Correlations among different platelet aggregation pathways in a group of healthy volunteers
Alejandro Carazo,
Marcel Hrubša,
Lukáš Konečný,
Catherine Gunaseelan,
Jaka Fadraersada,
Pavel Skořepa,
Markéta Paclíková,
František Musil,
Jana Karlíčková,
Lenka Javorská,
Kateřina Matoušová,
Lenka Kujovská Krčmová,
Alena Šmahelová,
Vladimír Blaha,
Přemysl Mladenka
Affiliations
Alejandro Carazo
Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Králové, Charles University, Hradec Králové, Czech Republic
Marcel Hrubša
Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Králové, Charles University, Hradec Králové, Czech Republic
Lukáš Konečný
Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Králové, Charles University, Hradec Králové, Czech Republic
Catherine Gunaseelan
Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Králové, Charles University, Hradec Králové, Czech Republic
Jaka Fadraersada
Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Králové, Charles University, Hradec Králové, Czech Republic
Pavel Skořepa
3rd Department of Internal Medicine-Metabolic Care and Gerontology, University Hospital and Faculty of Medicine in Hradec Králové, Charles University, Hradec Králové, Czech Republic
Markéta Paclíková
3rd Department of Internal Medicine-Metabolic Care and Gerontology, University Hospital and Faculty of Medicine in Hradec Králové, Charles University, Hradec Králové, Czech Republic
František Musil
Department of Occupational Medicine, University Hospital and Faculty of Medicine in Hradec Kralove, Charles University, Hradec Králové, Czech Republic
Jana Karlíčková
Department of Pharmacognosy and Pharmaceutical Botany, Faculty of Pharmacy in Hradec Králové, Charles University, Hradec Králové, Czech Republic
Lenka Javorská
Department of Clinical Biochemistry and Diagnostics, University Hospital Hradec Králové, Hradec Králové, Czech Republic
Kateřina Matoušová
Department of Clinical Biochemistry and Diagnostics, University Hospital Hradec Králové, Hradec Králové, Czech Republic
Lenka Kujovská Krčmová
Department of Clinical Biochemistry and Diagnostics, University Hospital Hradec Králové, Hradec Králové, Czech Republic
Alena Šmahelová
3rd Department of Internal Medicine-Metabolic Care and Gerontology, University Hospital and Faculty of Medicine in Hradec Králové, Charles University, Hradec Králové, Czech Republic
Vladimír Blaha
3rd Department of Internal Medicine-Metabolic Care and Gerontology, University Hospital and Faculty of Medicine in Hradec Králové, Charles University, Hradec Králové, Czech Republic
Přemysl Mladenka
Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Králové, Charles University, Hradec Králové, Czech Republic
AbstractPlatelet aggregation is a complicated process mediated by different signaling pathways. As the process is highly complex and apparently redundant, the relationships between these pathways are not yet fully known. The aim of this project was to study the interconnections among seven different aggregation pathways in a group of 53 generally healthy volunteers aged 20 to 66 years. Platelet aggregation was induced with thrombin receptor activating peptide 6 (TRAP), arachidonic acid (AA), platelet activating factor 16 (PAF), ADP, collagen, thromboxane A2 analogue U46619 or ristocetin (platelet agglutination) ex vivo in fasting blood samples according to standardized timetable protocol. Additionally, some samples were pre-treated with known clinically used antiplatelet drugs (vorapaxar, ticagrelor or acetylsalicylic acid (ASA)). Significant correlations among all used inducers were detected (Pearson correlation coefficients (rP): 0.3 to 0.85). Of all the triggers, AA showed to be the best predictor of the response to other inducers with rP ranging from 0.66 to 0.85. Interestingly, the antiplatelet response to ticagrelor strongly predicted the response to unrelated drug vorapaxar (rP = 0.71). Our results indicate that a response to one inducer can predict the response for other triggers or even to an antiplatelet drug. These data are useful for future testing but should be also confirmed in patients.