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Evidence that angiotensin-converting enzyme inhibitor use diminishes the need for coronary revascularization after stenting

Academic Article
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Overview

authors

  • Ellis, S. G.
  • Lincoff, A. M.
  • Whitlow, P. L.
  • Raymond, R. E.
  • Franco, I.
  • Schneider, J. P.
  • Topol, Eric

publication date

  • April 2002

journal

  • American Journal of Cardiology  Journal

abstract

  • Restenosis after stenting, in contrast to balloon angioplasty, is predominantly due to neointima formation. Angiotensin-converting enzyme (ACE) inhibitors diminish neointima formation in animal models of arterial injury. In an observational study, 1,598 patients who were treated from 1994 to 1997 with coronary stents and prospectively followed for clinical events were divided into 2 groups: those receiving ACE inhibitors at the time of stenting (n = 345) and those who did not (n = 1,253). Multivariate logistic regression was used to adjust for imbalances between populations with regard to elements relevant to risk of 12-month coronary revascularization, which was the primary study end point. After adjustment, ACE inhibitor usage remained significantly protective against revascularization (odds ratio [OR] 0.46, 95% confidence interval 0.29 to 0.73, p = 0.001). Protection was not observed in patients treated with balloon angioplasty alone during the same period (OR 1.06, p = 0.33), which is consistent with the results of prior randomized trials. ACE inhibitors appear to decrease late revascularization, possibly due to a reduction in restenosis after coronary stenting.

subject areas

  • Aged
  • Angioplasty, Balloon, Coronary
  • Angiotensin-Converting Enzyme Inhibitors
  • Case-Control Studies
  • Coronary Restenosis
  • Coronary Stenosis
  • Female
  • Humans
  • Logistic Models
  • Male
  • Middle Aged
  • Myocardial Revascularization
  • Prospective Studies
  • Sensitivity and Specificity
  • Stents
  • Time Factors
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Identity

International Standard Serial Number (ISSN)

  • 0002-9149

Digital Object Identifier (DOI)

  • 10.1016/s0002-9149(02)02242-7

PubMed ID

  • 11950431
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Additional Document Info

start page

  • 937

end page

  • 940

volume

  • 89

issue

  • 8

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