Relevant bibliographies by topics / Atherosclerotic calcification

Academic literature on the topic 'Atherosclerotic calcification'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Atherosclerotic calcification"

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Li, Yuan, Changqiu Wang, Anhuai Lu, Kang Li, Xiao Cheng, Chongqing Yang, Yanzhang Li, Yan Li, and Hongrui Ding. "A Comparative Study of Pathological Nanomineral Aggregates with Distinct Morphology in Human Aortic Atherosclerotic Plaques." Journal of Nanoscience and Nanotechnology 21, no. 1 (January 1, 2021): 547–54. http://dx.doi.org/10.1166/jnn.2021.18449.

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Calcification exists in atherosclerotic plaques in the form of nanomineral aggregates and is closely related to the development of atherosclerosis. Spheroidal and massive calcification are two major types of calcification found in atherosclerotic tissue. However, the exact difference between these two types of calcification is still not clear. Samples composed entirely of spheroidal calcifications and massive calcifications were isolated from aortic atherosclerotic plaques and tested using both bulk and microscopic analysis techniques. Scanning electron microscopy and transmission electron microscopy showed that spheroidal calcifications had a core–shell structure. Massive calcifications were composed of randomly arranged nanocrystals. Synchrotron radiation X-ray diffraction, Raman spectroscopy and selected area electron diffraction showed amorphous calcium phosphate, whitlockite and carbonate hydroxyapatite all existing in spheroidal calcification, while massive calcification only consisted of carbonate hydroxyapatite. We conclude that amorphous calcium phosphate may act as a precursor phase of spheroidal calcifications that eventually transforms into a crystalline phase, while whitlockite in lesions could aggravate the progression of atherosclerosis.
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Gade, Piyusha S., Riikka Tulamo, Kee-won Lee, Fernando Mut, Eliisa Ollikainen, Chih-Yuan Chuang, Bong Jae Chung, et al. "Calcification in Human Intracranial Aneurysms Is Highly Prevalent and Displays Both Atherosclerotic and Nonatherosclerotic Types." Arteriosclerosis, Thrombosis, and Vascular Biology 39, no. 10 (October 2019): 2157–67. http://dx.doi.org/10.1161/atvbaha.119.312922.

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Objective: Although the clinical and biological importance of calcification is well recognized for the extracerebral vasculature, its role in cerebral vascular disease, particularly, intracranial aneurysms (IAs), remains poorly understood. Extracerebrally, 2 distinct mechanisms drive calcification, a nonatherosclerotic, rapid mineralization in the media and a slower, inflammation driven, atherosclerotic mechanism in the intima. This study aims to determine the prevalence, distribution, and type (atherosclerotic, nonatherosclerotic) of calcification in IAs and assess differences in occurrence between ruptured and unruptured IAs. Approach and Results: Sixty-five 65 IA specimens (48 unruptured, 17 ruptured) were resected perioperatively. Calcification and lipid pools were analyzed nondestructively in intact samples using high resolution (0.35 μm) microcomputed tomography. Calcification is highly prevalent (78%) appearing as micro (<500 µm), meso (500 µm–1 mm), and macro (>1 mm) calcifications. Calcification manifests in IAs as both nonatherosclerotic (calcification distinct from lipid pools) and atherosclerotic (calcification in the presence of lipid pools) with 3 wall types: Type I—only calcification, no lipid pools (20/51, 39%), Type II—calcification and lipid pools, not colocalized (19/51, 37%), Type III—calcification colocalized with lipid pools (12/51, 24%). Ruptured IAs either had no calcifications or had nonatherosclerotic micro- or meso-calcifications (Type I or II), without macro-calcifications. Conclusions: Calcification in IAs is substantially more prevalent than previously reported and presents as both nonatherosclerotic and atherosclerotic types. Notably, ruptured aneurysms had only nonatherosclerotic calcification, had significantly lower calcification fraction, and did not contain macrocalcifications. Improved understanding of the role of calcification in IA pathology should lead to new therapeutic targets.
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Ragino, Yu I., E. V. Kashtanova, I. S. Murashov, A. M. Volkov, A. V. Kurguzov, E. V. Sadovski, N. A. Maslatsov, L. V. Scherbakova, A. M. Chernjavskii, and Ya V. Polonskaya. "The Study of Biochemical Factors of Calcification of Stable and Unstable Plaques in the Coronary Arteries of Man." Kardiologiia 60, no. 2 (March 5, 2020): 83–88. http://dx.doi.org/10.18087/cardio.2020.2.n775.

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Objective. The aim of the study was to study biochemical factors of calcification in stable and unstable plaques of coronary arteries and in the blood of patients with severe coronary atherosclerosis, to find associations of biochemical factors of calcification with the development of unstable atherosclerotic plaque.Materials and Methods. The study included 25 men aged 60,4±6,8 years who received coronary bypass surgery. In the course of the operation intraoperative indications in men were from coronary endarteriectomy (s) artery (a – d) and histological and biochemical analyses of the samples of the intima / media. Out of 85 fragments of intima / media of coronary arteries, 15 fragments of unchanged intima / media, 39 fragments of stable atheromatous plaque and 31 fragments of unstable plaque were determined. In homogenates of samples of intima / media (after measurement of protein by the method of Lowry) and in blood by ELISA were determined by biochemical factors of calcification: osteoprotegerin, osteocalcin, an osteopontin, osteonectin, as well as inflammatory factors (cytokines, chemokines).Results. A significant direct correlation (Spearman coefficient =0.607, p<0.01) between the stages of atherosclerotic focus development to unstable plaque and the degree of calcification of atherosclerotic focus development samples was found. There was an increased content of osteocalcin in stable and unstable plaques by 3.3 times in comparison with the unchanged tissue of intima / media of coronary arteries, as well as in samples with small and dust-like, with coarse-grained calcifications in comparison with samples without calcifications by 2.8 and 2.1 times, respectively. According to multivariate logistic regression analysis, the relative risk of unstable atherosclerotic plaque in the coronary artery is associated with a reduced content of osteocalcin (OR=0.988, 95 % CI 0.978–0.999, p=0.028). Also, the relative risk of calcifications in the atherosclerotic plaque in the coronary artery is associated with an increased content of osteocalcin (OR=1,008, 95 % CI 1,001–1,015, p=0,035). In men with severe coronary atherosclerosis, a significant inverse correlation was found (Spearman coefficient –0.386, p=0.022) between the content of osteoprotegerin in the vascular wall and in the blood.
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Seime, Till, Max van Wanrooij, Eva Karlöf, Malin Kronqvist, Staffan Johansson, Ljubica Matic, T. Christian Gasser, and Ulf Hedin. "Biomechanical Assessment of Macro-Calcification in Human Carotid Atherosclerosis and Its Impact on Smooth Muscle Cell Phenotype." Cells 11, no. 20 (October 18, 2022): 3279. http://dx.doi.org/10.3390/cells11203279.

