Mechanism of COVID-19-Induced Cardiac Damage from Patient, In Vitro and Animal Studies

Elizabeth A. V. Jones*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Purpose of ReviewThough patient studies have been important for understanding the disease, research done in animals and cell culture complement our knowledge from patient data and provide insight into the mechanism of the disease. Understanding how COVID causes damage to the heart is essential to understanding possible long-term consequences.Recent FindingsCOVID-19 is primarily a disease that attacks the lungs; however, it is known to have important consequences in many other tissues including the heart. Though myocarditis does occur in some patients, for most cases of cardiac damage, the injury arises from scarring either due to myocardial infarction or micro-infarction.The main focus is on how COVID affects blood flow through the coronaries. We review how endothelial activation leads to a hypercoagulative state in COVID-19. We also emphasize the effects that the cytokine storm can directly have on the regulation of coronary blood flow. Since the main two cell types that can be infected in the heart are pericytes and cardiomyocytes, we further describe the known effects on pericyte function and how that can further lead to microinfarcts within the heart. Though many of these effects are systemic, this review focuses on the consequences on cardiac tissue of this dysregulation and the role that it has in the formation of myocardial scarring.
Original languageEnglish
Pages (from-to)451-460
Number of pages10
JournalCurrent Heart Failure Reports
Volume20
Issue number5
Early online date1 Aug 2023
DOIs
Publication statusPublished - 1 Aug 2023

Keywords

  • COVID
  • Microthrombi
  • Pericyte
  • Heart
  • ANGIOTENSIN-CONVERTING ENZYME
  • SARS-COV-2 RECEPTOR ACE2
  • ENDOTHELIAL-CELLS
  • MYOCARDIAL INVOLVEMENT
  • NUCLEAR IMPORT
  • BLOOD-FLOW
  • PERICYTES
  • EXPRESSION
  • CAPILLARY
  • INFECTION

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