北京地区rt-PA静脉溶栓治疗超早期脑梗死患者临床分析

目的分析北京地区12所医院202例超早期脑梗死患者经不同剂量重组组织型纤溶酶原激活剂(rt- PA)静脉溶栓治疗后的疗效及其不良事件,探讨使用rt-PA的最佳剂量及其安全性与可行性。方法287例发病6h以内的脑梗死患者,男201例,女86例,年龄38～80岁,平均64岁。所有患者均伴有偏瘫,头颅CT未见出血及责任梗死灶,无溶栓禁忌证。202例接受rt-PA治疗,分为A组与B组,A组88例,给予rt-PA 0．9 mg/kg。B组114例,给予rt- PA0．6～0．8 mg/kg。C组(对照组)85例患者给予低分子右旋糖酐、复方丹参等治疗。分别比较治疗前与治疗后11d、21 d、90 d的美国国立卫生院神经功能缺损评分(NIHSS)、Barthel指数,并进行疗效评定。结果A组、B组分别与C组90 d的NIHSS评分、Barthel指数相比有显著差异。A组、B组及C组的基本痊愈及显著改善率分别为69%、77%及40%．A组、B组分别与C组脑出血的发生率为7．96%、4．38%及0%。症状性出血(4．55%、2．63%及0%),非症状性出血(2．63%、1．75%及0%)。结论超早期脑梗死静脉应用rt-PA溶栓治疗是安全有效的。不同剂量的rt-PA均减轻了脑梗死的致残率,但两组间无明显差异。中国人rt-PA溶栓治疗最佳剂量尚需要进一步进行大样本的前瞻性、多中心、随机对照研究．     

经导管局部溶栓治疗髂-股静脉血栓:58例回顾性分析

目的　探讨经导管局部溶栓治疗髂 股静脉血栓的效果及临床应用中的有关问题。资料与方法　对 5 8例髂 股静脉血栓形成患者 (病程 <4周 4 5例 ,>4周 13例 ) ,采取经导管血栓局部灌注尿激酶 ,尿激酶先团注2 5 0 0 0 0U ,然后以 12 5 0 0 0～ 15 0 0 0 0U/h持续灌注。结果　全组溶栓治疗时间 4～ 5 6h ,平均 36h ,尿激酶用量75 0 0 0 0～ 72 5 0 0 0 0U ,平均 4 70 0 0 0 0U。阻塞段完全开通 (残存狭窄率 <30 % )者 30例 ,部分开通者 2 3例 ,无效 5例 ,有效率达 91.4 %。对残存狭窄率 >30 %的 2 3例 ,14例行经皮球囊血管成形术 (PTA)治疗 ,9例行PTA及内支架治疗。 6例溶栓前放置下腔静脉过滤器。本组无严重并发症及肺栓塞发生。结论　经导管血栓局部灌注尿激酶是治疗髂 股静脉血栓的安全、有效方法。溶栓术后继续肝素全身抗凝治疗可增强溶栓疗效     

急性心肌梗塞静脉溶栓治疗冠脉再通者早期ST段再抬高的临床意义

急性心肌梗塞早期静脉溶栓治疗后，一些溶栓再通患者中，可见早期降低的ＳＴ段再度出现抬高现象。本文回顾溶栓成功者８１例，其中早期出现ＳＴ段再度抬高者２１例（占３５％），与ＳＴ段非再度抬高者相比，ＣＰＫ、ＣＰＫ－ＭＢ峰值，心功能及院内死亡率等无显著差异。笔者认为，此现象也为再通的标志之一。因此，急性心肌梗塞溶栓治疗的早期连续监测心电图对确认再通与否非常重要     

