From acute SARS-CoV-2 infection to pulmonary hypertension

Abstract

As the world progressively recovers from the acute stages of the coronavirus disease 2019 (COVID-19) pandemic, we may be facing new challenges regarding the long-term consequences of COVID-19. Accumulating evidence suggests that pulmonary vascular thickening may be specifically associated with COVID-19, implying a potential tropism of severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) virus for the pulmonary vasculature. Genetic alterations that may influence the severity of COVID-19 are similar to genetic drivers of pulmonary arterial hypertension. The pathobiology of the COVID-19-induced pulmonary vasculopathy shares many features (such as medial hypertrophy and smooth muscle cell proliferation) with that of pulmonary arterial hypertension. In addition, the presence of microthrombi in the lung vessels of individuals with COVID-19 during the acute phase, may predispose these subjects to the development of chronic thromboembolic pulmonary hypertension. These similarities raise the intriguing question of whether pulmonary hypertension (PH) may be a long-term sequela of SARS-COV-2 infection. Accumulating evidence indeed support the notion that SARS-COV-2 infection is indeed a risk factor for persistent pulmonary vascular defects and subsequent PH development, and this could become a major public health issue in the future given the large number of individuals infected by SARS-COV-2 worldwide. Long-term studies assessing the risk of developing chronic pulmonary vascular lesions following COVID-19 infection is of great interest for both basic and clinical research and may inform on the best long-term management of survivors.