolism / physiopathology

Substances

Troponin
Angiotensin-Converting Enzyme 2