Journal articles on the topic 'Atherosclerotic calcification'
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1
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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Bogdanov, L. A., N. Yu Osyaev, Yu D. Bogdanova, R. A. Mukhamadiyarov, A. R. Shabaev, А. V. Evtushenko, and A. G. Kutikhin. "Elemental analysis of valvular and atherosclerotic calcification." Complex Issues of Cardiovascular Diseases 10, no. 3 (September 25, 2021): 26–33. http://dx.doi.org/10.17802/2306-1278-2021-10-3-26-33.
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Aim. To analyze the topographic patterns of valvular and atherosclerotic calcification growth.Methods. Dysfunctional aortic valves (n = 18) and atherosclerotic plaques (n = 20) were fixed in formalin, postfixed in 1% osmium tetroxide, consecutively stained by 2% osmium tetroxide and 2% uranyl acetate, and embedded into epoxy resin (Epon) with the further grinding and polishing ofthe samples. Upon the counterstaining by lead citrate and sputter coating with carbon, samples were visualized by backscattered scanning electron microscopy. Elemental analysis was conducted via energy-dispersive X-ray spectroscopy. Measurement of Ca/P ratio within the mineral deposits was carried out employing a pool table principle (i.e., in the center of the deposit, in the near and far circumferences (clockwise), and in control regions around the mineral deposit). Topographic patterns of calcifications were modeled using the correlation analysis. Results. Significant correlation was revealed between the Ca/P ratio in the deposit center and in the near and far circumferences of deposit in both in valvular (r = 0,35-0,78 - near circumference; r = 0,63-0,69 - far circumference) and atherosclerotic mineral deposits (r = 0,37-0,56 - near circumference; r = 0,48-0,63 - far circumference), suggesting the hierarchical growth of cardiovascular calcification around the initial nucleation sites.Conclusion. Valvular and atherosclerotic calcifications development is concentric.
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Mitra, Noémi, Renáta Gerculy, Evelin Szabó, Diana Opincariu, Monica Chițu, and Imre Benedek. "The Impact of Coronary Artery Calcification on Long-Term Cardiovascular Outcomes." Journal of Interdisciplinary Medicine 6, no. 1 (March 1, 2021): 15–20. http://dx.doi.org/10.2478/jim-2021-0007.
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Abstract Decades of research and experimental studies have investigated various strategies to prevent acute coronary events. However, significantly efficient preventive methods have not been developed and still remains a challenge to determine if a coronary atherosclerotic plaque will become vulnerable and unstable. This review aims to assess the significance of plaque vulnerability markers, more precisely the role of spotty calcifications in the development of major cardiac events, given that coronary calcification is a hallmark of atherosclerosis. Recent studies have suggested that microcalcifications, spotty calcifications, and the presence of the napkin-ring sign are predictive vulnerable plaque features, and their presence may cause plaque instability.
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Aleksandrova, N., A. Aleksandrov, N. Nikitina, and V. Aleksandrov. "AB1349 CORRELATION OF CHRONIC INFLAMMATION MARKERS WITH ULTRASOUND SIGNS OF ATHEROSCLEROTIC HEART DISEASE AND BRACHIOCEPHALIC ARTERIES LESIONS IN RHEUMATOID ARTHRITIS." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 1781.1–1781. http://dx.doi.org/10.1136/annrheumdis-2022-eular.2264.
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BackgroundClinical and experimental data confirm the role of both systemic and arterial inflammation in potentiating atherosclerosis and increasing cardiovascular risk in patients with rheumatoid arthritis (RA) against the background of severe immunological disorders.ObjectivesTo study the severity of ultrasound signs of atherosclerotic lesions of brachiocephalic arteries and heart valve apparatus in patients with rheumatoid arthritis (RA).Methods57 patients with RA (50 women and 7 men; mean age 50,45±10,12 years old; mean duration of disease 9,2±6,8 years; DAS28 activity: low - 3,5%, medium - 86%, high - 10,5%) were examined. Laboratory examination included determination of serum IgG-RF, CRP, antibodies to cyclic citrullinated peptide (ACCP), antibodies to modified citrullinated vimentin (MCV), total antinuclear antibodies (ANA), and levels of proinflammatory cytokines (IL-1, IL-6, TNF-α, angiopoietin-like proteins types 2, 3, and 4 - ANGPTL 2, 3, 4) by enzyme immunoassay.Cardiac ultrasound examination was performed according to the traditional technique on an Accuvix V10 ultrasound diagnostic system (Samsung Medison, South Korea) equipped with a multifrequency microconvex transducer with a frequency of 2-4 MHz. All patients underwent duplex scanning of brachiocephalic arteries (BCA) with assessment of the severity of atherosclerotic changes (А0 - absence of BCA atherosclerosis, АI - isolated thickening of intima-media complex as a manifestation of non-stenotic BCA atherosclerosis, АII - presence of atherosclerotic plaques and artery stenosis as manifestation of stenotic BCA atherosclerosis). The following gradation was used to estimate the degree of cardiac valve calcification: 0 - no calcification, 1st degree - unexpressed calcification, 2nd degree - moderate calcification, 3rd degree - expressed calcification of cardiac valves.ResultsSigns of cardiovascular system lesions (pericarditis, heart valve lesions, cardiomyopathies, cardiac conduction pathway lesions, myocarditis, endocarditis, coronary arteritis etc.) were diagnosed in 28 (49,1%) RA patients. Heart valve dysfunction was manifested by mitral valve (MV) and/or aortic valve (AV) insufficiency in the majority of cases. In RA patients, ultrasound signs of cardiac valve calcification occurred in 40.4% (23/57) of cases; there was a high prevalence of aortic valve calcification of varying severity (19/23; 82.6%) and less detectable mitral valve calcification (12/23; 52.17%); patients with grade II-III cardiac valve calcification predominated (16/23; 69.6%); 5 patients (21.7%) had combined AV and MV lesions. In 25 (43.8%) patients with RA the signs of atherosclerosis of brachiocephalic arteries were determined: in 19 (33.3%) - non-stenotic (AI), in 6 (10.5%) - stenotic atherosclerosis (АII).No statistically significant correlations were found between changes of cardiac valve apparatus, BCA lesions and main clinical characteristics of RA (disease activity, erosions, RF and ACCP positivity). Increased levels of ANGPTL2 (χ2=4.6, p=0.032) were observed in the group of RA patients with cardiac valve lesions, and ANA (χ2=3.91, p=0.049) and elevated IL-6 (χ2=4.28, p=0.039) were detected more frequently in patients with signs of atherosclerotic lesions of BCA.The presence of autoimmune chronic inflammatory process is an independent sign of premature atherosclerosis development and causes the highest risk of atherosclerotic lesion of BCA and accelerates the processes of cardiac valve calcification in RA patients.ConclusionRegular echocardiography (with duplex scanning of BCA and heart valve examination) in RA patients can contribute to earlier identification of groups of patients possible requiring changes in therapeutic approaches to treatment and prevention of vascular accidents.Disclosure of InterestsNone declared
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Lerman, Daniel Alejandro, Sai Prasad, and Nasri Alotti. "Calcific Aortic Valve Disease: Molecular Mechanisms And Therapeutic Approaches." European Cardiology Review 10, no. 2 (2015): 108. http://dx.doi.org/10.15420/ecr.2015.10.2.108.
