Coronary thrombolysis

Sobel BE, Geltman EM, Tiefenbrunn AJ, Jaffe AS, Spadaro JJ, Jr., Ter-Pogossian MM et al. Improvement of regional myocardial metabolism after coronary thrombolysis induced with tissue-type plasminogen activator or streptokinase. Circulation 1984 69 983-990... [Pg.34]

Haskel EJ, Prager NA, Sobel BE, et al. Relative efficacy of antithrombin compared with antiplatelet agents in accelerating coronary thrombolysis and preventing early reocclusion. Circulation 1991 83 1048-1056. [Pg.125]

Bergmann SR, Lerch RA, Fox KAA, et al. Temporal dependence of beneficial effects of coronary thrombolysis characterized by positron emission tomography. Am J Med 1982 73 573-580. [Pg.137]

Verheugt FWA, Meijer A, Lagrand WK, Van Eenige MJ. Reocclusion the flip side of coronary thrombolysis. J Am Coll Cardiol 1996 27 766-773. [Pg.137]

In the initial study described by Gold et al. (1984), recombinant t-PA was characterized for its ability to lyse 2-hour-old thrombi. Tissue plasminogen activator was infused at doses of 4.3, 10, and 25 (ig/kg/min, i.v, and resulted in reperfusion times of 40, 31, and 13 minutes, respectively. Thus, in this model of canine coronary thrombosis, t-PA exhibited dose-dependent coronary thrombolysis. Furthermore, it is possible to study the effect of different doses of t-PA on parameters of systemic fibrinolytic activation, such as fibrinogen, plasminogen, and a2-antiplasmin, as well as to assess myocardial infarct size. For example, Kopia et al. (1988) demonstrated that SK elicited dose-dependent thrombolysis in this model. [Pg.286]

Subsequently, Gold et al. (1986, 1988) modified the model to study not only reperfusion, but also acute reocclusion. Clinically, reocclusion is a persistent problem after effective coronary thrombolysis, which is reported to occur in 15 15 % of patients (Goldberg... [Pg.286]

Gold HK, Coller BS, Yasuda T et al. (1988) Rapid and sustained coronary artery recanalization with combined bolus injection of recombinant tissue-type plasminogen activator and monoclonal antiplatelet Gp Ilb/IIIa antibody in a canine preparation. Circulation 77 670-677 Gold HK, Fallon JT, Yasuda T et al. (1984) Coronary thrombolysis with recombinant human tissue-type plasminogen activator. Circulation 70 700-707... [Pg.287]

Gold HK, Leinbach RC, Garabedian HD et al. (1986) Acute coronary reocclusion after thrombolysis with recombinant human tissue-type plasminogen activator prevention by a maintenance infusion. Circulation 73 347-352 Goldberg RK, Levine S, Fenster PE (1985) Management of patients after thrombolytic therapy for acute myocardial infarction. Clin Cardiol 8 455 159 Kopia GA, Kopaciewicz LJ, Ruffolo RR (1988) Coronary thrombolysis with intravenous streptokinase in the anesthetized dog a dose-response study. J Pharmacol Exp Ther 244 956-962... [Pg.287]

Integrilin) coronary thrombolysis improvement in lysis of occlusive thrombus et al. 1994 myocardial infarction -thrombolysis with tPA in incidence and speed of reperfusion et al. 1997... [Pg.316]

Collen D, Topol EJ, Tiefenbrunn AJ et al. (1984) Coronary thrombolysis with recombinant human tissue-type plasminogen activator a prospective, randomized, placebo-controlled trial. Circulation 70 1012-1017... [Pg.317]

Fitzgerald DJ, Wright F, FitzGerald GA (1989) Increased thromboxane biosynthesis during coronary thrombolysis evidence that platelet activation and thromboxane A2 modulate the response to tissue-type plasminogen activator in vivo. Circ Res 65 83-94... [Pg.317]

Cairns JA, Kennedy JW, Fuster V. Coronary thrombolysis. Chest 1998 114(5 Suppl) S634-57. [Pg.3407]

Important practical barriers have limited the widespread adoption of primary PCI for the treatment of STEMI. The fact that fewer than 25% of hospitals in the United States and fewer than 10% of hospitals in Europe have facilities for coronary angiography is a formidable factor (47,48). Several randomized, clinical triads signed to compare primary PCI with coronary thrombolysis for treatment of STEMI followed the... [Pg.7]

