Rozprawy doktorskie: „Coronary heart disease – Genetic aspects”

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McCaskie, Pamela Ann. "Multiple-imputation approaches to haplotypic analysis of population-based data with applications to cardiovascular disease". University of Western Australia. School of Population Health, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0160.

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[Truncated abstract] This thesis investigates novel methods for the genetic association analysis of haplotype data in samples of unrelated individuals, and applies these methods to the analysis of coronary heart disease and related phenotypes. Determining the inheritance pattern of genetic variants in studies of unrelated individuals can be problematic because family members of the studied individuals are often not available. For the analysis of individual genetic loci, no problem arises because the unit of interest is the observed genotype. When the unit of interest is the linear combination of alleles along one chromosome, inherited together in a haplotype, it is not always possible to determine with certainty the inheritance pattern, and therefore statistical methods to infer these patterns must be adopted. Due to genotypic heterozygosity, mutliple possible haplotype configurations can often resolve an individual's genotype measures at multiple loci. When haplotypes are not known, but are inferred statistically, an element of uncertainty is thus inherent which, if not dealt with appropriately, can result in unreliable estimates of effect sizes in an association setting. The core aim of the research described in this thesis was to develop and implement a general method for haplotype-based association analysis using multiple imputation to appropriately deal with uncertainty haplotype assignment. Regression-based approaches to association analysis provide flexible methods to investigate the influence of a covariate on a response variable, adjusting for the effects of other variables including interaction terms. ... These methods are then applied to models accommodating binary, quantitative, longitudinal and survival data. The performance of the multiple imputation method implemented was assessed using simulated data under a range of haplotypic effect sizes and genetic inheritance patterns. The multiple imputation approach performed better, on average, than ignoring haplotypic uncertainty, and provided estimates that in most cases were similar to those observed when haplotypes were known. The haplotype association methods developed in this thesis were used to investigate the genetic epidemiology of cardiovascular disease, utilising data for the cholesteryl ester transfer protein gene (CETP), the hepatic lipase (LIPC) gene and the 15- lipoxygenase (ALOX15) gene on a total of 6,487 individuals from three Western Australian studies. Results of these analyses suggested single nucleotide polymorphisms (SNPs) and haplotypes in the CETP gene were associated with increased plasma high-density lipoprotein cholesterol (HDL-C). SNPs in the LIPC gene were also associated with increased HDL-C and haplotypes in the ALOX15 gene were associated with risk of carotid plaque among individuals with premature CHD. The research presented in this thesis is both novel and important as it provides methods for the analysis of haplotypic associations with a range of response types, while incorporating information about haplotype uncertainty inherent in populationbased studies. These methods are shown to perform well for a range of simulated and real data situations, and have been written into a statistical analysis package that has been freely released to the research community.

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Fournier, Caroline. "Genetic investigation of vascular diseases in the French-Canadian population". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0030/MQ64355.pdf.

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Makubalo, Zola. "Mutation screening of candidate genes and the development of polymorphic markers residing on chromosome 19q13.3, the progressive familial heart block I gene search area". Thesis, Stellenbosch : Stellenbosch University, 2000. http://hdl.handle.net/10019.1/51838.

