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Dissertations / Theses on the topic 'Coronary heart disease – Pathogenesis'

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Published: 4 June 2021

Last updated: 3 February 2022

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1

Cao, Fei. "Chlamydia pneumoniae, toll-like receptors and pathogenesis of atherosclerotic heart disease." View the abstract Download the full-text PDF version (on campus access only), 2007. http://etd.utmem.edu/ABSTRACTS/2007-022-Cao-index.html.

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Thesis (Ph.D. )--University of Tennessee Health Science Center, 2007.
Title from title page screen (viewed on May 16, 2008 ). Research advisor: Gerald I. Byrne, Ph.D. Document formatted into pages (xi, 114 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 65-107).

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2

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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3

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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4

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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5

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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6

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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7

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
incomplete_metadata

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8

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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9

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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10

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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11

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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12

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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13

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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14

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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15

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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16

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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17

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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18

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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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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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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21

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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Hogg, Marilynne Audrey. "Women living with coronary heart disease, barriers to care." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0024/MQ51753.pdf.

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Zdravkovic, Slobodan. "Coronary heart disease in Swedish twins : quantitative genetic studies /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-771-5/.

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Järemo, Petter. "Platelets and the inflammatory response in coronary heart disease /." Linköping, 2003. http://www.bibl.liu.se/liupubl/disp/disp2003/med816s.pdf.

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Eriksson-Berg, Margita. "Hemostasis in middle-aged women with coronary heart disease /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-978-1/.

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Al-Khalili, Faris. "Coronary heart disease in women : diagnostic and prognostic markers /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4092-4/.

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McKeigue, Paul Matthew. "Epidemiology of coronary heart disease in Asians in Britain." Thesis, University College London (University of London), 1990. http://discovery.ucl.ac.uk/1350028/.

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In countries where people of South Asian origin have settled, unexpectedly high coronary heart disease rates have been recorded in South Asian men and women compared with other ethnic groups. In England high CHD mortality is shared by Gujarati Hindus, Punjabi Sikhs and Muslims from Pakistan and Bangladesh. The high CHD rates in these populations are unexplained by levels of smoking, blood pressure, plasma cholesterol or dietary fat intake. To test whether disturbances of haemostatic activity, lipoprotein metabolism or carbohydrate metabolism might underlie the high CHD mortality in South Asians, a population study in east London was undertaken. The results confirmed that the high CHD rates in South Asians compared with the native British population cannot be explained by differences in the distributions of blood pressure or plasma cholesterol. The hypothesis of a disturbance of haemostatic activity was not supported. A pattern of low plasma HDL cholesterol and high triglyceride levels, high serum insulin levels after a glucose load and high prevalence of non-insulin-dependent diabetes was identified in CD Bangladeshis. On the basis of these findings and a review of other recent work it is suggested that: (i) insulin resistance underlies these disturbances of lipoprotein and carbohydrate metabolism in Bangladeshis; (ii) this tendency to insulin resistance is a general pattern in South Asian populations overseas; and (iii) it is a possible underlying mechanism for the high rates of both CHD and diabetes in these populations. The planning of a large study to test this is described. Preliminary results confirm that a syndrome of metabolic disturbances related to insulin resistance, first identified in Bangladeshis, is present also in Gujaratis and Punjabis. This is associated with a striking tendency to central obesity in South Asians. These findings point to the aetiological role of insulin resistance in CHD and suggest possible strategies for prevention in South Asian communities.

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capewell, simon. "defining and addressing the burden of coronary heart disease." Thesis, University of Liverpool, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493051.

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Malik, Iqbal Saeed. "Assessment of the inflammatory burden in coronary heart disease." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.542947.

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Doshi, Sagar Navinchandra. "Homocysteine, folate and endothelial function in coronary heart disease." Thesis, Cardiff University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444121.

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Nicholson, Amanda Claire. "Psychological distress as a predictor of coronary heart disease." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406151.

