急性脑梗死患者脑微出血病变的相关因素分析
发布时间：2018-05-11 03:01
本文选题：急性脑梗死 + 脑微出血 ； 参考：《华北理工大学》2017年硕士论文
【摘要】：目的利用磁敏感加权成像(Susceptibility weighted imaging,SWI)序列对急性脑梗死患者进行脑微出血(Cerebral microbleeds,CMBs)扫描检查,了解CMBs在急性脑梗死患者中的患病及分布情况,并探讨急性脑梗死患者中CMBs发生的相关因素。方法收集2015年12月至2016年11月在唐山工人医院神经内科诊断为急性脑梗死,且经SWI序列扫描检查的患者124例。依据SWI扫描结果分为CMBs组和无CMBs组。患者均行T1WI、T2WI、FLAIR、DWI、SWI序列及MRA检查。记录检出CMBs组的人数、数目、分布情况。记录脑白质疏松严重程度及腔隙性梗死病灶个数。详细记录患者临床资料,包括年龄、性别、吸烟史、饮酒史、收缩压、舒张压、高血压病史、糖尿病史、卒中史、颈动脉硬化斑块情况等。化验空腹血糖、甘油三酯、总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、凝血酶原时间、纤维蛋白原、尿酸、高同型半胱氨酸等相关血液生化。参考TOAST标准,对急性脑梗死行亚型分组,记录各亚型中CMBs的例数。采用t检验或ManneWhitney U检验比较计量资料,计数资料的比较采用卡方检验或连续校正的卡方检验。运用单因素和多因素的二分类Logistic回归方法行急性脑梗死伴CMBs的相关因素分析。双向有序变量做Spearman相关性分析。结果1在124例急性脑梗死患者中,发现伴CMBs患者69例,占55.6%。共统计出CMBs的个数为548个,平均为7.94个。其中基底节/丘脑区CMBs的病灶个数最多,共217个,病例数也最多47例;其次为脑叶-皮层下CMBs的病灶个数为200个,病例数43例;最后是幕下区CMBs的病灶个数为131个,病例数38例。2 TOAST分型中小动脉闭塞型中CMBs患者有28例(40.6%),大动脉粥样硬化型种CMBs患者有27例(39.1%),心源性栓塞型中CMBs患者4例(5.8%),未明确原因型中CMBs患者10例(14.5%),在小动脉闭塞型中CMBs的发现率最高。3两组间在收缩压、高血压、卒中史、腔隙性梗死、脑白质疏松、颈动脉硬化斑块比较时,差异具有统计学意义(P㩳0.05)。4单因素的Logistic回归分析显示急性脑梗死患者中CMBs与收缩压(OR:1.639,95%CI:1.323-2.030,P0.001)、高血压病(OR:3.412,95%CI:1.593-7.307,P=0.002)、卒中史(OR:3.269,95%CI:1.121-9.531,P=0.030)、颈动脉硬化斑块(OR:2.215,95%CI:1.066-4.606,P=0.033)、腔隙性脑梗死(OR:3.575,95%CI:1.174-10.867,P=0.025)、脑白质疏松(OR:2.812,95%CI:1.352-5.850,P=0.006)存在相关性。5多因素Logistic回归分析结果表明,收缩压(调整OR:1.668,95%CI:1.320-2.108,P㩳0.001)、腔隙性梗死(调整OR:4.085,95%CI:1.027-16.246,P=0.046)、脑白质疏松(调整OR:2.681,95%CI:1.153-6.232,P=0.022)与急性脑梗死患者CMBs病变相关。6采用Spearman相关性分析结果表明,CMBs严重程度与腔隙性梗死分级及脑白质疏松严重程度均呈显著相关性关系(r=0.353,P㩳0.001;r=0.352,P㩳0.001)。结论1在急性脑梗死患者中,出现CMBs最多的部位是基底节/丘脑区。2急性脑梗死各亚型中,在小动脉闭塞型中CMBs的检出率最高。3收缩压、腔隙性梗死、脑白质疏松与急性脑梗死患者CMBs病变相关。4 CMBs严重程度与腔隙性梗死分级及脑白质疏松严重程度有关,且呈正相关性。
[Abstract]:Objective to investigate the incidence and distribution of CMBs in patients with acute cerebral infarction by using Susceptibility weighted imaging (SWI) sequence to scan the cerebral microhemorrhage (Cerebral microbleeds, CMBs) in patients with acute cerebral infarction, and to explore the related factors of CMBs in patients with acute cerebral infarction. Methods collect 2015 1. From February to November 2016, 124 cases of acute cerebral infarction were diagnosed as acute cerebral infarction in the Department of Neurology in Tangshan workers' hospital and were examined by SWI sequence scan. The results were divided into CMBs group and no CMBs group according to the results of SWI scan. The patients were all performed T1WI, T2WI, FLAIR, DWI, SWI sequence and MRA examination. The number, number and distribution of CMBs group were recorded. The serious leukoaraiosis was recorded. The number of degree and lacunar infarction focus. Detailed records of the patient's clinical data, including age, sex, smoking history, drinking history, systolic pressure, diastolic pressure, hypertension history, diabetes history, stroke history, carotid atherosclerotic plaque. Prothrombin time, fibrinogen, uric acid, high homocysteine and other related blood biochemistry. Refer to TOAST standard, subgroup of acute