IN-STENT STENOSIS: PATHOLOGY AND IMPLICATIONS FOR THE DEVELOPMENT OF DRUG ELUTING STENTS

"Neointima" formation within a stent also results from other mechanisms, such as axial movement of primary plaque displaced to adjacent artery segments by the original procedure.\n Indeed, a major concern with both brachytherapy and drug eluting stents relates to failure of complete vessel...

Full description

Saved in:
Bibliographic Details
Published in:British heart journal 2003-02, Vol.89 (2), p.218-224
Main Author: Bennett, Martin R
Format: Article
Language:English
Subjects:
Analysis
Angiogenesis Inhibitors - administration & dosage
Angioplasty
Biological and medical sciences
Blood clots
Blood platelets
Brachytherapy - methods
Care and treatment
Case studies
Cell adhesion & migration
Cell cycle
Cell growth
Collagen
Coronary Restenosis - pathology
Coronary Restenosis - prevention & control
Diseases of the cardiovascular system
Dissection
Drug dosages
Drug Implants - adverse effects
Drug therapy
Education in Heart
Gene expression
Graft Occlusion, Vascular - prevention & control
Health aspects
Humans
Immunosuppressive Agents - administration & dosage
Inflammation
Medical research
Medical sciences
Medicine, Experimental
Paclitaxel - administration & dosage
Pathology
Radiation therapy
Radioisotope brachytherapy
Radiotherapy. Instrumental treatment. Physiotherapy. Reeducation. Rehabilitation, orthophony, crenotherapy. Diet therapy and various other treatments (general aspects)
Sirolimus - administration & dosage
Smooth muscle
Stenosis
Stents
Thrombosis
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:"Neointima" formation within a stent also results from other mechanisms, such as axial movement of primary plaque displaced to adjacent artery segments by the original procedure.\n Indeed, a major concern with both brachytherapy and drug eluting stents relates to failure of complete vessel healing, with subsequent lack of re-endothelialisation and late thrombosis, and medial thinning with stent malapposition. [...]an ideal agent would exhibit specificity to the vessel intima, without having an effect on endothelial cells or medial VSMCs. A recent study of differential gene expression in human ISS versus medial VSMCs demonstrated increased expression of FKBP12 in ISS VSMCs. [...]rapamycin released to the vessel wall may preferentially bind to the intima, the receptor potentially acting as a "sink" and local reservoir for the drug.
ISSN:1355-6037
0007-0769
1468-201X
DOI:10.1136/heart.89.2.218