Yield of transcranial Doppler in acute cerebral ischemia.
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BACKGROUND AND PURPOSE: The objective of this study was to evaluate the yield of emergent transcranial Doppler (TCD) for the evaluation of acute cerebral ischemia. METHODS: We performed urgent bedside non-contrast-enhanced TCD in patients with acute cerebral ischemia before or immediately after baseline CT scanning. A fast-track scanning protocol (+info)
Economic assessment of tirofiban in the management of acute coronary syndromes in the hospital setting: an analysis based on the PRISM PLUS trial.
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AIMS: We analysed whether generalized use of tirofiban plus heparin and aspirin might save direct healthcare costs, as compared with heparin and aspirin alone, in patients with acute coronary ischaemic syndromes in Switzerland. METHODS AND RESULTS: We conducted an incremental cost-consequence analysis from the perspective of the admitting hospital for the period of the first 7 days. Costs were analysed for the management of refractory ischaemic conditions and myocardial infarctions, including incremental days on the general ward or intensive care unit, as well as necessary revascularization procedures, and expressed in Swiss francs (CHF) and European currency units (ECU). Drug costs were based on a loading dose of 0.4 micro x kg(-1) x min(-1)and a maintenance dose of 0.1 micro x kg(-1) x min(-1)for tirofiban at a cost of CHF 273.55 (ECU 166.50) per vial. Heparin was administered at a loading dose of 5000 U and a maintenance dose of 1000 U x h(-1). All calculations were standardized to 100 treated patients. The costs of managing ischaemic complications were based on typical practice patterns in Swiss hospitals. The incremental costs per patient of managing unstable angina patients with recurrent ischaemia or myocardial infarction were calculated as CHF 23 325 (ECU 14 198) and CHF 18 599 (ECU 11 321), respectively. The incremental drug costs amounted to CHF 82 065 (ECU 49 954). The additional use of tirofiban resulted in net savings of CHF 54 899 (ECU 33 418) per 100 patients, achieved through a reduction in the cost of treating refractory ischaemic conditions (CHF 79 306, ECU 48 275) and myocardial infarctions (CHF 57 658, ECU 35 097). CONCLUSION: Tirofiban is cost-saving in acute coronary ischaemic syndromes and improves the economics of managing these patients during the initial hospitalization. (+info)
Comparative antiplatelet effects of aspirin, vapiprost and GR144053, a GPIIb/IIIa antagonist, with a special reference to the role of platelet microaggregates.
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Microthrombi produced have a potential to form larger thrombi, leading to vascular occlusions. Recently, a new device to easily detect microaggregates using laser-light scattering (LS) has been developed. We adopted this device to comparatively evaluate the inhibitory effects of aspirin (1,3 or 10 mg kg(-1)), vapiprost (0.3, 1 or 3 mg kg(-1)) or GR144053 (0.1, 0.3 or 1 mg kg(-1)) on ex vivo aggregation of hamster platelets in relation to their in vivo antithrombotic effects. A transluminal thrombus was produced in the hamster femoral artery by the photochemical reaction. Each compound was injected i.v. as a bolus 10 min prior to the reaction, showing a dose-dependent antithrombotic effect, i.e. they prolonged the time before the artery occluded. At that time cyclic flow reductions occurred more marked when aspirin or vapiprost was given. At the end of experiments, blood was collected to evaluate the platelet aggregation using both the new LS device and the conventional optical density (OD) method. Many more small aggregates were still formed when the highest dose of aspirin or vapiprost was used as compared with that of GR144053, although suppression of the platelet aggregation using the OD method, prolongation of the occlusion time and the bleeding time were quite similar. In conclusion, a GPIIb/IIIa antagonist markedly suppressed the microthrombi and reduced the cyclic flow reduction. This further indicates the importance of small aggregates as triggers of thrombosis and shows that prevention of their formation may result in improved vascular patency after thrombotic insult. (+info)
Antithrombotic efficacy of the vitamin K antagonist fluindione in a human Ex vivo model of arterial thrombosis : effect of anticoagulation level and combination therapy with aspirin.
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Thrombin is a main mediator of arterial thrombus formation, and its inhibition is an important antithrombotic strategy. However, the place of vitamin K antagonists among the different therapeutic strategies for preventing arterial thrombus formation is still debated. We studied the antithrombotic efficacy of the vitamin K antagonist fluindione in a human ex vivo model of arterial thrombosis and determined whether aspirin enhances fluindione efficacy. Ten healthy male volunteers were randomly assigned to receive fluindione, alone or in combination with aspirin (325 mg/d). Fluindione was given at increasing doses to give a stable international normalized ratio (INR) between 1.5 and 2.0 and between 2.1 and 3.0. We induced arterial thrombus formation ex vivo by exposing collagen- or tissue factor (TF)-coated coverslips in a parallel-plate perfusion chamber to native blood for 3 minutes at an arterial wall shear rate of 2600 s(-1). Platelet and fibrin deposition were measured by immunoenzymatic methods. Fluindione inhibited thrombus formation on TF-coated coverslips in a dose-dependent manner by 50% and 80% at INR 1.5 to 2.0 and INR 2.1 to 3.0, respectively (P<0.05). Fluindione in combination with aspirin inhibited TF-induced thrombus formation in a comparable manner. Collagen-induced thrombus formation was not reduced in subjects treated by fluindione. It was reduced by 50% to 60% in those treated with fluindione plus aspirin, regardless of the level of anticoagulation (P<0.05). Thus, the effectiveness of fluindione for preventing arterial thrombosis is dependent on the nature of the thrombogenic trigger. Fluindione is very effective in preventing TF- but not collagen-triggered thrombus formation. Aspirin enhances the antithrombotic effectiveness of fluindione, because combined treatment interrupts both TF- and collagen-induced thrombus formation. (+info)
Prospective randomised comparison between thrombolysis, rescue PTCA, and primary PTCA in patients with extensive myocardial infarction admitted to a hospital without PTCA facilities: a safety and feasibility study.
