Advances in antithrombotic therapy of acute myocardial infarction.
The aim of the acute treatment of myocardial infarction is to restore, as promptly as possible, blood flow in the culprit vessel. Thrombolysis is a cornerstone of treatment, and direct coronary angioplasty (PTCA) is emerging as a valuable or even better alternative reperfusion strategy. The activation of hemostasis after plaque disruption, thrombolysis, or PTCA represents a strong rationale for the use of antithrombotic drugs. The results of the ISIS-2 trial and the data from the Antiplatelet Trialists' Collaboration indicated that aspirin is mandatory in patients with acute myocardial infarction and for secondary prevention. Recently, the efficacy of abciximab and other glycoprotein IIb/IIIa inhibitors was proven in the treatment of acute coronary syndromes and after PTCA, and their early use in patients with acute myocardial infarction is presently under evaluation. Anticoagulation with heparin appears to be only slightly effective in acute myocardial infarction not treated with thrombolysis; however, a rationale exists for its use in patients undergoing percutaneous and/or surgical revascularization and in conjunction with fibrin-specific thrombolytic agents. Further studies are under way on the possible usefulness of low-molecular-weight heparin. Direct antithrombin agents (hirudin, hirulog, and others) have been recently studied as an adjunct to thrombolysis. The data from these studies indicate the presence of a narrow therapeutic window, with only marginal advantage over heparin; studies with newer compounds are ongoing. Aspirin is still a mandatory drug in patients with acute myocardial infarction; the most promising agents in this setting seem to be glycoprotein IIb/IIIa inhibitors. Heparin and low-molecular-weight heparins are indicated in selected cases, and further studies are needed to assess the value of newer direct thrombin inhibitors.
Gensini
G F
GF
Internal Medicine, Azienda Ospedaliera Careggi, University of Florence, Italy.
Comeglio
M
M
Falai
M
M
D000077284:Abciximab; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D000925:Anticoagulants / Q000627:therapeutic use; D000991:Antithrombins / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D003326:Coronary Circulation / Q000187:drug effects; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006487:Hemostasis / Q000187:drug effects; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000628:therapy; 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; D016032:Randomized Controlled Trials as Topic; D011947:Receptors, Antigen, B-Cell / Q000037:antagonists & inhibitors; D011956:Receptors, Cell Surface / Q000037:antagonists & inhibitors; D015912:Thrombolytic Therapy / Q000379:methods*
D000911:Antibodies, Monoclonal; D000925:Anticoagulants; D000991:Antithrombins; D005343:Fibrinolytic Agents; D007140:Immunoglobulin Fab Fragments; 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; D006493:Heparin; D001241:Aspirin; D000077284:Abciximab