Patients with unstable angina present clinical characteristics of atherosclerotic plaque vulnerability, contrary to chronic coronary syndrome patients. The process of athersclerotic plaque destabilization is also regulated by microRNA particles. In this study, the investigation on expression levels of microRNAs inhibiting the expression of proteins that protect from atherosclerotic plaque progression (miR-92a inhibiting KLF2, miR-10b inhibiting KLF4, miR-126 inhibiting MerTK, miR-98 inhibiting IL-10, miR-29b inhibiting TGFβ1) was undertaken. A number of 62 individuals were enrolled-unstable angina (UA, = 14), chronic coronary syndrome (CCS, = 38), and healthy volunteers (HV, = 10). Plasma samples were taken, and microRNAs expression levels were assessed by qRT-PCR. UA patients presented significantly increased miR-10b levels compared to CCS patients (0.097 vs. 0.058, = 0.033). Moreover, in additional analysis when UA patients were grouped together with stable patients with significant plaque in left main or proximal left anterior descending ("UA and LM/proxLAD" group, = 29 patients) and compared to CCS patients with atherosclerotic lesions in other regions of coronary circulation ("CCS other" group, = 25 patients) the expression levels of both miR-10b (0.104 vs. 0.046; = 0.0032) and miR-92a (92.64 vs. 54.74; = 0.0129) were significantly elevated. , the study revealed significantly increased expression levels of miR-10b and miR-92a, a regulator of endothelial protective KLF factors (KLF4 and KLF2, respectively) in patients with more vulnerable plaque phenotypes.