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

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

Streptokinase remains the most widely used agent worldwide, largely because it is the cheapest. Because of cost considerations when the incremental cost of the use of accelerated TPA exceeds $35,000 (US) per life year added, and because an iatrogenically induced stroke in a patient who is otherwise likely to have a good outcome is unacceptable, streptokinase may be used in patients with small to moderate-sized infarctions and those aged less than 60 years. Streptokinase is the agent of choice in patients who have an increased risk of stroke and may be used in patients presenting after 6 hours. Streptokinase also may have a role in patients with cardiogenic shock. Administration of accelerated TPA is the treatment of choice in patients at high risk such as those with large anterior infarctions, the elderly, and patients with bypass grafts, and it is an alternative to urokinase when streptokinase has been administered previously. The most important approach is to treat as many patients as early as possible with thrombolytic therapy regardless of which agent is used. Thrombolytic therapy still is widely underused. More lives will be saved, regardless of which thrombolytic drug is used, by encouraging patients to present early, improving on the "door-to-needle" time, and treating more patients with a therapy that can save thousands of lives worldwide.
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PMID:Selecting a thrombolytic agent. 758 72

To clarify the efficacy and limitations of the intra-arterial local infusion of a high-dose fibrinolytic agent for acute embolic stroke, we analyzed the results of 44 patients and compared them with those of 51 patients treated with intracarotid (18 patients) or intravenous (33 patients) infusion therapy. Ten megaunits of recombinant tissue plasminogen activator or 24 x 10(4) IU of urokinase were administered through a microcatheter placed into or proximal to an embolus for 20 minutes. When arterial recanalization was not achieved, a second or third infusion was performed. The rates of complete and partial recanalization just after the local infusion were 52 and 32%, respectively. They were high in middle cerebral and basilar artery occlusion and low in internal carotid artery occlusion (69, 78, and 20%, respectively). In our use, there was no difference between tissue plasminogen activator and urokinase in restoring blood flow. The mean time interval from onset to recanalization in patients with middle cerebral artery occlusion showing marked improvement was 4.8 hours, and it was 5.8 hours with basilar artery occlusion. The size of infarction was reduced, and the outcome was good in patients with complete recanalization achieved. The incidence of hemorrhagic infarction within 24 hours was 22%, and only one patient clinically deteriorated. In the intracarotid infusion group (20 x 10(4) IU of urokinase for 30 min), only two patients showed partial recanalization without clinical improvement. The incidence of hemorrhagic infarction was 28%. The outcome in this group and the intravenous infusion group (18 x 10(4) IU of urokinase a day for 1 wk) was poor compared with that in the local infusion group showing complete recanalization. This preliminary study appears to suggest that intra-arterial local fibrinolytic therapy could be a new strategy for acute embolic stroke.
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PMID:Fibrinolytic therapy for acute embolic stroke: intravenous, intracarotid, and intra-arterial local approaches. 773 3

Seven prospective, epidemiological studies indicate plasma fibrinogen levels (over 300-350 mg/dl) as an important, independent cardiovascular risk factor for subsequent myocardial infarction and stroke. Furthermore, several clinical studies revealed an association between fibrinogen and both the angiographic and clinical degree of coronary heart disease. In addition, a significant relation of fibrinogen with the number of occluded coronary vessels was found. The following pathophysiologic mechanism are of particular importance: Fibrinogen is a main determinant of plasma viscosity and red cell aggregation. Both phenomena deteriorate blood fluidity especially in the microcirculation. Fibrinogen plays a central role in platelet aggregation and performs an essential substrate in the coagulation cascade. Thus, high fibrinogen levels may favor a hypercoagulable state resulting in final thrombotic events of cardiovascular disease. Fibrinogen is also involved in atherogenesis by stimulating proliferation and migration of smooth muscle cells. Several determinants of fibrinogen levels are known. Smoking is the strongest one in healthy persons. This clinically important effect is dose related. Consequently, cessation of smoking is a major step to lower fibrinogen and subsequently the individual cardiovascular risk. Reduction of overweight and maintenance of regular physical activity are further nonpharmacologic means. Fibrates decrease fibrinogen about 10-30% on an average. Finally, intermittent low-dose Urokinase for end-stages of coronary artery disease and LDL-apheresis (HELP) represent additional approaches to reduce fibrinogen.
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PMID:[Clinical significance of the cardiovascular risk factor fibrinogen in secondary prevention]. 776 17

