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Shafi, Shahida. "The uptake of low density lipoproteins by vessel walls in relation to atherosclerosis." Thesis, King's College London (University of London), 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338174.
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Peel, Andrew. "The development and application of a novel assay for apolipoprotein B-48." Thesis, University of Surrey, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334576.
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Isherwood, Samantha Gail. "Apolipoprotein B-48 as a marker for chylomicrons and their remnants : studies in the postprandial state." Thesis, University of Surrey, 1996. http://epubs.surrey.ac.uk/842779/.
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Dietary-derived lipoproteins, chylomicrons (CM) and CM remnants (CMR), have been implicated in the progression of cardiovascular disease. Retinyl esters are currently the most widely used method for monitoring CM metabolism. The availability, however, of a specific antisera to apo B-48, the protein uniquely associated with dietary-derived lipoproteins, has allowed more extensive investigation of CM and CMR metabolism. The effect of habitual, moderate levels of exercise (3 to 4 exercise sessions a week) on the lipaemic response to meals of varying fat content was assessed in young male subjects. Apo B-48, triacylglycerol (TAG) and retinyl ester were used as markers for CM particles. Active subjects had a lower response than an inactive group in all parameters measured over time after the meals. Lipoprotein lipase (LPL) activity levels measured at the end of the postprandial period were higher in the active group. The area under the time-response curves (AUC) for apo B-48 in the inactive group increased with increasing fat content of the meals, whereas the AUC for apo B-48 was the same after each meal in the active group. Validation of a specific ELISA for apo B-48 was carried out. Cross-reactivity of the antisera with low levels of apo B-100, the protein present on endogenous lipoproteins, was ruled out. The assay was specific and sensitive for measuring apo B-48 concentrations in the CM-enriched fractions. The use of the assay in the current format for plasma samples could not be fully assessed due to difficulties with isolating a pure, concentrated sample of apo B-100 and problems with reactivity between the secondary antibody used in the assay and plasma proteins. The assay was useful for showing postprandial patterns of changes in apo B-48 levels in plasma. The effects of meal frequency on the lipaemic response to a high fat test meal challenge were assessed in an intervention study. A nibbling diet was found to cause differences between the response of various parameters after the meal (NEFA-AUC, LPL activity, infranatant-TAG AUC and time to peak) compared with the normal meal frequency. The size and density distribution of CMR in plasma were investigated. Apo B-48 was found in the IDL and LDL fractions in both the postabsorptive and postprandial states. A comparison between the retinyl ester and apo B-48 responses in the postprandial studies showed that the time to peak retinyl ester level was delayed compared to apo B-48 and TAG. The importance of apo B-48 for studying the metabolism of CM and CMR metabolism was demonstrated.
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Junit, Sarni Mat. "Regulation of human HMGCoA reductase and LDL receptor gene expression in relation to coronary heart disease and diet." Thesis, University of Nottingham, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387665.
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Bolton, Jennifer Lynn. "Candidate genotypes in prediction of coronary heart disease." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/15877.
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Introduction There has been much discussion on personalised medicine; however use of genotype in risk prediction for coronary heart disease (CHD) has not resulted in appreciable improvements over non-genetic risk factors. The primary aim was to determine whether candidate single nucleotide polymorphisms (SNPs) identified from genome-wide association studies improved prediction of CHD over conventional risk factors (CRF). The secondary aim was to determine whether the use of apolipoproteins or lipoprotein(a) improved risk prediction of CHD. Methods Analyses used the Edinburgh Heart Disease Prevention Study (EHDPS), with 1592 men aged 30-59 and follow-up after 20 years; and the Edinburgh Artery Study (EAS), with 1592 men and women aged 54-75 and 15 years of follow-up. Candidate SNPs were identified by systematic literature reviews. CHD status was evaluated as severe (myocardial infarction or coronary revascularisation), and any (severe CHD, angina or non-specified ischaemic heart disease). Cox proportional hazards models were used to evaluate addition of candidate SNPs or lipids to models containing CRF. Results A group of genome-wide significant SNPs resulted in a non-significant improvement in C-index for severe CHD (0.038, p=0.082), and a significant improvement in C-index for any CHD (0.042, p=0.016); the associated net reclassification improvements (NRI) were 20.5% and 18.7%, respectively. Regression trees identified SNPs that were predictive of the remaining variance after adjusting for CRF; this resulted in a significant improvement in C-index for any CHD (0.031, p=0.008). The NRI were 11.0% and 9.6% for severe and any CHD, respectively. When compared with HDL cholesterol/total cholesterol, apolipoprotein AI/total cholesterol yielded a NRI of 3.3% for severe CHD. Lipoprotein(a) improved prediction of severe CHD, with a non-significant improvement in C-index (0.020, p=0.087), and NRI of 11.8%. Conclusion The results of this study indicate that a well selected group of candidate SNPs can improve risk prediction for CHD over-and-above CRF. The inclusion of lipoprotein(a), along with CRF, appeared to improve prediction of severe CHD, but not any CHD.
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Pocathikorn, Anothai. "Low density lipoprotein receptor-related protein (LRP) and its mRNA : influence of genetic polymorphisms, a fat load and statin therapy /." Connect to this title, 2005. http://theses.library.uwa.edu.au/adt-WU2006.0117.
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Mbewu, Anthony David. "Clinical and laboratory studies of lipoprotein (A) in coronary heart disease." Thesis, Queen Mary, University of London, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283731.
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Harris, Christopher Peter David. "Lipoprotein quality, anti-(xanthine oxidase) antibodies and coronary heart disease risk." Thesis, University of Bath, 1995. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.760669.
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Masoud, Mohamed Abdulsalam. "Validation of a recently proposed equation for the estimation of small, dense LDL particles from routine lipid measures in a population of mixed ancestry South Africans." Thesis, Cape Peninsula University of Technology, 2016. http://hdl.handle.net/20.500.11838/2490.
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Thesis (MSc (Biomedical Technology))--Cape Peninsula University of Technology, 2016.Cardiovascular diseases (CVD) are the leading cause of global mortality, of which over 75% occurred in low- and middle-income countries such as South Africa. The lipid profile, specifically decreased levels of high density lipoprotein cholesterol (HDL-C), elevated triglyceride levels and the presence of small-dense low density lipoprotein (sdLDL) has been reported associated with CVD. An increased number of sdLDL is also common in metabolic syndrome (MetS), visceral obesity and diabetes mellitus, the last a known risk factor for CVD. The modification of low density lipoprotein (LDL) size, or number of sdLDL particles, has been reported to significantly reduce CVD risk, but not conclusively so and needs further investigation. In this regard, sdLDL particles are seldom estimated routinely for clinical use because of financial and other limitations. Currently, an alternative approach for estimating sdLDL is to use equations derived from routine lipid measures, as has been proposed by several groups. However, there is a need for extensive evaluation of this equation across different ethnic and disease groups, especially since reports showed an inadequate performance of the equation in a Korean population. The aim of this study was to assess the performance of a recently proposed equation for the estimation of sdLDL in healthy and diabetic mixed ancestry South Africans. Furthermore, we also investigated the role of sdLDL as a cardiometabolic risk factor, as measured against known risk factors such as the glycemic and lipid profiles.
