Cardiovascular Tropism and Sequelae of SARS-CoV-2 Infection

Viruses. 2022 May 25;14(6):1137. doi: 10.3390/v14061137.

Abstract

The extrapulmonary manifestation of coronavirus disease-19 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), became apparent early in the ongoing pandemic. It is now recognized that cells of the cardiovascular system are targets of SARS-CoV-2 infection and associated disease pathogenesis. While some details are emerging, much remains to be understood pertaining to the mechanistic basis by which SARS-CoV-2 contributes to acute and chronic manifestations of COVID-19. This knowledge has the potential to improve clinical management for the growing populations of patients impacted by COVID-19. Here, we review the epidemiology and pathophysiology of cardiovascular sequelae of COVID-19 and outline proposed disease mechanisms, including direct SARS-CoV-2 infection of major cardiovascular cell types and pathogenic effects of non-infectious viral particles and elicited inflammatory mediators. Finally, we identify the major outstanding questions in cardiovascular COVID-19 research.

Keywords: COVID-19; SARS-CoV-2; cardiomyocyte; myocarditis; pericyte; post-acute sequelae of SARS-CoV-2 infection; thrombosis.

Publication types

  • Review
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • COVID-19*
  • Cardiovascular System*
  • Disease Progression
  • Humans
  • Pandemics
  • SARS-CoV-2
  • Tropism