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Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
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Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis

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641

The coagulopathy, endotheliopathy, and vasculitis of COVID-19

Toshiaki Iba1, Jean Marie Connors2, Jerrold H Levy3

  • 1Department of Emergency and Disaster Medicine, Juntendo University Graduate School of Medicine, 2-1-1 Hongo Bunkyo-ku, Tokyo, 113-8421, Japan. toshiiba@juntendo.ac.jp.

Inflammation Research : Official Journal of the European Histamine Research Society ... [Et Al.]
|September 12, 2020
PubMed

Insights

COVID-19-associated coagulopathy (CAC) involves elevated D-dimer and is linked to thrombotic complications. Endothelial damage from SARS-CoV-2 infection and inflammation drives CAC, necessitating control of thromboinflammation for better outcomes.

Area of Science:

  • * Infectious Diseases
  • * Hematology
  • * Pathophysiology

Background:

  • * COVID-19-associated coagulopathy (CAC) presents with elevated D-dimer and normal global coagulation markers.
  • * CAC is associated with increased thrombotic complications and disease severity in COVID-19 patients.

Purpose of the Study:

  • * To elucidate the pathophysiology of COVID-19-associated coagulopathy (CAC).
  • * To understand the mechanisms leading to unique coagulation changes in COVID-19.

Main Methods:

  • * Conducted a literature search on PubMed using keywords: COVID-19, SARS-CoV-2, coronavirus, coagulopathy, and thrombus.
  • * Selected 51 relevant articles for review.

Main Results:

  • * SARS-CoV-2 targets pneumocytes, immune cells, and vascular endothelial cells, causing alveolar damage and pulmonary microvascular thrombosis.
  • * Endotheliopathy, driven by direct viral infection and inflammatory pathways, leads to CAC, resulting in microvascular and macrovascular thrombosis.
  • * SARS-CoV-2 can induce vasculitis, presenting as a systemic inflammatory vascular disease, requiring novel therapies beyond anticoagulation.

Conclusions:

  • * Endothelial damage, from direct SARS-CoV-2 infection and inflammation, is the primary driver of CAC.
  • * Intensive control of thromboinflammation is crucial for improving outcomes in COVID-19 patients with CAC.
Abstract

Keywords:
COVID-19CoagulopathyEndotheliopathyThromboembolismVasculitis

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