Acute and Chronic Cardiovascular Manifestations of COVID-19: Role for Endotheliopathy.
John P CookeJohn H ConnorAbhishek JainPublished in: Methodist DeBakey cardiovascular journal (2021)
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.
Keyphrases
- coronavirus disease
- sars cov
- endothelial cells
- heart failure
- nitric oxide
- venous thromboembolism
- respiratory syndrome coronavirus
- left ventricular
- pulmonary hypertension
- cardiovascular disease
- high resolution
- intensive care unit
- liver failure
- staphylococcus aureus
- long non coding rna
- intellectual disability
- cell adhesion
- hepatitis b virus
- acute respiratory distress syndrome