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.
Full textHinshaw, 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.
Full textFulmer, 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.
Full textBennett, 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.
Full textKoulaouzidis, 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.
Full textМоскаленко, 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.
Full textDhore, 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.
Full textNicoll, 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.
Full textRadomychelski, 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.
Full textRosa, 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.
Full textCardiovascular 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
Garoff, Maria. "Carotid calcifications in panoramic radiographs in relation to carotid stenosis." Doctoral thesis, Umeå universitet, Institutionen för odontologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-119794.
Full textBakgrund Inom ramen för specialist- och allmäntandvård utförs panoramaröntgen-undersökningar dagligen på såväl barn som vuxna. En panoramaröntgenbild (PB) är en översiktsbild som är specifikt anpassad till att återge området för tänder och käkar. Utöver det, avbildas även delar av halsen och som bifynd ibland förkalkningar belägna i området för halspulsådern (karotiskärlet). Dessa förkalkningar kallas för karotisförkalkningar och är ett tecken på åderförkalkning. Åderförkalkning består i huvudsak av en fettrik plackansamling i kärlväggen. Placket kan med tiden förkalkas till varierande grad. Det är dessa förkalkningar vi kan se i PB. När en åderförkalkning ökar i volym kan den utgöra en förträngning i kärlet. Då förträngningen av kärldiametern är ≥ 50% benämns åderförkalkningar belägna i karotiskärlet för ”signifikanta karotisstenoser” (SKS). Graden av förträngning bedöms som regel med ultraljudsundersökning av halskärlen. Bitar av SKS kan lossna varvid det bildas små blodproppar. Eftersom halspulsådern försörjer främre hjärnhalvan med blod så kan dessa bitar täppa till ett av hjärnans blodförsörjande kärl och leda till stroke (slaganfall). För att minska risken att drabbas av stroke kan man ibland operera bort SKS (karotisplacket). Syfte Syftet med denna avhandling var att ta reda på (1) hur många av de patienter som blir undersökta med PB inom tandvården som uppvisar karotisförkalkningar, hur stor andel som har SKS samt utreda om patienter med förkalkningar i PB i större utsträckning är drabbade av hjärtkärlsjukdomar/risk faktorer, (2) hur ofta utopererade karotisplack innehåller kalk och hur ofta patienter med känd SKS uppvisar karotisförkalkningar i PB, (3) huruvida förkalkningsmängden i utopererade karotisplack är korrelerad till förträngningsgrad, och (4) huruvida det finns något specifikt radiografiskt utseende på karotisförkalkningar i PB som kan användas för att identifiera en större andel patienter med SKS bland patienter som uppvisar karotisförkalkningar i PB, det vill säga minska risken för att skicka patienter utan SKS på ultraljudsundersökning. Material och metoder Materialet bestod av två huvudgrupper av patienter. Grupp A bestod av patienter undersökta inom tandvården med PB som uppvisat karotisförkalkningar. Alla dessa patienter undersöktes med ultraljud för att bedöma förekomst av SKS. Den medicinska journalen granskades avseende tidigare förekomst av åderförkalkningsrelaterade sjukdomar och risk faktorer. En köns- och åldersmatchad kontrollgrupp utan karotisförkalkningar i PB analyserades på motsvarande sätt för jämförelse. Grupp B bestod av patienter med känd SKS som före operativt avlägsnande av karotisplack undersöktes med PB. PB granskades avseende förekomst av karotisförkalkning och utopererade karotisplack avseende kalkinnehåll. Förkalkningsmängden i de utopererade karotisplacken korrelerades dels till möjlighet att identifiera karotisförkalkning i PB samt till förträngningsgraden i kärlen. Karotisförkalkningarnas utseende delades in i grupper för att utvärdera om vissa utseenden i större utsträckning kunde associeras till förekomst av SKS. Resultat I Grupp A uppvisade 8/117 (7%) patienter SKS, alla var män, 8/64 (12%). Patienter med karotisförkalkningar i PB hade oftare åderförkalkningsrelaterade sjukdomar och risk faktorer (p < 0,001). I Grupp B hade 84% av patienterna med SKS karotisförkalkning i PB. Bland de utopererade karotisplacken innehöll 99% förkalkningar och förkalkningsvolymen varierade från 1-509 mm3. Möjligheten att upptäcka karotisförkalkning i PB var oberoende av om förkalkningsvolymen var stor eller liten. Förkalkningsvolymen var heller inte korrelerad till hur