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

Intracarotid urokinase infusion therapy was performed on 22 patients with evolving cerebral infarction due to acute thromboembolic occlusion of the middle cerebral artery. Mean time from onset of symptoms to start of infusion and mean dosage of urokinase were 4.5 hours and 927,000 units, respectively. Immediate recanalization was achieved in 10 patients (45%) after urokinase therapy. In patients with successful recanalization, rapid amelioration of symptoms followed the restoration of blood flow. Thrombolytic recanalization was associated with reduction of neurologic deficits and of computed tomography-demonstrable infarction volume. The reduction of infarction volume and functional outcome correlated highly with the degree of reflow. Hemorrhagic transformation of infarction occurred in four patients and controllable extracranial bleeding in three patients. These results support the safety and efficacy of urokinase therapy for acute thromboembolic occlusion of the middle cerebral artery.
Stroke 1988 Jul
PMID:Intracarotid urokinase with thromboembolic occlusion of the middle cerebral artery. 338 52

A 37-year-old man was admitted to our clinic 3 hours after the onset of cerebrovascular accident with right hemiparesis and total aphasia. On admission, we started combined administration of mannitol, vitamin E, phenytoin (Sendai Cocktail) and perfluorochemicals to protect ischemic brain. Left cerebral angiography revealed occlusion of the left middle cerebral artery involving its perforating arteries. Following the performance of angiography, vascular balloon catheter was introduced into the embolus, and fibrinolytic agent (urokinase) was continuously injected. Soon after the injection of 240,000 unit urokinase, recanalization of left middle cerebral artery was shown by repeated cerebral angiography performed 5.5 hours after the onset. On his clinical course, left hemiparesis and aphasia were improved step by step, and 1 week later, he could walk by himself with minor neurological deficits. Further examination revealed that myxoma was located on left atrium by echocardiography. Within 1 week, the patient was transferred to cardio-surgical unit, and myxoma was successfully removed. Now he is in good health and has returned to his job. Usually cerebral embolisms result from atrial myxoma cause severe cerebral infarction. Here we reported a case of cerebral embolism by myxoma and recanalized using fibrinolytic agent by balloon catheter injection. The damage will be reduced if the duration of occlusion is limited, so this method will be helpful to treat cerebral embolism.
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PMID:[A case of cerebral embolism caused by atrial myxoma--superselective fibrinolytic therapy]. 344 2

Human arteries and veins contract with hypoxia and deprivation of substrate provoked by increasing calcium inflow into the cell and reduced energy. Such spasm may be eliminated by phosphoenolpyruvate which loads up the cell's energy, blocking glycogen reduction at the same time. Reperfusion will then guarantee a sufficient energy stroke. Therapy should pursue the following steps: 1. Phosphoenolpyruvate infusion (1 X 10(-6) up to 1 X 10(-3) gm/ml in tyrodes solution pH 7.3) into the arterial branch, proximal and distal to the injury. 2. Subsequent treatment with vasodilating drugs and rheologically active substances. 3. Failed therapy after more than three hours warm ischemia could be due to autolytic processes and requires resection of the affected vessel. 4. The imbalance of the thrombolytic system with the so-called no reflow phenomenon could be due to a plasminogen activator's inhibitor released during hypoxia. Such cases may reasonably be treated by urokinase or by streptokinase plasminogen complex.
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PMID:[Vascular spasms in microsurgery]. 362 68

