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High Coronary Shear Stress in Patients With Coronary Artery Disease Predicts Myocardial Infarction Evolving insights into the role of local shear stress in late stent failure from neoatherosclerosis formation and plaque destabilization Role of local coronary blood flow patterns and shear stress on the development of microvascular and epicardial endothelial dysfunction and coronary plaque Implications of the local hemodynamic forces on the formation and destabilization of neoatherosclerotic lesions Role of endothelial dysfunction in determining angina after percutaneous coronary intervention: Learning from pathophysiology to optimize treatment TAVI Represents an Anti-Inflammatory Therapy via Reduction of Shear Stress Induced, Piezo-1-Mediated Monocyte Activation Transcatheter Aortic Valve Implantation Represents an Anti-Inflammatory Therapy Via Reduction of Shear Stress-Induced, Piezo-1-Mediated Monocyte Activation Endothelial ACKR3 drives atherosclerosis by promoting immune cell adhesion to vascular endothelium
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Original Research2018 Dec 1;272:7-12.

JOURNAL:Int J Cardiol. Article Link

Implications of the local hemodynamic forces on the formation and destabilization of neoatherosclerotic lesions

Torii R, Stettler R, Bourantas CV et al. Keywords: Endothelial shear stress; Neoatherosclerosis; Optical coherence tomography

ABSTRACT


OBJECTIVE - To examine the implications of endothelial shear stress (ESS) distribution in the formation of neoatherosclerotic lesions.

 

METHODS - Thirty six patients with neoatherosclerotic lesions on optical coherence tomography (OCT) were included in this study. The OCT data were used to reconstruct coronary anatomy. Blood flow simulation was performed in the models reconstructed from the stent borders which it was assumed that represented the lumen surface at baseline, immediate after stent implantation, and the estimated ESS was associated with the neointima burden, neoatherosclerotic burden and neointima characteristics. In segments with neointima rupture blood flow simulation was also performed in the model representing the lumen surface before rupture and the ESS was estimated at the ruptured site.

 

RESULTS - An inverse association was noted between baseline ESS and the incidence and the burden of neoatherosclerotic (β = -0.60, P < 0.001, and β = -4.05, P < 0.001, respectively) and lipid-rich neoatherosclerotic tissue (β = -0.54, P < 0.001, and β = -3.60, P < 0.001, respectively). Segments exposed to low ESS (<1 Pa) were more likely to exhibit macrophages accumulation (28.2% vs 10.9%, P < 0.001), thrombus (11.0% vs 2.6%, P < 0.001) and evidence of neointima discontinuities (8.1% vs 0.9%, P < 0.001) compared to those exposed to normal or high ESS. In segments with neointima rupture the ESS was high at the rupture site compared to the average ESS over the culprit lesion (4.00 ± 3.65 Pa vs 3.14 ± 2.90 Pa, P < 0.001).

 

CONCLUSIONS - Local EES is associated with neoatherosclerotic lesion characteristics, which suggests involvement of ESS in the formation of vulnerable plaques in stented segments.

 

Copyright © 2018 Elsevier B.V. All rights reserved.