stor förträngning av kärlet en SKS (≥ 50%) orsakat. Ett radiografiskt utseende på karotisförkalkningar i PB noterades i 65% av de halssidor som hade en SKS. Detta specifika radiografiska utseende återfanns dock även i 47% av halssidor utan SKS. Andelen falskt positiva patienter var således fortsatt hög. Slutsats Vi fann att 12% män med karotisförkalkningar i PB, undersökta i en generell population inom tandvården, uppvisar SKS. Patienter med karotisförkalkningar i PB uppvisar fler riskfaktorer och är oftare drabbade av hjärt-kärlsjukdomar än patienter utan karotisförkalkningar i PB. Majoriteten av patienter med SKS uppvisar karotisförkalkningar i PB och nära 100% av utopererade karotisplack innehåller kalk. Förkalkningsmängden påverkar inte möjligheten att upptäcka karotisförkalkning i PB. Förkalkningsmängd och specificerade radiografiska utseenden hos karotisförkalkningar i PB förutsäger inte SKS bättre än definitionen ”förkalkning ja eller nej”. Dessa parametrar kan således inte användas till att förfina urvalet bland patienter som uppvisar karotisförkalkning i PB mot högre andel patienter med SKS. Individer med karotisförkalkningar i PB bör uppmanas konsultera vården för undersökning av eventuella risk faktorer för hjärt-kärlsjukdom.
Fulmer, Makenzie. "Role of Cannabinoid Receptor Type 2 (CB2) in Late Stage Atherosclerosis." Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/etd/3328.
Full textBoon, Arthur Edwin. "Cardiac and vascular riskfactors in stroke the role of cardiac valve calcification and silent brain infarcts /." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1996. http://arno.unimaas.nl/show.cgi?fid=7392.
Full textIvanovski, Ognen. "New insights into atherosclerosis and vascular calcification in an experimental mouse model of chronic renal failure." Paris 6, 2006. http://www.theses.fr/2006PA066182.
Full textDube, Prabhatchandra R. "“Mechanisms of Calcification in Atherosclerosis: Role of Macrophages and the Transient Receptor Potential Canonical 3 (TRPC3) Channel”." University of Toledo Health Science Campus / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=mco1512574541600974.
Full textJashari, Fisnik. "Carotid artery disease : plaque features and vulnerability." Doctoral thesis, Umeå universitet, Kardiologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-111048.
Full textEccles, Bree A. "Effect of Cannabinoids on Osteogenic Differentiation of Cultured Vascular Smooth Muscle Cells." Digital Commons @ East Tennessee State University, 2017. https://dc.etsu.edu/honors/392.
Full textGrzesiak, Lucile. "Rôle de la leucine-rich alpha-2 glycoprotein 1 (LRG1) dans le développement de complications de plaque." Thesis, Toulouse 3, 2022. http://www.theses.fr/2022TOU30080.
Full textAtherosclerosis is the primary cause of cardiovascular disease. The development of plaque complications such as calcification and neo-angiogenesis strongly impacts plaque stability and is a good predictor of mortality in patients with atherosclerosis. Despite some known risk factors of plaque complications like diabetes mellitus and chronic kidney disease, the mechanisms involved are still not fully understood. We and others have identified that the concentration of circulating leucine-rich α-2 glycoprotein 1 (LRG1) was increased in diabetic and chronic kidney disease patients. Using Apolipoprotein E knockout (ApoE KO) mice fed with high fat diet, we showed that plasma LRG1 was also increased in a mouse model of atherosclerosis. We also observed that LRG1 was present in complicated calcified plaque in vivo and that LRG1 was preferentially localised in calcification areas in mice. This result was also confirmed in human carotid endarterectomy specimens. In vitro we showed that LRG1 expression was enhanced in endothelial cells by inflammatory mediators such as Tumor necrosis factor-alpha (TNF-α). Interestingly, LRG1 is known to bind a co-receptor of the Transforming growth factor beta (TGF-β) family, a pathway largely described to control the calcification process in vascular smooth muscle cells (VSMC). Accordingly, we researched the role of LRG1 on VSMC calcification and we identified that LRG1 was able to induce VSMC calcification in vitro by increasing calcium content and the expression of osteoblastic markers. In conclusion, our results identified for the first time a role of LRG1 on vascular calcification and suggest a role of this molecule in the development of plaque complications in patients with atherosclerosis
Mlih, Mohamed. "Implication de LRP1 et ShcA dans deux pathologies cardiovasculaires : l'arthérosclérose et l'insuffisance cardiaque." Thesis, Strasbourg, 2012. http://www.theses.fr/2012STRAJ086/document.
