An Update on Carotid Stent Trials and Perspectives

An Update on Carotid Stent Trials and Perspectives

Bertog Stefan , Franke Jennifer, Hornung Marius , Sievert Horst, Wunderlich Nina
Interventional Cardiology Volume 4 Issue1
Published: November 2009
download article View ebook

| More
dots

The presence of carotid artery stenosis is associated with an increased risk of stroke. Carotid endartectomy (CEA) has been demonstrated to reduce the stroke risk in standard-risk patients with symptomatic carotid stenosis as well as in asymptomatic patients, provided that the operative risk is low. The role of percutaneous carotid intervention is less clear. There are no trials that compare percutaneous carotid intervention with medical management. Although trial results comparing CEA with carotid artery stenting (CAS) are variable and/or controversial, some trials have demonstrated promising results and have fostered enthusiasm for the performance of ongoing trials comparing CAS with CEA. This article focuses on the results of completed trials and outlines ongoing and planned trials that aim to clarify the role of CAS in patients with carotid stenosis. In addition, potential unresolved problems associated with CAS, such as CAS in the elderly, in-stent restenosis and distal embolisation, are discussed.

Strokes are frequently devastating events with potentially fatal complications and significant disability, resulting in a major impact on the affected individual’s quality of life. It is well accepted that the presence of carotid stenosis is responsible for 20–30% of strokes.1 Great effort has therefore been invested in the search for treatments to reduce the stroke risk attributed to it. Although the mechanism of stroke related to carotid atherosclerosis is not entirely clear, analogous to the occurrence of an acute coronary syndrome, plaque rupture with subsequent thrombus adhesion followed by distal embolisation of either thrombotic material or atherosclerotic debris2 is most commonly thought to be the cause. With the aim of plaque removal or stabilisation, medical and interventional treatment options have been explored. It is assumed that, by stent implantation, the plaque composition is modified such that the plaque becomes less vulnerable to rupture and/or embolisation. This brief review will focus on carotid artery stenting (CAS). The discussion of the evolution of percutaneous treatment modalities would be incomplete without a brief summary of the extensive surgical experience prior to the advent of percutaneous treatment.

Evidence Following the Completion of Surgical Trials
Similar to the initial experience with percutaneous carotid intervention, the first carotid endarterectomy (CEA) in 19543 was followed by many years of mixed and controversial results4,5 until the performance of three important trials in the early 1990s: the North American Symptomatic Carotid Endarterectomy Trial (NASCET),6 the European Carotid Stenosis Trial (ECST)7 and the Veterans Affairs Cooperative trial.8 These trials unequivocally demonstrated a benefit of CEA for patients with symptomatic carotid stenosis greater than 50%.

In the presence of stenosis >69%, fewer than 10 patients needed to be treated with CEA to prevent one stroke, provided the surgical risk was 6% or less. This benefit included men and women, patients over 74 years of age and patients with contralateral carotid occlusion. As expected, in the following years the number of CEAs increased substantially, including in patients with asymptomatic carotid stenoses.

Keywords:
Carotid stenosis, carotid endarterectomy (CEA), carotid stenting, carotid angioplasty, carotid artery, carotid intervention

