期刊
JOURNAL OF CLINICAL MEDICINE
卷 10, 期 5, 页码 -出版社
MDPI
DOI: 10.3390/jcm10051024
关键词
extracellular vesicles; platelet reactivity; prostacyclin analogues; pulmonary arterial hypertension; thrombus formation
资金
- Centre of Postgraduate Medical Education, Warsaw, Poland [501-1-54-25-18]
- PRELUDIUM Grant of the Polish National Science Centre [2018/31/N/NZ7/02260]
- Netherlands Organisation for Scientific Research-Domain Applied and Engineering Sciences (NWO-TTW), research program VENI [15924]
The study showed that PAH patients treated with prostacyclin analogues had impaired platelet reactivity, EV release, and thrombus formation compared to those not receiving prostacyclin analogues.
(1) Background: Prostacyclin analogues (epoprostenol, treprostinil, and iloprost) induce vasodilation in pulmonary arterial hypertension (PAH) but also inhibit platelet function. (2) Objectives: We assessed platelet function in PAH patients treated with prostacyclin analogues and not receiving prostacyclin analogues. (3) Methods: Venous blood was collected from 42 patients treated with prostacyclin analogues (49.5 +/- 15.9 years, 81% female) and 38 patients not receiving prostacyclin analogues (55.5 +/- 15.6 years, 74% female). Platelet reactivity was analyzed by impedance aggregometry using arachidonic acid (AA; 0.5 mM), adenosine diphosphate (ADP; 6.5 mu M), and thrombin receptor-activating peptide (TRAP; 32 mu M) as agonists. In a subset of patients, concentrations of extracellular vesicles (EVs) from all platelets (CD61(+)), activated platelets (CD61(+)/CD62P(+)), leukocytes (CD45(+)), and endothelial cells (CD146(+)) were analyzed by flow cytometry. Platelet-rich thrombus formation was measured using a whole blood perfusion system. (4) Results: Compared to controls, PAH patients treated with prostacyclin analogues had lower platelet reactivity in response to AA and ADP (p = 0.01 for both), lower concentrations of platelet and leukocyte EVs (p <= 0.04), delayed thrombus formation (p <= 0.003), and decreased thrombus size (p = 0.008). Epoprostenol did not affect platelet reactivity but decreased the concentrations of platelet and leukocyte EVs (p <= 0.04). Treprostinil decreased platelet reactivity in response to AA and ADP (p <= 0.02) but had no effect on the concentrations of EVs. All prostacyclin analogues delayed thrombus formation and decreased thrombus size (p <= 0.04). (5) Conclusions: PAH patients treated with prostacyclin analogues had impaired platelet reactivity, EV release, and thrombus formation, compared to patients not receiving prostacyclin analogues.
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