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The current standard for adjunctive therapy with thrombolysis remains aspirin and heparin. Both of these medications came into use more than 50 yr ago when our understanding of the molecular biology underlying acute coronary syndromes was nonexistent. As we have deciphered the mechanisms underlying platelet activation and aggregation and thrombin generation and activity, we now stand at the thresh old of a new era in which exquisitely tailored pharmacotherapy can be used to inhibit the pathways leading to coronary artery thrombosis.

Platelet physiology has now been sufficiently dissected to allow us to specifically target and inhibit platelet adhesion, activation, and aggregation. While aspirin remains a vital component of acute myocardial infarction therapy, both ADP antagonists and GP IIb/IIIa inhibitors have emerged as powerful new adjunctive agents. Similarly, we now have at our disposal inhibitors both of thrombin generation and of thrombin activity and we are able to attack both fluid-phase and clot-bound thrombin.

Regardless of whether a patient with ST elevation myocardial infarction undergoes pharmacologic-based or catheter-based reperfusion, intensive antiplatelet therapy and proximal inhibition of the coagulation cascade are likely to be the mainstays of adjuvant therapy. As we continue to refine our knowledge, the next steps will be to design appropriate combinations of agents for each setting.

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