The primary cause of death in COVID-19 is progressive respiratory failure. However, there’s not much evidence that suggests molecular and morphologic transformations in the peripheral lungs of COVID-19 patients. The objective of this study is to evaluate the incidence of pulmonary vascular angiogenesis, thrombosis, and endothelialitis in COVID-19.

The researchers examined seven lungs obtained during the autopsy of patients who died from COVID-19 and compared them with patients who died from influenza-associated acute respiratory distress syndrome (ARDS), and ten uninfected, control lungs of the same age. The lungs were inspected using scanning electron microscopy, micro-computed tomographic imaging, direct multiplexed measurement of gene expression, and seven-color immunohistochemical analysis. 

The lungs of patients who died from COVID-19 and influenza-associated ARDS had diffused alveolar damage with perivascular T-cell infiltration on the peripheral side. The lungs of COVID-19 patients also demonstrated characteristic vascular features, indicating severe endothelial injury. The histologic analysis of pulmonary vessels also showed signs of extensive thrombosis and angiogenesis. The angiogenesis in the lungs of COVID-19 patients was 2.7 times higher than the lungs of ARDS patients. 

The research concluded that COVID-19 in humans was directly associated with pulmonary vascular angiogenesis, thrombosis, and endothelialitis. It was also concluded that angiogenesis was greater in COVID-19 than an equally-severe influenza infection.