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Editorial
. 2020 Dec;17(12):1528-1530.
doi: 10.1513/AnnalsATS.202008-1014ED.

COVID-19 and Pulmonary Arterial Hypertension: Early Data and Many Questions

Samar Farha  1 , Gustavo A Heresi  1
Affiliations
Editorial

COVID-19 and Pulmonary Arterial Hypertension: Early Data and Many Questions

Samar Farha et al. Ann Am Thorac Soc. 2020 Dec.
No abstract available

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Figures

Figure 1.
Figure 1.
Schematic representation of the different mechanisms that could modify coronavirus disease (COVID-19) illness in patients with pulmonary arterial hypertension (PAH). The renin–angiotensin pathway is dysregulated in PAH with decreased angiotensin-converting enzyme 2 (ACE-2) and angiotensin (Ang) (–7) levels. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) enters human cells via binding to ACE-2 receptor, which is expressed on various pulmonary cells including type II alveolar cells, macrophages, endothelial, smooth muscle cells, and perivascular pericytes. Reduced ACE-2 in PAH could impair viral entrance. However, higher angiotensin II levels could lead to worse lung injury and inflammation. The immune system plays a role in the pathogenesis of PAH with increased perivascular mast cells, macrophages, dendritic cells, and T cells and could modulate viral replication and/or the deleterious cytokine response induced by SARS-CoV-2. Another important hypothetical mechanism is the role of PAH-targeted therapies, mainly endothelin receptor antagonists (ERAs) and the nitric oxide (NO) pathway enhancers, phosphodiesterase type 5 inhibitors (PDE5-i), and soluble guanylate cyclase stimulators (sGCS). ERAs block the downregulation of ACE-2 by endothelin-1 (ET-1) and inhibit angiotensin II–induced vasoconstriction and lung injury. PAH-targeted therapies may also have antiinflammatory and antithrombotic effects. Inhaled NO has been shown to have an antimicrobial effect; however, it is unclear whether other therapies that increase signaling along the NO axis have the same effect. Lastly, PAH therapies are pulmonary vasodilators and could worsen ventilation–perfusion mismatch in COVID-19 lung injury.
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