To assess the effects of Xuesaitong soft capsules on platelet function, clinical efficacy, prognosis, and safety in the treatment of acute coronary syndrome, 400 patients with acute coronary syndrome who underwent PCI were treated with Xuesaitong soft capsules (mainly containing ginsenosides) for 12 weeks.
Patients diagnosed with acute ST-segment elevation myocardial infarction, acute non-ST-segment elevation myocardial infarction, or unstable angina according to Western medical standards. Inclusion Criteria.
Within 4 weeks post-PCI.
Aged between 18 and 80 years, both male and female.
Voluntarily participating in the clinical trial, having signed the informed consent form.
Uncontrolled hypertension after medication (systolic BP >180mmHg or diastolic BP > 110mmHg).
Increased bleeding risk: history of hemorrhagic stroke; intracranial aneurysm; major trauma or surgery within the past month (including Exclusion Criteria bypass surgery); active bleeding disorders.
History of gastrointestinal ulcers or significant gastrointestinal bleeding.
Severe organic heart disease, such as LVEF < 35% or NYHA/Killip heart function grade IV.
Parallel
Xuesaitong soft capsule (main ingredient is Panax notoginseng saponins)
DrugRoutine western medicine treatment (oral drug therapy and standard percutaneous coronary intervention) + Xuesaitong soft capsule, 0.33g/ tablets, 2 tablets each time, twice a day. The treatment period is 12 weeks.
placebo capsule
DrugRoutine western medicine treatment (oral drug therapy and standard percutaneous coronary intervention) + placebo capsule, 0.33g/ tablets, 2 tablets each time, twice a day. The treatment period is 12weeks.
Changes in thromboelastography induced by AA, including R value, K value , α angle , MA value , CI, TPI， LY30, and AAYZL, before and after treatment, as assessed by thromboelastography.
This outcome measure will assess changes in thromboelastography induced by AA, including R value (reaction time), K value (coagulation time), αangle (alpha angle), MA value (maximum amplitude), CI (coagulation index), TPI (thrombodynamic potential index)， LY30 (amplitude at 30 minutes), and AAYZL Percentage platelet clotting inhibition of AA), before and after treatment. Data will be summarized based on the change in levels of each marker from baseline to post-treatment, and any significant changes will be noted.
Changes in thromboelastography induced by ADP, including R value, K value , α angle , MA value , CI, TPI， LY30, and ADPYZL, before and after treatment, as assessed by thromboelastography.
This outcome measure will assess changes in thromboelastography induced by ADP, including R value (reaction time), K value (coagulation time), αangle (alpha angle), MA value (maximum amplitude), CI (coagulation index), TPI (thrombodynamic potential index)， LY30 (amplitude at 30 minutes), and ADPYZL（ Percentage platelet clotting inhibition of ADP), before and after treatment. Data will be summarized based on the change in levels of each marker from baseline to post-treatment, and any significant changes will be noted.
Changes in platelet granule markers, including platelet factor 4 (PF4) and β-thromboglobulin, before and after treatment, as assessed by ELISA
This outcome measure will assess changes in platelet granule markers, including platelet factor 4 (PF4) and β-thromboglobulin, before and after treatment. Both markers will be measured using enzyme-linked immunosorbent assay (ELISA) and reported in consistent units (pg/mL). Data will be summarized based on the change in levels of each marker from baseline to post-treatment, and any significant changes will be noted.
Changes in platelet surface activation markers and platelet-neutrophil aggregation before and after treatment, as assessed by flow cytometry
This outcome measure involves the detection of changes in platelet surface activation markers, including P-selectin (CD62P) and the GPIIb/IIIa complex (CD41/CD61), using flow cytometry. Additionally, platelet-neutrophil aggregation will be assessed by measuring the co-expression of CD41 (platelet marker) and CD15 (neutrophil marker). These analyses will quantify the impact of treatment on platelet activation and the interaction between platelets and neutrophils, with results presented as mean fluorescence intensity for each marker. Changes will be compared before and after treatment.
Changes in endothelial function markers, including plasma soluble vascular cell adhesion molecule 1 (VCAM-1), soluble intercellular adhesion molecule 1 (ICAM-1), vascular hemophilic factor (vWF), before and after treatment, as assessed by ELISA
This outcome measure will assess changes in platelet granule markers, including plasma soluble vascular cell adhesion molecule 1 (VCAM-1), soluble intercellular adhesion molecule 1 (ICAM-1), vascular hemophilic factor (vWF), before and after treatment. Both markers will be measured using enzyme-linked immunosorbent assay (ELISA) and reported in consistent units (pg/mL). Data will be summarized based on the change in levels of each marker from baseline to post-treatment, and any significant changes will be noted.
Changes in inflammatory markers, including serum hs-CRP, IL-11,IL-6,MCP-1,MMP-9,CD40L,before and after treatment, as assessed by ELISA.
Changes in inflammatory markers, including serum high-sensitivity C-reactive protein (hs-CRP), interleukin 11 (IL-11), interleukin 6 (IL-6), monocyte chemotactic protein 1 (MCP-1), matrix metalloproteinase-9 (MMP-9), and leukocyte differentiation antigen40 ligand (CD40L) before and after treatment. Both markers will be measured using enzyme-linked immunosorbent assay (ELISA) and reported in consistent units (pg/mL). Data will be summarized based on the change in levels of each marker from baseline to post-treatment, and any significant changes will be noted.
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