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Roland, Alexander. "Possible protection against cardiovascular disease by plant antioxidants : flavonoids, copper and low density lipoprotein." Thesis, University of Reading, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342119.
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Dane-Stewart, Cheryl Ann. "Postprandial lipoprotein metabolism in patients at high risk of coronary artery disease : effects of statin therapy." University of Western Australia. School of Medicine and Pharmacology, 2003. http://theses.library.uwa.edu.au/adt-WU2004.0061.
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[Formulae and special characters can only be approximated here. Please see the pdf version of the abstract for an accurate reproduction.] Atherosclerosis is a common degenerative disease in which the clinical manifestations are often through stroke or myocardial infarction. Some of the established risk factors for atherosclerosis include elevated plasma low-density lipoprotein (LDL)-cholesterol levels, obesity, diabetes mellitus (DM) and cigarette smoking. Of the risk factors, an elevation in plasma LDL is one of the most established and the most researched. This is partly a consequence of the deposition of cholesterol within arterial intima being a crucial step in the progression of atherosclerosis, combined with the finding that LDL particles are a major transporter of cholesterol in circulation. Recently there is increasing evidence showing a role of the other major transporter of cholesterol in circulation, chylomicron remnants, in the progression of atherosclerosis. The notion of atherosclerosis as a postprandial phenomenon has been further substantiated by the emergence of evidence showing a direct role of chylomicron remnants in arterial cholesterol deposition. Based on evidence that chylomicron remnants are proatherogenic, the suggestion arises that accumulation of postprandial lipoproteins in plasma may add another dimension of risk to the development of coronary artery disease (CAD). This thesis tests the general hypothesis that individuals with or at high risk of CAD have postprandial dyslipidaemia and that this metabolic abnormality is correctable with a class of lipid-lowering drugs called statins. To test the hypothesis, clinical studies were conducted in normolipidaemic CAD patients, heterozygous familial hypercholesterolaemia (FH) and postmenopausal women with type 2 DM. Determination of postprandial dyslipidaemia by comparison with control populations were conducted initially in each patient group (Studies 1, 3 and 5), followed by intervention studies investigating possible modulation of the dyslipidaemia with a statin (Studies 2, 4 and 6). Six observation statements based on case-control comparisons of postprandial lipaemia in patients with or at risk of CAD and the effects of statins on postprandial dyslipidaemia in the patient groups were derived from the general hypothesis. The observation statements were examined in the individual studies described below. Postprandial lipoprotein metabolism was assessed using a number of methods. For comparison of postprandial lipaemia in Studies 1 and 2, a classic oral fat challenge was utilised. As markers of chylomicrons and chylomicron remnants, retinyl palmitate and triglyceride were measured postprandially as well as apolipoprotein (apo) B48 concentrations, a specific marker of intestinal lipoproteins. ApoB48 was also measured in the fasting state and found to predict the postprandial responses of retinyl palmitate, triglyceride and apoB48. This suggested that fasting measurement of apoB48 could be used as a simple indicator of postprandial dyslipidaemia. Consequently for Studies 3 - 6, fasting apoB48 measurements were used as primary markers of postprandial dyslipidaemia. Other markers for chylomicrons and their remnants utilised were fasting plasma concentrations of remnant-like particle-cholesterol (RLP-C) and apoC-III. As well as these static markers, chylomicron remnant catabolism was measured using a stable isotope breath test. The breath test involves the intravenous injection of a chylomicron remnant-like emulsion labelled with ¹³C-oleate and measurement of enriched ¹³CO2 in expired breath by isotope ratio mass spectrometry. The fractional catabolic rate (FCR) of the injected emulsion was subsequently calculated using multi-compartmental modeling (SAAM II). The studies are presented in this thesis as published and unpublished works. In Study 1, postprandial lipoprotein metabolism was compared between 18 normolipidaemic CAD patients (cholesterol 4.54 ± 0.12 mmol/L, triglyceride 1.09 ± 0.16) with 13 asymptomatic healthy controls using an oral fat challenge. Normolipidaemic CAD patients had higher postprandial area-under-curve (AUC) for triglyceride (+34%, p=0.019), retinyl palmitate (+74%, p=0.032) and apoB48 (+36%, p<0.001). Fasting apoB48 was also higher (+41%, p=0.001) and found to correlate significantly with AUC of triglyceride (p=0.017), retinyl palmitate (p=0.001) and apoB48 (p<0.001). The data suggest that normolipidaemic CAD patients have increased concentrations of intestinal lipoproteins in the fasting and postprandial state. In addition to these findings, significant correlations of fasting apoB48 with postprandial markers (p<0.02) suggests the fasting marker to be a simpler surrogate marker for the degree of total postprandial lipaemia. Study 2 investigated the effect of atorvastatin treatment on postprandial dyslipidaemia found in the 18 near-normolipidaemic CAD patients from Study 1. The trial was conducted in a randomised, placebo-controlled design, using oral fat challenges before and after 12-weeks atorvastatin/placebo treatment. Compared with the placebo group, atorvastatin decreased the total postprandial AUC for iii triglyceride (-22%, p=0.05) and apoB48 (-34%, p=0.013). Fasting markers of apoB48 (-35%, p=0.019) and RLP-C (-36%, p=0.032) also decreased significantly. Atorvastatin was also found to increase LDL-receptor activity by +218% (p<0.001) as reflected in binding studies. The data suggest atorvastatin reduces the fasting levels of intestinal lipoproteins as well as total postprandial lipaemia, but without acute dynamic changes in postprandial lipaemia. The reduction in fasting and total postprandial lipoprotein levels could be partly attributed to an increase in LDL-receptor mediated removal from circulation. In Study 3, postprandial lipaemia was compared in 15 heterozygous FH patients with 15 healthy controls. FH patients had higher fasting concentrations of apoB48 (+56%, p<0.001) and RLP-C (+48%, p=0.003). The elevation in these fasting markers of chylomicrons and their remnants suggests FH patients have postprandial dyslipidaemia due to an accumulation of these particles in plasma. Study 4 examined the effects of long- (> 6 months) and short-term (4 weeks) simvastatin treatment on modulating postprandial dyslipidaemia found in the 15 FH patients from Study 3. Short- and long-term simvastatin treatment decreased the fasting concentrations of apoB48 (-29% and 15% respectively, p<0.05) and RLP-C (both -38%, p<0.001), but did not significantly alter the FCR of the injected chylomicron remnant-like emulsion. The data suggest that in heterozygous FH both long- and short-term simvastatin treatments decrease the fasting markers of postprandial lipoproteins by mechanisms that may not be mediated via processes differentiated by the 13CO2 breath test. This implies that the effect on postprandial lipaemia may be from a decrease in production and/or a possible increase in catabolism of triglyceride-rich lipoproteins (TRLs). In Study 5, postprandial lipaemia was compared in 24 postmenopausal women age and body mass index matched with 14 postmenopausal women with type 2 DM. Postmenopausal diabetic women were found to have higher fasting concentrations of apoB48 (+21%, p=0.021) and apoC-III (+16%, p=0.042) as well as lower FCR of the chylomicron remnant-like emulsion (-50%, p<0.001). The data suggest that postmenopausal diabetic women have postprandial dyslipidaemia, and that this is due to delayed catabolism of chylomicron remnants. Study 6 was an hypothesis-generating exercise examining the effects of 4-weeks pravastatin treatment on postprandial dyslipidaemia found in 7 postmenopausal women with type 2 DM from Study 5. Although plasma LDL-cholesterol was reduced (-19%, p=0.028), there were no significant effects found on fasting apoB48 concentrations (-12%, p=0.116) or the FCR of the chylomicron remnant-like emulsion (+38%, p=0.345). A larger sample size of patients and/or treatment with a more potent statin at a dosage known to affect chylomicron remnant metabolism would be required to demonstrate a significant reduction in postprandial dyslipidaemia in postmenopausal women with type 2 DM. The results of the above mentioned studies combined support the general hypothesis that postprandial dyslipidaemia is a feature of patients with or at risk of CAD. This defect may be demonstrated