title: [Drug-eluting coronary stents].
abstract: The first method of percutaneously treating a diseased vessel was developed by Dotter and Judkins in 1964. Andreas Grüntzig performed the first coronary angioplasty in 1977. In 1985 Palmaz et al. implanted the first balloon-mounted stent in a peripheral artery. Puel and Sigwart implanted the first human coronary stent in March 1986; it was a self-expanding mesh-like device. Schatz et al. applied some small modifications to the original Palmaz stent, which resulted in the first coronary stent available on the market, called Palmaz-Schatz stent. In 1987 Sigwart was the first to suggest the use of coronary stents in acute vessel occlusions during unsuccessful PTCA. Using the device it became possible to cover the intimal flap and to prevent elastic recoil. Because of the high incidence of subacute stent thromboses and the bleeding complications (aggressive anticoagulation regimens) these times the coronary stents were implanted only in order to avoid emergency CABG surgery. In 1993 BENESTENT and STRESS trials have proved that elective stent implantation can significantly reduce the incidence of restenosis. The dual antiplatelet therapy and the high pressure stent implantation technique dramatically reduced the incidence of subacute stent thrombosis. The treatment of coronary artery disease has undergone revolutionary changes in the past decade but remained the leading cause of mortality in the developed world. The most important limitation of PCI has been in-stent restenosis, which occurs in 20-40% of stent implantations. Clinically it results in recurrent ischemic episodes most often requiring repeat revascularisation (rePCI or CABG). With the use of drug-eluting stents the incidence of in-stent restenosis can be reduced dramatically, based on the currently available clinical trials it remains below 10%.
authors.affiliation: Gottsegen György Országos Kardiológiai Intézet, Hemodinamikai Osztály, Budapest.
authors.forename: Géza
authors.initials: G
authors.lastname: Fontos
mesh_terms: D002453:Cell Cycle / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000378:metabolism* / Q000628:therapy*; D023903:Coronary Restenosis / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D003362:Cost-Benefit Analysis; D003692:Delayed-Action Preparations / Q000627:therapeutic use; D006801:Humans; D006814:Hungary; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000473:pathology; D017239:Paclitaxel / Q000627:therapeutic use*; D011494:Protein Kinases / Q000187:drug effects; D020123:Sirolimus / Q000627:therapeutic use*; D015607:Stents / Q000191:economics / Q000592:standards; D058570:TOR Serine-Threonine Kinases; D016896:Treatment Outcome; D050257:Tubulin Modulators / Q000627:therapeutic use; D014481:United States
chemical_list: D003692:Delayed-Action Preparations; D050257:Tubulin Modulators; D011494:Protein Kinases; C546842:MTOR protein, human; D058570:TOR Serine-Threonine Kinases; D017239:Paclitaxel; D020123:Sirolimus