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Gorman, Donal Neilson. "Triglycerides, the APOA5-APOC3 locus and coronary heart disease." Thesis, University of Cambridge, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.707967.

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Wu, Kelvin Kwan Hoe. "Gene-nutrient interactions and risk of coronary heart disease." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.614117.

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Meng, Weihua. "Investigation of the genetic basis of coronary heart disease." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501377.

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Bhattacharyya, M. R. "Psychological and biological factors in acute coronary heart disease." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1444164/.

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Psychosocial factors are thought to contribute to the long term development of coronary artery disease (CAD), to the triggering of cardiac events in people with advanced disease, and to adaptation following acute coronary syndromes (ACS). My thesis presents three studies addressing different aspects of the relationship between emotional factors and CAD, using different methodologies. They focus on the role of negative emotions in vulnerability to myocardial ischaemia in daily life, the influence of acute emotional triggers of ACS on long term quality of life, and the effect of depression following ACS on a particularly important aspect of adaptation, namely return to work. The first study, called the Silent Ischaemia Study (SIS) investigated 88 out-patients with suspected CAD who underwent 24 hour ambulatory electrocardiogram (ECG) monitoring, together with saliva sampling and characterisation of daily life by a new method called the Day Reconstruction Method (DRM). The results indicated that in patients with definite CAD, depressed mood was associated with reduced high frequency and increased low frequency heart rate variability (HRV), suggestive of parasympathetic withdrawal. The Cortisol slope over the day was flatter in more depressed patients with CAD. Episodes of transient ischaemia and/or arrhythmia were also associated with increased negative affect, but their incidence was low, primarily because most patients were medicated with beta blockers. The second and third studies derive from the ACCENT (Acute Coronary Syndrome, Emotion and Triggers) study, exploring long term adaptation following ACS. Analyses showed that the likelihood of returning to work was negatively associated with depression immediately following ACS, independently of clinical and demographic factors, and that emotional triggers predicted elevated anxiety and poor mental health status at 12 and 36 months independently of covariates. In combination, these studies suggest that negative emotional status contribute both to the onset of acute cardiac events, and to adaptation following ACS.

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Leong, Yuk-yan Pauline, and 梁玉恩. "The effectiveness of exercise-based cardiac rehabilitation program for secondary prevention of coronary heart disease : a systematic review." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193828.

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Objective: To examine the effect of exercise-based cardiac rehabilitation program for secondary prevention of coronary heart disease on cardiac-related mortality, recurrent cardiovascular event and quality of life. Methods: All studies published between 1990 and 2013 in PubMed, and from 1980 to 2013 in EMBASE, which evaluated the effectiveness of exercise-based cardiac rehabilitation program for coronary heart disease. Using the specific keywords “Cardiac rehabilitation”, “Coronary heart disease” OR “Ischemic heart disease” [MeSH], “Exercise” OR “Physical activities” AND “Quality of life” OR “Mortality” AND Cardiovascular events” were searched. A total of 7randomized controlled trials out of 5,051articles from PubMed and 117 articles from EMBASE were included in this systematic review. The primary outcome measures used in the included seven studies were HRQOL, restenosis, cardiac event, cardiac related mortality. Similar demographic and clinical characteristics of the subjects between the intervention and the control groups were recorded. The studies were from five countries. The average age of the subjects in the seven studies was 61years, the average half of them have history of myocardial infarction. Though there were discrepancies among the results generated in the included studies, the potential benefits of exercise-based cardiac rehabilitation could be seen. Results: Compared with the non-exercise-based cardiac rehabilitation, patients allocated to the exercise-based cardiac rehabilitation program had greater improvement in HRQOL and reduction of cardiac events. The result of reducing restenosis was inconsistent. The cardiac related mortality is not significant difference between exercise-based and non-exercise-based cardiac rehabilitation.
published_or_final_version
Public Health
Master
Master of Public Health

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39

Thompson, Mary. "Coronary effects of endothelins." Thesis, University of Bath, 1995. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296580.