The capacity of intracarotid infusion of urokinase to salvage neurologic function in a baboon model of acute thrombotic stroke has been studied. The model consists of reversible eccentric balloon compression (3 hours) of the right middle cerebral artery (MCA) proximal to the take-off of the lenticulostriate arteries (LSA), resulting in in situ thrombosis of perforating branches supplying the right corpus striatum. Neurologic endpoints included quantitative assessment of neurologic function (NE), estimation of cerebral infarction volume by computerized tomographic (CT) scan, and carotid angiography. In untreated acute stroke control animals (n = 6), a persistent decrease in functional score (from 100 to 36 +/- 11) at 14 days and a defined region of cerebral infarction (volume = 3.2 +/- 1.5) were detected at 10 days. Intracarotid urokinase administered to five animals (1.2 X 10(6) IU over 60 min) following the 3 hour period of MCA occlusion improved neurologic function (NE = 50, 55, 85, 100, 100) and reduced infarction size (0.3, 0.5, 0.8, 0.7, 1.1 cm3, respectively) without evidence of intracranial hemorrhage. Systemic fibrinogenolysis was produced in all five treated animals. We conclude that thrombolytic therapy given within 3 hours of experimental thrombotic occlusion may salvage neurologic function and reduce cerebral infarction volume without CT scan detectable intracranial bleeding.
Stroke
PMID:The beneficial effect of intracarotid urokinase on acute stroke in a baboon model. 373 45

In 16 patients with recent myocardial infarction (3 to 12 week old) and with large left ventricular thrombi systemic thrombolysis with urokinase was performed. Left ventricular thrombi were diagnosed by two-dimensional echocardiography; in all patients the mural thrombus was located in the area of recent myocardial infarction. Each of three patients suffered an embolic episode before the initiation of thrombolytic therapy and the episode caused a stroke in one. Urokinase was infused intravenously at a rate of 60,000 U/hr for 2 to 8 days in combination with intravenous heparin (200 units/kg X 12 hr). Left ventricular thrombi were successfully lysed in 10 of 16 patients, as determined by two-dimensional echocardiography. In four of the six remaining patients only partial thrombolysis was achieved and in two thrombolytic treatment failed. There was no evidence of embolic events during thrombolysis in any of the 16 patients. The success of thrombolysis seemed to depend on the age of the thrombus: the thrombus was dissolved in eight of nine patients undergoing thrombolysis within 4 weeks of the acute myocardial infarction vs in two of seven patients receiving treatment later (p = .057). The presence of a left ventricular aneurysm or depressed left ventricular function also appeared to reduce the likelihood of successful thrombolysis. All patients were discharged on oral anticoagulants. At 6 months follow-up (n = 9) no recurrence of left ventricular thrombus was found. These results show that left ventricular thrombi can be safely lysed by intravenous urokinase. However, for better definition of the risk and benefit of this new therapy further investigation is necessary.
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PMID:Lysis of left ventricular thrombi with urokinase. 400 22

Out of 46 patients who had undergone acute coronary angiography in 41 a definitive acute myocardial infarction was present. In 31 complete and in 10 cases subtotal obliterations of the infarct-related coronary artery were found. 14 patients had a one-vessel-disease, 8 a two-vessel-disease, but 19 a three-vessel-disease. In these 41 patients with acute myocardial infarction a subsequent intracoronary fibrinolysis therapy with streptokinase or urokinase immediately followed, which was successful in 33 patients (80.5%). Coronarographically neither a recanalization or a marked improvement of luminal patency of the infarct-related coronary artery could be proved. In 4 patients an additional guidewire thrombus perforation was necessary. The intracoronary fibrinolysis lasted maximally 2 hours (average total dosage 121.000 +/- 45.000 U streptokinase) and was essentially well tolerated. Only 3 patients of the treatment group died. 20 patients underwent a repeated angiography on average 8 1/2 months after fibrinolysis therapy, out of this group in 10 successfully treated patients comparable quantitative angiographic investigations are present. Heart index, stroke volume and systolic ejection fraction improved significantly. The percental size of the non-contracting area of the myocardium decreased statistically significantly. The recanalized coronary arteries were still patent at control.
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PMID:[Results of local intracoronary fibrinolysis in acute myocardial infarct and the effects of reperfusion on the function of the left ventricle]. 652 81