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Thesis (MSc)--Stellenbosch University, 2000.
ENGLISH ABSTRACT: Progressive familial heart block type I (PFHBI) is a cardiac ventricular conduction disorder of unknown cause associated with risk of sudden death, which has been described in several South African families. Clinically, PFHBI is characterised by right bundle branch block on ECG, which may progress to complete heart block, necessitating pacemaker implantation. The disease shows an autosomal dominant pattern of inheritance with evidence of genetic anticipation. Using genetic linkage analysis, the PFHBI-causative gene was mapped to a 10 eentimorgan (cM) gene-rich area of chromosome (C) 19q13.3, which has, subsequently, been reduced to 7cM by fine mapping with polymorphic dinucleotide (CA)n short tandem repeat (STR) markers. Several attractive candidate genes, including muscle glycogen synthase (GSY 1) and histidine-rich calcium binding protein (HRC), lie within this region. The aim of the present study was two-fold: 1) to identify and characterise tetranucleotide (AAAT)n STRs within the PFHBI critical region that could be developed as polymorphic markers for use in genetic fine mapping and 2) to screen selected regions of GSY 1and HRC, positional candidate genes, for the presence ofPFHBI-causing mutation(s). Cosmids harbouring CI9q13.3 insert DNA were screened for the presence of (AAAT)n STRs by dot blot and Southern blot hybridisation using a radiolabelled (AAAT)lO oligonucleotide probe. To characterise the harboured (AAAT)n STRs, the positively hybridising fragments identified by Southern blot were sub-cloned, sequenced and primers designed from the unique repeat-flanking sequences. These primers were used to genotype the (AAAT)n repeat locus to assess its polymorphic nature in a panel of unrelated individuals. Alternatively, vectorette PCR, a rapid method of identifying repeat sequences and obtaining the flanking sequences in large inserts, was employed to develop polymorphic markers from the positively hybridising clones. Selected exons of GSY1 and HRC were screened for the presence of potentially disease-causing mutations by PCR-SSCP analysis and direct sequencing, respectively, in PFHBI-affected and unaffected family members. Of the available cosmid clones that gave strong signals on dot blot and Southern blot hybridisation, three, 29395, 24493 and 20381, were located within the critical PFHBI area and were used for marker development. An interrupted (AAAT)n repeat motif (n less than 5) was identified in cosmid 29395, however, the repeat locus was not polymorphic in the tested population. No (AAAT)n motif, single or repeated was observed in the partial sequence of the sub-cloned fragment of cosmid 24493. Using vectorette peR, no repeated (AAAT)n motif was identified on sequencing the generated products in either cosmid 24493 or 2038l. However, diffuse single AAAT motifs were detected in both cosmids. Exons 4, 5, 11, 12 and 16 of GSY 1, containing domains that are conserved across species, and the conserved eterminus- encoding exons 2-6 of HRC were selected for screening for potential PFHBI-causing mutation(s). However, no sequence variations were detected. The interrupted (AAAT)n repeat identified in cosmid 29395 was not polymorphic, which confirmed reports that complex repeats, especially those containing AAAT motifs of less than 6 repeats, are not polymorphic. One possible explanation for the absence of a repeated AAAT motif in cosmids 24493 and 20381, which both gave positive hybridisation signals, is that the low annealing temperature of the AfT -rich repeat-anchored primers used in vectorette peR may have resulted in transient annealing to the diffuse single AAAT motifs detected on sequencing. The screened regions of candidate genes GSYI and HRC were excluded from carrying the disease-causing mutation(s). The availability of new sequence data generated by the Human Genome Project will influence future strategies to identify the PFHBI gene. Electronic searches will allow identification of STR sequences for development of polymorphic markers and gene annotation will allow selection of new candidate genes for mutation screening.
AFRIKAANSE OPSOMMING: Sien volteks vir opsomming

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Kuek, Conchita Maria. "Hereditary haemochromatosis and the C282Y genotype : implications in diagnosis and disease". University of Western Australia. School of Surgery and Pathology, 2003. http://theses.library.uwa.edu.au/adt-WU2004.0024.

