Ticlopidine is a novel and specific antiplatelet agent with a mechanism of action different from and superior to that of aspirin, which is a non-cyclic oxidase inhibitor. It has a strong inhibitory effect on platelet aggregation induced by low and high concentrations of adenosine phosphate (ADP). In addition to inhibiting ADP-induced second-phase aggregation, it also completely inhibits first-phase aggregation, and inhibits platelet aggregation induced by low-dose arachidonic acid, thromboxane A2 analogs, collagen, thrombin and platelet-activating factor (PAF). It can prolong the bleeding time by 3-5 times. It also reduces the platelet adhesion and release response. In this study, ASA alone inhibited the aggregation induced by AA and TIC alone inhibited the aggregation induced by ADP, which is related to the different antiaggregation mechanisms of both. TIC mainly blocks ADP-mediated platelet activation, which is a widely involved component in most of the early steps of the platelet activation pathway. The present study showed that when ASA was combined with TIC, it showed specific inhibition of both AA and ADP, acting as a summative effect. When A50 was combined with T125, the inhibition of ADP and AA was stronger than that of A100 and T250, respectively, suggesting an additive and synergistic effect. Since platelets are likely to be exposed to multiple agonists during true thrombosis in vivo, it is reasonable to combine antiplatelet agents with different mechanisms. In addition, ASA has a rapid onset of action, with significant platelet inhibition after 1 h of administration of common tablets; whereas TIC can have significant platelet inhibition only 24-48 h after multiple doses, with a peak of about 3 d to 1 week [9]; when ASA is combined with TIC, it also plays a complementary role in terms of time. A beneficial effect on thrombotic stent obstruction has been seen within 3 d after coronary stent placement [7], and this need is also present in secondary prevention of ischemic cerebrovascular disease, especially TIA. Severe neutropenia occurs in approximately 1% to 2% of patients taking TIC, the vast majority within the first 2 to 3 months, and usually resolves after withdrawal, but is not always reversible after discontinuation, causing physicians to be apprehensive about the use of TIC. However, it has also been reported that ASA is still safe in combination with TIC under regular routine blood and liver function monitoring [9]. In this paper, after removing patients with early onset neutropenia, no late onset neutropenia occurred in any group taking the drug for more than six months. Therefore, we recommend that routine blood tests be performed once or twice a week at the beginning, with longer intervals and at least 3 months of follow-up depending on the situation. Monitoring of patients taking TIC should be as important as anticoagulation; ASA is effective and economical, but gastrointestinal reactions at high doses also affect compliance with the drug. In this paper, we show that the use of small doses of both ASA and TIC reduces the adverse effects of the respective dose increases and enhances the antiplatelet effect of both. As the affordability of patients also affects the compliance of treatment, according to our national situation and according to the condition, the combination of ASA 50mg·d-1 and TIC 125mg·d-1 can be considered as an option for secondary prevention of I-CVD with a better price/effectiveness ratio and relative safety for patients who need intensive anti-poly therapy under regular blood monitoring for an appropriate long period of time. CVD secondary prevention is an option. After the patient’s condition has stabilized and the combination has been used for a period of time, the treatment can be considered to be changed to ASA alone according to the situation. Current studies suggest that enteral aspirin can reduce the incidence of cerebrovascular disease by 15% and the incidence of stroke and death in men by 48%. Therefore, enteric aspirin is an effective drug for the treatment of blood flow disorders [1]. It inhibits platelet aggregation induced by ADP, collagen, thrombin, arachidonic acid, and prostaglandin endoperoxide, and inhibits platelet aggregation induced by exogenous and endogenous ADP. In clinical use, it is significantly better than enteric aspirin in reducing blood viscosity and has fewer side effects on gastrointestinal bleeding than enteric aspirin. No signs of gastrointestinal bleeding were found in a patient with gastric ulcer during the last 3 months of use, and no signs of rebleeding were found in a patient who had used enteral aspirin to cause gastrointestinal bleeding. There was no recurrence of cerebrovascular disease in the group using Valtrex during the 1-year follow-up period. In the group using enteric aspirin alone, there were 5 recurrences of cerebrovascular disease within 1 year. However, for elderly patients who cannot tolerate aspirin, they can be switched to Vaccinium. Anti-platelet drugs are divided into: (1) cyclooxygenase inhibitors: aspirin, ibuprofen, indobufen, thiopiridone, trifloxacin; (2) phosphodiesterase inhibitors: pansentin; (3) platelet calcium channel inhibitors: sulodexide; (4) thromboxane synthase inhibitors: picotamide; (5) ADP receptor antagonists: ticlopidine and clopidogrel. Currently, aspirin, ticlopidine and clopidogrel are used more frequently. Clopidogrel is an acetate derivative of ticlopidine, both of which are non-competitive ADP inhibitors that irreversibly bind ADP receptors on the platelet surface, and ADP binding is an indispensable process for platelet membrane glycoprotein IIb/IIIa activation, thus acting as an anti-platelet agent. Due to structural changes, clopidogrel has 6-fold higher antiplatelet activity than ticlopidine. In a recent meta-analysis of 13,827 patients, clopidogrel was found to reduce the incidence of ischemic events (OR = 0.73) and mortality (OR = 0.57) compared to ticlopidine, with a much higher safety profile (ticlopidine caused granulocytopenia and thrombocytopenia in 2-3% of patients compared to 0.1-0.26% for clopidogrel). (0.1%-0.26%).