Evidence map›Paper›PMID 38151494›Full record

ArticleScientific reports2023

Antithrombotic and prohemorrhagic actions of different concentrations of apixaban in patients exposed to single and dual antiplatelet regimens.

Julia Martinez-Sanchez, Leticia Castrillo, Didac Jerez, Sergi Torramade-Moix, Marta Palomo, Guiomar Mendieta, M Urooj Zafar, Ana Belén Moreno-Castaño, Pablo Sanchez, Juan Jose Badimon and 3 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 61% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. 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

13 authors at 4 institutions in 2 countries.

Julia Martinez-Sanchez *Hemostasis and Erythropathology LaboratoryHematopathologyDepartment of Pathology, Centre de Diagnostic Biomedic (CDB), Hospital Clinic de Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Barcelona, Spain.
Leticia Castrillo *Department of Cardiology, ICCV, Hospital Clinic de Barcelona, IDIBAPS, Universitat de Barcelona, Villarroel 170, 08036, Barcelona, Spain.
Didac JerezHemostasis and Erythropathology LaboratoryHematopathologyDepartment of Pathology, Centre de Diagnostic Biomedic (CDB), Hospital Clinic de Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Barcelona, Spain.
Sergi Torramade-MoixHemostasis and Erythropathology LaboratoryHematopathologyDepartment of Pathology, Centre de Diagnostic Biomedic (CDB), Hospital Clinic de Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Barcelona, Spain.
Marta PalomoHemostasis and Erythropathology LaboratoryHematopathologyDepartment of Pathology, Centre de Diagnostic Biomedic (CDB), Hospital Clinic de Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Barcelona, Spain.
Guiomar MendietaDepartment of Cardiology, ICCV, Hospital Clinic de Barcelona, IDIBAPS, Universitat de Barcelona, Villarroel 170, 08036, Barcelona, Spain.
M Urooj ZafarDepartment of Medicine, AtheroThrombosis Research Unit (ATRU), Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, USA.
Ana Belén Moreno-CastañoHemostasis and Erythropathology LaboratoryHematopathologyDepartment of Pathology, Centre de Diagnostic Biomedic (CDB), Hospital Clinic de Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Barcelona, Spain.
Pablo SanchezDepartment of Marine Biology and Oceanography, Institut de Ciències del Mar, Spanish National Research Council, Barcelona, Spain.
Juan Jose BadimonDepartment of Medicine, AtheroThrombosis Research Unit (ATRU), Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, USA.
Maribel Diaz-RicartHemostasis and Erythropathology LaboratoryHematopathologyDepartment of Pathology, Centre de Diagnostic Biomedic (CDB), Hospital Clinic de Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Barcelona, Spain.
Gines EscolarHemostasis and Erythropathology LaboratoryHematopathologyDepartment of Pathology, Centre de Diagnostic Biomedic (CDB), Hospital Clinic de Barcelona, Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona, Barcelona, Spain.
Mercè RoquéDepartment of Cardiology, ICCV, Hospital Clinic de Barcelona, IDIBAPS, Universitat de Barcelona, Villarroel 170, 08036, Barcelona, Spain. mroque@clinic.cat.
Hospital Clínic de Barcelona · ESConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESIcahn School of Medicine at Mount Sinai · USInstitut de Ciències del Mar · ES

Funding

ERISTA (Bristol Myers Squibb and Pfizer) ERISTA2016Fundació la Marató de TV3 202026-10Generalitat de Catalunya 2017-SGR675, CERCAInstituto de Salud Carlos III FIS PI19/00888José Carreras Leukämie-Stiftung 03R/2019
6 · The paper itself

Abstract

We evaluated modifications in the hemostatic balance of different concentrations of apixaban (APIX) in 25 healthy donors and 53 patients treated with aspirin (ASA, n = 21), ASA and clopidogrel (ASA + CLOPI, n = 11), or ASA and ticagrelor (ASA + TICA, n = 21). Blood samples from participants were spiked ex vivo with apixaban 0 (APIX0), 40 (APIX40), and 160 ng/mL (APIX160). We assessed the effects of APIX on (1) clot formation, by ROTEM thromboelastometry; (2) thrombin generation primed by platelets; and (3) platelet and fibrin interactions with a thrombogenic surface, in a microfluidic model with circulating blood. APIX caused dose-related prolongations of clotting time with minimal impact on other ROTEM parameters. Thrombin generation was significantly inhibited by APIX160, with ASA + TICA actions showing the strongest inhibition (p < 0.01 vs APIX0). Microfluidic studies showed that APIX160 was more potent at suppressing platelet and fibrin interactions (p < 0.001 vs. APIX0). APIX40 demonstrated a consistent antithrombotic action but with a favorable protective effect on the structural quality of fibrin. APIX potentiated the antithrombotic effects of current antiplatelet regimens. APIX at 40 ng/mL, enhanced the antithrombotic action of single or dual antiplatelet regimens but was more conservative for hemostasis than the 160 ng/mL concentration.

Indexed as

Fibrinolytic AgentsThrombinAspirinBlood PlateletsFibrinHumansPlatelet Aggregation InhibitorsPyrazolesPyridonesapixabanAspirinFibrinFibrinolytic AgentsPlatelet Aggregation InhibitorsPyrazolesPyridonesThrombin

Identifiers

PMID38151494
PMCPMC10752876
OpenAlexW4390268267

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.