The Kinetics of Platelet-derived Microparticles in Patients with ST Segment Elevation Acute Myocardial Infarction under Pharmacological Suppression of Platelet Aggregation

Scientific Research Question: Platelet derived microparticles (PDMP) are associated with the presence and severity of cardiovascular disorders, especially those with atherothrombotic component. The effect of acute coronary ischemia, necrobiosis and necrosis on PDMP release and vise versa is not fully understood, as well as impact of antiplatelet therapy on this process. We suppose that the PDMP kinetics in acute coronary syndrome (ACS) way serves as a key for deciphering the pathogenetic role of PDMP in intracoronary thrombosis and its possible clinical impact.

Methodology: 130 patients with ACS (30 … 86 yo) treated with aspirin + P2Y12 inhibitor were involved in the study. Size distribution and zeta potential of microparticles (MP) in circulation were measured by means of the Zetasizer Nano ZS Analyser. PDMP and thrombopoietin (TPO) levels were serially measured by ELISA: at admission to cardiac intensive care unit; on the second and seventh days. Platelet aggregation and secretion was assessed by impedance and luminescence aggregometry by Chronolog-700.

Findings: According to particles size there were detected three MP pools in ACS patients circulation: 1st - 35–70 nm, 2nd - 9–21 nm and 3d - 300 nm and larger. The peaks intensity differed in patients with unstable angina vs ST elevation myocardial infarction (STEMI): 1 - 78.8 (75.6; 84.5) vs 89.8 (82.7; 98.45)%, p = 0.000; 2 - (17.4 (12.7; 20.6) vs 12.0 (4.2; 15.4)%, p = 0.007). Peak 2 intensity positively correlated with platelet count (R = 0.435, p < 0.05). PDMP levels in STEMI measured at admission varied from 2.3 ng/mL up to 119.4 ng/mL. During the 7-days observation there was statistically significant change in PDMP, which depended on the initial PDMP level. In patients with PDMP level lower than 12,7 ng/mL it was monotonous increase (KW test p = 0.000); in patients with PDMP 12,7 - 39,5 ng/mL after PDMP increase on the second day of observation, it maintained on the relatively constant level (KW test p = 0.027); and in patients with initial PDMP level > 39,85 ng/mL it remained constant during all the observation period. Those subgroups of STEMI patients differed in age, MPV and D-dimer (KW test p = 0.049; 0.034 and 0.042 relatively). We failed to detect any association between PDMP level and studied platelet aggregation and secretion parameters. PDMP level at the seventh day revealed a strong positive correlation with initial values of TPO (R = 0,608, p < 0,05).

Conclusions: Received results illustrate the presence of MP from at least three cell sources including platelets in circulation of ACS patients. Pharmacological suppression of platelet aggregation resulted in leveling of the PDMP release in STEMI patients. Obtained data suggest an impact of platelet production on PMPD kinetics. In STEMI patients treated with double antiplatelet therapy PDMP release correlated with severity of intracoronary thrombosis, but not via platelet mechanism.