Endothelialitis plays a central role in the pathophysiology of severe COVID-19 and its cardiovascular complications

Acta Cardiol. 2021 Apr;76(2):109-124. doi: 10.1080/00015385.2020.1846921. Epub 2020 Nov 19.


This clinical review paper discusses the pathophysiology of the pulmonary and cardiovascular manifestations of a SARS-CoV-2 infection and the ensuing implications on acute cardiovascular care in patients presenting with a severe COVID-19 syndrome admitted to an intensive acute cardiac care unit. The high prevalence of old age, obesity, diabetes, hypertension, heart failure, and ischaemic heart disease in patients who develop a severe to critical COVID-19 syndrome suggests shared pathophysiological mechanisms. Pre-existing endothelial dysfunction and an impaired innate immune response promote the development by the viral infection of an acute endothelialitis in the pulmonary microcirculation complicated by abnormal vasoconstrictor responses, luminal plugging by inflammatory cells, and intravascular thrombosis. This endothelialitis extends into the systemic circulation what may lead to acute myocardial injury, myocarditis, and thromboembolic complications both in the arterial and venous circulation.

Keywords: COVID-19; SARS-CoV-2; adult respiratory distress syndrome; cytokine storm; diabetes; endothelialitis; endothelium; microcirculation; obesity; thrombosis; ventilation.

Publication types

  • Review

MeSH terms

  • COVID-19 / complications*
  • COVID-19 / epidemiology
  • Cardiovascular Diseases / epidemiology
  • Cardiovascular Diseases / etiology*
  • Endothelium, Vascular / pathology*
  • Global Health
  • Humans
  • Incidence
  • Pandemics*
  • SARS-CoV-2*