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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-one patients with acute cerebral infarction were treated with the thrombolytic agent urokinase for either a single or a double infusion period, each of ten hours. The effects of urokinase therapy administered at dosage rates of 1,200, 1,500 or 1,700 CTA urokinase units per pound of body weight per hour were followed by serial blood coagulation and other biochemical studies. In the dosage used, urokinase produced a prompt sustained increase, 20-fold to 40-fold, of plasma thrombolytic activity with relatively minor disturbance of the blood coagulation system. Nevertheless, hemorrhagic complications occurred in several patients and distinctly favorable therapeutic effects were not observed.
Stroke
PMID:A pilot study of urokinase therapy in cerebral infarction. 126 5

Four patients undergoing urokinase infusion therapy for acute occlusive cerebrovascular disease had intracerebral hemorrhage in the ischemic hemisphere. Three patients died during the acute phase of their illness and an autopsy was performed on two. The pathogenesis of cerebral bleeding in these case reports is discussed.
Stroke
PMID:Intracranial bleeding associated with urokinase therapy for acute ischemic hemispheral stroke. 126 6

We report on 10 patients with thromboembolic occlusion of the middle cerebral artery (MCA) who underwent local thrombolytic therapy. Six patients developed a MCA occlusion during long-standing interventional neuroradiological procedures, while four had a proven or suspected cardio-embolic stroke. Streptokinase or urokinase was applied by a microcatheter placed into the thrombus within six hours of clinical onset. Complete or partial revascularization was achieved in all patients. Recovery was complete in seven and partial in three of the patients. In two patients, minor haemorrhagic transformation of the infarct occurred, which did not lead to neurological deterioration. It is concluded that in a selected group of patients with MCA occlusion, local thrombolytic therapy represents a safe and effective therapy.
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PMID:Local thrombolytic therapy for thromboembolic occlusion of the middle cerebral artery. 135 78

We have tested the feasibility of local intraarterial thrombolytic therapy in ischemic stroke in the carotid artery territories observed within 5 h of the onset of symptoms. Only 5 of 615 consecutive patients were enrolled. They were 1 man and 4 women aged 50 to 75 years. Angiography disclosed occlusion of the M2 tract in one, of the M3 tract in one, of the carotid siphon in one of M4 tract in two. Intraarterial urokinase was infused at a mean dosage of 560,000 units close to the site of occlusion. Four of them had partial or complete recanalisation at early angiographic control and were independent at 6th month control. The one who did not demonstrate recanalisation was confined to a wheelchair. One patient, who had recanalisation, sustained a hemorrhagic transformation of the brain ischemia not interfering with outcome. Our experience, at the light of the low rate of enrollment, despite the results, suggest that intraarterial thrombolysis may be a therapeutic tool for selected patients with stroke in the carotid artery territories and not a routinary treatment for them.
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PMID:Local intraarterial thrombolysis for acute stroke in the carotid artery territories. 141 52

Retrograde thrombosis of feeding arteries is a potentially catastrophic complication occasionally reported following resection of arteriovenous malformations (AVM's). No successful therapy for this condition, which causes postoperative stroke, has previously been reported. A case of retrograde thrombosis of the left middle cerebral artery immediately following resection of a parietal AVM is reported in a patient with a retained intra-arterial catheter from preoperative embolization. The administration of urokinase within 4 hours of surgery resulted in dramatic clinical and angiographic improvement without hemorrhagic complications. While urokinase is considered highly experimental in this setting, this case demonstrates that thrombolytic agents should be viewed as therapeutic options worthy of further investigation.
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PMID:Intra-arterial urokinase for treatment of retrograde thrombosis following resection of an arteriovenous malformation. Case report. 158 4