Intracerebral hemorrhagic transformation is one of the most important complications of thrombolytic therapy for acute ischemic stroke. The relationship between changes in markers for the coagulation and fibrinolytic systems and occurrence of hemorrhagic transformation was determined after local intra-arterial thrombolytic therapy using urokinase (UK) (24 patients) or recombinant tissue plasminogen activator (t-PA) (10 patients) within 6 hours of onset. All 34 patients had no hypodensity areas on initial computed tomography scans. Plasma concentrations of fibrinogen-fibrin degradation products (FDP), fibrinogen, alpha 2-plasmin inhibitor (alpha 2-PI), plasmin-alpha 2 plasmin inhibitor complex (PIC), thrombin-antithrombin III complex (TAT), and D-dimer were measured. Hemorrhagic transformation occurred in seven patients (21%) with complete or partial recanalization; four in the UK group and three in the t-PA group. Doses of the thrombolytic agents did not correlate with the incidence of hemorrhagic transformation. The FDP levels in the hemorrhagic transformation group treated with UK significantly increased immediately and 1 hour after the therapy. The alpha 2-PI activities decreased and PIC levels increased in both the hemorrhagic transformation and the nonhemorrhagic groups after the therapy. The TAT levels in both groups tended to be higher than the normal range, but there was no significant difference from the pretreatment levels. The D-dimer levels in the hemorrhagic transformation group were higher than those in the nonhemorrhagic group at 24 hours after the therapy. Furthermore, the D-dimer levels were significantly higher in patients with complete recanalization compared with those with none or partial recanalization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in coagulation and fibrinolytic system after local intra-arterial thrombolysis for acute ischemic stroke. 777 Jan 6

Thrombolysis with tissue plasminogen activator (tPA) and hypothermia are two potential treatment modalities for acute ischemic stroke. Many investigators are studying these modalities both in the laboratory and in clinical trials. Because these modalities each appear to show benefit in animal models, there is considerable interest in studying combined therapy with both thrombolysis and hypothermia. However, it is known that alterations in the coagulation system can occur with decreased body temperature. Clinicians have frequently observed bleeding problems when patients are subjected to hypothermia for a variety of reasons. Hypothermia induced coagulopathy has been attributed to a variety of factors. Hypothermia can cause platelet dysfunction, inhibition of clotting factors, increased fibrinolysis and endogenous production of a heparin-like factor. Groups who studied fibrinolysis and temperature, however, found the opposite to be the case. Clot lysis studies with streptokinase showed increased fibrinolysis at higher temperatures. Data by Mumme suggested that the peak fibrinolytic activity of streptokinase was at 40 degrees C, but at 43 degrees C fibrinolytic activity was decreased. Rijken et al studied plasminogen activation with tissue plasminogen activator (tPA), urokinase and streptokinase at extremely low temperatures. They found less plasminogen activation and fibrinogen degradation at 25 degrees C compared to 37 degrees C, but negligible differences at 10 degrees C, 0 degrees C and -8 degrees C. To our knowledge, there is no data studying the fibrinolytic activity of tissue plasminogen activator (tPA) at temperature ranges between 25-37 degrees C which is the range of temperatures used clinically for therapeutic purposes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thrombolysis with tissue plasminogen activator (tPA) is temperature dependent. 777 62

This is a case report of a 47-year-old man admitted with a 7-month history of disequilibrium, multiple reversible vertebrobasilar ischemic attacks, and one submaximal completed stroke in the left posterior inferior cerebellar artery distribution. Vertebrobasilar ischemic attacks continued despite anti-coagulation, and orthostatic symptomatology suggested a significant hemodynamic component contributing to the posterior circulation ischemia. Angiography confirmed bilateral high-grade stenoses of the intracranial vertebral arteries. A right intracranial vertebral artery endarterectomy was performed with electroencephalographic and somatosensory evoked potential monitoring and protection with barbiturate infusion. The arteriotomy was closed with a vein patch. Postoperatively, the endarterectomy site thrombosed. This thrombosis was completely reversed with 220,000 U of urokinase selectively infused intra-arterially at the site of thrombosis. This procedure was not complicated by hemorrhage or distal embolization. The vertebral artery was confirmed to be patent 24 hours and 7 days after the urokinase injection. The patient sustained a borderzone infarction in the right cerebellar hemisphere without neurological deficits and was discharged home well.
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PMID:Successful treatment of an acute thrombosis of an intracranial vertebral artery endarterectomy with urokinase. 783 54

