进展性卒中危险因素的临床分析

目的探讨进展性卒中的危险因素。方法回顾性分析进展性卒中78例患者的临床资料,并随机抽取同期住院的非进展性缺血性卒中患者72例作为对照组。对两组患者的血压、山糖、体温、周围血白细胞、血脂、血浆纤维蛋白原、经颅多普勒超声和颈部血管彩超进行分析。结果进展组与对照组比较：①两组高血压病史差异无统计学意义,发病后用降压药使平均动脉压24h内下降30％后的病情加重者,进展组有27例（34．6％）,对照组有4例（5．6％）,两组间差肄有统计学意义（P〈0．01）。②进展组有糖尿病史者51例（65．4％）,对照组有16例（22．2％）,两组间差异有统计学意义（P〈0．01）。③进展组人院后体温〉37．5℃者有23例（29．5％）,对照组有6例（8．3％）;进展组周围白细胞〉10×10。／L者有45例（57．7％）,对照绀有12例（16．7％）,两组间差异均有统计学意义（P〈0．01）。④进展组有高脂血症者56例（71．8％）,对照组有50例（69．4％）,两组间差异无统计学意义（P〉0．05）。⑤进展组患者血浆纤维蛋白原为（5．1±1．8）g／L,对照组为（2．3±1．4）g／L,两者比较差异有统计学意义（P〈0．01）。⑥两组大血管狭窄发生率分别为53．8％和20．8％,差异有统计学意义（P〈0．01）。进展组颈动脉斑块总检出数为68个,检出率为87．2％。低或不规则回声威块数为31个,检出率为59．7％。溃疡斑块检出数为33个,检出率为42．3％。对照组的检出率为69．4％。低或不规则回声斑块数和检出率分别为16个和22．2％;溃疡斑块检出数为7个,检出率为9．7％,两者比较差异有统计学意义（P〈0．05）。结论过度降版、糖尿病、感染、高纤维蛋白原水平、大动脉狭窄、颈动脉不稳定斑块是进展性卒中的危险因素。

Clinical analysis of risk factors for progressive stroke

Objective To investigate the risk factors for patients with progressive stroke （PS）. Methods The clinical data of 78 patients with PS were analyzed retrospectively, and 72 patients with non-progressive stroke were selected randomly over the same period of hospitalization as the control group. The blood pressure, glucose, body temperature, peripheral blood leukocytes, lipids, fibrinogen, TCD and carotid duplex ultrasound in patients of the 2 groups were analyzed. Results As compared between the PS group and the control group： ①There was no significant difference in the history of hypertension between the 2 groups. Twenty-seven （34. 6% ） of the patients whose mean arterial pressure was reduced by 30% with antihypertensive drugs within 24 hours ＇after the symptom onset were in the PS group and 4 （5.6%） were in the control group; the difference between the two groups was statistically significant （P 〈 0. 01 ）.②There were 51 patients （65.4%） with a history＂ of diabetes in the PS group and 16 （22.2%） in the control group; there was significant difference between the two groups （P 〈 0.01 ）. ③The body temperature of 23 patients （29.5%） was over 37.5% Mter admission in the PS group, and there were 6 patients （8.3%） in the control group. The peripheral blood leukoeytes of 45 patients （57. 7% ） were 〉 10 ×10^9/L in the PS group, and there were 12 patients （ 16. 7% ） in the control group; there was significant difference between the two groups （P 〈 0.01 ）.④56 patients （71.8%） with hyperlipidemia were in the PS group, and 50 （69.4%） were in the control group ; there was no significant difference between the two groups （ P 〉 0. 05 ）.⑤The fibrinogen was 5. 1 ± 1. 8 g/L in the PS group, and it was 2. 3 ± 1, 4 g/L in the control group; the difference was statistically significant between the 2 groups （P 〈0. 01 ）. （The stenosis rate of large blood vessels in both groups was 53.8% and 20.8%, respectively. The difference was statistically significant （ P 〈 0. 01 ）. The total number of carotid artery plaque detected in the PS group was 68 （87. 2% ） ; the number of soft plaques was 31 （59. 7% ） ; and the number of ulcer plaques detected were 33 （42. 3% ）, while the detection rate of the control group was 69. 4%, the number of soft plaque and the detection rate were 16 and 22. 2%, respectively; the number of ulcer plaques detected and detection rate were 7 and 9. 7%. The difference was statistically significant between the 2 groups （P 〈 0. 05）. Conclusion Excessive lowering of blood pressure, diabetes, infection, high fibrinogen level, large artery stenosis, and unstable carotid plaque are the risk factors for PS.