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Intimal calcification and vascular stiffening are predominant features of end-stage atherosclerosis. However, their role in atherosclerotic plaque instability and how the extent and spatial distribution of calcification influence plaque biology remain unclear. We recently showed that extensive macro calcification can be a stabilizing feature of late-stage human lesions, associated with a reacquisition of more differentiated properties of plaque smooth muscle cells (SMCs) and extracellular matrix (ECM) remodeling. Here, we hypothesized that biomechanical forces related to macro-calcification within plaques influence SMC phenotype and contribute to plaque stabilization. We generated a finite element modeling (FEM) pipeline to assess plaque tissue stretch based on image analysis of preoperative computed tomography angiography (CTA) of carotid atherosclerotic plaques to visualize calcification and soft tissues (lipids and extracellular matrix) within the lesions. Biomechanical stretch was significantly reduced in tissues in close proximity to macro calcification, while increased levels were observed within distant soft tissues. Applying this data to an in vitro stretch model on primary vascular SMCs revealed upregulation of typical markers for differentiated SMCs and contractility under low stretch conditions but also impeded SMC alignment. In contrast, high stretch conditions in combination with calcifying conditions induced SMC apoptosis. Our findings suggest that the load bearing capacities of macro calcifications influence SMC differentiation and survival and contribute to atherosclerotic plaque stabilization.
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Cretoiu, Dragos, Ruxandra Florentina Ionescu, Robert Mihai Enache, Sanda Maria Cretoiu, and Silviu Cristian Voinea. "Gut Microbiome, Functional Food, Atherosclerosis, and Vascular Calcifications—Is There a Missing Link?" Microorganisms 9, no. 9 (September 9, 2021): 1913. http://dx.doi.org/10.3390/microorganisms9091913.

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The gut microbiome is represented by the genome of all microorganisms (symbiotic, potential pathogens, or pathogens) residing in the intestine. These ecological communities are involved in almost all metabolic diseases and cardiovascular diseases are not excluded. Atherosclerosis, with a continuously increasing incidence in recent years, is the leading cause of coronary heart disease and stroke by plaque rupture and intraplaque hemorrhage. Vascular calcification, a process very much alike with osteogenesis, is considered to be a marker of advanced atherosclerosis. New evidence, suggesting the role of dietary intake influence on the diversity of the gut microbiome in the development of vascular calcifications, is highly debated. Gut microbiota can metabolize choline, phosphatidylcholine, and L-carnitine and produce vasculotoxic metabolites, such as trimethylamine-N-oxide (TMAO), a proatherogenic metabolite. This review article aims to discuss the latest research about how probiotics and the correction of diet is impacting the gut microbiota and its metabolites in the atherosclerotic process and vascular calcification. Further studies could create the premises for interventions in the microbiome as future primary tools in the prevention of atherosclerotic plaque and vascular calcifications.
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Balanescu, Serban, Violeta Claudia Bojinca, Adrian Iancu, Mihai Bojinca, and Andra Balanescu. "Postmenopausal Calcium and Vitamin D Supplements Controversy: Do They Increase Cardiovascular Risk?" Revista de Chimie 69, no. 4 (May 15, 2018): 956–60. http://dx.doi.org/10.37358/rc.18.4.6236.

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Calcium and vitamin D are prescribed in women with osteopenia-osteoporosis to prevent fractures. These bone events increase morbidity and mortality justifying therapy to prevent bone loss. These elderly patients also have cardiovascular risk factors, atherosclerosis and vascular calcifications. Multiple trials demonstrated a relationship between the latter, coronary events and cardiovascular mortality. In these patients, ectopic tissue mineralization may worsen cardiovascular outcome. Calcium intake correlates neither with serum calcium, vascular calcification nor cardiovascular events. However serum calcium-phosphate product is related to vascular calcification and outcome. The main cause for vascular calcification is systemic inflammation and local atherosclerotic process with specific interactions between macrophages and smooth muscle cells. This review examines calcium intake, serum calcium concentration, systemic and vascular inflammation, the mechanisms of vascular calcification and their impact on cardiovascular outcome.
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Bakhshian Nik, Amirala, Hooi Hooi Ng, Manuel Garcia Russo, Francesco Iacoviello, Paul R. Shearing, Sergio Bertazzo, and Joshua D. Hutcheson. "The Time-Dependent Role of Bisphosphonates on Atherosclerotic Plaque Calcification." Journal of Cardiovascular Development and Disease 9, no. 6 (May 25, 2022): 168. http://dx.doi.org/10.3390/jcdd9060168.

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Atherosclerotic plaque calcification directly contributes to the leading cause of morbidity and mortality by affecting plaque vulnerability and rupture risk. Small microcalcifications can increase plaque stress and promote rupture, whereas large calcifications can stabilize plaques. Drugs that target bone mineralization may lead to unintended consequences on ectopic plaque calcification and cardiovascular outcomes. Bisphosphonates, common anti-osteoporotic agents, have elicited unexpected cardiovascular events in clinical trials. Here, we investigated the role of bisphosphonate treatment and timing on the disruption or promotion of vascular calcification and bone minerals in a mouse model of atherosclerosis. We started the bisphosphonate treatment either before plaque formation, at early plaque formation times associated with the onset of calcification, or at late stages of plaque development. Our data indicated that long-term bisphosphonate treatment (beginning prior to plaque development) leads to higher levels of plaque calcification, with a narrower mineral size distribution. When given later in plaque development, we measured a wider distribution of mineral size. These morphological alterations might be associated with a higher risk of plaque rupture by creating stress foci. Yet, bone mineral density positively correlated with the duration of the bisphosphonate treatment.
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Saba, Luca, Valentina Nardi, Riccardo Cau, Ajay Gupta, Hooman Kamel, Jasjit S. Suri, Antonella Balestrieri, et al. "Carotid Artery Plaque Calcifications: Lessons From Histopathology to Diagnostic Imaging." Stroke 53, no. 1 (January 2022): 290–97. http://dx.doi.org/10.1161/strokeaha.121.035692.

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The role of calcium in atherosclerosis is controversial and the relationship between vascular calcification and plaque vulnerability is not fully understood. Although calcifications are present in ≈50% to 60% of carotid plaques, their association with cerebrovascular ischemic events remains unclear. In this review, we summarize current understanding of carotid plaque calcification. We outline the role of calcium in atherosclerotic carotid disease by analyzing laboratory studies and histopathologic studies, as well as imaging findings to understand clinical implications of carotid artery calcifications. Differences in mechanism of calcium deposition express themselves into a wide range of calcification phenotypes in carotid plaques. Some patterns, such as rim calcification, are suggestive of plaques with inflammatory activity with leakage of the vasa vasourm and intraplaque hemorrhage. Other patterns such as dense, nodular calcifications may confer greater mechanical stability to the plaque and reduce the risk of embolization for a given degree of plaque size and luminal stenosis. Various distributions and patterns of carotid plaque calcification, often influenced by the underlying systemic pathological condition, have a different role in affecting plaque stability. Modern imaging techniques afford multiple approaches to assess geometry, pattern of distribution, size, and composition of carotid artery calcifications. Future investigations with these novel technologies will further improve our understanding of carotid artery calcification and will play an important role in understanding and minimizing stroke risk in patients with carotid plaques.
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Vancheri, Federico, Giovanni Longo, Sergio Vancheri, John S. H. Danial, and Michael Y. Henein. "Coronary Artery Microcalcification: Imaging and Clinical Implications." Diagnostics 9, no. 4 (September 23, 2019): 125. http://dx.doi.org/10.3390/diagnostics9040125.

