English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

ince stent thrombosis (ST) is one of the serious and mortal complications after percutaneous coronary intervention (PCI), especially drug-eluting stent (DES) implantation, we are eager that the means of predicting and preventing ST be established. Several studies have reported an association between inflammation and stent thrombogenicity. In a clinical setting, Hwang et al1 reported a positive association between elevated levels of interleukin (IL)-6, a marker of inflammation, and DES thrombosis. In their study, plasma levels of monocyte chemoattractant protein-1, tumor necrosis factor-α, and IL-6 were compared between ST patients and matched controls. The levels of these 3 cytokines were similar in the ST group, compared to the control group. When divided into quartiles, however, the patients with the highest quartile of IL-6 showed a significantly higher rate of ST, compared to the control group. In addition, the highest IL-6 quartile was an independent predictor of ST in the multivariate analysis. In that study, blood samples were collected when the patients in both groups were in a stable condition (ie, at least 3 months after the index procedure in the control group and at least 3 months after development of ST in the ST group) in order to avoid conditions that may interfere with baseline levels of biomarkers such as myocardial infarction, procedural issues, and medications used in the treatment of ST. Regarding the mechanism by which IL-6 but not other inflammatory markers was specifically associated with ST, they discuss promotion by IL-6 of tissue factor expression from endothelial cells and circulating monocytes, which is responsible for thrombogenecity. This study demonstrated that the trend in the relationship between IL-6 level and ST was more conspicuous in early ST patients or ST in clopidogrel-treated patients, compared to late ST patients or ST patients without clopidogrel treatment. Since the pathological and morphological mechanisms of late ST in DES patients are mainly attributed to lack of re-endothelialization as the vascular healing process, excessive fibrin deposition, acquired stent malapposition, and antiplatelet drug discontinuation,2,3 the predictive value of IL-6 for ST might be weak in late ST patients or ST patients without clopidogrel treatment. In the case of late ST, acquired stent malapposition, poor re-endothelialization and antiplatelet drug discontinuation would be rather better predictors.

Stent Thrombosis After Drug Eluting Stent Implantation