Effect of heparin on coronary arterial patency after thrombolysis with tissue plasminogen activator in acute myocardial infarction

Unfractionated and Low-Molecular-Weight Heparin as Adjuncts to Thrombolysis in Aspirin-Treated Patients With ST-Elevation Acute Myocardial Infarction

“…There is also evidence of improved infarct-related coronary artery patency when intravenous UFH is added to fibrin-specific thrombolytic agents. 19,36,43 However, in 2 of these trials, patients treated with intravenous UFH did not receive aspirin, 19,36 whereas in the third study, 43 in which all patients received aspirin, there was only a modest impact of intravenous UFH on patency. Trials of other antithrombotic agents (eg, glycoprotein IIb/IIIa inhibitors) suggest that improved patency does not necessarily translate into improved clinical outcomes.…”

Randomized Comparison of Enoxaparin, a Low-Molecular-Weight Heparin, With Unfractionated Heparin Adjunctive to Recombinant Tissue Plasminogen Activator Thrombolysis and Aspirin

“…9,10 As a result of distinct pharmacologic and pharmacokinetic profiles of some LMWHs compared with UFH, they may offer benefits in this indication, but no previous early angiographic studies have directly compared the two classes of antithrombotic agents as adjuncts to thrombolysis in AMI. In the Fragmin in Acute Myocardial Infarction (FRAMI) study, subcutaneous dalteparin started 8 hours after thrombolysis with streptokinase in patients with acute anterior myocardial infarction provided a significant reduction in left ventricular thrombus formation 9 days after the acute event.…”

“…[1][2][3][4][5][6][7][8][9][10] Specifically, the use of antithrombotic drugs, traditionally unfractionated heparin (UFH), and aspirin are intended to decrease the phenomenon of new fibrin formation during the lytic process.…”

Importance of modulating balance of procoagulant and fibrinolytic activity to success of antithrombotic therapy.

“…Thus, even when intense fibrinolytic activity is induced in patients with myocardial infarction, increases in procoagulant activity appear to be an important determinant of recurrent thrombosis.1-3 Results of recent clinical trials are consistent with the importance of conjunctive therapy with aspirin and heparin in patients given fibrinolytic agents. [4][5][6][7][8][9] See p 2454 data support the hypothesis that the natural history of thrombosis and the response to treatment are mediated by the relative balance of procoagulant and fibrinolytic activity. Recent advances in defining the specific mechanisms that regulate procoagulant and fibrinolytic activity have led to the development of novel agents that offer the potential of even more precise modulation of anticoagulant and fibrinolytic activity as a means of inhibiting thrombosis.…”