Imaging of the unstable plaque

Tan, Kiat Tsong; Lip, Gregory Y.H.

doi:10.1016/j.ijcard.2007.11.054

Cited by 20 publications

(12 citation statements)

References 60 publications

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“…Atherosclerosis is a progressive (and inflammatory ) disease (Altman 2003; Binder et al 2002; Blake and Ridker 2001; Duewell et al 2010; Dwyer et al 2004; Forrester 2002, 2004; Gieseg et al 2009; Grainger 2007; Hansson 2001, 2005; Himmelfarb et al 2002; Kibel et al 2008; Kunsch and Medford 1999; Libby 2002; Libby et al 2002; Madamanchi et al 2005a, b; Mullenix et al 2005; Nigro et al 2006; Packard and Libby 2008; Paoletti et al 2004; Popa et al 2007; Rader and Daugherty 2008; Ridker et alet al 2004; Ross 1999; Schleicher and Friess 2007; Subramanian and Ferrante 2009; Sullivan 2009; Tan and Lip 2008; Tang et al 2009; Taqueti et al 2006; Tedgui and Mallat 2006; van Leuven et al 2008; van Oostrom et al 2004; Willerson and Ridker 2004; Young et al 2002) characterized by the accumulation of both oxidised lipids and various fibrous elements in arteries, often as plaques (Lusis 2000; Stocker and Keaney 2004). Several lines of evidence point to the involvement of iron in these processes:

Both iron and oxidised lipids (de Valk and Marx 1999; Smith et al 1992) are found in atherosclerotic lesions (Altamura and Muckenthaler 2009; Brewer 2007; Chau 2000; Fernandes de Godoy et al 2007; Gajda et al 2008; Halliwell 2009; Horwitz et al 1998; Kazi et al 2008; Lee et al 1998; McRae et al 2009; Rajendran et al 2007; Ramakrishna et al 2003; Roijers et al 2005; Smith et al 1992; Stadler et al 2004; Stanley et al 2006; Stocker and Keaney 2005; Sullivan 2009; Watt et al 2006; Wolff et al 2004; Yuan and Li 2008)

Iron depletion by dietary or other means delays the formation of such lesions...

…”

Section: Iron Deposition and Disease: Cause Or Effect? The Case Of Atmentioning

confidence: 99%

Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson’s, Huntington’s, Alzheimer’s, prions, bactericides, chemical toxicology and others as examples

2010

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Exposure to a variety of toxins and/or infectious agents leads to disease, degeneration and death, often characterised by circumstances in which cells or tissues do not merely die and cease to function but may be more or less entirely obliterated. It is then legitimate to ask the question as to whether, despite the many kinds of agent involved, there may be at least some unifying mechanisms of such cell death and destruction. I summarise the evidence that in a great many cases, one underlying mechanism, providing major stresses of this type, entails continuing and autocatalytic production (based on positive feedback mechanisms) of hydroxyl radicals via Fenton chemistry involving poorly liganded iron, leading to cell death via apoptosis (probably including via pathways induced by changes in the NF-κB system). While every pathway is in some sense connected to every other one, I highlight the literature evidence suggesting that the degenerative effects of many diseases and toxicological insults converge on iron dysregulation. This highlights specifically the role of iron metabolism, and the detailed speciation of iron, in chemical and other toxicology, and has significant implications for the use of iron chelating substances (probably in partnership with appropriate anti-oxidants) as nutritional or therapeutic agents in inhibiting both the progression of these mainly degenerative diseases and the sequelae of both chronic and acute toxin exposure. The complexity of biochemical networks, especially those involving autocatalytic behaviour and positive feedbacks, means that multiple interventions (e.g. of iron chelators plus antioxidants) are likely to prove most effective. A variety of systems biology approaches, that I summarise, can predict both the mechanisms involved in these cell death pathways and the optimal sites of action for nutritional or pharmacological interventions.

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Iron depletion by dietary or other means delays the formation of such lesions...

