Response to Damiani and colleagues

Diehl, J J; Péron, N.; Philippe, Aurélien; Smadja, David

doi:10.1186/s13613-020-00757-6

Cited by 2 publications

(2 citation statements)

References 6 publications

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“…Taken together, these results underline the hypothesis of severe microvascular dysfunction and thrombosis in ARDS. In a similar way to non-COVID-19 ARDS patients, such results could reinforce the hypothesis of similar alterations at the lung level, favoring a high number of ventilated alveoli with no or severely diminished perfusion [ 4 , 216 , 217 ].…”

Section: Perfusion Defects In Covid-19 Ards Lungs: Intensivist’s Point Of View On Endothelium and Pulmonary Vasculaturesupporting

confidence: 74%

COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects

et al. 2021

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Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is presenting as a systemic disease associated with vascular inflammation and endothelial injury. Severe forms of SARS-CoV-2 infection induce acute respiratory distress syndrome (ARDS) and there is still an ongoing debate on whether COVID-19 ARDS and its perfusion defect differs from ARDS induced by other causes. Beside pro-inflammatory cytokines (such as interleukin-1 β [IL-1β] or IL-6), several main pathological phenomena have been seen because of endothelial cell (EC) dysfunction: hypercoagulation reflected by fibrin degradation products called D-dimers, micro- and macrothrombosis and pathological angiogenesis. Direct endothelial infection by SARS-CoV-2 is not likely to occur and ACE-2 expression by EC is a matter of debate. Indeed, endothelial damage reported in severely ill patients with COVID-19 could be more likely secondary to infection of neighboring cells and/or a consequence of inflammation. Endotheliopathy could give rise to hypercoagulation by alteration in the levels of different factors such as von Willebrand factor. Other than thrombotic events, pathological angiogenesis is among the recent findings. Overexpression of different proangiogenic factors such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (FGF-2) or placental growth factors (PlGF) have been found in plasma or lung biopsies of COVID-19 patients. Finally, SARS-CoV-2 infection induces an emergency myelopoiesis associated to deregulated immunity and mobilization of endothelial progenitor cells, leading to features of acquired hematological malignancies or cardiovascular disease, which are discussed in this review. Altogether, this review will try to elucidate the pathophysiology of thrombotic complications, pathological angiogenesis and EC dysfunction, allowing better insight in new targets and antithrombotic protocols to better address vascular system dysfunction. Since treating SARS-CoV-2 infection and its potential long-term effects involves targeting the vascular compartment and/or mobilization of immature immune cells, we propose to define COVID-19 and its complications as a systemic vascular acquired hemopathy.

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Section: Perfusion Defects In Covid-19 Ards Lungs: Intensivist’s Point Of View On Endothelium and Pulmonary Vasculaturesupporting

confidence: 74%

COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects

et al. 2021

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“…In COVID-19, this link between VWF and pulmonary microthrombosis requires further confirmation. A way to highlight this link could be measuring VWF:Ag at multiple time points during the hospitalization of severe COVID-19 patients and evaluate its correlation with advanced respiratory monitoring parameters established to mirror the pulmonary microcirculation dysfunction such as pulmonary physiological dead space and its sub-components airway dead-space and alveolar dead-space [32,33].…”

Section: Discussionmentioning

confidence: 99%

Circulating Von Willebrand factor and high molecular weight multimers as markers of endothelial injury predict COVID-19 in-hospital mortality

et al. 2021

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Background Coronavirus disease 2019 (COVID-19) is a respiratory disease associated with endotheliitis and microthrombosis. Objectives To correlate endothelial dysfunction to in-hospital mortality in a bi-centric cohort of COVID-19 adult patients. Methods Consecutive ambulatory and hospitalized patients with laboratory-confirmed COVID-19 were enrolled. A panel of endothelial biomarkers and von Willebrand factor (VWF) multimers were measured in each patient ≤ 48 h following admission.Results Study enrolled 208 COVID-19 patients of whom 23 were mild outpatients and 189 patients hospitalized after admission. Most of endothelial biomarkers tested were found increased in the 89 critical patients transferred to intensive care unit. However, only von Willebrand factor antigen (VWF:Ag) scaled according to clinical severity, with levels significantly higher in critical patients (median 507%, IQR 428-596) compared to non-critical patients (288%, 230-350, p < 0.0001) or COVID-19 outpatients (144%, 133-198, p = 0.007). Moreover, VWF high molecular weight multimers (HMWM) were significantly higher in critical patients (median ratio 1.18, IQR 0.86-1.09) compared to non-critical patients (0.96, 1.04-1.39, p < 0.001). Among all endothelial biomarkers measured, ROC curve analysis identified a VWF:Ag cut-off of 423% as the best predictor for in-hospital mortality. The accuracy of VWF:Ag was further confirmed in a Kaplan-Meier estimator analysis and a Cox proportional Hazard model adjusted on age, BMI, C-reactive protein and d-dimer levels. Conclusion VWF:Ag is a relevant predictive factor for in-hospital mortality in COVID-19 patients. More than a biomarker, we hypothesize that VWF, including excess of HMWM forms, drives microthrombosis in COVID-19.

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Response to Damiani and colleagues

Cited by 2 publications

References 6 publications

COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects

COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects

Circulating Von Willebrand factor and high molecular weight multimers as markers of endothelial injury predict COVID-19 in-hospital mortality

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