scholarly journals Relation between plaque type, plaque thickness, blood shear stress, and plaque stress in coronary arteries assessed by X-ray Angiography and Intravascular Ultrasound

2012 ◽  
Vol 39 (12) ◽  
pp. 7430-7445 ◽  
Author(s):  
Simone Balocco ◽  
Carlo Gatta ◽  
Marina Alberti ◽  
Xavier Carrillo ◽  
Juan Rigla ◽  
...  
2006 ◽  
Vol 10 (4) ◽  
pp. 615-631 ◽  
Author(s):  
Andreas Wahle ◽  
John J. Lopez ◽  
Mark E. Olszewski ◽  
Sarah C. Vigmostad ◽  
Krishnan B. Chandran ◽  
...  

Author(s):  
Jin Suo ◽  
Michael McDaniel ◽  
Habib Samady ◽  
Don Giddens

Atherosclerosis is a disease characterized by arterial plaques that include several components of which the necrotic core has been recognized as an important indicator of the likelihood of plaque rupture [1]. In the present study, the relation of hemodynamic wall shear stress (WSS) to necrotic core localization in the left coronary artery of patients was investigated using intravascular ultrasound (IVUS) and computational fluid dynamics (CFD). An innovative 3D measuring technique was developed and was successfully used to reconstruct coronary arteries in patients based on angiographic images and echo ultrasound slices from IVUS. The reconstruction includes lumen, external elastic membrane (EEM) and spatial distribution of plaque components such as fibrous tissue, necrotic core and calcium. WSS distribution in the vessel segment was computed by CFD, and the relative locations of necrotic core and WSS were determined. Results to date support the hypothesis that a greater necrotic core in coronary plaques is associated with areas of low WSS. The methodology developed has implications for the study of plaque progression and the prediction of likelihood of plaque rupture.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Johannes Rieber ◽  
Thomas Redel ◽  
Holger Hetterich ◽  
Tobias Potzger ◽  
Konstantin Nikolaou ◽  
...  

Beyond classic risk parameters non physiologic or oscillating wall shear stress (WSS) has been proven to act as a local factor for initiation and progression of atherosclerosis as well as for plaque rupture. Direct measurement of WSS in-vivo is difficult and restricted to animal models. Computational fluid dynamics (CFD) is a validated tool to compute flow parameters and WSS. For this purpose an exact model of the underlying patient specific geometry of the coronary tree is a prerequisite. Using 3D-IVUS or modern multislice computed tomographic coronary angiography (CTA) with submilimeter resolution these data can be provided. The aim of this study was to 1.) demonstrate feasibility of in-vivo CFD calculation of human coronaries based on CTA and 2.) to correlate the findings with radio frequency tissue information derived by intravascular ultrasound. We prospectively included 10 patients with suspected coronary artery disease who received CTA (Dual source 64 slice CT) and invasive conventional coronary angiography. Intravascular ultrasound and ECG-triggered radio frequency analysis (VH) was attempted in all three epicardial vessels. In the CTA-dataset the coronaries were segmented and a mesh model for CFD was generated. CFD calculations were performed using a commercial available software package with laminar flow and blood as a Newtonian fluid as boundary conditions. Coronary models were stationary with rigid vessel walls, while the pulsatile inflow characteristics was derived from invasive Doppler velocity measurement. Flow pattern calculations, vessel wall shear stress and IVUS analysis were successfully performed in 24/30 and 17/30 coronary arteries. The presence of high shear stress and non turbulent flow was inversely correlated with the presence of plaque as determined by intravascular ultrasound. No correlation of any CFD parameter with the radio frequency tissue information could yet be observed. The findings of the present study demonstrate the feasibility of assessing fluid tissue interactions in human coronary arteries using CTA and its correlation to invasive findings. The possible impact of CFD parameters on risk- and treatment stratification has to be determined in a large scale prospective trial.


Author(s):  
Runlei Ma ◽  
Marly van Assen ◽  
Daan Ties ◽  
Gert Jan Pelgrim ◽  
Randy van Dijk ◽  
...  