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[Truncated abstract. Please see the pdf format for the complete text.] The discovery of the C282Y mutation and its role in the development of hereditary haemochromatosis has allowed a greater understanding into the effects of iron overload and its involvement in other conditions such as diabetes and heart disease. It has also allowed the better classification of heterozygotes, who were previously only diagnosed through the use of family studies. There are however, areas of conflict between phenotyping and genotyping methods. My research involved examining the relationship between Haemochromatosis and certain diseases such as diabetes and heart disease; genotyping versus phenotyping discrepancies and the possible interaction of secondary mutations. In Chapter 3 a population study was undertaken with the aim of comparing genotyping versus phenotyping methods as well as increasing general practitioner awareness regarding hereditary haemochromatosis and its diagnosis. It was determined that a minimum of 5000 subjects would be required to give the study sufficient power. Individuals were to be between the ages of 20—40 years, and thus presumably presymptomatic. Participation was entirely voluntary and a consent form was to be signed. Recruitment of subjects proved to be difficult and there was a selective bias towards individuals already displaying symptoms of haemochromatosis. In total less than a 100 subjects were recruited for the study. There were several issues encountered in the implementation of this study. Firstly the number of GPs participating was probably insufficient to recruit the subjects required. A more extensive campaign was probably required to enroll more GPs. Secondly it is very difficult for a busy GP to find the time necessary to explain the study to each of his patients and to get them to sign the consent form. Finally a bias developed in some of the requests. The subjects participating in this study were supposed to be random but in many cases the GPs had enrolled them in the study because they had symptoms of iron overload. In effect the biggest obstacle this study faced was the recruitment of subjects. Due to the small number of subjects little statistical data could be obtained from this study. It was noted, however, that genotyping methods detected two individuals who were homozygous for the C282Y mutation. Both also had increased transferrin saturation levels. Phenotyping detected 5 individuals with increased transferrin saturation. The three others detected via phenotyping were C282Y heterozygotes. Haemochromatosis has long been though to be related to the development of diabetes due to the effect of iron overload on the pancreas. If this is so it would be logical to assume that the prevalence of haemochromatosis would be higher in a diabetic population. Chapter 4 examined the possibility that diabetics have a higher frequency of the C282Y mutation. A population group consisting of 1355 diabetics was genotyped for the C282Y mutation and iron studies were performed on all heterozygotes and C282Y homozygotes. Initial findings indicated that there was a significant difference between the diabetic and control population. However, this finding was the opposite of what was expected, there seemed to be a decreased frequency of the Y allele in the diabetic population rather than an increased one. The control and diabetic populations were not matched in terms of ethnicity. The removal of the ethnic bias in the diabetic population altered the statistics so there was no longer a significant difference between the two groups. This study highlighted the importance of using appropriate control populations as comparison groups. The final results of the study indicated that there was no significant difference between the diabetic population and the control population. This would seem to indicate that there is not an increased occurrence of the C282Y mutation in the diabetic population when compared to the control group. Chapter 5 considered the possible association between C282Y heterozygosity and cardiovascular disease as well as the potential for early mortality. Several recent studies have indicated that C282Y heterozygosity may be a risk factor for the development of atherosclerosis, possibly on the basis of increased iron loading. Using a control population and a population of individuals with known coronary events the incidence of the C282Y mutation was compared against other risk factors. C282Y heterozygosity did not appear to be a risk factor for atherosclerosis. There was however, a statistically significant link between increased ferritin in women and carotid plaques. A population of elderly women was genotyped in order to examine the effects of C282Y heterozygosity on longevity. The first hypothesis addressed in chapter 5 was that C282Y heterozygosity was a risk factor for the development of coronary heart disease.

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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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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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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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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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Net, J. B. van der. "Towards genetic prediction of coronary heart disease in familial hypercholesterolemia". [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2009. http://hdl.handle.net/1765/14566.

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Sarwar, Nadeem. "Emerging molecular and genetic risk factors for coronary heart disease". Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611549.

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Zhang, Qiuping. "Genetic variants of lipid transport genes, dyslipidaemia and coronary heart disease". Thesis, Queen Mary, University of London, 1997. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1642.