using fasting apoB48 as an indicator of the degree of postprandial lipaemia. Postprandial dyslipidaemia may reflect a reduction in catabolism, as suggested with the breath test in type 2 DM, and/or an over overproduction of chylomicrons. Both these mechanisms would also increase competition for lipolysis and clearance pathways between hepatically and intestinally-derived lipoproteins. The exact mechanisms by which postprandial dyslipidaemia occurs are yet to be determined. Statins appear to improve defective postprandial lipaemia in patients with or at risk of CAD, which is in agreement with the general hypothesis. The effectiveness of a statin is dependant on their potency in inhibiting cholesterol biosynthesis and increasing receptor mediated clearance of LDL and chylomicron remnants. The studies conducted in this thesis show that postprandial dyslipidaemia can be reduced by statins but not to the extent demonstrated in controls. However, the demonstrated reduction in fasting and total postprandial lipaemia translates to a lowering in overall arterial exposure to circulating proatherogenic particles. The elevation in fasting and postprandial levels of proatherogenic chylomicron remnants found in the patient groups described in this thesis indicates another dimension to their risk of coronary disease. The reductions in the overall levels of proatherogenic particles in patients with or at high CAD risk, infers a possible reduction in the risk of coronary disease in these patients.
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Wideman, Laurie. "Postprandial lipemia in abdominally obese and non-obese males." Virtual Press, 1993. http://liblink.bsu.edu/uhtbin/catkey/845959.
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Recent research has shown that the combination of high triglyceride (TG) levels and low high density lipoprotein (HDL) levels, significantly increases the incidence of coronary artery disease (CAD). The incidence of CAD is also increased in abdominally obese individuals. To assess differences in postprandial TG clearance patterns between abdominally obese (AO) and controls (C), fourteen healthy, normolipidemic males (seven controls and seven abdominally obese) completed an oral fat loading test (78 grams of fat). Blood samples were collected every hour for eight hours. Abdominally obese individuals had significantly greater TG values, significantly lower total HDL and HDL2 values and significantly greater area under the TG curve (p = 0.03). Time to reach peak TG and time to reach baseline TG values did not differ between the two groups, even though fewer AO individuals reached baseline within eight hours. The data from the present investigation indicate that increased time to clear TG in AO individuals may be one pathway that increases the incidence of CAD in this group.School of Physical Education
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Tavridou, Anna. "Lipoprotein (a) in population-based samples of South Asian and European adults in Newcastle upon Tyne." Thesis, University of Newcastle Upon Tyne, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297575.
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Wilson, Heather Marion. "High density lipoprotein subspecies and the control of lipoprotein metabolism in relation to coronary heart disease." Thesis, University of Aberdeen, 1990. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU031961.
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The concept that high plasma concentrations of high density lipoproteins (HDL) offers protection against coronary heart disease has been challenged on epidemiological grounds. This dispute may arise as a result of the heterogeneous nature of HDL in which only some subspecies exert a protective function while the major portion has a neutral role. In order to test this hypothesis, the distribution of HDL subfractions in 100 myocardial infarction (MI) survivors was examined within 12 hours of the onset of chest pain and before post-MI changes in lipoproteins occurred. These patients were shown to have a significantly lower percentage distribution of apoprotein E-rich HDL measured by heparin-Sepharose affinity chromatography, and of HDL2b estimated by gradient gel electrophoresis, yet a higher percentage distribution of HDL3c than a similarly sized group of healthy control subjects. At six months post-MI follow-up with an appropriate improvement in lifestyle, as well as therapeutic treatment, there was a significant increase in the percentage distribution of apoprotein E-rich HDL and of HDL2b and a significant decrease in HDL3c, with no alteration in total HDL or any other lipoprotein component. Measurement of these HDL subfractions may thus provide a better indicator of coronary risk than of total plasma cholesterol, which is frequently employed for this purpose, but was found indistinguishable between the two groups in the present study. Such subfractions also provide useful information into the underlying causes of atherosclerosis. The apoprotein E-rich subfraction of HDL which was shown to be reduced in MI survivors, was further separated into several, more discrete subfractions by heparin-Sepharose affinity chromatography, using a judicious choice of eluting solvents. The separated subfractions differed in mean particle diameter and in lipid and apoprotein composition. The fraction designated HDL2b was shown to comprise three main species which may serve different roles in coronary protection.
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Brooks, Catriona. "The effects of dietary fatty acids on lipoprotein lipase activity and gene expression." Thesis, University of Surrey, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265101.
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Thompson, Alexander John. "Assessing associations of lipoprotein-associated phospholipase A₂ (Lp-PLA₂) with coronary heart disease risk." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611726.
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Slunga, Lisbeth. "Serum lipoprotein(a) in relation to ischemic heart disease and associated risk factors." Doctoral thesis, Umeå universitet, Klinisk kemi, 1993. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-101298.
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Lipoprotein(a) (Lp(a)) consists of an LDL-like particle and the specific protein apo(a), which is very similar to plasminogen. Apo(a) contains repeated kringle structures and a serine protease domain, which cannot be activated by t-PA. Lp(a) is considered to be a predictor for atherosclerotic disease. It has been found incorporated in atherosclerotic plaques and inhibits in vitro fibrinolysis. Lp(a) was determined in 1527 randomly selected individuals participating in the Northern Sweden WHO-MONICA project. A weak but significant relation between Lp(a) and increasing age was found. Menopausal status was the strongest independent predictor of Lp(a) level in women. Fibrinogen was independently related to Lp(a) in both sexes. Only a minor fraction of Lp(a) variance could be explained for in a multiple regression model, which is in agreement with the contention that Lp(a) is highly genetically determined. Lp(a) was determined in 1571 patients investigated with coronary angiography because of suspected severe coronary artery disease (CAD). Patients with proven CAD at elective angiography had significantly higher Lp(a) than patients without significant CAD or healthy controls. Lp(a) was found to be an independent discriminator of CAD in both sexes. HLA-DR genotype 13 or 17 was found more frequently in 30 male patients with angiographic CAD at young age (< 50 years) than in 30 age matched controls. These genotypes were common in patients with high Lp(a) levels, which indicates that Lp(a) may be related to immunological processes. The reaction of Lp(a) was investigated in 32 patients with acute myocardial infarction (AMI). Lp(a) increased during the first week, but the response was comparatively weak. Individual Lp(a) responses were heterogeneous and no correlations to infarct size or changes in the acute phase proteins were found. In a randomized cross-over study on 36 hypercholesterolaemic patients treated with simvastatin/placebo during 12+12 weeks Lp(a) did not change significantly, but patients with high Lp(a) levels at baseline tended to develop further increased Lp(a). To conclude, Lp(a) was found to be an independent predictor of angiographic CAD in both men and women. Lp(a) levels are primarily genetically determined and only a small fraction of Lp(a) variance could be explained by other factors in this study. Lp(a) may be related to HLA DR types and immunological processes involved in atherosclerotic disease. Lp(a) increased slightly during the first week of AMI, but was not related to changes in the acute-phase proteins. The effective LDL-lowering agent simvastatin did not influence Lp(a) significantly.Diss. (sammanfattning) Umeå : Umeå universitet, 1993, härtill 5 uppsatser.