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Lee, Hang-ling Justine. "An exploratory study of the psycho-social stress of coronary heart disease patients /." Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2233094X.

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41

Sitt, Wing-hung Edward, and 薛穎雄. "Is the validity of non-invasive computerized tomography coronary angiography equivalent to invasive coronary angiography for theevaluation of coronary artery disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39724578.

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42

Liu, Longjian. "Population based studies of fibrinogen in relation to other coronary heart disease risk factors, coronary heart disease and diabetes mellitus in Hong Kong /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19926583.

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43

Michael, Sze-Yuan. "The role of cytokines in the pathogenesis of coronary artery disease." Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.502766.

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44

Gan, Wenqi. "Traffic-related air pollution, community noise, and coronary heart disease." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/38091.

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Cardiovascular disease is the leading cause of death worldwide. Recent evidence suggests associations between exposure to air pollution and community noise and cardiovascular disease mortality. While road traffic is a major common source for air pollution and community noise in urban areas, studies of their joint effects on the risk of cardiovascular disease have been limited. Linked administrative databases from the British Columbia health insurance system were used to assemble a population-based cohort to investigate the independent and joint effects of traffic-related air pollution and community noise on coronary heart disease (CHD) mortality. The cohort included all residents aged 45-85 years who resided in metropolitan Vancouver, Canada, for at least 5 years at baseline (N~400,000). During a 4-year follow-up period, CHD death cases were identified from the provincial death registration database. Distances from residences to major roads were first used as a surrogate for exposure to traffic-related pollution. Living close to major roads was associated with CHD mortality and changes in distances to major roads were associated with altered CHD mortality risk in an exposure-response fashion. Both traffic-related air pollution and noise could be responsible for these associations. Subsequently, land use regression models were used to estimate residential exposure to major traffic-related air pollutants including black carbon, PM₂.₅, NO₂, and NO. Black carbon concentrations were associated with CHD mortality, with a clear exposure-response relationship. No robust associations were found with other air pollutants. A noise prediction model was then used to estimate annual average community noise levels at each person’s residence. Community noise and black carbon were independently associated with CHD mortality: an interquartile range elevation in noise (6.6 dB(A)) and black carbon (0.97×10–⁵/m) was associated with a 6% (95% CI, 1-11%) and a 4% (95% CI, 1-8%) increase in coronary mortality, respectively. There was no discernable linear exposure-response relationship between community noise and CHD mortality. Together, these analyses suggest that traffic-related fine particulate air pollution, indicated by black carbon, and traffic noise may both be responsible for observed associations between exposure to road traffic and cardiovascular disease.

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45

Ashton, Emma Louise, and emma ashton@deakin edu au. "Effects of dietary constituents on coronary heart disease risk factors." Deakin University. School of Biological and Chemical Sciences, 2000. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20061207.153511.

