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Mechanisms of Pulmonary Vasculopathy in Acute and Long-Term COVID-19: A Review
Marianne Riou1,2, Florence Coste3, Alain Meyer1,2
1Translational Medicine Federation of Strasbourg (FMTS), University of Strasbourg, CRBS, Team 3072 "Mitochondria, Oxidative Stress and Muscle Protection", 1 rue Eugène Boeckel, CS 60026, 67084 Strasbourg, France.
Insights
Coronavirus disease 2019 (COVID-19) causes pulmonary vascular damage through mechanisms like thrombosis and endotheliitis. This vascular injury may also contribute to long COVID symptoms, including pulmonary hypertension.
Area of Science:
- Cardiovascular Medicine
- Pulmonology
- Infectious Diseases
Background:
- Coronavirus disease 2019 (COVID-19) remains a significant public health issue.
- The pandemic revealed specific pulmonary vascular disorders associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.
Purpose of the Study:
- To review the pathological mechanisms of pulmonary vascular damage during acute COVID-19.
- To explore the potential role of this damage in the pathophysiology of long COVID.
Main Methods:
- This review synthesizes current literature on COVID-19's impact on the pulmonary vasculature.
- Pathological mechanisms discussed include thromboembolic events, coagulopathy, endotheliitis, and hypoxic pulmonary vasoconstriction.
Main Results:
- COVID-19 can lead to both venous and arterial thrombotic disease, including severe acute pulmonary embolism.
- Direct viral effects on endothelial cells and indirect inflammatory responses contribute to pulmonary vasculopathy.
- Pulmonary vascular damage and pulmonary hypertension are hypothesized sequelae of acute infection.
Conclusions:
- COVID-19-induced pulmonary vascular damage is multifactorial, involving thrombosis and endothelial dysfunction.
- Persistent pulmonary vascular changes may underlie long COVID symptoms such as dyspnea and pulmonary hypertension.
Abstract:
Despite the end of the pandemic, coronavirus disease 2019 (COVID-19) remains a major public health concern. The first waves of the virus led to a better understanding of its pathogenesis, highlighting the fact that there is a specific pulmonary vascular disorder. Indeed, COVID-19 may predispose patients to thrombotic disease in both venous and arterial circulation, and many cases of severe acute pulmonary embolism have been reported. The demonstrated presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) within the endothelial cells suggests that direct viral effects, in addition to indirect effects of perivascular inflammation and coagulopathy, may contribute to pulmonary vasculopathy in COVID-19. In this review, we discuss the pathological mechanisms leading to pulmonary vascular damage during acute infection, which appear to be mainly related to thromboembolic events, an impaired coagulation cascade, micro- and macrovascular thrombosis, endotheliitis and hypoxic pulmonary vasoconstriction. As many patients develop post-COVID symptoms, including dyspnea, we also discuss the hypothesis of pulmonary vascular damage and pulmonary hypertension as a sequela of the infection, which may be involved in the pathophysiology of long COVID.
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