…”

Section: Iron Deposition and Disease: Cause Or Effect? The Case Of Atmentioning

confidence: 99%

Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson’s, Huntington’s, Alzheimer’s, prions, bactericides, chemical toxicology and others as examples

2010

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“…In estimating heritability, we first adjusted each raw trait for a covariate set of age, sex, and body weight, regardless of their significance for that trait, and then normalized and standardized the covariate-adjusted residual prior to statistical genetic analysis. Heritability, h2, was estimated as the proportion of residual variance explained by pedigree relationships (i.e., h2 = σ2 G /sigma2 P , where σ2 G represents the additive genetic, and α2 P the residual phenotypic, variances); significance was assessed by comparison with a model in which heritability was fixed at zero. Simulations, using the same pedigree and data (i.e., lysate protein levels) structure as in this study demonstrated we had 80% power to detect h2=0.21 as significantly different from zero (at α=0.05; M.C.Mahaney, unpublished observations).…”

Section: Methodsmentioning

confidence: 99%

“…Heritability, h2, was estimated as the proportion of residual variance explained by pedigree relationships (i.e., h2 = σ2 G /sigma2 P , where σ2 G represents the additive genetic, and α2 P the residual phenotypic, variances); significance was assessed by comparison with a model in which heritability was fixed at zero. Simulations, using the same pedigree and data (i.e., lysate protein levels) structure as in this study demonstrated we had 80% power to detect h2=0.21 as significantly different from zero (at α=0.05; M.C.Mahaney, unpublished observations). Bivariate models were used to estimate correlation coefficients for the endothelial cell traits with various metabolic traits, and significance of the correlation was assessed by comparison with a model in which the traits were forced to be uncorrelated.…”

Section: Methodsmentioning

confidence: 99%

“…The expressions of E-selectin, ICAM-1 and VCAM-1 were increased 12.2-, 41.4- and 3.5-fold, respectively (p<0.0001). The quantitative levels of several traits were heritable after TNF-α stimulation: h2=0.244 ( P =0.017) for IL-8 and h2=0.278 ( P =0.0028) for E-selectin in culture medium, h2=0.207 ( P =0.034) for ICAM-1; and h2=0.369 ( P =0.00015) for VCAM-1 expression on EC surfaces. Furthermore, a significant heritability was observed for lysate protein level, which is a measure of cell growth rate, with (h2=0.639, P =0.00021) or without (h2=0.511, P =0.00069) TNF-α stimulation.…”

mentioning

confidence: 99%

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Genetic Regulation of Endothelial Inflammatory Responses in Baboons

Rainwater

Shi

Mahaney

et al. 2010

ATVB

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Objective-To investigate the genetic contributions to the expression of cell surface adhesion molecules on endothelial cells (ECs) and to the release by ECs of chemokines, which are responsible for local inflammation. Methods and Results-Monocyte adhesion to ECs and transmigration across the endothelial barrier are the key steps in the formation of atherosclerotic plaques and the rupture of the existing plaques. Biopsy specimens were obtained from the femoral arteries of 131 pedigreed baboons (65 males and 66 females) aged 10.4Ϯ1.5 years (meanϮSD); arterial ECs were harvested and cultured up to the second passage and then subjected to in vitro challenge with tumor necrosis factor (TNF) ␣, 10 ng/mL, or vehicle for 4 hours. Endothelial surface adhesion molecules were measured using flow cytometry, and chemokines released by the ECs were measured by immunoassay. In response to TNF-␣ treatment, interleukin 8 and monocyte chemoattractant protein-1 released by ECs were increased 3.4-and 26-fold, respectively (PϽ0.001).

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“…Current knowledge of coronary artery disease progression has significantly evolved and the interest has been focused on the development of new imaging techniques for the early detection of vulnerable lesions, which are ultimately responsible for the majority of acute cardiovascular events [2,3].…”

Section: Introductionmentioning

confidence: 99%

Intravascular Thermography for Assessing Vulnerable Plaques

Toutouzas

Drakopoulou

Synetos

et al. 2010

curr cardiovasc imaging rep

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Atherosclerosis and its cardiovascular complications remain the leading cause of death in developed countries. Current knowledge of coronary artery disease progression has significantly evolved and the interest has been focused on the development of new imaging techniques for the early detection of vulnerable lesions. Intracoronary thermography is a method that detects local plaque inflammation. Clinical studies with intracoronary thermography have enlightened the diagnostic algorithm of high-risk or "vulnerable" plaque. The current shortcomings, however, of intracoronary thermography limit the clinical application of the method. Future technological achievements will hopefully lead to the detection of inflamed plaques, thus determining the role of inflammation in plaque destabilization and directing local and/or systemic therapy in patients with coronary artery disease.

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Imaging of the unstable plaque

Cited by 20 publications

References 60 publications

Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson’s, Huntington’s, Alzheimer’s, prions, bactericides, chemical toxicology and others as examples

Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson’s, Huntington’s, Alzheimer’s, prions, bactericides, chemical toxicology and others as examples

Genetic Regulation of Endothelial Inflammatory Responses in Baboons

Intravascular Thermography for Assessing Vulnerable Plaques

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