74例急性脑梗死患者血小板和凝血功能以及血脂变化的研究

Observation of changes of platelet, coagulation function and blood lipids in 74 patients with acute cerebral infarction

目的探讨急性脑梗死患者血小板各参数、凝血功能及血脂的变化。方法选择本院住院的急性脑梗死患者74例为急性脑梗死组，以同期本院65例健康查体者作为健康对照组。两组均空腹取静脉血，测定血小板各参数、凝血功能及血脂水平。结果与健康对照组比较，脑梗死组血小板计数（PLT）明显减少（×10’／L：191．01±62．65比234．54±77．60），平均血小板体积[MPV（f1）：16．51±1．37比10．16±1．76]及血小板分布宽度[PDW：（22．74±3．71）％比（13．02±2．96）％]明显增大（均P〈0．05），血小板比容（PET：0．40±0．14比0．37±0．14）、大血小板比例（P—LCR：0．37±0．10比0．32±0．09）比较差异均无统计学意义（均P〉0．05）；活化部分凝血活酶时间[APTT（s）：29．13±4．66比36．32±3．84]、凝血酶原时间[PT（s）：11．38±1．27比12．49±0．92]则明显缩短（均P〈0．05）；纤维蛋白原[Fib（g／L）：5．11±0．82比3．37＋0．73]及D-二聚体（μg／L：790．23±471．69比377．29±140．41）均明显增高（均P〈0．05），凝血酶原活动度[（92．28±15．33）％比（107．69±12．03）％]、凝血酶时间[TT（s）：16．04±2．06比15．66±1．74]、凝血酶原国际标准化比值（PT-INR，0．96±0．15比1．02±0．15）比较差异均无统计学意义（均P〉0．05）；总胆固醇[TC（mmol／L）：5．31±1．06比3．84±0．80]、甘油三酯[TG（mmol／L）：3．20±1．39比2．29±0．77]及低密度脂蛋白[LDL（mmol／L）：3．05±0．60比2．29±0．77]均明显增高（均P〈0．05），高密度脂蛋白[HDL（mmol／L）：0．71±0．17比0．75±0．20]比较差异无统计学意义（P〉0．05）。结论血小板质和量的异常、凝血功能改变及脂代谢的紊乱是急性脑梗死的重要发病因素。

Objective To explore the changes of platelet parameters, coagulation function and blood lipids of patients with acute cerebral infarction. Methods Seventy-four patients with acute cerebral infarction were enrolled as the observation group, and 65 healthy people during the same period were chosen as the controls. Venous blood was collected at fast, and the platelet parameters, coagulation function and blood lipids were determined in both groups. Results The platelet count （PLT） of the acute cerebral infarction group was obviously decreased compared with that of the healthy control group （ ×10^9/L ： 191.01±62.65 vs. 234.54±77.60）, while the mean platelet volume [ MPV （fl）： 16.51±1.37 vs. 10.16±1.76] and platelet distribution width [ PDW： （22.74±3.71） % vs. （13.02±2.96） %] were significantly higher than those in the healthy control group （all P〈0.05）. Plateletocrit （PCT ： 0.40±0.14 vs. 0.37±0.14） and platelet large cell ratio （P-LCR ： 0.37±0.10 vs. 0.32±0.09）had no statistically significant differences compared with those of the healthy control group （both P〉 0.05）. Activated partial thromboplastin time [ APTT （s） ： 29.13±4.66 vs. 36.32±3.84] and plasma prothrombin time [ PT （s） ： 11.38±1.27 vs. 12.49±0.92] were obviously shorter in cerebral infarction group than those in healthy control group （both P〈0.05） ; fibrinogen [ Fib （g/L） ： 5.11± 0. 82 vs. 3.37±0.73 ] and D-Dimer （μg/L ： 790.23 ± 471.69 vs. 377.29± 140.41 ） were significantly higher than those in healthy control group （both P〈0.05）. Prothrombin activity [ （92.28± 15.33） % vs. （ 107.69± 12.03） %], thrombin time [ TT （s） ： 16.04±2.06 vs.15.66± 1.74] and prothrombin time-international normalized ratio （PT-INR ： 0.96± 0.15 vs. 1.02± 0.15 ） had no statistical differences compared with those of the control group （all P〉0.05） ; Total cholesterol [ TC （mmol/L） ： 5.31±1.06 vs. 3.84±0.80], triglyceride [ TG （mmol/L） ： 3.20＋1.39 vs. 2.29±0.77] and low-density lipoprotein [ LDL （mmol/L） ：3.05±0.60 vs. 2.29±0.77] were obviously higher in cerebral infarction group than those in healthy control group （all P〈0.05）. High-density lipoprotein [ HDL （mmol/L）： 0.71±0.17 vs. 0.75±0.20 ] had no statistical difference compared with that of the healthy control group （P 〉 0.05）. Conclusion The abnormality of the quality and number with platelet, the change of coagulation function and dyslipidemia were the important factors in the pathogenesis of acute cerebral infarction.