Ferrite-encapsulated nanoparticles with stable photothermal performance for multimodal imaging-guided atherosclerotic plaque neovascularization therapy

2021 ◽  
Author(s):  
Zhuowen Yang ◽  
Jianting Yao ◽  
Jianxin Wang ◽  
Cong Zhang ◽  
Yang Cao ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Multimodal Imaging ◽  
Plaque Rupture ◽  
Pathological Angiogenesis ◽  
Atherosclerotic Plaque Rupture ◽  
Encapsulated Nanoparticles

Pathological angiogenesis is a critical contributor to atherosclerotic plaque rupture. However, there are few effective theranostic strategies to stabilize plaques by suppressing neovascularization. A polymeric nanosystem using 3 nm manganese...

scholarly journals Applicability of Recent Dyslipidemia Guidelines in Clinical Practice

2019 ◽  
Vol 5 (1 (P)) ◽  
pp. 43
Author(s):  
Erwinanto Erwinanto
Keyword(s):  
Myocardial Infarction ◽  
Atherosclerotic Plaque ◽  
Coronary Flow ◽  
Cardiovascular Events ◽  
Ldl Cholesterol ◽  
Plaque Rupture ◽  
Heart Association ◽  
Plaque Stabilization ◽  
Plaque Regression ◽  
Atherosclerotic Plaque Rupture

Atherosclerotic plaque rupture is closely related to acute coronary syndromes.Stabilization of atherosclerotic plaque which slashes plaque rupture is as importantas regression ofplaque size for reducing cardiovascular events. Dyslipidemia therapy targeting to decrease LDL cholesterol reduces cardiovascular events such as acute myocard infarct, stroke, and death which are suggested to be the result of plaque stabilization. Dyslipidemia therapy also regress atherosclerotic plaque into a smaller volume. Plaque regression improves coronary flow responsible for the reduction of myocardial infarction incidence in patients with coronary heart disease (CHD).This paper consists of two parts. The first part discusses the evidence of cardiovascular event reduction with statin. The second part describes dyslipidemia management based on the 2017 Indonesian Heart Association (PERKI) Guideline on the Management of Dyslipidemia

Atherosclerotic plaque rupture: a fatigue process?

2000 ◽  
Vol 55 (6) ◽  
pp. 480-484 ◽  
Author(s):  
A.J. Bank ◽  
A. Versluis ◽  
S.M. Dodge ◽  
W.H. Douglas
Keyword(s):  
Atherosclerotic Plaque ◽  
Plaque Rupture ◽  
Fatigue Process ◽  
Atherosclerotic Plaque Rupture

Computational Analysis of Atherosclerotic Plaque Vulnerability Due to Hemodynamic Effects

2007 ◽  
Author(s):  
Ramses Galaz ◽  
Rosaire Mongrain ◽  
Valerie Pazos ◽  
Richard Leask ◽  
Jean Claude Tardif
Keyword(s):  
Atherosclerotic Plaque ◽  
Plaque Rupture ◽  
Developed Countries ◽  
Mechanical Failure ◽  
Myocardial Infarctions ◽  
Plaque Morphology ◽  
Myocardial Tissue ◽  
Physical Interaction ◽  
Tissue Properties ◽  
Atherosclerotic Plaque Rupture

Atherosclerotic plaque rupture has been extensively associated with acute myocardial infarctions, the leading cause of death in developed countries. When a plaque ruptures in the coronary arteries, it often leads to a clot formation that restricts the flow of blood downstream of the coronaries causing damage to the myocardial tissue. Hemodynamic factors combined with certain plaque morphologies and material properties play an important role in the mechanical failure of the plaque [1]. It is essential for clinicians to understand the vulnerability of plaques and the particular physiological conditions that lead to their mechanical failure. Our study focused on understanding the physical interaction between blood flow, plaque morphology and tissue properties to assess the plaque’s degree of vulnerability.

scholarly journals BIRC6 Is Associated with Vulnerability of Carotid Atherosclerotic Plaque

2020 ◽  
Vol 21 (24) ◽  
pp. 9387
Author(s):  
Iraide Alloza ◽  
Andrea Salegi ◽  
Jorge Mena ◽  
Raquel Tulloch Navarro ◽  
César Martin ◽  
...  
Keyword(s):  
Atherosclerotic Plaque ◽  
Plaque Rupture ◽  
Negative Regulator ◽  
Mrna Levels ◽  
Nucleotide Polymorphisms ◽  
Carotid Atherosclerotic Plaque ◽  
Single Nucleotide ◽  
Distribution Width ◽  
Asymptomatic Subjects ◽  
Atherosclerotic Plaque Rupture

Carotid atherosclerotic plaque rupture can lead to cerebrovascular accident (CVA). By comparing RNA-Seq data from vascular smooth muscle cells (VSMC) extracted from carotid atheroma surgically excised from a group of asymptomatic and symptomatic subjects, we identified more than 700 genomic variants associated with symptomatology (p < 0.05). From these, twelve single nucleotide polymorphisms (SNPs) were selected for further validation. Comparing genotypes of a hospital-based cohort of asymptomatic with symptomatic patients, an exonic SNP in the BIRC6 (BRUCE/Apollon) gene, rs35286811, emerged as significantly associated with CVA symptomatology (p = 0.002; OR = 2.24). Moreover, BIRC6 mRNA levels were significantly higher in symptomatic than asymptomatic subjects upon measurement by qPCR in excised carotid atherosclerotic tissue (p < 0.0001), and significantly higher in carriers of the rs35286811 risk allele (p < 0.0001). rs35286811 is a proxy of a GWAS SNP reported to be associated with red cell distribution width (RDW); RDW was increased in symptomatic patients (p < 0.03), but was not influenced by the rs35286811 genotype in our cohort. BIRC6 is a negative regulator of both apoptosis and autophagy. This work introduces BIRC6 as a novel genetic risk factor for stroke, and identifies autophagy as a genetically regulated mechanism of carotid plaque vulnerability.

Sign in / Sign up

Export Citation Format

Share Document