Full textCardiovascular disease is the number one cause of death worldwide. A better understanding of the pathophysiological mechanisms is necessary. In this thesis we are focused on two cardiovascular diseases: atherosclerosis and heart failure. Recently, we identified the LRP1 receptor and the adapter protein ShcA as two proteins involved in two of these cardiovascular diseases. We have shown that ShcA exerts a protective role against heart failure. Mutant mice lacking ShcA in the heart exhibit a dilated cardiomyopathy with reduced cardiac contractility. Myocyte ultrastructure analysis shows that Shc A is essential to maintain sarcomeric intégrity in early embryonic heart development. in last part we have shown vascular calcification in the absence of PPARgamma requires expression of LRP1 in vascular smooth muscle cells. LRP1 promotes a Wnt5a-dependent prochondrogenic pathway. We show that PPARgamma protects against vascular calcification by inducing the expression of secreted frizzled-related protein-2 (Sfrp2, wich functions as a Wnt5a antagonist
Zecchin, Mathilde. "Le rôle du récepteur nucléaire Rev-erb-α dans les maladies inflammatoires : la régulation circadienne du complexe inflammasome NLRP3 dans l'hépatite fulminante et l'inhibition du développement de l'athérosclérose et de la calcification vasculaire." Thesis, Lille, 2018. http://www.theses.fr/2018LILUS057.
Full textAtherosclerosis is chronic inflammatory disease of the vascular wall, which consists inthe accumulation of Low Density Lipoproteins (LDL) into the vascular wall triggering theinternalization of leucocytes. Recruited monocytes differentiate into macrophages to removeLDL through the so-called reverse cholesterol transport pathway. However, when flux isimpaired, lipid-laden macrophages become foam cells leading to their apoptosis or necrosis.Their lipid content and cellular debris are then released in the extracellular matrix, thus formingthe necrotic core. In addition, laden-cholesterol crystals trigger lysosomal damage inmacrophage, which activates the NLRP3 inflammasome complex. NLRP3 inflammasome isinvolved in the maturation of the pro-caspase 1, which subsequently cleaves the pro- IL1B andpro-IL18 into mature IL1B and IL18. These interleukins are then released and stimulate thesecretion of interferon γ by CD4+ T cells, leading to the proliferation and the migration ofSmooth Muscle Cells (SMC) toward the necrotic core to form the fibrous cap. In addition tothe numerous risk factors of cardiovascular diseases such as diabetes or smoking, disruption ofdaily rhythms, as seen in shiftwork, increases the incidence of these diseases. Beyond its majorrole in metabolism and inflammation control, the nuclear receptor Rev-erb-α is also a corecomponent of the molecular clock. Altogether, it thus represents a putative therapeutic target inthe treatment of such multifactorial diseases related to clock impairment. My work shows thatthe deletion of Rev-erbα in a murine model of atherosclerosis (LDLr-/-) leads to an increase inplasma lipid levels and accelerates atherogenesis. In addition, Rev-erb-α regulates the circadianexpression of the NLRP3 pathway components as well as the subsequent secretion of IL1B andIL18 in primary human and mouse macrophages. At the molecular level, Rev-erb-α directlyrepresses the NLRP3 pathway, whereas Rev-erbα deficiency enhances its activation. Thismechanism may regulate the circadian susceptibility to inflammatory stimuli depending on thetime of challenge in acute inflammation models such as fulminant hepatitis or peritonitis. Theabsence of Rev-erbα also induces the expression of Nlrp3, Il1β and Il18 in models of chronicinflammation such as atherosclerosis as well as the expression of NLRP3 in lesionalmacrophages. In addition, IL1B and IL18 stimulate the differentiation of SMCs into osteoblastlikecells that form intimal calcification. It is noteworthy that Rev-erbα deletion in LDLr-/- miceis associated to an increase in lesion calcification in vivo, while the absence of Rev-erb-α inprimary SMCs increases their differentiation into osteoblasts and the formation of calciumdeposit in vitro. Interestingly, this differential effect observed on calcium deposition in vitro isexacerbated when primary SMCs are stimulated in culture with IL1B. Therefore, Rev-erb-α may be involved not only in macrophage-mediated IL1B production but also in the sensing ofsuch signal by SMCs. Conversely, treatment with Rev-erb ligands inhibits these effects. Thiswork emphasizes the key role of Rev-erb-α in the circadian regulation of the inflammatoryresponse and in the development of cardiovascular diseases, thus identifying Rev-erb-α as anew therapeutic target that act on several aspects of the pathology
Harada, Paulo Henrique Nascimento. "Avaliação da associação da gordura pericárdica medida pela tomografia computadorizada com o escore de cálcio coronário em pacientes renais crônicos não dialíticos." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-23112015-164730/.