digitalisering@umu
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Kanjana, Hongtong Supranee Changbumrung. "Platelet fatty acids and lipoprotein (a) in subjects with coronary heart disease and healthy controls /." Abstract, 2003. http://mulinet3.li.mahidol.ac.th/thesis/2546/46E-Kanjana-H.pdf.
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Gagné, S. Eric. "Identification and the relationship between mutations in the lipoprotein lipase gene, dyslipidemia and coronary heart disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0009/NQ38889.pdf.
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Erqou, Sebhat. "Lipoprotein(a) and the risk of vascular disease." Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/225182.
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Background: Lipoprotein(a) [Lp(a)] is composed of a low density-lipoprotein (LDL) particle and a glycoprotein molecule known as apolipoprotein(a) [apo(a)]. Apo(a) exists in several differently-sized isoforms and is responsible for the unique properties of Lp(a). Although Lp(a) has been known for the past 40 years its relationship with coronary heart disease (CHD) has not been characterized in sufficient detail. Whether Lp(a) causes CHD is not clear. Furthermore, the role of apo(a) isoform variation and other sources of Lp(a) heterogeneity (e.g., level of oxidized phospholipids) in Lp(a)-disease association has not been determined. Objectives: To characterize in detail the association of circulating Lp(a) levels with the risk CHD To assess the nature of Lp(a)-CHD association using an integrative genetic study To explore the role of Lp(a) heterogeneity in its association with CHD Data sources: 1. The Emerging Risk Factors Collaboration (ERFC) database (36 studies, 127,000 participants) 2. The European Prospective Investigation of Cancer – Norfolk (EPIC-Norfolk) study (2200CHD cases, 2200 controls) 3. The Pakistani Risk of Myocardial Infarction Study (PROMIS) (1800 MI cases and 1800 controls) 4. Systematic quantitative reviews of published epidemiological studies Results: ERFC data - Analyses of cross-sectional data on up to 127,000 participants (predominantly of European descent) demonstrated that Lp(a) is generally not strongly correlated with known CHD risk factors. Weakly positive correlations were observed with LDL-cholesterol, apolipoprotein B100 and fibrinogen. Levels were over 2-fold higher in Blacks compared to Whites. Analyses of available data on repeat measurements in 6600 participants demonstrated that Lp(a) values have very high long-term within-person consistency (regression dilution ratio ~ 0.9). Outcome data involved 9300 incident CHD events, 1900 ischaemic strokes and 8100 nonvascular deaths. The risk ratio for CHD per 1SD higher Lp(a) concentration, adjusted for age, sex, lipids and other conventional vascular risk factors, was 1.13 (95% CI, 1.09-1.18). The corresponding risk ratios for ischaemic stroke and nonvascular death were 1.10 (1.02 – 1.18) and 1.01 (0.98-1.05), respectively. Data were too limited to assess association in nonwhites. PROMIS data – the adjusted odds ratio for MI in South Asians was comparable to that of Europeans. EPIC-Norfolk genetic data - The odds ratio for CHD per 1-SD higher Lp(a) concentration, after adjustment for cardiovascular risk factors, was 1.37 (1.20-1.56). Tagging SNPs rs10455872 and rs11751605 (minor allele frequency: 8% and 18%, respectively) were associated with 207% (95% CI, 188 - 227%) and 38% (31 - 46%) higher Lp(a) concentrations per copy of minor allele, respectively. These SNPs accounted for 35% and 5% of the variation in circulating Lp(a) levels, respectively, and were associated with an odds ratio for CHD of 1.34 (1.14-1.58) and 1.17 (1.04-1.33), respectively. The observed SNP-CHD associations were consistent with expected odds ratios corresponding to the Lp(a) effect of the SNPs. Systematic reviews – meta-analysis of published data from 40 studies (11,300 cases, 47,000 controls) demonstrated that people with smaller apo(a) isoforms have about a 2-fold higher risk of CHD or ischemic stroke than those with larger isoforms. Meta-analysis of published data from 10 studies (1500 cases, 10,200 controls) showed that people in the top third of baseline distribution of oxidized LDL levels have a 1.8-fold higher risk of CHD than those in bottom third. EPIC-Norfolk biomarker data – Levels of oxidized phospholipids were strongly correlated with Lp(a) concentration (r = 0.7, p-value < 0.0001). One SD higher concentration of oxidized phospholipids was associated with an adjusted odds ratio for CHD of 1.31 (1.15-1.49). The risk ratio was no longer significant after adjustment for Lp(a) concentration (1.08; 95% CI, 0.91-1.29). Conclusion: Lp(a) concentration is specifically, continuously and independently associated with the risk of ischaemic vascular outcomes. Available evidence supports the causal role of the particle in CHD. Lp(a) appears to induce vascular damage through causal mechanisms that involve apo(a) isoforms and oxidized phospholipids. A comprehensive study of markers of Lp(a) heterogeneity should help to understand the full impact of Lp(a) on cardiovascular diseases. In addition, further study is needed in nonwhites to assess the relevance of the factor to vascular disease risk in these populations.
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Stensel, David J. "The effects of brisk walking on endurance fitness, lipoprotein metabolism and other risk factors for coronary heart disease." Thesis, Loughborough University, 1993. https://dspace.lboro.ac.uk/2134/25597.
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This thesis examines the potential of a one year programme of brisk walking to influence endurance fitness, lipoprotein metabolism and other risk factors for coronary heart disease (CHD) in previously sedentary, middle-aged men. Seventy-two asymptomatic males were recruited into the study and randomly allocated on a two to one basis into either a walking group (n = 48) or a control group (n = 24). Walkers were asked to build up to an average of 45 minutes of brisk walking per day and maintain this level thereafter. Control subjects continued with their habitual lifestyle. Both groups undertook not to change their dietary habits. Maximum oxygen uptake (V0₂max) was predicted at base line, three, six and 12 months from submaximal heart rate and oxygen uptake data during treadmill walking. Endurance fitness was assessed at similar intervals by measuring heart rate and blood lactate concentration during standardised submaximal treadmill walking. Serum concentrations of total cholesterol, high density lipoprotein cholesterol, apoproteins A-I and B, triglycerides and lipoprotein(a) were measured at each observation point. Additionally, plasma fibrinogen, resting arterial blood pressure and indices of pulmonary function were determined. Differences in the response of walkers and controls over time were examined using two way analysis of variance for repeated measures employing the 5% level of significance. Adherence to the walking programme was high and 42 of the walkers (88%) remained in the study for the year completing an average of 28 ± 9 (mean ± SD) minutes of brisk walking each day (self-report). The response of the walkers over time was significantly different to that of the controls for predicted V0₂max and for heart rate and blood lactate concentration during standardised submaximal exercise indicating that brisk walking favourably influenced endurance fitness. No significant differences were observed between groups for any of the lipoprotein variables or other CHD risk factors monitored during the study. It was concluded that brisk walking did not influence established CHD risk factors in this group of previously sedentary middle-aged men despite the evidence of improved endurance fitness.
