Microvesicles from patients with acute coronary syndrome enhance platelet aggregation

• Published in: Scandinavian journal of clinical and laboratory investigation Vol. 79; no. 7; pp. 507 - 512
• Main Authors: Kafian, Sam, Wallén, Håkan, Samad, Bassem A., Mobarrez, Fariborz
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis 03.10.2019
• Subjects: acute coronary syndrome; Microvesicles; multiple electrode aggregometry; percutaneous coronary intervention; platelets aggregation; percutaneous coronary intervention; acute coronary syndrome; platelets aggregation; Microvesicles; multiple electrode aggregometry
• ISSN: 0036-5513; 1502-7686; 1502-7686
• DOI: 10.1080/00365513.2019.1663554

Microvesicles (MVs) released from leukocytes, platelets and endothelial cells are elevated in patients with acute coronary syndrome (ACS). In the present study, we assessed the potential pro-aggregatory properties of MVs obtained from ACS patients. Thus, we divided the patients into two groups based on clopidogrel-responsiveness, i.e. high on-treatment platelet reactivity (HPR; n = 16), and low or normal on-treatment platelet reactivity (non-HPR; n = 14), respectively. MVs from patients were obtained by high-speed centrifugation, and the pro-aggregatory effect of MVs added to fresh isolated platelets from healthy subjects were analyzed by 96-well microplate aggregometry. MVs from HPR patients significantly enhanced spontaneous platelet aggregation around two times more than MVs from non-HPR patients. The pro-aggregatory effect of three out of four MV phenotypes correlated to MV-concentrations as determined by flow cytometry. Furthermore, MVs from patients with diabetes mellitus (n = 9) had a stronger pro-aggregatory effect compared to MVs from those without diabetes (n = 21; p = .025 between groups). In conclusion, MVs from ACS patients with clopidogrel non-responsiveness enhance platelet aggregation, as do MVs from ACS patients with diabetes. Thus, MVs from patients with hyperreactive platelets boost platelet aggregation. Blocking MV-formation may reduce platelet hyperreactivity.