分析低分子肝素对缺血性脑卒中患者ADP通道药物抑制率及AA通道药物抑制率的影响

Effect analysis of low molecular weight heparin on ADP pathway inhibition rate and AA pathway inhibition rate in patients with ischemic stroke

目的 分析低分子肝素(LMWH)对缺血性脑卒中患者二磷酸腺苷(ADP)通道药物抑制率及花生四烯酸(AA)通道药物抑制率的影响。方法 1008例缺血性脑卒中患者,按照最大振幅(MA)值分为血小板功能亢进组(92例)和血小板功能正常组(916例),比较两组ADP通道药物抑制率和AA通道药物抑制率。按照患者是否使用过LMWH治疗分为未应用LMWH组(549例)和应用LMWH组(459例),比较两组ADP通道药物抑制率及AA通道药物抑制率。结果 血小板功能亢进组ADP通道抑制率为(48.72±31.19)%,高于血小板功能正常组的(36.72±28.89)%,差异有统计学意义(P<0.05);血小板功能亢进组AA通道抑制率为(83.80±29.59)%,低于血小板功能正常组的(86.26±28.06)%,但差异无统计学意义(P>0.05)。应用LMWH组ADP通道抑制率为(36.55±28.61)%,未应用LMWH组为(39.32±30.06)%;应用LMWH组AA通道抑制率为(86.98±26.60)%,未应用LMWH组为(84.92±29.98)%。应用LMWH组与未应用LMWH组ADP通道抑制率与AA通道抑制率比较,差异均无统计学意义(P>0.05)。结论 缺血性脑卒中患者采用LMWH治疗时LMWH可增强血小板活化,且不会使缺血性脑卒中患者血栓弹力图血小板图(TEGPM)的ADP通道药物抑制率下降。

Objective To analyze the effect of low molecular weight heparin(LMWH) on adenosine diphosphate(ADP) pathway inhibition rate and arachidonic acid(AA) pathway inhibition rate in patients with ischemic stroke. Methods A total of 1008 patients with ischemic stroke were divided into hyperthyroidism group(92 cases) and normal platelet function group(916 cases) according to the maximum amplitude(MA) value.The ADP pathway inhibition rate and AA pathway inhibition rate of the two groups were compared. Patients were divided into non-LMWH group(549 cases) and the LMWH group(459 cases) according to whether they had been treated with LMWH or not, and the ADP pathway inhibition rate and AA pathway inhibition rate were compared between the two groups. Results The ADP pathway inhibition rate in the hyperthyroidism group was(48.72±31.19)%, which was higher than(36.72±28.89)% in the normal platelet function group, and the difference was statistically significant(P<0.05). The AA pathway inhibition rate in the hyperthyroidism group was(83.80±29.59)%, which was lower than(86.26±28.06)% in the normal platelet function group, but the difference was not statistically significant(P>0.05). The ADP pathway inhibition rate in the LMWH group was(36.55±28.61)%, while that in the non-LMWH group was(39.32±30.06)%;the AA pathway inhibition rate was(86.98±26.60)% in the LMWH group and(84.92±29.98)% in the non-LMWH group. There was no statistically significant difference in the ADP pathway inhibition rate and AA pathway inhibition rate between the LMWH group and the non-LMWH group(P>0.05). Conclusion For patients with ischemic stroke, LMWH can enhance platelet activation without reducing the ADP pathway inhibition rate detected by thrombelastography platelet mapping(TEGPM) in patients.