心肌显像联合冠状动脉造影及组织学检查在评价Ad-HGF治疗猪心肌梗死疗效中的价值

目的探讨心肌静息显像联合冠状动脉造影及组织学检查在评价重组腺病毒-肝细胞生长因子（Ad—HGF）治疗猪实验性心肌梗死中的价值。方法低、中、高剂量Ad—HGF治疗组[Ad-HGF剂量依次为10^8，4×10^8，5×10^9空斑形成单位（PFU）／点；均分10点注射]，生理盐水对照组及空白对照组小型猪各5头，分别于治疗前后行静息心肌显像及冠状动脉造影，并于治疗后行组织学检查。结果空白对照组及生理盐水对照组治疗前后心肌灌注及Rentrop评分无明显变化。各Ad-HGF治疗组治疗后心肌灌注及Rentrop评分较治疗前改善，低、中、高剂量组治疗前后冠状动脉左回旋支（LCX）供血节段得分分别为7．8±1．3和16．4±1．1（低），8．2±1．6和17．6±0．9（中），8．4±1．5和19．0±0．7（高）；各组治疗前后LCX供血区域Rentrop评分分别为0．80±0．16和1．66±0．15（低），0．94±0．11和2．16±0．11]（中），0．90±0．22和2．22±0．19（高）。3组治疗前后数据比较差异均有统计学意义（P〈0．01）。各Ad-HGF治疗组及空白对照组治疗后血管数量明显多于生理盐水对照组。结论用心肌静息显像联合冠状动脉造影及组织学检查评价Ad-HGF治疗猪心肌梗死的疗效有价值。     

急性脑梗死诱发全身炎症反应综合征致多器官功能障碍综合征的临床研究

目的　探讨急性脑梗死 (ACI)诱发全身炎症反应综合征 (SIRS)致多器官功能障碍综合征(MODS)的发病机制 ,以及血清肿瘤坏死因子 (TNF α)、白细胞介素 (IL 1) β含量变化在ACI诱发SIRS发生、发展并向MODS转化的临床意义。方法　 6 8例ACI患者根据病情变化分为 3组 ,其中单纯性ACI(SACI组 ) 36例 ,ACI致SIRS(SIRS组 ) 32例 ,ACI致SIRS后发展为MODS(MODS组 ) 2 4例 ;应用酶联免疫吸附法 (ELISA法 )分别测定患者不同病程中血清TNF α、IL 1β值 ,并与对照组 (为 2 8名同期健康体检者 )比较。 结果　 (1) 6 8例ACI中 4 7.0 6 %发生SIRS;SIRS时 75 %发生MODS。 (2 )血清TNF α、IL 1β的含量MODS 组 >SIRS组 >SACI组 >对照组 ,各组间比较 ,差异具有极显著性 (均P <0 0 1)。MODS重症者 (积分≥ 9分 )血清TNF α、IL 1β含量高于轻症者 (积分 <9分 ) (均P <0 0 1) ;MODS死亡者血清TNF α、IL 1β含量高于存活者 (均 P <0 0 1)。结论　 (1)ACI后出现SIRS可导致MODS的发生。 (2 )患者血清TNF α、IL 1β水平异常变化可作为判断ACI致SIRS、MODS病情进展、预后及转归的一项指标     

急性心肌梗死患者J波的临床研究

目的　研究心电图有 J波的急性心肌梗死 ( AMI)患者的临床情况。方法　选择住院的急性心肌梗死患者 10 2例 ,心电图有 J波者 5 0例为研究组 ,心电图无 J波者 5 2例为对照组 ,比较两组临床情况。结果　心电图有 J波组比心电图无 J波组发生胸闷 ( 3 0 /5 0∶ 2 0 /5 2 ,P<0 .0 5 )、前壁心肌梗死 ( 2 8/5 0∶ 18/5 2 ,P<0 .0 5 )、合并糖尿病 ( 14/5 0∶ 4/5 2 ,P<0 .0 5 )、超声心动图检查发生舒张功能减低 ( 2 4/5 0∶ 14/5 2 ,P<0 .0 5 )、心电图检查发现室性心动过速 ( 11/5 0∶ 1/5 1,P<0 .0 5 )者多。结论　心电图有 J波者比心电图无 J波者临床情况差 ,易于发生严重心律失常     