Full textPericardial fat (PF), a component of visceral adipose tissue has been consistently related to coronary atherosclerosis in the general population. This study evaluated the association between PF and coronary artery calcification (CAC) in non-dialysis dependent chronic kidney disease (CKD) patients. This is a post-hoc cross sectional analysis of the baseline of a prospective cohort of 117 outward CKD patients without manifest coronary artery disease (age, 56.9 ± 11.0 years, 64,1% males, 95.1% hypertensive, 25.2% diabetics, 15.5% ever smokers, CKD stage 2 to 5 with estimated glomerular filtration rate 36.8 ± 18.1 ml/min). CAC scores, PF volume and abdominal visceral fat (AVF) areas were measured by computed tomography. The association of PF as a continuous variable with the presence of CAC was analyzed by multivariate logistic regression. CAC (calcium score >0) was present in 59.2% patients. On the comparison with patients with no CAC, those with CAC were 10 years older on average, had a higher proportion of male gender (78.7% vs. 42.9%, p < 0.001), and had higher values of waist circumference (95.9 ± 10.7 versus 90.2 ± 13.2 cm, p=0.02), PF volumes (224.8±107.6 versus 139.1±85.0 cm³, p < 0.01) and AVF areas (109.2 ± 81.5 versus 70.2 ± 62.9 cm², p=0.01). In the multivariate analysis, adjusting for age, gender, diabetes, smoking and, left ventricular concentric hypertrophy, PF was significantly associated with the presence of CAC (OR: 1.88 95% CI: 1.03-3.43 per standard deviation, p=0.04). PF remained associated with CAC even after additional adjustments for estimated glomerular filtration rate or serum phosphorus (OR: 1.85 95% CI: 1.00-3.42, p=0.05). PF is independently associated with CAC in non-dialysis dependent CKD patients
Ribeiro, Giovana Gomes. "Calcificação prematura de artérias coronárias no lúpus eritematoso sistêmico: associação com duração de doença e densidade mineral óssea." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5145/tde-16062009-164313/.
Full textObjective: To evaluate the relevance of traditional cardiovascular risk factors (CVR), disease-related risk factors and bone mineral density (BMD) for premature coronary artery calcification (CAC) in young female systemic lupus erythematosus (SLE). Methods: Ninety-four female SLE patients 5 years disease duration and age <45 years were consecutively selected for this study. Cardiovascular risks (CVR) analyzed were: diabetes mellitus, arterial hypertension, dyslipoproteinemia, smoking, body mass index (BMI), ovarian and renal insufficiency. SLE-related risk factors evaluated were: disease duration, ACR criteria, modified SLICC/ACR (excluding atherosclerosis-related scores), SLEDAI, glucocorticoid and cyclophosphamide treatment. Bone mineral density (BMD) in whole body, lumbar spine and femoral neck was assessed by dual X ray absorptiometry (DXA). Coronary artery calcification was determined using the 16-slice multidetector computed tomography. Results: Premature coronary artery calcification was identified in 12 (12.7%) patients and was associated with a higher frequency of patients with CVR (p=0.008), a higher mean number of CVR (p=0.003), mean age (p= 0.025), mean disease duration (p=0.011) and mean SLICC (p=0.011). Individual analysis of CVR demonstrated that the presence of menopause (p= 0.036), dyslipidemia (p= 0.003) and hypertension (p=0.006) were significantly associated with coronary calcification. Additionally, premature calcification was associated with a lower whole body BMD (p=0.013). Multiple logistic regression analysis using CVR, age, disease duration, SLICC and whole body BMD revealed that only disease duration (p=0.042) and whole body BMD (p=0.023) remained significant factors for coronary calcification. Conclusion: We have identified that disease duration and decreased BMD are independent predictors for premature coronary calcification in young women with SLE, suggesting a common underlying mechanism
Laurinavicius, Antonio Gabriele. "Avaliação da aterosclerose subclínica em portadores de HDL-colesterol marcadamente elevado." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-06062016-103124/.
