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.

Potential therapeutic targets for COVID-19 complicated with pulmonary hypertension: a bioinformatics and early validation study

“…Chronic thromboembolic pulmonary hypertension may be more likely to occur in people with COVID-19 if microthrombi are present in their lung arteries during the acute phase. These parallels prompt the fascinating hypothesis that chronic SARS-CoV-2 infection may lead to PH [11,12]. Overactivated platelets cause cytokine storms and thrombosis, and studies have shown that platelets that express pro-in ammatory molecules and that carry viral RNA are particularly likely to be highly active [13].…”

Pulmonary Hypertension in Underrepresented Minorities: A Narrative Review

“…It has been widely reported that minority patients and those from lower socioeconomic backgrounds had worse outcomes during the COVID-19 pandemic [ 51 ]. Although evidence remains limited, recent studies have demonstrated the onset of pulmonary hypertension and right ventricular dysfunction after acute COVID-19 infection, with these hemodynamic effects potentially implicated in the symptoms associated with “post-COVID syndromes” [ 52 , 53 ]. As our understanding of the chronic consequences of COVID-19 infections improves, COVID-19 survivors may become a notable subgroup of Group 3 PH whose management should be considered in a distinct way.…”

SARS-CoV-2 spike protein receptor-binding domain perturbates intracellular calcium homeostasis and impairs pulmonary vascular endothelial cells

“…During prolonged infection, persistent pulmonary vascular damage and microthrombus accumulation could together drive prolonged pulmonary vascular inflammation and remodeling, indicating PH as a long COVID complication that deserves further evaluation and attention. 25 , 26 Previous studies have addressed that endothelial damage play vital roles to initiate the pulmonary vascular remodeling and PH. Endothelial cell death leads to imbalance between cell apoptosis and proliferation, which emerges and promotes the establishment of lumen-occluding lesions.…”