{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T21:11:27Z","timestamp":1790457087811,"version":"4.1.0"},"reference-count":39,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2026,2,21]],"date-time":"2026-02-21T00:00:00Z","timestamp":1771632000000},"content-version":"vor","delay-in-days":1239,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.atsjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To compare lung parenchymal and vascular alterations between patients with fatal COVID-19 pneumonia and other DAD-causing etiologies using a multidimensional approach.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>This autopsy cohort consisted of consecutive patients with COVID-19 pneumonia (n\u2009=\u200920) and with respiratory failure and histologic DAD (n\u2009=\u200921; non\u2013COVID-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 (CVasc) in different microscopic compartments. Respiratory mechanics and gas-exchange parameters were evaluated longitudinally in patients with ARDS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>In premortem CT, patients with COVID-19 showed more dilated vasculature when all lung segments were evaluated (P\u2009=\u20090.001) compared with controls with DAD. Histopathology revealed vasculopathic changes, including hemangiomatosis-like changes (P\u2009=\u20090.043), thromboemboli (P\u2009=\u20090.0038), pulmonary infarcts (P\u2009=\u20090.047), and perivascular inflammation (P\u2009&amp;lt;\u20090.001). Generalized estimating equations revealed significant regional differences in the lung microarchitecture among all DAD-causing entities. COVID-19 showed a larger overall CVasc range (P\u2009=\u20090.002). Alveolar-septal congestion was associated with a significantly shorter time to death from symptom onset (P\u2009=\u20090.03), length of hospital stay (P\u2009=\u20090.02), and increased ventilatory ratio [an estimate for pulmonary dead space fraction (Vd); p\u2009=\u20090.043] in all cases of ARDS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>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 Vd and clinical outcomes in ARDS in general.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.202109-2150oc","type":"journal-article","created":{"date-parts":[[2022,6,7]],"date-time":"2022-06-07T16:41:46Z","timestamp":1654620106000},"page":"857-873","update-policy":"https:\/\/doi.org\/10.1164\/crossmarkpolicies","source":"Crossref","is-referenced-by-count":39,"title":["Vasculopathy and Increased Vascular Congestion in Fatal COVID-19 and Acute Respiratory Distress Syndrome"],"prefix":"10.1093","volume":"206","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9230-8747","authenticated-orcid":false,"given":"Julian A.","family":"Villalba","sequence":"first","affiliation":[{"name":"James Homer Wright Pathology Laboratories"},{"name":"Department of Pathology, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caroline F.","family":"Hilburn","sequence":"additional","affiliation":[{"name":"James Homer Wright Pathology Laboratories"},{"name":"Department of Pathology, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle A.","family":"Garlin","sequence":"additional","affiliation":[{"name":"Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts"},{"name":"Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Grant A.","family":"Elliott","sequence":"additional","affiliation":[{"name":"Unboxed Systems LLC, West Palm Beach, Florida"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5300-0571","authenticated-orcid":false,"given":"Yijia","family":"Li","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keiko","family":"Kunitoki","sequence":"additional","affiliation":[{"name":"Harvard T. 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