References:
  1. DeBakey ME, J Endovasc Surg, 1996;3:4.
  2. Fisher CM, Medicine (Baltimore), 1957; 6:169–209.
  3. Eastcott HH, Pickering GW, Rob CG, Lancet, 1954;267:994–6.
  4. Fields WS, Maslenikov V, Meyer JS, et al., JAMA, 1970; 211:1993–2003.
  5. Shaw DA, Venables GS, Cartlidge NE, et al., J Neurol Sci, 1984;64:45–53.
  6. National Institute of Neurological Disorders and Stroke Stroke and Trauma Division. North American Symptomatic Carotid Endarterectomy Trial (NASCET) investigators, Stroke, 1991;22:816–17.
  7. European Carotid Surgery Trialists’ Collaborative Group, Lancet, 1991;337:1235–43.
  8. Mayberg MR, Wilson SE, Yatsu F, et al., JAMA, 1991;266:3289–94.
  9. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study, JAMA, 1995;273:1421–8.
  10. Halliday A, Mansfield A, Marro J, et al., Lancet,2004;363:1491–1502.
  11. Wennberg DE, Lucas FL, Birkmeyer JD, et al., JAMA, 1998;279:1278–81.
  12. Tu JV, Wang H, Bowyer B, et al., Stroke, 2003;34:2568–73.
  13. Mathias K, Mittermayer C, Ensinger H, ROFO Fortschr Geb Rontgenstr Nuklearmed 1980;133:258–61.
  14. Mathias K, Angio, 1981;3:47–50.
  15. Mathias K. In: Al-Mubarak N, Roubin GS, Iyer SS, Vitek J, eds, Carotid Artery Stenting: Current Practice and Techniques, Philadelphia, Lippincott Williams and Wilkins, 2004:1–22.
  16. Roubin GS, New G, Iyer SS, et al., Circulation, 2001;103:532–7.
  17. Wholey MH, Al-Mubarek N, Wholey MH, Catheter Cardiovasc Interv, 2003;60:259–66.
  18. Kastrup A, Gröschel K, Krapf H, et al., Stroke, 2003;34:813–19.
  19. Theiss W, Hermanek P, Mathias K, et al., Stroke, 2004;35:2134–9.
  20. Bosiers M, Peeters P, Deloose K, et al., J Cardiovasc Surg (Torino), 2005;46:241–7.
  21. CaRESS Steering Committee, J Endovasc Ther, 2003;10:1021–30.
  22. CaRESS Steering Committee, J Vasc Surg, 2005;42:213–19.
  23. Gray WA, Hopkins LN, Yadav S, et al., J Vasc Surg, 2006;44:258–68.
  24. White CJ, Iyer SS, Hopkins LN, et al., Catheter Cardiovasc Interv, 2006;67:503–12.
  25. Safian RD, Bresnahan JF, Jaff MR, et al., J Am Coll Cardiol, 2006;47:2384–9.
  26. Hopkins LN, CABERNET (oral presentation), EuroPCR. Paris, France, 2005.
  27. Gray WA, Yadav J, Hopkins LN, et al., American College of Cardiology Annual Scientific meeting, Atlanta, 2006.
  28. Naylor AR, Bolia A, Abbott RJ, et al., J Vasc Surg, 1998;28: 326–34.
  29. Alberts M, Stroke, 2001;32:325d.
  30. Lancet, 2001;357:1729–37.
  31. Brooks WH, McClure RR, Jones MR, et al., J Am Coll Cardiol, 2001;38:1589–95.
  32. Yadav JS, Cleve Clin J Med, 2004;71(Suppl. 1):S45–6.
  33. Gurm HS, Yadav JS, Fayad P, et al., N Engl J Med, 2008;358:1572–9.
  34. Brooks WH, McClure RR, Jones MR, et al., Neurosurgery, 2004;54:318–24, discussion 324–5.
  35. SPACE Collaborative Group: Ringleb PA, Allenberg J, Brückmann H, et al., Lancet, 2006;368:1239–47.
  36. Eckstein HH, Ringleb P, Allenberg JR, et al., Lancet Neurol, 2008;7:893–902.
  37. Mas JL, Chatellier G, Beyssen B, et al., N Engl J Med, 2006;355:1660–71.
  38. Mas JL, Trinquart L, Leys D, et al., Lancet Neurol, 2008;7:885–92.
  39. Hobson RW, 2nd, Howard VJ, Roubin GS, et al., J Vasc Surg, 2004;40:952–7.
  40. Hobson RW, 2nd, Howard VJ, Roubin GS, et al., J Vasc Surg, 2004;40:1106–11.
  41. Mathiesen EB, Waterloo K, Joakimsen O, et al., Neurology, 2004;62:695–701.
  42. Johnston SC, O’Meara ES, Manolio TA, et al., Ann Intern Med, 2004;140:237–47.
  43. Sztriha LK, Nemeth D, Sefcsik T, et al., J Neurol Sci, 2009;283:36–40.
  44. Crawley F, Clifton A, Buckenham T, et al., Stroke, 1997;28:2460–64.
  45. Crawley F, Stygall J, Lunn S, et al., Stroke, 2000;31:1329–34.
  46. González A, Piñero P, Martínez E, et al., Neurol Res, 2005;27(Suppl. 1):S79–83.
  47. Hammer FD, Lacroix V, Duprez T, et al., J Vasc Surg, 2005;42:847–53, discussion 853.
  48. Jaeger H, Mathias K, Drescher R, et al., Cardiovasc Intervent Radiol, 2001;24:249–56.
  49. Feiwell RJ, Besmertis L, Sarkar R, et al., AJNR Am J Neuroradiol, 2001;22:646–9.
  50. Jordan WD, Jr., Voellinger DC, Doblar DD, et al., Cardiovasc Surg, 1999;7:33–8.
  51. Boltuch J, Sabeti S, Amighi J, et al., J Endovasc Ther, 2005;12:538–47.
  52. Castriota F, Cremonesi A, Manetti R, et al., J Endovasc Ther, 2002;9:786–92.
  53. Coggia M, Goëau-Brissonnière O, Duval JL, et al., J Vasc Surg, 2000;31:550–57.
  54. Rapp JH, Pan XM, Sharp FR, et al., J Vasc Surg, 2000;32:68–76.
  55. Moody DM, Bell MA, Challa VR, et al., Ann Neurol, 1990;28:477–86.
  56. Henry M, Henry I, Klonaris C, et al., J Endovasc Ther, 2002;9:1–13.
  57. Roubin GS, Yadav S, Iyer SS, et al., Am J Cardiol, 1996;78:8–12.
  58. Wholey MH, Wholey MH, Tan WA, et al., J Endovasc Ther, 2001;8:341–53.
  59. Qureshi AI, Luft AR, Janardhan V, et al., Stroke, 2000;31:376–82.
  60. Mehran R, Roubin G, New G, American Heart Association Meeting. Anaheim, CA, 2001.
  61. Wholey MH, Wholey M, Mathias K, et al., Catheter Cardiovasc Interv, 2000;50:160–67.
  62. Yadav JS, Roubin GS, Iyer S, et al., Circulation, 1997;95:376–81.
  63. Shawl F, Kadro W, Domanski MJ, et al., J Am Coll Cardiol, 2000;35:1721–8.
  64. Shawl FA, Curr Opin Cardiol, 2002;17:671–76.
  65. Willfort-Ehringer A, Ahmadi R, Gschwandtner ME, et al., J Endovasc Ther, 2002;9:299–307.
  66. Lal BK, Semin Vasc Surg, 2007;20:259–66.
  67. Mathur A, Roubin GS, Iyer SS, et al., Circulation, 1998;97:1239–45.
  68. Henry M, Henry I, Polydorou A, et al., Catheter Cardiovasc Interv, 2008;72:309–17.
  69. Setacci C, de Donato G, Chisci E, et al., J Endovasc Ther, 2006;13:302–9.
  70. Chiam PT, Roubin GS, Iyer SS, et al., Catheter Cardiovasc Interv, 2008;72:318–24.

Copyright® 2004 - 2010 Business Briefings, Ltd. All rights reserved.
Touch Cardiology is for informational purposes and should not be considered medical advice, diagnosis or treatement recommendations.