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Strategies to prevent acute coronary and cerebrovascular events are based on accurate identification of patients at increased cardiovascular (CV) risk who may benefit from intensive preventive measures. The majority of acute CV events are precipitated by the rupture of the thin cap overlying the necrotic core of an atherosclerotic plaque. Hence, identification of vulnerable coronary lesions is essential for CV prevention. Atherosclerosis is a highly dynamic process involving cell migration, apoptosis, inflammation, osteogenesis, and intimal calcification, progressing from early lesions to advanced plaques. Coronary artery calcification (CAC) is a marker of coronary atherosclerosis, correlates with clinically significant coronary artery disease (CAD), predicts future CV events and improves the risk prediction of conventional risk factors. The relative importance of coronary calcification, whether it has a protective effect as a stabilizing force of high-risk atherosclerotic plaque has been debated until recently. The extent of calcium in coronary arteries has different clinical implications. Extensive plaque calcification is often a feature of advanced and stable atherosclerosis, which only rarely results in rupture. These macroscopic vascular calcifications can be detected by computed tomography (CT). The resulting CAC scoring, although a good marker of overall coronary plaque burden, is not useful to identify vulnerable lesions prone to rupture. Unlike macrocalcifications, spotty microcalcifications assessed by intravascular ultrasound or optical coherence tomography strongly correlate with plaque instability. However, they are below the resolution of CT due to limited spatial resolution. Microcalcifications develop in the earliest stages of coronary intimal calcification and directly contribute to plaque rupture producing local mechanical stress on the plaque surface. They result from a healing response to intense local macrophage inflammatory activity. Most of them show a progressive calcification transforming the early stage high-risk microcalcification into the stable end-stage macroscopic calcification. In recent years, new developments in noninvasive cardiovascular imaging technology have shifted the study of vulnerable plaques from morphology to the assessment of disease activity of the atherosclerotic lesions. Increased disease activity, detected by positron emission tomography (PET) and magnetic resonance (MR), has been shown to be associated with more microcalcification, larger necrotic core and greater rates of events. In this context, the paradox of increased coronary artery calcification observed in statin trials, despite reduced CV events, can be explained by the reduction of coronary inflammation induced by statin which results in more stable macrocalcification.
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Polonskaya, Yana V., Elena V. Kashtanova, Ivan S. Murashov, Aleksei V. Kurguzov, Evgeny V. Sadovski, Nikolay A. Maslatsov, Ekaterina M. Stakhneva, Alexander M. Chernyavskii, and Yuliya I. Ragino. "The Influence of Calcification Factors and Endothelial-Dysfunction Factors on the Development of Unstable Atherosclerotic Plaques." Diagnostics 10, no. 12 (December 11, 2020): 1074. http://dx.doi.org/10.3390/diagnostics10121074.

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Background: This study aimed to evaluate changes in markers of calcification and of endothelial dysfunction during the development of calcification and instability of atherosclerotic plaques and to identify associations of calcification factors with the formation of unstable plaques. Methods: We analyzed 44 male patients with coronary atherosclerosis who underwent endarterectomy in coronary arteries during coronary bypass surgery. The endarterectomy material (intima/media) was examined using histological and biochemical methods, and the stability and calcification degree of atherosclerotic plaques were assessed. In homogenates of the tissue samples and in blood, concentrations of osteoprotegerin, osteocalcin, osteopontin, osteonectin, monocyte-chemoattractant protein type 1 (MCP-1), soluble vascular cell adhesion molecule 1 (sVCAM-1), and E-selectin were determined by enzyme immunoassays. Results: Unstable atherosclerotic plaques proved to be calcified more frequently (80.4% of plaques) than stable ones (45.0%). Osteonectin, E-selectin, and sVCAM-1 levels were lower in unstable plaques and plaques with large calcification deposits. Osteocalcin content increased with the increasing size of the calcification deposits in plaque. Blood osteocalcin concentration directly correlated with osteocalcin concentration in atherosclerotic plaques and was higher in the blood of patients with calcified plaques in coronary arteries. Conclusions: The results provide the basis for further research on the suitability of osteocalcin as a potential biomarker of an unstable calcified atherosclerotic plaque in a coronary artery.
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Dissertations / Theses on the topic "Atherosclerotic calcification"

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Sim, Alisia Mara. "Detection of calcification in atherosclerotic plaques using optical imaging." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/33151.

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PET imaging, using the bone tracer Na18F, allows the non-invasive location of atherosclerotic plaques that are at risk of rupture. However, the spatial resolution of PET is only 4-5 mm, limiting the mechanistic information this technique can provide. In this thesis, the use of fluorescence and Raman imaging to elucidate the mechanism of micro-calcification within atherosclerotic plaques has been investigated. A number of fluorescent probes to detect fluoride and calcium have been synthesised. One of the fluoride probes has been shown to be selective for fluoride however, the concentration of fluoride required to activate the probe is order of magnitudes higher than the amount of Na18F used for PET imaging making it problematic to use for future studies. On the other hand, a calcium probe has been shown to: selectively bind to hydroxyapatite (HAP); permit visualisation and quantification of HAP in both vascular and bone cell models; and effectively stain cultured aortic sections and whole mouse aorta for OPT imaging. Building on these preliminary data, fluorescence imaging and immunohistochemistry (IHC) imaging of both healthy and atherosclerotic tissue that were previously subjected to PET imaging, were successfully carried out showing the ability of the probe to detect HAP in human vascular tissue. IHC staining for Osteoprotegerin (OPG) and Osteopontin (OPN), two bone proteins recently detected in vascular tissue, showed the co-localization of OPG with the probe. Conversely, the OPN was shown to localize in areas surrounding high OPG and probe signal. To determine the exact composition of vascular calcification, Raman spectroscopy was also used. It is believed that the biosynthetic pathway to HAP passes through a series of transitional states; each of these has different structural characteristics which can be studied using Raman spectroscopy. In particular, HAP has a strong characteristic Raman peak at 960 cm-1. An increase in HAP concentration has been detected by Raman in both calcified cell models and aortic sections. When human vascular tissue was analysed, an additional peak at 973 cm-1 was present suggesting the presence of whitlockite (WTK) in this tissue as well as HAP.
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Hinshaw, Kaitlyn. "The Role of Type-2 Cannabinoid Receptors in Calcification of Atherosclerotic Lesions." Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/honors/98.

