Downstream coronary effects of drug-eluting stents.


Journal Article

BACKGROUND: Antiproliferative agents used in drug-eluting stents (DES) attenuate atherosclerosis, yet DES implantation has been linked to endothelial dysfunction. The downstream effects of DES on new lesion formation have not been previously directly examined. We sought to compare the development of de novo stenoses and need for treatment in the downstream coronary vessel of patients treated with DES or a bare-metal stent. METHODS: Angiographic images and procedural information were prospectively collected on 463 adults who underwent implantation of a single stent in a proximal coronary artery, had an appropriate control vessel for comparison, and subsequently returned for intervention. Propensity matching identified 89 pairs of patients. End points were defined as angiographic identification of a de novo stenosis or need for secondary intervention in the downstream vessel within 12 months of initial intervention. RESULTS: In the overall (P < .01) and propensity-matched cohort (P = .01), there was reduced risk of new lesions downstream to DES. No difference was seen in respective control vessels (P = .14 and P = .99). A reduced need for downstream intervention with DES was seen in both the overall (P = .01) and propensity-matched cohorts (P = .04). No difference was seen in the control vessels (P = .98 and P = .36). Multivariate proportional hazards modeling of known atherosclerosis risk factors identified stent type as the sole predictor for downstream lesions (P < .01) and downstream events (P = .02). CONCLUSIONS: Patients receiving DES appear less likely to develop downstream stenoses and events compared with patients receiving bare-metal stents, suggesting beneficial downstream drug delivery.

Full Text

Duke Authors

Cited Authors

  • Krasuski, RA; Cater, GM; Devendra, GP; Wolski, K; Shishehbor, MH; Nissen, SE; Oberti, C; Ellis, SG

Published Date

  • October 2011

Published In

Volume / Issue

  • 162 / 4

Start / End Page

  • 764 - 771.e1

PubMed ID

  • 21982671

Pubmed Central ID

  • 21982671

Electronic International Standard Serial Number (EISSN)

  • 1097-6744

Digital Object Identifier (DOI)

  • 10.1016/j.ahj.2011.08.001


  • eng

Conference Location

  • United States