Amerikanische Gesellschaft für Hirudotherapie

Dabigatran enhances platelet reactivity and platelet thrombin receptor expression in patients with atrial fibrillation.

Research article published in Journal of thrombosis and haemostasis : JTH (2017)

Zuletzt aktualisiert: June 18, 2026Geprüft von: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Research reportKlinische StudienArzneimittelentwicklungAchilles et al. · Journal of thrombosis and haemostasis : JTH, 2017

Abstract

UNLABELLED: Essentials Whether or not dabigatran enhances the risk of myocardial infarction is under discussion. We measured platelet reactivity and thrombin receptor expression in dabigatran patients. Platelet reactivity and thrombin receptor expression is enhanced during dabigatran treatment. This should be considered when choosing the optimal direct oral anticoagulant for individuals. SUMMARY: Background The direct oral anticoagulant (DOAC) dabigatran is a direct thrombin inhibitor. Its landmark trial, the RE-LY study, observed a trend towards a higher incidence of myocardial infarctions (MIs) in dabigatran-treated patients. Since then, there have been discussions on whether dabigatran increases the risk of MI. Objective In this study, we aimed to assess platelet reactivity and platelet thrombin receptor expression in dabigatran-treated patients. Methods We conducted a cross-sectional study in 13 hospitalized patients with planned initiation of dabigatran medication. Platelet reactivity was measured by light-transmission aggregometry and platelet thrombin receptor expression was measured by flow cytometry analysis. Results Platelet reactivity was higher after initiation of dabigatran medication as compared with baseline (baseline 44 ± 24% vs. dabigatran 70 ± 25%). Accordingly, the density of both platelet thrombin receptors (protease activated receptor [PAR]-1 and PAR-4) on platelets increased during dabigatran treatment (PAR1, baseline 63 ± 11% vs. dabigatran 70 ± 10%; PAR4, baseline 1.1 ± 0.5% vs. dabigatran 1.6 ± 0.9%). Conclusions Dabigatran increases platelet reactivity by enhancing the thrombin receptor density on platelets. This finding should be considered while choosing the optimal DOAC in individualized medicine.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal ArticleResearch Support, Non-U.S. Gov't
Indexed MeSH termsAdministration, OralAgedAnticoagulantsArachidonic AcidAtrial FibrillationBlood PlateletsCollagenCross-Sectional StudiesDabigatranFemaleFlow CytometryGene Expression Regulation

Zusammenfassung

Essentials Whether or not dabigatran enhances the risk of myocardial infarction is under discussion. We measured platelet reactivity and thrombin receptor expression in dabigatran patients.

Warum dies für die Hirudotherapie relevant ist

This cross-sectional study of 13 hospitalized patients with planned initiation of dabigatran medication assessed platelet reactivity by light-transmission aggregometry and platelet thrombin receptor expression by flow cytometry, finding that dabigatran treatment was associated with increased platelet reactivity and enhanced density of both platelet thrombin receptors (PAR-1 and PAR-4) compared to baseline. The abstract describes dabigatran as a direct thrombin inhibitor but does not mention hirudin, leeches, hirudotherapy, or any connection to the leech secretome. There is no defensible leech link in this article.

Zitation

Dabigatran enhances platelet reactivity and platelet thrombin receptor expression in patients with atrial fibrillation.

Achilles et al. · Journal of thrombosis and haemostasis : JTH, 2017

Verwandter klinischer Kontext

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