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Introduction: Atherosclerosis is a chronic inflammatory disease characterized by the buildup of cholesterol, fat and other debris within arterial walls. Atherosclerotic lesions undergo a calcification process with similarities to bone remodeling. In mice, the type-2 cannabinoid receptor (CB2) is known to regulate bone remodeling processes and has also been shown to alter atherosclerotic lesion characteristics. However, the role of CB2 in lesion calcification is still unclear. CB2 modulates bone remodeling by affecting differentiation of osteogenic precursor cells; thus we hypothesize that CB2 alters lesion calcification by altering osteoblastogenesis and osteoclastogenesis of precursor cells of vascular origin. To test this hypothesis, we studied the role of CB2 receptor in mediating osteoclastogenesis and osteoblastogenesis from murine monocyte/macrophage and smooth muscle cell lines in vitro. Methods: RAW264.7 cells are a murine monocyte/macrophage cell line known to undergo osteoclastogenesis in response to receptor activator of nuclear factor kappa B ligand (RANKL). RAW264.7 cells were cultured in media containing RANKL and supplemented with either CB2 agonists or antagonists. Effects on RANKL-induced osteoclastogenesis were then evaluated by measuring the osteoclast marker enzyme tartrate-resistant acid phosphatase (TRAP) activity and further verified by microscopic quantitation of multi-nucleate TRAP-positive osteoclasts. MOVAS-1 cells are a murine vascular aortic smooth muscle cell line known to differentiation into osteoblasts when cultured in osteogenic media. MOVAS-1 cells were cultured in osteogenic media supplemented with CB2 agonists or antagonists. Effects on osteoblastogenesis were evaluated by measuring marker enzyme activity. Alizarin red staining was performed to visualize and quantitate effects on calcium deposition. Results: RAW264.7 cells treated with Win55, 212-2, a nonselective CB agonist, or HU-308, a selective CB2 agonist, displayed a dose-dependent decrease in RANKL-induced TRAP activity. Co-administration of a CB2-selective antagonist (SR144528), but not a CB1-selective antagonist (AM251), blocked this effect. Visual quantitation of multinucleated TRAP-positive cells confirmed Win55,212-2 treatment reduced osteoclastogenesis in RANKL-treated RAW264.7 cells. Induction of osteoblastic differentiation of MOVAS-1 cells, as determined by ALP activity, was enhanced by supplementation with Win55, 212-2 or 2-archidonyl glycerol. Co-administration of SR144528, but not AM251, reduced the induction of ALP activity in MOVAS-1 cells by Win55,212-2 and 2-AG. Alizarin red staining revealed increased calcium deposition in cultures of MOVAS-1 cells treated with Win55,212-2 compared to those cultured in osteogenic medium without Win55,212-2. Conclusions: These results demonstrate that CB2 activation can affect osteogenic differentiation of vascular cells in vitro. These results support the hypothesis that CB2 signaling promotes lesion calcification by altering the balance of osteoclastic and osteoblastic differentiation of vascular precursors.
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Fulmer, Makenzie L., Emilee Englehaupt, Chris Garst, and Stacy D. Brown. "Type 2 Cannabinoid Receptor Deficiency is Associated with Atherosclerotic Lesion Calcification in Ldr-null Mice." Digital Commons @ East Tennessee State University, 2016. https://dc.etsu.edu/etsu-works/5271.

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Background: Calcification of atherosclerotic plaques is associated with vulnerability to rupture and increased risk of myocardial infarction. The mechanism of plaque calcification is unclear, but has been shown to be a cell-mediated process involving complex signaling pathways affecting the osteogenic transcription factor Runt-related transcription factor 2 (Runx2). The type-2 cannabinoid receptor (CB2) modulates processes involved in bone remodeling and our prior studies determined that CB2 alters the composition of early lesions in hyperlipidemic Ldlr-/- mice; however, the function of CB2 in plaque calcification is unknown. Therefore, we tested the hypothesis that CB2 modulates plaque calcification by evaluating the effects of systemic CB2 gene deletion on lesion calcification and aortic expression of Runx2 in Ldlr-/- mice. Results: Groups (n≥8) of 8-week old CB2+/+Ldlr-/- (WT) and CB2-/- Ldlr-/- (CB2-/-) mice were fed a high fat diet (HFD) for up to 24 weeks. Standard blood plasma analysis showed no difference in HFD-induced hyperlipidemia between WT and CB2-/- mice. Aortic levels of endocannabinoids, anandamide and 2-archidonylglycerol, were significantly elevated after 12 weeks of HFD feeding as determined by LC-MS/MS. En face analysis revealed the extent of atherosclerosis in the aortic arch and thoracic aorta did not differ between WT and CB2-/- mice, but was ~1.9-fold greater in the abdominal aortas of CB2-/- mice (17.0±1.3% vs 9.0±1.3%, p=0.002). Calcification of aortic root lesions was ~2.3 fold greater in CB2-/- mice compared to WT mice (12.9±1.1% vs 5.6±1.2%, p=0.002) as revealed by von Kossa staining. Western blot analysis showed significantly increased expression of Runx2 in aortas of WT mice compared to CB2-/- after 20 weeks of HFD (2.55±0.25 fold, p Conclusion: Systemic CB2 deficiency enhances lesion calcification and is associated with altered aortic expression of Runx2. These results provide novel mechanistic insights into the function of CB2 signaling in the pathogenesis of atherosclerosis and vascular calcification that may lead to the development of therapies aimed at stabilizing calcified plaque.
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Bennett, Brian J. "Chondroplastic conversion and calcification of advanced atherosclerotic lesions : the impact of bone regulatory proteins and diet /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/6602.

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Koulaouzidis, George. "Investigation of the origin of the coronary artery calcification process and its relationship to the atherosclerotic cardiovascular disease." Doctoral thesis, Umeå universitet, Institutionen för folkhälsa och klinisk medicin, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-83450.

