The 1918 influenza killed approximately 50 million people in a few short years, and now, the world is facing another pandemic. In December 2019, a novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused an international outbreak of a respiratory illness termed coronavirus disease 2019 (COVID-19) and rapidly spread to cause the worst pandemic since 1918. Recent clinical reports highlight an atypical presentation of acute respiratory distress syndrome (ARDS) in COVID-19 patients characterized by severe hypoxemia, an imbalance of the renin–angiotensin system, an increase in thrombogenic processes, and a cytokine release storm. These processes not only exacerbate lung injury but can also promote pulmonary vascular remodeling and vasoconstriction, which are hallmarks of pulmonary hypertension (PH). PH is a complication of ARDS that has received little attention; thus, we hypothesize that PH in COVID-19-induced ARDS represents an important target for disease amelioration. The mechanisms that can promote PH following SARS-CoV-2 infection are described. In this review article, we outline emerging mechanisms of pulmonary vascular dysfunction and outline potential treatment options that have been clinically tested.
【저자키워드】 COVID-19, acute lung injury, renin angiotensin system, respiratory viral infection, cytokine release storm, Endothelin, Kallikrein–Kinin System, hypoxic-adenosinergic response, 【초록키워드】 coronavirus disease, SARS-CoV-2, ARDS, coronavirus, pandemic, SARS-COV-2 infection, Respiratory illness, Lung injury, Novel coronavirus, outbreak, International, vascular dysfunction, disease, mechanism, acute respiratory distress, pulmonary hypertension, Atypical, COVID-19 patient, acute respiratory syndrome, Vascular, potential treatment option, syndrome, severe hypoxemia, hallmark, vasoconstriction, recent, highlight, tested, described, caused, spread to, clinically, characterized, promote, increase in, 1918 influenza, exacerbate, 【제목키워드】 ARDS, pulmonary, target, respiratory, Potential,