Full textHDL-c is a negative cardiovascular risk factor and its plasma concentration is inversely related to the incidence of cardiovascular events. However, evidence of benefit among subjects with HDL-c levels above the 95th percentile of the general population is still scarce and the impact of hyperalphalipoproteinemia (HALP) on cardiovascular risk continues to represent matter of debate in the medical literature. Some studies with specific populations indicated an increased cardiovascular risk associated with HALP. In addition, other reports identified groups of patients with marked hypoalphalipoproteinemia and longevity. Hence, there could be a dissociation between HDL-c levels and cardiovascular risk in certain populations, possibly due to dysfunctional HDL particles. The aim of this study was to investigate the role of HALP phenotype in determining cardiovascular risk; to compare the prevalence of subclinical cardiovascular disease, assessed by ultrasound measurement of Carotid Intima-Media Thickness (CIMT) among patients with HDL-c >= 90mg/dL (HALP group) and patients with HDL-c currently considered normal (40-50mg/dL for men and 50-60mg/dL for women); and to evaluate HDL functionality in patients with HALP through the study of its composition, its cholesterol efflux capacity, and its anti-inflammatory and antioxidant activity; correlating those characteristics with the presence of subclinical cardiovascular disease assessed by CIMT, Pulse Wave Velocity (PWV) and Coronary Artery Calcification (CAC). To answer these questions, the present study was articulated into two arms: Arm 1: ELSA-Brasil study cohort analysis in order to assess HALP prevalence in a general population, defining demographic, anthropometric and metabolic profile of HALP individuals; and comparing the prevalence of subclinical vascular disease among HALP subjects with controls with normal HDL-c. Arm 2: Recruitment of 80 healthy volunteers with HALP to study the correlation between subclinical vascular disease and HDL functionality in this group. Our study led to four main conclusions: 1) markedly elevated HDL-c is associated with lower CIMT compared to the control group with normal HDL-c levels. Although individuals with HALP display a more favorable metabolic profile than subjects with normal HDL-c, the association between CIMT and HALP was independent of traditional risk factors, indicating that the lower prevalence of subclinical vascular disease in this group is only partially justified by the lower prevalence of cardiovascular risk factors; 2) Although HALP can be regarded as an atheroprotective phenotype, there are individuals with markedly elevated levels of HDL-c who develop cardiovascular disease. Our results indicate good correlation of the three methods here adopted to study subclinical vascular disease among HALP patients: CIMT, VOP and CAC; 3) Traditional risk factors continue to exert their weight in determining cardiovascular risk in patients with HALP. Age, smoking, hypertension, hypertriglyceridemia and high levels of LDL-c were significantly associated with the presence of subclinical vascular disease among HALP individuals; 4) the assessment of the HDL composition and functionality in patients with HALP may allow to identify individuals specifically more susceptible to atherosclerosis. Our results indicate that, in particular, cholesterol efflux capacity, the anti-inflammatory activity of HDL, and triglyceride transfer capacity were independently associated with lower CIMT in HALP individuals, while higher levels of Apo A-IV were associated with a greater burden of subclinical cardiovascular disease
Miranda, Érique José Peixoto de. "Associação entre doença tireoidiana subclínica, aterosclerose coronariana, índice de espessura de médio-íntima carotídea e rigidez arterial aórtica em análise transversal do Estudo Longitudinal de Saúde do Adulto (ELSA-Brasil)." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5169/tde-19062017-154141/.
