Coronary-Artery Stent

Abstract

The use of percutaneously introduced prosthetic devices to maintain the luminal integrity of diseased blood vessels was proposed by Dotter and Judkins in 1964 (2), well before the introduction of coronary angioplasty by Gruntzig et al 1997.(3) Palmaz et al introduced the use of balloon- mounted stents (as used in coronary arteries today) in peripheral arteries in 1985.(4) Schatz et al subsequently modified the palmaz-stent, which led to the development of the first commercially successful stent, the palmaz-schatz stent.(5) One such device was a metal tube or" Scaffold" that was inserted. Puel and Sigwart were the first to implant a stent in humans after balloon angioplasty in March 1986. Sigwart and colleagues were also the first to describe the use of this stent in 1987 for emergency vessel closure during balloon angioplasty.(6) In 1994 the first Palmaz-Schatz stent was approved for use in the United States.(7) Over the next decade, several generations of bare metal stents were developed, with each succeeding one being more flexible and easier to deliver to narrowing.(7) Early observation trials highlighted problems associated with the use of stents, in particular, a high incidence of subacute occlusion, despite aggressive anticoagulation regimens that prolonged hospital stays and that were difficult to control and occasionally led to serious events.(1) In 1993 two important randomized trialscompared the Palmaz-schatz stent with angioplasty, establishing the elective placement of coronary stents as a standard treatment. (BENESTENT, STRESS) Although the implantation of an intracoronary stent prevents the acute recoil and post-injury arterial shrinkage associated with balloon angioplasty, it increases the risk of subacute thrombosis (3.7 percent of patients, a value higher than that seen with balloon angioplasty alone) and, more importantly, replaces the atherosclerotic coronary disease with the more severe iatrogenic condition of in-stent neointimal hyperplasia, that is, the growth of scar tissue inside the stent through the cell-cycle pathway, and as a result, the proliferation and migration of vascular smoothmuscle cells.(1) This in-stent restenosis occurs in about 25% of cases of bare metal implantation, typically at six months, necessitating a repeat procedure.( 7) A recent meta-analysis of 29 published, randomized studies involving 9918 patients and comparing balloon angioplasty with routine coronary stenting with bare stents confirmed that stenting reduces restenosis and repeat intervention, but dose not reduce mortality or MI.(8) Once a role for elective stent implantation was established, the next goal was to overcome the compplications of subacute thrombosis and neointimal hyperplasia through pharmacologic and physical means. Various biologically inert surfaces coatings, such as carbon, platinum, phosphorylcholine, and gold, have beenapplied to stainless-steel stents in an attempt to reduce thrombosis and restenosis, but the effectiveness of these strategies has not been proven in clinical trials. Significat reduction of stent thrombosis with heparincoated stents has been reported from a single center study.(9)