High Coronary Shear Stress in Patients With Coronary Artery Disease Predicts Myocardial Infarction

Kumar, Arnav; Thompson, Elizabeth; Lefieux, Adrien; Molony, David; Davis, Emily; Chand, Nikita; Fournier, Stéphane; Lee, Hee Su; Suh, Jon; Sato, Kimi; Ko, Yi An; Molloy, Daniel L.; Chandran, Karthic; Hosseini, Hossein; Sk, Gupta; Μιλκασ, Αναστασιοσ; Gogas, Bill D.; Chang, Hyuk Jae; Min, James K.; Fearon, William F.; Veneziani, Alessandro; Giddens, Don P.; King, Spencer B.; Bruyne, Bernard De; Samady, Habib

doi:10.1016/j.jacc.2018.07.075

Cited by 144 publications

(97 citation statements)

References 37 publications

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“…There is increasing evidence that haemodynamic-associated biomechanical forces increase plaque vulnerability and may lead to destabilization causing a clinical event. [35][36][37][38] The most extensively studied biomechanical forces are endothelial shear stress (ESS), plaque structural stress, and axial plaque stress. 7,35,39,40 In addition, a fluid-structure interaction model is being developed to define pulsatility as a determinant of the risk of plaque rupture (Supplementary material online, Appendix-Impact of local haemodynamic forces on plaque biology).…”

Section: Imaging Of the High-risk/culprit Coronary Plaquementioning

confidence: 99%

“…36 It has been also shown that high wall shear stress in the upstream part of a plaque may contribute to the prognostic value of fractional flow reserve to predict myocardial infarction. 37 Although CFD is a powerful research tool, such analysis requires numerous assumptions and procedures, including three-dimensional reconstruction of the vessel, meshing, and solving the Navier-Stokes equation. The principles of appropriate ESS computation and its potential clinical implications have been described in detail elsewhere.…”

Section: Imaging Of the High-risk/culprit Coronary Plaquementioning

confidence: 99%

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Vulnerable plaques and patients: state-of-the-art

Tomaniak

Katagiri

Modolo

et al. 2020

European Heart Journal

121

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Despite advanced understanding of the biology of atherosclerosis, coronary heart disease remains the leading cause of death worldwide. Progress has been challenging as half of the individuals who suffer sudden cardiac death do not experience premonitory symptoms. Furthermore, it is well-recognized that also a plaque that does not cause a haemodynamically significant stenosis can trigger a sudden cardiac event, yet the majority of ruptured or eroded plaques remain clinically silent. In the past 30 years since the term ‘vulnerable plaque’ was introduced, there have been major advances in the understanding of plaque pathogenesis and pathophysiology, shifting from pursuing features of ‘vulnerability’ of a specific lesion to the more comprehensive goal of identifying patient ‘cardiovascular vulnerability’. It has been also recognized that aside a thin-capped, lipid-rich plaque associated with plaque rupture, acute coronary syndromes (ACS) are also caused by plaque erosion underlying between 25% and 60% of ACS nowadays, by calcified nodule or by functional coronary alterations. While there have been advances in preventive strategies and in pharmacotherapy, with improved agents to reduce cholesterol, thrombosis, and inflammation, events continue to occur in patients receiving optimal medical treatment. Although at present the positive predictive value of imaging precursors of the culprit plaques remains too low for clinical relevance, improving coronary plaque imaging may be instrumental in guiding pharmacotherapy intensity and could facilitate optimal allocation of novel, more aggressive, and costly treatment strategies. Recent technical and diagnostic advances justify continuation of interdisciplinary research efforts to improve cardiovascular prognosis by both systemic and ‘local’ diagnostics and therapies. The present state-of-the-art document aims to present and critically appraise the latest evidence, developments, and future perspectives in detection, prevention, and treatment of ‘high-risk’ plaques occurring in ‘vulnerable’ patients.