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Calcification occurs in atherosclerotic vascular lesions and in the aortic valve. Calcific aortic valve disease (CAVD) is a slow, progressive disorder that ranges from mild valve thickening without obstruction of blood flow, termed aortic sclerosis, to severe calcification with impaired leaflet motion, termed aortic stenosis. In the past, this process was thought to be ‘degenerative’ because of time-dependent wear and tear of the leaflets, with passive calcium deposition. The presence of osteoblasts in atherosclerotic vascular lesions and in CAVD implies that calcification is an active, regulated process akin to atherosclerosis, with lipoprotein deposition and chronic inflammation. If calcification is active, via pro-osteogenic pathways, one might expect that development and progression of calcification could be inhibited. The overlap in the clinical factors associated with calcific valve disease and atherosclerosis provides further support for a shared disease mechanism. In our recent research we used an in vitro porcine valve interstitial cell model to study spontaneous calcification and potential promoters and inhibitors. Using this model, we found that denosumab, a human monoclonal antibody targeting the receptor activator of nuclear factor-κB ligand may, at a working concentration of 50 μg/mL, inhibit induced calcium deposition to basal levels.
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Burnett, John R., and Samuel D. Vasikaran. "Cardiovascular disease and osteoporosis: is there a link between lipids and bone?" Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 39, no. 3 (May 1, 2002): 203–10. http://dx.doi.org/10.1258/0004563021902134.
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Atherosclerotic heart disease and osteoporosis are both diseases of old age. Evidence is accumulating for a link between vascular and bone disease. Calcification is a common feature of atherosclerotic plaques, and osteoporosis is associated with both atherosclerosis and vascular calcification. However, the relationship of vascular calcification to the pathogenesis of atherosclerosis remains incompletely understood. Hormone replacement therapy has beneficial effects in the prevention of both atherosclerosis and osteoporosis. Bisphosphonates inhibit bone resorption and are used in the treatment of osteoporosis, whereas the statins inhibit cholesterol biosynthesis and are used for the treatment of atherosclerosis. We have reviewed recent advances in the knowledge of the actions of bisphosphonates and statins at the cellular, molecular and end-organ levels in order to examine the relationship between cardiovascular disease and osteoporosis and to explore the link between lipids and bones. These studies suggest that the mechanism of actions of these two classes of drugs at the cellular level may not be mutually exclusive. There are some early clinical data to complement these findings, suggesting that statins increase bone density and bisphosphonates may have a beneficial effect in vivo on plasma lipid levels and on the atherosclerotic process. Properly designed prospective studies that examine the effect of statins on bone density and fractures, as well as the effects of bisphosphonates on lipid profiles, atherosclerotic progression and cardiovascular morbidity and mortality are needed to define clearly the clinical effects and potential new roles for these agents.
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Lu, Hong, Mary Sheppard, and Alan Daugherty. "Calcification in atherosclerotic lesions." Current Opinion in Lipidology 27, no. 5 (October 2016): 543–44. http://dx.doi.org/10.1097/mol.0000000000000344.
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Shioi, A., K. Mori, S. Jono, T. Wakikawa, Y. Hiura, H. Koyama, Y. Okuno, Y. Nishizawa, and H. Morii. "Mechanism of atherosclerotic calcification." Zeitschrift f�r Kardiologie 89, no. 14 (February 1, 2000): S075—S079. http://dx.doi.org/10.1007/s003920070103.
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Hernyes, Anita, Marton Piroska, Bence Fejer, Laszlo Szalontai, Helga Szabo, Bianka Forgo, Adam L. Jermendy, et al. "Overlapping Genetic Background of Coronary Artery and Carotid/Femoral Atherosclerotic Calcification." Medicina 57, no. 3 (March 9, 2021): 252. http://dx.doi.org/10.3390/medicina57030252.
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Background and objectives: Multivessel atherosclerosis and its genetic background are under-investigated, although atherosclerosis is seldom local and still causes high mortality. Alternative methods to assess coronary calcification (CAC) might incorporate genetic links between different arteries’ atherosclerotic involvement, however, co-occurrences of coronary calcification have not been investigated in twins yet. Materials and Methods: We assessed the heritability of radio morphologically distinct atherosclerotic plaque types in coronary (non-enhanced CT, Agatston score), carotid, and femoral arteries (B-mode ultrasound) in 190 twin subjects (60 monozygotic, 35 dizygotic pairs). Four-segment scores were derived in order to assess the dissemination of the distinct plaque types in the carotid and femoral arteries taking bilaterality into account. We calculated the genetic correlation between phenotypically correlating plaque types in these arteries. Results: CAC and dissemination of calcified plaques in the carotid and femoral arteries (4S_hyper) were moderately heritable (0.67 [95% CI: 0.37–1] and 0.69 [95% CI: 0.38–1], respectively) when adjusted for age and sex. Hypoechoic plaques in the carotid and femoral arteries showed no heritability, while mixed plaques showed intermediate heritability (0.50 [95% CI: 0–0.76]). Age and sex-adjusted phenotypic correlation between CAC and 4segm_hyper was 0.48 [95% CI: 0.30–0.63] and the underlying genetic correlation was 0.86 [95% CI: 0.42–1]. Conclusions: Calcification of atherosclerotic plaques is moderately heritable in all investigated arteries and significant overlapping genetic factors can be attributed to the phenotypical resemblance of coronary and carotid or femoral atherosclerotic calcification. Our findings support the idea of screening extracoronary arteries in asymptomatic individuals. We also propose a hypothesis about primarily carotid-coronary and femoral-coronary atherosclerosis as two distinct genetic predispositions to co-localization.
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Seime, Till, Asim Cengiz Akbulut, Moritz Lindquist Liljeqvist, Antti Siika, Hong Jin, Greg Winski, Rick H. van Gorp, et al. "Proteoglycan 4 Modulates Osteogenic Smooth Muscle Cell Differentiation during Vascular Remodeling and Intimal Calcification." Cells 10, no. 6 (May 21, 2021): 1276. http://dx.doi.org/10.3390/cells10061276.
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Calcification is a prominent feature of late-stage atherosclerosis, but the mechanisms driving this process are unclear. Using a biobank of carotid endarterectomies, we recently showed that Proteoglycan 4 (PRG4) is a key molecular signature of calcified plaques, expressed in smooth muscle cell (SMC) rich regions. Here, we aimed to unravel the PRG4 role in vascular remodeling and intimal calcification. PRG4 expression in human carotid endarterectomies correlated with calcification assessed by preoperative computed tomographies. PRG4 localized to SMCs in early intimal thickening, while in advanced lesions it was found in the extracellular matrix, surrounding macro-calcifications. In experimental models, Prg4 was upregulated in SMCs from partially ligated ApoE−/− mice and rat carotid intimal hyperplasia, correlating with osteogenic markers and TGFb1. Furthermore, PRG4 was enriched in cells positive for chondrogenic marker SOX9 and around plaque calcifications in ApoE−/− mice on warfarin. In vitro, PRG4 was induced in SMCs by IFNg, TGFb1 and calcifying medium, while SMC markers were repressed under calcifying conditions. Silencing experiments showed that PRG4 expression was driven by transcription factors SMAD3 and SOX9. Functionally, the addition of recombinant human PRG4 increased ectopic SMC calcification, while arresting cell migration and proliferation. Mechanistically, it suppressed endogenous PRG4, SMAD3 and SOX9, and restored SMC markers’ expression. PRG4 modulates SMC function and osteogenic phenotype during intimal remodeling and macro-calcification in response to TGFb1 signaling, SMAD3 and SOX9 activation. The effects of PRG4 on SMC phenotype and calcification suggest its role in atherosclerotic plaque stability, warranting further investigations.