直接冠状动脉内支架安置术和r-SK静脉溶栓治疗急性心肌梗死的对比研究

①目的　比较急性心肌梗死 (AMI)病人直接冠状动脉内支架安置和重组链激酶 (r SK)静脉溶栓治疗的临床疗效。②方法　对初次发病 1 2h以内的 1 0 5例AMI病人 ,随机给予直接冠状动脉内支架安置 (支架组 ,6 0例 )和静脉r SK溶栓 (溶栓组 ,5 5例 )治疗。观察两组梗死相关血管再通成功率、心肌梗死溶栓试验 (TIMI)Ⅲ级血流发生率、平均住院天数、住院病死率 ,出院前二维超声心动图测定并推算左心室射血分数 (LVEF)和梗死区室壁运动指数 (RWMI) ,出院后 6个月病死率、LVEF和RWMI。③结果　支架组与溶栓组相比较 ,梗死相关血管再通率显著提高、TIMIⅢ级血流发生率显著增加、平均住院天数显著缩短、住院病死率显著降低 (χ2 =5 .4 2 4～2 8.931 ,t=7.90 1 ,P <0 .0 5、0 .0 1 ) ;出院前LVEF和RWMI ,两组间存在显著差异 (t =3.2 91、2 .1 2 7,P <0 .0 5、0 .0 1 ) ;出院后 6个月病死率、LVEF和RWMI ,两组比较无显著差异。出院后 6个月LVEF、RWMI与出院前比较 ,支架组与溶栓组均有显著改善 (t=2 .1 92～ 4 .6 1 1 ,P <0 .0 5、0 .0 1 )。④结论　与静脉r SK溶栓治疗相比 ,直接冠状动脉内支架安置术治疗AMI,可更有效地再通梗死相关血管、降低住院病死率、更有效地保护病人心脏功能     

Influence of heparin on fibrinogen and D-dimer plasma levels in acute myocardial infarction treated with streptokinase

The purpose of this study was to investigate whether, to whatextent, and through which mechanisms intravenous heparin, administeredbefore and after streptokinase, affects the plasma levels ofD-dimer and fibrinogen in myocardial infarction. Data concerningmortality and incidence of coronary recanalization in patientsreceiving heparin and thrombolytic therapy after acute myocardialinfarction are controversial; furthermore, the mechanisms throughwhich heparin acts in combination with thrombolytic therapyare unclear. Thirty-eight patients with acute myocardial infarctiontreated with streptokinase were considered. Nineteen of themreceived, immediately before the beginning of thrombolytic treatment,a bolus of heparin (100 U. kg¹ intravenously) and, 2 h later,intravenous heparin in doses raising the partial thromboplastintime to 2-2.5 times the normal value (Group 1); the remaining19 did not receive anticoagulant treatment (Group 2). Multipledeterminations of plasma D-dimer and fibrinogen levels wereobtained in all patients before, and in the seven days followingthrombolytic treatment. Six hours after streptokinase, fibrinogendecreased from 304 ± 34 to 61 ± 34 mg. dt¹ inGroup 1 and from 312 ± 29 to 38 ±21 mg. dt¹ inGroup 2 (P<002 versus Group 1). The same difference betweengroups persisted at the 12th and at the 18th hour. D-dimer values,from 0-5 ± 01 \ig. dl¹ in Group 1 and 04 ±01 fig.dt¹ in Group 2, increased at the 1st hour to 37.2 ± 36.5fig. dt¹ and 52.2 ± 39.8 µg. dl¹, respectively.A peak value was reached in both groups at the 6th hour, whichwas followed by a slow decrease. A significant difference betweenthe two groups (P<0.05) was observed at the 1st, 2nd, 4thand 6th hour. An inverse correlation between maximal changesof fibrinogen and of D-dimer was found in both groups (r= 0.89,P<0.001 in Group 1; r=-0.81, P<0.001 in Group 2). The relationship between D-dimer and fibrinogen variations afterstreptokinase and changes induced by heparin, support the hypothesisthat the decrease of fibrinogen, following thrombolysis, isnot only the consequence of its direct degradation, but alsothe result of its transformation by streptokinase into fibrin,fibrin cross-linked (with facilitation of thrombogenic condition)and then into the stable catabolite, D-dimer. These data confirma thrombogenic effect of streptokinase therapy; this tendencycan be limited by prompt use of high doses of heparin.     