纤溶酶原激活剂抑制物-1及其基因多态性与急性心肌梗死的相关性研究

目的：研究纤溶酶原激活剂抑制物－1（PAI－1）活性及其等位基因多态性与急性心肌梗死（AMI）之间的关系，从基因水平揭示AMI发病的危险因素。方法：AMI组55例、对照组48例健康者分别应用特异性寡核苷酸点膜杂交技术，进行PAI－1启动子区4G／5G多态性分析，用发色底物法测定血浆PAI－1活性。结果：AMI组和对照组中4G／4G基因型的血浆PAI－1活性水平最高，与4G／5G基因型、5G／5G基因型比较有显著性差异（P＜0．01）。AMI组中4G／4G纯合子基因型频率明显高于对照组（P＜0．05）。结论：血浆PAI－1活性增高是AMI发病的危险因素之一，4G／4G纯合子基因型是AMI发病的危险基因型。     

阻断大脑中动脉建立大鼠局灶性脑梗塞模型的观察

通过经颅阻断大鼠大脑中动脉制成局灶性脑缺血动物模型。大脑中动脉阻塞后大鼠均出现各种神经病学征象。氯化三苯基四氮唑染色发现梗塞区位于皮质及基底节。光镜和电镜观察大脑中动脉阻塞后脑组织的病理改变,发现梗塞区不同程度的细胞和间质变性坏死。结果表明该模型是比较理想的局灶性脑缺血模型.     

Ultrasound for the assessment of the embolic risk of carotid plaques

In a prospective study we compared duplex-ultrasound characteristics of symptomatic internal carotid artery (ICA) stenoses with cranial computerized tomographic (CCT) findings in 82 patients suffering from completed or transient middle cerebral artery symptoms. The aim was to assess the pathogenic role of ICA plaque morphology and the potential embolic risk of ICA plaques. The degree of carotid stenosis was estimated by spectral analysis of the pulsed Doppler signal. The CCT findings were classified as being either normal, lacunar lesions, hemodynamically induced low-perfusion infarctions, or territorial embolic infarctions. According to their ultrasonic features we characterized the ICA plaque surface as smooth or irregular and their structure as homogeneous or heterogeneous. Plaques with an irregular surface and heterogeneous echogenicity dominated significantly in CCT-territorial infarctions (p < 0.01), whereas hemodynamically induced low-perfusion infarctions showed no relationship with any plaque characteristic. High degree ICA stenoses (> 50>%) dominated in both territorial infarctions and low-perfusion infarctions, as compared to ipsilateral normal CCT or lacunes (p < 0.05). Normal CCT and lacunar infarctions were associated with homogeneous and smooth plaques (both p < 0.05). We conclude that > 50% ICA stenoses can cause both hemodynamically induced low-perfusion infarctions as well as thromboembolic territorial infarctions, whereas ulcerated and heterogeneous plaques constitute a high risk factor for arterio-arterial embolic stroke. Furthermore, carotid ultrasound may help to estimate the clinical significance of carotid lesions.     

The validity of a simple clinical classification of acute ischaemic stroke

The aim of the study reported here was to test the validity of a simple clinical classification of acute ischaemic stroke (Oxfordshire Community Stroke Project, OCSP) in predicting the site and size of cerebral infarction on computed tomography (CT). Consecutive patients admitted to hospital with acute ischaemic stroke were prospectively identified and classified into one of four clinical syndromes according to the OCSP classification, blind to the result of CT. The CT brain scans were classified blind to the clinical features into those demonstrating: small, medium or large cortical infarcts; small or large subcortical infarcts in the anterior circulation territory; and posterior cerebral circulation territory infarcts. A total of 108 patients were included. A recent infarct was seen. on the CT scan in 91 patients (84%), and the clinical classification correctly predicted the site and size of the cerebral infarct in 80 of these (88%; 95% confidence interval 77–92%). The positive predictive value was best for large cortical infarcts (0.94) and worst for small subcortical infarcts (0.63). The OCSP clinical classification is a reasonably valid way of predicting the site and size of cerebral infarction on CT and can, therefore, be used very early after stroke onset before the infarct appears on the scan.     