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Kashtanova, Elena V., Yana V. Polonskaya, and Yulia I. Ragino. "Calcification and atherosclerosis of the coronary arteries." Terapevticheskii arkhiv 93, no. 1 (January 10, 2021): 84–86. http://dx.doi.org/10.26442/00403660.2021.01.200598.
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Calcification is a very common phenomenon in the coronary arteries, which is part of the atherosclerotic process, and the degree of calcification can predict clinical outcomes in patients at high risk of coronary events. Both the degree of calcification and the patterns of its distribution are of prognostic importance, but the relationship of coronary artery calcification with atherosclerotic plaque instability is extremely complex and not fully understood. This article is devoted to the study of calcification markers and their influence on the development of atherosclerotic foci.
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Masenko, V. L., A. N. Kokov, S. E. Semenov, and O. L. Barbarash. "Noninvasive evaluation of density of coronary and carotid calcification in patients with type 2 diabetes mellitus." Journal of radiology and nuclear medicine 99, no. 6 (January 2, 2019): 310–18. http://dx.doi.org/10.20862/0042-4676-2018-99-6-310-318.
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Objective. To estimate the density of calcium deposits of atherosclerotic plaques of coronary and carotid arteries in patients with diabetes mellitus (DM) type 2 using multislice computed tomography (MSCT).Material and methods. 251 patients with multifocal atherosclerosis (MA) were examined using MSCT. Determined equivalent density of calcium deposits (EDCD) atherosclerotic plaque of coronary and carotid arteries.Results. According to the data of MSCT in patients with MA irrespective of concomitant diabetes was a high incidence of calcification of the coronary and carotid arteries. In Group 1 EDCD coronary arteries was 0.235 (0.214; 0.254) mg/mm3, in the group 2 - 0,219 (0,192; 0,242) mg/mm3. EDCD of carotid arteries in patients with diabetes was 0.183 (0.171; 0.193) mg/mm3, in patients without diabetes - 0.226 (0.199; 0.247) mg/mm3. There was a significant difference in the groups EDCD values for coronary (p = 0.017), and the carotid (p = 0.000003) artery.Conclusion. Using index EDCD obtained on the basis of routine MSCT coronary and carotid arteries in patients with MA with DM compared with those without diabetes had significantly higher density calcifications in projection of coronary and low density of calcium deposits carotid arteries without regard to the degree of Agatston calcification scale.
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Liang, Yingquan, Guilan Chen, Feng Zhang, Xiaoxiao Yang, Yuanli Chen, Yajun Duan, Maoyun Yu, Shuang Zhang, and Jihong Han. "Procyanidin B2 Reduces Vascular Calcification through Inactivation of ERK1/2-RUNX2 Pathway." Antioxidants 10, no. 6 (June 5, 2021): 916. http://dx.doi.org/10.3390/antiox10060916.
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Vascular calcification is strongly associated with atherosclerotic plaque burden and plaque instability. The activation of extracellular signal-regulated kinase 1/2 (ERK1/2) increases runt related transcription factor 2 (RUNX2) expression to promote vascular calcification. Procyanidin B2 (PB2), a potent antioxidant, can inhibit ERK1/2 activation in human aortic smooth muscle cells (HASMCs). However, the effects and involved mechanisms of PB2 on atherosclerotic calcification remain unknown. In current study, we fed apoE-deficient (apoE−/−) mice a high-fat diet (HFD) while treating the animals with PB2 for 18 weeks. At the end of the study, we collected blood and aorta samples to determine atherosclerosis and vascular calcification. We found PB2 treatment decreased lesions in en face aorta, thoracic, and abdominal aortas by 21.4, 24.6, and 33.5%, respectively, and reduced sinus lesions in the aortic root by 17.1%. PB2 also increased a-smooth muscle actin expression and collagen content in lesion areas. In the aortic root, PB2 reduced atherosclerotic calcification areas by 75.8%. In vitro, PB2 inhibited inorganic phosphate-induced osteogenesis in HASMCs and aortic rings. Mechanistically, the expression of bone morphogenetic protein 2 and RUNX2 were markedly downregulated by PB2 treatment. Additionally, PB2 inhibited ERK1/2 phosphorylation in the aortic root plaques of apoE−/− mice and calcified HASMCs. Reciprocally, the activation of ERK1/2 phosphorylation by C2-MEK1-mut or epidermal growth factor can partially restore the PB2-inhibited RUNX2 expression or HASMC calcification. In conclusion, our study demonstrates that PB2 inhibits vascular calcification through the inactivation of the ERK1/2-RUNX2 pathway. Our study also suggests that PB2 can be a potential option for vascular calcification treatment.
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Angulo, Jesús, Thao Nguyen-Khoa, Ziad A. Massy, Tilman Drüeke, and Jean Serra. "MORPHOLOGICAL QUANTIFICATION OF AORTIC CALCIFICATION FROM LOW MAGNIFICATION IMAGES." Image Analysis & Stereology 22, no. 2 (May 3, 2011): 81. http://dx.doi.org/10.5566/ias.v22.p81-89.
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Atherosclerotic and medial vascular calcifications are frequent in chronic renal failure patiens and predict their increased cardiovascular mortality. Experimental models for mice have been recently developed in order to study these disorders. The aim of this paper is to present the morphological image processing algorithms developed for the semi-automated measurement of calcification from sections of aorta stained using von Kossa's silver nitrate procedure and acquired at low magnification power (x 2.5) on colour images. The approach is separated into two sequential phases. First, the segmentation is aimed to extract the calcification structures and on the other hand to demarcate the region of the atherosclerotic lesion within the tissue. The segmentation yields the image data which is the input to the second phase, the quantification. Calcified structures are measured inside and outside the lesion using a granulometric curve which allows the calculation of statistical parameters of size. The same operator computes the shape of the lesion. The relative proportion of the area of calcification is also calculated respectively for the atherosclerotic lesion area and the area outside such lesions. In conclusion, the here developed method allows quantification of vascular calcified deposits in mouse aorta. This method will be useful for the quantitative assessment of pathological vascular changes in animals and man.
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Healy, Abigail, Joshua M. Berus, Jared L. Christensen, Cadence Lee, Chris Mantsounga, Willie Dong, Jerome P. Watts, et al. "Statins Disrupt Macrophage Rac1 Regulation Leading to Increased Atherosclerotic Plaque Calcification." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 3 (March 2020): 714–32. http://dx.doi.org/10.1161/atvbaha.119.313832.