cerebral infarction, record the number of CMBs in each subtype. Use t test or ManneWhitney U test to compare the measurement data, the count data are compared with chi square test or continuous correction of Chi Square test. The correlation factors of acute cerebral infarction with CMBs were analyzed with two classified Logistic regression methods with single factor and multiple factors. Spearman correlation analysis was done with bidirectional ordered variables. Results in 1 of 124 patients with acute cerebral infarction, 69 patients with CMBs were found, accounting for a total of 548 CMBs, with an average of 7.94. The basal ganglia / thalamus was in the 124 cases of acute cerebral infarction. The number of lesions in the area CMBs was the most, a total of 217, and the number of cases was 47. The number of lesions in the subcortical CMBs was 200, the number of cases was 43, and the number of the lesions in the subscreen CMBs was 131, the number of cases 38 cases of.2 TOAST type middle and small artery occlusion was 28 cases (40.6%), and the large atherosclerotic CMBs patients had 27. Cases (39.1%), 4 cases (5.8%) of CMBs patients with cardiogenic embolism, 10 cases (14.5%) of undefined cause type CMBs patients, and the highest detection rate of CMBs in the occlusion type of arterioles was of systolic pressure, hypertension, stroke history, lacunar infarction, leukoaraiosis, and carotid arteriosclerosis plaque comparison, the difference was statistically significant (P? 0.05).4 single factor Logistic regression analysis showed that CMBs and OR:1.639,95%CI:1.323-2.030 (P0.001) in patients with acute cerebral infarction, hypertension (OR:3.412,95%CI:1.593-7.307, P=0.002), stroke history (OR:3.269,95%CI:1.121-9.531, P=0.030), carotid atherosclerotic plaque (OR: 2.215,95%CI:1.066-4.606, P=0.033), lacunar cerebral infarction (OR:3.575,95%CI:1.174-10.8) 67, P=0.025), OR:2.812,95%CI:1.352-5.850 (P=0.006) associated.5 multiple factor Logistic regression analysis showed that systolic pressure (adjusted OR:1.668,95%CI:1.320-2.108, P? 0.001), lacunar infarction (adjusted OR:4.085,95%CI:1.027-16.246, P= 0.046), leukoaraiosis (OR:2.681,95%CI:1.153-6.232, P=0.022) and acute The Spearman correlation analysis of CMBs pathological changes in cerebral infarction patients showed that the severity of CMBs was significantly correlated with the severity of lacunar infarction and the severity of leukoaraiosis (r=0.353, P? 0.001; r=0.352, P? 0.001). Conclusion 1 in patients with acute cerebral infarction, the most CMBs is the acute brain of the basal ganglia / thalamus region. Among the infarct subtypes, the detection rate of CMBs in the arteriole occlusion was the highest.3 systolic pressure, lacunar infarction, and leukoaraiosis associated with CMBs lesions in patients with acute cerebral infarction, the severity of.4 CMBs was related to the severity of lacunar infarction and the severity of leukoaraiosis.
【学位授予单位】：华北理工大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R743.3
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