Endothelial compromise by SARS-CoV-2


  • Heather Mason
  • Univadis Medical News
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SARS-CoV-2 facilitates endotheliitis in several organs, in addition to the host’s inflammatory response, according to results from a case series (n=3) reported in the Lancet. Two of the patients died.

According to current literature, SARS-CoV-2 infects the host through angiotensin-converting enzyme 2 (ACE2) receptors which are present in lung, heart, kidney, intestinal and endothelial tissues. Upon microscopic examination of these tissues from each subject, the investigators found viral elements within endothelial cells and accumulation of inflammatory cells, with evidence of endothelial and inflammatory cell death. This evidence suggests that SARS-CoV-2 facilitates endotheliitis in several organs in addition to the host’s inflammatory response. The authors also propose that induction of apoptosis and pyroptosis could be associated with the endothelial cell injury they observed. Therefore, endotheliitis caused by COVID-19 could underlie the systemically impaired microcirculation and some of the clinical manifestations seen in this disease.

These findings could support the use of endothelium-stabilising therapies that can also impact viral replication, such as anti-inflammatory anti-cytokine drugs, ACE inhibitors, and statins. Such an approach could be particularly useful for patients at high-risk for COVID-19 (males, smokers, hypertensives, diabetics, obese, and individuals with cardiovascular disease) that tend to have endothelial dysfunction.