靶向寡肽溶栓剂

对靶向寡肽溶栓剂P6A(ARPAK)及其衍生物、RGD肽及含有自由基伪肽的靶向溶栓作用进行综述。P6A是纤溶酶原的降解产物之一,具有增加血管通透性和溶栓作用。P6A的衍生物及P6A代谢产物具有更强的溶栓作用。血栓形成中,RGD序列是纤维蛋白原与血小板结合的关键序列。将RGD序列与溶栓寡肽结合,构成了具有靶向溶栓作用的杂交寡肽。在溶栓治疗中,血流再灌注生成的大量自由基会对组织造成损伤,将自由基清除剂与溶栓寡肽结合可得到具有溶栓和自由基清除双向功能的溶栓伪肽。因为溶栓处是产生大量自由基的部位,所以含自由基清除剂的溶栓伪肽可将自由基清除剂带到自由基堆积部位,体现了靶向内涵。     

TAT和GMP-140在急性心肌梗塞患者溶栓治疗中的应用价值

目的探讨急性心肌梗塞溶栓治疗中凝血酶-抗凝血酶复合物(TAT)和血小板α-颗粒膜蛋白(GMP-140)动态变化及临床应用价值.方法以健康人为正常对照组(n=48),随机选择6h内急性心肌梗塞患者48例,用150万U尿激酶进行溶栓治疗,并按临床再通标准分为再通组(n=30),未通组(n=18),分别在溶栓前、溶栓后2h、4h、24h、48h采用酶联免疫吸附双抗体夹心法测定血浆TAT和GMP-140水平,观察其动态变化.结果患者组治疗前TAT水平(14.56±1.04)μg/L、GMP-140水平(12.50±1.05)ng/ml,较正常对照组(2.15±0.89)μg/L、(8.39±1.33)ng/ml显著升高(P<0.05),治疗后2h再通组GMP-140水平达到峰值(22.17±2.05)ng/ml,4h后TAT到达峰值(46.67±5.79)μg/L(P<0.05)后逐渐下降,持续至少3天,但仍高于正常对照组.未通组二项指标持续缓慢上升,48h达到峰值.结论急性心肌梗塞溶栓治疗前后TAT、GMP-140水平变化对判断疗效有一定指导意义.     

Thrombolytic and antithrombotic effects of the low-molecular-weight heparin-serotonin complex

Thrombolytic activity of the low-molecular-weight heparin-serotonin complex is tested in rats. Thrombi are formed in the left jugular vein. The complex, its components, or normal saline is injected in the right jugular vein 5 min after thrombosis. The complex exhibits high thrombolytic activity in comparison with the control (normal saline) and similar to that of heparin. Antithrombotic activity of the complex is higher than that of heparin, normal saline, and serotonin. Thrombolytic and antithrombotic activities of the complex may be associated with its non-enzyme fibrinolytic activity. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 122, No. 11, pp. 530–532, November, 1996     

Efficacy and tolerance of recombinant tissue-type plasminogen activator in patients with thrombotic or embolic occlusions of leg-arteries

Summary The efficacy and safety of recombinant tissue-type plasminogen activator (rt-PA) was evaluated in 46 patients with thrombembolic arterial occlusions in leg arteries. rt-PA was given over 1–4 h with a maximum dose of 18 mg. The effect of rt-PA treatment was determined as patency of the occluded arteries in 44 different patients 14 days after treatment. In 41 patients at least one artery was recanalized (93%) by rt-PA, and in almost half of these patients (48%) no residual stenosis were detected after the lytic treatment. A slight residual stenosis was detected in 29% of the patients and a severe residual stenosis in 21%. An additional treatment with percutaneous transluminal angioplasty was performed in 23 of the 44 patients and successful in 21 (91%). In 8 patients an addition catheter-embolectomy was performed. No difference in patency rate was detected between patients with thrombotic and those with embolic occlusions. The age of the occlusion influenced the patency rate; occlusions under the age of 5 weeks showed a patency rate of 96% compared to 82% in older occlusions. The length of the occlusion did not have any influence on the outcome of the rt-PA treatment. From the results of this open study we conclude that a dose of up to 18 mg of rt-PA is both safe and effective in the treatment of thromboembolic occlusions in leg arteries.Abbreviations rt-PA recombinant tissue-type plasminogen activator - GGT gamma-glutamyltransferase - SGOT aspartate aminotransferase - SGPT alanine aminotransferase - LDH lactate dehydrogenase - PTA percutaneous transluminal angioplasty Dedicated to Prof. Dr. N. Zöllner on the occasion of his 70th birthday