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Wang, Xiao Suo. "A novel ELISA to detect methionine sulfoxide-containing apolipoprotein A-I." Connect to full text, 2009. http://hdl.handle.net/2123/5423.
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Thesis (Ph. D.)--University of Sydney, 2009.Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Discipline of Pathology, Faculty of Medicine. Title from title screen (viewed Sept. 30, 2009) Includes bibliography. Also available in print form.
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Bartholomew, Ciera Lynn. "Weekly One-Day Water-Only Fasting Interventional Trial for Low-Density Lipoprotein Cholesterol Reduction (WONDERFUL)." BYU ScholarsArchive, 2021. https://scholarsarchive.byu.edu/etd/8880.
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Purpose: Fasting has been promoted as a method of preventing disease and aging for thousands of years. With heart disease being a leading cause of death in the U.S., researchers have explored the effects of fasting on variables that influence cardiovascular disease (CVD), like LDL cholesterol. Therefore, the purpose of this study was to assess the effects of weekly water-only fasting on LDL cholesterol (LDL-C) in men and women with metabolic risk factors for CVD. Methods: This study was a randomized control trial in adult men and women. Participants were randomized to fasting (treatment) or normal diet (control). The fasting protocol consisted of four weeks of two 24-hour water-only fasts, followed by 22 weeks of once-weekly water-only 24-hour fasts. Measurements such as height, weight, waist circumference and LDL-C were assessed at baseline, 4 weeks, 13 weeks, and 26 weeks. Results: Intermittent fasting (n = 50) and control (n = 53) participants were 49.3 ± 12.0 and 47.0 ± 9.8 years, respectively, predominantly females (66.0% and 67.9%), overweight (103 ± 24 and 100 ± 21 kg), and with mild LDL-C elevation (124 ± 19 and 128 ± 20 mg/dL). Change in weight was −1.70 ± 4.69 (kg) in the fasting group and 0.20 ± 3.45 (kg) in the control group and not different between conditions (p = 0.06). There was no condition-by-period interaction for LDL-C (p = 0.06). Similarly, the change in LDL-C from baseline to follow-up was not different between conditions (t = −0.538, p = 0.59; Cohens D = 0.12) Conclusions: A once-per-week intermittent fasting regimen did not reduce weight or LDL-C. Further research of such fasting regimens is needed to evaluate their potential impact on cardiometabolic health.
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Pocathikorn, Anothai. "Low density lipoprotein receptor-related protein (LRP) and its mRNA : influence of genetic polymorphisms, a fat load and statin therapy." University of Western Australia. School of Surgery and Pathology, 2006. http://theses.library.uwa.edu.au/adt-WU2006.0117.
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[Truncated abstract] The low density lipoprotein receptor-related protein (LRP), a member of the low-density lipoprotein (LDL) receptor gene family is involved in numerous biological processes including lipoprotein metabolism. This thesis concerns investigations into some aspects of LRP metabolism/regulation and possible roles in coronary artery disease (CAD). Specific aims were: to investigate the association between polymorphisms in the LRP gene and in its associated protein, the lipoprotein receptor-associated protein (RAP), with the risk of CAD; to extensively examine the influence of the LRP exon 22 C200T polymorphism on lipid metabolism; to develop and characterise assays for the mRNA expression of LRP and 2 other genes relevant to lipid metabolism, the LDL receptor (LDLR), and HMG CoA reductase (HMGCR); and finally, to apply the latter techniques to studies on the influence of genetic variation in LRP, and dietary and drug interventions, on LRP, LDLR and HMGCR mRNA expression in nucleated blood cells from healthy human subjects. Six hundred CAD subjects and 700 similarly aged controls were genotyped for 8 LRP gene polymorphisms as well as for the RAP V311M polymorphism. ... In the final phase of my studies, I examined the influence of 4 weeks therapy with a cholesterol lowering drug, an HMGCR inhibitor, atorvastatin (20mg daily), on the mRNA expression of LDLR, LRP and HMGCR in human nucleated blood cells. Twelve normal Caucasian male subjects aged 49 ? 5 (SD) years were studied. Plasma total cholesterol and LDL-C decreased by averages of 29 % and 41 % after the 4 week period. This was accompanied by an elevation in LDLR mRNA expression by approximately 30 35 %. In contrast, there was no significant effect on LRP and HMGCR mRNA expression. In conclusion, the original findings in this thesis included: demonstration of a strong influence of the LRP exon 22 C200T polymorphism on coronary artery disease and LDLR expression, but without a clear effect on fasting or postprandial lipid levels; data on the biological variation in LDLR and LRP gene expression in nucleated blood cells from normal subjects; the influence of an oral fat load on the expression viii of these genes, finding that LDLR was significantly depressed; and finally, the observation that statin therapy upregulated LDLR in nucleated blood cells.
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Jeyarajah, Elias Joseph. "Development and Validation of a 1H NMR Method for Lipoprotein Quantification and Coronary Heart Disease Risk Assessment." NCSU, 2005. http://www.lib.ncsu.edu/theses/available/etd-05032005-105307/.
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There is abundant evidence that the subclasses within a given lipoprotein class differ in their associations with coronary heart disease. Since subclass distributions can vary widely from person to person, individuals with the same levels of LDL cholesterol and HDL cholesterol may be at different cardiovascular risk and respond differently to dietary and drug therapy. Unfortunately, existing laboratory methods of subclass measurement are too time-consuming and expensive to be used in routine clinical practice. Using a new approach to lipoprotein analysis that exploits the natural proton NMR spectroscopic differences exhibited by lipoprotein particles of different size, we have developed a new quantitative NMR technology for use in clinical laboratory medicine. The newly developed NMR LipoProfile assay rapidly and simultaneously quantifies the lipoprotein subclass particle concentrations of 10 lipoprotein species (3 VLDL, IDL, 3 LDL and 3 HDL) with good intraassay and interassay precision. Extensive validation studies were conducted that established robustness of the NMR lipoprotein particle assay. The average particle sizes of the major lipoprotein classes determined by NMR correlate very well with those estimated by gradient gel electrophoresis. Emerging clinical data from several coronary disease outcome studies indicate that NMR-derived lipoprotein particle parameters are superior predictors of cardiovascular disease risk compared to traditional cholesterol risk factors. The speed and efficiency of NMR lipoprotein subclass profiling make it a potentially valuable research tool and cost-effective means of assessing and managing heart disease risk in the general population.