Full textIntroduction: Subclinical thyroid disease includes subclinical hypothyroidism and subclinical hyperthyroidism. Association between subclinical thyroid disease and cardiovascular morbidity and mortality is controversial and data about the relationship between those clinical conditions and subclinical atherosclerosis is scarce. Objectives: This study aims to evaluate the association between subclinical thyroid disease, coronary artery calcification (CAC), coronary artery disease (CAD), mean common carotid intima-media thickness (IMT) and carotid-femoral pulse wave velocity (cf-PWV) in the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). Methods: We included euthyroid subjects, defined as TSH between 0.4 and 4.0 mIU/l and FT4 between 0.8 and 1.9 ng/dL, and individuals with subclinical hypothyroidism, defined as TSH > 4.0 mIU/l and normal FT4, and subclinical hyperthyroidism, defined as TSH < 0.4 mIU/L and normal FT4. We excluded individuals with other thyroid disorders, subjects who used medication that altered thyroid function, subjects with past of cardiovascular disease. In computed angiotomography analysis, we have excluded subjects with subclinical hyperthyroidism because of the small sample, and in cf-PWV analysis, we have excluded individuals with chronic kidney disease, use of anti-hypertensive and diuretics. The association between TSH quintiles was evaluated in logistic regression models for CAC and CAD, and the association between IMT, cf-PWV (as continuous variables or as factor, categorized at 75th sample\'s percentile) and TSH levels or subclinical thyroid diseases was evaluated by multivariate logistic and linear regression models. All models were adjusted for demographic variables and cardiovascular risk factors. Results: CAC analysis included 3,836 subjects, median of age 49 years (IQR=44-56), 1,999 (52.1%) women. CAC > 100 was independently associated with first quintile of TSH, using the third quintile as the reference (adjusted OR=1.57, 95% CI=1.05-2.35, P=0.027). Computed angiotomography analysis included 796 subjects, median of age 55 years (IQR=48-60), 406 (51%) women. CAD and CAC > 0 was independently associated with first quintile in comparison with third quintile (adjusted OR=1.73, 95% CI=1.08-2.79, P=0.023 and adjusted OR=1.76, 95% CI=1.09-2.82, P= 0.02, respectively), but not with burden of disease. In IMT analysis, 8,623 subjects were included, median of age 50 years (IQR=45-57 years), 4,624 (53.6%) women in the subclinical hypothyroidism subanalysis, and 8,193, median age 50 years (IQR = 44-57 years), 4,382 (53.5%) women, in the subclinical hyperthyroidism subanalysis. Subclinical hypothyroidism, but not subclinical hyperthyroidism, was independently associated with IMT as continuous variable (beta=0.010, IC 95%=0.0004-0.019, P=0.041) or as factor categorized at 75th percentile adjusted for age, sex and race (adjusted OR=1.30, 95% CI=1.07-1.61, P=0.010). In cf-PWV analysis, 8,341 subjects were included, median of age 50 years (IQR=44-56 years), 4,383 (52.5%) women in the subclinical hypothyroidism subanalysis, and 7,790, median age 50 years (IQR = 44-57 years), 4,191 (53.8%) women in subclinical hyperthyroidism subanalysis. Cf- PWV was not associated with subclinical thyroid disease. Conclusion: In separated analysis, CAC and CAD was independently associated with first quintile of TSH using the third as the reference; IMT was independently associated with subclinical hypothyroidism, and cf-PWV was not associated with subclinical thyroid diseases
Ahmad, Pamela. "The Effect of Ddr1 Deletion on the Expression of Genes Involved in Atherosclerotic Vascular Remodeling and on the Development of Atherosclerotic Calcification." Thesis, 2008. http://hdl.handle.net/1807/16797.
Full text"Serum high-sensitivity C-reactive protein concentration of Chinese chronic-renal-failure patients with atherosclerotic vascular disease or cardiac valve calcification." 2002. http://library.cuhk.edu.hk/record=b5895944.
Full textThesis (M.Sc.)--Chinese University of Hong Kong, 2002.
Includes bibliographical references (leaves 85-93).
Abstracts in English and Chinese.
