Evidence map›Paper›PMID 32558620›Full record

ReviewVascular medicine (London, England)2020

COVID-19-associated coagulopathy: An exploration of mechanisms.

Meaghan E Colling, Yogendra Kanthi

Open access · hybridAbstract readReview
In one paragraph

Review in Vascular medicine (London, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed, 5 pooled it
39.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

145 citing papers in PubMed, 5 syntheses or guidelines pooled it, 284 citations in OpenAlex.

  1. Pooled it
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  3. Meta-analysis of cardiac markers for predictive factors on severity and mortality of COVID-19.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2021
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85 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Meaghan E CollingDivision of Intramural Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Yogendra KanthiDepartment of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan, and Ann Arbor Veterans Administration Healthcare System, Ann Arbor, MI, USA.ORCID 0000-0002-5660-5194
National Institutes of Health · USUniversity of Michigan · US

Funding

Purinergic regulation of Innate Immunity to promote Venous HomeostasisR01HL150392 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PINSKY, DAVID J. · 2020 to 2024
$2.2M
CD39 in Vein Graft ArterializationK08HL131993 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KANTHI, YOGENDRA · 2016 to 2020
$837k
NHLBI NIH HHS K08 HL131993NHLBI NIH HHS R01 HL150392
6 · The paper itself

Abstract

An ongoing global pandemic of viral pneumonia (coronavirus disease [COVID-19]), due to the virus SARS-CoV-2, has infected millions of people and remains a threat to many more. Most critically ill patients have respiratory failure and there is an international effort to understand mechanisms and predictors of disease severity. Coagulopathy, characterized by elevations in D-dimer and fibrin(ogen) degradation products (FDPs), is associated with critical illness and mortality in patients with COVID-19. Furthermore, increasing reports of microvascular and macrovascular thrombi suggest that hemostatic imbalances may contribute to the pathophysiology of SARS-CoV-2 infection. We review the laboratory and clinical findings of patients with COVID-19-associated coagulopathy, and prior studies of hemostasis in other viral infections and acute respiratory distress syndrome. We hypothesize that an imbalance between coagulation and inflammation may result in a hypercoagulable state. Although thrombosis initiated by the innate immune system is hypothesized to limit SARS-CoV-2 dissemination, aberrant activation of this system can cause endothelial injury resulting in loss of thromboprotective mechanisms, excess thrombin generation, and dysregulation of fibrinolysis and thrombosis. The role various components including neutrophils, neutrophil extracellular traps, activated platelets, microparticles, clotting factors, inflammatory cytokines, and complement play in this process remains an area of active investigation and ongoing clinical trials target these different pathways in COVID-19.

Indexed as

BetacoronavirusBlood Coagulation DisordersCoronavirus InfectionsCOVID-19HumansPandemicsPneumonia, ViralSARS-CoV-2anticoagulationantiplateletCOVID-19inflammationneutrophilsthrombosisvascular endotheliumvenous thromboembolism (VTE)

Identifiers

PMID32558620
PMCPMC7306998
OpenAlexW3036107018

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.