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Paavola, T. (Timo). "Associations of low HDL cholesterol level and premature coronary heart disease with functionality and phospholipid composition of HDL and with plasma oxLDL antibody levels." Doctoral thesis, Oulun yliopisto, 2019. http://urn.fi/urn:isbn:9789526223360.
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Abstract Coronary heart disease (CHD) is a clinical manifestation of atherosclerosis. It is a major cause of mortality and morbidity both in Finland and globally. Even after the best known treatments a significant residual risk of CHD remains. A low plasma HDL cholesterol level (HDL, high-density lipoprotein) is a common lipid abnormality in patients affected by premature CHD and also a component of the metabolic syndrome, a cluster of risk factors for atherosclerosis associated with central obesity. In this study, a phenotype of low HDL cholesterol level and premature CHD was investigated in two Northern Finnish family populations. The aim was to find new biological factors accounting for the elevated CHD risk in the phenotype. In the subjects of family population I, plasma levels of antibodies (IgG, IgM, IgA) against experimental epitopes (malondialdehyde-acetaldehyde-modified, copper-oxidized) of oxidized LDL (low-density lipoprotein) particles were measured. In the subjects of family population II, capacity of HDL fractions (total HDL, HDL2 and HDL3) to accept cholesterol from a THP-1 experimental foam cell model was assayed (cholesterol efflux). In addition, a phospholipid composition of their HDL fractions (HDL2 and HDL3) was measured using liquid chromatography-mass spectrometry. The antibody levels were not related to CHD or to HDL cholesterol level. Instead, the cholesterol efflux to HDL2 fraction was clearly impaired in CHD, which was associated with the low HDL cholesterol level of the patients. The impaired cholesterol efflux to HDL2 fraction was primarily in conjunction with the metabolic syndrome. The phospholipid composition of HDL fractions was different between the affected and the non-affected subjects. As an example, characteristic of the metabolic syndrome were elevated contents of palmitic, palmitoleic or oleic acids relative to linoleic acid in lysophosphatidylcholines and phosphatidylcholines. In conclusion, the HDL fraction is both functionally and compositionally modified in the phenotype of low HDL cholesterol level and premature CHD. Especially the cholesterol efflux capacity of the HDL2 fraction and thus its many functional properties may be impaired. There are many characteristic features in the phospholipid composition of the HDL in the phenotype which were detected in HDL2 and HDL3 fractionsTiivistelmä Sepelvaltimotauti on ateroskleroosin kliininen ilmenemismuoto. Se on merkittävimpiä kuolleisuuden ja sairastavuuden aiheuttajia niin Suomessa kuin maailmalla. Parhaillakin tunnetuilla hoidoilla sepelvaltimotaudille jää huomattava jäännösriski. Plasman matala HDL-kolesterolitaso (HDL, high-density lipoprotein) on yleinen lipidipoikkeavuus varhaista sepelvaltimotautia sairastavilla ja myös eräs metabolisen oireyhtymän, eli keskivartalolihavuuteen liittyvän ateroskleroosin riskitekijäkasauman, komponentti. Tässä väitöskirjassa tutkittiin matalan HDL-kolesterolitason ja varhaisen sepelvaltimotaudin fenotyyppiä kahdessa pohjoissuomalaisessa sukuaineistossa. Tavoitteena oli löytää uusia biologisia tekijöitä fenotyypin kohonneen sepelvatimotautiriskin taustalta. Ensimmäisen aineiston henkilöiden plasmasta mitattiin vasta-ainetasoja (IgG, IgM, IgA) LDL-hiukkasten (LDL, low-density lipoprotein) kokeellisia hapettuneita epitooppeja (malonidialdehydi-asetaldehydi-modioitu ja kuparilla hapetettu LDL) vastaan. Toisessa aineistossa mitattiin henkilöiden HDL-fraktioiden (kokonais-HDL, HDL2 ja HDL3) kykyä saada aikaan kolesterolin ulosvirtausta kokeellisesta THP-1 vaahtosolumallista. Lisäksi heidän HDL-fraktioidensa (HDL2, HDL3) fosfolipidikoostumus mitattiin nestekromatografi-massaspektrometri-laitteistolla. Vasta-ainetasot eivät liittyneet sepelvaltimotautiin tai HDL-kolesterolitasoon. Sen sijaan kolesterolin ulosvirtaus HDL2-fraktioon oli selkeästi alentunut sepelvaltimotaudissa, mikä liittyi potilaiden pieneen HDL-kolesterolipitoisuuteen. Alentunut ulosvirtaus HDL2-fraktioon liittyikin ensisijaisesti metaboliseen oireyhtymään. HDL-fraktioiden fosfolipidikoostumus erosi terveiden ja sairaiden välillä. Esimerkiksi metabolisessa oireryhtymässä tunnusomaista oli lysofosfatidyylikoliinien ja fosfatidyylikoliinien sisältämän palmitiinihapon, palmitoleiinihapon tai oleiinihapon suurentunut määrä suhteessa niiden sisältämän linoleenihapon määrään. Loppupäätelmä on, että matalan HDL-kolesterolitason ja varhaisen sepelvaltimotaudin fenotyypin HDL-fraktio on sekä toiminnaltaan että koostumukseltaan muuntunut. Erityisesti HDL2-fraktion kyky saada aikaan kolesterolin ulosvirtausta ja näin ollen sen monet toiminnalliset ominaisuudet voivat olla alentuneet. Fenotyypin HDL:n fosfolipidikoostumuksessa on monia tunnusomaisia piirteitä, joita havaittiin sekä HDL2- että HDL3-fraktiossa
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Sedgwick, Matthew J. "The effect of high-fat meals and exercise on endothelial function and triacylglycerol concentrations in adolescent boys." Thesis, Loughborough University, 2013. https://dspace.lboro.ac.uk/2134/12827.