Six patients with extensive hand and forearm thromboembolic disease were treated by means of intraarterial infusion of urokinase, with good clinical results. Four significant complications occurred, including a possible stroke. Embolization of pericatheter thrombus was a possible etiologic factor in this case. Antegrade brachial artery puncture should be used in the setting of prolonged upper extremity thrombolytic therapy to avoid the cerebral vasculature. Thrombolysis is an effective technique for tissue salvage in cases of inoperable hand thrombosis.
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PMID:Extensive thromboembolic disease of the hand and forearm: treatment with thrombolytic therapy. 179 58

In a randomized trial of the effects on in-hospital mortality of intravenous urokinase plus heparin versus heparin alone, 2,531 patients with acute myocardial infarction in 89 coronary care units were enrolled for greater than 30 months. Patients admitted within 4 hours of the onset of pain were randomized to receive either intravenous urokinase (a bolus dose of 1 million U repeated after 60 minutes) plus heparin (a bolus dose of 10,000 U followed by 1,000 IU/hour for 48 hours) or heparin alone (infused at the same rate). Complete data were obtained in 2,201 patients (1,128 taking urokinase and 1,073 taking heparin). At 16 days, overall hospital mortality was 8% in the urokinase and 8.3% in the heparin group (p = not significant). Among patients with anterior infarction, mortality was 10.3% in the urokinase and 13.9% in the heparin group (p = 0.09; relative risk = 0.73). The incidence of major bleeding (urokinase 0.44%, heparin 0.37%) as well as the overall incidence of stroke (urokinase 0.35%, heparin 0.20%) was similar in the 2 groups. The rates of major in-hospital cardiac complications (reinfarction, postinfarction angina) were also similar.
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PMID:Comparison of intravenous urokinase plus heparin versus heparin alone in acute myocardial infarction. Urochinasi per via Sistemica nell'Infarto Miocardico (USIM) Collaborative Group. 154 77

Recent trials of myocardial reperfusion using single-agent thrombolytic therapy and sequential cardiac catheterization have supported a conservative approach to the patient with acute myocardial infarction. To evaluate combination thrombolytic therapy and the role of a previously untested strategy for the aggressive use of cardiac catheterization, we performed a multicenter clinical trial with a 3 x 2 factorial design in which 575 patients were randomly allocated to one of three drug regimens--tissue-type plasminogen activator (t-PA) (n = 191), urokinase (n = 190), or both (n = 194) - and one of two catheterization strategies--immediate catheterization with angioplasty for failed thrombolysis (n = 287) or deferred predischarge catheterization on days 5-10 (n = 288). Patients with contraindications to thrombolytic therapy, cardiogenic shock, or age of more than 75 years were excluded. Global left ventricular ejection fraction was well preserved and almost identical at predischarge catheterization (54%), regardless of the catheterization or thrombolytic strategy used (p = 0.98). Combination thrombolytic therapy was associated with a less complicated clinical course, most clearly documented by a lower rate of reocclusion (2%) compared with urokinase (7%) and t-PA (12%) (p = 0.04) and a lower rate of recurrent ischemia (25%) compared with urokinase (35%) and t-PA (31%). When a composite clinical end point (e.g., death, stroke, reinfarction, reocclusion, heart failure, or recurrent ischemia) was examined, combination thrombolytic therapy was associated with greater freedom from any adverse event (68%) compared with either single agent (urokinase, 55%; t-PA, 60%) (p = 0.04) and with a less complicated clinical course when the composite clinical end points were ranked according to clinical severity (p = 0.024). Early patency rates were greater with combination therapy, although predischarge patency rates after considering interventions to maintain patency were similar among drug regimens. No difference in bleeding complication rates was observed with any thrombolytic regimen. The aggressive catheterization strategy led to an overall early patency rate of 96% and a predischarge patency rate of 94% compared with a 90% predischarge patency in the conservative strategy (p = 0.065). The aggressive strategy improved regional wall motion in the infarct region (-2.16 SDs/chord) compared with deferred catheterization (-2.49 SDs/chord) (p = 0.004). More patients treated with the aggressive strategy were free from adverse outcomes (67% versus 55% in the conservative strategy, p = 0.004), and the clinical course was less complicated when the adverse outcomes were ranked according to severity (p = 0.016). No significant increase in use of blood products resulted from the aggressive strategy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Evaluation of combination thrombolytic therapy and timing of cardiac catheterization in acute myocardial infarction. Results of thrombolysis and angioplasty in myocardial infarction--phase 5 randomized trial. TAMI Study Group. 202 33

