Pulmonary Arterial Thrombosis in COVID-19 With Fatal Outcome

Lax, Sigurd; Skok, Kristijan; Zechner, Peter; Kessler, Harald H.; Kaufmann, Norbert; Koelblinger, Camillo; Vander, Klaus; Bargfrieder, Ute; Trauner, Michael

doi:10.7326/m20-2566

Cited by 678 publications

(485 citation statements)

References 48 publications

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“…However, our nding seems to be supported by a recent meta-analysis on 11,590 COVID-19 patients, according to which smokers have higher odds of COVID-19 progression than never smokers (25). Intriguingly, all the predictors of mortality that we identi ed are linked to prothrombotic status; this might be particularly relevant in COVID-19, in which arterial and venous thrombosis seems to play a pivotal role in determining a worse prognosis (26).…”

Section: Discussionsupporting

confidence: 72%

Fatality rate and predictors of mortality in a large Italian cohort of hospitalized COVID-19 patients

Team

Sainaghi

2020

Preprint

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Substantial discrepancies are evident in the clinical features and natural history of coronavirus disease 2019 (COVID-19), among different countries, so we aimed to evaluate the fatality rate and to identify predictors of mortality in a cohort of hospitalized patients. We performed a retrospective multicenter cohort study on medical records of patients admitted between 1st March and 28th April 2020, involving three hospitals in Northern Italy. We included 1697 patients older than 18 years of age and with a confirmed diagnosis of SARS-CoV-2 infection by reverse-transcriptase polymerase chain reaction (RT-PCR). During the study period we observed 504 deaths, with a CFR of 29.7%. We further looked for predictors of mortality in a subset of 486 patients (239 males, 59%); the median age of the study population was 71 [58-80] years. Among demographic and clinical variables considered, age, a diagnosis of cancer, obesity and current smoking independently predicted mortality. When laboratory data were added to the model, age, the diagnosis of cancer, and the baseline PaO2/FiO2 ratio were independent predictors of mortality. During the COVID-19 outbreak, the CFR of hospitalized patients in Northern Italy was high, approaching 30%. The identification of mortality predictors might contribute to better stratification of individual patient risk.

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Section: Discussionsupporting

confidence: 72%

Fatality rate and predictors of mortality in a large Italian cohort of hospitalized COVID-19 patients

Team

Sainaghi

2020

Preprint

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“…autopsies performed in COVID-19 patients at a medical center in Austria, with nuclear pleomorphism in cholangiocytes and ductular proliferation. 47 Despite this evidence, COVID-19 patients with liver damage do not exhibit severe alterations in gamma-glutamyl transferase (GGT) or alkaline phosphatase (ALP) levels. 48 Instead, moderate elevations of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are observed, suggesting a direct effect on hepatocytes.…”

Section: Direct Cytopathic Effects Of Sars-cov-2 On Parenchymal Cellsmentioning

confidence: 99%

Direct or Collateral Liver Damage in SARS-CoV-2–Infected Patients

et al. 2020

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Liver injury can result from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection with more than one-third of COVID-19 patients exhibiting elevated liver enzymes. Microvesicular steatosis, inflammation, vascular congestion, and thrombosis in the liver have been described in autopsy samples from COVID-19 patients. Several factors, including direct cytopathic effect of the virus, immune-mediated collateral damage, or an exacerbation of preexisting liver disease may contribute to liver pathology in COVID-19. Due to its immunological functions, the liver is an organ likely to participate in the viral response against SARS-CoV-2 and this may predispose it to injury. A better understanding of the mechanism contributing to liver injury is needed to develop and implement early measures to prevent serious liver damage in patients suffering from COVID-19. This review summarizes current reports of SARS-CoV-2 with an emphasis on how direct infection and subsequent severe inflammatory response may contribute to liver injury in patients with and without preexisting liver disease.

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“…One of the key clinical features of COVID19 is upregulation of the pro-thrombotic phenotype and microvascular complications, leading to COVID19-associated coagulopathy (7). This is characterized by venous, arterial, and microvascular thrombosis despite the use of anti-coagulant therapies (32)(33)(34)(35)(36)(37)(38). Our study provides compelling evidence of COVID19 associated changes in coagulation-related gene expression levels that may exacerbate thrombosis caused by endothelial cell injury and platelet activation in COVID19+ ICU patients (7).…”

Section: Discussionmentioning

confidence: 78%

Transcriptional Profiling of Leukocytes in Critically Ill COVID19 Patients: Implications for Interferon Response and Coagulation

Gill

Santos

O’Gorman

et al. 2020

Preprint

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Background: COVID19 is caused by the SARS-CoV-2 virus and has been associated with severe inflammation leading to organ dysfunction and mortality. Our aim was to profile the transcriptome in leukocytes from critically ill patients positive for COVID19 compared to those negative for COVID19 to better understand the COVID19 associated host response. For these studies, all patients admitted to our tertiary care intensive care unit (ICU) suspected of being infected with SARS-CoV-2, using standardized hospital screening methodologies, had blood samples collected at the time of admission to the ICU. Transcriptome profiling of leukocytes via ribonucleic acid sequencing (RNAseq) was then performed and differentially expressed genes as well as significantly enriched gene sets were identified.Results: We enrolled seven COVID19+ (PCR positive, 2 SARS-CoV-2 genes) and seven age- and sex-matched COVID19- (PCR negative) control ICU patients. Cohorts were well-balanced with the exception that COVID19- patients had significantly higher total white blood cell counts and circulating neutrophils and COVID19+ patients were more likely to suffer bilateral pneumonia. The mortality rate for this cohort of COVID19+ ICU patients was 29%. Transcriptional analysis revealed that when compared to COVID19- patients, the altered transcriptional responses of leukocytes in critically ill COVID19+ ICU patients appeared to be associated with multiple interrelated outcomes, including but not limited to robust interferon (IFN)-associated transcriptional responses, a marked decrease in the transcriptional activity of genes contributing to protein synthesis and the dysregulated expression of genes that contribute to coagulation, platelet activation, Toll-like receptor activation, neurotrophin signalling, and protein SUMOylation/ubiquitination. Conclusions: Our findings demonstrate that critically ill COVID19+ patients on day 1 of admission to the ICU display a unique leukocyte transcriptional profile that distinguishes them from COVID19- patients, providing guidance for future targeted studies exploring novel prognostic and therapeutic aspects of COVID19.

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Pulmonary Arterial Thrombosis in COVID-19 With Fatal Outcome

Cited by 678 publications

References 48 publications

Fatality rate and predictors of mortality in a large Italian cohort of hospitalized COVID-19 patients

Fatality rate and predictors of mortality in a large Italian cohort of hospitalized COVID-19 patients

Direct or Collateral Liver Damage in SARS-CoV-2–Infected Patients

Transcriptional Profiling of Leukocytes in Critically Ill COVID19 Patients: Implications for Interferon Response and Coagulation

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