出血性脑梗死危险因素的Logistic回归分析

目的 探讨出血性脑梗死的危险因素。方法 根据专业知识确定与出血性脑梗死有关的因素，采用非条件Logistic回归确定危险因素。结果 大面积梗死灶、使用抗凝剂或溶栓治疗、糖尿病史是出血性脑梗死的独立危险因素，与年龄、高血压史、高血脂关系不大。结论 大面积脑梗死、使用抗凝剂或溶栓、糖尿病患者发生梗死后出血的几率增大，及时行影像学检查可以早期发现。     

出血性脑梗死影响因素分析

目的 探讨出血性脑梗死的影响因素.方法 分析本院2003-05～2005-04收治的78例出血性脑梗死病人的临床资料.结果 脑梗死后出血与脑栓塞、大面积脑梗死、皮层梗死、合并高血糖、溶栓治疗有关.结论 急性脑梗死病人存在大面积脑梗死、皮层梗死、高血糖等危险因素及进行溶栓治疗时,应密切观察病情,及时复查CT或MRI,以早期发现出血性梗死,及时调整治疗方案.     

出血性脑梗死的相关因素分析

目的探讨出血性脑梗死的相关因素。方法回顾性分析本院近8年来收住的925例脑梗死病人的临床资料。结果脑梗死后出血与大面积梗死、合并房颤、皮质梗死相关,且大面积脑梗死是其中最强的危险因素,而与患者的性别、年龄、病前是否长期使用抗血小板药(>半年),病后是否使用抗凝剂、血管扩张剂、抗血小板药,是否合并有高血压、糖尿病、二尖瓣病变,既往有无脑梗死病史无关。结论对大面积脑梗死、合并房颤疑为脑栓塞或皮质梗死病人宜密切动态观察,注意梗死后出血的可能,及时复查头颅CT以调整治疗方案。     

出血性脑梗死的相关危险因素分析

目的探讨出血性脑梗死的相关危险因素。方法回顾性分析本院2007-09~2010-08收住的685例脑梗死患者的临床资料。结果出血性脑梗死组患者在大面积梗死、房颤、高血压、高血糖等方面的发生率均高于同期非出血性脑梗死组。结论大面积梗死、房颤、高血压、高血糖等是出血性脑梗死的相关危险因素。     

出血性脑梗死36例临床分析

目的 :探讨出血性脑梗死患者的临床特点 ,发病机制及预防策略。方法 :回顾性分析 3 6例出血性脑梗死患者的临床资料。结果 :大面积梗死者 16例 ,原梗死灶出血 2 0例 ,梗死后第 2周发生出血 8例 ,第一周内发生出血 19例。出血性脑梗死中分水岭梗死不少见 ,并发高血糖者是发生出血性梗死后的一个重要危险因素。出血性脑梗死病例头痛发生率高 ,注意临床观察 ,及时复查CT ,以利诊断。结论 :需溶栓的病例 ,可先行SPECT检查进行筛选 ,再定治疗方案。     

出血性脑梗死36例临床分析

目的：探讨出血性脑梗死患者的临床特点，发病机制及预防策略。方法：回顾性分析36例出血性脑梗死患者的临床资料，结果：大面积梗死患16例，原梗死灶出血20例，梗死后第2周发生出血8例，第一周内发生出血19例，出血性脑梗死中分水岭梗死不少见，并发高血糖者是发生出血性梗死后的一个重要危险因素。出血性脑梗死病例头痛发生率高。注意临床观察，及时复查CT，以利诊断。结论：需溶栓的病例，可先行SPEGT检查进行筛选。再定治疗方案。     

