In vivo assessment of the relationship between shear stress and necrotic core in early and advanced coronary artery disease

Jj, Wentzel; Jc, Schuurbiers; N, Gonzalo Lopez; Fj, Gijsen; Ag, van der Giessen; Hc, Groen; Dijkstra, Jouke; Hm, Garcia-Garcia; Pw, Serruys

doi:10.4244/eijv9i8a165

Cited by 40 publications

(38 citation statements)

References 23 publications

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“…ESS has been implicated in atherosclerosis development and progression [6] and is correlated with high risk plaque characteristics [8]. Key to its estimation is the coronary artery lumen 3D model.…”

Section: Discussionmentioning

confidence: 99%

“…Low ESS is an independent predictor of increased plaque burden, plaque progression and luminal narrowing in both animals [3-5] and humans [6, 7]. Conversely, high ESS has been associated with plaque transition to an unstable phenotype [6] and with high risk plaque characteristics [8]. Autopsy [9] and clinical [10] studies have also shown that the majority of high-risk plaques occur in the proximal portions of the major coronary arteries [11-13].…”

Section: Introductionmentioning

confidence: 99%

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Quantifying the effect of side branches in endothelial shear stress estimates

et al. 2016

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Background and aims Low and high endothelial shear stress (ESS) is associated with coronary atherosclerosis progression and high-risk plaque features. Coronary ESS is currently assessed via computational fluid dynamic (CFD) simulation in the lumen geometry determined from invasive imaging such as intravascular ultrasound and optical coherence tomography. This process typically omits side branches of the target vessel in the CFD model as invasive imaging of those vessels is not clinically-indicated. The purpose of this study was to determine the extent to which this simplification affects the determination of those regions of the coronary endothelium subjected to pathologic ESS. Methods We determined the diagnostic accuracy of ESS profiling without side branches to detect pathologic ESS in the major coronary arteries of 5 hearts imaged ex vivo with CT angiography. ESS of the three major coronary arteries was calculated both without (test model), and with (reference model) inclusion of all side branches >1.5 mm in diameter, using previously-validated CFD approaches. Diagnostic test characteristics (accuracy, sensitivity, specificity and negative and positive predictive value [NPV/PPV]) with respect to the reference model were assessed for both the entire length as well as only the proximal portion of each major coronary artery, where the majority of high-risk plaques occur. Results Using the model without side branches overall accuracy, sensitivity, specificity, NPV and PPV were 83.4%, 54.0%, 96%, 95.9% and 55.1%, respectively to detect low ESS, and 87.0%, 67.7%, 90.7%, 93.7% and 57.5%, respectively to detect high ESS. When considering only the proximal arteries, test characteristics differed for low and high ESS, with low sensitivity (67.7%) and high specificity (90.7%) to detect low ESS, and low sensitivity (44.7%) and high specificity (95.5%) to detect high ESS. Conclusions The exclusion of side branches in ESS vascular profiling studies greatly reduces the ability to detect regions of the major coronary arteries subjected to pathologic ESS. Single-conduit models can in general only be used to rule out pathologic ESS.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Quantifying the effect of side branches in endothelial shear stress estimates

et al. 2016

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“…In the carotid circulation, ulceration of carotid plaques, visible on angiography or on pathological examination, was seen most often in regions where WSS was highest [43] and the inflammatory burden was severe [44]. In line with the experimental and autopsy studies, longitudinal and cross-sectional human coronary and carotid studies have shown an increase in plaque necrotic core, calcium [35], and strain [45], development of expansive remodeling [35,46], presence of IPH [47], large necrotic core [34,46,48], a necrotic core in contact with the lumen [48], and napkin-ring sign [46] in areas exposed to high WSS. Meanwhile, some data show that WSS might not have the same role in development of plaque erosion as it has in the development of plaque rupture [9,10].…”

Section: High Wall Shear Stressmentioning

confidence: 96%

High wall shear stress and high-risk plaque: an emerging concept

Eshtehardi

Brown

Bhargava

et al. 2017

Int J Cardiovasc Imaging

124

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In recent years, there has been a significant effort to identify high-risk plaques in vivo prior to acute events. While number of imaging modalities have been developed to identify morphologic characteristics of high-risk plaques, prospective natural-history observational studies suggest that vulnerability is not solely dependent on plaque morphology and likely involves additional contributing mechanisms. High wall shear stress (WSS) has recently been proposed as one possible causative factor, promoting the development of high-risk plaques. High WSS has been shown to induce specific changes in endothelial cell behavior, exacerbating inflammation and stimulating progression of the atherosclerotic lipid core. In line with experimental and autopsy studies, several human studies have shown associations between high WSS and known morphological features of high-risk plaques. However, despite increasing evidence, there is still no longitudinal data linking high WSS to clinical events. As the interplay between atherosclerotic plaque, artery, and WSS is highly dynamic, large natural history studies of atherosclerosis that include WSS measurements are now warranted. This review will summarize the available clinical evidence on high WSS as a possible etiological mechanism underlying high-risk plaque development.

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“…progression and rupture (1,17). The complete scaffold integration into the vascular wall has shaped a neoplaque phenotype that resulted from the complex interaction of pre-existing plaque, morphological changes of the pre-existing plaque subject to dynamic local rheological factors (18,19), strut resorption, and neointima formation (8). We visually characterized neoplaque using standardized OCT criteria (7).…”

Section: Figure 2 Quantifying Signal-rich Layer Thickness In Differenmentioning

confidence: 99%

OCT Assessment of the Long-Term Vascular Healing Response 5 Years After Everolimus-Eluting Bioresorbable Vascular Scaffold

Καρανάσος

Şimşek

Gnanadesigan

et al. 2014

Journal of the American College of Cardiology

Self Cite

104

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At long-term BVS follow-up, we observed a favorable tissue response, with late luminal enlargement, side-branch patency, and development of a signal-rich, low-attenuating tissue layer that covered thrombogenic plaque components. The small size of the study and the observation of a different tissue response in 1 patient warrant judicious interpretation of our results and confirmation in larger studies.

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In vivo assessment of the relationship between shear stress and necrotic core in early and advanced coronary artery disease

Abstract: With the advancement of disease, necrotic core is less often located at low WSS regions, but exposed to high WSS, which is probably the result of lumen narrowing. Necrotic core in contact with the lumen was most frequently exposed to high WSS.

Cited by 40 publications

References 23 publications

Quantifying the effect of side branches in endothelial shear stress estimates

Quantifying the effect of side branches in endothelial shear stress estimates

High wall shear stress and high-risk plaque: an emerging concept

OCT Assessment of the Long-Term Vascular Healing Response 5 Years After Everolimus-Eluting Bioresorbable Vascular Scaffold

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