Why the study?
Does ex vivo treatment with epigallocatechin-3-gallate (EGCG) reduce platelet aggregation and adhesion in patients taking aspirin, clopidogrel, ticagrelor, or no anti-platelet medication?
Does ex vivo treatment with epigallocatechin-3-gallate (EGCG) reduce platelet aggregation and adhesion in patients taking aspirin, clopidogrel, ticagrelor, or no anti-platelet medication?
Ex vivo EGCG inhibits platelet aggregation and adhesion but does not further suppress aggregation in patients already taking specific anti-platelet agents, suggesting a potential complementary anti-platelet effect without increasing bleeding risk.
May augment ex vivo antiplatelet effects with standard agents; hypothesis-generating, clinical trials needed before any practice consideration.
Background/Aims: Although epigallocatechin-3-gallate (EGCG), which is found in high contents in the dried leaves of green tea, has been reported to have an anti-platelet effect, synergistic effects of EGCG in addition to current anti-platelet medications remains to be elucidated. Methods: Blood samples were obtained from 40 participants who took aspirin (ASA, n = 10), clopidogrel (CPD, n = 10), ticagrelor (TCG, n = 10) and no anti-platelet medication (Control, n = 10). Ex vivo platelet aggregation and adhesion under various stimulators were analyzed by multiple electrode aggregometry (MEA) and Impact-R systems. PAC-1 and P-selectin expressions in human platelets were analyzed by flow cytometry. Results: In MEA analysis, adenosine diphosphate (ADP) and thrombin receptor activating peptide (TRAP)-induced platelet aggregations were lower in the CPD and the TCG groups; arachidonic acid (AA)-induced platelet aggregation was lower in the ASA group, whereas collagen (COL)-induced platelet aggregations were comparable among four groups. EGCG significantly reduced ADP-and COL-induced platelet aggregation in dose-dependent manner (ADP, p = 0.04; COL, p < 0.01). There were no additional suppressions of platelet aggregation stimulated by AA in the ASA group, and by ADP in the CPD and TCG groups. Moreover, EGCG suppressed shear stress-induced platelet adhesion on Impact-R, and had no effect on P-selectin and PAC-1 expressions. Conclusions: Ex vivo treatment of EGCG inhibited platelet adhesion and aggregation without changes in P-selectin and PAC-1 expression. There was no additional suppressions in platelet aggregation stimulated by AA in the ASA group and ADP in the CPD and TCG groups.
No takes yet. Share an insight, caveat, or question.
Joo et al. (2017) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: