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Coronary microvascular dysfunction pathophysiology in COVID-19.

Jie Yin1, Shaoshen Wang2, Yang Liu1

  • 1Institute of Cardiovascular Disease Research, Xuzhou Medical University, Xuzhou, China.

Microcirculation (New York, N.Y. : 1994)
|May 20, 2021
PubMed
Summary

This review explores how COVID-19 causes coronary microvascular dysfunction (CMD) through inflammation, RAAS imbalance, and nerve issues. Understanding these mechanisms is key to managing cardiovascular symptoms in COVID-19 patients.

Keywords:
COVID-19SARS-CoV-2coronary microvascular dysfunction

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Area of Science:

  • Cardiology
  • Infectious Diseases
  • Pathophysiology

Background:

  • Endothelial dysfunction is increasingly recognized in COVID-19 pathogenesis.
  • Coronary microvascular dysfunction (CMD) is a significant factor in cardiovascular disease (CVD), sharing risk factors with COVID-19.
  • Common risk factors for both CVD and COVID-19 include age, hypertension, diabetes mellitus, and obesity.

Purpose of the Study:

  • To review the pathophysiology of CMD in the context of COVID-19.
  • To explore the mechanisms linking COVID-19 infection to coronary microvascular changes.
  • To synthesize current evidence on how COVID-19 affects the coronary microvasculature.

Main Methods:

  • Review of recent scientific literature and evidence.
  • Analysis of COVID-19 mechanisms including renin-angiotensin-aldosterone-systems (RAAS) imbalance, systemic inflammation, immune responses, endothelial dysfunction, and coagulatory disorders.
  • Examination of CMD pathophysiology from five distinct perspectives related to COVID-19.

Main Results:

  • SARS-CoV-2 entry disrupts local RAAS and Kallikrein-kinin-systems, decreasing ACE2 levels.
  • COVID-19-associated hyper-inflammation and a pro-thrombotic state lead to coronary microvascular obstruction.
  • Hypoxia from pneumonia/ARDS causes oxidative stress and sympathetic nerve activation in coronary microvessels.
  • Autonomic dysfunction and endothelial-perivascular cell interactions contribute to CMD in COVID-19 patients.

Conclusions:

  • Multiple interconnected mechanisms, including RAAS imbalance, inflammation, hypoxia, and autonomic dysfunction, contribute to CMD in COVID-19.
  • These mechanisms can act sequentially or intermittently, leading to cardiovascular symptoms.
  • Further research is needed to fully elucidate the underlying molecular pathogenesis of CMD in COVID-19.