MicroRNA dynamics and their link to platelet function following acute ST-segment elevation myocardial infarction

Reduced effect of antiplatelet therapy has been observed in patients with ST-segment elevation myocardial infarction (STEMI). MicroRNA (miR) expression may serve as biomarkers for platelet function and the effect of antiplatelet therapy.

In acute STEMI patients, we investigated changes in miR expression from the acute event to a more stable phase, and evaluated their association with platelet function at both time points to assess their potential as biomarkers of antiplatelet therapy efficacy.

Patients admitted with acute STEMI for primary percutaneous coronary intervention were included and treated according to guidelines. Samples were collected within 24 h after admission and at 2-3 months after enrolment. Expression of candidate miRs, platelet reactivity markers evaluated by flow cytometry, platelet impedance aggregometry and serum thromboxane B₂ were measured at both time points.

Samples were obtained in 44 STEMI patients. Two miRs (miR-15a-5p and miR-21-5p) showed lower, whereas five (miR-26b-5p, miR-126-3p, miR-150-5p, miR-223-3p and miR-423-5p) showed higher expression at follow-up than at baseline. At baseline, miR-26b-5p expression consistently correlated with the expression of the fibrinogen receptor on activated platelets, across different agonists (rho: from 0.29 to 0.32, p < 0.05). At follow-up, miR-93-5p expression was associated with platelet aggregation using various agonists (rho: from -0.39 to -0.47, p < 0.02).

Seven miRs were differentially expressed at follow-up compared to baseline. Several miRs were linked to platelet function at baseline and follow-up, suggesting that a single miR may not be sufficient as a biomarker for platelet function and the effect of antiplatelet therapy.