scholarly journals Spectral Differences Between Normal and Atherosclerotic Aorta

2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Nikolay Korovin
Keyword(s):  
Laser Energy ◽  
Spectral Characteristics ◽  
Vascular Wall ◽  
Laser Angioplasty ◽  
Tissue Interactions ◽  
Atherosclerotic Lesions ◽  
Coronary Artery Atherosclerosis ◽  
Normal Vessel ◽  
Technique Development ◽  
Development Result

Ischemic heart disease associated with coronary artery atherosclerosis is a leading cause ofdeath in the world today. In addition to standard treatments such as balloon angioplasty, laser mediated angioplasty is being considered as a potential adjuvant or replacement. Nevertheless, experiments and clinical experience have demonstrated that laser angioplasty is associated with damage to normal vessel tissue, which can cause serious complications. To study the possibility of minimizing these effects by directing laser energy more specifically to atherosclerotic lesions, data concerning the spectral characteristics of normal and diseased artery are necessary. In the current study, the absorbance, reflection and fluorescence spectra of normal and atherosclerotic aortic wall tissue are defined, revealing that (i) spectral characteristics of atherosclerotic aorta wall samples are significantly differed from that of healthy vascular wall samples and (ii) based on a spectral analysis of vascular wall, it is possible to distinguish morphological types of atherosclerotic plaques (i.e., lipidic, calcified). The current study contributes to a more complete understanding of laser-tissue interactions that may, following more experimentation and technique development, result in an improvement of clinical laser angioplasty technique.

Laser

2010 ◽  
pp. 568-585
Author(s):  
Peter O’Kane ◽  
Simon Redwood
Keyword(s):  
Balloon Angioplasty ◽  
Clinical Case ◽  
Laser Energy ◽  
Medical Application ◽  
Laser Angioplasty ◽  
Case Examples ◽  
Tissue Interactions ◽  
Percutaneous Coronary ◽  
Catheter Technology ◽  
Carbon Dioxide Co2

The first medical application of laser was reported by Dr Leon Goldman who, in 1962, reported the use of ruby and carbon dioxide (CO2) lasers in dermatology. In cardiovascular disease, early laser use was confined to cadaver vessels, animal models, and arteries located in freshly amputated limbs, until eventually work progressed to the use of laser energy to salvage an ischaemic limb in 1984. The concept of using laser to remove atherosclerotic material in coronary arteries developed as an alternative strategy to simply modifying the shape of an obstructed lumen as occurs with simple balloon angioplasty. Expectations grew that this new biomedical technology may overcome the low success rate and high complication rate of lesions considered non-ideal for balloon angioplasty. However, initial successful reports could not be replicated. Furthermore, underdeveloped catheter technology and limited appreciation of laser/tissue interactions meant that a cure for restenosis was not in fact discovered and laser coronary angioplasty became isolated to only a few centres in the world. However, more recently with advancement in both catheter technology and technique, excimer coronary laser angioplasty (ELCA) has been rediscovered for use in specific subsets of percutaneous coronary interventions (PCIs). This chapter outlines the basic principles of ELCA and important practical aspects for using the device in contemporary PCI. A discussion of the current indications for clinical use follows and these are highlighted by clinical case examples.

scholarly journals Nitric oxide function in atherosclerosis

1997 ◽  
Vol 6 (1) ◽  
pp. 3-21 ◽  
Author(s):  
K. E. Matthys ◽  
H. Bult
Keyword(s):  
Nitric Oxide ◽  
Leukocyte Adhesion ◽  
Atherosclerotic Lesion ◽  
Vascular Wall ◽  
Early Event ◽  
No Production ◽  
Oxygen Intermediates ◽  
Atherosclerotic Lesions ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Atherosclerosis is a chronic inflammatory process in the intima of conduit arteries, which disturbs the endothelium-dependent regulation of the vascular tone by the labile liposoluble radical nitric oxide (NO) formed by the constitutive endothelial nitric oxide synthase (eNOS). This defect predisposes to coronary vasospasm and cardiac ischaemia, with anginal pain as the typical clinical manifestation. It is now appreciated that endothelial dysfunction is an early event in atherogenesis and that it may also involve the microcirculation, in which atherosclerotic lesions do not develop. On the other hand, the inflammatory environment in atherosclerotic plaques may result in the expression of the inducible NO synthase (iNOS) isozyme. Whether the dysfunction in endothelial NO production is causal to, or the result of, atherosclerotic lesion formation is still highly debated. Most evidence supports the hypothesis that constitutive endothelial NO release protects against atherogenesis e.g. by preventing smooth muscle cell proliferation and leukocyte adhesion. Nitric oxide generated by the inducible isozyme may be beneficial by replacing the failing endothelial production but excessive release may damage the vascular wall cells, especially in combination with reactive oxygen intermediates.