Although thrombolytic agents were discovered nearly 60 years ago, it is only within the past decade that the clinical use of these agents has revolutionized the treatment of acute myocardial infarction. There are four currently available agents approved for use in treatment of myocardial infarction: streptokinase, urokinase, tissue plasminogen activator, and anistreplase. Although each of these agents works in a unique fashion, the common end point of therapy is the dissolution of a fibrin clot by the conversion of plasminogen to plasmin. A number of clinically measurable end points have been used to determine the effectiveness of these agents in the treatment of acute myocardial infarction, including mortality, reperfusion, patency, left ventricular function, left ventricular volumes, and quantitative creatine kinase isoenzyme analysis. Secondary end points have included bleeding and stroke, as well as recurrent ischemic events. Numerous clinical studies have demonstrated the effectiveness of all of these agents in achieving the desired end points and comparative studies, including several large-scale trials, have failed to differentiate among these agents with regard to efficacy. Newer dosing regimens for currently available thrombolytic agents, as well as new thrombolytic agents, are currently under active investigation and will be the subject of intense research over the next few years. Despite the lack of consensus as to which agent is superior, it is clear that thrombolytic therapy for acute myocardial infarction is the treatment of choice.
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PMID:Thrombolytic therapy: then and now. 191 23

Thrombolytic agents are aimed at restoring arterial patency thus reducing the risk of cerebral infarction in case of arterial occlusion by blood thrombus or embolus. A review of data from the literature is presented, and the authors have tried to answer the following questions: 1) What are the probabilities of early mortality (first 30 days) and of morbidity due to untreated or medically (thrombolysis excluded) treated cerebral infarction? 2) What are the morbidity and mortality rates after systemic thrombolysis or selective intraarterial thrombolysis? 3) Are the results of thrombolysis affected by the site of arterial occlusion (carotid or vertebrobasilar system)? 4) Does thrombolysis increase the risk of cerebral haemorrhage? 5) Can thrombolysis be regarded as an effective treatment and, if so, in which cases? This study of systemic thrombolysis yielded a mean mortality rate of 22.2%, with satisfactory functional outcome in 58.2% of the survivors. The corresponding figures for selective intraarterial thrombolysis were 29.7% and 84.5% respectively. However when the arterial territories occluded were taken into account, they became 10.4% and 84.4% respectively in the carotid system and 61.5% and 85.00% in the vertebrobasilar system. Comparisons between the natural history of cerebral infarctions, as far as it is known, and the results of thrombolysis suggest that thrombolytic agents are: 1) probably justified by the selective intraarterial route when the occlusion lies in the carotid system; 2) not indicated by the systemic route with urokinase or streptokinase but trials with tPA are being performed. These conclusions, however, must be interpreted with caution as they rest on general data leaving out a number of factors that are often neglected in reports particularly the exact site of arterial occlusion, chiefly in the vertebrobasilar system. From 3 limited cohorts it was possible to evaluate at about 14% the mortality rate in thrombolysis for basilar artery occlusion. This figure, compared with the 70-80% estimate found in the literature for untreated occlusions, suggests that the selective intraarterial thrombolysis may perhaps be indicated also in basilar artery occlusions. It must be noted that selective intraarterial thrombolysis is still an exceptional treatment which requires sophisticated techniques, highly qualified neuroradiologists and prompt application i.e. emergency stroke units.
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PMID:[Thrombolytic agents in cerebral infarctions]. 202 56


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