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Naturopathic Medicine and the Prevention and Treatment of Cardiovascular Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
The localized inflammatory milieu leads to migration of smooth muscle cells into the intima and replicating. Soon a fibrous cap appears in the surface of the artery lining, and an atherosclerotic plaque is formed. Over time, the plaque continues to grow until eventually it either ruptures and a clot breaks off or it blocks the entire artery.
Spectral CT Imaging Using MARS Scanners
Published in Katsuyuki Taguchi, Ira Blevis, Krzysztof Iniewski, Spectral, Photon Counting Computed Tomography, 2020
Aamir Y. Raja, Steven P. Gieseg, Sikiru A. Adebileje, Steven D. Alexander, Maya R. Amma, Fatemeh Asghariomabad, Ali Atharifard, Benjamin Bamford, Stephen T. Bell, Srinidhi Bheesette, Anthony P. H. Butler, Philip H. Butler, Pierre Carbonez, Alexander I. Chernoglazov, Shishir Dahal, Jérôme Damet, Niels J. A. de Ruiter, Robert M. N. Doesburg, Brian P. Goulter, Joseph L. Healy, Praveen K. Kanithi, Stuart P. Lansley, Chiara Lowe, V. B. H. Mandalika, Emmanuel Marfo, Aysouda Matanaghi, Mahdieh Moghiseh, Raj K. Panta, Hannah M. Prebble, Nanette Schleich, Emily Searle, Jereena S. Sheeja, Rayhan Uddin, Lieza Vanden Broeke, V. S. Vivek, E. Peter Walker, Michael F. Walsh, Manoj Wijesooriya
Cardiovascular disease is very much an inflammatory disease that is aggravated by elevated levels of cholesterol ester-carrying low-density lipoproteins (LDLs) in the blood [81]. The LDLs passing through the artery wall appear to become altered, either through oxidation or aggregation to become a form of “high-uptake LDL” that is rapidly taken up by inflammatory macrophage cells recruited into the plaques [82, 83]. These cholesterol-filled macrophages make up a significant part of the atheroma mass, along with T-cells and cholesterol-filled smooth muscle cells. As part of the inflammatory response, these cells release additional oxidants, so exacerbating the process by making more oxidized LDL. In advanced plaques, which typically start forming in late to middle aged patients, the cholesterol filled macrophages start to die through a necrotic process. The dying cells lyse open releasing the cellular contents into the extracellular space of the plaque. The resulting necrotic core region is rich in cholesterol esters and is usually covered by covered by a fibrous cap of proteins and connective tissue cells. If this complex structure is ruptured, usually due to thinning of the fibrous cap, the exposed plaque contents cause blood clotting within the artery.
Atherosclerosis and Mechanical Forces
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
A plaque ruptures if the local stress exceeds the strength of the fibrous cap. The balance between local stress and fibrous cap strength is determined by the intrinsic properties of individual plaque (vulnerability) and by the extrinsic forces on the plaque (trigger force). Plaque geometry plays an important role in this relationship, as it determines the distribution and magnitude of hemodynamic forces, as well as the distribution of internal stresses (Kwak 2014; Lee 2017).
Neurotrophins in carotid atherosclerosis and stenting
Published in Annals of Medicine, 2023
Teodora Yaneva-Sirakova, Latchezar Traykov, Kiril Karamfiloff, Ivo Petrov, Julieta Hristova, Dobrin Vassilev
Carotid ultrasound was done with Vivid E95 General Electric linear transducer 7–13 MHz with reference to the national and European recommendations. We used the NASCET method for assessment [16–19]. With reference to the cited recommendations, [20] we used the following definitions:Unstable plaque – with heterogenous structure with high risk for embolization.Stable plaque – homogenous structure, smooth surface, and good fibrous cap.Symptomatic patient – with transitory visual or neurological symptoms, non-specific symptoms which may be associated with brain ischemia.Non-significant plaque – less than 50% and without characteristics of unstable or high-risk, with peak systolic velocity less than 125 cm/sec and ratio Internal carotid artery/common carotid artery less than 2.5.
Achieving coronary plaque regression: a decades-long battle against coronary artery disease
Published in Expert Review of Cardiovascular Therapy, 2022
Venkat S. Manubolu, Matthew J. Budoff
Technological advancements in cardiovascular imaging, including both invasive and noninvasive modalities, have increased our understanding of the biology of coronary atherosclerosis, plaque development, and progression to event-prone plaques. Traditionally invasive angiography was used in early 1990´s to evaluate the effect of statins on plaque progression, which was measured in terms of changes in luminal diameter and percentage stenosis. This was replaced by the invention of intravascular ultrasound (IVUS) [25,26]. Several clinical trials conducted in the early 2000s utilized gray scale IVUS, which allowed transmural imaging of the complete artery wall and enabled both early diagnosis of atherosclerosis and accurate measurement of plaque volumes. Subsequently, the development of novel IVUS-based post-processing techniques such as virtual histology IVUS (VH-IVUS), iMAP-IVUS, and Integrated Backscatter IVUS improved assessment of coronary plaque composition and enabled us to follow changes in plaque overtime. Intravascular optical coherence tomography (OCT) is another intracoronary imaging technique that uses emission and reflection of near-infrared light to produce cross-sectional images of coronary arteries in order to evaluate the plaque characteristics. OCT has approximately 10-fold greater resolution than ultrasound-based techniques with a resolution of 4–20 um. This makes it an ideal imaging modality to identify the thin fibrous cap (defined as <65 um) in patients with thin-cap fibroatheroma. This imaging modality has primarily been used to evaluate vulnerable plaque characteristics.
Histopathological and ultrastructural study of carotid atherosclerotic plaques: a study of four cases
Published in Ultrastructural Pathology, 2021
Ru Yong-xin, Zhang Xue-bin, Dong Shu-xu, Zhang Yongqiang, Li Ying, Liu Jing, Gao Ying-dai, Shang Hong-Cai, Brian Eyden
In the upper regions of the fibrous cap, the slender cells lying between the bundles of collagen fibers had an elongate nucleus, rER, myofilaments with densities, and an irregular lamina on the surface. Some of them exhibited degenerated features such as osmiophilic ceroid and vacuoles in the cytoplasm. Necrotic cells, which contained organelle remains, lipid droplets and foci of dissolved myofilaments were distributed among the collagen fibers. Fibronexus structures with straight myofilaments abutting dense plaques on the membrane were found in the slender cells in the upper regions also. The elongated foam cells with plentiful lipid droplets and fewer myofilaments were often found in the deeper regions of the fibrous caps. All of them possessed fibronectin fibrils or multilayered lamina on the surface (Figure 10).