scholarly journals Biomarkers of Carotid Stenosis

2021 ◽  
Vol 3 (1) ◽  
pp. 104-130
Author(s):  
Sergey G. Sсherbak ◽  
Tatyana A. Kamilova ◽  
Svetlana V. Lebedeva ◽  
Dmitry A. Vologzhanin ◽  
Alexander S. Golota ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Carotid Stenosis ◽  
Plaque Rupture ◽  
Early Recognition ◽  
Clinical Problem ◽  
Vascular Wall ◽  
Inflammatory Factors ◽  
Atherosclerotic Lesions ◽  
Important Clinical Problem ◽  
Definition Of

Early recognition of rupture-prone atherosclerotic lesions in patients with high-graded carotid stenosis is an important clinical problem for preventing ischemic stroke. Various pathophysiological mechanisms are responsible for the progression and instability of plaques, such as changes in lipid composition, infiltration by immunoinflammatory cells and degradation of the extracellular matrix of the vascular wall by matrix metalloproteinases, enhanced inflammatory response and plaque neovascularization. These features are the main cause of plaque rupture and, as a consequence, neurologic symptoms. Therefore, matrix metalloproteinases and inflammatory factors can serve as possible markers for patients with severe unstable stenosis of carotid arteries. Due to the heterogeneity of atherosclerotic lesions, only one biomarker is not enough to reliably predict the development of a stroke. The use of a combination of biomarkers is better correlated with clinical data and, therefore, exceeds the analysis of individual factors. To increase the overall sensitivity and specificity and more reliable diagnosis of stroke in patients with symptomatic and asymptomatic carotid stenosis, the biomarker panel should include independent biomarkers. Further preclinical experiments and clinical trials are needed to assess the significance and precise definition of the threshold levels of such biomarkers before they can be used in clinical practice.

Abstract 028: Endothelial Nogo-B Controls Sphingolipid de novo Biosynthesis to Impact Coronary Artery Atherosclerosis

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Yi Zhang ◽  
Linda Sasset ◽  
Ren Xu ◽  
Matthew Blake Greenblatt ◽  
Annarita Di Lorenzo
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Vascular Inflammation ◽  
High Cholesterol Diet ◽  
Serine Palmitoyltransferase ◽  
Atherosclerotic Lesions ◽  
Coronary Artery Atherosclerosis ◽  
Artery Disease

Coronary artery disease is a leading cause of myocardial infarction (MI) worldwide. Alterations in sphingolipid levels have been linked to atherosclerosis although specific molecular mechanisms are poorly understood. Recently, we discovered that endothelial Nogo-B, a membrane protein of the ER, regulates vascular functions by inhibiting serine palmitoyltransferase (SPT), the rate-limiting enzyme of the de novo sphingolipid biosynthesis. Mice lacking Nogo-B are resistant to hypertension and heart failure. Here, we employed a novel model of coronary atherosclerotic lesions induced by hypercholesterolemia and hypertension, well-known risk factors for atherosclerosis. To this aim, transverse aortic constriction (TAC) surgery was performed in mice lacking endothelial Nogo-B in ApoE -/- background and ApoE -/- mice as control. ApoE -/- mice developed coronary atherosclerotic lesions within 6 weeks following TAC, (without the need of long-term high-cholesterol diet) and 70% of the mice died of MI at 6-week post-TAC. On the contrary, mice lacking Nogo-B specifically in endothelial cells were markedly resistant to the development of coronary atherosclerotic lesions and MI (20%). Mechanistically, in the absence of endothelial Nogo-B, the biosynthesis of sphingolipids, particularly S1P, is upregulated, protecting the endothelium from hypertension and hypercholesterolemia-triggered vascular inflammation and atherogenesis. This study identifies an important and novel role of endothelial Nogo-B-dependent regulation of sphingolipid de novo biosynthesis in the coronary atherosclerosis, a primary cause of myocardial infarction.