Intra-carotid urokinase (UK) infusion in 20 patients with acute internal carotid artery (ICA) territorial ischemic stroke achieved immediate recanalization in 45% and the clinical outcome in patients with recanalization was superior to that of patients without recanalization. The procedure was most effective in patients with smaller arterial occlusions: 7 of 10 patients with MCA branch occlusions (M2 to M4) achieved recanalization compared to only 2 of 10 with distal ICA or M1 occlusions, which should be an important issue for the critical evaluation of the efficacy of thrombolytic therapy (TT). Hemorrhagic transformation was observed in 9 patients on CT scan; petechial hemorrhage in 5 and intraparenchymal hematoma formation in 4. Among 4 patients with hematoma formation, clinical deterioration was seen in 3 cases and the angiography at the immediate end of the UK infusion showed recanalization in only one patient. The average dose of UK in patients with parenchymal hematoma formation was higher than that of patients without hemorrhagic transformation (123.3 x 10(4) units vs 101 x 10(4) units). The administration of a large dose of UK, probably more than 100 x 10(4) units, and the absence of immediate recanalization seemed to increase the risk of parenchymal hematoma formation. Despite the effort of investigators, the in-hospital time delay for the TT was significant which was mainly related to the time consuming preparation for angiography especially during night. A more effective system for the earlier intervention of acute ischemic stroke needs to be developed.
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PMID:Intra-carotid thrombolytic therapy in acute ischemic stroke of carotid arterial territory. 800 97

Thrombolytic therapy has been proposed in the treatment of cerebrovascular occlusive disease. Early clinical experiences with Urokinase and Streptokinase raised concern about the risk of hemorrhagic complications. More recently, tissue plasminogen activator (tPA) has been evaluated experimentally with promising results. Its clinical utilization has been recently initiated. A review of experimental and clinical data on thrombolysis in cerebral ischemia is presented. TPA treatment produced recanalization and clinical improvement in several patients. The rate of intracranial hemorrhagic complications is similar to the incidence of spontaneous hemorrhagic conversion of ischemic infarction. Nevertheless, large placebo-controlled clinical trials are necessary to further define the efficacy and the optimal modality of administration of tPA in thromboembolic stroke.
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PMID:Thrombolysis in cerebral ischemia. A review of clinical and experimental data. 830 72

Stroke is one of the leading causes of death in the industrial nations of the world. Up to now, there has been no therapeutic strategy available which has been proven by controlled clinical trials. In the majority of acute stroke patients acute thrombosis contributes to carotid and vertebrobasilar arterial occlusions. Therefore, significant interest has focused on the possible value of fibrinolytic therapy in acute stroke. The principal goal is the rapid lysis of occluding thrombus with a minimum risk of intracranial or systemic hemorrhage. Clinical investigations on thrombolysis in cerebrovascular ischemia included different plasminogen-activators such as urokinase, streptokinase, and tissue plasminogen activator, either given systemically or locally via an intraarterial catheter. The pivotal trials conducted so far have revealed a wide range of recanalization rates, an acceptable safety and, also, encouraging effects on neurologic outcome. Thrombolysis itself carries the risk of intracranial bleeding, a practical limitation of this approach in acute stroke. On the other hand, hemorrhagic infarction and parenchymatous hematoma are natural consequences of thromboembolic stroke, possibly as a result of persistent occlusion of an artery. Hemorrhage following thrombolysis seems to show the same features seen in untreated patients and with an incidence similar to that in untreated patients. Future developments in thrombolysis in acute stroke should include improved early recruitment of patients, evaluation of noninvasive techniques in the pretreatment assessment of patients, the evaluation of advanced invasive techniques for delivery of the thrombolytic agent and assessment of combined treatment strategies. Clinical studies evaluating these strategies are currently under way.
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PMID:Thrombolytic intervention in acute thrombotic and embolic stroke. 832 15


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