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Objective: Calcification of atherosclerotic plaque is traditionally associated with increased cardiovascular event risk; however, recent studies have found increased calcium density to be associated with more stable disease. 3-hydroxy-3-methylglutaryl coenzymeA reductase inhibitors or statins reduce cardiovascular events. Invasive clinical studies have found that statins alter both the lipid and calcium composition of plaque but the molecular mechanisms of statin-mediated effects on plaque calcium composition remain unclear. We recently defined a macrophage Rac (Ras-related C3 botulinum toxin substrate)–IL-1β (interleukin-1 beta) signaling axis to be a key mechanism in promoting atherosclerotic calcification and sought to define the impact of statin therapy on this pathway. Approach and Results: Here, we demonstrate that statin therapy is independently associated with elevated coronary calcification in a high-risk patient population and that statins disrupt the complex between Rac1 and its inhibitor RhoGDI (Rho GDP-dissociation inhibitor), leading to increased active (GTP bound) Rac1 in primary monocytes/macrophages. Rac1 activation is prevented by rescue with the isoprenyl precursor geranylgeranyl diphosphate. Statin-treated macrophages exhibit increased activation of NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells), increased IL-1β mRNA, and increased Rac1-dependent IL-1β protein secretion in response to inflammasome stimulation. Using an animal model of calcific atherosclerosis, inclusion of statin in the atherogenic diet led to a myeloid Rac1-dependent increase in atherosclerotic calcification, which was associated with increased serum IL-1β expression, increased plaque Rac1 activation, and increased plaque expression of the osteogenic markers, alkaline phosphatase and RUNX2 (Runt-related transcription factor 2). Conclusions: Statins are capable of increasing atherosclerotic calcification through disinhibition of a macrophage Rac1–IL-1β signaling axis.
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Demer, Linda, Jeffrey Hsu, and Yin Tintut. "Murine Models of Atherosclerotic Calcification." Current Drug Targets 9, no. 3 (March 1, 2008): 224–28. http://dx.doi.org/10.2174/138945008783755539.
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Demer, Linda L., Andrew P. Sage, and Yin Tintut. "Nanoscale Architecture in Atherosclerotic Calcification." Arteriosclerosis, Thrombosis, and Vascular Biology 28, no. 11 (November 2008): 1882–84. http://dx.doi.org/10.1161/atvbaha.108.175711.
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Vieceli Dalla Sega, Francesco, Francesca Fortini, Paolo Severi, Paola Rizzo, Iija Gardi, Paolo Cimaglia, Claudio Rapezzi, Luigi Tavazzi, and Roberto Ferrari. "Cardiac Calcifications: Phenotypes, Mechanisms, Clinical and Prognostic Implications." Biology 11, no. 3 (March 9, 2022): 414. http://dx.doi.org/10.3390/biology11030414.
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There is a growing interest in arterial and heart valve calcifications, as these contribute to cardiovascular outcome, and are leading predictors of cardiovascular and kidney diseases. Cardiovascular calcifications are often considered as one disease, but, in effect, they represent multifaced disorders, occurring in different milieus and biological phenotypes, following different pathways. Herein, we explore each different molecular process, its relative link with the specific clinical condition, and the current therapeutic approaches to counteract calcifications. Thus, first, we explore the peculiarities between vascular and valvular calcium deposition, as this occurs in different tissues, responds differently to shear stress, has specific etiology and time courses to calcification. Then, we differentiate the mechanisms and pathways leading to hyperphosphatemic calcification, typical of the media layer of the vessel and mainly related to chronic kidney diseases, to those of inflammation, typical of the intima vascular calcification, which predominantly occur in atherosclerotic vascular diseases. Finally, we examine calcifications secondary to rheumatic valve disease or other bacterial lesions and those occurring in autoimmune diseases. The underlying clinical conditions of each of the biological calcification phenotypes and the specific opportunities of therapeutic intervention are also considered and discussed.
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Aengevaeren, Vincent L., Arend Mosterd, Sanjay Sharma, Niek H. J. Prakken, Stefan Möhlenkamp, Paul D. Thompson, Birgitta K. Velthuis, and Thijs M. H. Eijsvogels. "Exercise and Coronary Atherosclerosis." Circulation 141, no. 16 (April 21, 2020): 1338–50. http://dx.doi.org/10.1161/circulationaha.119.044467.
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Physical activity and exercise training are effective strategies for reducing the risk of cardiovascular events, but multiple studies have reported an increased prevalence of coronary atherosclerosis, usually measured as coronary artery calcification, among athletes who are middle-aged and older. Our review of the medical literature demonstrates that the prevalence of coronary artery calcification and atherosclerotic plaques, which are strong predictors for future cardiovascular morbidity and mortality, was higher in athletes compared with controls, and was higher in the most active athletes compared with less active athletes. However, analysis of plaque morphology revealed fewer mixed plaques and more often only calcified plaques among athletes, suggesting a more benign composition of atherosclerotic plaques. This review describes the effects of physical activity and exercise training on coronary atherosclerosis in athletes who are middle-aged and older and aims to contribute to the understanding of the potential adverse effects of the highest doses of exercise training on the coronary arteries. For this purpose, we will review the association between exercise and coronary atherosclerosis measured using computed tomography, discuss the potential underlying mechanisms for exercise-induced coronary atherosclerosis, determine the clinical relevance of coronary atherosclerosis in middle-aged athletes and describe strategies for the clinical management of athletes with coronary atherosclerosis to guide physicians in clinical decision making and treatment of athletes with elevated coronary artery calcification scores.
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Burger, Fabienne, Daniela Baptista, Aline Roth, Karim J. Brandt, Rafaela Fernandes da Silva, Fabrizio Montecucco, François Mach, and Kapka Miteva. "Single-Cell RNA-Seq Reveals a Crosstalk between Hyaluronan Receptor LYVE-1-Expressing Macrophages and Vascular Smooth Muscle Cells." Cells 11, no. 3 (January 25, 2022): 411. http://dx.doi.org/10.3390/cells11030411.
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Background: Atherosclerosis is a chronic inflammatory disease where macrophages participate in the progression of the disease. However, the role of resident-like macrophages (res-like) in the atherosclerotic aorta is not completely understood. Methods: A single-cell RNA sequencing analysis of CD45+ leukocytes in the atherosclerotic aorta of apolipoprotein E–deficient (Apoe−/−) mice on a normal cholesterol diet (NCD) or a high cholesterol diet (HCD), respecting the side-to-specific predisposition to atherosclerosis, was performed. A population of res-like macrophages expressing hyaluronan receptor LYVE-1 was investigated via flow cytometry, co-culture experiments, and immunofluorescence in human atherosclerotic plaques from carotid artery disease patients (CAD). Results: We identified 12 principal leukocyte clusters with distinct atherosclerosis disease-relevant gene expression signatures. LYVE-1+ res-like macrophages, expressing a high level of CC motif chemokine ligand 24 (CCL24, eotaxin-2), expanded under hypercholesteremia in Apoe−/− mice and promoted VSMC phenotypic modulation to osteoblast/chondrocyte-like cells, ex vivo, in a CCL24-dependent manner. Moreover, the abundance of LYVE-1+CCL24+ macrophages and elevated systemic levels of CCL24 were associated with vascular calcification and CAD events. Conclusions: LYVE-1 res-like macrophages, via the secretion of CCL24, promote the transdifferentiation of VSMC to osteogenic-like cells with a possible role in vascular calcification and likely a detrimental role in atherosclerotic plaque destabilization.
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Henein, Michael Y., Sergio Vancheri, Gani Bajraktari, and Federico Vancheri. "Coronary Atherosclerosis Imaging." Diagnostics 10, no. 2 (January 24, 2020): 65. http://dx.doi.org/10.3390/diagnostics10020065.
