尿激酶溶栓联合介入术治疗急性脑梗死51例

目的评价急性脑梗死动脉内溶栓结合动脉溶栓后残余狭窄球囊扩张、支架置入术治疗的疗效。方法 51例急性脑梗死病人采取超选择接触性溶栓,尿激酶(UK)用微量泵以1×104U/min持续泵入,总量为60×104U～100×104U。在泵入尿激酶的过程中,通过导引导管造影,了解闭塞血管再通情况。结果颈动脉系统血管闭塞43例,椎-基底动脉系统闭塞2例。脑血管造影未发现明显的血管闭塞6例。颈内动脉闭塞再通率为63.64%;大脑中动脉闭塞再通率为63.63%;大脑中动脉分支闭塞再通率为55.56%;大脑前动脉闭塞(前交通动脉未开放)的1例再通;椎-基底动脉系统闭塞2例全部部分再通。动脉溶栓后颈内动脉残余明显狭窄3例行球囊扩张支架置入术。临床症状完全恢复正常或有明显好转的33例(64.71%)。结论动脉内接触性溶栓结合动脉溶栓后残余狭窄球囊扩张、支架置入术治疗急性脑梗死能明显提高治愈率,减少致残率,是安全、可靠、有效的治疗方法。     

发病24h内症状性颅内外大动脉狭窄或闭塞急诊支架治疗的临床观察

急性脑梗死的治疗有静脉溶栓、动脉溶栓、抗血小板药物、扩容等,但是国内对于症状性脑动脉狭窄行支架治疗研究甚少,本文就2例发病24 h内从中获益的患者进行分析.     

后循环脑梗死患者静脉溶栓后不同治疗方法的效果对比

目的探讨静脉溶栓后即刻抗凝、即刻抗血小板聚集与24 h后抗血小板聚集在治疗后循环梗死患者的临床效果。方法发病4~9 h的后循环脑梗死患者65例随机分为行静脉溶栓后即刻抗凝组18例、即刻抗血小板聚集组22例与24 h后抗血小板聚集组25例。采用美国国立卫生研究院脑卒中量表(NIHSS)评分观察临床症状改善情况,评价治疗后24 h和7 d治疗效果。结果治疗24 h和治疗7 d的疗效比较,即刻抗血小板聚集组有效率高于24 h后抗血小板聚集组,即刻抗凝组有效率明显高于即刻抗血小板聚集、24 h后抗血小板聚集组(P0.05)。结论后循环梗死患者病情危重,不一定完全按照指南,可根据自身情况,尝试溶栓后即刻给予抗凝或抗血小板聚集的联合治疗。     

急性脑梗死溶栓治疗的血管再通率

评价急性脑梗死的溶栓治疗的效果。使闭塞的脑血管再通是溶栓治疗的基础。开展急性脑梗死的溶栓治疗 ,需要探讨急性脑梗死的血管闭塞率和自然再通率 ,了解动脉和静脉溶栓治疗的血管再通率 ,以及影响溶栓治疗血管开通的因素。针对上述有关问题 ,我们结合自己的临床实践进行了文献系统综述     

老年椎-基底动脉闭塞患者院内死亡危险因素分析

随着老龄人口的增多，脑梗死的发病率也相应增多，从而导致脑梗死病死亡率的上升。分析急性脑梗死患者病变情况，认识其规律和相关影响因素，对于临床采取相应措施以降低其死亡率，争取良好的功能性恢复具有重要指导意义。椎一基底动脉闭塞约占脑梗死的20％，但有很高的死亡率，经早期溶栓抗凝抗血小板聚集治疗，血管再通部分患者可脱离生命危险，但血管再通后部分患者可出现再次闭塞、各种感染、营养不良、电解质紊乱、脏器衰竭等，没有血管再通的死亡率高达70％～90％。本文着重探讨椎一基底动脉闭塞的老年患者院内死亡的危险因素及对生存有益的因素。     

超选择动脉内溶栓治疗急性脑梗死46例疗效观察

目的评价超选择性动脉溶栓治疗急性期脑梗死的疗效及安全性。方法对46例发病6h内的急性脑梗死患者给予尿激酶超选择性动脉内溶栓治疗,分别于溶栓前,溶栓后24h、14d、3个月行NIHSS评分,3个月时行改良Rankin评分（mRS）。结果造影发现闭塞38例,溶栓后血管再通33例（完全再通21例,部分再通12例）;溶栓后各时间点NIHSS评分均明显下降（P均〈0．05）,3个月时mRS评分≤3分者28例;其间颅内出血2例,死亡3例。结论超选择性动脉内溶栓能提高闭塞血管再通率,改善患者预后。     

