Ticagrelor Inhibits Toll-Like and Protease-Activated Receptor Mediated Platelet Activation in Acute Coronary Syndromes.


Journal

Cardiovascular drugs and therapy
ISSN: 1573-7241
Titre abrégé: Cardiovasc Drugs Ther
Pays: United States
ID NLM: 8712220

Informations de publication

Date de publication:
02 2020
Historique:
pubmed: 18 2 2020
medline: 21 10 2020
entrez: 17 2 2020
Statut: ppublish

Résumé

Since ticagrelor inhibits the cellular uptake of adenosine, thereby increasing extracellular adenosine concentration and biological activity, we hypothesized that ticagrelor has adenosine-dependent antiplatelet properties. In the current study, we compared the effects of ticagrelor and prasugrel on platelet activation in acute coronary syndrome (ACS). Platelet surface expression of P-selectin and activated glycoprotein (GP) IIb/IIIa in response to adenosine diphosphate (ADP), the toll-like receptor (TLR)-1/2 agonist Pam3CSK4, the TLR-4 agonist lipopolysaccharide (LPS), the protease-activated receptor (PAR)-1 agonist SFLLRN, and the PAR-4 agonist AYPGKF were measured by flow cytometry in blood from 80 ticagrelor- and 80 prasugrel-treated ACS patients on day 3 after percutaneous coronary intervention. Residual platelet aggregation to arachidonic acid (AA) and ADP were assessed by multiple electrode aggregometry and light transmission aggregometry. ADP-induced platelet activation and aggregation, and AA-induced platelet aggregation were similar in patients on ticagrelor and prasugrel, respectively (all p ≥ 0.3). Further, LPS-induced platelet surface expression of P-selectin and activated GPIIb/IIIa did not differ significantly between ticagrelor- and prasugrel-treated patients (both p > 0.4). In contrast, Pam3CSK4-induced platelet surface expression of P-selectin and activated GPIIb/IIIa were significantly lower in ticagrelor-treated patients (both p ≤ 0.005). Moreover, SFLLRN-induced platelet surface expression of P-selectin and activated GPIIb/IIIa were significantly less pronounced in patients on ticagrelor therapy compared to prasugrel-treated patients (both p < 0.03). Finally, PAR-4 mediated platelet activation as assessed by platelet surface expression of activated GPIIb/IIIa following stimulation with AYPGKF was significantly lower in patients receiving ticagrelor (p = 0.02). Ticagrelor inhibits TLR-1/2 and PAR mediated platelet activation in ACS patients more strongly than prasugrel.

Identifiants

pubmed: 32062795
doi: 10.1007/s10557-019-06932-7
pii: 10.1007/s10557-019-06932-7
pmc: PMC7093367
doi:

Substances chimiques

P-Selectin 0
Platelet Aggregation Inhibitors 0
Platelet Glycoprotein GPIIb-IIIa Complex 0
Purinergic P2Y Receptor Antagonists 0
Receptors, Proteinase-Activated 0
SELP protein, human 0
Toll-Like Receptors 0
Prasugrel Hydrochloride G89JQ59I13
Ticagrelor GLH0314RVC

Types de publication

Comparative Study Journal Article Observational Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

53-63

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Auteurs

Patricia P Wadowski (PP)

Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.

Constantin Weikert (C)

Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.

Joseph Pultar (J)

Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.

Silvia Lee (S)

Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.

Beate Eichelberger (B)

Department of Blood Group Serology and Transfusion Medicine, Medical University of Vienna, Vienna, Austria.

Renate Koppensteiner (R)

Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.

Irene M Lang (IM)

Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria.

Simon Panzer (S)

Department of Blood Group Serology and Transfusion Medicine, Medical University of Vienna, Vienna, Austria.

Thomas Gremmel (T)

Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria. thomas.gremmel@meduniwien.ac.at.
Department of Internal Medicine, Cardiology and Nephrology, Landesklinikum Wiener Neustadt, Wiener Neustadt, Austria. thomas.gremmel@meduniwien.ac.at.

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Classifications MeSH