2009
DOI: 10.1136/hrt.2009.175455
|View full text |Cite
|
Sign up to set email alerts
|

Relationship between plasma inflammatory markers and plaque fibrous cap thickness determined by intravascular optical coherence tomography

Abstract: There is an inverse linear correlation between fibrous cap thickness and plasma levels of inflammatory markers. The plasma hs-CRP concentration is the strongest independent predictor of TCFA.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2
1

Citation Types

1
25
0
1

Year Published

2010
2010
2014
2014

Publication Types

Select...
7
1

Relationship

0
8

Authors

Journals

citations
Cited by 43 publications
(27 citation statements)
references
References 16 publications
1
25
0
1
Order By: Relevance
“…Inflammation not only promotes the occurrence of atherosclerosis and participates in the formation of vulnerable plaque [1][2][3], but also promotes the occurrence of ACS. As a pro-inflammatory cytokine, IL-18 plays a central role in the inflammatory reaction [4], accelerating atherosclerosis progress, promoting atherosclerotic plaque transforming into vulnerable plaque phenotype which would make the occurrence of ACS [12][13][14]. IL-10 is a major anti-inflammatory cytokine, which can inhibit the activity of inflammatory cells and down-regulate the expression and biological activity of inflammatory cytokines, thus inhibiting the occurrence and development of ACS [8,14].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Inflammation not only promotes the occurrence of atherosclerosis and participates in the formation of vulnerable plaque [1][2][3], but also promotes the occurrence of ACS. As a pro-inflammatory cytokine, IL-18 plays a central role in the inflammatory reaction [4], accelerating atherosclerosis progress, promoting atherosclerotic plaque transforming into vulnerable plaque phenotype which would make the occurrence of ACS [12][13][14]. IL-10 is a major anti-inflammatory cytokine, which can inhibit the activity of inflammatory cells and down-regulate the expression and biological activity of inflammatory cytokines, thus inhibiting the occurrence and development of ACS [8,14].…”
Section: Discussionmentioning
confidence: 99%
“…The mechanism of vulnerable plaque formation promoted by IL-18 may be: (1) IL-18 stimulates the release of a variety of pro-inflammatory mediators (such as TNF, IL-1b, IL-6, and iNOS etc.). These inflammatory factors, promote the macrophage apoptosis in atherosclerotic plaque [16][17][18], increase the lipid core in plaque; (2) macrophages activated by IL-18 can secrete matrix metalloproteinase and collagen, which can make the fibrous cap become thinner [12]. The current results of this study showed that the plasma IL-10 level in patients with ACS was lower than in those without ACS, suggesting that IL-10 may suppress the occurrence of ACS.…”
Section: Discussionmentioning
confidence: 99%
“…A key feature of unstable plaque is thin-cap atherosclerosis, and recent data remind us that the inflammatory environment is an important determinant of instability, an OCT study showing a clear association between the cap thickness of plaques and inflammatory plasma markers such as high-sensitivity C-reactive protein (61).…”
Section: Intravascular Imaging-clinical Benefit?mentioning
confidence: 99%
“…60 A key feature of unstable plaque is thin-cap atherosclerosis, and recent data remind us that the inflammatory environment is an important determinant of instability, an OCT study showing a clear association between the cap thickness of plaques and inflammatory plasma markers such as high-sensitivity C-reactive protein. 61 …”
Section: Intravascular Imagingdclinical Benefit?mentioning
confidence: 99%