Role of Cardiac Ganglia in the Prevention of Coronary Atherosclerosis: An Analytical Examination of cholesterol-fed Rabbits

Atherosclerosis represents a complex disease which encompasses all the components of the vascular wall. Nevertheless, according to all known theories of the pathogenesis of atherosclerosis, the key role in this process belongs to the endothelial cells, i.e. the changes that they are subjected to especially during the initial stage of the lesion. In this review we have attempted, according to the results of our continuous research and numerous data from available modern literature, to show the cytohistological characteristics of endothelial cells, as well as the changes they are subjected to in all stages of atherosclerosis. In the first part we have reviewed the ultrastructure, function and pathology of the endothelium, subcellular organization of the endothelial cells, their specific characteristics, micro compartments and intercellular junctions. In the second part we have described the morphological and functional changes of endothelial cells during atherosclerosis. Special attention is given to the role of endothelial cells in the development of the initial stage of lesion: endothelial dysfunction, factors that cause the increased expression of adhesion molecules in endothelial cells and mechanisms that cause leukocytes to migrate through the endothelial layer to subendothelial connective tissue in the early stage of atherosclerosis.

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Abstract 192: A Hypothesis on Initiation of Coronary Atherosclerosis: The Role of Intimal Neovascularization and Proliferation. Do Lipoproteins Invade Coronary Tunica Intima from the Opposite Site?

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.32.suppl_1.a192 ◽

2012 ◽

Vol 32 (suppl_1) ◽

Author(s):

Vladimir M Subbotin

Keyword(s):

Coronary Atherosclerosis ◽

Binding Capacity ◽

Good Reason ◽

Single Layer ◽

Vasa Vasorum ◽

Great Expectations ◽

Diffuse Intimal Thickening ◽

Arterial Intima ◽

Capillary Bed

Objectives Tremendous success of statins in coronary atherosclerosis (CA) prevention offered great expectations for extended protection and effective therapeutics. However, stalled progress in pharmaceutical treatment gives a good reason to review whether the hypothesis underlining our efforts is consistent with undoubted facts on coronary artery in normal and diseased forms. Analysis An accepted hypothesis states that CA is initiated by endothelial dysfunction due to inflammation and high levels of LDL, followed by lipids and macrophage penetration into arterial intima and plaque formation. It is crucial to highlight that normal coronary intima is not a single-layer endothelium covering thin acellular compartment, as is commonly claimed in most publications, but always appears as a multi-layer cellular compartment, or diffuse intimal thickening (DIT), where cells are arranged in a few dozens layers. Since it is unanimously agreed that LDL invade DIT from lumen, the initial depositions ought to be most proximal to blood, i.e. in inner DIT layers. The facts show that the opposite is true, and lipids are deposited in the outer DIT. This contradiction is resolved by noting that normal DIT is always avascular, receiving oxygen and nutrients by diffusion from lumen, whereas in CA outer DIT is always neovascularized from adventitial vasa vasorum . Proteoglycan biglycan, confined to outer DIT of normal and diseased coronary, has high binding capacity for LDL. However, normal DIT is avascular, whereas in CA biglycan of outer DIT layers appears in direct contact with blood and extract lipoproteins. These facts explain patterns and mechanisms of CA initiation, which is not unique: normally avascular cornea accumulates lipoproteins after neovascularization, resulting in lipid keratopathy. The author offers a hypothesis on neovascularization. Cells in coronary DIT possess high proliferative capacity. Excessive cell replication increases DIT thickness, impairs diffusion, resulting in hypoxia of outer DIT. Hypoxia induces neovascularization of outer DIT layers, where biglycan extracts LDL from newly formed capillary bed, initiating CA. Conclusion Controls of cell proliferation and neovascularization in coronary DIT should be a priority of our research.

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Abstract 466: Vascular Claudin-11 Plays a Protective Role for Human Atherosclerosis Progression

Circulation Research ◽

10.1161/res.127.suppl_1.466 ◽

2020 ◽

Vol 127 (Suppl_1) ◽

Author(s):

Eun Hee Kim ◽

Moon Hee Jung ◽

Man Seok Park ◽

Kang Ho Choi ◽

Su Jin Lee ◽

...

