ObjectiveTo explore the relationship of platelet-activating factors and vascular endothelial activity markers to lacunar infarction (LI).MethodsA total of 100 inpatients diagnosed with LI in Shaanxi Provincial People’s Hospital between March 2018 and February 2019 were included, and 100 matched healthy controls were collected. Basic information, clinical baseline data, laboratory examinations, cerebral MRI and treatment data were collected after admission. The platelet-activating factors (platelet membrane glycoprotein Ⅱb/Ⅲa receptor and P-selectin) and vascular endothelial activity markers [von Willebrand factor (vWF), homocysteine (HCY), and high-sensitivity C-reactive protein (hsCRP)] levels of patients with LI were detected one month and three months after onset, and those of the control group were decteted when they were selected. SPSS 25.0 software was used for statistical analysis.ResultsAt one month after onset, there was no statistically significant difference in the levels of platelet activating factors between the LI group and the control group [platelet membrane glycoprotein Ⅱb/Ⅲa receptor: (2.84±1.00)% vs. (2.59±0.96)%, P=0.065; P-selectin: (3.05±0.63)% vs. (2.98±0.59)%, P=0.419], while the differences in the levels of vascular endothelial activity markers between the two groups were statistically significant [vWF: (141.80±17.60) vs. (124.63±10.65) ng/mL, P<0.001; hsCRP: (5.53±1.37) vs. (2.17±0.55) mg/L, P<0.001; HCY: (18.76±4.07) vs. (15.81±2.63) mmol/L, P<0.001]. At three months after onset, 94 LI patients were followed up. The levels of vWF and hsCRP between the 100 patients one month after onset and the 94 patients three months after onset were statistically different [(vWF: (141.80±17.60) vs. (134.86±13.35) ng/mL, P=0.002; hsCRP: (5.53±1.37) vs. (2.63±0.55) mg/L, P<0.001], but there was no statistically significant difference between the two time points in the levels of HCY or platelet-activating factors (P>0.05).ConclusionChronic platelet activation may not play a core role in LI pathophysiology, and endothelial dysfunction may be one of the pathological mechanisms of LI.