Collen D, Topol EJ, Tiefenbrunn AJ, Gold HK, Weisfeldt ML, Sobel BE, Leinbach RC, Brinker JA, Ludbrook PA, Yasuda 1, Bulkley BH, Robison AK, Hutter AM Jr, Bell WR, Spadaro JJ Jr, Khaw BA, Gross-bard EB. Coronary thrombolysis with recombinant human tissue-type plasminogen activator a prospective, randomized, placebo-controUed trial. Circulation 1984 70 1012-1017. [Pg.21]

Van de Werf F, Ludbrook PA, Bergmann SR, Tiefenbrunn AJ, Fox KAA, de Geest H, Verstraete M, Collen D, Sobel BE. Coronary thrombolysis with tissue-type plasminogen activator in patients with evolving myocardial infarction. N Engl J Med 1984 310 609-613. [Pg.21]

National Heart Foundation of Australia Coronary Thrombolysis Group. Coronary thrombolysis and myocardial salvage by tissue plasminogen activator given up to 4 hours after onset of myocardial infarction. Lancet 1988 1 203-208. [Pg.22]

Sobel BE, Hirsh J. Principles and practice of coronary thrombolysis and conjunctive treatment. Am J Cardiol 1991 68 382-388. [Pg.27]

Sobel BE. Interpretation of results of clinical trials in coronary thrombolysis. Fibrinolysis Proteolysis 1997 11 17-21. [Pg.30]

Development Impact and Limitations of Coronary Thrombolysis Milestones in Pharmacological Reperfusion Therapy... [Pg.33]

Sobel BE, Nachowiak DA, Fry ETA, Bergmann SR, Torr SR. Paradoxical attenuation of fibrinolysis attributable to plasminogen steal and its implications for coronary thrombolysis. Coronary Artery Dis 1991 1 111-119. [Pg.60]

Bode C, Smalling RW, Berg G, et al. Randomized comparison of coronary thrombolysis achieved with double-bolus reteplase (recombinant plasminogen activator) and front-loaded, accelerated alteplase (recombinant tissue plasminogen activator) in patients with acute myocardial infarction. Circulation 1996 4 891-898. [Pg.63]

Prewitt RM, Gn S, Garber PJ, Ducas J. Marked systemic hypotension depresses coronary thrombolysis induced by intracoronary administration of recombinant tissue-type plasminogen activator. J Am Coll Cardiol 1992 20 1626-1633. [Pg.110]

Other factors. Approximately 40% of patients do not exhibit normal (TIMI 3) flow in the region of supply of the infarct artery 90 minutes after thrombolysis (7,8). These observations support the concept that a combination of percutaneous coronary intervention plus coronary thrombolysis may be optimal for restoring and maintaining flow in the infarct-related artery. [Pg.121]

Smalling RW, Bode C, Kalbfleisch J, et al. More rapid, complete, and stable coronary thrombolysis with bolus administration of reteplase compared with alteplase infusion in acute myocardial infarction. RAPID Investigators. Circulation 1995 91 2725-2732. [Pg.146]

Coronary Thrombolysis in Perspective Principles Underlying Conjunctive and Adjunctive Therapy, edited by Burton E. Sobel and Desire Collen... [Pg.249]

Refinements and improvements in pharmacologic ( thrombolysis ) and mechanical approaches ( primary angioplasty ) to recanalization have been impressive. Randomized clinical trials and registries have been used to compare and contrast the two, but assessment of both in combination lay dormant until quite recently. Improvements in coronary thrombolysis and coronary interventions now make reassessment of pharmacoinvasive therapy particularly desirable. Reassessment is indicated given the inherent limitations, when used alone, in both pharmacologic (failure to restore flow adequately) and mechanical approaches (unavoidable delay that can prolong the time to initiation of reperfusion). [Pg.257]

Section I of this book describes 1) the conceptual basis underlying pharmacoinvasive therapy, 2) the efficacy and limitations of each of its two components when used alone, and 3) the reductions in mortality that have been accomplished with each. Section II addresses the failure of early trials to demonstrate the benefit of combinations of balloon angioplasty coupled with antecedent coronary thrombolysis. [Pg.257]

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