急性脑梗死后认知功能障碍的相关危险因素分析

目的观察急性脑梗死后认知功能障碍的危险因素,为早期预防和早期治疗提供依据。方法急性脑梗死290例患者,应用MMSE筛查出入院3d内发生认知功能障碍者,观察急性脑梗死后认知功能障碍的发生率,并对影响其发生的危险因素进行分析。结果急性脑梗死后认知功能障碍的发生率22.9%;年龄、糖尿病史、卒中或TIA史、多发性脑梗死、梗死面积大、左半球梗死为急性脑梗死后认知功能障碍发生的危险因素。结论急性脑梗死后认知功能障碍发生率较高;年龄、卒中或TIA史、糖尿病史、多发性脑梗死体积、梗死面积大、左半球梗死为急性脑梗死后认知功能障碍发生的危险因素。     

影响急性脑梗死出血性转化的危险因素

目的探讨急性脑梗死的出血性转化的危险因素。方法收集2012年1月~2015年1月在湖北省恩施州利川市人民医院神经内科住院的急性脑梗死患者的临床及实验室检查资料,并在入院后10 d内行头颅CT复查,采用多变量logistic回归分析确定出血性转化的独立危险因素。结果共纳入345例急性脑梗死患者,其中男205例,女140例,101例发生出血性转化。出血性转化组的年龄、脑梗死体积、脑卒中史或TIA史、高血压病、糖尿病、抗凝药和房颤的比例均显著高于非出血性转化组(P0.05),而2组抗血小板聚集药、他汀类、高脂血症史、吸烟或饮酒史无明显差异(P0.05)。多变量logistic回归分析显示年龄(OR=1.168,95%,CI=1.059~3.412;P=0.021)、梗死体积(OR=3.461,95%C1=1.317~6.270;P=0.044)和房颤(OR=1.284,95%C1=1.117~2.903;P=0.015)为出血性转化的独立危险因素。结论急性脑梗死患者出血性转化的发生率为29.3%,年龄、脑梗死体积和房颤为出血性转化的独立危险因素,绝大多数出血性转化不会加重临床症状,临床症状加重的患者主要是脑实质血肿型。     

出血性脑梗死危险因素分析

通过对31例经头颅CT扫描证实的出血性脑梗死患者的回顾性分析，以期获得对该病较全面的认识，从而有利于预防和早期诊断与治疗。本组31例出血性脑梗死中属皮质型9例、血肿型7例、梗死灶内渗血型15例。高龄、高血压、糖尿病、心房纤颤为出血性脑梗死的危险因素，大面积校死易发生出血性病变。     

出血性脑梗死相关因素的探讨

目的:探讨出血性脑梗死(HI)发病的相关因素、临床特点及发病机制;方法:对365例脑梗死病人进行回顾性分析。分为HI组和NHI组;脑栓塞组和脑血栓形成组;溶栓治疗组和非溶栓治疗组,应用X2检验。结果:HI发生率为14.52％。HI发生率大灶梗死与小灶梗死比较,无显著性差异;大灶梗死与腔隙性梗死比较,有显著性差异;小灶梗死与腔隙性梗死比较,有显著性差异;脑栓塞组与脑血栓形成组比较,有显著性差异;溶栓治疗组与非溶栓治疗组比较,有显著性差异。患者年龄、高血压、高血糖、高血脂等脑梗死常见危险因素,HI组与NHI组无差异。结论:脑栓塞、梗死面积大及溶栓治疗与HI发生密切相关,可示为HI发生的主要危险因素。而患者年龄、高血压、高血糖、高血脂等脑梗死常见危险因素与HI的发生无明显相关性。     