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cell ◽

Muscle Cell ◽

Coronary Atherosclerosis ◽

Tube Formation ◽

Total N ◽

Tube Formation Assay ◽

Junction Protein

Background and Aims: The expression and the role of tight junction protein, Claudin-11 (CLDN11) in vasculat smooth muscle cell (vSMC) is unknown. Methods: To understand the role of CLDN11 in the vSMC, we transfected siRNA-CLDN11 into human coronary vascular smooth muscle cell line (hCSMC). cDNA microarray using Agilent Human mRNA arrays, immunocytochemistry, tube formation assay, FACS, and cell cycle analysis were performed 7 days after CLDN11 knock-down. To know the role of CLDN11 in the human cardiovascular system, we obtained vascular smooth muscle layer from autopsied left anterior descending artery and CLDN11 mRNA expression was evaluated following modified AHA Consensus Classification Based on Morphologic Descriptions (three groups, total n=45). Results: CLDN11 was well expressed in vascular smooth mucscle layer in immunohistochemisty and western blot analysis. We observed the angiogenesis (CXCL8, SOX17, HEY1), cell proliferation (EGR3, ITGB2), and extracellular matrix (BMPER, WNT1) associated gene expression. Following CLDN11-siRNA transfection, the tube formation assay and proliferating cellular phase was markedly increased in siRNA treatment group (p<0.01, respectively). In the human sample, CLDN11 expression was inversely correlated with the progression of coronary atherosclerosis (p=0.0026), and the sudden cardiac death with complicated coronary atherosclerosis (p<0.05). Conclusions: These results indicate that CLDN11 could tightly regulate the vascular smooth muscle physiology. And CLDN11 might play a certain role for atherosclerosis propagation to regulate the vSMCs plasticity and possible new etiology for cardiovascular events.

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The role of adventitia in coronary atherosclerosis: results of echocardiographic imaging of the left anterior descending coronary artery

Journal of the American College of Cardiology ◽

10.1016/s0735-1097(02)81103-2 ◽

2002 ◽

Vol 39 ◽

pp. 246 ◽

Cited By ~ 1

Author(s):

Irmina Gradus-Pizlo ◽

Brian Bigelow ◽

Yousuf Mahomed ◽

Stephen G. Sawada ◽

Karen Rieger ◽

...

Keyword(s):

Coronary Artery ◽

Coronary Atherosclerosis

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Prognostic Value of Residual Syntax Score after Percutaneous Coronary Intervention in Multivessel Coronary Artery Disease

Indian Journal of Cardiovascular Disease in Women WINCARS ◽

10.1055/s-0039-3400204 ◽

2019 ◽

Vol 04 (03) ◽

pp. 133-141

Author(s):

Sunitha Aramalla ◽

Indrani Garre ◽

Shabbir Ali Shaik ◽

P. Hemanth Harish

Keyword(s):

Coronary Artery Disease ◽

Percutaneous Coronary Intervention ◽

Clinical Outcomes ◽

Coronary Atherosclerosis ◽

Coronary Intervention ◽

Multivessel Coronary Artery Disease ◽

Percutaneous Coronary ◽

The Difference ◽

Artery Disease

Abstract Background Residual SYNTAX (Synergy between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery) Score (RSS) is an objective measure for the assessment of degree and complexity of residual stenosis after the percutaneous coronary intervention (PCI). Aim The study aimed at evaluating the role of angiographic complete (CR) and incomplete (ICR) revascularization on clinical outcomes in patients undergoing PCI for multivessel coronary artery disease (MVCAD). The study sought to investigate the role of initial and residual severity of coronary atherosclerosis in prognostication of patients with MVCAD who underwent PCI. Material and Methods We retrospectively recruited 135 patients having MVCAD who underwent PCI. Coronary angiogram was used to assess the severity of coronary atherosclerosis. From the angiographic data baseline (BSS) and RSS were calculated. Subjects having a RSS of 0 were defined as having CR, and those having RSS > 0 are defined as ICR group. The study population was subgrouped into two groups as follows: CR, 0 (n = 17, 23%); ICR, >0 to 4 (n = 89, 47.2%). Clinical outcomes were measured, which included major adverse cardiac and cerebrovascular events (MACE) at 1 year. Results Among the study subjects mean age was 57.25 ± 17.55. About 76.3% were males, and 23.7% were females. About 89.4% had diabetes, 88.6% had hypertension as risk factors, and 95.8% were smokers.The mean values of BSS and RSS were 20.2 ± 9.2 and 4.1 ± 7.0, respectively. Based on RSS the individuals were divided into two groups as follows: CR, 0 (n = 17, 23%); ICR, > 0 to 4 (n = 89, 47.2%), > 4 to 8 (n = 16, 21.6%), > 8 (n = 13, 17.55%). After 1 year, three patients lost the follow-up. Among the remaining 132 patients, those with higher BSS had more mortality and morbidity, and the difference is statistically significant (MACE in ≥23 vs. <23, p = 0.000755); 10 patients in the ICR group had MACE compared with 1 patient in CR group(5.8% in CR group vs. 8.6% in ICR group, p-value of 0.38); however, the difference was not statistically significant. However, higher RSS acts as an indirect marker of increasing morbidity and mortality when compared within the tertiles, and the difference was statistically significant (RSS 1–4 group vs. > 4 MACE, p = 0.0009559, RSS < 8 vs. >8 MACE, p = 0.00000172). Conclusions This study proved that both BSS and higher RSS help to foretell the risk of adverse clinical outcomes in individuals with MVCAD who underwent PCI. RSS, which is an indirect marker of residual atherosclerosis, that is, ICR, had a positive correlation MACE after PCI.

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