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The objectives of this thesis are: a) To examine racial/ethnic differences in coronary artery calcification (CAC) and CAD, between symptomatic South Asians and Caucasians, matched for age, gender and conventional cardiovascular risk factors, b) To assess, using a meta-analysis model, the natural history of and stability of measurements of coronary artery calcium scoring (CACs) based on data collected from two large published trials: St Francis and EBEAT, c) To investigate the prevalence of coronary artery calcification in individuals with CT evidence for AVC, mitral valve calcification (MAC) or of both of them (AVC+MAC), d) To assess any potential association between premature CAD (<55 years in first-degree male relatives and <65 years in first-degree female relatives) and CAC in a large cohort of asymptomatic individuals. We found that coronary artery calcification is more extensive and diffuse in symptomatic patients of South Asian ethnic origin as compared to Caucasians, despite similar conventional risk factors for CAD. This is more evident in those >50 years of age, suggesting potential genetic or other risk factors yet to be determined. The natural history of coronary artery calcification was overtime progression in the majority of subjects, irrespective of gender. The higher variability in RCA measurements could be related to the low baseline CACs or exaggerated movement of the right side atrioventricular ring, whereas those for LCA brances are influenced by the branch allocation of the CACs. Valve calcification is not isolated but involve also and the coronary arteries. The presence of calcification in the aortic valve or combined aortic and mitral valves predicted coronary artery calcification. Additionally patients in whom both valves have become calcified tend to have severe coronary artery calcification. And finally, there is no relationship between the prevalence and extent of coronary artery calcification and the presence of family history of coronary heart disease in asymptomatic individuals with none of the conventional risk factors for atherosclerosis.
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Москаленко, Роман Андрійович, Роман Андреевич Москаленко, Roman Andriiovych Moskalenko, Анатолій Миколайович Романюк, Анатолий Николаевич Романюк, Anatolii Mykolaiovych Romaniuk, Інна-Маргарита Сергіївна Закорко, et al. "Biomechanical properties studying of atherosclerotic aortic wall with micro and macrocalcifications." Thesis, Springer, 2017. http://essuir.sumdu.edu.ua/handle/123456789/75151.

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Objective: In the aortic wall calcification occurs as a pattern o f micro and macrocalcification changing significantly aortic wall biomechanical properties. The aim o f the w ork is biom echanical properties studying of aortic wall in the conditions of macro and microcalcification.
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Dhore, Cherida Rachel. "Molecular regulation of vascular calcification." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 2005. http://arno.unimaas.nl/show.cgi?fid=6374.

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Nicoll, Rachel. "Insights into the relationship between coronary calcification and atherosclerosis risk factors." Doctoral thesis, Umeå universitet, Institutionen för folkhälsa och klinisk medicin, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-124909.

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Introduction Coronary artery disease (CAD) is the most common cause of death in Europe and North America and early detection of atherosclerosis is a clinical priority. Diagnosis of CAD remains conventional angiography, although recent technology has introduced non-invasive imaging of coronary arteries using computed tomographic coronary angiography (CTCA), which enables the detection and quantification of coronary artery calcification (CAC). CAC forms within the arterial wall and is usually found in or adjacent to atherosclerotic plaques and is consequently known as sub-clinical atherosclerosis.  The conventional cardiovascular (CV) risk factors used to quantify the estimated 10-year coronary event risk comprise dyslipidaemia, hypertension, diabetes mellitus, obesity, smoking and family history of CAD. Nevertheless, their relationship with significant (>50%) stenosis, their interaction with the CAC score and their predictive ability for CAC presence and extent has not been fully determined in symptomatic patients.   Methods   For Papers 1-4 we took patients from the Euro-CCAD cohort, an international study established in 2009 in Umeå, Sweden. The study data gave us the CAC score and the CV risk factor profile in 6309 patients, together with angiography results for a reduced cohort of 5515 patients. In Papers 1 and 2 we assessed the risk factors for significant stenosis, including CAC as a risk factor. Paper 2 carried out this analysis by geographical region: Europe vs USA and northern vs southern Europe. Paper 3 investigated the CV risk factors for CAC presence, stratified by age and gender, while Paper 4 assessed the CV risk factors for CAC extent, stratified by gender.  In paper 5 we carried out a systematic review and meta-analysis of all studies of the risk factor predictors of CAC presence, extent and progression in symptomatic patients. From a total of 884 studies, we identified 10 which fitted our inclusion criteria, providing us with a total of 15,769 symptomatic patients. All 10 were entered in the systematic review and 7 were also eligible for the meta-analysis.   Results Paper 1:           Among risk factors alone, the most powerful predictors of significant coronary stenosis were male gender followed by diabetes, smoking, hypercholesterolaemia, hypertension, family history of CAD and age; only obesity was not predictive. When including the log transformed CAC score as a risk factor, this proved the most powerful predictor of >50% stenosis, but hypercholesterolaemia and hypertension lost their predictive ability. The conventional risk factors alone were 70% accurate in predicting significant stenosis, the log transformed CAC score alone was 82% accurate but the combination was 84% accurate and improved both sensitivity and specificity.  Paper 2:           Despite some striking differences in profiles between Europe and the USA, the most important risk factors for >50% stenosis in both groups were male gender followed by diabetes. When the log CAC score was included as a risk factor, it became by far the most important predictor of >50% stenosis in both continents, followed by male gender. In the northern vs southern Europe comparison the result was similar, with the log CAC score being the most important predictor of >50% stenosis in both regions, followed by male gender.  Paper 3:           Independent predictors of CAC presence in males and females were age, dyslipidaemia, hypertension, diabetes and smoking, with the addition of family history of CAD in males; obesity was not predictive in either gender. The most important predictors of CAC presence in males were dyslipidaemia and diabetes, while among females the most important predictors of CAC presence were diabetes followed by smoking. When analysed by age groups, in both males and females aged <70 years, diabetes, hypertension and dyslipidaemia were predictive, with diabetes being the strongest; in females aged <70 years, smoking was also predictive. Among those aged ≥70 years, the results are completely different, with only dyslipidaemia being predictive in males but smoking and diabetes were predictive in females.  Paper 4:           In the total cohort, age, male gender, diabetes, obesity, family history of CAD and number of risk factors predicted an increasing CAC score, with the most important being male gender and diabetes. In males, hypertension and dyslipidaemia were also predictive, although diabetes was the most important predictor. Diabetes was similarly the most important risk factor in females, followed by age and number of risk factors. Among patients with CAC, hypertension, dyslipidaemia and diabetes predicted CAC extent in both males and females, with diabetes being the strongest predictor in males followed by dyslipidaemia, while diabetes was also the strongest predictor in females, followed by hypertension. Quantile regression confirmed the consistent predictive ability of diabetes.  Paper 5:           In the systematic review, age was strongly predictive of both CAC presence and extent but not of CAC progression. The results for CAC presence were overwhelmed by data from one study of almost 10,000 patients, which found that white ethnicity, diabetes, hypertension and obesity were predictive of CAC presence but not male gender, dyslipidaemia, family history or smoking. With respect to CAC extent, only male gender and hypertension were clearly predictive, while in the one study of CAC progression, only diabetes and hypertension were predictive. In the meta-analysis, hypertension followed by male gender, diabetes and age were predictive of CAC presence, while for CAC extent mild-moderate CAC was predicted by hypertension alone, whereas severe CAC was predicted by hypertension followed by diabetes.   Conclusion Our investigation of the Euro-CCAD cohort showed that the CAC score is far more predictive of significant stenosis than risk factors alone, followed by male gender and diabetes, and there was little benefit to risk factor assessment over and above the CAC score for >50% stenosis prediction. Regional variations made little difference to this result. Independent predictors of CAC presence were dyslipidaemia and diabetes in males and diabetes followed by smoking in females. The risk factor predictors alter at age 70. The most important risk factor predictors of CAC extent were male gender and diabetes; when analysed by gender, diabetes was the most important in both males and females. Our studies have consistently shown the strong predictive ability of male gender in the total cohort and diabetes in males and females and this is reflected in the meta-analysis, which also found hypertension to be independently predictive. Interestingly, dyslipidaemia does not appear to be a strong risk factor.
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Radomychelski, I., Анатолій Миколайович Романюк, Анатолий Николаевич Романюк, Anatolii Mykolaiovych Romaniuk, Артем Михайлович Піддубний, Артем Михайлович Поддубный, Artem Mykhailovych Piddubnyi, et al. "Investigation of the presence of neutrophils and macrophages in the tissues of calcified aorta affected by atherosclerosis." Thesis, Springer, 2020. https://essuir.sumdu.edu.ua/handle/123456789/81352.