列线图风险预测模型评估未溶栓治疗的出血转化和脑梗死再发风险

目的建立列线图风险预测模型评估未溶栓治疗的出血转化和脑梗死再发风险。方法回顾性分析未给予溶栓治疗的脑梗死病人118例,单因素回归分析得到发生出血转化(HT)的危险因素,多因素回归Logistic分析出独立危险因素,同时利用R软件构建未溶栓治疗的出血转化和脑梗死再发风险的列线图预测模型。结果年龄(OR=4.084,95%CI:1.583~8.746)、高血压(OR=6.056,95%CI:2.065~17.762)、房颤(OR=3.347,95%CI:1.239~9.041)、NIHSS评分(OR=2.754,95%CI:1.226~6.187)、低密度脂蛋白(OR=2.659,95%CI:1.040~6.799)、大面积脑梗死(OR=5.652,95%CI:1.622~19.698)是未溶栓治疗患者发生出血转化和脑梗死再发的独立危险因素,以此6个独立危险因素构建列线图预测风险模型,并验证该模型的精确度,预测结果和实际值基本相同,C-index为0.850(95%CI:0.832~0.878),表明风险预测模型准确度较高。结论年龄、高血压、房颤、NIHSS评分、低密度脂蛋白、大面积脑梗死是未溶栓治疗患者发生出血转化和脑梗死再发的独立危险因素,本研究建立的风险预测模型准确度高,对于提高未溶栓治疗的患者发生出血转化和脑梗死的诊治有一定的指导价值。     

非栓塞性脑梗死的出血性转化(附19例分析)

目的 探讨非栓塞性脑梗死患者发生出血性转化(hemorrhagic transformation,HT)的病因、临床特点及治疗.方法 回顾性分析19例非栓塞性脑梗死患者的临床资料.结果 患者平均年龄为76.4岁,大面积脑梗死(95%)是主要病因,高血压(74%)、糖尿病(53%)亦有较高的发生率.结论 非栓塞性脑梗死的HT常发生在高龄及大面积脑梗死,高血压、糖尿病亦是重要的病因,多为晚发型出血,预后相对较好.

Abstract：

Objective To investigate the etiological factors, clinical characteristics and cures of patients with nonembolic cerebral infarction after cerebral infarction. Methods The clinical data of 19 patients with non-embolic cerebral infarction were analyzed retrospectively. Results The average age of patients was 76.4 and the major risk factor was massive cerebral infarction (95%). While hypertension (74%) and diabetes mellitus (53%) were also the risk factors of nonembolic cerebral infarction. Conclusions Hemorrhagic transformation after non-embolic cerebral infarction usually occurs in patients with old age and massive cerebral infarction. Hypertension and diabetes mellitus are also the major risk factors for hemorrhagic transformation after non-embolic cerebral infarction, mainly with delayed onset and better outcomes.     

大脑中动脉高密度征与大面积脑梗死预后的相关性研究

目的探讨大脑中动脉高密度征(HMCAS)与大面积脑梗死预后的关系。方法回顾性分析我院139例大面积脑梗死患者的影像学及临床资料。结果根据OCSP分型:98例(98/139)完全前循环梗死(TACI),41例(41/139)部分前循环梗死(PACI)。据首次CT检查中是否出现HMCAS分两组,HMCAS组58例(58/139);非HMCAS组81例(81/139);所有患者因不符合溶栓指征未行溶栓治疗,其中34例(34/139)患者发生梗死后出血。HMCAS组伴出血者21例(21/58),死亡者11例(11/58),非HMCAS组伴出血者13例(13/81),死亡者5例(5/81)。HMCAS组的出血率、死亡率明显高于非HMCAS组。差异具有统计学意义(χ2出血率=7.43,χ2死亡率=5.43,P0.05)。大面积脑梗死患者出现HMCAS,其伴梗死后出血的发生率和死亡率均高于无HMCAS患者。结论 HMCAS出现可以作为脑梗死预测梗死后出血的指标之一,并可提示大面积脑梗死预后不佳。     

