Acute myocardial infarction (AMI) is one of the leading causes of morbidity and mortality worldwide, while early diagnosis still represents an upmost priority. While platelet activation is critical for AMI pathogenesis, the role of platelet microRNAs (pmiRNAs) as biomarkers for AMI is unclear. Furthermore, correlations between the levels of pmiRNAs and indices of platelet activity are also unknown. Expression of platelet miR-1, miR-21, miR-126, miR-150 and miR-223 were prospectively assessed in 20 ST-segment elevation myocardial infarction (STEMI) patients, and 40 healthy volunteers. Platelet reactive units (PRU) were assessed with cartridge analyzer, and vasodilator-stimulated phosphoprotein (VASP) was measured by flow cytometry. There were no significant changes in pmiR-1 expression. Expressions of pmiR-21 and pmiR-126 were decreased, while pmiR-150 and pmiR-223 were increased in STEMI patients when compared to controls (all p < 0.01). However, only pmiR-126 exhibited correlation with plasma cardiac troponin I (r = - 0.556, p = 0.011) in STEMI. There was no correlation between pmiRNAs with PRU or VASP during admission, or at 48 h post-stenting. Among tested pmiRNAs, pmiR-126 may serve as a potential novel biomarker for STEMI, while pmiR-1, pmiR-21, pmiR-150, and pmiR-223 were not particularly useful. Moreover, since assessed pmiRNA expression did not correlate well with platelet activity indices their potential diagnostic utility is quite limited.
Keywords: Acute myocardial infarction; Antiplatelet therapy; Biomarkers; Platelet microRNAs; Platelet reactivity.