Home > Journals > Minerva Cardioangiologica > Past Issues > Minerva Cardioangiologica 2007 April;55(2) > Minerva Cardioangiologica 2007 April;55(2):199-211

CURRENT ISSUE
 

JOURNAL TOOLS

eTOC
To subscribe PROMO
Submit an article
Recommend to your librarian
 

ARTICLE TOOLS

Reprints

 

REVIEWS   

Minerva Cardioangiologica 2007 April;55(2):199-211

Copyright © 2007 EDIZIONI MINERVA MEDICA

language: English

Stent thrombosis in the era of drug eluting stents

Kawaguchi R., Angiolillo D. J., Futamatsu H., Suzuki N., Bass T. A., Costa M. A.

Division of Cardiology and Cardiovascular Imaging Core Laboratories University of Florida, Jacksonville, FL, USA


PDF


Despite a marked reduction in restenosis and the need for repeat revascularization procedures with the use of drug-eluting stents (DES), the risk for stent thrombosis remains of serious concern. Although the safety profiles of DES dose not seem to differ from those of bare metal stent (BMS) in the acute and subacute phases following coronary intervention, recent data suggest a potential increase of thrombotic events late after DES deployment. The main factors associated with late stent thrombosis remain elusive. Delayed re-endothelialization, hypersensitivity reaction, technical and mechanical factors and hypercoagulability have all been proposed as contributing factors. It is unlikely that any of these variables alone can cause stent thrombosis, as the incidence of each factor is much higher than the currently known rates of DES thrombosis. Further, temporal appearances of the thrombotic events represent a challenge to our understanding of re-endothelialization, as one would expect that endothelial coverage would be higher in the later phases after treatment. New expanded definitions of stent thrombosis, which also include events secondary to repeat revascularization, have been proposed to provide a better comparative endpoint between BMS and DES. Such clinical attempt to characterize stent thrombosis is valuable, but does not provide much insight into the pathophysiology and intrinsic thrombotic risk of each device. A true progress in this field will only be possible after we improve our understanding of the patho-physiology of very late stent thromboses, which may differ from events occurring earlier after treatment. The incidence of stent thrombosis remains rare, but its potential catastrophic consequences should remind clinicians and scientists to make every effort to develop strategies and technologies for its prevention. The topic of stent thrombosis in the era of DES will be reviewed in this article.

top of page