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Coronary Heart Disease (CHD) is a major cause of death in Western countries. Mediterranean and Asian populations have a lower risk of death from CHD compared to Westernised population, as do vegetarian versus omnivorous populations. Dietary constituents of traditional diets consumed by these populations are thought to influence both the classical risk factors for CHD, and the more recently identified risk factors, such as oxidative modification of low density lipoprotein (LDL), LDL particle size, arterial compliance and haemostatic factors. The aim of this thesis was to examine the effects of several food components, particularly soybean and monounsaturated fat (MUFA), on CHD risk factors through 3 carefully controlled dietary interventions, and a cross-sectional study. A randomised crossover dietary intervention study was conducted in 42 healthy males to investigate the effect on CHD risk factors of replacing lean meat with tofu, a soybean product regularly consumed by Asian populations, while controlling all other dietary factors. The tofu diet resulted in significantly lower total cholesterol and triacylglycerol levels compared to the lean meat diet, and LDL particles that were more resistant to in vitro oxidative modification. However, insulin, fibrinogen, factor VII, and lipoprotein (a) were not significantly different on the 2 diets. A postprandial study was subsequently conducted to investigate any acute effects of a tofu test meal on the oxidative modification of LDL in 16 male subjects. There was no significant difference between the susceptibility of LDL to oxidative modification before and after the tofu meal. Twenty eight healthy subjects completed a separate randomised crossover dietary intervention comparing a high MUFA fat diet, using an Australian high oleic sunflower oil, with a low fat, high carbohydrate diet on CHD risk factors. The high MUFA oil diet significantly increased high density lipoprotein cholesterol compared to the low fat diet as well as producing LDL that were more resistant to oxidative modification. Neither the size of the LDL particle nor arterial compliance were significantly different on the 2 diets. Twelve matched pairs of vegetations and omnivores were also studies to compare the habitual diet of a low and higher risk population group, to compare their risk factors and identify dietary constituents that may explain the differences. The vegetarians consumed less saturated fat (SFA) and dietary cholesterol while consuming more polyunsaturated fat, dietary fibre and vitamin E compared to omnivores. The vegetarians had lower total cholesterol, LDL cholesterol and triacylglycerol levels compared to the omnivores and had LDL particles that were more resistant to in vitro oxidation. These findings contribute to our knowledge about the dietary constituents that can alter some CHD risk factors in healthy subjects, and which could reduce the risk of developing CHD. Investigations in high risk groups might reveal even more benefits.

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46

Dunn, Jeremy. "Genetic influences on the premature development of coronary heart disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq24837.pdf.

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47

Stamp, Kelly D. "Advanced registered nurse practitioners' judgments of coronary heart disease risk." [Tampa, Fla] : University of South Florida, 2006. http://purl.fcla.edu/usf/dc/et/SFE0001811.

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48

Aarabi, Mohsen. "Risk stratification of coronary heart disease in UK South Asians." Thesis, University of Sheffield, 2007. http://etheses.whiterose.ac.uk/6084/.

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It is clear that South Asians living in the West have substantially greater relative (coronary heart disease) CHD mortality and morbidity than the general population. Despite this current risk functions based on classical risk factors alone underestimate risk in non-diabetic South Asians. After reviewing the available literature for longitudinal studies exploring the relationship between South Asian ethnicity, as an independent factor, and CHD an adjustment factor suitable for use with the paper- based risk prediction functions was derived. The exploration of possible explanations for the excess risk identified dysglycaemia as one possible explain. Adding 10 years to age, although crude and based on the single prospective study, provides adequate sensitivity and specificity to take into account an "ethnicity factor" accounting for average excess risk in individual UK South Asians. Using this adjustment it was shown that more South Asian men and women, living in the UK, are candidates to receive lipid-lowering therapy for primary and secondary prevention than their Caucasian counterparts. Although the evidence base for a CVD risk estimation procedure in South Asians is slight it is better that they have their risk estimated, albeit with less precision, than be excluded. The present work provides a properly researched evidence base. Moreover, it provides its own very simple, but 1. practice acceptable, adjustment for currently used paper risk estimation tools. Acceptance of ant1hypertensives as a primary prevention treatment was looked at in the South Asians community. South Asians are at least equally accepting of treatment as Caucasians when given information about the personal impact of CVD and the effect and tolerability of antihypertensive treatment. With South Asians having a greater need and at least equal acceptance of preventive therapy, they should receive more such treatment. Current evidence suggests that this is not the case and targeted intervention may be needed. Further research is still required in many areas such as risk factors, risk estimation and recalibration, lifestyle intervention, and efficacy of preventive drug therapy in ethnic minorities. Because this population is at high risk, the benefits of appropriate research will also be high.

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49

Patterson, Christopher Charles. "Survivorship models applied to the study of coronary heart disease." Thesis, Queen's University Belfast, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336126.

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50

McCoy, Patience R. "Perceived versus actual risk of coronary heart disease in women." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3318517.

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