To investigate the efficacy of Polivir combined with low molecular heparin in the treatment of transient ischemic attack (TIA).160 patients were randomly divided into treatment group (82 cases) and control group (78 cases).The treatment group applied Polivir 75mgqdx30day, low molecular heparin sodium 5000u ihq12hx10day; the control group used only aspirin, dehydrating agent, statin and so on. Results There were significant differences in whole blood viscosity, fibrinogen (Fg), thrombus precursor protein (TpP), CRP, platelet aggregation rate, platelet count and the number of cases of cessation of TIA episodes (p<0.05) in the treatment group compared with the control group. The combination of the two drugs has a synergistic effect and is safe and effective, which can effectively control the transformation of TIA to cerebral infarction. Transient ischemic attack (TIA) is one of the most important causes of complete cerebral infarction, which was once called the intermittent breaking of the brain, and some people compare it to angina attack in cardiology. From February 2005 to October 2006, 160 patients with transient ischemic attack were treated with Polivir combined with low molecular heparin with remarkable efficacy, which is now reported as follows: All the cases were hospitalized in our hospital, and met the diagnostic criteria formulated by the Fourth National Conference on Cerebrovascular Disease. Among them, 88 cases were male and 72 cases were female, aged 39-72 years old, with an average of 57.1 years old. There were 65 cases of TIA in the internal carotid artery system (32 cases of monoparesis or hemiparesis, 21 cases of limb numbness or hyperalgesia, 10 cases of aphasia, and 6 cases of monocular blackout); and 95 cases of TIA in the vertebral basilar artery system (89 cases of vertigo, 6 cases of ataxia, and 9 cases of tilting episodes) with an average number of TIAs of 2.8 episodes and an episode time of >1 h in 95 cases, and an episode duration of 3-74 h, with an average duration of 17 h. All of them were subject to TCD, MRI, MRA, DW1 and other examinations were performed. 112 cases of TCD examination found spasm or ischemia of the vertebrobasilar artery, which was in line with 88.3% of the domestic reports, 78 cases of MRA examination had a positive finding, which was in line with 53.3% of the domestic reports [1], 89 cases of MRI found lacunar infarcts, and 52 cases of DW1 showed abnormalities. The patients were randomly divided into treatment and control groups (1) 82 cases in the treatment group (Polivir combined with low molecular heparin group), of which 32 cases had an ABCD score >6; (2) 78 cases in the control group, of which 29 cases had an ABCD score >6. The difference in age and gender between the two groups was statistically significant (p>0.05). TIA is a group of clinical manifestations caused by peripheral hypoperfusion due to microthrombosis, vasospasm or hemodynamic changes on the basis of atherosclerotic lesions. Despite the rapid recovery of clinical symptoms and signs, repeated episodes of cerebral ischemia can cause pathologic damage to brain tissues, resulting in cerebral infarction. The traditional definition of time stipulates that TIA episodes should not exceed 24 h. However, with the accumulation of clinical data, it has been found that common TIA episodes only last for 1 min on average, and usually do not last for more than 5 min, and the American neurologists have put forward a new concept of not exceeding 1 h. TIA has been shown to cause strokes in 5.3% of the patients within 2 d after the onset of an episode, and 1/9 of the patients develop strokes within 3 months, so it is crucial to stop this process. It is crucial to stop this process.Increased CRP may be one of the pathological bases of ischemic changes accompanying TIA in the elderly and may independently predict stroke mortality. Measurement of Fg and TpP levels in patients with TIA can facilitate timely prevention and intervention in the occurrence and development of TIA, and can also be used to evaluate the effectiveness of treatment. There are many causes of TIA, and atherosclerosis is the most important one. Atherosclerosis and thrombosis is a multifactorial and causal process, in which platelet activation and fibrinogen bridging play an important role in thrombus formation and expansion. Platelets are activated by three pathways (1) ADP pathway (2) thromboxane A2 pathway (3) platelet-activating factor (pAF) pathway. A national survey on antiplatelet drugs showed that 71.9% of patients used aspirin. However, aspirin resistance is attracting increasing attention. There is evidence that clopidogrel may be slightly more effective than aspirin in preventing further vascular events [7]. Polivir selectively inhibits ADP binding to its receptor and secondary ADP-mediated activation of the mucin GPIIb/IIIa complex, with irreversible effects on platelet ADP receptors. Low molecular heparin promotes t-pA release, shortens euglobulin lysis time, facilitates fibrin degradation, and prevents the conversion of fibrinogen to fibrin, while lower fibrinogen levels reduce the substrate for thrombosis. In recent years, low molecular heparin has brought anticoagulation back into clinical use 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, which can effectively control the transformation of TIA to cerebral infarction without toxic side effects, and has good compliance and clinical effects, which is worthy of clinical promotion.