Coronary artery thrombolysis

Rebello SS, Bentley RG, Morgan SR, et al. Antithrombotic efficacy of a novel factor Xa inhibitor, FXV673, in a canine model of coronary artery thrombolysis. Br J Pharmacol 2001 133 1 190-1198. 

Saitoh S,SaitoT,Otake A, Owada T, Mitsugi M, HasfaimotoH.MaruyamaY Cilostazol, anovel cydic AMP pbos diodiesterase inhibitor, prevents reocdusion after coronary arterial thrombolysis with recombinant tissue-type plasminogen activator. Arteriosder Thromb 1993 13 563-570. 

Mickelson JK, Simpson PI, Cronin M, Homeister JW, Laywell E, Kitzen J, Lucchesi BR Antiplatelet antibody (7E3 ((ab IJ prevents rethrombosis after recombinant tissue-type plasminogen activator-induced coronary artery thrombolysis in a canine model. Circulation (1990) 81 617-627. 

Abbreviations AMI, acute myocardial infarction GUSTO, Global Use of Strategies to Open Occluded Coronary Arteries SK, streptokinase TIMI, thrombolysis in myocardial infarction tPA, tissue plasminogen activator UFH, unfractionated heparin. ... 

Thrombosis in stenosed human coronary arteries is one of the most common thrombotic diseases leading to unstable angina, acute myocardial infarction or sudden death. Treatment with angioplasty, thrombolysis, or bypass grafts can expose new thrombogenic surfaces and re-thrombosis may occur. The mechanisms responsible for this process include interactions of platelets with the damaged arterial wall and platelet aggregation. 

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... 

Eccleston D, Topol EJ. Inhibitors of platelet glycoprotein Ilb/IIIa as augmenters of thrombolysis. Coronary Artery Dis 1995 6 947-955. 

Coller BS. Augmentation of thrombolysis with antiplatelet drugs. Coronary Artery Disease 1995 6911-914. 

Adrie C. Bloch KD. Moreno PR et al (1996) Inhaled nitric oxide increase coronary artery patency after thrombolysis Circulation 94 1919-1926. 

De ite differmces in their mechanisms of action and in vitro activities, pentasaccharide, DX-9065a and TAP have been shown to be effective antithrombotic agents in experimental models of venous thrombosis, coronary artery occlusion, arterial thrombolysis and acute reocclusion, restenosis after angioplasty, dialysis, and DIG. Pentasaccharide has also demonstrated measurable antithrombotic effects in human trials. Both TAP and DX-9065a produce measurable in vitro anticoagulant effects. In contrast, pentasaccharide does not produce an anticoagulant effect by the typical clot based assays. Thus, with fector Xa inhibitors there is not necessarily a correlation between current lab assays and antithrombotic efficacy as there is with heparin. 

Thrombolysis may also be valuable in persistent unstable angina and especially where eirteriography demonstrates substantial thrombus in coronary arteries. 

Zabel M, Hohnloser SH, Koster W, Prinz M, Kasper W, Just H, et ai. Analysis of creatine kinase, CK-2, myoglobin, and troponin T time-activity curves for early assessment of coronary artery reperfusion after intravenous thrombolysis. Circulation 1993 87 1542-50. 

Corbalan R, Prieto JC, Chavez E, Nazzal C, Cumsille F, Krucoff M. Bedside markers of coronary artery patency and shortterm prognosis of patients with acute myocardial infarction and thrombolysis. Am Heart J 1999 138 533. 

Pinney SP, Rabbani LE. Myocardial infarction in patients with normal coronary arteries proposed pathogenesis and predisposing risk factors. J Thromb Thrombolysis 2001 11 11. 

ACS = acute coronary syndrome CAD = coronary artery disease CHD = coronary heart disease DM = diabetes mellitus HTN = hypertension Ml = myocardial Infarction TIMI = Thrombolysis in Myocardial Infarction. 

Electrically induced thrombosis [41], [42], [43] electrode placed directly into a coronary artery causing endothelial disruption Platelet rich, but significant fibrin/ red cell content Coronary artery blood flow (e.g. electromagnetic flow probe) Efficacy of antithrombotic agents adjunctive agents in thrombolysis... 

Thrombin induced thrombosis [48] stenosis, endothelial damage (by arterial clamping) and thrombin/blood injection Fibrin and red cell rich initial thrombus platelet rich reocclusion Coronary artery blood flow Adjunctive agents in thrombolysis (but not for effects on lysis of platelet rich thrombus)... 

Everted coronary artery graft with stenosis [48] Platelet rich (rt-PA resistant) Coronary blood flow Adjunctive agents in thrombolysis of rt-PA resistant platelet rich thrombus... 

In a model of thrombin induced thrombosis in the dog coronary artery, 7E3F(ab )2 (0.8mg/kg i.v.) markedly accelerated thrombolysis with recombinant tissue plasminogen activator (rtPA), and fully prevented reocclusion [153]. Similar models were used to show the inferiority of aspirin and dipyr-amidole in the dog coronary artery [154], or of aspirin in the baboon femoral artery [155], compared with 7E3F(ab )2 as adjunctive agents to thrombolysis with rtPA. However, in another dog study using this model, the thrombin in-... 

The IMPACT-AMI phase I/II trial investigated the combination of various doses of integrilin (36-180 g/kg i.v. bolus and 0.2-0.75/rg/kg/min 24h infusion) with thrombolysis using tPA, aspirin and heparin [15,168]. Although an improvement in coronary artery patency at 90min was observed with the highest dose, no significant benefit in clinical outcomes was... 

Aronow WS Thrombolysis and antithrombotic therapy for coronary artery disease. Clin Geriatr Med... 

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. 

Bleich SD, Nichols T, Schumacher R, et al. Effect of heparin on coronary arterial patency after thrombolysis with tissue plasminogen activator in acute myocardial infarction. Am J Cardiol 1990 66 1412-1417. 

Our patient population was predominantly male, consistent with the demography of the UAE and the protection conferred in premenopausal women from accelerated coronary artery disease as well as the age distribution of the population. Thus, the number of women studied was very low. Several studies have shown that when thrombolysis is initiated less than 3 hours after the onset of chest pain, mortality is remarkably low (11,12). Most of our patients were treated early. The mean time from onset of chest pain to treatment was 3.25 hours. This would, to some extent, account for the low mortality. 

Schomig A, Ndrepepa G, MehilU J, et al. Therapy-dependent influence of time-to-treatment interval on myocardial salvage in patients with acute myocardial infarction treated with coronary artery stenting or thrombolysis. Circulation 2003 108 1084-1088. 

Gore JM, Granger CB, Simoons ML, Sloan MA, Weaver WD, White HD, Barbash Gl, Van de Werf F, Aylward PE, Topol FJ, et al. Stroke after thrombolysis. Mortality and functional outcomes in the GUSTO-I trial. Global Use of Strategies To Open Occluded Coronary Arteries. Circulation. 1995 92 2811-2818. 

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