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Cardiovascular complications are rapidly emerging as a key threat in coronavirus disease 2019 (COVID-19) in addition to respiratory disease. Intriguingly, SARS-CoV-2 can directly infect engineered human blood vessel organoids in vitro.[4] Here we demonstrate endothelial cell involvement across vascular beds of different organs in a series of patients with COVID-19 (further case details are provided in the appendix). She developed progressive respiratory failure due to COVID-19 and subsequently developed multi-organ failure and needed renal replacement therapy. [Extracted from the article]

We thank Cynthia Goldsmith and colleagues for their interest in our recent Correspondence.[1] We described autopsy findings from patients who had died from COVID-19 and showed a systemic endotheliitis with evidence of loss of integrity of the endothelial monolayer.[1] The framework of endotheliitis provides an explanation for the unique predilection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in those individuals with hypertension, diabetes, or established cardiovascular disease, a group known to have pre-existing endothelial dysfunction. In another recent study,[6] virus-like particles in patients with confirmed SARS-CoV-2 infection were 70-110 nm in diameter. This notwithstanding, these observed particles in patients with COVID-19 should be best designated as virus-like particles because definitive assignment of these structures as SARS-CoV-2 virions requires immuno-EM. [Extracted from the article]