Details

Autor(en) / Beteiligte

• Villalba, Julian A
• Hilburn, Caroline F
• Garlin, Michelle A
• Elliott, Grant A
• Li, Yijia
• Kunitoki, Keiko
• Poli, Sergio
• Alba, George A
• Madrigal, Emilio
• Taso, Manuel
• Price, Melissa C
• Aviles, Alexis J
• Araujo-Medina, Milagros
• Bonanno, Liana
• Boyraz, Baris
• Champion, Samantha N
• Harris, Cynthia K
• Helland, Timothy L
• Hutchison, Bailey
• Jobbagy, Soma
• Marshall, Michael S
• Shepherd, Daniel J
• Barth, Jaimie L
• Hung, Yin P
• Ly, Amy
• Hariri, Lida P
• Turbett, Sarah E
• Pierce, Virginia M
• Branda, John A
• Rosenberg, Eric S
• Mendez-Pena, Javier
• Chebib, Ivan
• Rosales, Ivy A
• Smith, Rex N
• Miller, Miles A
• Rosas, Ivan O
• Hardin, Charles C
• Baden, Lindsey R
• Medoff, Benjamin D
• Colvin, Robert B
• Little, Brent P
• Stone, James R
• Mino-Kenudson, Mari
• Shih, Angela R

Titel

Vasculopathy and Increased Vascular Congestion in Fatal COVID-19 and Acute Respiratory Distress Syndrome

Ist Teil von

• American journal of respiratory and critical care medicine, 2022-10, Vol.206 (7), p.857-873

Ort / Verlag

United States: American Thoracic Society

Erscheinungsjahr

2022

Quelle

MEDLINE

Beschreibungen/Notizen

• The leading cause of death in coronavirus disease 2019 (COVID-19) is severe pneumonia, with many patients developing acute respiratory distress syndrome (ARDS) and diffuse alveolar damage (DAD). Whether DAD in fatal COVID-19 is distinct from other causes of DAD remains unknown. To compare lung parenchymal and vascular alterations between patients with fatal COVID-19 pneumonia and other DAD-causing etiologies using a multidimensional approach. This autopsy cohort consisted of consecutive patients with COVID-19 pneumonia (  = 20) and with respiratory failure and histologic DAD (  = 21; non-COVID-19 viral and nonviral etiologies). Premortem chest computed tomography (CT) scans were evaluated for vascular changes. Postmortem lung tissues were compared using histopathological and computational analyses. Machine-learning-derived morphometric analysis of the microvasculature was performed, with a random forest classifier quantifying vascular congestion (C ) in different microscopic compartments. Respiratory mechanics and gas-exchange parameters were evaluated longitudinally in patients with ARDS. In premortem CT, patients with COVID-19 showed more dilated vasculature when all lung segments were evaluated (  = 0.001) compared with controls with DAD. Histopathology revealed vasculopathic changes, including hemangiomatosis-like changes (  = 0.043), thromboemboli (  = 0.0038), pulmonary infarcts (  = 0.047), and perivascular inflammation (  < 0.001). Generalized estimating equations revealed significant regional differences in the lung microarchitecture among all DAD-causing entities. COVID-19 showed a larger overall C range (  = 0.002). Alveolar-septal congestion was associated with a significantly shorter time to death from symptom onset (  = 0.03), length of hospital stay (  = 0.02), and increased ventilatory ratio [an estimate for pulmonary dead space fraction ( ); = 0.043] in all cases of ARDS. Severe COVID-19 pneumonia is characterized by significant vasculopathy and aberrant alveolar-septal congestion. Our findings also highlight the role that vascular alterations may play in and clinical outcomes in ARDS in general.