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Drug-eluting intracoronary stents: General principles

J Dawn Abbott, MD, FACC
Donald Cutlip, MD
Section Editor
Stephan Windecker, MD
Deputy Editor
Gordon M Saperia, MD, FACC


Drug-eluting stents (DES) reduce the rate of restenosis and, accordingly, target lesion revascularization compared to bare metal stents (BMS). DES consist of a standard metallic stent, a polymer coating, and an anti-restenotic drug (eg, sirolimus or a derivative of sirolimus or paclitaxel) that is mixed within the polymer and is released over a period of weeks to months after implantation to reduce the local proliferative healing response. DES types currently approved for use in the United States are shown in a table (table 1). The sirolimus-eluting stent is no longer manufactured and several stents have been redesigned since their initial approval.

This topic will present the mechanisms of benefit of DES and discuss a few procedural and safety issues. The discussions of the comparison of DES to BMS and of one DES to another are found elsewhere. (See "Clinical use of intracoronary bare metal stents" and "Comparison of drug-eluting intracoronary stents".)


Late lumen loss and restenosis after nonstent interventions are caused by a combination of acute recoil, negative remodeling (arterial contraction) of the treated segment, and local neointimal hyperplasia. In contrast, late lumen loss after stenting is due solely to in-stent neointimal hyperplasia, as the main benefit of stents is to prevent recoil and negative remodeling. Stents retain a larger acute lumen diameter (than balloon angioplasty) that offsets the reduction in lumen diameter from neointimal hyperplasia. (See "Intracoronary stent restenosis", section on 'Pathogenesis'.)

The restenosis benefit of drug-eluting stents (DES) compared to bare metal stent (BMS) results from inhibition of in-stent neointimal hyperplasia [1], which is reflected as a lesser degree of late in-stent lumen loss at six to nine months (0.1 to 0.4 versus 0.9 to 1.0 mm with BMS) [2-5]. Neointimal suppression is sustained at two years [6].

Biologic characteristics of the four available antirestenotic drugs that have been used in DES include [7]:

