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BACKGROUNDThe 2019 novel coronavirus, or severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which results in coronavirus disease 2019 (COVID-19), has been declared a pandemic and is severely affecting the provision of health care services all over the world. 1 Health care workers are at higher risk because this virus is very easily spread, especially through the kind of close contact involved in the performance of echocardiographic studies. The virus carries relatively high mortality and morbidity risk, particularly for certain populations (the elderly, the chronically ill, the immunocompromised, and possibly pregnant women). 2 Given the risk for cardiovascular complications in the setting of COVID-19, including preexisting cardiac disease, acute cardiac injury, and drug-related myocardial damage, 3 echocardiographic services will likely be required in the care of patients with suspected or confirmed COVID-19. Consequently, echocardiography providers will be exposed to SARS-CoV-2.Sonographers, nurses, advance practice providers, and physicians have a duty to care for patients and are at the front lines in the battle against disease. We are at high risk, particularly when we participate in This document is endorsed by the following

BACKGROUND The 2019 novel coronavirus, or severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which results in coronavirus disease 2019 (COVID-19), has been declared a pandemic and is severely affecting the provision of health care services all over the world (1). Health care workers are at higher risk because this virus is very easily spread, especially through the kind of close contact involved in the performance of echocardiographic studies. The virus carries relatively high mortality and morbidity risk, particularly for certain populations (the elderly, the chronically ill, the immunocompromised, and possibly pregnant women) (2). Given the risk for cardiovascular complications in the setting of COVID-19, including preexisting cardiac disease, acute cardiac injury, and drug-related myocardial damage, (3) echocardiographic services will likely be required in the care of patients with suspected or confirmed COVID-19. Consequently, echocardiography providers will be exposed to SARS-CoV-2.

Background-Vasoactive intestinal peptide (VIP), a pulmonary vasodilator and inhibitor of vascular smooth muscle proliferation, has been reported absent in pulmonary arteries from patients with idiopathic pulmonary arterial hypertension (PAH). We have tested the hypothesis that targeted deletion of the VIP gene may lead to PAH with pulmonary vascular remodeling. Methods and Results-We examined VIP knockout (VIP Ϫ/Ϫ ) mice for evidence of PAH, right ventricular (RV) hypertrophy, and pulmonary vascular remodeling. Relative to wild-type control mice, VIP Ϫ/Ϫ mice showed moderate RV hypertension, RV hypertrophy confirmed by increased ratio of RV to left ventricle plus septum weight, and enlarged, thickened pulmonary artery and smaller branches with increased muscularization and narrowed lumen. Lung sections also showed perivascular inflammatory cell infiltrates. No systemic hypertension and no arterial hypoxemia existed to explain the PAH. The condition was associated with increased mortality. Both the vascular remodeling and RV remodeling were attenuated after a 4-week treatment with VIP. Conclusions-Deletion of the VIP gene leads to spontaneous expression of moderately severe PAH in mice during air breathing.Although not an exact model of idiopathic PAH, the VIP Ϫ/Ϫ mouse should be useful for studying molecular mechanisms of PAH and evaluating potential therapeutic agents. VIP replacement therapy holds promise for the treatment of PAH, and mutations of the VIP gene may be a factor in the pathogenesis of idiopathic PAH. (Circulation.

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