[Prevention of in-stent restenosis: towards an in situ treatment?].
The use of intracoronary stents represent a major breakthrough in the armamentarium of interventional cardiology. Stents reduce significantly the incidence of recurrent stenosis (in-stent restenosis) via an improved post-procedure luminal diameter and an abrogation of the constrictive remodeling of the arterial wall. However, stent-related arterial injury results in intense proliferative and inflammatory responses and severe intimal hyperplasia, which, in 20% to 40% of the patients, may end up with clinically significant in-stent restenosis. Efficient prevention of in-stent restenosis has yet to be found. Systemic treatments have failed because they don't take into account the specific physiopathology and, most importantly, the focal nature of in-stent intimal hyperplasia. Hence, local prevention appears to be a straightforward approach to the unsolved issue of in-stent restenosis. In situ beta- or gamma-irradiation (brachytherapy) has received much attention as a curative treatment of in-stent restenosis but is not indicated for prevention. In contrast, drug-releasing stents have been tested in experimental models and have already provided very promising results in randomized clinical trials. Most of clinical studies have been performed with the antiproliferative agents sirolimus and paclitaxel, but other agents are under scrutiny. In addition, important research is carried out, in which the efficacy of antiproliferative genes is investigated. Clearly, drug-releasing stents are on the verge of profoundly modifying our practice of interventional cardiology. However, several questions remain unanswered as regard to the long term efficacy/toxicity and the cost-effectiveness of this new approach.
Mazighi
Mikaël
M
Service de Cardiologie et Inserm U.460, Hôpital Bichat, 46, rue Henri Huchard, 75018 Paris, France.
Gouëffic
Yann
Y
Scheuble
Aliocha
A
Feldman
Laurent J
LJ
D000818:Animals; D023903:Coronary Restenosis / Q000188:drug therapy / Q000473:pathology / Q000517:prevention & control*; D016503:Drug Delivery Systems; D006801:Humans; D006965:Hyperplasia; D017239:Paclitaxel / Q000031:analogs & derivatives / Q000627:therapeutic use; D020123:Sirolimus / Q000627:therapeutic use; D015607:Stents; D017539:Tunica Intima / Q000473:pathology
D017239:Paclitaxel; D020123:Sirolimus