Authors: L.A. McKeown
COVID-19 Autopsies Put Endothelial Damage, Angiogenesis in the Spotlight
The still-forming picture suggests significantly more new-vessel growth in the lung than would be expected from a typical flu.
More autopsy reports on COVID-19 patients, some from the United States, are helping researchers piece together a picture of a virus that damages endothelial cells, causing a clotting disorder that can lead to deep vein thrombosis and pulmonary emboli.
“These people are in a hypercoagulant state, and early anticoagulation is important,” said Louis Maximilian Buja, MD (UTHealth, Houston, TX), lead author on a recent autopsy paper in Cardiovascular Pathology. “I think what’s going to happen is some kind of cocktail of combined therapies is going to evolve that’s going to give these people a better shot at surviving compared to just the respirator alone.”
As TCTMD recently reported, German researchers looking at 12 autopsies of COVID-19 patients found a substantial number of deaths were related to pulmonary embolism despite the patients having no prior evidence of thrombosis. In their autopsy study of patients from five centers in the United States, Buja and colleagues report major pulmonary thromboemboli with pulmonary infarcts and/or hemorrhage in five of 23 patients and a pattern of cardiac comorbidity similar to what was seen in the German study.
“The pathogenesis of COVID-19 pulmonary disease involves binding of SARS-CoV-2 virus to ACE2 receptors to pneumocytes and endothelial cells, leading to development of acute lung injury manifest as [diffuse alveolar damage],”
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