In this small, yet interesting series, we observe angiogenesis could differentiate pulmonary physiopathology by Covid-19 vs. from viral infections of similar severity (such as influenza).
Being quite small, we can hardly consider it universal, or whether it could have clinical impact. Meanwhile, we keep learning about the new virus.
Progressive respiratory failure is the main cause of death by Covid-19. Despite the interest in this new disease, we know little about the morphological and molecular changes produced by this infection.
The study looked at 7 lungs obtained from autopsies of Covid-19 patients and compared them to other 7 lungs obtained from patients who had died of acute respiratory distress syndrome (ARDS) secondary to influenza A(H1N1) infection. Researchers analyzed immunohistochemical characteristics, electron microscopy, and gene expression, among other things.
Both viruses produced a histologic pattern in the peripheral lung characterized by diffuse alveolar damage with perivascular T-cell infiltration. However, Covid-19 patients showed other distinctive characteristics such as severe endothelial injury associated to intracellular presence and completely destroyed cell membranes.
Histologic analysis of lung vessels showed microangiopathy and diffuse thrombosis.
Intra alveolar microthrombi were 9 times more frequent in Covid-19 patients, compared against influenza patients (p<0.001).
In addition, there was new vessel growth produced mainly by intussusceptive angiogenesis. This phenomenon was 2.7 times more frequent in Covid-19 vs. influenza patients (p<0.001).
Pulmonary angiogenesis could be a distinctive characteristic of the new coronavirus. The universality and clinical implication of this finding require further study.
Original Title: Pulmonary Vascular Endothelialitis, Thrombosis, and Angiogenesis in Covid-19.
Reference: Maximilian Ackermann et al. N Engl J Med. 2020, Online ahead of print. doi: 10.1056/NEJMoa2015432.
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