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Identifying patients at increased risk of coronary artery disease, before the atherosclerotic complications become clinically evident, is the aim of cardiovascular prevention. Imaging techniques provide direct assessment of coronary atherosclerotic burden and pathological characteristics of atherosclerotic lesions which may predict the progression of disease. Atherosclerosis imaging has been traditionally based on the evaluation of coronary luminal narrowing and stenosis. However, the degree of arterial obstruction is a poor predictor of subsequent acute events. More recent techniques focus on the high-resolution visualization of the arterial wall and the coronary plaques. Most acute coronary events are triggered by plaque rupture or erosion. Hence, atherosclerotic plaque imaging has generally focused on the detection of vulnerable plaque prone to rupture. However, atherosclerosis is a dynamic process and the plaque morphology and composition may change over time. Most vulnerable plaques undergo progressive transformation from high-risk to more stable and heavily calcified lesions, while others undergo subclinical rupture and healing. Although extensive plaque calcification is often associated with stable atherosclerosis, the extent of coronary artery calcification strongly correlates with the degree of atherosclerosis and with the rate of future cardiac events. Inflammation has a central role in atherogenesis, from plaque formation to rupture, hence in the development of acute coronary events. Morphologic plaque assessment, both invasive and non-invasive, gives limited information as to the current activity of the atherosclerotic disease. The addition of nuclear imaging, based on radioactive tracers targeted to the inflammatory components of the plaques, provides a highly sensitive assessment of coronary disease activity, thus distinguishing those patients who have stable disease from those with active plaque inflammation.
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Ruiz, Jessica L., Joshua D. Hutcheson, Luis Cardoso, Amirala Bakhshian Nik, Alexandra Condado de Abreu, Tan Pham, Fabrizio Buffolo, et al. "Nanoanalytical analysis of bisphosphonate-driven alterations of microcalcifications using a 3D hydrogel system and in vivo mouse model." Proceedings of the National Academy of Sciences 118, no. 14 (April 1, 2021): e1811725118. http://dx.doi.org/10.1073/pnas.1811725118.
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Vascular calcification predicts atherosclerotic plaque rupture and cardiovascular events. Retrospective studies of women taking bisphosphonates (BiPs), a proposed therapy for vascular calcification, showed that BiPs paradoxically increased morbidity in patients with prior acute cardiovascular events but decreased mortality in event-free patients. Calcifying extracellular vesicles (EVs), released by cells within atherosclerotic plaques, aggregate and nucleate calcification. We hypothesized that BiPs block EV aggregation and modify existing mineral growth, potentially altering microcalcification morphology and the risk of plaque rupture. Three-dimensional (3D) collagen hydrogels incubated with calcifying EVs were used to mimic fibrous cap calcification in vitro, while an ApoE−/− mouse was used as a model of atherosclerosis in vivo. EV aggregation and formation of stress-inducing microcalcifications was imaged via scanning electron microscopy (SEM) and atomic force microscopy (AFM). In both models, BiP (ibandronate) treatment resulted in time-dependent changes in microcalcification size and mineral morphology, dependent on whether BiP treatment was initiated before or after the expected onset of microcalcification formation. Following BiP treatment at any time, microcalcifications formed in vitro were predicted to have an associated threefold decrease in fibrous cap tensile stress compared to untreated controls, estimated using finite element analysis (FEA). These findings support our hypothesis that BiPs alter EV-driven calcification. The study also confirmed that our 3D hydrogel is a viable platform to study EV-mediated mineral nucleation and evaluate potential therapies for cardiovascular calcification.
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Faggiano, Andrea, Gloria Santangelo, Stefano Carugo, Gregg Pressman, Eugenio Picano, and Pompilio Faggiano. "Cardiovascular Calcification as a Marker of Increased Cardiovascular Risk and a Surrogate for Subclinical Atherosclerosis: Role of Echocardiography." Journal of Clinical Medicine 10, no. 8 (April 13, 2021): 1668. http://dx.doi.org/10.3390/jcm10081668.
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The risk prediction of future cardiovascular events is mainly based on conventional risk factor assessment by validated algorithms, such as the Framingham Risk Score, the Pooled Cohort Equations and the European SCORE Risk Charts. The identification of subclinical atherosclerosis has emerged as a promising tool to refine the individual cardiovascular risk identified by these models, to prognostic stratify asymptomatic individuals and to implement preventive strategies. Several imaging modalities have been proposed for the identification of subclinical organ damage, the main ones being coronary artery calcification scanning by cardiac computed tomography and the two-dimensional ultrasound evaluation of carotid arteries. In this context, echocardiography offers an assessment of cardiac calcifications at different sites, such as the mitral apparatus (including annulus, leaflets and papillary muscles), aortic valve and ascending aorta, findings that are associated with the clinical manifestation of atherosclerotic disease and are predictive of future cardiovascular events. The aim of this paper is to summarize the available evidence on clinical implications of cardiac calcification, review studies that propose semiquantitative ultrasound assessments of cardiac calcifications and evaluate the potential of ultrasound calcium scores for risk stratification and prevention of clinical events.
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Lee, Cadence F., Rachel E. Carley, Celia A. Butler, and Alan R. Morrison. "Rac GTPase Signaling in Immune-Mediated Mechanisms of Atherosclerosis." Cells 10, no. 11 (October 20, 2021): 2808. http://dx.doi.org/10.3390/cells10112808.
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Coronary artery disease caused by atherosclerosis is a major cause of morbidity and mortality around the world. Data from preclinical and clinical studies support the belief that atherosclerosis is an inflammatory disease that is mediated by innate and adaptive immune signaling mechanisms. This review sought to highlight the role of Rac-mediated inflammatory signaling in the mechanisms driving atherosclerotic calcification. In addition, current clinical treatment strategies that are related to targeting hypercholesterolemia as a critical risk factor for atherosclerotic vascular disease are addressed in relation to the effects on Rac immune signaling and the implications for the future of targeting immune responses in the treatment of calcific atherosclerosis.
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YIU, KAI-HANG, SILUN WANG, MO-YIN MOK, GAIK-CHENG OOI, PEK-LAN KHONG, CHAK-SING LAU, and HUNG-FAT TSE. "Relationship Between Cardiac Valvular and Arterial Calcification in Patients with Rheumatoid Arthritis and Systemic Lupus Erythematosus." Journal of Rheumatology 38, no. 4 (February 1, 2011): 621–27. http://dx.doi.org/10.3899/jrheum.100844.
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Objective.Cardiac valvular calcification has been linked with systemic atherosclerosis in the general population. The prevalence and relationship with arterial calcification in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) is unknown. We investigated the prevalence of valvular calcification in patients with RA and SLE and its relationship with arterial atherosclerotic calcification.Methods.We compared aortic valve calcification (AVC), mitral valve calcification (MVC), and systemic vascular bed calcification using multidetector computed tomography in 110 patients (mean age 46.5 ± 9.4 yrs, 97 women) with RA (n = 58) or SLE (n = 52) and 60 age and sex-matched healthy controls.Results.Patients with RA and SLE, combined, had significantly higher prevalence of AVC (21.8% vs 3.3% in controls; p < 0.01), MVC (19.1% vs 0% in controls; p < 0.01), and arterial calcification in different vascular beds (all p < 0.05). AVC was not associated with any specific clinical characteristics, but MVC was associated with older age, hypertension, C-reactive protein level, and duration of disease. The presence of MVC was independently associated with coronary calcification and calcification in any vascular bed upon adjustment with clinical measures.Conclusion.Our study demonstrated that cardiac valvular calcification is more prevalent in patients with RA and SLE compared with healthy controls. The presence of MVC, but not AVC, independently predicted the occurrence of premature atherosclerosis with arterial calcification in patients with RA and SLE.
