Flow parameters in normal left coronary artery tree. Implication to atherogenesis

Soulis, Johannes V.; Giannoglou, George D.; Parcharidis, George E.; Louridas, George

doi:10.1016/j.compbiomed.2006.06.006

Cited by 30 publications

(12 citation statements)

References 54 publications

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“…The atherosclerotic materials probably move within the sub-endothelial layer into regions of low WP. Along the vessel, at regions where low WSS and locally low WP occur, the effect of blood flow resistance, due to increased blood molecular viscosity, gives rise to increased contact time between the atherogenic particles of the blood and the endothelium [26,27]. The components of the WPG possibly have different effects upon endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…The components of the WPG possibly have different effects upon endothelial cells. The WPG as well as the WSS gradient in space and in the phase of the cardiac cycle may represent important local modulators of endothelial gene expression in atherogenesis [27,28]. The WPG acting on the endothelium gives rise to a torque development resulting in the redistribution of the initially accumulated atheromatic material within the sub-endothelial layer [26].…”

Section: Discussionmentioning

confidence: 99%

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Correlations of coronary plaque wall thickness with wall pressure and wall pressure gradient: a representative case study

et al. 2012

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BackgroundThere are two major hemodynamic stresses imposed at the blood arterial wall interface by flowing blood: the wall shear stress (WSS) acting tangentially to the wall, and the wall pressure (WP) acting normally to the wall. The role of flow wall shear stress in atherosclerosis progression has been under intensive investigation, while the impact of blood pressure on plaque progression has been under-studied.MethodThe correlations of wall thickness (WT) with wall pressure (WP, blood pressure on the lumen wall) and spatial wall pressure gradient (WPG) in a human atherosclerotic right coronary artery were studied. The pulsatile blood flow was simulated using a three dimensional mathematical model. The blood was treated as an incompressible viscous non-Newtonian fluid. The geometry of the artery was re-constructed using an in vivo intravascular ultrasound (IVUS) 44-slice dataset obtained from a patient with consent obtained. The WT, the WP and the WPG were averaged on each slice, respectively, and Pearson correlation analysis was performed on slice averaged base. Each slice was then divided into 8 segments and averaged vessel WT, WP and WPG were collected from all 352 segments for correlation analysis. Each slice was also divided into 2 segments (inner semi-wall of bend and outer semi-wall of bend) and the correlation analysis was performed on the 88 segments.ResultsUnder mean pressure, the Pearson coefficient for correlation between WT and WP was r = − 0.52 (p < 0.0001) by 2-segment analysis and r = − 0.81 (p < 0.0001) by slice averaged analysis, respectively. The Pearson coefficient for correlation between WT and WPG was r = 0.30 (p = 0.004) by 2-segment analysis and r = 0.45 (p = 0.002) by slice averaged analysis, respectively. The r-values corresponding to systole and diastole pressure conditions were similar.ConclusionsResults from this representative case report indicated that plaque wall thickness correlated negatively with wall pressure (r = −0.81 by slice) and positively with wall pressure gradient (r = 0.45). The slice averaged WT has a strong linear relationship with the slice averaged WP. Large-scale patient studies are needed to further confirm our findings.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Correlations of coronary plaque wall thickness with wall pressure and wall pressure gradient: a representative case study

et al. 2012

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“…46 There is a paucity of high-resolution flow measurements, particularly in coronary arteries. However flow models based upon vessel geometry predict greater complexity of flow characteristics, including flow separation, in the proximal regions of coronary arteries 47–48 . Asynchrony of wall shear stress and circumferential strain (CS) during a cardiac cycle in the coronary artery system exposes the coronary endothelium to a significantly different hemodynamic environment than the non-coronary endothelium.…”

Section: Discussionmentioning

confidence: 99%

Coronary Artery Endothelial Transcriptome In Vivo

Civelek

Manduchi

Riley

et al. 2011

Circ Cardiovasc Genet

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Background Endothelial function is central to the localization of atherosclerosis. The in vivo endothelial phenotypic footprints of arterial bed identity and site-specific athero-susceptibility are addressed. Methods and Results 98 endothelial cell samples from 13 discrete coronary and non-coronary arterial regions of varying susceptibilities to atherosclerosis were isolated from 76 normal swine. Transcript profiles were analyzed to determine the steady state in vivo endothelial phenotypes. An unsupervised systems biology approach utilizing weighted gene co-expression networks determined highly correlated endothelial genes. Connectivity network analysis identified 19 gene modules, 12 of which showed significant association with circulatory bed classification. Differential expression of 1,300 genes between coronary and non-coronary artery endothelium suggested distinct coronary endothelial phenotypes with highest significance expressed in gene modules enriched for biological functions related to endoplasmic reticulum (ER) stress and unfolded protein binding, regulation of transcription and translation, and redox homeostasis. Furthermore, within coronary arteries comparison of endothelial transcript profiles of susceptible proximal regions to protected distal regions suggested the presence of ER stress conditions in susceptible sites. Accumulation of reactive oxygen species (ROS) throughout coronary endothelium was greater than in non-coronary endothelium consistent with coronary artery ER stress and the lower endothelial expression of anti-oxidant genes in coronary arteries. Conclusions Gene connectivity analyses discriminated between coronary and non-coronary endothelial transcript profiles and identified differential transcript levels associated with increased ER and oxidative stress in coronary arteries, consistent with enhanced susceptibility to atherosclerosis.

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“…The features of complicated plaque could be considered as a central attribute of a lesion that allows progression of haemodynamic injury to the endothelium, 28 on the one hand, and of increased deposition of atheromatous material in the subintima, on the other. Atherosclerotic plaques occur at sites of disturbed blood flow; this activates extracellular matrixspecific signals that determine patterns of integrin dominance.…”

Section: Complicated Plaquementioning

confidence: 99%

Complicated atheromatous plaque as integral atherogenesis

Agius

2006

J Clin Pathol

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Flow parameters in normal left coronary artery tree. Implication to atherogenesis

Cited by 30 publications

References 54 publications

Correlations of coronary plaque wall thickness with wall pressure and wall pressure gradient: a representative case study

Correlations of coronary plaque wall thickness with wall pressure and wall pressure gradient: a representative case study

Coronary Artery Endothelial Transcriptome In Vivo

Complicated atheromatous plaque as integral atherogenesis

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