Intimal hyperplasia: Slow but deadly

B. Mills, T. Robb, D. F. Larson

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

Intimal hyperplasia is the leading cause of long-term failure in coronary artery bypass vein grafting, coronary artery stenting, angioplasty, arteriovenous fistula for dialysis, and allograft transplantation. Intimal hyperplasia is a product of vascular smooth muscle cell proliferation, migration through the internal elastic lamina, and deposition of extracellular matrix proteins driven by growth factors in the vasculature. This vascular pathology results in a progressive diminution of the vessel lumen and serves as a site for thrombosis and atherosclerotic lesions. A key cell type in the initiation of intimal hyperplasia is the vascular endothelial cell, which appears to have down-stream effects on the vascular smooth muscle proliferation and migration. Currently, the only means available for prevention of intimal hyperplasia is through inhibition of mammalian target of rapamycin (mTOR) with the immunosuppressant rapamycin. mTOR integrates up-stream signals from growth factors such as IL-2 and senses the cellular nutrient and energy levels and redox status. This presentation will discuss the potential means of preserving the vascular endothelial cell and, thereby, reducing the development of intimal hyperplasia in our open-heart surgical patients.

Original languageEnglish (US)
Pages (from-to)520-528
Number of pages9
JournalPerfusion (United Kingdom)
Volume27
Issue number6
DOIs
StatePublished - Nov 2012

Keywords

  • Kruppel-like factor
  • cytokines
  • endothelial cell
  • inflammation
  • lymphocyte
  • remodeling
  • vascular smooth muscle cell

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging
  • Safety Research
  • Cardiology and Cardiovascular Medicine
  • Advanced and Specialized Nursing

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