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Coronary heart disease (CHD) is one of the most common causes of death in Western Countries. Genetic factors playa major role in the aetiology of CHD, however, the primary defects responsible for the disease have not been identified in most cases. With the application of recombinant DNA technology, it is possible to analyse the putative aetiological role of candidate genes. The role of the Lipoprotein Lipase (LPL) gene and the Apolipoprotein AI-CIII-AIV gene cluster were examined in German and Chinese controls, dyslipidaemics and arteriopaths (coronary artery disease and/or peripheral artery disease). Analyses of four allelic distributions (HindIlI-RFLP, Ser447_Ter, Asp9-Asn and Asn291_Ser mutations) of the LPL gene in German and Chinese populations with or without arterial disease did not show any significant frequency differences. In the German group, plasma triglycerides and VLDL-triglycerides were lower in subjects possessing the Ser447_Ter mutation (p=0.06 and < 0.05 respectively), this mutation was also significantly less frequent in the highest tertiles for triglycerides (p<0.02) and VLDL(P<0.04). The Ser447_Ter variant was found at lower frequencies in the Chinese lipaemic subjects. In addition, two disease related genetic variants (Asp9-Asn and Asn291 _Ser) in Europeans were not found in the Chinese group (P<0.03). Analyses of four genotypic distributions (the ApoAI PstI, MspI, XmnI RFLPs and the ApoCIII G3175_C variant) of the ApoAI-CIII-AIV gene cluster in German and Chinese populations with or without arterial disease did not show any significant differences. However, significant associations between high triglyceride, VLDL, TGIHDL ratio and the PstI RFLP at the ApoAI gene were shown in the German group (p=O.OOl, p<0.02 and p<0.04). In the Chinese group, the rare alleles of the Apo CIII G3175 -C variant and the Apo AI MspI polymorphic variant were both found more frequently in the upper tertile distributions for apo CIII levels and plasma triglyceride/HDL ratios (p<0.05 and p<0.04 respectively). The frequencies of two disease related RFLPs of the ApoAI gene (detected Pane 2 b with Mspl and Xmnl) and the ApoC1I1 G3175 -C variant were significantly different (p<0.0006, p<0.004 and p<0.003 respectively) between Chinese and German control groups. Out of eighteen French patients with diabetes m., obesity and severe hypertriglyceridaemia, eight subjects were found to possess mutations at the LPL gene locus by direct DNA sequencing. Three of these: Argl92_Ter (C829_ T); Phe351 _Leu (C1308_ G) and Thr361 -Thr (C1338 _ A) had not previously been described. Thr361_ Thr appears to be a common population polymorphism whose allele frequency in normolipidaemic diabetics was found to be 0.120 (162 chromosomes studied). The others are all rare at frequencies of <0.01 and may contribute to the phenotype by impairi~g clearance of plasma triglycerides. In eleven of the most lipaemic Chinese subjects, Thr361_Thr (C1338_A) was observed, additionally, the previously published mutations, Ala261_ Thr and Ser447 -Ter, were also noticed. Finally, a Finnish kindred, with premature coronary heart disease and decreased HDL cholesterol levels, was identified having an ApoAI variant (Lys107 ~~) by Single-Strand Conformation Polymorphisms (SSCP) and direct DNA sequencing. This variant was caused by a 3 bp deletion of nucleotides 1396 through 1398 in exon 4 of the ApoAI gene. Ten family members were heterozygous for this mutation. Mean serum apoAI and apoAII levels in heterozygotes were reduced by 18% and 220/0, and cholesteryl ester transfer protein activity (CETP) was reduced by 25% compared with unaffected family members (both p<0.05) respectively, while the plasma lecithin:cholesterol acyltransferase (LCAT) activity did not show any difference between heterozygotes and unaffected family members. The ability of the isolated apoAI variant to serve as a co-factor for LCAT in vitro did not differ from that of normal apoAI.

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Ashton, Emma Louise, i 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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Björnstedt, Bennermo Marie. "On the genetic variation of interleukin-6 in health and coronary heart disesase /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-253-5/.

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Abdul-Majid, Hariyati Shahrima. "Psychological aspects of recovery from coronary heart disease among patients in Malaysia". Thesis, University of Surrey, 2001. http://epubs.surrey.ac.uk/843015/.

