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Role of Low Endothelial Shear Stress and Plaque Characteristics in the Prediction of Nonculprit Major Adverse Cardiac Events: The PROSPECT Study Coronary Microcirculation in Ischemic Heart Disease Low shear stress induces vascular eNOS uncoupling via autophagy-mediated eNOS phosphorylation Angiographic derived endothelial shear stress: a new predictor of atherosclerotic disease progression Low Endothelial Shear Stress Predicts Evolution to High-Risk Coronary Plaque Phenotype in the Future: A Serial Optical Coherence Tomography and Computational Fluid Dynamics Study Local Low Shear Stress and Endothelial Dysfunction in Patients With Nonobstructive Coronary Atherosclerosis Evolving understanding of the heterogeneous natural history of individual coronary artery plaques and the role of local endothelial shear stress Flow-Regulated Endothelial S1P Receptor-1 Signaling Sustains Vascular Development Prediction of progression of coronary artery disease and clinical outcomes using vascular profiling of endothelial shear stress and arterial plaque characteristics: the PREDICTION Study Low shear stress induces endothelial reactive oxygen species via the AT1R/eNOS/NO pathway
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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.