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The presence of aortic calcification causes severe tissue overstretching. Neutrophils and macrophages promote experimental abdominal aortic aneurysm formation. Aim: to compare the number of neutrophils andmacrophages in the tissue of the atherosclerotic aorta with calcification and without it.
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Rosa, Mickael. "Athérosclérose et sténose valvulaire aortique : implication des macrophages et des cellules interstitielles de valve dans les calcifications cardiovasculaires." Thesis, Lille 2, 2016. http://www.theses.fr/2016LIL2S046.

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Les pathologies cardiovasculaires sont le plus souvent l’aboutissement des processus liés à l’athérosclérose. Elles représentent la première cause de morbi-mortalité dans le monde et leur incidence s’accroit avec le vieillissement de la population et l’expansion de facteurs de risques comme le diabète ou l’obésité. La sténose valvulaire aortique (SVA) est la valvulopathie la plus fréquente dans les pays développés présentant de nombreux points communs avec l’athérosclérose vasculaire. En plus des facteurs de risque, les lésions valvulaires et les lésions vasculaires partagent des similitudes dans les processus physiopathologiques impliqués comme l’inflammation, la fibrose, l’angiogenèse et la calcification. Ce dernier processus apparait dans les stades avancés des pathologies liées à l’athérosclérose et joue un rôle critique via son implication dans la stabilité de la plaque ou l’épaississement des cuspides valvulaires aortiques. Les macrophages, cellules issues de la différenciation des monocytes infiltrés, jouent un rôle prépondérant dans ces lésions via les phénotypes classiques (M1) et alternatifs (M2). Néanmoins cette dichotomie ne reflète pas complètement la variété de leur plasticité et les différents phénotypes induits notamment par le microenvironnement des monocytes/macrophages (zones riches en lipides, zones riches en fer ou zones riches en calcification). Dans la valve aortique, les cellules interstitielles de valve (VIC) forment la population cellulaire la plus présente au sein de la valve aortique. Ces cellules jouent un rôle déterminant dans le maintien du tissu valvulaire, mais également dans les processus de calcification menant à la SVA. Dans un premier temps, cette thèse a pour but d’étudier la capacité des macrophages à former des ostéoclastes, cellules responsables de la dégradation de la matrice osseuse, au sein des plaques d’athérosclérose. Dans un second temps, ce travail se focalisera sur les processus de calcification de la valve aortique via l’étude du rôle de la leptine dans les calcifications valvulaires (étude a priori) puis dans une étude transcriptomique sans a priori de VIC issues de valve sténosées et non-sténosées. Nos résultats sur les macrophages montrent ex vivo que les cellules en bordure des calcifications vasculaires sont des macrophages alternatifs de type M2. In vitro, ces cellules sont incapables de se différencier en ostéoclastes et de résorber une matrice osseuse. Pour l’étude de l’effet de la leptine sur les VIC, nous montrons que la leptine sérique est plus élevée chez des patients présentant une SVA, nous confirmons que la leptine et son récepteur sont exprimés au sein des valves aortiques et que la leptine favorise la différenciation ostéoblastique des VIC de manière dépendante des voies Akt et ERK. Enfin, l’étude transcriptomique a permis de mettre en évidence une nouvelle voie métabolique dérégulée dans les VIC. Cette enzyme est sous exprimée dans les VIC issues de valves pathologiques et dans les zones calcifiées des valves aortiques sténosées. Par ailleurs, le traitement des VIC par le produit de cette enzyme en milieu procalcifiant inhibe la calcification. Cette thèse met en avant de nouveaux indices sur les processus de calcification observés dans les plaques d’athérosclérose et les valves aortiques sténosées. Ces résultats décrivent l’impossibilité des M2 à former des ostéoclastes capables de résorber les calcifications. Il sera intéressant d’étudier le phénotype des macrophages en bordure des calcifications des valves aortiques sténosées. D’autre part, il sera intéressant d’étudier l’origine de la leptine dans la valve et son mécanisme d’action sur les VIC. Enfin, ce travail a mis à jour une nouvelle voie métabolique, impliquée dans le développement des calcifications valvulaires, qui pourrait constituer une voie thérapeutique innovante dans le traitement médicamenteux de la SVA
Cardiovascular diseases (CVD) are the most often outcome of atherosclerosis processes. CVD are the first leading cause of death rate with an increasing incidence due to ageing populations and expansion of risk factors such as diabetes mellitus or obesity. Aortic valve stenosis (AVS) is the most frequent valvulopathy in developed countries sharing common points with vascular atherosclerosis. More than only risk factors, valvular and vascular lesions share common pathophysiological processes implicated in the development of the disease such as inflammation, fibrosis, angiogenesis and calcification. This last process appears in late stages of atherosclerosis diseases and play critical roles via implication in plaque stability or thickening of the aortic valve. Macrophages are cells deriving from infiltrated monocytes, playing an important role in the inflammatory state of lesions via classical (M1) or alternative phenotypes (M2) phenotypes. Nevertheless, this dichotomy does not reflect completely the variety of their plasticity and different phenotypes induced by the microenvironment of monocytes/macrophages (lipid riche zone, iron riche zone or calcium rich zone). In the aortic valve, valvular interstitial cells (VIC) are the most prominent cell type found in the aortic valve. These cells play a major role not only in the valve tissue homeostasis but also in the calcification processes leading to AVS. In a first part, the aim of this thesis is to elucidate the ability of macrophages to differentiate into osteoclasts, cell type responsible for bone matrix remodeling, inside atherosclerosis plaques. In a second part, this work will focus on the calcification processes occurring in the aortic valve via the study of the role of leptin in valvular calcification (association study) and then in a transcriptomic analysis of VIC isolated from calcified versus non calcified aortic valves (genome-wide expression study). Our results about macrophages show that ex vivo cell surrounding vascular calcification are alternative M2 macrophages. In vitro, these cells are no able to differentiate into true osteoclasts nor to resorb calcium deposits. Concerning the role of leptin on VIC, the results show that serum leptin is higher in patients with AVS, leptin and its receptors are expressed in the aortic valves and leptin enhances the osteoblast différenciation of VIC in an Akt and ERK dependant manner. Finally, the transcriptomic analysis allowed to highlight a new pathway deregulated in VIC. This enzyme is underexpressed in VIC isolated from calcified aortic valves and in the calcified zonesAbstract4of stenosed aortic valves. Otherwise, treating VIC with the product of this enzyme in a procalcifying medium inhibits calcification processes.This thesis highlights new insights into the calcification processes occurring in atherosclerosis lesions and calcified aortic valves. These results describe that M2 macrophages cannot differentiate into osteoclasts and reverse calcification formation inside atherosclerosis plaques. In parallel, it would be interesting to study the macrophages phenotypes surrounding calcium deposits in stenosed aortic valves. Then, it will be interesting to decipher the origin of leptin and its precise mechanism of action on VIC. Finally this work points out a new metabolic pathway implicated in the development of valvular calcification which could be a medical treatment of SVA
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Books on the topic "Atherosclerotic calcification"

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Covic, Adrian, Mugurel Apetrii, Luminita Voroneanu, and David J. Goldsmith. Vascular calcification. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0120_update_001.

