• François Potus, Vicky Mai, Marius Lebret, Simon Malenfant, Emilie Breton-Gagnon, Annie C Lajoie, Olivier Boucherat, Sébastien Bonnet, and Steeve Provencher.
• Pulmonary Hypertension Research Group, Centre de Recherche de l'Institut Universitaire de Cardiologie et Pneumologie de Quebec City, Quebec, Canada.
• Am. J. Physiol. Lung Cell Mol. Physiol. 2020 Aug 1; 319 (2): L277-L288.

AbstractIn the last few months, the number of cases of a new coronavirus-related disease (COVID-19) rose exponentially, reaching the status of a pandemic. Interestingly, early imaging studies documented that pulmonary vascular thickening was specifically associated with COVID-19 pneumonia, implying a potential tropism of the virus for the pulmonary vasculature. Moreover, SARS-CoV-2 infection is associated with inflammation, hypoxia, oxidative stress, mitochondrial dysfunction, DNA damage, and lung coagulopathy promoting endothelial dysfunction and microthrombosis. These features are strikingly similar to what is seen in pulmonary vascular diseases. Although the consequences of COVID-19 on the pulmonary circulation remain to be explored, several viruses have been previously thought to be involved in the development of pulmonary vascular diseases. Patients with preexisting pulmonary vascular diseases also appear at increased risk of morbidity and mortality. The present article reviews the molecular factors shared by coronavirus infection and pulmonary vasculature defects, and the clinical relevance of pulmonary vascular alterations in the context of COVID-19.

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