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From angiotensin-converting enzyme 2 disruption to thromboinflammatory microvascular disease: A paradigm drawn from

R Vinci1, D Pedicino2, F Andreotti3

  • 1Department of Cardiovascular and Pulmonary Sciences, Catholic University of the Sacred Heart, Rome, Italy.

International Journal of Cardiology
|November 12, 2020
PubMed

Insights

The novel coronavirus disease (COVID-19) is characterized by angiotensin-converting enzyme 2 disruption and thromboinflammatory microangiopathy. This can lead to widespread microvascular plugging, ischemia, and organ failure, representing a potentially fatal vascular disease.

Area of Science:

  • Pathology
  • Virology
  • Cardiovascular Science

Background:

  • Clinical, autopsy, experimental, and molecular data on COVID-19 are reviewed.
  • Distinctive features of COVID-19 include angiotensin-converting enzyme 2 (ACE2) disruption and thromboinflammatory microangiopathy.

Purpose of the Study:

  • To review and consolidate current data on COVID-19.
  • To highlight the role of thromboinflammatory microangiopathy in COVID-19 pathogenesis.

Main Methods:

  • Review of existing clinical, autopsy, experimental, and molecular data related to COVID-19.

Main Results:

  • Viral entry into microvessels disrupts the renin-angiotensin system and causes endothelial injury.
  • Activation of the complement cascade and release of von Willebrand factor induce thromboinflammatory reactions.
  • Widespread microvascular plugging can result in ischemia and organ failure.

Conclusions:

  • COVID-19 data support a paradigm of potentially fatal thromboinflammatory microvascular disease.
  • Thromboinflammatory microangiopathy is a critical, under-recognized aspect of severe COVID-19.

Keywords:
2019 coronavirusComplementRenin-angiotensin systemThromboinflammatory microangiopathyvon Willebrand factor

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