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Am J Respir Crit Care Med ; 2022 Jun 07.
Article in English | MEDLINE | ID: covidwho-1879167


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 non-viral 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 On premortem CT, COVID-19 patients showed more dilated vasculature when evaluating all lung segments (p=0.001) compared to DAD-controls. 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.

Hum Pathol ; 125: 18-22, 2022 07.
Article in English | MEDLINE | ID: covidwho-1778168


Placental pathology can identify characteristic features of specific infectious pathogens. The histopathology of acute SARS-CoV-2 placental infection and exposure without infection has been well described. However, whether the characteristic placental pathology persists after the acute phase of the infection is less clear. We retrospectively identified 67 COVID-19-recovered pregnant patients who had placental pathology available. After reviewing the gross and histopathology, we categorized the findings and studied the placentas for evidence of chronic infection by immunohistochemistry for the spike protein of the virus. We found these placentas showed significantly increased prevalence of maternal and a trend towards significance of fetal vascular malperfusion when compared to a control group of placentas examined for the sole indication of maternal group B streptococcal colonization. None of the COVID-19-recovered placentas showed expression of the viral spike protein; therefore, we found no evidence of persistent infection of the placenta in women with a history of COVID-19 during their pregnancy. We conclude that recovery from a SARS-CoV-2 infection during pregnancy puts the pregnancy at risk for specific pathology.

COVID-19 , Pregnancy Complications, Infectious , Female , Humans , Placenta/pathology , Pregnancy , Pregnancy Complications, Infectious/pathology , Retrospective Studies , SARS-CoV-2 , Spike Glycoprotein, Coronavirus
Mod Pathol ; 34(7): 1345-1357, 2021 07.
Article in English | MEDLINE | ID: covidwho-1137760


COVID-19 has been associated with cardiac injury and dysfunction. While both myocardial inflammatory cell infiltration and myocarditis with myocyte injury have been reported in patients with fatal COVID-19, clinical-pathologic correlations remain limited. The objective was to determine the relationships between cardiac pathological changes in patients dying from COVID-19 and cardiac infection by SARS-CoV-2, laboratory measurements, clinical features, and treatments. In a retrospective study, 41 consecutive autopsies of patients with fatal COVID-19 were analyzed for the associations between cardiac inflammation, myocarditis, cardiac infection by SARS-CoV-2, clinical features, laboratory measurements, and treatments. Cardiac infection was assessed by in situ hybridization and NanoString transcriptomic profiling. Cardiac infection by SARS-CoV-2 was present in 30/41 cases: virus+ with myocarditis (n = 4), virus+ without myocarditis (n = 26), and virus- without myocarditis (n = 11). In the cases with cardiac infection, SARS-CoV-2+ cells in the myocardium were rare, with a median density of 1 cell/cm2. Virus+ cases showed higher densities of myocardial CD68+ macrophages and CD3+ lymphocytes, as well as more electrocardiographic changes (23/27 vs 4/10; P = 0.01). Myocarditis was more prevalent with IL-6 blockade than with nonbiologic immunosuppression, primarily glucocorticoids (2/3 vs 0/14; P = 0.02). Overall, SARS-CoV-2 cardiac infection was less prevalent in patients treated with nonbiologic immunosuppression (7/14 vs 21/24; P = 0.02). Myocardial macrophage and lymphocyte densities overall were positively correlated with the duration of symptoms but not with underlying comorbidities. In summary, cardiac infection with SARS-CoV-2 is common among patients dying from COVID-19 but often with only rare infected cells. Cardiac infection by SARS-CoV-2 is associated with more cardiac inflammation and electrocardiographic changes. Nonbiologic immunosuppression is associated with lower incidences of myocarditis and cardiac infection by SARS-CoV-2.

COVID-19/pathology , Aged , Anticoagulants/therapeutic use , Autopsy , COVID-19/blood , COVID-19/drug therapy , Echocardiography , Electrocardiography , Female , Humans , Immunosuppressive Agents/therapeutic use , Male , Myocarditis/pathology , Myocarditis/virology , Myocardium/pathology , Retrospective Studies , SARS-CoV-2/physiology