The incidence of early progression of acute cerebral infarction is 16% to 40%, with a high rate of disability and death, which is a difficult clinical treatment point. Early progression is mostly in the 48-72h after the onset of neurological deficit symptoms gradually aggravated, reaching a peak in 3-5d. In the clinical anterior circulation cerebral infarction in the onset of the proportion of absolute dominance, so the early progression of anterior circulation cerebral infarction has become a hot spot of concern for clinicians. The atherosclerotic type of large arteries is predominant in the etiology, which is considered to be related to the presence of unstable plaques in the intracranial and extracranial arteries, poorly controlled hypertension, hyperglycemic status, and history of stroke, some of which are considered to be important factors in the early progression of acute cerebral infarction. The vascular factors of early progression of acute cerebral infarction in the anterior circulation are mainly considered to be the prolongation of the end of the in situ thrombus, the failure to rapidly establish the lateral branches of cerebral arteries, and the lack of cerebral circulatory reserve power, causing the increase of the hypoperfused area in the infarcted region leading to the progression of the disease and the clinical manifestation of progressive neurological deterioration. Actively inhibiting the spread of emboli, rescuing the ischemic semidarkation zone and preventing the expansion of the infarct area are the keys to improve the poor prognosis of early progression of cerebral infarction. The specific treatment for acute cerebral infarction is revascularization therapy, but the timing is missed in most patients due to time constraints and other factors. Prolonged emboli, increased platelet aggregation rate, diminished fibrinolytic system function, and activated coagulation system are closely associated with early progression of anterior circulation cerebral infarction, according to which theoretical anticoagulation and antiplatelet aggregation combination therapy needs to be investigated in such patients with cerebral infarction. Although some patients with early progression of anterior circulation cerebral infarction can be treated with revascularization after a rigorous evaluation, most patients in the real world still do not benefit from it, and secondary prevention is the only option for such patients. The classical antiplatelet aggregation drug aspirin is most widely used in clinical practice as a secondary prevention agent for the purpose of preventing atherosclerotic plaque growth. Agatroban is a new anticoagulant drug with anticoagulant and adjuvant thrombolytic effects on local thrombus. Agatroban can prolong the activated partial thromboplastin time (APTT) or activated clotting time (ACT) with a half-life of only 39-51 min [11]; after stopping the drug for 2-4 h, APTT can return to baseline levels, and the effect of thrombin inhibition can last for 12-24 h. Agatroban is metabolized in the liver, and the drug dose should be adjusted appropriately in patients with hepatic insufficiency, while age, gender, and renal function have no significant effect on The effects of age, gender and renal function on pharmacokinetic parameters are not obvious. Studies have shown that argatroban has a rapid onset and significant efficacy in improving neurological deficits, significantly improving patients’ ability to perform daily living activities and reducing disabling effects at 6 months of onset [12]. Combined antithrombotic therapy with aspirin and argatroban can theoretically both control the formation of white thrombus and inhibit the development of red thrombus, which can more effectively prevent thrombotic events