Elevated Expression of Serum Endothelial Cell Adhesion Molecules in COVID-19 Patients

Tong, Ming; Jiang, Yu; Xia, Da; Xiong, Ying; Zheng, Qiang; Chen, Fang; Zou, Lianhong; Xiao, Wen; Zhu, Yimin

doi:10.1093/infdis/jiaa349

Cited by 180 publications

(171 citation statements)

References 13 publications

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“…An autopsy report showed the presence of viral particles and apoptotic bodies in the vascular endothelium (208). Studies have shown elevated expression of endothelial and platelet activation markers ICAM1, VCAM1, P-selectin, sCD40L and thrombomodulin in COVID-19 patients when compared to controls (220,223). These data suggest that the direct SARS-CoV-2 viral infection also induces procoagulant factors that favor vascular thrombosis.…”

Section: Indirect Effect Of Sars-cov-2 Infection On Triggering Cardiomentioning

confidence: 97%

Immune Mechanisms in Cardiovascular Diseases Associated With Viral Infection

2020

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Influenza virus infection causes 3-5 million cases of severe illness and 250,000-500,000 deaths worldwide annually. Although pneumonia is the most common complication associated with influenza, there are several reports demonstrating increased risk for cardiovascular diseases. Several clinical case reports, as well as both prospective and retrospective studies, have shown that influenza can trigger cardiovascular events including myocardial infarction (MI), myocarditis, ventricular arrhythmia, and heart failure. A recent study has demonstrated that influenza-infected patients are at highest risk of having MI during the first seven days of diagnosis. Influenza virus infection induces a variety of pro-inflammatory cytokines and chemokines and recruitment of immune cells as part of the host immune response. Understanding the cellular and molecular mechanisms involved in influenza-associated cardiovascular diseases will help to improve treatment plans. This review discusses the direct and indirect effects of influenza virus infection on triggering cardiovascular events. Further, we discussed the similarities and differences in epidemiological and pathogenic mechanisms involved in cardiovascular events associated with coronavirus disease 2019 (COVID-19) compared to influenza infection.

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Section: Indirect Effect Of Sars-cov-2 Infection On Triggering Cardiomentioning

confidence: 97%

Immune Mechanisms in Cardiovascular Diseases Associated With Viral Infection

2020

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“…Furthermore, the proinflammatory cytokines released in patients with COVID-19 promote vascular endothelial cell apoptosis, PMT, vascular leakage, alveolar edema, and ultimately hypoxia [66]. Proinflammatory cytokines can also increase the expression of adhesion molecules that in turn results in endothelial activation, procoagulant effects and pro-adhesive changes [67]. All these molecular changes can impaire microvascular flow and, consequently, alter ventilation/perfusion ratio.…”

Section: The Role Of Endothelial Injurymentioning

confidence: 99%

Pulmonary embolism in patients with coronavirus disease-2019 (COVID-19) pneumonia: a narrative review

Sakr

Giovini

Léone

et al. 2020

Ann. Intensive Care

175

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Background Preliminary reports have described significant procoagulant events in patients with coronavirus disease-2019 (COVID-19), including life-threatening pulmonary embolism (PE). Main text We review the current data on the epidemiology, the possible underlying pathophysiologic mechanisms, and the therapeutic implications of PE in relation to COVID-19. The incidence of PE is reported to be around 2.6–8.9% of COVID-19 in hospitalized patients and up to one-third of those requiring intensive care unit (ICU) admission, despite standard prophylactic anticoagulation. This may be explained by direct and indirect pathologic consequences of COVID-19, complement activation, cytokine release, endothelial dysfunction, and interactions between different types of blood cells. Conclusion Thromboprophylaxis should be started in all patients with suspected or confirmed COVID-19 admitted to the hospital. The use of an intermediate therapeutic dose of low molecular weight (LMWH) or unfractionated heparin can be considered on an individual basis in patients with multiple risk factors for venous thromboembolism, including critically ill patients admitted to the ICU. Decisions about extending prophylaxis with LMWH after hospital discharge should be made after balancing the reduced risk of venous thromboembolism (VTE) with the risk of increased bleeding events and should be continued for 7–14 days after hospital discharge or in the pre-hospital phase in case of pre-existing or persisting VTE risk factors. Therapeutic anticoagulation is the cornerstone in the management of patients with PE. Selection of an appropriate agent and correct dosing requires consideration of underlying comorbidities.

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“…TO THE EDITOR—We read with great interest the recent study by Tong et al, who demonstrated the increased expression of endothelial cell adhesion molecules is correlated to coronavirus disease 2019 (COVID-19) severity and may contribute to coagulation dysfunction [ 1 ]. The authors examined the expression of 3 endothelial cell adhesion molecules by enzyme-linked immunosorbent assays (ELISA), including vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion protein-1 (VAP-1).…”

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confidence: 99%