Hemorrhagic complications of thrombolytic therapy in experimental stroke

Recent success with thrombolytic therapy for acute myocardial infarction has stimulated interest in its use for stroke. To determine the hemorrhagic potential of thrombolytic therapy in experimental cerebral infarction, we compared a group of tissue plasminogen activator-treated rabbits (n = 4) with 2 groups of streptokinase-treated rabbits (n = 6 in each), as well as with 3 groups of heparin-treated rabbits (n = 5 in each) and untreated controls (n = 12). Focal cerebral infarction was produced in rabbits by occlusion of the right common carotid and middle cerebral arteries coupled with 2 hours of halothane-induced hypotension. Treatment with heparin or thrombolytic agents began 24 hours after occlusion. One additional group was treated with streptokinase 1 hour after occlusion (n = 6) to determine the hemorrhagic potential of thrombolytic agents in evolving infarction. Rabbits were killed 29-33 hours after occlusion, and brain sections were examined using light microscopy. The results demonstrate that microscopic hemorrhage is frequently present in infarcted tissue irrespective of treatment. Gross cerebral hemorrhage did not occur in untreated rabbits or in rabbits treated with streptokinase 1 hour after occlusion. Only rabbits treated with streptokinase, tissue plasminogen activator, or excessive doses of heparin 24 hours after occlusion, at a time when cerebral infarction was well established, exhibited gross hemorrhage in the area of infarction. These data suggest that treatment of ischemic stroke with thrombolytic agents carries an increased risk of cerebral hemorrhage unless the agents are given early after the onset of symptoms.     

Thrombolysis and stroke. Past and future

Investigators have tried to limit ischemic cerebral infarct size by pharmacologic and surgical means with mixed results. Thrombolytic (fibrinolytic) therapy has been used in the past with unfavorable outcome. With advances in clinical and radiologic assessment and new knowledge of the pathophysiology of brain ischemia, thrombolytic therapy has now become a feasible pharmacologic intervention in acute stroke. Central nervous system hemorrhage, the most dreaded complication of fibrinolytic therapy, is rare in patients with acute myocardial infarction favorably treated with these agents. Risk of hemorrhagic transformation of ischemic cerebral infarcts is related to size, location, and age of patient. Anticoagulation therapy may increase its size, but not its likelihood. The development of clot-specific agents, such as tissue-type plasminogen activator, and careful patient selection make fibrinolytic therapy safe and potentially effective in acute stroke.     

Hemorrhagic transformation in cerebral embolism

We studied the mechanism of hemorrhagic infarction after acute cerebral embolism in 160 patients by brain computed tomography and angiography. Hemorrhagic infarction during the month after the embolic event was evident in 65 patients (40.6%). Initial angiography a median of 1.5 (range 1-60) days after the event revealed occlusion of the cerebral arteries in 117 of 142 patients (82.4%), and reopening of the vessels was observed in 56 (94.9%) of 59 patients who had follow-up angiography a median of 20 (range 3-47) days after the event. The incidence of hemorrhagic infarction was higher in patients greater than or equal to 70 years old (31 of 61, 50.8%) than in those aged 50-69 years (27 of 72, 37.5%) or less than 50 years (seven of 27, 25.9%) (greater than or equal to 70 vs. less than 50, p less than 0.05). In patients with moderate or large infarcts, hemorrhagic infarction developed in 50.0% or 51.5%, respectively, while in those with small infarcts it developed in only 2.9% (p less than 0.05). No correlation was found between hemorrhagic infarction and history of hypertension or blood pressure during the acute stage of stroke. Thrombolytic and/or anticoagulant therapy did not affect the incidence of hemorrhagic infarction (40.0% with vs. 40.7% without therapy) but tended to cause massive hematoma. Our results indicate that hemorrhagic transformation in cerebral embolism is caused not only by reopening of the occluded vessels but also by other factors such as age and size of the infarct. Hypertension per se seems to be less important for hemorrhagic infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Factors affecting haemorrhagic transformation in middle cerebral artery infarctions.