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Vascular calcification (VC) is a common feature of patients with advanced CKD and it could be, at least in part, the cause of increased cardiovascular mortality in these patients. From a morphologic point of view, there are at least two types of pathologic calcium phosphate deposition in the arterial wall—namely, intima calcification (mostly associated with atherosclerotic plaques) and media calcification (associated with stiffening of the vasculature, resulting in significantly adverse cardiovascular outcomes). Although VC was viewed initially as a passive phenomenon, it appears to be a cell-mediated, dynamic, and actively regulated process that closely resembles the formation of normal bone tissue, as discovered recently. VC seems to be the result of the dysregulation of the equilibrium between promoters and inhibitors. The determinants are mostly represented by altered calcium and phosphorus metabolism, secondary hyperparathyroidism, vitamin D excess, high fibroblast growth factor 23, and high levels of indoxyl sulphate or leptin; meanwhile, the inhibitors are vitamin K, fetuin A, matrix G1a protein, osteoprotegerin, and pyrophosphate. A number of non-invasive imaging techniques are available to investigate cardiac and vascular calcification: plain X-rays, to identify macroscopic calcifications of the aorta and peripheral arteries; two-dimensional ultrasound for investigating the calcification of carotid arteries, femoral arteries, and aorta; echocardiography, for assessment of valvular calcification; and, of course, computed tomography technologies, which constitute the gold standard for quantification of coronary artery and aorta calcification. All these methods have a series of advantages and limitations. The treatment/ prevention of VC is currently mostly around calcium-mineral bone disease interventions, and unproven. There are interesting hypotheses around vitamin K, Magnesium, sodium thiosulphate and other potential agents.
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Guzik, Tomasz J., and Rhian M. Touyz. Vascular pathophysiology of hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0019.

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Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.
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Book chapters on the topic "Atherosclerotic calcification"

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Boström, Kristina, and Linda L. Demer. "Mechanism of Atherosclerotic Calcification." In Drugs Affecting Lipid Metabolism, 35–42. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0311-1_4.

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Anderson, H. C., D. H. McGregor, and A. Tanimura. "Mechanisms of Calcification in Atherosclerosis." In Pathobiology of the Human Atherosclerotic Plaque, 235–49. New York, NY: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4612-3326-8_15.

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Faggiano, Pompilio, and Eugenio Picano. "Cardiovascular Calcification and Carotid Intima-media Thickness in Atherosclerosis." In Cardiovascular Calcification, 17–32. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81515-8_2.

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Riyahi-Alam, S., U. Morbiducci, H. Katano, K. Yokoyama, S. Ali, A. Audenino, and F. Molinari. "Preoperative in silico analysis of atherosclerotic calcification vulnerability in carotid artery stenting using Finite Element Analysis by considering Agatston score." In IFMBE Proceedings, 881–84. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19387-8_215.

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Mackey, Rachel H., Lakshmi Venkitachalam, and Kim Sutton-Tyrrell. "Calcifications, Arterial Stiffness and Atherosclerosis." In Atherosclerosis, Large Arteries and Cardiovascular Risk, 234–44. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000096744.

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Zhu, Beili. "Atherosclerosis Models with Cell-Mediated Calcification." In Methods in Pharmacology and Toxicology, 75–90. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-095-3_4.

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Zeb, Irfan, and Matthew J. Budoff. "Coronary Calcification: Roles in Risk Prediction and Monitoring Therapies." In Imaging Coronary Atherosclerosis, 145–54. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0572-0_11.

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Hutcheson, Joshua D., and Elena Aikawa. "Optical Molecular Imaging of Inflammation and Calcification in Atherosclerosis." In Cardiovascular Imaging, 107–20. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09268-3_5.

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Radfar, Azar, Jack P. Andrews, Marc R. Dweck, Jagat Narula, and Ahmed Tawakol. "Clinical Molecular Imaging of Inflammation and Calcification in Atherosclerosis." In Atlas of Nuclear Cardiology, 513–30. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-49885-6_14.

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Thompson, Randall C., Chris J. Rowan, Nicholas W. Weis, M. Linda Sutherland, Caleb E. Finch, Michaela Binder, Charlotte A. Roberts, and Gregory S. Thomas. "Cardiovascular disease (CVD) in ancient people and contemporary implications." In Palaeopathology and Evolutionary Medicine, 222–38. Oxford University Press, 2022. http://dx.doi.org/10.1093/oso/9780198849711.003.0012.

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Cardiovascular diseases (CVD), principally coronary artery disease and stroke, are the leading cause of death throughout the globe. Atherosclerosis (hardening and narrowing) of the coronary arteries results in blockages that cause myocardial infarction (i.e. necrosis of heart muscle). The majority of strokes are also caused by obstructive atherosclerosis in the arteries leading to and within the brain. Atherosclerosis is considered by many to be a modern-day disease secondary to contemporary lifestyles. However, in recent years it has been confirmed as a much older disease with a longer evolutionary history. This conclusion has been reached by the discovery of evidence found in naturally mummified individuals living 3000 years ago in what is now modern-day Sudan. This evidence demonstrates vascular calcifications which, based on morphology, anatomic location and scanning electron microscopy, are atherosclerotic in origin. Confirmatory computed tomography (CT) scans by the HORUS team and other research groups of the mummified remains of people from Egypt, Peru, North America, Europe and Asia dating back over 5000 years also demonstrate arterial calcification. These CT findings have the same radiographic characteristics and appear in the same anatomic locations as modern-day patients with atherosclerosis, which is the underlying cause of myocardial infarction and most deaths from cardiac disease. These findings of vascular calcification in mummified individuals from cultures across the globe not only demonstrate that atherosclerosis cannot solely be attributed to modern-day lifestyles, but also raise questions as to the evolutionary and cultural factors that may have predisposed humans to atherosclerosis.
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Conference papers on the topic "Atherosclerotic calcification"

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Sim, Alisia M., Nabil A. Rashdan, Cui Lin, Fabio Nudelman, Marc Dweck, Vicky E. MacRae, and Alison N. Hulme. "1 Detection of calcification in atherosclerotic plaques using optical imaging." In The Scottish Cardiovascular Forum 2018, 3rd February 2018, Trinity Biomedical Science Institute, Trinity College Dublin Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-scf.1.