scholarly journals The P387 Thrombospondin-4 Variant Promotes Accumulation of Macrophages in Atherosclerotic Lesions

2019 ◽  
Author(s):  
Santoshi Muppala ◽  
Mohammed Tanjimur Rahman ◽  
Irene Krukovets ◽  
Dmitriy Verbovetskiy ◽  
Elzbieta Pluskota ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Smooth Muscle Actin ◽  
Vascular Inflammation ◽  
Cutting Temperature ◽  
Vascular Wall ◽  
Alpha Smooth Muscle Actin ◽  
Knock Out ◽  
Atherosclerotic Lesions ◽  
Thrombospondin 4

AbstractAimsThrombopspondin-4 (TSP4) is a pro-angiogenic protein that has been implicated in tissue remodeling and local vascular inflammation. TSP4 and, in particular, its SNP variant, P387 TSP4, have been associated with cardiovascular disease.Macrophages are central to initiation and resolution of inflammation and development of atherosclerotic lesions, but the effects of the P387 TSP4 on macrophages remain essentially unknown. We examined the effects of the P387 TSP4 variant on macrophages in cell culture andin vivoin a murine model of atherosclerosis. Further, the levels and distributions of the twoTSP4 variants were assessed in human atherosclerotic arteries.Methods and ResultsInApoE−/−/P387-TSP4 knock-in mice, atherosclerotic lesions accumulated more macrophages than lesions bearing A387 TSP4. The levels of inflammatory markers were increased in lesions ofApoE−/−/P387-TSP4 knock-in mice compared toApoE−/−mice. Lesions in human arteries from individuals carrying the P387 variant had higher levels of TSP4 and higher macrophage accumulation. P387 TSP4 was more active in supporting adhesion of cultured human and mouse macrophages in experiments using recombinant TSP4 variants and in cells derived from P387-TSP4 knock-in mice.ConclusionsTSP4 supports the adhesion of macrophages and their accumulation in atherosclerotic lesions. P387 TSP4 is more active in supporting these pro-inflammatory events in the vascular wall, which may contribute to the increased association of P387 TSP4 with cardiovascular disease.AbbreviationsBSA, bovine serum albumin; DMSO, dimethyl sulfoxide; ECM, extracellular matrix;Thbs4−/−, thrombospondin-4 gene knock-out; WT, wild type; P387-TSP4 KI, P387TSP4knock-in mice; OCT, Optimum Cutting Temperature; vWF, von Willebrand factor; α-SMA, alpha-smooth muscle actin; Egr2, Early Growth Response 2; PBS, Phosphate Buffer saline; DMEM, Dulbecco’s Modified Eagle Medium.

Quantifying the Motion of Murine Epicardial Coronary Arteries

2008 ◽  
Author(s):  
David S. Long ◽  
Hui Zhu ◽  
Morton H. Friedman
Keyword(s):  
Risk Factors ◽  
Coronary Arteries ◽  
Mechanical Stresses ◽  
Intimal Thickening ◽  
High Cholesterol ◽  
Additional Risk ◽  
Atherosclerotic Lesions ◽  
Coronary Artery Atherosclerosis ◽  
Obesity Hypertension ◽  
Accumulation Of Lipids

Coronary artery atherosclerosis is a leading cause of morbidity and mortality in western societies. Atherosclerosis is a progressive fibroinflammatory disease identified by intimal thickening, the focal accumulation of lipids, fibrous elements, and cellular elements within the walls of large arteries. These lesions preferentially develop at arterial branches, the outer walls of bifurcations, and the inner walls of curved sections; the cause of this focal vasculopathy is not fully understood. It is, however, understood from epidemiological and clinical studies that individual susceptibility to the development and progression of atherosclerotic lesions is influenced by “traditional” systemic risk factors, including smoking, diabetes mellitus, obesity, hypertension, and high cholesterol. However, these risk factors cannot account for half of the variability in occurrence of this disease; this indicates additional risk factors have not been identified. One prevalent explanation of the focal nature of the disease is that the local fluid mechanical stresses at the walls of coronary arteries, as well as mechanical stresses within the vessel wall, may mediate the phenotype of endothelial cells thereby producing atherosusceptible sites. Therefore, it has been speculated [1] that certain aspects of arterial geometry and motion, which vary substantially among individuals, may increase an individual’s susceptibility to developing atherosclerosis — “geometric risk factors”.

