IIb/IIIa receptor blockade in acute myocardial infarction.
To appreciate the clinical potential of antiplatelet therapy in the treatment of patients with acute myocardial infarction (MI), it is important to understand the mechanism and pathophysiology of acute MI and to understand the role that platelets play in the process of acute thrombus formation. Recognition of the limitations of current therapy has sparked intense interest in the development of more potent platelet inhibitors such as antagonists of the platelet glycoprotein (GP) IIb/IIIa receptor. Because this receptor represents the final common pathway of platelet aggregation, it emerges as a very attractive therapeutic target for phamacologic interventions. The purpose of this review is to summarize the results of recent large-scale clinical trials that use GP IIb/IIIa antagonist therapy in patients with acute MI both as an adjunct to percutaneous coronary interventions and as an adjunct to exogenously administered fibrinolytic therapy. As an adjunct to percutaneous coronary interventions, GP IIb/IIIa antagonists have shown significant benefit in the prevention of composite end points of death, MI, and emergency revascularization. As an adjunct to fibrinolytic agents, GP IIb/IIIa antagonists enhance the speed and degree of reperfusion achievable pharmacologically. Although the potential risk of bleeding remains a concern (particularly with higher doses of streptokinase), recent phase II trials such as TIMI 14 and SPEED suggest considerable potential for these potent antiplatelet agents in the medical treatment of patients with acute MI.
Ferguson
J J
JJ
St. Luke's Episcopal Hospital, Texas Heart Institute, Houston, USA.
Taqi
K
K
D015906:Angioplasty, Balloon, Coronary; D001792:Blood Platelets / Q000502:physiology; D002986:Clinical Trials as Topic; D017322:Clinical Trials, Phase II as Topic; D003131:Combined Modality Therapy; D003328:Coronary Thrombosis / Q000209:etiology / Q000503:physiopathology; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006470:Hemorrhage / Q000139:chemically induced; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D015425:Myocardial Reperfusion; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D019038:Platelet Glycoprotein GPIb-IX Complex; D010980:Platelet Membrane Glycoproteins; D011947:Receptors, Antigen, B-Cell / Q000037:antagonists & inhibitors*; D011956:Receptors, Cell Surface / Q000037:antagonists & inhibitors*; D015996:Survival Rate; D015912:Thrombolytic Therapy; D013997:Time Factors
D005343:Fibrinolytic Agents; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D019038:Platelet Glycoprotein GPIb-IX Complex; D010980:Platelet Membrane Glycoproteins; D011947:Receptors, Antigen, B-Cell; D011956:Receptors, Cell Surface; C032193:glycoprotein receptor GPIb-IX