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Vasculopathy and Increased Vascular Congestion in Fatal COVID-19 and Acute Respiratory Distress Syndrome.
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.
  • Villalba JA; James Homer Wright Pathology Laboratories.
  • Hilburn CF; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
  • Garlin MA; James Homer Wright Pathology Laboratories.
  • Elliott GA; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
  • Li Y; Center for Systems Biology, Massachusetts General Hospital, Boston, Massachusetts.
  • Kunitoki K; Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, New York.
  • Poli S; Unboxed Systems LLC, West Palm Beach, Florida.
  • Alba GA; Division of Infectious Diseases, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
  • Madrigal E; Harvard T. H. Chan School of Public Health, Boston, Massachusetts.
  • Taso M; Department of Psychiatry.
  • Price MC; Department of Medicine, Mount Sinai Medical Center, Miami Beach, Florida.
  • Aviles AJ; Division of Pulmonary and Critical Care Medicine, Department of Medicine, Department of Medicine.
  • Araujo-Medina M; James Homer Wright Pathology Laboratories.
  • Bonanno L; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
  • Boyraz B; Division of MRI Research, Department of Radiology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
  • Champion SN; Division of Thoracic Imaging and Intervention, Department of Radiology.
  • Harris CK; James Homer Wright Pathology Laboratories.
  • Helland TL; James Homer Wright Pathology Laboratories.
  • Hutchison B; Immunopathology Research Laboratory, and.
  • Jobbagy S; James Homer Wright Pathology Laboratories.
  • Marshall MS; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
  • Shepherd DJ; James Homer Wright Pathology Laboratories.
  • Barth JL; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
  • Hung YP; James Homer Wright Pathology Laboratories.
  • Ly A; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
  • Hariri LP; C. S. Kubik Laboratory for Neuropathology, Department of Pathology, Massachusetts General Hospital Charlestown HealthCare Center, Charlestown, Massachusetts.
  • Turbett SE; Miami-Dade County Medical Examiner Department, Miami, Florida.
  • Pierce VM; James Homer Wright Pathology Laboratories.
  • Branda JA; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
  • Rosenberg ES; James Homer Wright Pathology Laboratories.
  • Mendez-Pena J; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
  • Chebib I; James Homer Wright Pathology Laboratories.
  • Rosales IA; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
  • Smith RN; James Homer Wright Pathology Laboratories.
  • Miller MA; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
  • Rosas IO; James Homer Wright Pathology Laboratories.
  • Hardin CC; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
  • Baden LR; James Homer Wright Pathology Laboratories.
  • Medoff BD; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
  • Colvin RB; James Homer Wright Pathology Laboratories.
  • Little BP; James Homer Wright Pathology Laboratories.
  • Stone JR; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
  • Mino-Kenudson M; James Homer Wright Pathology Laboratories.
  • Shih AR; Department of Pathology, Harvard Medical School, Boston, Massachusetts.
Am J Respir Crit Care Med ; 206(7): 857-873, 2022 10 01.
Article in English | MEDLINE | ID: covidwho-2053494
ABSTRACT
Rationale 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.

Objective:

To compare lung parenchymal and vascular alterations between patients with fatal COVID-19 pneumonia and other DAD-causing etiologies using a multidimensional approach.

Methods:

This autopsy cohort consisted of consecutive patients with COVID-19 pneumonia (n = 20) and with respiratory failure and histologic DAD (n = 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 (CVasc) in different microscopic compartments. Respiratory mechanics and gas-exchange parameters were evaluated longitudinally in patients with ARDS. Measurements and Main

Results:

In premortem CT, patients with COVID-19 showed more dilated vasculature when all lung segments were evaluated (P = 0.001) compared with controls with DAD. Histopathology revealed vasculopathic changes, including hemangiomatosis-like changes (P = 0.043), thromboemboli (P = 0.0038), pulmonary infarcts (P = 0.047), and perivascular inflammation (P < 0.001). 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 = 0.002). Alveolar-septal congestion was associated with a significantly shorter time to death from symptom onset (P = 0.03), length of hospital stay (P = 0.02), and increased ventilatory ratio [an estimate for pulmonary dead space fraction (Vd); p = 0.043] in all cases of ARDS.

Conclusions:

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.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Pneumonia / Respiratory Distress Syndrome / Vascular Diseases / COVID-19 Type of study: Cohort study / Etiology study / Experimental Studies / Observational study / Prognostic study / Randomized controlled trials Topics: Long Covid Limits: Humans Language: English Journal: Am J Respir Crit Care Med Journal subject: Critical Care Year: 2022 Document Type: Article

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Pneumonia / Respiratory Distress Syndrome / Vascular Diseases / COVID-19 Type of study: Cohort study / Etiology study / Experimental Studies / Observational study / Prognostic study / Randomized controlled trials Topics: Long Covid Limits: Humans Language: English Journal: Am J Respir Crit Care Med Journal subject: Critical Care Year: 2022 Document Type: Article