ACKNOWLEDGEMENTS --- p.4
SUMMARY --- p.5
ABBREVIATIONS --- p.9
LIST OF TABLES --- p.11
LIST OF FIGURES --- p.13
Chapter CHAPTER I --- INTRODUCTION --- p.14
Chapter 1.1 --- The Historical Aspects of C-Reaction Protein --- p.15
Chapter 1.2 --- Biochemistry of CRP --- p.16
Chapter 1.3 --- Physiology of CRP --- p.18
Chapter 1.4 --- Current Clinical Applications of Serum CRP Assay --- p.19
Chapter 1.5 --- Recent Findings of CRP --- p.21
Chapter 1.5.1 --- Pathophysiology of atherosclerosis --- p.22
Chapter 1.5.2 --- A nother atherogenic risk factor: hs- CRP --- p.26
Chapter 1.5.3 --- Can hs-CRP replace other risk factors? --- p.30
Chapter 1.5.4 --- Altering hs-CRP result in medication --- p.32
Chapter 1.6 --- Methods of Measurement of CRP Concentration --- p.33
Chapter 1.7 --- Analytical Considerations in the Measurement of hs-CRP --- p.34
Chapter CHAPTER II --- OBJECTIVES AND SIGNIFICANCE --- p.36
Chapter 2.1 --- Objectives --- p.37
Chapter 2.2 --- Issues and Problems --- p.37
Chapter 2.3 --- Significance and Value of this Study --- p.38
Chapter CHAPTER III --- MA TERIALS AND METHODS I Setting up the serum hs-CRP assay on the Hitachi 911 Analyzer --- p.39
Chapter 3.1 --- Materials --- p.40
Chapter 3.1.1 --- Reagents from Roche Diagnostics --- p.40
Chapter 3.1.2 --- Reagents for the Beckman Coulter Array ® Analyzer --- p.40
Chapter 3.1.3 --- In-house reagents --- p.41
Chapter 3.2. --- Apparatus and Equipment --- p.41
Chapter 3.2.1 --- Hitachi 911 Analyzer --- p.41
Chapter 3.2.2 --- Beckman Coulter Array ® 360 Analyzer --- p.42
Chapter 3.3 --- The Tina-quant a C-Reactive Protein (Latex) Ultrasensitive Assay --- p.42
Chapter 3.3.1 --- Priniciple of the Dual-Radius Enhanced Latex (DuREL´ёØ) technology --- p.42
Chapter 3.3.2 --- Assessment of Analytical Performance --- p.45
Chapter CHAPTER IV --- MA TERIALS AND METHODS II Serum hs-CRP in Chinese chronic-renal-failure patients with atherosclerotic vascular disease or cardiac valve calcification --- p.48
Chapter 4.1 --- Patient Recruitment --- p.49
Chapter 4.2. --- Blood Specimens --- p.49
Chapter 4.3 --- Assay Methods --- p.50
Chapter 4.3.1 --- hs-CRP --- p.50
Chapter 4.3.2 --- TC --- p.50
Chapter 4.3.3 --- TG --- p.51
Chapter 4.3.4 --- HDL-C --- p.51
Chapter 4.3.5 --- LDL-C --- p.52
Chapter 4.3.6 --- Apo A-1 --- p.52
Chapter 4.3.7 --- Apo B --- p.53
Chapter 4.3.8 --- Lp(a) --- p.53
Chapter 4.4 --- Ultrasound measurement of carotid artery inter-media thickness --- p.53
Chapter 4.5 --- Statistical analysis --- p.54
Chapter CHAPTER V --- RESUTLSI Setting up the serum hs-CRP assay on the Hitachi 911 Analyzer --- p.55
Chapter 5.1 --- Imprecision --- p.56
Chapter 5.2 --- Linearity --- p.56
Chapter 5.3 --- Recovery --- p.56
Chapter 5.4 --- Detection Limit --- p.57
Chapter 5.5 --- Carry-over --- p.57
Chapter CHAPTER VI --- RESULTS II Serum hs-CRP in Chinese chronic-renal-failure patients with atherosclerotic vascular disease or cardiac valve calcification --- p.63
Chapter 6.1 --- Patient Recruitment --- p.64
Chapter 6.2 --- Chinese chronic-renal-failure patients with AVD --- p.64
Chapter 6.3 --- Chinese chronic-renal-failure patients with CVC --- p.65
Chapter CHAPTER VII --- DISCUSSION I Performance of the serum hs-CRP assay on the Hitachi 911 Analyzer --- p.75
Chapter 7.1 --- "Imprecision, Detection Limit, Linearity, and Recovery of hs-CRP Assay" --- p.76
Chapter 7.1.1 --- Imprecision --- p.76
Chapter 7.1.2 --- Detection Limit --- p.76
Chapter 7.1.3 --- Linearity --- p.76
Chapter 7.1.4 --- Recovery --- p.77
Chapter 7.2 --- Overall Performance --- p.77
Chapter CHAPTER VIII --- DISCUSSION II Serum hs-CRP in Chinese chronic-renal-failure patients with atherosclerotic vascular disease or cardiac valve calcification --- p.79
Chapter 8.1 --- CAPD Patients --- p.80
Chapter 8.2 --- Serum hs-CRP Concentration of AVD and CVC Patients --- p.81
Chapter 8.3 --- Other risk factors in AVD and CVC Patients --- p.82
Chapter 8.4 --- Conclusion --- p.83
REFERENCES --- p.85
Lee, Guan-Lin, and 李冠霖. "The Role of TLR2 and TLR4 in Atherosclerosis and Vascular Calcification." Thesis, 2016. http://ndltd.ncl.edu.tw/handle/9v349a.
