title: Pharmacological approaches for the prevention of restenosis after percutaneous coronary intervention.
abstract: A large number of drug trials for prevention of restenosis have been conducted with many showing little or conflicting benefit. Antiplatelets such as aspirin, ticlopidine and thromboxane A2 receptor inhibitors have not shown a clear benefit. Similarly, antithrombotics, either acting indirectly such as heparin, or as direct thrombin inhibitors such as hirudin and hirulog, do not prevent restenosis. Trials with ACE inhibitors, HMG-CoA reductase inhibitors and fish-oil supplements have yielded inconclusive results. The antiproliferatives, angiopeptin, trapidil and tranilast have shown some benefit in small-scale studies. Other drug classes of potential benefit include the glycoprotein IIb/IIIa receptor antagonists, inhibitors of the early coagulation cascade, calcium channel blockers and nitric oxide donors. Drug research into restenosis prevention has been hampered by problems with the definition of restenosis and the applicability in humans of animal models. Although no single drug has conclusively proven effective yet, the promise of a number of agents, together with other nonpharmacological strategies will likely result in further reductions in the incidence of restenosis.
authors.affiliation: Department of Cardiology, Cleveland Clinic Foundation, OH 44195-5033, USA.
authors.forename: J
authors.initials: J
authors.lastname: Lefkovits
authors.forename: E J
authors.initials: EJ
authors.lastname: Topol
mesh_terms: D000077284:Abciximab; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D000925:Anticoagulants / Q000627:therapeutic use; D002317:Cardiovascular Agents / Q000627:therapeutic use; D003251:Constriction, Pathologic; D017023:Coronary Angiography; D003327:Coronary Disease / Q000517:prevention & control / Q000628:therapy*; D003331:Coronary Vessels / Q000187:drug effects* / Q000473:pathology*; D004195:Disease Models, Animal; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D009842:Oligopeptides / Q000627:therapeutic use; D010456:Peptides, Cyclic; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D010980:Platelet Membrane Glycoproteins / Q000627:therapeutic use; D012008:Recurrence; D013004:Somatostatin / Q000031:analogs & derivatives / Q000627:therapeutic use; D014192:Trapidil / Q000627:therapeutic use
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000911:Antibodies, Monoclonal; D000925:Anticoagulants; D002317:Cardiovascular Agents; D000960:Hypolipidemic Agents; D007140:Immunoglobulin Fab Fragments; D009842:Oligopeptides; D010456:Peptides, Cyclic; D010975:Platelet Aggregation Inhibitors; D010980:Platelet Membrane Glycoproteins; C060347:lanreotide; D013004:Somatostatin; D014192:Trapidil; D000077284:Abciximab