Since a myocardial infarction is typically caused by a thrombus occluding a coronary artery, thrombolytic agents and anticoagulants are part of the drug regimen used to treat heart disease.  Thrombolytic agents convert plasminogen to plasmin, an enzyme that breaks down fibrin, the major constituent of clots.  Tissue plasminogen activator (tPA) acts at the site of the clot as it is activated by fibrin; other fibrinolytic agents act more systemically.  Anistreplase is a complex of streptokinase and plasminogen which gives it some fibrin specificity and increases its half-life.  Since these agents promote fibrinolysis, hemorrhage is a risk.  Consequently, these agents should not be given prior to surgery or to patients with a bleeding history.  Examples of thrombolytic agents include tissue plasminogen activator (Activase), urokinase (Abbokinase), streptokinase (Streptase), anistreplase/APSAC (Eminase), reteplase (Retavase).  Reteplase is a recombinant form of human tissue plasminogen activator in which the molecule has been genetically altered to contain 357 of the 527 amino acids of the original protein [1].

Thrombolytic antagonists are agents that inhibit plasminogen activators.  They are used to reduce or prevent hemorrhage.  They enhance hemostasis (clotting) when fibrinolysis is contributing to a bleeding problem.  They should not be used in conditions such as disseminated intravascular coagulation (DIC) in which active intravascular clotting is occurring.  Examples of these agents include amiocaproic acid (Amicar), tranexamic acid (Amstat). 

Anticoagulants inhibit the production of fibrin by interfering with the coagulation cascade.  Heparin binds to antithrombin III (AT-III)which then inactivates thrombin and other proteases involved in blood clotting.  Coumadin (warfarin) acts as a vitamin K antagonist and, thus, inhibits the synthesis of vitamin K-dependent coagulation factors (II, VII, IX, and X) [2].  Due to their mechanisms of action, these anticoagulants act to prevent venous thrombosis [2].  Heparin is not absorbed in the GI tract.  Consequently, it is given by injection.  Coumadin is an oral anticoagulant.  Heparin is rapid-acting whereas coumadin has a delayed onset of action.  Accordingly, heparin is used in situations that require a quick response, and coumadin is used for long-term prophylaxis.

The antiplatelet drugs suppress platelet aggregation and are most effective at preventing arterial thrombosis [2].  These agents include aspirin, dextrans, dipryridamole (Persantine), ticlopidine (Ticlid), clopidogrel (Plavix), abciximab (Reopro), and eptifibatide (Integrilin).  Most of aspirin’s effects are attributed to its inhibition of cyclooxygenase (COX-1 and COX-2), an enzyme required for the synthesis of thromboxane A-2, the chemical that causes platelets to clump [3].  Dextrans bind to platelets reducing their adhesiveness.  They also reduce factor VIII-Ag Von Willebrand factor, thereby decreasing platelet function.  Dipryridamole inhibits the uptake of adenosine leading to increased cAMP levels, which inhibits platelet function.  The thienopyridines, ticlopidine and clopidogrel, block the ADP receptor found on the surface of platelets.  Blocking the ADP receptor prevents ADP from attaching to the receptor and the platelets from clumping [3].  Abciximab and eptifibatide prevent clumping by inhibiting the platelet receptor for glycoprotein IIb/IIIa [3].  Daily aspirin ingestion (£325 mg/day) is commonly recommended as primary prophylaxis of myocardial infarction, prevention of reinfarction, and prevention of strokes in patients who have a history of transient ischemic attacks (TIAs) [2].

References

1.  Wooster, M. B. and Luzier, A. B.  (1999)  Reteplase: A New thrombolytic for the Treatment of Acute Myocardial Infarction.  Journal: Ann Pharmacother.  33:318-24.

2.  Lehne, R. A. (1998). Pharmacology for Nursing Care, 3rd Ed. Philadephia: W. B. Saunders Co.

3.  http://www.medicinenet.com/aspirin_beta_blockers_and_ace_inhibitors/article.htm