The Research Of Clinical Effects Of Sodium Ozagrel On Treating Transient Ischemic Attack

Objective: TIA is the recurrent, transient neurologic impairmentinduced by lack of cerebral blood supply. TIA is the premonition ofcerebral infarction, treament to it in time is importan to preventischemic stroke. In recent years, sodium ozagrel, an antiplateletaggregation medicine, has been accepted gradually to be used intreating TIA. The present research confirmed the mechanism ofsodium ozagrel (the Thromboxane A2 synthase inhibitor) on treatingTIA and identified the treatment theoretic basis through detecting thealteration of TXB2 and 6-Keto-PGF1α levels in plasma,hemorrheology, TCD, imageology and therapeutical effects on TIApatients, which has provided rationale for extensive application infuture clinical work. Methods: 98 TIA patients in our hospital in the period from2004, 1ry to 2005, 1ry were divided into two groups randomly,treatment group (sodium ozagrel, 57cases) and control group(arasaponin, 41cases) and all the patients accepted the treatment for14 days. The levels of TXB2 and 6-Keto-PGF1α in plasma weremeasured by radioimmune method before and after medicinetreatment. Blood viscosity was investigated by LBY-N6B automaticmulti-function blood rheometer before and after treatment. Inaddition, we detected intracranial major arteries blood flow withTCD and assessed the clinical effect. Results: Before treament the average level of TXB2 in all patients washigher compared to the normal level obviously, while the level of6-Keto-PGF1α was lower than normal. Sodium ozagrel caused asignificant decrease of the level of TXB2 (p<0.001) with concomitantincrease in 6-Keto-PGF1α (p<0.001). However, the levels of TXB2and 6-Keto-PGF1α were invariable in control group before and afterlulutong administration (p>0.05). Difference were consideredsignificant at p<0.001 between treatment group and control groupafter treatment.Blood clotting routine examaination results: Before treamentthe average level of FBG in plasma in all patients was a little higherthan the normal level. Sodium ozagrel caused decrease of the levelof FBG (p<0.01), while in control group the levels of FBG wereinvariable before and after lulutong administration (p>0.05).Difference were considered significant at p<0.01 between treatmentgroup and control group after treatment. The clotting time in twogroups was not change obviously before and after therapy.Hemorrheologic index results: There were no significantdifference in each item of hemorrheologic index (p>0.05) betweentreatment group and controls pretherapy. High blood viscosity,middle blood viscosity, low blood viscosity, plasma viscosity,hematocrit and erythrocyte aggregation index were higher thannormal in all patients pretherapy. After 14 days treatment, each itemabove decreased obviously, and erythrocyte deformability indexincreased than before in both treatment group and controls (p<0.01).The changed level of index did not differ when compared betweentwo groups (p>0.05).TCD examination results: TCD outcome of 44 carotid arterysystem TIA patients (73.3%) showed abnormality, most of whichappeared fast blood flow velocity, including 20 patients in treatmentgroup (60.6%) and 16 cases in controls (66.7%), and many caseswere accompanied with the spectral changes. Abnormity happend inmiddle cerebral artery was most common. While in 38 vertebra-basalartery system TIA patients, TCD outcome of 26 cases (68.4%),including 10 patients in treatment group (41.7%) and 6 in controls(42.9%), occurred abnormality, most of which manifested slowblood flow velocity with spectral changes. There were no significantdifference between treatment group and controls after medicineadministrantion (p>0.05). The affection on blood vessel didn't varyevidently in all patients with abnormal TCD outcome.Imageology examination results: Abnormal rate of MRI reached81.6% (80 patients) which was higher than 56.1% in CT (55patients). The presentation rate of ischemic focus conformed withsymptom of TIA was 28.4% (36 patients). It has been confirmed byimageology that pathological changes were mostly small lacunarinfarction located at the basal ganglia and corona radiata.Clinical effect assessment results: All 98 patients were followedup 1 year. In treatment group, 57 cases, total excellence rate(recovery+excellence) reached 76.4%, total effective rate(recovery+excellence+utility) was 91.2%, 4 patients (7%) developedto cerebral infarction. While in control group, total excellence ratewas 31.8%, total effective rate was 73.1%, which were lower thanthe treatment group, and 7 patients (17.07%) developed to cerebralinfarction.Conclusions: 1. Sodim ozagrel caused a significant decrease ofTXB2 with a concomitant increase in 6-Keto-PGF1α level in plasma,so the balance between TXA2 and PGI2 in TIA patients could beadjusted appropriately. Simultaneously, it could inhibit the plateletaggregation and prevent the thrombus formation.2. Sodium ozagrel had the function of accelerating the transitspeed of erythrocyte in plasma, increasing blood-supply of tissue andameliorating microcirculation by degrading erythrocyte aggregationand blood viscosity, and improving erythrocyte deformability.3. Though sodium ozagrel could dilate vessel lightly, it had notreatment effect on angiostenosis. We could apply sodium ozagrel ondelaying attack temporarily in TIA patients with obviousangiostenosis, but it is by no means the ultimate way to solve thisproblem.4. Sodium ozagrel could reduce the incidence of completestroke in TIA patients and the attack frequency of TIA, it had thepredominant clinical effects with well safety.5. Sodium ozagrel can be applied on treating TIA when it isdifficult to judge the type in early period of TIA, it had the certaintherapeutic effects on both microembolization and hemodynamicstype TIA.