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Literature review current through: Nov 2017. | This topic last updated: Mar 02, 2016.
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  1. Costa MA, Simon DI. Molecular basis of restenosis and drug-eluting stents. Circulation 2005; 111:2257.
  2. Moses JW, Leon MB, Popma JJ, et al. Sirolimus-eluting stents versus standard stents in patients with stenosis in a native coronary artery. N Engl J Med 2003; 349:1315.
  3. Schofer J, Schlüter M, Gershlick AH, et al. Sirolimus-eluting stents for treatment of patients with long atherosclerotic lesions in small coronary arteries: double-blind, randomised controlled trial (E-SIRIUS). Lancet 2003; 362:1093.
  4. Stone GW, Ellis SG, Cox DA, et al. A polymer-based, paclitaxel-eluting stent in patients with coronary artery disease. N Engl J Med 2004; 350:221.
  5. Mauri L, Orav EJ, O'Malley AJ, et al. Relationship of late loss in lumen diameter to coronary restenosis in sirolimus-eluting stents. Circulation 2005; 111:321.
  6. Aoki J, Colombo A, Dudek D, et al. Peristent remodeling and neointimal suppression 2 years after polymer-based, paclitaxel-eluting stent implantation: insights from serial intravascular ultrasound analysis in the TAXUS II study. Circulation 2005; 112:3876.
  7. Stefanini GG, Holmes DR Jr. Drug-eluting coronary-artery stents. N Engl J Med 2013; 368:254.
  8. Grube E, Sonoda S, Ikeno F, et al. Six- and twelve-month results from first human experience using everolimus-eluting stents with bioabsorbable polymer. Circulation 2004; 109:2168.
  9. Räber L, Wohlwend L, Wigger M, et al. Five-year clinical and angiographic outcomes of a randomized comparison of sirolimus-eluting and paclitaxel-eluting stents: results of the Sirolimus-Eluting Versus Paclitaxel-Eluting Stents for Coronary Revascularization LATE trial. Circulation 2011; 123:2819.
  10. Baber U, Mehran R, Sharma SK, et al. Impact of the everolimus-eluting stent on stent thrombosis: a meta-analysis of 13 randomized trials. J Am Coll Cardiol 2011; 58:1569.
  11. Nebeker JR, Virmani R, Bennett CL, et al. Hypersensitivity cases associated with drug-eluting coronary stents: a review of available cases from the Research on Adverse Drug Events and Reports (RADAR) project. J Am Coll Cardiol 2006; 47:175.
  12. Otsuka F, Yahagi K, Ladich E, et al. Hypersensitivity reaction in the US Food and Drug Administration-approved second-generation drug-eluting stents: histopathological assessment with ex vivo optical coherence tomography. Circulation 2015; 131:322.
  13. Fujimaki T, Kato K, Fukuda S, et al. Acute interstitial pneumonitis after implantation of paclitaxel-eluting stents: a report of two fatal cases. Int J Cardiol 2011; 148:e21.
  14. Shin HW, Nam CW, Kim H, et al. Zotarolimus-eluting stent-induced hypersensitivity pneumonitis. Korean J Intern Med 2013; 28:108.
  15. Alfonso F, Pérez-Vizcayno MJ, Ruiz M, et al. Coronary aneurysms after drug-eluting stent implantation: clinical, angiographic, and intravascular ultrasound findings. J Am Coll Cardiol 2009; 53:2053.
  16. Aoki J, Kirtane A, Leon MB, Dangas G. Coronary artery aneurysms after drug-eluting stent implantation. JACC Cardiovasc Interv 2008; 1:14.
  17. Subramaniam KG, Akhunji Z. Drug eluting stent induced coronary artery aneurysm repair by exclusion. Where are we headed? Eur J Cardiothorac Surg 2009; 36:203.
  18. Halkin A, Mehran R, Casey CW, et al. Impact of moderate renal insufficiency on restenosis and adverse clinical events after paclitaxel-eluting and bare metal stent implantation: results from the TAXUS-IV Trial. Am Heart J 2005; 150:1163.
  19. Garg P, Charytan DM, Novack L, et al. Impact of moderate renal insufficiency on restenosis and adverse clinical events after sirolimus-eluting and bare metal stent implantation (from the SIRIUS trials). Am J Cardiol 2010; 106:1436.
  20. Simsek C, Magro M, Boersma E, et al. Impact of renal insufficiency on safety and efficacy of drug-eluting stents compared to bare-metal stents at 6 years. Catheter Cardiovasc Interv 2012; 80:18.
  21. Tomai F, Ribichini F, De Luca L, et al. Randomized Comparison of Xience V and Multi-Link Vision Coronary Stents in the Same Multivessel Patient With Chronic Kidney Disease (RENAL-DES) Study. Circulation 2014; 129:1104.
  22. Kastrati A, Dibra A, Mehilli J, et al. Predictive factors of restenosis after coronary implantation of sirolimus- or paclitaxel-eluting stents. Circulation 2006; 113:2293.
  23. Carrozza JP Jr. Sirolimus-eluting stents: does a great stent still need a good interventionalist? J Am Coll Cardiol 2004; 43:1116.
  24. Lemos PA, Saia F, Ligthart JM, et al. Coronary restenosis after sirolimus-eluting stent implantation: morphological description and mechanistic analysis from a consecutive series of cases. Circulation 2003; 108:257.
  25. Fujii K, Mintz GS, Kobayashi Y, et al. Contribution of stent underexpansion to recurrence after sirolimus-eluting stent implantation for in-stent restenosis. Circulation 2004; 109:1085.
  26. Takebayashi H, Kobayashi Y, Mintz GS, et al. Intravascular ultrasound assessment of lesions with target vessel failure after sirolimus-eluting stent implantation. Am J Cardiol 2005; 95:498.
  27. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation 2007; 116:1736.