tetano
Editor, Senior Moderator
Methodist Debakey Cardiovasc J
. 2021 Dec 15;17(5):53-62.
doi: 10.14797/mdcvj.1044. eCollection 2021.
Acute and Chronic Cardiovascular Manifestations of COVID-19: Role for Endotheliopathy
John P Cooke[SUP] 1 [/SUP], John H Connor[SUP] 2 [/SUP], Abhishek Jain[SUP] 3 4 [/SUP]
Affiliations
Abstract
SARS-CoV-2, the virus that causes coronavirus disease 19 (COVID-19), is associated with a bewildering array of cardiovascular manifestations, including myocardial infarction and stroke, myocarditis and heart failure, atrial and ventricular arrhythmias, venous thromboembolism, and microvascular disease. Accumulating evidence indicates that a profound disturbance of endothelial homeostasis contributes to these conditions. Furthermore, the pulmonary infiltration and edema, and later pulmonary fibrosis, in patients with COVID-19 is promoted by endothelial alterations including the expression of endothelial adhesion molecules and chemokines, increased intercellular permeability, and endothelial-to-mesenchyme transitions. The cognitive disturbance occurring in this disease may also be due in part to an impairment of the blood-brain barrier. Venous thrombosis and pulmonary thromboembolism are most likely associated with an endothelial defect caused by circulating inflammatory cytokines and/or direct endothelial invasion by the virus. Endothelial-targeted therapies such as statins, nitric oxide donors, and antioxidants may be useful therapeutic adjuncts in COVID-19 by restoring endothelial homeostasis.
Keywords: SARS-CoV-2; cerebrovascular attack; deep venous thrombosis; dementia; endothelium; myocardial infarction; myocarditis; nitric oxide; pulmonary embolism.
. 2021 Dec 15;17(5):53-62.
doi: 10.14797/mdcvj.1044. eCollection 2021.
Acute and Chronic Cardiovascular Manifestations of COVID-19: Role for Endotheliopathy
John P Cooke[SUP] 1 [/SUP], John H Connor[SUP] 2 [/SUP], Abhishek Jain[SUP] 3 4 [/SUP]
Affiliations
- PMID: 34992723
- PMCID: PMC8680072
- DOI: 10.14797/mdcvj.1044
Abstract
SARS-CoV-2, the virus that causes coronavirus disease 19 (COVID-19), is associated with a bewildering array of cardiovascular manifestations, including myocardial infarction and stroke, myocarditis and heart failure, atrial and ventricular arrhythmias, venous thromboembolism, and microvascular disease. Accumulating evidence indicates that a profound disturbance of endothelial homeostasis contributes to these conditions. Furthermore, the pulmonary infiltration and edema, and later pulmonary fibrosis, in patients with COVID-19 is promoted by endothelial alterations including the expression of endothelial adhesion molecules and chemokines, increased intercellular permeability, and endothelial-to-mesenchyme transitions. The cognitive disturbance occurring in this disease may also be due in part to an impairment of the blood-brain barrier. Venous thrombosis and pulmonary thromboembolism are most likely associated with an endothelial defect caused by circulating inflammatory cytokines and/or direct endothelial invasion by the virus. Endothelial-targeted therapies such as statins, nitric oxide donors, and antioxidants may be useful therapeutic adjuncts in COVID-19 by restoring endothelial homeostasis.
Keywords: SARS-CoV-2; cerebrovascular attack; deep venous thrombosis; dementia; endothelium; myocardial infarction; myocarditis; nitric oxide; pulmonary embolism.