动脉溶栓治疗基底动脉闭塞后血管再通的影响因素

基底动脉闭塞直接影响脑干的供血，并且直接累及穿支动脉，因侧支循环代偿较差，故常被视为致命性脑梗死的最主要原因。然而，最初对于老年人群的研究认为，基底动脉闭塞属于少见疾病，而后通过全脑血管造影，发现本病并不少见。对于基底动脉闭塞，若采取传统方法，如降纤治疗、抗凝治疗和抗血小板聚集治疗，通常难以及时使基底动脉的血管再通，病死率高达80％～90％。因此，20世纪80年代开始，基底动脉闭塞后动脉溶栓治疗才得以逐步开展和不断完善。我们回顾20余年基底动脉闭塞的动脉溶栓治疗的相关文献，初步探讨血管再通及其临床意义。     

静脉溶栓桥接动脉内取栓治疗颅内大血管急性闭塞的效果分析

目的探讨静脉溶栓桥接动脉内取栓开通颅内大血管急性闭塞的安全性和有效性。方法回顾性分析首都医科大学宣武医院2016年1月至9月采用静脉溶栓桥接动脉内取栓模式治疗的63例颅内大血管急性闭塞患者的临床资料,静脉溶栓开始时间在发病≤4.5 h,血管内治疗开始时间(股动脉穿刺)在发病≤6 h。根据取栓方式将其分为单纯支架取栓组(41例)和支架联合抽吸取栓组(22例),两组患者在性别构成、平均年龄、闭塞部位及入院美国国立卫生研究院卒中量表(NIHSS)评分方面差异无统计学意义(均P0.05)。采用改良脑梗死溶栓试验(m TICI)评价血管开通效果,分析静脉桥接下两种动脉内治疗方式的血管再通时间,取栓次数,入院时、术后72 h和90 d的NIHSS评分,术中及术后并发症发生情况。结果 (1)单纯支架取栓组中,前循环闭塞37例(90.2%),后循环闭塞4例(9.8%);支架联合抽吸取栓组中,前循环闭塞20例(90.9%),后循环闭塞2例(9.1%),组间差异无统计学意义(P0.05)。治疗后患者大血管均获得良好开通(m TICI分级:Ⅱb~Ⅲ级)。(2)单纯支架取栓组血管平均再通时间为(86±11)min,平均动脉取栓次数为(2.8±0.9)次;术后并发症发生率为14.6%(症状性出血5例,心源性死亡1例),90 d随访mRS(0~2分)患者占51.2%(21/41)。支架联合抽吸取栓组血管平均再通时间为(83±11)min,平均动脉取栓次数为(2.2±0.8)次,术后并发症发生率为13.6%(症状性出血2例,心源性死亡1例),90 d随访mRS(0~2分)患者占59.1%(13/22)。两组以上指标比较,差异均有统计学意义(均P0.05)。结论静脉溶栓桥接单纯支架取栓和支架联合抽吸取栓均能快速使颅内闭塞大血管获得再通,并且支架联合抽吸取栓具有更好的再通率。但两种技术在改善患者临床预后方面尚有待进一步研究。     

急性颈内动脉闭塞症介入治疗11例

急性颈内动脉(ICA)闭塞多发生在动脉粥样硬化狭窄的基础上,出现急性ICA闭塞,从而导致急性脑梗死,是最严重的脑血管病之一,如不积极治疗其后果往往是严重的,甚至危及病人生命,常规静脉溶栓往往难以使闭塞血管完全再通,即使静脉溶栓后血管暂时恢复供血,但术后再闭塞可能性很大,但     

静脉溶栓联合负荷量阿司匹林治疗内囊预警综合征一例

内囊预警综合征(CWS)是一组临床罕见的脑血管病综合征,易进展为急性脑梗死。该研究报道1例以发作性右侧肢体无力伴言语模糊起病的CWS患者,予阿替普酶静脉溶栓治疗后,仍反复频发刻板样短暂性脑缺血发作,评估获益后,静脉溶栓24 h内予负荷剂量阿司匹林抗血小板聚集治疗,患者症状得到控制,但对静脉溶栓24 h内能否启动抗血小板聚集治疗尚需大规模数据进一步探讨。     