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Tajbakhsh, Amir, Petri T. Kovanen, Mahdi Rezaee, Maciej Banach, and Amirhossein Sahebkar. "Ca2+ Flux: Searching for a Role in Efferocytosis of Apoptotic Cells in Atherosclerosis." Journal of Clinical Medicine 8, no. 12 (November 21, 2019): 2047. http://dx.doi.org/10.3390/jcm8122047.
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In atherosclerosis, macrophages in the arterial wall ingest plasma lipoprotein-derived lipids and become lipid-filled foam cells with a limited lifespan. Thus, efficient removal of apoptotic foam cells by efferocytic macrophages is vital to preventing the dying foam cells from forming a large necrotic lipid core, which, otherwise, would render the atherosclerotic plaque vulnerable to rupture and would cause clinical complications. Ca2+ plays a role in macrophage migration, survival, and foam cell generation. Importantly, in efferocytic macrophages, Ca2+ induces actin polymerization, thereby promoting the formation of a phagocytic cup necessary for efferocytosis. Moreover, in the efferocytic macrophages, Ca2+ enhances the secretion of anti-inflammatory cytokines. Various Ca2+ antagonists have been seminal for the demonstration of the role of Ca2+ in the multiple steps of efferocytosis by macrophages. Moreover, in vitro and in vivo experiments and clinical investigations have revealed the capability of Ca2+ antagonists in attenuating the development of atherosclerotic plaques by interfering with the deposition of lipids in macrophages and by reducing plaque calcification. However, the regulation of cellular Ca2+ fluxes in the processes of efferocytic clearance of apoptotic foam cells and in the extracellular calcification in atherosclerosis remains unknown. Here, we attempted to unravel the molecular links between Ca2+ and efferocytosis in atherosclerosis and to evaluate cellular Ca2+ fluxes as potential treatment targets in atherosclerotic cardiovascular diseases.
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Mal’kov, Oleg A., Alena A. Govorukhina, Anna Yu Afineevskaya, and Yuriy G. Burykin. "The Role of Calcification in the Pathogenesis of Inflammatory Reaction in the Arterial Wall (Exemplified by the Vessels of the Neck and Head in Adults)." Journal of Medical and Biological Research, no. 4 (December 1, 2021): 435–43. http://dx.doi.org/10.37482/2687-1491-z081.
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Calcification provoked by inflammation accompanies many comorbid conditions (including atherosclerosis and fibromuscular dysplasia). What is more, they mutually aggravate each other. The aim of this study was to reveal the patterns of calcification of the arteries of the neck and head in patients with clinical manifestations of vascular disorders of varying severity in inflammatory and non-inflammatory diseases. Materials and methods. A total of 155 patients were examined (mean age 49.1 ± 16.3 years) using computed tomography. The subjects were divided into three groups according to the severity of functional changes in the arterial bed: 1) no vascular obstruction (n = 43); 2) arterial obstruction ≤ 50 % according to NASCET criteria (n = 55); 3) arterial obstruction > 50 % (n = 57). A visual analysis of atherosclerotic lesions of the vessels of the neck and head revealed that the calcification was a dystrophic type of intimal lesion in almost half of the cases (44 %). A visual analysis of stenosis caused by fibromuscular dysplasia showed that calcium deposition is not typical of this process. The absence of calcium phosphate deposition in this case was associated with genetic connective tissue abnormalities. Results. We created a flowchart representing the pathogenesis of artery wall calcification in chronic inflammation. In addition, we revealed previously not described in the literature links between the processes of osteoporosis, progression of biomineralization of atherosclerotic plaques, and decalcification of plaques, which allowed us to indirectly assess their degree of maturation. The results of the study indicate that artery calcification could be considered as a possible marker of the progression of atherosclerosis. For citation: Mal’kov O.A., Govorukhina A.A., Burykin Yu.G., Afineevskaya A.Yu. The Role of Calcification in the Pathogenesis of Inflammatory Reaction in the Arterial Wall (Exemplified by the Vessels of the Neck and Head in Adults). Journal of Medical and Biological Research, 2021, vol. 9, no. 4, pp. 435–443. DOI: 10.37482/2687-1491-Z081
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Bogdanov, L. A., N. Yu Osyaev, V. E. Markova, R. A. Mukhamadiyarov, A. R. Shabaev, and A. G. Kutikhin. "Elemental analysis insights into atherosclerotic calcification." Сибирский научный медицинский журнал 41, no. 1 (March 4, 2021): 81–90. http://dx.doi.org/10.18699/ssmj20210108.
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Higgins, Catherine L., Seth A. Marvel, and Joel D. Morrisett. "Quantification of Calcification in Atherosclerotic Lesions." Arteriosclerosis, Thrombosis, and Vascular Biology 25, no. 8 (August 2005): 1567–76. http://dx.doi.org/10.1161/01.atv.0000172017.79441.73.
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Boström, Kristina, Karol E. Watson, William P. Stanford, and Linda L. Demer. "Atherosclerotic calcification: Relation to developmental osteogenesis." American Journal of Cardiology 75, no. 6 (February 1995): 88B—91B. http://dx.doi.org/10.1016/0002-9149(95)80020-s.
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Osyaev, N. Yu, L. A. Bogdanov, R. A. Mukhamadiyarov, A. R. Shabaev, D. K. Shishkova, V. E. Markova, O. V. Gruzdeva, and A. G. Kutikhin. "Regularities of plaque stabilization in various scenarios of neointimal calcification and vascularization." Russian Journal of Cardiology 26, no. 6 (July 16, 2021): 4051. http://dx.doi.org/10.15829/1560-4071-2021-4051.
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Aim. To study the relationships between phenotypes of extracranial arteries' plaques (stable/unstable), their calcification and its causes, in particular, vascularization.Material and methods. The study included 88 patients: patients (n=44) with ischemic stroke and those (n=44) with chronic brain ischemia. In all subjects, the parameters of systemic mineral homeostasis were assessed (total and ionized calcium, phosphate, total protein, albumin, and calcification propensity). Atherosclerotic plaques have been obtained during carotid endarterectomy, fixed in formalin, postfixed in 1% osmium tetroxide, stained in 2% osmium tetroxide, dehydrated in ascending ethanol series and acetone, stained with 2% alcoholic uranyl acetate and embedded into epoxy resin with its further polymerization. Epoxy resin blocks were grinded, polished, counterstained with Reynolds' lead citrate and sputter coated with carbon. Sample visualization was performed employing backscattered scanning electron microscopy. Number and area of calcium deposits and neointimal vessels were quantified using ImageJ. Statistical analysis was carried out using Mann-Whitney U-test and Spearman's rank correlation coefficient.Results. It was found that area of neointimal calcification, but not number of calcium deposits, was associated with the stable plaque phenotype. The stabilizing effect of calcification was manifested in retarding stenosis associated with plaque rupture and stroke. Calcification extent directly correlated with total and local plaque vascularization, which have been associated with unstable and stable plaque phenotype, respectively. In addition, plaque calcification negatively correlated with total protein and albumin, thereby reflecting the impaired systemic mineral homeostasis.Conclusion. Atherosclerotic plaque calcification and active local vascularization reduce stenosis extent and stabilize plaque. In contrast, total plaque calcification contributes to the atherosclerosis progression and promotes major acute cardiovascular events.
