Evidence map›Paper›PMID 32586214›Full record

ReviewCirculation research2020

The Emerging Threat of (Micro)Thrombosis in COVID-19 and Its Therapeutic Implications.

James D McFadyen, Hannah Stevens, Karlheinz Peter

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05036824 (Intensive Dose Tinzaparin in Hospitalized COVID19 Patients), which is not on this map. Cited by 348 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
348citing papers in PubMed, 6 pooled it
12.8field-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.

NCT05036824 unknown statusnot on this mapstarted 2021, after this paper: background citation

Intensive Dose Tinzaparin in Hospitalized COVID19 Patients

TypeobservationalSponsorUniversity Hospital of PatrasRan2021 to 2022Enrolled300ConditionsCovid19, HospitalizationArmstinzaparin
3 · Its place in the literature

Who cites it

348 citing papers in PubMed, 6 syntheses or guidelines pooled it, 613 citations in OpenAlex.

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  12. Five-year cardiovascular outcomes following COVID-19-associated carditis.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
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288 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

3 authors at 1 institution in 1 country.

James D McFadyen *From the Atherothrombosis and Vascular Biology Program, Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia (J.D.M., H.S., K.P.).
Hannah Stevens *From the Atherothrombosis and Vascular Biology Program, Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia (J.D.M., H.S., K.P.).
Karlheinz PeterDepartment of Cardiology (K.P.), Alfred Hospital, Melbourne, Victoria, Australia.
Baker Heart and Diabetes Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The recent emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the ensuing global pandemic has presented a health emergency of unprecedented magnitude. Recent clinical data has highlighted that coronavirus disease 2019 (COVID-19) is associated with a significant risk of thrombotic complications ranging from microvascular thrombosis, venous thromboembolic disease, and stroke. Importantly, thrombotic complications are markers of severe COVID-19 and are associated with multiorgan failure and increased mortality. The evidence to date supports the concept that the thrombotic manifestations of severe COVID-19 are due to the ability of SARS-CoV-2 to invade endothelial cells via ACE-2 (angiotensin-converting enzyme 2), which is expressed on the endothelial cell surface. However, in patients with COVID-19 the subsequent endothelial inflammation, complement activation, thrombin generation, platelet, and leukocyte recruitment, and the initiation of innate and adaptive immune responses culminate in immunothrombosis, ultimately causing (micro)thrombotic complications, such as deep vein thrombosis, pulmonary embolism, and stroke. Accordingly, the activation of coagulation (eg, as measured with plasma D-dimer) and thrombocytopenia have emerged as prognostic markers in COVID-19. Given thrombotic complications are central determinants of the high mortality rate in COVID-19, strategies to prevent thrombosis are of critical importance. Several antithrombotic drugs have been proposed as potential therapies to prevent COVID-19-associated thrombosis, including heparin, FXII inhibitors, fibrinolytic drugs, nafamostat, and dipyridamole, many of which also possess pleiotropic anti-inflammatory or antiviral effects. The growing awareness and mechanistic understanding of the prothrombotic state of COVID-19 patients are driving efforts to more stringent diagnostic screening for thrombotic complications and to the early institution of antithrombotic drugs, for both the prevention and therapy of thrombotic complications. The shifting paradigm of diagnostic and treatment strategies holds significant promise to reduce the burden of thrombotic complications and ultimately improve the prognosis for patients with COVID-19.

Indexed as

AnticoagulantsCoronavirus InfectionsCOVID-19HumansImmunity, InnatePandemicsPlatelet Aggregation InhibitorsPneumonia, ViralThrombosisAnticoagulantsPlatelet Aggregation Inhibitorscoronavirusmortalitystrokethrombosisviruses

Identifiers

PMID32586214
PMCPMC7386875
OpenAlexW3037447982

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.