静脉联合超选择动脉溶栓治疗急性缺血性脑卒中的疗效及安全性

目的观察静脉联合超选择动脉溶栓治疗缺血性脑卒中的疗效及安全性。方法回顾分析2003年8月~2005年8月急性缺血性脑卒中患者67例,随机分为观察组34例和对照组33例,分别给予静脉联合动脉溶栓和单纯动脉溶栓治疗,比较两组患者间疗效。结果观察组与对照组再通率间差异有非常显著性意义(P<0·01);观察组发病3h内与3~6h溶栓患者再通率间差异有显著性意义(P<0·05)。结论静脉联合超选择动脉溶栓治疗缺血性脑卒中能明显提高闭塞血管的再通率,疗效好,见效快,明显改善预后,是治疗急性缺血性脑卒中有效和相对安全的方法。     

Pathogenesis of impending myocardial infarction and acute myocardial infarction: clinical and angiographic evaluation of coronary thrombosis as a precipitating factor

In order to investigate the role of coronary thrombosis as a precipitating factor of acute myocardial infarction (AMI), we examined coronary angiographic findings in 89 patients with AMI taken within 24 hours of the onset and in 42 patients with prolonged angina attack of impending myocardial infarction (impending MI) taken within 50 hours of the last angina attack. Furthermore, in the patients with impending MI, the effects of intracoronary and intravenous thrombolytic therapy and anticoagulant therapy used to prevent impending MI from developing into AMI, were also studied. (1) In 72 of 89 patients (81%) with AMI, coronary thrombi were detected angiographically. The thrombi were detected most frequently (88%) in angiographs taken within 3 hours of onset. (2) In 23 of 42 patients with impending MI, coronary thrombi were detected angiographically. In 6 patients with coronary thrombi who underwent intracoronary thrombolysis during angina attack, occlusive coronary thrombi in ischemia-related vessels were the observed, and recanalization by thrombolysis with intracoronary urokinase infusion relieved chest pain and improved ECG changes. (3) The incidence of AMI in 42 patients with impending MI who were treated with intracoronary and intravenous thrombolytic therapy and anticoagulant therapy was significantly less than in the conventional therapy group (80 patients) (11.9% vs. 27.5%; p less than 0.05). In 4 of 5 patients with developing AMI, coronary thrombi were detected angiographically in the acute phase of impending MI. These results indicate that coronary thrombosis plays an important role not only in the precipitation of impending MI but also in the development of impending MI to AMI.     

Randomized,placebo-controlled study of Lamifiban with thrombolytic therapy for the treatment of acute myocardial infarction: Rationale and design for the Platelet Aggregation Receptor Antagonist Dose Investigation and Reperfusion Gain in Myocardial Infarction (PARADIGM) study

The benefits of thrombolytic therapy in the treatment of acute myocardial infarction are incontrovertible. Large-scale studies combining angiographic and clinical endpoints have demonstrated a perfusion-mortality relationship, with the highest survival rate among patients with early restoration of TIMI grade 3 coronary arterial flow. Despite advances in thrombolytic strategies, a substantial number of patients fail to rapidly achieve and maintain adequate coronary perfusion with thrombolysis. Conjunctive therapy with aspirin has proven useful in thrombolytic regimens, likely countering the heightened platelet activity central to acute coronary syndromes. The antiplatelet effect of aspirin is relatively weak compared with that of glycoprotein IIb/IIIa platelet receptor antagonists, which block the final common pathway of platelet aggregation. Lamifiban is a nonpeptide glycoprotein IIb/IIIa receptor antagonist. In early experimental studies, Lamifiban in combination with thrombolytic therapy has been shown to effectively restore coronary arterial patency, and phase I and phase II data have shown its use to be safe. To determine the optimal dose with regard to safety and efficacy of Lamifiban to be used with thrombolytic therapy in a large-scale trial, a phase II study is underway. The Platelet Aggregation Receptor Antagonist Dose Investigation and Reperfusion Gain in Myocardial Infarction (PARADIGM) study is a randomized, placebo-controlled study of Lamifiban in 400 patients receiving thrombolysis as treatment for acute myocardial infarction. By studying 90-minute angiography, platelet aggregation, continuous electrocardiography, and clinical outcome in PARADIGM, important insights will be obtained to determine the optimal dose of Lamifiban for phase III study. We provide the background and rationale for the study of Lamifiban in PARADIGM and other ongoing studies in acute coronary syndromes.     