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Chistiakov, Dimitry A., Veronika A. Myasoedova, Alexandra A. Melnichenko, Andrey V. Grechko, and Alexander N. Orekhov. "Calcifying Matrix Vesicles and Atherosclerosis." BioMed Research International 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/7463590.
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Artery calcification is a well-recognized predictor of late atherosclerotic complications. In the intima media, calcification starts with apoptosis of vascular smooth muscle cells (VSMCs) and the release of calcifying matrix vesicles with diameter of 0.5–15 μm that can be observed microscopically. In complicated plaques, calcification is generally less frequent. Calcifying vesicles are released by proatherosclerotic VSMCs into the collagen-rich matrix. The vesicles can penetrate into the intima media and protrude into the arterial lumen and thereby may represent a potential cause of atherothrombosis. In calcified fibrolipid plaques, the rate of calcification is increased but is followed with healing of a lesion rupture and exhibited by further erosion and/or intimal thickening. Generally, calcification directly correlates with the apoptosis of VSMCs and macrophages accompanied by the release of osteogenic matrix vesicles. This is a hallmark of atherosclerosis-related apoptosis of VSMCs that is commonly released in plaque stabilization.
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Böhm, Elsa Wilma, Maria Pavlaki, Georgios Chalikias, Dimitrios Mikroulis, George S. Georgiadis, Dimitrios N. Tziakas, Stavros Konstantinides, and Katrin Schäfer. "Colocalization of Erythrocytes and Vascular Calcification in Human Atherosclerosis: A Systematic Histomorphometric Analysis." TH Open 05, no. 02 (April 2021): e113-e124. http://dx.doi.org/10.1055/s-0041-1725042.
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Abstract Background Intimal calcification typically develops in advanced atherosclerosis, and microcalcification may promote plaque progression and instability. Conversely, intraplaque hemorrhage and erythrocyte extravasation may stimulate osteoblastic differentiation and intralesional calcium phosphate deposition. The presence of erythrocytes and their main cellular components (membranes, hemoglobin, and iron) and colocalization with calcification has never been systematically studied. Methods and Results We examined three types of diseased vascular tissue specimens, namely, degenerative aortic valve stenosis (n = 46), atherosclerotic carotid artery plaques (n = 9), and abdominal aortic aneurysms (n = 14). Biomaterial was obtained from symptomatic patients undergoing elective aortic valve replacement, carotid artery endatherectomy, or aortic aneurysm repair, respectively. Serial sections were stained using Masson–Goldner trichrome, Alizarin red S, and Perl's iron stain to visualize erythrocytes, extracelluar matrix and osteoid, calcium phosphate deposition, or the presence of iron and hemosiderin, respectively. Immunohistochemistry was employed to detect erythrocyte membranes (CD235a), hemoglobin or the hemoglobin scavenger receptor (CD163), endothelial cells (CD31), myofibroblasts (SMA), mesenchymal cells (osteopontin), or osteoblasts (periostin). Our analyses revealed a varying degree of intraplaque hemorrhage and that the majority of extravasated erythrocytes were lysed. Osteoid and calcifications also were frequently present, and erythrocyte membranes were significantly more prevalent in areas with calcification. Areas with extravasated erythrocytes frequently contained CD163-positive cells, although calcification also occurred in areas without CD163 immunosignals. Conclusion Our findings underline the presence of extravasated erythrocytes and their membranes in different types of vascular lesions, and their association with areas of calcification suggests an active role of erythrocytes in vascular disease processes.
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Vehmas, Tapio, Asta Hiltunen, Leena Kivisaari, and Päivi Leino-Arjas. "Atherosclerotic and pleural calcifications are related among asbestos-exposed workers." European Journal of Cardiovascular Prevention & Rehabilitation 15, no. 5 (October 2008): 599–601. http://dx.doi.org/10.1097/hjr.0b013e328309a224.
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Methods We studied the relationship between calcified chest atherosclerosis and pleural plaques among 505 construction workers with computed tomography. The extent and thickness of pleural plaques and the score of visceral pleural thickening were estimated, as was calcification of both pleural disease and chest atherosclerosis. Results Adjusted for age, BMI, smoking, and asbestos exposure, pleural calcification was associated with calcification in coronary arteries ( P < 0.001) and in the aorta ( P < 0.001). Conclusion These associations may be due to susceptibility factors common to both conditions. Calcification in pleural plaques may be a hint of atherosclerosis at least among asbestos-exposed people.
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Lassen, Jean Bismuth, Bækgaard, and Christoffersen. "Intraluminale Kalkbildung der abdominalen Aorta." Vasa 29, no. 4 (November 1, 2000): 282–84. http://dx.doi.org/10.1024/0301-1526.29.4.282.
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A patient who had no evidence of atherosclerotic disease and had never been hypertensive, presented with symptoms usually associated with gallstone disease. A large intraluminal calcification in the juxtarenal aorta was found to be the probable cause of these symptoms. The aorta was otherwise free of atherosclerotic changes. Although it could not be identified with certainty, this calcification could have developed secondary to a single ulcerated atheroma.
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Selwaness, Mariana, Quirijn van den Bouwhuijsen, Francesco U. S. Mattace-Raso, Germaine C. Verwoert, Albert Hofman, Oscar H. Franco, Jacqueline C. M. Witteman, Aad van der Lugt, Meike W. Vernooij, and Jolanda J. Wentzel. "Arterial Stiffness Is Associated With Carotid Intraplaque Hemorrhage in the General Population." Arteriosclerosis, Thrombosis, and Vascular Biology 34, no. 4 (April 2014): 927–32. http://dx.doi.org/10.1161/atvbaha.113.302603.
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Objective— The relation between arterial stiffness and atherosclerosis, and specifically the influence of arterial stiffness on plaque composition, is largely unknown. In a population-based study, we investigated the association between arterial stiffness and the presence and composition of carotid atherosclerotic plaques. Approach and Results— Arterial stiffness was measured in 6527 participants (67.0±8.6 years) using aortic pulse wave velocity (PWV). Presence of carotid atherosclerotic plaques was assessed with ultrasound. Subsequently, 1059 subjects with carotid plaques (>2.5 mm) underwent MRI to assess plaque composition (presence of intraplaque hemorrhage, lipid, and calcification). Generalized estimation equation analyses adjusted for age, sex, mean arterial pressure, heart rate, carotid wall thickening, pulse pressure, and traditional cardiovascular risk factors were used to study the association between PWV and the presence and composition of carotid atherosclerotic plaques. In multivariable analysis, higher PWV was independently related to higher prevalence of carotid atherosclerotic plaque on ultrasound (odds ratio for highest quartile of PWV compared with lowest quartile, 1.24 [95% confidence interval, 1.02–1.51]). Furthermore, higher PWV was associated with intraplaque hemorrhage (age- and sex-adjusted odds ratio per SD increase in PWV, 1.20 [1.04–1.38] and calcification, 1.18 [1.03–1.35]), but not with lipid. After adjustment for cardiovascular risk factors, PWV remained significantly associated with intraplaque hemorrhage (1.20 [1.01–1.43]). Additional adjustment for pulse pressure did not materially affect the effect estimate (1.19 [1.00–1.42]). Conclusions— Higher PWV is associated with presence and composition of carotid atherosclerotic plaques, in particular with intraplaque hemorrhage. These findings provide further clues for understanding the development of vulnerable atherosclerotic plaque.