Laser angioplasty: controlled delivery of argon laser energy.

Radiology ◽  
1988 ◽  
Vol 167 (2) ◽  
pp. 463-465 ◽  
Author(s):  
L A Nordstrom ◽  
W R Castaneda-Zuniga ◽  
C C Lindeke ◽  
T M Rasmussen ◽  
D K Burnside
Keyword(s):  
Laser Energy ◽  
Argon Laser ◽  
Laser Angioplasty ◽  
Controlled Delivery

scholarly journals Sphingosine kinase-2 prevents macrophage cholesterol accumulation and atherosclerosis by stimulating autophagic lipid degradation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kazuhiro Ishimaru ◽  
Kazuaki Yoshioka ◽  
Kuniyuki Kano ◽  
Makoto Kurano ◽  
Daisuke Saigusa ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Lipid Droplets ◽  
Heart Diseases ◽  
Sphingosine Kinase ◽  
Vascular Wall ◽  
Coronary Heart Diseases ◽  
Sphingosine Kinase 2 ◽  
Atherosclerotic Lesions ◽  
Novel Target ◽  
Membrane Components

AbstractAtherosclerosis is the major cause of ischemic coronary heart diseases and characterized by the infiltration of cholesterol-accumulating macrophages in the vascular wall. Although sphingolipids are implicated in atherosclerosis as both membrane components and lipid mediators, the precise role of sphingolipids in atherosclerosis remains elusive. Here, we found that genetic deficiency of sphingosine kinase-2 (SphK2) but not SphK1 aggravates the formation of atherosclerotic lesions in mice with ApoE deficiency. Bone marrow chimaera experiments show the involvement of SphK2 expressed in bone marrow-derived cells. In macrophages, deficiency of SphK2, a major SphK isoform in this cell type, results in increases in cellular sphingosine and ceramides. SphK2-deficient macrophages have increases in lipid droplet-containing autophagosomes and autolysosomes and defective lysosomal degradation of lipid droplets via autophagy with an impaired luminal acidic environment and proteolytic activity in the lysosomes. Transgenic overexpression of SphK1 in SphK2-deficient mice rescued aggravation of atherosclerosis and abnormalities of autophagosomes and lysosomes in macrophages with reductions of sphingosine, suggesting at least partial overlapping actions of two SphKs. Taken together, these results indicate that SphK2 is required for autophagosome- and lysosome-mediated catabolism of intracellular lipid droplets to impede the development of atherosclerosis; therefore, SphK2 may be a novel target for treating atherosclerosis.

scholarly journals Novel Insights into the Vasoprotective Role of Heme Oxygenase-1

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Emanuela Marcantoni ◽  
Luigia Di Francesco ◽  
Melania Dovizio ◽  
Annalisa Bruno ◽  
Paola Patrignani
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Vascular Wall ◽  
Heme Oxygenase 1 ◽  
Antiinflammatory Effect ◽  
Atherosclerotic Lesions ◽  
Inflammatory Processes ◽  
Cox 2 ◽  
Endogenous Antioxidant

Cardiovascular risk factors contribute to enhanced oxidative stress which leads to endothelial dysfunction. These events trigger platelet activation and their interaction with leukocytes and endothelial cells, thus contributing to the induction of chronic inflammatory processes at the vascular wall and to the development of atherosclerotic lesions and atherothrombosis. In this scenario, endogenous antioxidant pathways are induced to restrain the development of vascular disease. In the present paper, we will discuss the role of heme oxygenase (HO)-1 which is an enzyme of the heme catabolism and cleaves heme to form biliverdin and carbon monoxide (CO). Biliverdin is reduced enzymatically to the potent antioxidant bilirubin. Recent evidence supports the involvement of HO-1 in the antioxidant and antiinflammatory effect of cyclooxygenase(COX)-2-dependent prostacyclin in the vasculature. Moreover, the role of HO-1 in estrogen vasoprotection is emerging. Finally, possible strategies to develop novel therapeutics against cardiovascular disease by targeting the induction of HO-1 will be discussed.

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