Disease relevance of Thrombolytic Therapy

• METHODS: We randomly assigned 612 patients with symptomatic pulmonary embolism who did not require thrombolytic therapy or embolectomy to either subcutaneous low-molecular-weight heparin (tinzaparin) given once daily in a fixed dose or adjusted-dose, intravenous unfractionated heparin [1].
• The recent demonstrations that thrombolytic therapy with plasminogen activators can result in substantial reductions in mortality from coronary thrombosis have generated considerable interest in the properties of fibrinolytic enzymes [2].
• Mortality at 1 year with combination platelet glycoprotein IIb/IIIa inhibition and reduced-dose fibrinolytic therapy vs conventional fibrinolytic therapy for acute myocardial infarction: GUSTO V randomized trial [3].
• Randomised double-blind placebo-controlled trial of thrombolytic therapy with intravenous alteplase in acute ischaemic stroke (ECASS II). Second European-Australasian Acute Stroke Study Investigators [4].
• The role of intracoronary thrombus in unstable angina: angiographic assessment and thrombolytic therapy during ongoing anginal attacks [5].

Psychiatry related information on Thrombolytic Therapy

• CONCLUSIONS: Compared with other post-MI treatment interventions, cardiac rehabilitation is more cost-effective than thrombolytic therapy, coronary bypass surgery, and cholesterol lowering drugs, though less cost-effective than smoking cessation programs [6].

High impact information on Thrombolytic Therapy

• CONCLUSION: Combination therapy (abciximab and reteplase) did not reduce mortality over 1 year compared with fibrinolytic therapy with reteplase alone [3].
• The study population consisted of 432 patients presenting within 6 hours of onset of symptoms of first acute myocardial infarction who met ECG criteria that allowed estimation of myocardial area at risk before treatment with thrombolytic therapy and who had thallium-201 myocardial infarct-size measurements performed several weeks after infarction [7].
• Age and outcome with contemporary thrombolytic therapy. Results from the GUSTO-I trial. Global Utilization of Streptokinase and TPA for Occluded coronary arteries trial [8].
• The purpose of the present study was to evaluate the safety and efficacy of adjunctive therapy with poloxamer 188 in patients receiving thrombolytic therapy for acute myocardial infarction [9].
• Activated partial thromboplastin time was prolonged similarly in each group after thrombolytic therapy [10].

Chemical compound and disease context of Thrombolytic Therapy

• Dobutamine-responsive wall motion and non-Q-wave infarction may be very useful for accurately identifying reversible dysfunction early after thrombolytic therapy for acute MI [11].
• The severity of hypokinesia at follow-up study correlated with the magnitude of peak serum creatine kinase (r = -0.71), indicating that thrombolytic therapy initiated within 2 hours after the onset of symptoms improves regional left ventricular function and reduces infarct size more than later therapy does [12].
• It is concluded that serial planar technetium-99m isonitrile myocardial imaging in patients with acute myocardial infarction undergoing thrombolytic therapy offers a new quantitative noninvasive approach for assessment of the initial risk zone as well as the success of reperfusion [13].
• We have investigated the coronary vasodilator responses to nitrates in the early stages of acute myocardial infarction before, during and after the administration of thrombolytic therapy [14].
• METHODS AND RESULTS: C1-inhibitor therapy was started not earlier than 6h after acute myocardial infarction, in order to prevent interference with thrombolytic therapy [15].

Biological context of Thrombolytic Therapy

• These findings may help explain u-PA-mediated physiological fibrinolysis and have implications for therapeutic thrombolysis with scu-PA [16].
• Hirudin and a small peptidomimetic analog--hirulog--are being developed as alternatives to heparin for the treatment of unstable angina, for prevention of abrupt closure and restenosis following coronary angioplasty, for prevention of deep vein thrombosis after major orthopedic surgery, and as an adjunct to fibrinolytic therapy [17].
• The discovery that tissue plasminogen activator can promote neuronal degeneration has uncovered a novel pathway leading to neuronal cell death and raises important issues concerning the use of tissue plasminogen activator as a thrombolytic therapy for stroke [18].
• Profound inhibition of platelet aggregation with monoclonal antibody 7E3 Fab after thrombolytic therapy. Results of the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) 8 Pilot Study [19].
• The monitoring of changes in the blood coagulation and fibrinolytic systems during thrombolytic therapy with recombinant tissue-type plasminogen activator (rt-PA) may be complicated by artifacts due to in vitro activation after blood collection and to interference of other agents (e.g., heparin) in the assays [20].

