To investigate the efficacy of polivi combined with low molecular heparin in the treatment of progressive cerebral infarction. Methods 105 patients were randomly divided into treatment group (55 cases) and control group (50 cases), treatment group applied Polivi Polivi 300mgst, followed by 75mgqdx30day, low molecular heparin sodium 4100u ihq12hx10day; control group used low molecular heparin alone. Results There was a significant difference between the treatment group and the control group in terms of apparent efficiency and total efficiency (p<0.05). Conclusion The combination of the two drugs has a synergistic effect and is safe and effective, which can effectively control the development of progressive cerebral infarction. Progressive cerebral infarction as a clinical type of cerebral infarction, it is difficult to control the development of the disease with the current conventional treatment, has a high rate of disability and death, and is easy to lead to medical disputes, our hospital has applied the combination of boleolevir and low molecular heparin to treat 105 progressive cerebral infarction with remarkable efficacy from 2004 to 2006, and it is now reported as follows. 1. Targets and Methods Targets: patients with acute cerebral infarction whose onset of disease occurs in 48 hours, patients whose onset of disease occurs in 24 hours, and patients whose onset of disease occurs in 24 hours. Patients with cerebral infarction, progressive aggravation of focal neurological deficit symptoms within 24 hours of onset, cerebral hemorrhage, subarachnoid hemorrhage and hemorrhagic infarction, and history of hemorrhagic disease were confirmed and excluded by cranial CT. All patients met the diagnostic criteria revised by the Fourth National Academic Conference on Cerebrovascular Disease. They were randomly divided into treatment group and control group. (1) Treatment group 55 cases in the group of Polivir combined with hypocretin, 30 men, 25 women, age 35-75 years old, average 56.4 years (2) Control group 50 cases in the group of hypocretin alone, 28 men, 22 women, age 37-78 years old, average 58.22 years old, the difference between the age and gender of the two groups of patients was not significant (p>0.05). METHODS: Treatment Methods Treatment group Polivir 300mgst (Hangzhou Sanofi Aventis Minsheng Pharmaceutical Co., Ltd.), followed by 75mg qdx30day. low molecular heparin (Tianjin Hongri Pharmaceutical Co., Ltd.) 4100u ihq12hx10day. simultaneous application of aspirin, dehydrating agents, lowering blood pressure and other treatments. In the control group, only aspirin, dehydrating agent and hypotension were used. Observation Methods According to the “Clinical Neurological Deficiency Degree (NDS) Scoring Criteria for Stroke Patients” and “Clinical Efficacy Scoring Criteria” adopted by the National Cerebrovascular Disease Academic Conference in 1995, the scores were made before, after, 14 and 30 days of treatment, respectively. The clinical efficacy scoring criteria were scored before, after, 14 days and 30 days of treatment. Criteria for assessment of efficacy (1) Basic recovery: 91%-100% reduction in NDS and 0 grade of disability (2) Significant improvement: 46%-90% reduction in NDS and 1-3 grade of disability (3) Progress: 18%-45% reduction in NDS and 1 grade of recovery of disability (4) No change: No change in NDS or no reduction or increase of 17% or less in NDS, and no recovery or aggravation of disability (5) Deterioration of NDS and increase of 18% or more in NDS before treatment and 14 days after treatment, respectively. The blood rheology, prothrombin time, fibrinogen, platelet aggregation rate and cholesterol were measured before, after, 14 days and 30 days of treatment, and the cranial CT was immediately rechecked if the condition worsened in the course of treatment. Progressive stroke, or stroke progression, usually refers to neurological deficit or deterioration that occurs in a few hours to a few days after a stroke. It accounts for about 26%-43% of ischemic strokes [1]. Incomplete occlusion or adequate side branch compensation within 6 hours of stroke onset in progressive strokes shows only partial symptoms of the occluded vessel. Due to the reduced activity of the fibrinolytic system, hypercoagulability, hyperlipidemia, etc., the further development of vascular occlusion destroys the collateral circulation in the semi-dark zone, enlarges the extent of the occluded cerebral artery, and results in the necrosis of some of the still viable central zones. Symptoms are further aggravated. The main causes include advanced age, early admission, arterial stenosis of more than 50%, reduced cerebral perfusion, poor establishment of collateral circulation, thrombus growth, and high blood viscosity. The more accepted mechanism is irreversible damage to the semidarktic band, but most progressive strokes lose the opportunity for thrombolysis, so anticoagulation and antiplatelet aggregation are particularly important. Thrombosis is a multifactorial and causal process, in which platelet activation and fibrinogen bridging play an important role in thrombus formation and expansion. In the acute phase of cerebral infarction, platelets are activated by three pathways (1) ADP pathway (2) thromboxane A2 pathway (3) platelet activating factor (pAF) pathway. Polivir can selectively inhibit the binding of ADP to its receptor and the secondary ADP-mediated activation of the mucin GPIIb/IIIa complex, and its effect on platelet ADP receptor is irreversible. The results of pharmacokinetic study suggest that it takes 7 days for polivir, 75mg/d, to achieve the maximal inhibition of platelet aggregation (about 70%), whereas a loading dose of 300mg can achieve the maximal inhibition of platelet aggregation within 3 hours. Maximum inhibition of platelet aggregation (approximately 80%) was achieved within 3 hours with a loading dose (300 mg). Low molecular heparin can promote the release of t-pA, shorten the time of euglobulin dissolution, promote the degradation of fibrin, and prevent the conversion of fibrinogen into fibrin, and at the same time, the reduction of the level of fibrinogen reduces the substrate of thrombus formation, thus preventing the thrombus that has already been formed from further prolonging and expanding, and preventing the formation of micro thrombus around the ischemic semidecentralized zone, and preventing the progression of incomplete cerebral infarction to complete cerebral infarction. In recent years, low molecular heparin has been reintroduced into the clinical use of anticoagulation therapy because of its good antithrombotic effect, high bioavailability, long half-life, and few adverse effects (especially bleeding). In addition high doses of heparin can inhibit platelet aggregation and release. The results of this study show that the combination of the two drugs has a synergistic effect and is safe and effective in controlling the development of progressive stroke.