Full text國防醫學院
生命科學研究所
105
Abnormal activation of components of the innate immune system, such as Toll-like receptor (TLR), has been implicated in the pathological progression of metabolic inflammatory diseases including atherosclerosis and vascular calcification. Functional phenotype of vascular smooth muscle cells (VSMCs) is considered to be a vital event in the pathophysiology of atherosclerosis. Despite substantial evidence supporting the pathogenic role of TLR2 and TLR4 in the progression of vascular diseases, their roles in the regulation of VSMC function remains unclear. The goal of the present study was to elucidate the mechanism by which TLR2 and TLR4 regulate VSMC function and phenotypic switching. Migration assay revealed that activation of TLR2 and TLR4 by their specific agonists induced VSMCs migration. Inhibition experiments indicated that IL-6 secretion and VSMC migration induced by agonists of TLR2 and TLR4 were mediated through the activation of p38 mitogen-associated protein kinase (p38 MAPK) and extracellular signal–regulated kinase (ERK) 1/2 signaling. Neutralizing anti-IL-6 antibodies abrogated TLR2 and TLR4-driven VSMC migration and F-actin polymerization. Blockade of p38 MAPK or ERK1/2 signaling cascade inhibited agonists of TLR2 and TLR4-mediated activation of cAMP response element binding protein (CREB). Moreover, siRNA-mediated suppression of CREB production repressed IL-6 production and VSMC migration-induced by TLR2 and TLR4. Rac-1 inhibitor suppressed TLR2 and 4-driven VSMC migration but not IL-6 production. Further experiments with inhibitors and siRNA found that TLR4 activates PI3K/ATK signaling to induce F-spondin expression, subsequently controls CREB-mediated IL-6 production to promote VSMC migration. These findings provide mechanismistic insights into the essential role of F-spondin in VSMC function and atherosclerosis. In addition to VSMC migration, agonists of TLR2 and TLR4 also promoted VSMC chondrogenesis and calcification as demonstrated by Alcian blue and Alizarin red S (ARS) staining. Neutralizing anti-IL-6 antibodies attenuated TLR2 and TLR4-mediated VSMC chondrogenesis, but did not affect VSMC calcification. Interestingly, TLR2 and TLR4 activated c-Jun N-terminal kinases (JNKs) - and ERK1/2 signaling to downregulate calcification inhibitor, osteoprotegerin (OPG) levels, which in turn not only promoted VSMC chondrogenesis but also trigged VSMCs calcification. Importantly, the lower OPG level and increased atherogenic calcification were clearly detected in high-fat diet (HFD)-fed ApoE-/- mice compared with HFD-fed ApoE-/-Tlr2-/- mice. Based on our findings, we concluded that, upon specific ligand binding, both TLR2 and TLR4 activate MAPKs to trigger VSMC migration and VSMC chondrogenesis, which in turn progressively triggers atherogenesis and atherogenic calcification.
Akers, Emma Jill. "The role of lipoproteins in vascular calcification and plaque stabilisation." Thesis, 2021. https://hdl.handle.net/2440/133847.
Full textThesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2021
Irkle, A., A. T. Vesey, D. Y. Lewis, J. N. Skepper, Joseph Bird, M. R. Dweck, F. R. Joshi, et al. "Identifying active vascular microcalcification by 18F-sodium fluoride positron emission tomography." 2015. http://hdl.handle.net/10454/10328.
Full textVascular calcification is a complex biological process that is a hallmark of atherosclerosis. While macrocalcification confers plaque stability, microcalcification is a key feature of highrisk atheroma and is associated with increased morbidity and mortality. Positron emission tomography and X-ray computed tomography (PET/CT) imaging of atherosclerosis using 18F-sodium fluoride (18F-NaF) has the potential to identify pathologically high-risk nascent microcalcification. However, the precise molecular mechanism of 18F-NaF vascular uptake is still unknown. Here we use electron microscopy, autoradiography, histology and preclinical and clinical PET/CT to analyse 18F-NaF binding. We show that 18F-NaF adsorbs to calcified deposits within plaque with high affinity and is selective and specific. 18F-NaF PET/CT imaging can distinguish between areas of macro- and microcalcification. This is the only currently available clinical imaging platform that can non-invasively detect microcalcification in active unstable atherosclerosis. The use of 18F-NaF may foster new approaches to developing treatments for vascular calcification.