title: Pharmacologic prevention of acute ischemic complications of coronary angioplasty.
abstract: The risk of acute coronary occlusion following percutaneous transluminal coronary angioplasty (PTCA) has remained high despite the traditional use of heparin and aspirin. Interest has focused on newer strategies for preventing intracoronary thrombus formation, which is an important mechanism of abrupt vessel closure. Pretreatment with thrombolytic agents has failed vigorous testing in double-blind trials. Retrospective and observational studies have indicated that pretreatment with intravenous heparin is of benefit in patients with unstable symptoms, but prolonged infusion after angioplasty increases bleeding complications without improving outcomes. Subcutaneous heparin may be safer, but has not proved more effective. Oral dipyridamole has shown no advantage over aspirin, although there is evidence to suggest a benefit when given intravenously. Direct thrombin inhibitors (such as hirudin and hirulog) are associated with fewer early complications compared with heparin, but have yielded no apparent long-term benefit. The use of the antiplatelet drug ticlopidine is increasing, although long-term data are lacking. A great deal of recent interest has focused on newer antiplatelet agents, particularly the glycoprotein IIB/IIIa receptor inhibitor c7E3 Fab. In a large-scale trial, c7E3 significantly reduced the 30-day rate of mortality and cardiac events, and these benefits were maintained at 6 mo. This drug, unlike other antiplatelet agents, inhibits the final common pathway of platelet aggregation, which influences not only acute closure but has lasting effects for at least 6 mo. This may reflect a reduction in restenosis, although this remains to be proven. This article gives a brief overview of the pharmacologic agents available for the prophylaxis and treatment of acute ischemic complications of PTCA.
authors.affiliation: Cardiothoracic Unit, Northern General Hospital National Health Service Trust, Sheffield, United Kingdom.
authors.forename: N
authors.initials: N
authors.lastname: Wheeldon
authors.forename: D
authors.initials: D
authors.lastname: Cumberland
mesh_terms: D000077284:Abciximab; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D003251:Constriction, Pathologic; D003327:Coronary Disease / Q000209:etiology / Q000517:prevention & control*; D005343:Fibrinolytic Agents / Q000627:therapeutic use*; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D013927:Thrombosis / Q000209:etiology / Q000517:prevention & control; D013988:Ticlopidine / Q000627:therapeutic use
chemical_list: D000911:Antibodies, Monoclonal; D005343:Fibrinolytic Agents; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D006493:Heparin; D013988:Ticlopidine; D001241:Aspirin; D000077284:Abciximab