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The aim of this research was to identify psychological factors associated with outcomes of coronary heart disease (CHD) among patients in Malaysia. The research tested whether a model of psychological factors found to predict recovery from CHD in the West would be applicable in a collectivistic society such as Malaysia. Among the research questions posed were whether self-referent beliefs, coping styles and locus of control constructs would predict affective status for patients at the time of hospitalisation, and whether these psychological constructs would predict patients' affective status, functional status and quality of life up to nine months posthospitalisation. The research also looked at whether behavioural intentions assessed at the time of hospitalisation predict attendance at cardiac rehabilitation programmes (CRP) and the use of complementary medicine after hospital discharge. A series of studies were conducted to answer the research questions formulated based on the model developed for each study. Study 1 assessed the reliability and validity of measures developed in the West when used on a healthy Malaysian sample (N = 97). Study 2 examined the concurrent relationships among psychological variables assessed at the time of hospitalisation for 97 cardiac patients. Study 3 examined the longitudinal relationships among variables assessed in patients at the hospital and outcome variables assessed up to six months post-hospitalisation (n = 26). Study 4 (N = 77) determined the concurrent relationships among psychological variables assessed in posthospitalisation patients, and compared the psychological characteristics between posthospitalisation patients and the in-hospital patients in Study 2. A notable feature of the findings obtained from Studies 2, 3 and 4 was that whilst some psychological variables were predictive of outcome variables, others failed to support findings obtained in the West. Self-referent beliefs, for example, significantly predicted intention to attend CRP but did not significantly predict actual attendance. In addition, negative affect was relatively low for patients at in- and post-hospital assessments. Accordingly, Study 5 (N = 300) was conducted to explore possible origins of the lack of consistent findings of the studies on Malaysian cardiac samples. It assessed perceptions of illness constructs in healthy individuals. The findings of this study revealed that perceptions of illness constructs were predictive of healthful behaviors. The findings also revealed the importance of looking at specific cultural factors such as spiritual beliefs in explaining treatment-seeking behaviours in non-Western societies such as Malaysia. In conclusion, the findings of this research project highlighted the importance of studying health and illness-related behaviors within the socio-cultural contexts in which the illness occurs. Although models developed in the West may be applicable in these non-Western, collectivistic societies, the constructs assessed may not be sufficient in accounting for the variance in explaining psychological and behavioral outcomes of illness. Thus, in addition to the constructs found to be predictive of these outcomes on Western patients, psychological studies done in Malaysia should also assess mental representations of illness that are specific to Malaysians.

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Lluís, Ganella Carla 1984. "Genetic factors associated with coronary heart disease and analysis of their predictive capacity". Doctoral thesis, Universitat Pompeu Fabra, 2012. http://hdl.handle.net/10803/84185.