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Section: Imaging Of the High-risk/culprit Coronary Plaquementioning

confidence: 99%

Section: Imaging Of the High-risk/culprit Coronary Plaquementioning

confidence: 99%

Vulnerable plaques and patients: state-of-the-art

Tomaniak

Katagiri

Modolo

et al. 2020

European Heart Journal

121

View full text Add to dashboard Cite

show abstract

“…29 patients with myocardial infarction (MI) were matched with a control group (n = 29) who did not have MI to study ESS in the coronary lesions. However, in this study in patients with stable CAD, high ESS proximal to the lesion had a significant incremental value to FFR in predicting myocardial infarction [52].These detailed observations highlight the importance of ESS-whether high or low in natural history and progression of CAD.…”

Section: Invasive Coronary Angiography and Ivusmentioning

confidence: 46%

Physiology and coronary artery disease: emerging insights from computed tomography imaging based computational modeling

Eslami

Thondapu

Karády

et al. 2020

Int J Cardiovasc Imaging

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Improvements in spatial and temporal resolution now permit robust high quality characterization of presence, morphology and composition of coronary atherosclerosis in computed tomography (CT). These characteristics include high risk features such as large plaque volume, low CT attenuation, napkin-ring sign, spotty calcification and positive remodeling. Because of the high image quality, principles of patient-specific computational fluid dynamics modeling of blood flow through the coronary arteries can now be applied to CT and allow the calculation of local lesion-specific hemodynamics such as endothelial shear stress, fractional flow reserve and axial plaque stress. This review examines recent advances in coronary CT image-based computational modeling and discusses the opportunity to identify lesions at risk for rupture much earlier than today through the combination of anatomic and hemodynamic information.

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“…The haemodynamic environment exquisitely regulates the behaviour of endothelial cells: it modulates metabolism, cell shape, cytoskeleton arrangement, proliferation, permeability, response to inflammatory stimuli and apoptosis [25][26][27][28][29]. Thus, haemodynamics strongly influences plaque development, progression and features of lesions that determine their propensity to rupture [30][31][32][33]. Emerging evidence also supports the involvement of haemodynamics in endothelial erosion.…”

Section: Introductionmentioning

confidence: 98%

A pivotal role for Nrf2 in endothelial detachment- implications for endothelial erosion of stenotic plaques

Satta

McElroy

Langford-Smith

et al. 2019

Preprint

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Endothelial erosion of atherosclerotic plaques and resulting thrombosis causes approximately 30% of acute coronary syndromes (ACS). As changes in the haemodynamic environment strongly influence endothelial function and contribute to plaque development, we reconstructed the coronary artery geometries of plaques with thrombi overlying intact fibrous caps from 17 ACS patients and performed computational fluid dynamic analysis. The results demonstrated that erosions frequently occur within areas of stenosis exposed to elevated flow. We recapitulated this flow environment in vitro, exposing human coronary artery endothelial cells to elevated flow and modelled smoking (a risk factor for erosion) by exposure to a combination of aqueous cigarette smoke extract and TNFα. This treatment induced endothelial detachment, which increased with pharmacological activation of the antioxidant system controlled by transcription factor Nrf2 (encoded by NFE2L2). The expression of Oxidative Stress Growth INhibitor genes OSGIN1 and OSGIN2 increased under these conditions and also in the aortas of mice exposed to cigarette smoke. Sustained high level expression of OSGIN1+2 resulted in cell cycle arrest, induction of senescence, loss of focal adhesions and actin stress fibres, and dysregulation of autophagy. Overexpression of either Nrf2 or OSGIN1+2 induced cell detachment, which did not depend on apoptosis, and could be partially rescued by inhibition of HSP70 using VER-155008, or AMP kinase activation using metformin. These findings demonstrate that under elevated flow, smokinginduced hyperactivation of Nrf2 can trigger endothelial cell detachment, highlighting a novel mechanism that could contribute to ACS involving endothelial erosion overlying stenotic plaques.

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High Coronary Shear Stress in Patients With Coronary Artery Disease Predicts Myocardial Infarction

Cited by 144 publications

References 37 publications

Vulnerable plaques and patients: state-of-the-art

Vulnerable plaques and patients: state-of-the-art

Physiology and coronary artery disease: emerging insights from computed tomography imaging based computational modeling

A pivotal role for Nrf2 in endothelial detachment- implications for endothelial erosion of stenotic plaques

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