Abstract:Objective To explore the differences in platelet aggregation level induced by peripheral blood arachidonic acid (AA), adenosine diphosphate (ADP) and collagen (COL) in different classifications of cerebral infarction, and to evaluate their correlation with carotid intima-media thickness (IMT) and plaque formation. Methods A total of 80 patients with cerebral infarction admitted to Neurology Department of the Second People's Hospital of Pingdingshan were enrolled as cerebral infarction group between April 2022 and February 2025. According to TOAST classification criteria, they were divided into large artery atherosclerosis (LAA group, n=40), cardiogenic embolism (CE group, n=24) and small artery occlusion (SAO group, n=16). According to carotid IMT by carotid ultrasound, they were divided into plaque formation group (n=38), intima thickening group (n=24) and normal intima group (n=18). The general data and laboratory indexes in patients with cerebral infarction were collected and compared. The related factors of cerebral infarction classifications were analyzed by Logistic regression analysis, and diagnostic value of platelet aggregation rate in carotid plaque formation was evaluated by ROC curves. Results There was no significant difference in gender, age, diabetes mellitus or drinking among LAA group, CE group and SAO group (P>0.05), but there were significant differences in the incidences of hypertension and arrhythmia, total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and platelet aggregation rate induced by AA, ADP and COL among the three groups (P<0.05). Logistic regression analysis showed that hypertension history, increased platelet aggregation rate induced by AA, ADP and COL, and decreased HDL-C were influencing factors of cerebral infarction classifications (P<0.05). In plaque formation group, intima thickening group and normal intima group, HDL-C level was gradually increased, while platelet aggregation rate induced by AA, ADP and COL was gradually decreased (P<0.05). ROC curves analysis showed that area under ROC curve (AUC) values of platelet aggregation rate induced by AA, ADP and COL in the diagnosis of plaque formation were 0.674, 0.826 and 0.679, respectively (P<0.05). Conclusion The platelet aggregation rate induced by peripheral blood AA, ADP and COL is different in different classifications of cerebral infarction, which is significantly increased in LAA especially. The platelet aggregation rate is closely related to carotid IMT and plaque formation, which can be applied as an important auxiliary index to evaluate cerebral infarction types and plaque risks.