CBS 2019
CBSMD教育中心
中 文

Shear Stress

Abstract

Recommended Article

Low shear stress induces vascular eNOS uncoupling via autophagy-mediated eNOS phosphorylation Role of local coronary blood flow patterns and shear stress on the development of microvascular and epicardial endothelial dysfunction and coronary plaque Comparison Of High Shear Stress-Induced Thrombotic And Thrombolytic Effect Between Aspirin, Clopidogrel And Very Low Dose Rivaroxaban And Aspirin, Ticagrelor Treatments In Patients With Acute Coronary Syndrome Evolving insights into the role of local shear stress in late stent failure from neoatherosclerosis formation and plaque destabilization Low shear stress induces endothelial reactive oxygen species via the AT1R/eNOS/NO pathway Role of Low Endothelial Shear Stress and Plaque Characteristics in the Prediction of Nonculprit Major Adverse Cardiac Events: The PROSPECT Study Transcatheter Aortic Valve Implantation Represents an Anti-Inflammatory Therapy Via Reduction of Shear Stress-Induced, Piezo-1-Mediated Monocyte Activation Implications of the local hemodynamic forces on the formation and destabilization of neoatherosclerotic lesions
|<< 1 2 3 >>|

Original Research2018 Oct;33(4):360-371.

JOURNAL:Cardiovasc Interv Ther. Article Link

Effect of low-density lipoprotein cholesterol on the geometry of coronary bifurcation lesions and clinical outcomes of coronary interventions in the J-REVERSE registry

Murasato Y, Kinoshita Y, J-REVERSE investigators et al. Keywords: Bifurcation angle; Coronary bifurcation lesion; Intravascular ultrasound; Low-density lipoprotein cholesterol

ABSTRACT

 

We investigated the effect of low-density lipoprotein cholesterol (LDL-C) on the geometry of coronary bifurcationlesions. A total of 300 non-left main bifurcation lesions in 298 patients from J-REVERSE registry were classified according to statin treatment status at admission (NT, non-treated; ST, statin-treated) and were further subdivided based on LDL-C levels with a cutoff of 100 mg/dL (NT-high, n = 76 lesions; NT-low, n = 46; ST-high, n = 99 and ST-low, n = 79). In addition, a group with strict control of LDL-C (< 70 mg/dL) was defined (ST-SC; n = 19). The NT-high group had higher angled bifurcations compared to that in the NT-low group (59.1° ± 21.5° vs. 50.3° ± 18.6°, p = 0.02). In the multivariate analysis, NT-high group was an independent factor contributing on generation of higher angled (> 80°) lesion (odds ratio 3.77, 95% CI 1.05-13.5, p = 0.04). The NT-low group had more men (95.6 vs. 81.6%, p = 0.03), and greater plaque volume in the distal main vessel (7.1 ± 3.2 mm3/mm vs. 5.7 ± 2.7 mm3/mm, p = 0.02), compared to those in the NT-high group. LDL-C was more likely to remain high after statin treatment in younger patients (65.3 ± 3.6 years vs. 68.6 ± 8.4 years, p = 0.02) and current smokers (36.7 vs. 16.9%, p = 0.004). The ST-SC group had limited luminal volume expansion compared to that in the ST-high group (proximal: 6.7 ± 1.4 mm3/mm vs. 7.7 ± 2.3 mm3/mm, p = 0.04; distal: 5.3 ± 1.5 mm3/mm vs. 6.5 ± 1.9 mm3/mm, p = 0.04), regardless of similar plaque volumes. Elevated LDL-C is likely to promote the generation of higher angled bifurcation lesions and multiple risk factors lead to a more progressed bifurcation lesion even in patients with lower LDL-C levels.