Anatomical context of Thrombolytic Therapy

• Dipyridamole echocardiography test. A new tool for detecting jeopardized myocardium after thrombolytic therapy [21].
• METHODS: We studied 12 consecutive patients (men/women = 5/7, age 58.8 +/- 14.9 years) who experienced one or more episodes of stuck bileaflet mitral valve over a 33-month period and received thrombolytic therapy with streptokinase, urokinase or tissue-type plasminogen activator [22].
• In this paper, we report a case of dilated cardiomyopathy with right atrial thrombi and pulmonary artery thromboemboli, in which regression of thromboemboli followed fibrinolytic therapy, and normalization of left ventricular dimensions and function were documented at echocardiographic follow-up [23].
• Color-flow imaging sonography of portal and hepatic vein flow to monitor fibrinolytic therapy with r-TPA for veno-occlusive disease following myeloablative treatment [24].
• METHODS: Thirty-two patients (mean age, 56 years) with acute intracranial internal carotid artery occlusion were studied clinically and with CT and angiography before and after thrombolytic therapy with intravenous alteplase (n = 16), superselective intraarterial alteplase (n = 8), and superselective intraarterial urokinase (n = 8) [25].

Associations of Thrombolytic Therapy with chemical compounds

• Substantial increases in the use of thrombolytic therapy, heparin, aspirin, and coronary angioplasty paralleled the survival trends [26].
• Many phase II trials have supported the potential of combined fibrinolytic therapy and platelet glycoprotein IIb/IIIa inhibition for improving reperfusion [27].
• Nitrates, beta-blockers, calcium blockers, fibrinolytic therapy, and coronary angioplasty have not been adequately evaluated [28].
• Multistage dobutamine echocardiography can be performed safely early after thrombolytic therapy [11].
• After 1 month of rigorous anticoagulation by intravenous heparin and subsequent oral warfarin or after the same period of treatment by antiplatelet agents, we repeated CAG in all patients except for one, who died 6 days after thrombolytic therapy [29].

Gene context of Thrombolytic Therapy

• Co-administration of tPA and a specific inhibitor of CPR, such as potato carboxypeptidase inhibitor, which does not affect CPN, may be useful in thrombolytic therapy [30].
• However, the high frequency of bleeding observed with alteplase in this trial suggests that patients should be carefully selected before thrombolytic therapy is given [31].
• When the patients were divided into subgroups based on whether or not they received thrombolytic therapy on admission to hospital, no significant difference in PON1 levels was observed [32].
• Thrombin-activatable fibrinolysis inhibitor (TAFI) is an important regulator of fibrinolysis, and inhibitors of this enzyme have potential use in antithrombotic and thrombolytic therapy [33].
• Drainage irrigation and fibrinolytic therapy was followed by a fall in CSF TGF-beta1 [34].

Analytical, diagnostic and therapeutic context of Thrombolytic Therapy

• Among patients receiving thrombolytic therapy, concomitant pharmacotherapy included intravenous heparin (96.9%), aspirin (84.0%), intravenous nitroglycerin (76.0%), oral beta-blockers (36.3%), calcium channel blockers (29.5%), and intravenous beta-blockers (17.4%) [35].
• To evaluate the association of smoking with mortality during hospitalization after thrombolytic therapy and 6 months afterward, we analyzed the results of the International Tissue Plasminogen Activator/Streptokinase Mortality Trial. METHODS AND RESULTS [36].
• Application of the F-104 ELISA to monitor the course of Aalpha chain proteolysis in a small study population of patients undergoing thrombolytic therapy for myocardial infarction (n = 14) showed that the loss of fibrinogen-associated F-104 immunoreactivity was a very early marker (within 15 to 30 minutes) of in vivo fibrinogenolysis [37].
• Immunoblotting studies of the A alpha chain proteolysis that occurs during thrombolytic therapy indicated that alpha C fragments, similar in size and epitope content to those isolated from purified fibrinogen, were released in vivo early during fibrinolytic system activation [38].
• Finally, patients with acute myocardial infarction who receive intravenous thrombolytic therapy are candidates for predischarge exercise thallium-201 scintigraphy for risk stratification and detection of residual ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)[39]

References