老年急性心肌梗塞病人PTF_(v1)的分析

本文分析91例60岁以上急性心肌梗塞(AMI)病人的心电图 V_1导联上 P 波的终末电势(PTFv_1)由 V_1导联的负向 P 波深度×宽度求得,单位为 mm·s。正常值≥-0.03mm·s,本组 PTFv_1异常者共44例,占48.4%,与 AMI 病人的年龄、梗塞部位、面积扩大及泵衰竭的增重有很大关系。经过治疗,随着病情的好转 PTFv_1可恢复正常。因此,PTFv_1对老年 AMI 的预后判断具有很大的意义。     

Heart failure: Effects of beta receptor antagonists on left ventricular function in patients with clinical evidence of heart failure after myocardial infarction. A double-blind comparison of metoprolol and xamoterol Echocardiographic results from the Metoprolol and Xamoterol Infarction Study (MEXIS)

Two hundred and ten patients with clinical evidence of heartfailure, developing after an acute myocardial infarction, wererandomized to treatment with the ß₁ antagonist metoprolol50–100mg b.i.d. (n=106) or the ß₁ partial agonistxamoterol 100–200 mg bid. (n=104). Left ventricular systolicand diastolic function were assessed with echocardiography andtransmitral Doppler cardiography before and after 3 and 12 monthsof double-blind treatment. E-point septal separation and percent left ventricular fractional shortening were used as indicesof systolic function. The ratio between peak early and latemitral diastolic flow (E/A ratio) and isovolumic relaxationtime were used as indices of diastolic function. In the xamoterol group, there was a deterioration in E-pointseptal separation (P<0·05). A difference between thetreatment groups was present both at 3 months (E-point septalseparation 11·4 vs 13·0 mm, P<0·0l,fractional short ening 271 vs 252%, P<005) and 12 months(E-point septal separation Ill vs 13·2 mm, P<0·05fractional shortening 26·9 vs 25·0%, P<0·05).E/A ratio increased in the metoprolol group (P<0·05)but not in the xamoterol group. At 3 months there was a significantdifference (0·85 vs 0·67, P<0·005 betweenthe groups but not at 12 months. In comparison with the ß₁-receptor antagonist metoprolol,the ß₁ partial agonist xamoterol impaired left ventricularsystolic function in patients with clinical evidence of heartfailure after an acute myocardial infarction.     

Blood-brain barrier dysfunction in Binswanger’s disease; an immunohistochemical study

Binswanger’s disease is pathologically characterized by a combination of diffuse cerebrovascular white matter lesions and lacunar infarcts in the basal ganglia and white matter. Although a blood-brain barrier (BBB) dysfunction has been implicated in the pathogenesis of these white matter (WM) lesions, few authors have addressed this problem. In the present study, we describe BBB dysfunction and its regional differences in the brains of Binswanger’s disease patients. Twelve brains from Binswanger’s disease patients (group III) were examined and compared with those from five patients with non-neurological disease (group I) and five cortical infarct patients without significant WM lesions (group II). Immunohistochemistry was performed for glial fibrillary acidic protein and vimentin as astroglial cell markers, and for immunoglobulins, complements and fibrinogen as extravasated serum protein markers. The grading scores for IgG extravasation were significantly higher in group III as compared to group I, in both the periventricular WM and the subcortical WM (P < 0.01). In group III, the scores in the periventricular WM and subcortical WM were significantly higher than in the subcortical U fibers and cerebral cortex (P < 0.01 for the periventricular WM; P < 0.001 for the subcortical WM), respectively. Clasmatodendritic astroglia, which had swollen cell bodies and large cytoplasmic vacuoles with disintegrated processes, incorporated the serum components IgG, IgM, C3d, C1q and fibrinogen, both in the periventricular WM and subcortical WM in 5 out of 12 (42%) Binswanger’s disease brains. These results indicate that WM lesions in Binswanger’s disease are accompanied by BBB dysfunction, although it remains uncertain whether BBB dysfunction is secondary to either chronic cerebral ischemia or arterial hypertension. Received: 25 April 1997 / Revised, accepted: 21 July 1997