Evidence map›Paper›PMID 35471714›Full record

ReviewClinical and experimental medicine2023

Pathophysiology of deep vein thrombosis.

Simón Navarrete, Carla Solar, Roberto Tapia, Jaime Pereira, Eduardo Fuentes, Iván Palomo

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical and experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
25.0field-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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.

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10 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

6 authors at 2 institutions in 1 country.

Simón NavarreteThrombosis Research Center, Medical Technology School, Department of Clinical Biochemistry and Immunohaematology, Faculty of Health Sciences, Universidad de Talca, Av. Lircay s/n, 3460000, Talca, Chile.ORCID http://orcid.org/0000-0001-5296-1215
Carla SolarThrombosis Research Center, Medical Technology School, Department of Clinical Biochemistry and Immunohaematology, Faculty of Health Sciences, Universidad de Talca, Av. Lircay s/n, 3460000, Talca, Chile.
Roberto TapiaMedicine School, Universidad de Talca, Talca, Chile.
Jaime PereiraDepartment of Hematology-Oncology, School of Medicine, Pontificia Universidad Católica de Chile, Santiago, Chile.
Eduardo FuentesThrombosis Research Center, Medical Technology School, Department of Clinical Biochemistry and Immunohaematology, Faculty of Health Sciences, Universidad de Talca, Av. Lircay s/n, 3460000, Talca, Chile.
Iván PalomoThrombosis Research Center, Medical Technology School, Department of Clinical Biochemistry and Immunohaematology, Faculty of Health Sciences, Universidad de Talca, Av. Lircay s/n, 3460000, Talca, Chile. ipalomo@utalca.cl.
University of Talca · CLPontificia Universidad Católica de Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deep venous thrombosis is a frequent, multifactorial disease and a leading cause of morbidity and mortality. Most of the time deep venous thrombosis is triggered by the interaction between acquired risk factors, such as hip fracture, pregnancy, and immobility, and hereditary risk factors such as thrombophilias. The mechanisms underlying deep venous thrombosis are not fully elucidated; however, in recent years, important advances have shed light on the role of venous flow, endothelium, platelets, leukocytes, and the interaction between inflammation and hemostasis. It has been described that the alteration of venous blood flow produces endothelial activation, favoring the adhesion of platelets and leukocytes, which, through tissue factor expression and neutrophil extracellular traps formation, contribute to the activation of coagulation, trapping more cells, such as red blood cells. Thus, the concerted interaction of these phenomena allows the formation and growth of the thrombus. In this work, the main mechanisms involved in the pathophysiology of deep vein thrombosis will be described.

Indexed as

Venous ThrombosisBlood CoagulationBlood PlateletsHumansInflammationLeukocytesCoagulationDVTEndotheliumLeukocytePlateletVenous valves

Identifiers

PMID35471714
OpenAlexW4224435868

What OpenQuestion holds

Textmetadata
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.