Evidence map›Paper›PMID 33625645›Full record

ArticleJournal of thrombosis and thrombolysis2021

Global coagulation assays in healthy controls: are there compensatory mechanisms within the coagulation system?

Hui Yin Lim, Brandon Lui, Mark Tacey, Carly Selan, Geoffrey Donnan, Louise M Burrell, Harshal Nandurkar, Prahlad Ho

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In one paragraph

Article in Journal of thrombosis and thrombolysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Global coagulation assays in hypercoagulable states.Journal of thrombosis and thrombolysis · 2022
    Review
  7. Global coagulation assays in patients with diabetes mellitus.Research and practice in thrombosis and haemostasis · 2021
    Article
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

8 authors at 5 institutions in 1 country.

Hui Yin LimDepartment of Haematology, Northern Hospital, 185 Cooper St, Epping, VIC, 3076, Australia. huiyin.lim@nh.org.au.ORCID http://orcid.org/0000-0003-2455-3155
Brandon LuiDepartment of Haematology, Northern Hospital, 185 Cooper St, Epping, VIC, 3076, Australia.
Mark TaceyThe Northern Hospital, Epping, VIC, Australia.
Carly SelanAustralian Centre for Blood Diseases, Monash University, Melbourne, VIC, Australia.
Geoffrey DonnanThe Melbourne Brain Centre, Royal Melbourne Hospital, University of Melbourne, Parkville, VIC, Australia.
Louise M BurrellDepartment of Medicine, Austin Health, University of Melbourne, Heidelberg, VIC, Australia.
Harshal NandurkarAustralian Centre for Blood Diseases, Monash University, Melbourne, VIC, Australia.
Prahlad HoDepartment of Haematology, Northern Hospital, 185 Cooper St, Epping, VIC, 3076, Australia.
The University of Melbourne · AUAustralian Centre for HIV and Hepatitis Virology Research · AUNorthern Health · AUNorthern Hospital · AUThe Royal Melbourne Hospital · AU

Funding

National Health and Medical Research Council APP1151535
6 · The paper itself

Abstract

Global coagulation assays (GCAs) may provide a more comprehensive individual hemostatic profiling. We aim to evaluate GCAs (thromboelastography, thrombin generation) in healthy controls, and correlate results with age, gender, lipid status, tissue factor pathway inhibitor (TFPI) and P-selectin. Blood samples were collected from healthy controls (> 18 years of age) not taking anticoagulation or antiplatelet agents and without known cardiovascular disease. Thromboelastography (TEG) was performed on citrated whole blood while calibrated automated thrombogram (CAT), P-selectin (endothelial marker) and TFPI (principle inhibitor of tissue factor-initiated coagulation) were performed on platelet-poor plasma. 153 healthy controls (mean age 42 years, 98 females (64%)) were recruited. Female controls demonstrated more hypercoagulable TEG and CAT parameters while those over 50 years of age demonstrated more hypercoagulable TEG parameters despite comparable thrombin generation. Paradoxically, individuals with "flattened" thrombin curves (lower velocity index (rate of thrombin generation) despite preserved endogenous thrombin potential (amount of thrombin)) were more likely to be male (49% vs 20%, p = 0.003) with increased low-density lipoprotein cholesterol (3.3 vs 2.6 mmol/L, p = 0.003), P-selectin (54.2 vs 47.3 ng/mL, p = 0.038) and TFPI (18.7 vs 8.6 ng/ml, p = 0.001). In addition to reduced velocity index and thrombin peak, controls in the highest TFPI tertile also demonstrated a poorer lipid profile. GCAs can detect subtle changes of the hemostatic profile. Interestingly, reduced thrombin generation was paradoxically associated with increased cardiovascular risk factors, possibly attributable to increased TFPI. This finding may suggest compensation by the coagulation system in response to endothelial activation and represent a biomarker for early cardiovascular disease. A larger prospective study evaluating these assays in the cardiovascular disease population is ongoing.

Indexed as

Cardiovascular DiseasesHemostaticsBlood Coagulation TestsFemaleHumansMaleProspective StudiesP-SelectinThrombinHemostaticsP-SelectinThrombinBlood coagulation testsCardiovascular diseaseThrombinThromboelastographyTissue factor pathway inhibitor

Identifiers

PMID33625645
OpenAlexW3132611423

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.