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Canton, Gador, Dalin Tang, Daniel S. Hippe, and Chun Yuan. "Distensibility of the Atherosclerotic Carotid Artery: Relationship With Plaque Burden and Composition?" In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80845.

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Arterial distensibility is a marker that can measure vessel wall functional and structural changes resulting from atherosclerosis [5] with applications including estimation of mechanical properties of the wall for biomechanical models. Although arterial segments affected by atherosclerosis are characterized by marked stiffening [2], little is known about the relationship between local specific atherosclerotic plaque features and wall stiffness. In particular, calcification has been shown to be associated with greater wall stiffness, however, this relationship is not consistent in different arterial segments [1,6]. For the carotid arteries, a more thorough understanding of the role of plaque features in determining wall stiffness might be offered by magnetic resonance imaging (MRI). Multi-contrast, high resolution MRI is an established imaging tool to quantify the components of carotid lesions, as well as plaque burden [8,9]. In addition, CINE MRI has been proven to be a reliable tool to measure arterial distensibility [3], an index frequently used to measure stiffness. In this study, our goals were to use MRI to characterize subject-specific wall stiffness in vivo in atherosclerotic carotid arteries, and to analyze the relation between stiffness and plaque burden and composition. CINE MRI was used to measure vessel wall stiffness; whereas a multi-contrast MRI protocol was applied to characterize vessel wall morphology and composition.
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Wei, Wei, Xiang Li, Qifa Zhou, K. Kirk Shung, and Zhongping Chen. "Combined intravascular photoacoustic and ultrasound imaging imaging of atherosclerotic calcification in human artery." In SPIE BiOS, edited by Fred S. Azar and Xavier Intes. SPIE, 2012. http://dx.doi.org/10.1117/12.909228.

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Florea, A., A. Morgenroth, J. Bucerius, L. Schurgers, and FM Mottaghy. "Non-invasive identification of inflammation and micro-calcification as markers of atherosclerotic plaque vulnerability." In NuklearMedizin 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1708256.

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Liu, Jiamin, Jianhua Yao, Mohammadhadi Bagheri, Veit Sandfort, and Ronald M. Summers. "A Semi-Supervised CNN Learning Method with Pseudo-class Labels for Atherosclerotic Vascular Calcification Detection." In 2019 IEEE 16th International Symposium on Biomedical Imaging (ISBI). IEEE, 2019. http://dx.doi.org/10.1109/isbi.2019.8759189.

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Florea, A., JP Sigl, A. Morgenroth, A. Vogg, S. Sahnoun, OH Winz, J. Bucerius, LJ Schurgers, and FM Mottaghy. "Sodium [18F]-Fluoride PET can non-invasively identify calcification as a marker of atherosclerotic plaque vulnerability." In NuklearMedizin 2021 – digital. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1726771.

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Chellamuthu, Karthik, Jiamin Liu, Jianhua Yao, Mohammadhadi Bagheri, Le Lu, Veit Sandfort, and Ronald M. Summers. "Atherosclerotic vascular calcification detection and segmentation on low dose computed tomography scans using convolutional neural networks." In 2017 IEEE 14th International Symposium on Biomedical Imaging (ISBI 2017). IEEE, 2017. http://dx.doi.org/10.1109/isbi.2017.7950544.

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Tang, Dalin, Chun Yang, Jie Zheng, Pamela K. Woodard, Kristen Billiar, Zhongzhao Teng, and Richard Bach. "3D In Vivo IVUS-Based Anisotropic FSI Models With Cyclic Bending for Human Coronary Atherosclerotic Plaque Mechanical Analysis." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204700.

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Assessing atherosclerotic plaque vulnerability based on limited in vivo patient data has been a major challenge in cardiovascular research and clinical practice. Considerable advances in medical imaging technology have been made in recent years to identify vulnerable atherosclerotic carotid plaques in vivo with information about plaque components including lipid-rich necrotic pools, calcification, intraplaque hemorrhage, loose matrix, thrombosis, and ulcers, subject to resolution limitations of current technology [1]. Image-based computational models have also been developed which combine mechanical analysis with image technology aiming for more accurate assessment of plaque vulnerability and better diagnostic and treatment decisions [2]. However, 3D models with fluid-structure interactions (FSI), cyclic bending and anisotropic properties based on in vivo IVUS images for human coronary atherosclerotic plaques are lacking in the current literature. In this paper, we introduce 3D FSI models based on in vivo IVUS images to perform mechanical analysis for human coronary plaques. Cyclic bending is included to represent deformation caused by cardiac motion. An anisotropic material model was used for the vessel so that the models would be more realistic for more accurate computational flow and stress/strain predictions.
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Santos, Leonardo Daniel Reis, Omar Pereira de Almeida Neto, Michelle Franco Macedo de Lima, and Nathália Varano. "Left atrial myxoma and transient ischemic attacks: case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.205.

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Context: Cardiac tumors are rare and myxomas are the most prevalent between them. Although histologically benign, they may cause severe effects given their intracardiac location. Unspecific symptoms compromise the diagnosis, leading to complications such as changes in the cerebral vascular dynamics. Case report following the CARE guidelines. Case report: A 62-year-old woman was admitted to a high complexity hospital in Minas Gerais, with history of unstable angina, aphasia, right hemiparesis, dysarthria, claiming precordialgia with strong intensity. Complained hyporexia and weight loss during the last month. Medical history of 7 transient ischemic attacks (TIA) in the last two years. Physical examination with no abnormalities. Chest x-ray and transesophageal echocardiogram showed bilateral neovascularization and 4.9 x 2.9 cm dimension mass in the left atrium. Coronary angiography revealed proximal calcification and atherosclerotic plaque occluding 40% of the flux in the middle third of the anterior descending artery, pointing to the coexistence of coronary disease and left atrial myxoma. The occurrence of a TIA was determined and the prescription of an anticoagulant to avoid future embolic events. A surgical approach was necessary. Biopsy concluded myxoid and hyaline-rich stroma tumor, evident vascular system, star-shaped cells isolated or forming small groups, confirming myxoma diagnosis. After a ten-day hospitalization, the patient was clinically stable, and was discharged after health education. Conclusion: Cardiac tumors such as myxomas lead to important cerebral vascular consequences, so that the clinical investigation is essential to the differential diagnosis between a stroke and the TIA, to provide adequate treatment and disease prevention.
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Udachkina, H., D. Novikova, T. Popkova, E. Markelova, I. Kirillova, and E. Gerasimova. "SAT0653 Relationship between cardiac valvular calcification, carotid atherosclerosis, and coronary calcification in patients with rheumatoid arthritis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5447.

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