Abstract Objectives To investigate the association of pericoronary adipose tissue mean attenuation (PCATMA) with coronary artery disease (CAD) characteristics on coronary computed tomography angiography (CCTA). Methods We retrospectively investigated 165 symptomatic patients who underwent third-generation dual-source CCTA at 70kVp: 93 with and 72 without CAD (204 arteries with plaque, 291 without plaque). CCTA was evaluated for presence and characteristics of CAD per artery. PCATMA was measured proximally and across the most severe stenosis. Patient-level, proximal PCATMA was defined as the mean of the proximal PCATMA of the three main coronary arteries. Analyses were performed on patient and vessel level. Results Mean proximal PCATMA was −96.2 ± 7.1 HU and −95.6 ± 7.8HU for patients with and without CAD (p = 0.644). In arteries with plaque, proximal and lesion-specific PCATMA was similar (−96.1 ± 9.6 HU, −95.9 ± 11.2 HU, p = 0.608). Lesion-specific PCATMA of arteries with plaque (−94.7 HU) differed from proximal PCATMA of arteries without plaque (−97.2 HU, p = 0.015). Minimal stenosis showed higher lesion-specific PCATMA (−94.0 HU) than severe stenosis (−98.5 HU, p = 0.030). Lesion-specific PCATMA of non-calcified, mixed, and calcified plaque was −96.5 HU, −94.6 HU, and −89.9 HU (p = 0.004). Vessel-based total plaque, lipid-rich necrotic core, and calcified plaque burden showed a very weak to moderate correlation with proximal PCATMA. Conclusions Lesion-specific PCATMA was higher in arteries with plaque than proximal PCATMA in arteries without plaque. Lesion-specific PCATMA was higher in non-calcified and mixed plaques compared to calcified plaques, and in minimal stenosis compared to severe; proximal PCATMA did not show these relationships. This suggests that lesion-specific PCATMA is related to plaque development and vulnerability. Key Points • In symptomatic patients undergoing CCTA at 70 kVp, PCATMAwas higher in coronary arteries with plaque than those without plaque. • PCATMAwas higher for non-calcified and mixed plaques compared to calcified plaques, and for minimal stenosis compared to severe stenosis. • In contrast to PCATMAmeasurement of the proximal vessels, lesion-specific PCATMAshowed clear relationships with plaque presence and stenosis degree.


2021 ◽  
Vol 73 (1) ◽  
Author(s):  
Magdy Algowhary ◽  
Mohammed Aboel-Kassem F. Abdelmegid

Abstract Background Stent manufacturers always record stent shortening data while they do not record stent elongation data. The aim of this study is to identify both stent shortening and elongation occurring after deployment in the coronary arteries and know their percentage. Results The length of coronary stents was measured by intravascular ultrasound (IVUS) by (1) edge-to-edge (E-E) length, measured from the appearance of the first distal strut to the last proximal strut, and (2) area-to-area (A-A) length, measured from the first distal struts seen at more than one IVUS quadrant to the last proximal struts seen at more than one IVUS quadrant. Stent shortening was defined as both E-E and A-A lengths were shorter than the manufacturer box-stated length (shortened group). Stent elongation was defined as both E-E and A-A lengths were longer than the manufacturer box-stated length (elongated group), otherwise unchanged group. Consecutive 102 stents deployed in ischemic patients were included. Stent elongation was detected in 67.6% (69 stents), and shortening was detected in 15.7% (16 stents), while unchanged stents were detected in 16.7% (17 stents). Although the 3 groups had similar box-stated length and predicted foreshortened length, they had significantly different measurements by IVUS, p<0.001 for each comparison. Differences from box-stated length were 1.9±1.4mm, −1.4±0.4mm, and 0.4±0.3mm, respectively, p<0.001. The elongated group had significantly longer differences from the corresponding box-stated and predicted foreshortened lengths, while the shortened group had significantly shorter differences from the corresponding box-stated length and similar foreshortened length. By multinomial regression analysis, the plaque-media area and stent deployment pressure were the independent predictors of the stent length groups, p=0.015 and p=0.026, respectively. Conclusions Change in stent length is not only shortening—as mentioned in the manufacturer documents—but also stent elongation. Stent elongation is dominant, and the most important predictors of longitudinal stent changes are plaque-media area and stent deployment pressure.


Author(s):  
Karol Calò ◽  
Giuseppe De Nisco ◽  
Diego Gallo ◽  
Claudio Chiastra ◽  
Ayla Hoogendoorn ◽  
...  

Atherosclerosis at the early stage in coronary arteries has been associated with low cycle-average wall shear stress magnitude. However, parallel to the identification of an established active role for low wall shear stress in the onset/progression of the atherosclerotic disease, a weak association between lesions localization and low/oscillatory wall shear stress has been observed. In the attempt to fully identify the wall shear stress phenotype triggering early atherosclerosis in coronary arteries, this exploratory study aims at enriching the characterization of wall shear stress emerging features combining correlation-based analysis and complex networks theory with computational hemodynamics. The final goal is the characterization of the spatiotemporal and topological heterogeneity of wall shear stress waveforms along the cardiac cycle. In detail, here time-histories of wall shear stress magnitude and wall shear stress projection along the main flow direction and orthogonal to it (a measure of wall shear stress multidirectionality) are analyzed in a representative dataset of 10 left anterior descending pig coronary artery computational hemodynamics models. Among the main findings, we report that the proposed analysis quantitatively demonstrates that the model-specific inlet flow-rate shapes wall shear stress time-histories. Moreover, it emerges that a combined effect of low wall shear stress magnitude and of the shape of the wall shear stress–based descriptors time-histories could trigger atherosclerosis at its earliest stage. The findings of this work suggest for new experiments to provide a clearer determination of the wall shear stress phenotype which is at the basis of the so-called arterial hemodynamic risk hypothesis in coronary arteries.


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