Thrombolytic therapy was carried out on four patients with brain stem stroke due to thromboembolism of the vertebrobasilar system. Diagnosis was confirmed by angiography. Clinical and instrumental findings indicated a very poor prognosis. Two of these patients were treated with urokinase and the other two with streptokinase for periods ranging from 16 to 44 hours. The interval between onset of symptoms and start of therapy was less than 10 hours for three of these patients. All made a gradual and almost complete recovery after only a few hours of treatment, and only one presented minimal residual neurological disability. The condition of the fourth patient, who started therapy four days after the first episode, remained unchanged until he died 16 hours later. Our observations suggest that thrombolytic therapy may be useful in treating recent acute life-threatening brain stem stroke.
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PMID:Thrombolytic therapy for thromboembolism of vertebrobasilar artery. 661 85

Elevation in the plasma concentration of fibrinogen in coronary heart disease (CHD) and in stroke has been found to be due to increased biosynthesis and turnover. The pathway of the increased turnover of fibrinogen is via formation of fibrin. A new method for detecting and measuring intravascular fibrin has shown a highly significant elevation in these patients. These elevated levels of fibrin formation, or intravascular clotting, are associated with depressed fibrinolysis or clot lysis. This increased formation of fibrin in the patient is not responsive to conventional oral anticoagulant therapy with Coumadin (Na Warfarin). Prospective studies on over 1,500 patients have shown elevated plasma fibrinogen to have at least as strong an association with cardiovascular death as raised cholesterol. Increased plasma fibrin is highly susceptive to control with low dose heparin and urokinase. These discoveries should provide the health care field with a new basis for detecting early warning signs of CHD and thrombotic stroke and for more effective preventive therapy.
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PMID:Haemostatic factors and coronary heart disease. 716 89

Thrombolytic therapy mimics and enhances physiological fibrinolysis. The following substances are presently available for clinical use: the nonphysiological thrombolytics streptokinase, the APSAC (acylated plasminogen-streptokinase activator complex), the physiological plasminogen activators urokinase and tissue plasminogen activator (t-PA). Whereas the first three systematically activate the fibrinolytic system, t-PA possesses relative fibrin selectivity. The fibrin-selective active pro-urokinase has not yet been officially approved for the treatment of thromboembolic diseases, but it is being clinically tested. Fibrinolytic therapy has an established place in the management of acute myocardial infarction and of massive pulmonary embolism. When an acute deep venous thrombosis is diagnosed with a proximal extension into the popliteal vein, thrombolytic therapy is clearly superior to heparin. The lysis has proven to be an effective form of treatment of peripheral occlusive arterial disease. Local thrombolytic therapy is an option for acute and chronic femoro-popliteal occlusions involving the trifurcation into the calf arteries and for embolic occlusions of the same segment in patients with contraindications to surgical therapy. First study results of thrombolytic therapy of stroke are promising.
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PMID:[Fibrinolytic agents--who benefits when?]. 748 76

Patients with a recent (less than 10 days) proximal deep vein thrombosis of the leg or pelvis are candidates for thrombolysis as the major benefit over heparin seems to be the prevention of the postphlebitic limb, an aim which is still not proven in a satisfactory manner. Nonocclusive thrombi appear to lyse more readily than occlusive thrombi. For this indication the optimal dose regimens for the three thrombolytic drugs (streptokinase, urokinase, alteplase) are not established. Acute massive pulmonary embolism with hypotension or shock should be treated with thrombolytic drugs and, pending the outcome in the first hour, be considered for pulmonary embolectomy. Major acute pulmonary embolism with haemodynamic instability responds well to thrombolysis. Whether thrombolysis is superior to heparin in subacute intermediate pulmonary embolism has not been proven unequivocally in terms of mortality or clinically important endpoints. Systemic administration of thrombolytic drugs for peripheral arterial occlusion has been abandoned for catheter-directed and intraoperative intra-arterial repeated bolus or short-term infusions. The efficacy and safety of intravenous thrombolytic treatment following a major ischaemic stroke is presently being tested in large scale trials; its use must be restricted to experimental protocols.
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PMID:Thrombolytic therapy of non-cardiac disorders. 754 71


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