نتایج جستجو برای: plaque inflammation

تعداد نتایج: 203595  

Journal: :Stroke 2011
Hannah Gardener Ashley Beecham Digna Cabral Danielle Yanuck Susan Slifer Liyong Wang Susan H Blanton Ralph L Sacco Suh-Hang Hank Juo Tatjana Rundek

BACKGROUND AND PURPOSE The genetic influence on carotid atherosclerotic plaque is mostly unknown. This study examines the association between carotid plaque and single nucleotide polymorphisms in selected genes implicated in inflammation and endothelial function. METHODS A total of 43 genes (197 single nucleotide polymorphisms) involved in inflammation and endothelial function were interrogat...

Journal: :Arteriosclerosis, thrombosis, and vascular biology 2004
David L Brown Kavita K Desai Babak A Vakili Chadi Nouneh Hsi-Ming Lee Lorne M Golub

BACKGROUND Vulnerable plaque demonstrates intense inflammation in which macrophages secrete matrix metalloproteinases (MMPs) that degrade the fibrous cap, ultimately leading to rupture, in situ thrombosis, and an associated clinical event. Thus, inhibition of MMP activity or more general suppression of vascular inflammation are attractive targets for interventions intended to reduce plaque rupt...

2018
Jah Yeon Choi Jiheun Ryu Hyun Jung Kim Joon Woo Song Joo Hee Jeon Dae-Hee Lee Dong Joo Oh Dae-Gab Gweon Wang-Yuhl Oh Hongki Yoo Kyeongsoon Park Jin Won Kim

Rationale: Atherosclerotic plaque is a chronic inflammatory disorder involving lipid accumulation within arterial walls. In particular, macrophages mediate plaque progression and rupture. While PPARγ agonist is known to have favorable pleiotropic effects on atherogenesis, its clinical application has been very limited due to undesirable systemic effects. We hypothesized that the specific delive...

2002
J. H. F. Rudd E. A. Warburton T. D. Fryer H. A. Jones J. C. Clark N. Antoun P. Johnström P. Davenport P. J. Kirkpatrick B. N. Arch J. D. Pickard P. L. Weissberg

Background—Atherosclerotic plaque rupture is usually a consequence of inflammatory cell activity within the plaque. Current imaging techniques provide anatomic data but no indication of plaque inflammation. The glucose analogue [F]-fluorodeoxyglucose (FDG) can be used to image inflammatory cell activity non-invasively by PET. In this study we tested whether FDG-PET imaging can identify inflamma...

2004
David L. Brown Kavita Desai Babak A. Vakili Chadi Nouneh Hsi-Ming Lee Lorne M. Golub

Background—Vulnerable plaque demonstrates intense inflammation in which macrophages secrete matrix metalloproteinases (MMPs) that degrade the fibrous cap, ultimately leading to rupture, in situ thrombosis, and an associated clinical event. Thus, inhibition of MMP activity or more general suppression of vascular inflammation are attractive targets for interventions intended to reduce plaque rupt...

Journal: :The Journal of invasive cardiology 1997
Srivatsa Holmes

The current study describes the histopathology of angiographic chronic total occlusions including residual lumen patency, intimal plaque composition, patterns of neovascular channel formation, intimal plaque calcification, and cellular inflammation, analyzed according to occlusion duration and intimal plaque type (fibrocalcific vs. lipid laden vs. mixed). Histologic findings are related to prev...

Journal: :Journal of the American College of Cardiology 2010
James H F Rudd Jagat Narula H William Strauss Renu Virmani Josef Machac Mike Klimas Nobuhiro Tahara Valentin Fuster Elizabeth A Warburton Zahi A Fayad Ahmed A Tawakol

Inflammation is a determinant of atherosclerotic plaque rupture, the event leading to most myocardial infarctions and strokes. Although conventional imaging techniques identify the site and severity of luminal stenosis, the inflammatory status of the plaque is not addressed. Positron emission tomography imaging of atherosclerosis using the metabolic marker fluorodeoxyglucose allows quantificati...

Journal: :Journal of nuclear medicine : official publication, Society of Nuclear Medicine 2011
Leon J Menezes Carl W Kotze Obi Agu Toby Richards Jocelyn Brookes Vicky J Goh Manuel Rodriguez-Justo Raymondo Endozo Richard Harvey Syed W Yusuf Peter J Ell Ashley M Groves

UNLABELLED Inflammation and angiogenesis are hypothesized to be important factors contributing to plaque vulnerability, whereas calcification is suggested to confer stability. To investigate this in vivo, we combined CT angiography and PET and compared the findings with immunohistochemistry for patients undergoing carotid endarterectomy. METHODS Twenty-one consecutive patients (18 men, 3 wome...

Journal: :Arteriosclerosis, thrombosis, and vascular biology 2006
Rikin A Trivedi Chinthake Mallawarachi Jean-Marie U-King-Im Martin J Graves Jo Horsley Martin J Goddard Andrew Brown Liqun Wang Peter J Kirkpatrick John Brown Jonathan H Gillard

BACKGROUND Inflammation within atherosclerotic lesions contributes to plaque instability and vulnerability to rupture. We set out to evaluate the use of a macrophage labeling agent to identify carotid plaque inflammation by in vivo magnetic resonance imaging (MRI). METHODS AND RESULTS Thirty patients with symptomatic severe carotid stenosis scheduled for carotid endarterectomy underwent multi...

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