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The thesis investigated the effect of exercise on endothelial function (measured as flow-mediated dilation (FMD)) and triacylglycerol concentrations following the ingestion of a high-fat breakfast and lunch in adolescent boys. The validity of measuring lipid and lipoprotein concentrations from a capillary blood sample, and the reproducibility of the postprandial FMD and triacylglycerol concentration responses to the high-fat meals, was established. The effects of prior continuous moderate-intensity exercise (60 min walking at 60% V̇O₂peak), repeated very short duration sprints (40 x 6 s maximal effort cycle sprints) and accumulated moderate-intensity exercise (6 x 10 min running at 70% V̇O₂peak) on endothelial function and triacylglycerol concentrations in adolescent boys were then established across three studies, each consisting of two, 2-day main trials (control and exercise). On day 1, participants were either inactive or completed the prescribed exercise. On day 2, FMD and triacylglycerol concentrations were measured prior to, and following, ingestion of a high-fat breakfast and lunch. In each control trial FMD was reduced (signifying endothelial dysfunction), compared to fasting, by 20-32% and 24-33% following the high-fat breakfast and lunch. Following continuous moderate-intensity exercise, repeated very-short duration sprints and accumulated moderate-intensity exercise these reductions were only 8% and 10% (main effect trial, P = 0.002; main effect time, P = 0.023; interaction effect trial x time, P = 0.088), 2% and 5% (main effect trial, P = 0.012; main effect time, P = 0.004; interaction effect trial x time, P = 0.003) and 1% and 3% (main effect trial, P = 0.020; main effect time, P < 0.001; interaction effect trial x time, P = 0.014) respectively. The continuous moderate-intensity exercise and repeated very short duration sprints also significantly reduced the total area under the triacylglycerol concentration versus time curve by 22% (Control vs. Exercise; 12.68 (sem 1.37) vs. 9.84 (sem 0.75) mmol L-1 6.5h, P = 0.018) and 13% (Exercise vs. Control: 8.65 (sem 0.97) vs. 9.92 (sem 1.16) mmol L-1 6.5h, P = 0.023). The accumulated moderate-intensity exercise also reduced the total area under the triacylglycerol concentration versus time curve by 11%, but this reduction was not significant (Control vs. Exercise: 10.71 (sem 0.94) vs. 9.56 (sem 0.67) mmol L-1 6.5h, respectively, P = 0.183). The experimental evidence from these studies emphasise that exercise might offer an acceptable, non-pharmacological means of influencing CHD risk when individuals are young. The results of these studies can help shape future physical activity guidelines.
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Chatterjee, Cynthia. "Purinergic Signaling and Autophagy Regulate the Secretion of High-Density Lipoprotein and Hepatic Lipase." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/24027.
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Dyslipidemia can be a comorbidity of both insulin-resistance and atherosclerosis. Hypertriglyceridemia is common in hyperglycemia and is associated with hypoalphalipoproteinemia (low HDL) and with altered nucleotide or purinergic signaling. We therefore hypothesized that extracellular nucleotides may affect hepatic lipoprotein metabolism. Our studies confirm this view and show that nucleotides regulate cellular proteolytic pathways in liver cells and thereby control lipoprotein secretion and their metabolism by hepatic lipase (HL).
Treatment of liver cells with the nucleotide, adenosine diphosphate (ADP), stimulates VLDL-apoB100 and apoE secretion, but blocks HDL-apoA-I and HL secretion. ADP functions like a proteasomal inhibitor to block proteasomal degradation and stimulate apoB100 secretion. Blocking the proteosome is known to activate autophagic pathways. The nucleotide consequently stimulates autophagic degradation in liver cells and increases cellular levels of the autophagic proteins, LC3 and p62. Confocal studies show that ADP increases cellular LC3 levels and promotes co-localization of LC3 and apoA-I in an autophagosomal degradation compartment. ADP acts through the G-protein coupled receptor, P2Y13, to stimulate autophagy and block both HDL and HL secretion. Overexpression of P2Y13 increases cellular LC3 levels and blocks the induction of both HDL and HL secretion, while P2Y13 siRNA reduce LC3 protein levels and cause up to a ten-fold stimulation in HDL and HL secretion. P2Y13 gene expression regulates autophagy through the insulin receptor (IR-β). A reduction in P2Y13 expression increases the phosphorylation of IR-β and protein kinase B (Akt) >3-fold, while increasing P2Y13 expression inhibits the activation of IR-β and Akt. Experiments with epitope-labeled apoA-I and HL show that activation of purinergic pathways has no effect on the internalization and degradation of extracellular apoA-I and HL, which confirms the view that nucleotides primarily impact intracellular protein transport and degradation. In conclusion, elevated blood glucose levels may promote dyslipidemia by stimulating purinergic signaling through P2Y13 and IR-β and perturbing the intracellular degradation and secretion of both HDL and VLDL.
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Brouilette, Scott Wayne. "Telomeres and coronary heart disease." Thesis, University of Leicester, 2004. http://hdl.handle.net/2381/29899.
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Using mean telomere length as a marker of biological age, I show that: 1. Subjects with premature myocardial infarction (MI) have significantly shorter telomeres than age-sex matched, healthy, controls. The mean telomere length in MI subjects was similar to controls almost 11 years older. 2. Healthy young adult children of families with a strong history of premature MI have shorter telomeres than age matched children of families without such a history. 3. Shorter telomere lengths are associated with increase risk of subsequent CHD events in a prospective study. This analysis was carried out on samples collected in the West of Scotland Coronary Prevention Study (WOSCOPS). This randomised blinded trial was designated to examine the benefits of statin treatment on preventing CHD and showed a 30% reduction of events in those treated with pravastatin. Interestingly, my analysis showed that this benefit of statin is only seen in those subjects at higher risk of CHD based on their telomere length.;As the final part of the thesis I carried out a quantitative linkage trait (QTL) analysis in sib-pairs in an attempt to identify genetic loci regulating telomere length. I report the mapping of a major QTL on chromosome 12 that determines almost 50% of the inter-individual variation in mean telomere length.;These findings support a novel "telomere" hypothesis of CHD. They indicate that telomere biology is intimately linked to the genetic aetiology and pathogenesis of CHD. Specifically, the findings suggest that (i) those individuals born with shorter telomeres may be at increased risk of CHD (ii) rather than individual genes, a more global structural property of the genetic material may explain the familial basis of CHD (iii) variation in telomere length may explain, in part, the variable age of onset of CHD. The findings provide several new avenues for future research.
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Lee, Chi-hang. "Microvascular obstruction following percutaneous coronary intervention for coronary artery disease." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43278723.
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Danesh, John. "Chronic infection and coronary heart disease." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326020.
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Kounali, Daphne. "Early growth and coronary heart disease." Thesis, University of Southampton, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436926.
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Heiser, Claire Anne. "Personality predictors of coronary heart disease." Thesis, Virginia Polytechnic Institute and State University, 1985. http://hdl.handle.net/10919/50027.
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Fifty percent of the diagnosed cases of coronary heart disease in the United States are of unknown etiology. This study proposed that five personality traits— achievement, dominance, aggression, succorance and Critical Parent—differentiate individuals with coronary heart disease manifestations. The ultimate goal of this research was to formulate a predictive profile of at-risk individuals of developing coronary heart disease.
Cardiac rehabilitation units' participants from across the United States were recruited as subjects. Randomly selected cardiac rehabilitation units were sent an initial letter inquiring whether their staff would be willing to participate in the study by administering the instruments to their participants. Eight units from each of the 50 states were contacted. A total of fourteen units agreed to participate. One hundred sixty-nine subjects completed the Demographic Data Questionnaire and the Adjective Check List.
Five scale scores, representing the five personality differentials, were analyzed. Comparison of the male subject population (n=135) and the male normative population (n=198) revealed no significant differences in terms of the five traits. Comparison of diagnostic subgroups of the subject population also revealed no significant differences.
It was concluded that the subject population did not differ significantly from the normative population in terms of the five traits assess by the instrument used. The goal of a predictive profile was not realized due to this lack of findings.Master of Science
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Lee, Chi-hang, and 李志恆. "Microvascular obstruction following percutaneous coronary interventionfor coronary artery disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43278723.
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Zapanta, Laurence (Laurence F. ). "Heart rate variability in mice with coronary heart disease." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/34118.
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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2005.Includes bibliographical references (leaves 69-71).