Platelet activation during thrombolysis and percutaneous transluminal coronary angioplasty in the acute phase of myocardial infarction

To clarify the mechanism of recanalization and reocclusion in thrombolysis and percutaneous transluminal coronary angioplasty (PTCA), the plasma concentrations of beta-thromboglobulin (beta-TG), thromboxane B2 (TXB2) and platelet aggregation adenosine diphosphate (ADP) (2 microM/ml, collagen 2 micrograms/ml) were assessed in 11 normal subjects and in 19 patients with acute myocardial infarction whose infarct-related vessels were recanalized by thrombolysis and/or PTCA. In patients with acute myocardial infarction, the plasma concentrations of beta-TG and TXB2 were significantly higher than those in normal subjects (beta-TG: 128 +/- 132 ng/ml vs 38 +/- 17 ng/ml, TXB2: 131 +/- 154 pg/ml vs 36 +/- 18 pg/ml). Collagen-induced platelet aggregation decreased significantly in patients with acute myocardial infarction; whereas, ADP-induced platelet aggregation showed no significant difference. Infarct-related vessels recanalized by thrombolysis (seven patients: group 1) and PTCA (seven patients: group 2) were patent on the follow-up angiograms. Infarct-related vessels were reoccluded in five patients immediately after PTCA or during the follow-up angiography (group 3). Beta-TG and TXB2 did not change before and after recanalization in groups 1 and 2, but increased significantly after recanalization in group 3 (beta-TG: 155 +/- 185 ng/ml----269 +/- 233 ng/ml, TXB2: 104 +/- 87 pg/ml----169 +/- 91 pg/ml). Platelet aggregation did not differ significantly among the three groups. We concluded that platelets are not activated during thrombolysis and/or PTCA in cases without reocclusion, while platelets are markedly activated during PTCA in cases with reocclusion. Thus, it is suggested that platelet activation plays an important role in the mechanism of reocclusion.     

Experimental treatments for acute ischaemic stroke

Treatments for acute ischaemic stroke continue to evolve. Experimental approaches to restore cerebral perfusion include techniques to augment recanalising therapies, including combination of antiplatelet agents with intravenous thrombolysis, bridging therapy of combining intravenous with intra-arterial thrombolysis, and trials of new thrombolytic agents. Trials with MRI selection criteria are underway to expand the window of opportunity for thrombolysis. Sonothrombolysis and novel endovascular mechanical devices to retrieve or dissolve acute cerebral occlusions are being tested. Approaches to improve cerebral perfusion with other devices and induced hypertension are also being considered. Although numerous neuroprotective agents have not shown benefit, trials of hypothermia, magnesium, caffeinol, high doses of statins, and albumin are continuing. The findings of these randomised trials are anticipated to allow improved treatment of patients with acute stroke.     

New approaches to treatment of myocardial infarction

Survival of patients with acute transmural infarction is largely related to the size of the myocardial infarction. The goal of thrombolytic therapy in acute myocardial infarction is maximal salvage of myocardium by reestablishment of flow in the occluded infarct-related artery and the establishment and maintenance of a patent infarct-related artery. Results of randomized trials show a significant reduction in mortality in patients who have undergone thrombolysis. A patent infarct-related artery, even in the absence of a change in left ventricular function, is associated with reduced mortality. The Thrombolysis in Myocardial Infarction Trial and the European Cooperative Trial showed that recombinant tissue-type plasminogen activator is superior to streptokinase in reestablishing flow in a totally occluded artery. Experimental and clinical evidence suggests that thrombolysis and thrombosis occur simultaneously, and that lysis appears to increase both thrombin and platelet activity. Effective reduction of thrombosis accelerates thrombolysis. Rethrombosis after thrombolysis is due to anchored residual thrombus, which alters the hemorrheology of blood flow and produces a highly thrombogenic substrate that is largely due to residual fibrin-bound thrombin. Platelet deposition is directly related to severity of residual stenosis and shear rate. Thrombin appears to be the most potent of the 5 potential stimulators of platelet activation during arterial thrombosis. Proper anticoagulation can play an important role in reducing thrombosis. Experimental evidence strongly supports the use of heparin during and after thrombolysis. A recently reported study shows continued reduction of residual stenosis after 1 month of vigorous anticoagulation with intravenous heparin and subsequent oral anticoagulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