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The main expansion of the discovery of genetic variants associated with complex diseases has occurred during the last decade. This expansion has been accompanied, and in some sense motivated, by the desire to use this information to improve the predictive capacity of many diseases with an unidentified familial component, including coronary heart disease (CHD), with the aim of translating this genetic knowledge into clinical practice. This doctoral thesis is structured in two lines of investigation that address distinct aspects of this issue, first to evaluate the possible role of genetic variation in a candidate gene in modulating CHD risk, and second to evaluate whether genetic information can be used to improve risk assessment tools used in clinical practice. In the first research line (described in Part I), we investigate the contribution of genetic variation in one of the most widely-studied genes in cardiovascular genetics, ESR1, which encodes the Oestrogen receptor α protein. We provide a solid meta-analysis of evidence regarding the most widely-studied variant in this gene and we further explore the role of a broad range of common and uncommon variants in this gene in CHD risk. Using these approaches, we find no evidence of association between the genetic variants studied and CHD risk. However, although we can confidently accept that common genetic polymorphisms are not associated with cardiovascular disease, we cannot discard the possibility that other types of variation in this gene (for instance epigenetic variation) could modify susceptibility to cardiovascular disease, or that other elements of this pathway are associated with an increased risk of CHD. In this research I have provided a reliable answer to this long running unanswered question in cardiovascular genetics, allowing research to re-focus on other elements of this system or other pathways. In the second line, we explored the possible utility of genetic information obtained from genome-wide association studies (GWAS) in prediction of 10-year risk of CHD events by adding this information to cardiovascular risk functions. We have followed the recommendations proposed by the American Heart Association for evaluating the utility of novel biomarkers in clinical practice, and have demonstrated that although the magnitudes of the effects of these genetic variants on CHD risk are modest, there is a tendency towards improvement in the capacity of the risk functions to predict future CHD events. The translation of genetic information into clinical practice was one of the main motivations for the investment in genome-wide association studies, and my research represents one of the first efforts to explore this possibility.
L’expansió principal pel que fa al descobriment de variants genètiques associades amb malalties complexes s’ha dut a terme durant la última dècada. Aquesta expansió ha estat acompanyada, i d’alguna forma motivada, pel desig d’usar aquesta informació per millorar la capacitat de predicció d’aquelles malalties on hi és present un cert component familiar però en les que no es coneixien les variants que conferien un major risc de patir la malaltia, entre elles la cardiopatia isquèmica (CI). La present tesis doctoral està estructurada en dues línies d’investigació que avaluen el possible rol d’un gen candidat en la susceptibilitat de la CI i també avalua la millora en la capacitat de predicció d’un esdeveniment coronari de les eines usades habitualment en la pràctica clínica mitjançant la inclusió d’informació genètica. Més concretament, la primera línea d’investigació es centra en la contribució de la variació genètica en un dels gens més estudiats en relació amb CI: el gen que codifica pel receptor d’estrogens alfa (ESR1). En aquesta línea hem proveït un sòlid meta-anàlisis entre la variant més àmpliament estudiada d’aquest gen i risc coronari i també hem explorat el paper de la majoria de les variants comunes descrites en aquest gen i risc de CI. Mitjançant cap dels anàlisis hem trobat evidència d’associació entre les variants genètiques en aquest gen i el risc de CI. No obstant això, i encara que podem acceptar que les variants genètiques comunes d’aquest gen no estan associades amb esdeveniments coronaris, no podem descartar que altres tipus de variació en aquest gen (com per exemple variació epigenètica) pugui estar modificant la susceptibilitat a patir un esdeveniment coronari, ni tampoc que altres elements de la mateixa cadena de senyalització estiguin associats amb la malaltia. En la segona línea d’investigació, hem explorat el possible paper de les variants genètiques, obtingudes mitjançant estudis d’associació global del genoma (GWAS), en la millora de la capacitat de predicció a 10 anys dels esdeveniments coronaris, mitjançant la seva addició en les funcions de risc cardiovascular clàssiques. Hem seguit les recomanacions proposades per la American Heart Association per l’avaluació en la pràctica clínica de nous biomarcadors, i hem demostrat que, tot i que la magnitud de l’associació d’aquestes variants és modesta, hi ha una tendència cap a la millora de la capacitat de predicció de les funcions de risc.

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Jain, Ravi. "Intelligent techniques for the diagnosis of coronary artery disease /". Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phj248.pdf.

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Ho, Lai-yi Ada, i 何麗儀. "Does social support influence coronary heart disease prognosis?: a meta-analysis". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B39724116.

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Patel, Riyaz. "Beyond genome wide discovery : an exploration of novel genetic variants for coronary heart disease". Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/38470/.

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Recent developments spurred on by the Human Genome Project have for the first time permitted genome wide association studies leading to identification of multiple novel variants for complex diseases. This thesis consists of a series of studies exploring recent genetic findings for coronary heart disease (CHD) within the broader context of the promises of the genomic era that new findings would ultimately lead to 1) Identification of new disease mechanisms 2) Permit genotype based risk prediction and 3) Promote development of novel and targeted therapies based on genotype. We sought to address these questions, using the Emory Genebank, a collection of angiographically phenotyped subjects with stored blood samples and long-term follow up. We first refined the phenotype for CHD to help understand underlying mechanism and demonstrated differential associations between 8 novel risk variants including 9p21, and sub-phenotypes of CHD and thereby proposed differing mechanisms of risk for these loci. With two non-CHD cohorts we then demonstrated further association between one particular risk variant at 6p24 and the intermediate phenotype of arterial elasticity and related this to a potential novel mechanism of risk. Despite significant association with first events in population cohorts, we showed that these risk variants including 9p21 have limited value in secondary risk prediction, failing to demonstrate any association with prospective events in our cohort as single markers or when combined into a cumulative genetic risk score. Finally in subjects carrying leukotriene pathway CHD risk variants, we administered an oral leukotriene synthesis inhibitor and after just 4 week of therapy observed significant improvement in their endothelial function. In summary, these studies demonstrate the value of refining the phenotype to understand potential mechanisms, the complexities of genetic risk prediction and the feasibility and benefit of targeting therapy based on risk genotype.