Heart rate variability (HRV), the beat-to-beat fluctuation of the heart rate, is a non-invasive test that measures the autonomic regulation of the heart. Assessment of HRV has been shown to predict the risk of mortality in patients after an acute myocardial infarction. Recently, the Krieger lab at MIT developed genetically engineered double knockout (dKO) mice that develop coronary artery disease accompanied by spontaneous myocardial infarctions and die at a very young age. This thesis investigated whether HRV could function as a prognostic indicator in the dKO mouse. A novel method for estimating physiological state of the mouse from the electrocardiogram using an innovative activity index was developed in order to compare HRV variables at different times while controlling for physiologic state. Traditional time and frequency domain variables were used to assess the prognostic power of HRV. Results have shown that none of the HRV variables were helpful in predicting mortality in the dKO mice. Mean heart rate showed some prognostic power, but it was not consistent in all the dKO mice. Finally, the activity index developed in this thesis provided a reliable metric for activity in mice as validated by a camera with motion detection.
by Laurence Zapanta.
S.M.
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Bhandari, Sanjay. "The impact of ethnicity on lipoproteins in coronary artery disease." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/40018.
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Coronary artery disease (CAD) is a leading cause of mortality in the UK, with individuals of South Asian origin at intensified risk, owing to a higher prevalence of diabetes, culminating in an atherogenic phenotype. The epidemiological evidence supporting a protective role for high density lipoprotein-cholesterol in CAD, has failed to be realised in the ILLUMINATE/AIM-high trials. The paradigm has shifted towards an appreciation of the quality of the lipoprotein particles, rather than arbitrary levels. Lipoproteins contain unique protein cargoes, mediating roles in coagulation, redox and inflammation. The objective of this study was to explore differences in the low abundant protein cargo of lipoproteins between South Asian and Caucasian patients with CAD, to further understand the differential risk. A novel lipoaffinity resin was explored and optimised for efficient and reliable lipoprotein pull-down from plasma. Samples were analysed using a label-free bottom-up proteomic approach on an ion-mobility enabled mass spectrometer. Statins remain the cornerstone for prevention of CAD. In a sub-study, statin therapy was associated with the modulation of proteins concerned with the cytoskeletal architecture, cell proliferation and inflammation, in patients with hypercholesterolemia. The controversial link between statin use and new onset diabetes may be explained a depletion of adipsin, a potent insulin secretagogue. In a further sub-study, lipoproteins of CAD patients were enriched with pro-inflammatory mediators compared with age and sex matched controls. A model comprising of 7 proteins accurately predicted CAD status. In the discovery study, lipoproteins of South Asians were enriched with pro-thrombotic and pro-inflammatory mediators, compared with sex-matched Caucasians with stable CAD. Plasma carboxypeptidase B2 was significantly higher in South Asians compared to Caucasians with CAD in verification studies, contributing to impaired fibrinolysis and potentially to their excess risk. The lipoproteomic cargo undergoes subtle changes in CAD, with various dysregulated proteins independently influenced by ethnicity.
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Rose, Edward Leslie. "Coronary heart disease in patients with peripheral vascular disease." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305544.
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Bagés, Nuri. "Psychosocial risk factors and coronary heart disease." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 2000. http://arno.unimaas.nl/show.cgi?fid=6899.
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Chandola, Tarani. "Social inequality in coronary heart disease outcomes." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285007.
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Freitag, Daniel Franz. "Inflammatory pathways and coronary heart disease risk." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648461.
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Du, Ying. "Ischemic and pharmacological preconditioning of rat myocardium : effects on ischemia-reperfusion injury /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BICH%202005%20DU.
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Ho, Lai-yi Ada. "Does social support influence coronary heart disease prognosis? : a meta-analysis /." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/b39724116.
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Dorn, Karen LaVonne Toft. "Circulatory, hormonal, and metabolic effects of arbutamine compared to exercise in persons with known or suspected coronary artery disease /." This resource online, 1994. http://scholar.lib.vt.edu/theses/available/etd-06062008-164634/.
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Guibert, Remy L. "Death certificate coding variation and coronary heart disease." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66229.
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Huff, Natasha Clare. "Coronary heart disease and the socio-economic environment." Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339634.
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Tinati, Mohammad Ali. "Time-frequency and time-scale analysis of phonocardiograms with coronary artery disease before and after angioplasty /." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09pht587.pdf.
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Bose, Jolly. "Percutaneous transluminal coronary angioplasty (PTCA) in the treatment of coronary artery disease in Hong Kong : procedural success, complications and long-term follow-up /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2084282X.
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Sitt, Wing-hung Edward. "Is the validity of non-invasive computerized tomography coronary angiography equivalent to invasive coronary angiography for the evaluation of coronary artery disease." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38479606.
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Liu, Longjian, and 劉隆健. "Population based studies of fibrinogen in relation to other coronary heart disease risk factors, coronary heart disease and diabetesmellitus in Hong Kong." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31237447.
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Shi, Fang. "Abnormalities of low-density lipoprotein metabolism in patients with coronary artery disease." Diss., The University of Arizona, 1991. http://hdl.handle.net/10150/185596.
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Studies have shown that hypercholesterolemia is a risk for cardiovascular disease; however, some normocholesterolemic individuals still develop coronary atherosclerosis. This project was undertaken to investigate the association of abnormalities of low density lipoprotein (LDL) metabolism, in the absence of hypercholesterolemia, with the development of coronary artery disease (CAD). Mononuclear leukocytes (MNL), HL-60 cells and 1,25-dihydroxyvitamin D₃-induced HL-60 macrophages were used as model systems to study the effect of an altered LDL composition on cellular lipoprotein and sterol metabolism. LDL and MNL were isolated from patients with and without CAD. The mean rate of LDL degradation was 1.7-fold higher in CAD-MNL than in control-MNL (P < 0.05), independent of the LDL source. The increased LDL degradation rate in CAD-MNL appeared to be due to an increased LDL receptor activity of CAD-MNL and not to an increased CAD-LDL interaction with the receptor since LDL isolated from patients with and without CAD had similar in vitro degradation rates by HL-60 cells and D₃-induced HL-60 macrophages. LDL from CAD patients (CAD-LDL) contained significantly less cholesteryl ester per particle than LDL from control subjects (Control-LDL). The ability of CAD-LDL and Control-LDL to regulate sterol and lipoprotein metabolism was compared in HL-60 cells. The results indicate that CAD-LDL exhibited reduced abilities to suppress receptor-mediated LDL degradation and to activate acyl-CoA:cholesterol acyltransferase as compared to Control-LDL. There was no significant difference in the rate of sterol synthesis between cells treated with CAD-LDL and Control-LDL. The data support the hypothesis that cholesteryl ester-poor CAD-LDL exhibits a decreased ability to down-regulate LDL receptor activity which could in part account for the observed increase in LDL degradation by MNL from CAD patients. A noncompetitive enzyme-linked immunosorbent assay (ELISA) was developed to measure plasma apolipoproteins (apo) A-I and B. The results indicate that a reduced plasma apo A-I level was associated with CAD patients even if there were no significant differences in the levels of high density lipoprotein cholesterol when compared with individuals without CAD.