Antithrombotic therapy in acute coronary syndromes

Current therapy of acute coronary syndromes (i.e., unstable angina and non-Q-wave myocardial infarction, Q-wave myocardial infarction) consists of thrombolytic, anti-platelet, and anti-coagulant therapy. In most cases of acute coronary syndromes, the pathogenesis is a mural thrombus formation on a ruptured or eroded atherosclerotic plaque. Both platelets and thrombin play an essential role in the pathophysiology of acute coronary syndromes. Aspirin and heparin are essential treatments for patients with acute coronary syndromes. Novel thrombin and platelet inhibitors have been developed and demonstrated useful effects for improving both acute and long-term clinical outcomes in acute coronary syndromes. Tissue plasminogen activator is the compound for effective thrombolytic therapy. New developments like reteplase and TNK-tPA can be administered as bolus injection and result in rapid reperfusion. Combination of thrombolytic therapy and glycoprotein IIb/IIIa inhibitors seem to accelerate and improve reperfusion. Clopidogrel as anti-aggregatory compound demonstrated profound effects following stent implantation as well as in patients with aspirin intolerance. Administration of glycoprotein IIb/IIIa inhibitors like abciximab, eptifibatide, tirofiban results in reduction of cardiovascular events in patients with unstable angina and following coronary intervention. Low-molecular-weight heparins like enoxiparin and dalteparin seem to be more effective than heparin, and their use is evolving in patients with unstable angina. Anti-thrombin therapy with hirudin results in slight reduction of cardiovascular events in combination with tolerable safety profile. It has yet to be determined which combination of agents and procedural strategies most significantly reduces mortality and serious events in patients with acute coronary syndromes.