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OBJECTIVE: To assess the safety and feasibility of acute transport followed by rescue percutaneous transluminal coronary angioplasty (PTCA) or primary PTCA in patients with acute myocardial infarction initially admitted to a hospital without PTCA facilities. DESIGN: In a multicentre randomised open trial, three regimens of treatment of acute large myocardial infarction were compared for patients admitted to hospitals without angioplasty facilities: thrombolytic treatment with alteplase (75 patients), alteplase followed by transfer to the PTCA centre and (if indicated) rescue PTCA (74 patients), or transfer for primary PTCA (75 patients). RESULTS: Between 1995 and 1997 224 patients were included. Baseline characteristics were distributed evenly. Transport to the PTCA centre was without severe complications in all patients. Mean (SD) delay from onset of symptoms to randomisation was 130 (75) minutes and from randomisation to angiography 90 (25) minutes. Death or recurrent infarction within 42 days occurred in 12 patients in the thrombolysis group, in 10 patients in the rescue PTCA group, and in six patients in the primary PTCA group. These differences were not significant. CONCLUSIONS: Acute transfer for rescue PTCA or primary PTCA in patients with extensive myocardial infarction is feasible and safe. Efficacy of rescue PTCA or primary PTCA in this setting will have to be tested in larger series before this approach can be implemented as "routine treatment" for patients with extensive myocardial infarction. (+info)
Thrombotic thrombocytopenic purpura associated with ticlopidine therapy.
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A patient who developed thrombotic microangiopathy while on ticlopidine therapy is reported. Thrombotic microangiopathy resolved with discontinuation of the drug and treatment with plasma exchange and has not recurred during 10 months of follow-up. The emerging data on the risk of developing thrombotic microangiopathy while on Ticlopidine and the possible mechanisms underlying this association are reviewed. The need for careful monitoring of the platelet count and hematocrit in addition to the white cell count during the first 3 months of therapy with this drug is emphasized. It is important that nephrologists, who are frequently called upon to diagnose thrombotic microangiopathy, be aware of its association with ticlopidine. Other drug-induced syndromes of thrombotic microangiography are also considered and compared, with respect to possible mechanisms of disease in each case. (+info)
Cocaine induced myocardial infarction.
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The case of a 29 year old man who presented with chest pains after the use of cocaine is reported. The diagnosis of myocardial infarction was made on the electrocardiogram changes and lactate dehydrogenase profile. The diagnosis may be overlooked if there is no direct questioning about the use of drugs such as cocaine. Diazepam has an important role in the management of cardiac complications after cocaine use and should be used early in management. The use of thrombolysis should be a joint decision between the emergency physician and cardiologist. (+info)
The state of lipid peroxidation and antioxidants following thrombolytic therapy with rt-PA and streptokinase in acute myocardial infarction.
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The role of reactive oxygen products in myocardial damage caused by ischemia-reperfusion has been established in a number of studies performed in animals models. However, studies showing the development of increased free radicals following effective myocardial reperfusion in humans are scarce. In the present study, both the increase of lipid peroxidation (LPO) following early stage thrombolytic therapy which is the current treatment issue performed after acute myocardial infarct (AMI) and the plasma levels of vitamin E and C (chain braker antioxidants) were investigated parallel to time. Forty patients with AMI who were admitted to hospital within six hours from the beginning of symptoms were included in the study and divided into two groups; group 1 (recombinant tissue-Plasminogen Activator, rt-PA group) and group 2 (streptokinase group). Serial serum specimens were drawn before and 30, 90 minutes and 24 hours after thrombolytic therapy for the investigation of LPO, vitamin E and C levels. Echocardiographic examination was performed on the tenth day to evaluate the functions of the left ventricle. Plasma levels of lipid peroxides (LPO) were found to increase 90 minutes after thrombolytic therapy in each group, while the levels of vitamins E and C showed significant decreases. The difference between the two groups was not significant. Similar to this finding, no significant difference in the ejection fraction values was observed between the groups. Further, no correlation was observed between the ejection fraction and LPO values at the 90th minute which is considered to be the time of successful thrombolysis. In conclusion, the occurrence of a series of biochemical changes confirming an increase in free radical development of peripheral blood was observed. Although the decrease in vitamin E and C levels suggests the need for supplementation of these vitamins along with the thrombolytic therapy, the fact that at least a week is needed for an increase of tissue levels of vitamin E confirms the opinion that the daily prophylactic doses of these vitamins is suitable for the decrease of AMI risk. (+info)