尿激酶及阿司匹林对血浆α-颗粒膜蛋白140的影响及意义

目的：探讨急性心肌梗塞（ＡＭＩ）患者尿激酶静脉溶栓及阿司匹林口服治疗前后血小板活性的动态变化及与血管再通的关系。方法：８０例ＡＭＩ患者,随机分成溶栓组及溶栓＋阿司匹林组各４０例,于溶栓前及溶栓后２、６、１２、２４小时测定血浆中α－颗粒膜蛋白１４０（ＧＭＰ－１４０）浓度,依临床间接指标（３８例行冠状动脉造影）判定血管再通,比较两组间及两组中再通与未通患者血浆ＧＭＰ－１４０浓度的动态变化。正常对照组６０例。结果：ＡＭＩ患者溶栓前后血浆ＧＭＰ－１４０浓度均明显高于正常对照组。两个溶栓组溶栓后再通与未通患者均呈现不同浓度的动态变化。血管再通,则血浆ＧＭＰ－１４０浓度降低,血管未通,血浆ＧＭＰ－１４０浓度升高;阿司匹林对血浆ＧＭＰ－１４０浓度无影响。结论：ＡＭＩ后血小板高度活化,血浆ＧＭＰ－１４０浓度与血栓形成、溶解及再通密切相关;阿司匹林不是抑制血小板活化的理想药物。     

Fiberoptic study on the effects of transluminal angioplasty in experimental occlusive arterial thrombosis

Percutaneous transluminal coronary angioplasty has been proposed as definitive therapy for coronary recanalization of occluded coronary arteries in patients with acute myocardial infarction (AMI). The effects of transluminal angioplasty (TA) on experimental occlusive canine arterial thrombi that closely simulated the clinical condition was examined by a fiberoptic method. Experimental arterial thrombosis was produced by endothelial denudation and induction of luminal stenosis. Eighteen dogs that showed total occlusion of the iliac artery with thrombi were evaluated. Seven dogs (group A) with 6-hour-old thrombi received 20,000 IU/kg intravenous urokinase (UK) but did not show recanalization. TA was performed with a Gruentzig or Simpson-Robert balloon catheter and its effect was evaluated by a vascular fibroscope. Eight dogs (group B) with 6-hour-old thrombi underwent primary TA. After TA, less than 50% luminal obstruction with residual thrombi was visualized in five dogs (71%) of group A and four dogs (50%) of group B. Residual thrombi showed a doughnut-like or globular type shape and consisted of dense fibrin networks and compact platelet aggregates. All dogs in group B received 20,000 IU/kg intravenous UK after TA, but most of them showed progression of thrombus size despite UK infusion. In conclusion, the results suggest (1) that TA is effective in recanalization of an occluded artery with aged thrombus that is resistant to thrombolytic therapy and (2) that vascular fiberscope is a useful method for evaluation of the effects of TA on occlusive arterial thrombus.     

Reappraising the role of immediate intervention following thrombolytic recanalization in acute myocardial infarction

Early studies indicated that after successful thrombolytic recanalization, adjunctive percutaneous transluminal coronary angioplasty (PTCA) was not appropriate, even when a significant residual stenosis was present. The aim of this study was to assess in-hospital clinical outcomes of patients with acute myocardial infarction (AMI) who underwent successful recanalization after thrombolytic therapy. The relation between repeat AMI/unstable angina and the severity of the stenosis, as well as other angiographic and clinical features was also examined. One hundred patients with AMI of <10 hours underwent coronary angiography 2 hours after receiving thrombolytic therapy. Salvage PTCA +/- stenting was performed if recanalization was unsuccessful (Thrombolysis In Myocardial Infarction [TIMI] trial grade 0 to 2), and no PTCA was undertaken if there was brisk anterograde flow (TIMI 3). Angiographic analysis was performed to assess the severity of the residual lesion, as well as the presence or absence of thrombus. Forty patients had unsuccessful recanalization, and of these, 36 underwent attempted PTCA. Of the 60 patients with TIMI 3 flow, 15 required repeat angiography and PTCA after repeat AMI (n = 13) or unstable angina (n = 2) within 5 days. Receiver-operating characteristic analysis indicated an optimum percent diameter stenosis predictor of 85% for repeat AMI/unstable angina. There was no additional relation to age, gender, time to thrombolysis, the infarct-related artery, or the presence of culprit lesion thrombus. After recanalization, a high-grade stenosis >85% is common (n = 25, 42.4%). This is associated with a 54% repeat AMI/unstable angina risk-a ninefold increase in the incidence of such events than in patients with lesions <85%. Thus, patients with narrowings >85% may benefit from early intervention rather than a conservative approach. Narrowings <85% have a 94% probability of no repeat AMI/unstable angina and do not require early intervention.