OBJECTIVE: Haemorrhagic transformation (HT) affects treatment and prognosis in patients with acute ischaemic stroke. The factors affecting haemorrhagic transformation in infarcts due to occlusion of middle cerebral artery (MCA) stem or branch were investigated. MATERIALS AND METHODS: Of 412 patients who were followed in our clinic between January 2001 and December 2001 with acute ischaemic stroke, 86 patients with occlusion in MCA stem or branch were enrolled in this study. These patients were divided into 2 groups, those with HT (n = 35) and without HT (n = 51). Age, sex, systemic arterial hypertension, diabetes mellitus, blood glucose level in the acute period, renal and liver function tests, systolic and diastolic arterial blood pressure in the acute period, previous cerebrovascular disease, leukoaraiosis, modified Rankin Disability Score (mRDS) and stroke subtype were evaluated. RESULTS: High blood glucose level in the acute period and presence of leukoaraiosis on cranial computerized (CCT) tomography were detected as risk factors in development of HT. HT was seen more frequently in MCA stem infarction than branch infarction. mRDS were worse in the group with HT. In multivariate analysis, there were independent relationships between mean blood glucose level on admission, mRDS, presence of diabetes mellitus, and MCA stem infarction and development of haemorrhagic transformation in patients with MCA territorial infarction.     

非溶栓急性脑梗死患者出血转化相关危险因素的Meta分析

目的通过Meta分析研究非溶栓急性脑梗死患者出血转化(HT)相关危险因素,为临床上早期识别、预防提供循证医学依据。方法检索PubMed、EMBASE、the Cochrane Library、CNKI、万方、维普、CBM数据库,筛选非溶栓急性脑梗死患者HT相关危险因素的文献,运用Revman 5.3和Stata 14软件对纳入的文献进行Meta分析。结果纳入的16项研究中总样本量7045例,HT组986例,非HT组6059例。Meta分析各危险因素的合并OR值及95%CI分别为:男性0.81(0.68,0.96),年龄0.70(-0.16,1.55),心房颤动3.35(2.25,4.48),高血压0.82(0.67,1.01),糖尿病1.23(0.96,1.52),高脂血症1.24(0.53,2.91),卒中史1.33(0.98,1.79),饮酒史1.30(0.84,1.99),吸烟史1.92(1.19,3.10),抗血小板治疗0.67(0.29,1.56),抗凝治疗2.18(1.15,4.12),大面积梗死4.08(2.40,6.94),血糖1.08(0.67,1.49),收缩压7.07(-3.51,17.55),舒张压0.61(-1.26,2.49),总胆固醇-0.17(-0.31,-0.03),三酰甘油-0.12(-0.21,-0.04),低密度脂蛋白-0.01(-0.21,0.18),高密度脂蛋白0.04(0.01,0.08),血小板计数4.93(-18.44,28.31),NIHSS评分2.94(1.41,4.47)。结论心房颤动、大面积梗死、吸烟、抗凝治疗及NIHSS评分为非溶栓急性脑梗死患者HT的危险因素。男性、高密度脂蛋白、总胆固醇及三酰甘油为非溶栓急性脑梗死患者HT的保护性因素。年龄、高血压、糖尿病、卒中史、高脂血症、低密度脂蛋白、血糖、收缩压、舒张压、饮酒、抗血小板治疗及血小板计数与非溶栓急性脑梗死患者HT无关。     

Are hypertension or cardiac embolism likely causes of lacunar infarction?

We tested the hypothesis that hypertension is more common and cardiac embolism less common in patients with lacunar infarction than in patients with other types of cerebral infarction. We studied risk factor profiles in a series of 102 consecutive patients with a lacunar infarct and 202 consecutive patients with a carotid artery-distribution infarct involving the cortex registered in the Oxfordshire Community Stroke Project, a community-based study of first-ever stroke. The two groups did not differ in the prevalence of prestroke hypertension (defined in a number of ways) or in the prevalence of markers of sustained hypertension. The presence of atrial fibrillation and a history of myocardial infarction, particularly during the 6 weeks before the stroke, were significantly more common in the group with carotid-distribution infarcts involving the cortex. There was no significant difference in the prevalence of other accepted risk factors for ischemic stroke, including previous transient ischemic attack, cervical bruit, diabetes mellitus, peripheral vascular disease, or cigarette smoking. Our results suggest that hypertension is no more important in the development of lacunar infarction than it is in the development of other types of ischemic stroke that are presumed to be due to atherosclerotic thromboembolism in a major cerebral artery. Our data support the autopsy evidence that cardioembolic occlusion is an unusual cause of lacunar infarction.