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McRobb, L., D. J. Handelsman, and A. K. Heather. "Androgen-Induced Progression of Arterial Calcification in Apolipoprotein E-Null Mice Is Uncoupled from Plaque Growth and Lipid Levels." Endocrinology 150, no. 2 (February 1, 2009): 841–48. http://dx.doi.org/10.1210/en.2008-0760.
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Arterial calcification has prognostic significance for cardiovascular outcomes, but its pathogenesis remains unclear. Calcification increases with age, but its prevalence in men suggests hormonal influence. In this study we analyzed the effect of exogenous androgens on calcification of advanced atherosclerotic lesions in the arterial tree of gonadally intact 34-wk-old male and female apolipoprotein E-null mice. Testosterone (T) increased calcification 3- to 4-fold (P < 0.05) in lesions of the innominate artery and aortic sinus. A nonaromatizable androgen, dihydrotestosterone, also increased lesion calcification in the innominate artery (2.4-fold, P < 0.05) but not the aortic sinus. The androgen-induced effects were independent of sex and occurred despite corresponding reductions in plaque area, the latter correlating inversely with increased serum high-density lipoprotein cholesterol levels. Androgen-induced calcification in the innominate artery was observed with up-regulation of local androgen receptor (AR) expression in response to T and dihydrotestosterone for both males and females but neither androgen influenced innominate artery estrogen receptor (ER)-α or -β expression in either sex. Conversely, T-induced calcification in the aortic sinus was associated with down-regulation of ERα but not ERβ expression in both sexes, whereas androgen-induced AR expression was increased in female but decreased in male mice. This study demonstrates for the first time that calcification of advanced atherosclerotic lesions is an androgen-sensitive process and postulates potential roles for both AR- and ER-mediated pathways in androgen-induced vascular calcification. We demonstrate a novel direct link between vascular calcification and the major male hormone, T, uncoupled from conventional relationships with plaque growth and lipid levels. Calcification of advanced atherosclerotic lesions is an androgen-sensitive process whereby testosterone uncouples conventional relationships between plaque growth and lipid levels.
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Donovan, Andrea, Mark Schweitzer, Jenny Bencardino, Catherine Petchprapa, Jodi Cohen, and Gina Ciavarra. "Correlation between Rotator Cuff Tears and Systemic Atherosclerotic Disease." Radiology Research and Practice 2011 (2011): 1–7. http://dx.doi.org/10.1155/2011/128353.
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The purpose of this study was to investigate the association of aortic arch calcification, a surrogate marker of atherosclerosis, with rotator cuff tendinosis and tears given the hypothesis that decreased tendon vascularity is a contributing factor in the etiology of tendon degeneration. A retrospective review was performed to identify patients ages 50 to 90 years who had a shoulder MRI and a chest radiograph performed within 6 months of each other. Chest radiographs and shoulder MRIs from 120 patients were reviewed by two sets of observers blinded to the others' conclusions. Rotator cuff disease was classified as tendinosis, partial thickness tear, and full thickness tear. The presence or absence of aortic arch calcification was graded and compared with the MRI appearance of the rotator cuff. The tendon tear grading was positively correlated with patient age. However, the tendon tear grading on MRI was not significantly correlated with the aorta calcification scores on chest radiographs. Furthermore, there was no significant correlation between aorta calcification severity and tendon tear grading. In conclusion, rotator cuff tears did not significantly correlate with aortic calcification severity. This suggests that tendon ischemia may not be associated with the degree of macrovascular disease.
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Shaprynskyi, V. V., and O. G. Urvan. "Morphological features of structural rearrangement of atherosclerotic plaque in patients with occlusive-stenotic diseases of the main arteries." Reports of Vinnytsia National Medical University 26, no. 3 (September 29, 2022): 354–58. http://dx.doi.org/10.31393/reports-vnmedical-2022-26(3)-01.
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Annotation. According to the set goal of the work, we analyzed the results of morphological studies of atherosclerotic plaque in patients with occlusive-stenotic diseases of the arteries of the lower extremities as a consequence of obliterating atherosclerosis. The material of the study was fragments of the arteries of 12 patients affected by atherosclerotic plaque, taken during open surgical interventions on different arterial segments, and in 8 cases, autopsy material of atherosclerotic plaques of the femoral and tibial arteries was selected. The histological research method is applied. It is established that atherosclerotic plaque in the process of its development goes through a number of stages from lipid spot to atheromatosis, calcification and fibrosis with the development of complications such as ulceration, hemorrhage, thrombosis. In addition, the severity of atherosclerotic plaque leads to vascular stenosis and significant local or systemic hemodynamic changes, and thus determines the indications for a particular type of surgery for occlusive-stenotic diseases of the main arteries.
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Stakhneva, Ekaterina M., Irina A. Meshcheryakova, Evgeny A. Demidov, Konstantin V. Starostin, Evgeny V. Sadovski, Sergey E. Peltek, Michael I. Voevoda, Alexander M. Chernyavskii, Alexander M. Volkov, and Yuliya I. Ragino. "A Proteomic Study of Atherosclerotic Plaques in Men with Coronary Atherosclerosis." Diagnostics 9, no. 4 (November 7, 2019): 177. http://dx.doi.org/10.3390/diagnostics9040177.
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Background: To study the changes in protein composition of atherosclerotic plaques at different stages of their development in coronary atherosclerosis using proteomics. Methods: The object of research consisted of homogenates of atherosclerotic plaques from coronary arteries at different stages of development, obtained from 15 patients. Plaque proteins were separated by two-dimensional electrophoresis. The resultant protein spots were identified by the matrix-assisted laser desorption ionization method with peptide mass mapping. Results: Groups of differentially expressed proteins, in which the amounts of proteins differed more than twofold (p < 0.05), were identified in pools of homogenates of atherosclerotic plaques at three stages of development. The amounts of the following proteins were increased in stable atherosclerotic plaques at the stage of lipidosis and fibrosis: vimentin, tropomyosin β-chain, actin, keratin, tubulin β-chain, microfibril-associated glycoprotein 4, serum amyloid P-component, and annexin 5. In plaques at the stage of fibrosis and calcification, the amounts of mimecan and fibrinogen were increased. In unstable atherosclerotic plaque of the necrotic–dystrophic type, the amounts of human serum albumin, mimecan, fibrinogen, serum amyloid P-component and annexin were increased. Conclusion: This proteomic study identifies the proteins present in atherosclerotic plaques of coronary arteries by comparing their proteomes at three different stages of plaque development during coronary atherosclerosis.
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Boström, Kristina I., Jiayi Yao, Pierre J. Guihard, Ana M. Blazquez-Medela, and Yucheng Yao. "Endothelial-mesenchymal transition in atherosclerotic lesion calcification." Atherosclerosis 253 (October 2016): 124–27. http://dx.doi.org/10.1016/j.atherosclerosis.2016.08.046.
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