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19

Karackattu, Sharon Liz. "Genetic approaches to studying coronary heart disease in SR-BI/apoE double knockout mice". Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/34279.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2006.
"February 2006."
Includes bibliographical references.
Coronary heart disease (CHD) is a major healthcare concern in both developed and developing nations. The principal cause of CHD is atherosclerosis, the buildup of fatty deposits in vessel walls. SR-BI/apoE double knockout (dKO) mice are a novel mouse model of human CHD, exhibiting spontaneous coronary occlusive atherosclerosis, myocardial infarction, cardiac dysfunction and premature death. This model represents a unique system in which to study the two principal underlying mechanisms of atherosclerosis and CHD, inflammation and lipoprotein lipid metabolism. The first part of this thesis demonstrates that B- and T-lymphocytes do not play a significant role in development or progression of atherosclerosis or CHD in SR-BI/apoE dKO mice. More importantly, this study eliminates B- and T-lymphocyte-driven immunoglobulin-mediated inflammation as a significant mechanism instigating or exacerbating myocardial injury in dKO mice. Strikingly, the mice generated for this study also demonstrate that genetic background influences both average lifespan and lifespan variability of dKO mice. The second study investigates alterations in lipoprotein metabolism on CHD and demonstrates that hepatic lipase deficiency, despite raising plasma cholesterol levels, retards development of both aortic and coronary occlusive atherosclerosis in dKO mice.
(cont.) This reduction in atherosclerosis is associated with delayed onset and/or progression of hypertrophy, myocardial infarction and cardiac dysfunction as well as a 37% extension in lifespan. Both of these studies, along with others, suggest SR-BI/apoE dKO mice experience atherosclerotic coronary-occlusion-induced ischemic heart disease and that they may be a valuable tool in which to investigate the etiology of as well as influences of genetic, environmental and pharmacologic manipulations on CHD.
by Sharon Liz Karackattu.
Ph.D.

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20

Robinson, Simon David. "Environmental, genetic and inflammatory factors modifying endothelial function in patients with coronary heart disease". Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/29340.

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Outcome measures: In a well characterised cohort of patients with stable CHD: athero-thrombotic events during follow-up; t-PA genotype; inflammatory cytokines; acute t-PA release and forearm blood flow 9FBF) during intra-brachial infusion of vaso-agonists. Results: Net t-PA release was 91% lower in the patients who experienced death, MI, CVA or hospitalisation for myocardial ischaemia (p ≤ 0.02) over a median follow-up 34 months. This novel finding validates the application of the forearm model to studying the pathophysiological changes observed in coronary heart disease and suggests that the acute endogenous fibrinolytic capacity is important in determining future cardiovascular risk. Despite confirming previous reports of impaired t-PA release and reduced FBF responses in cigarette smokers (p ≤ 0.05), we found no effect of a number of t-PA genetic polymorphisms on acute t-PA release. In subjects with established CHD, inter-individual differences in t-PA release appear to predominantly reflect the presence of environment factors such as cigarette smoking. Intra-brachial infusion of tumour necrosis factor-α impaired NO-dependent vasodilation (p < 0.001), increased basal t-PA concentrations and doubled bradykinin induced t-PA release (p=0.006). This suggests a pathosphysiological mechanism whereby circulating levels of inflammatory cytokines are directly related to plasma t-PA concentrations and the risk of future cardiovascular events. Pharmacological interventions with anti-cytokine therapies may have a therapeutic role in subjects at risk of acute coronary syndromes. Despite augmenting the effects of basal nitric oxide release and a direct NO donor (p<0.05), a bolus and intravenous infusion of sildenafil did not affect either endothelium-dependent vasodilation or acute t-PA release. Sildenafil does not modify acute t-PA release and phosphodiesterase type 5 inhibitors are unlikely to reverse the generalised vascular dysfunction seen in patients with coronary heart disease.

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21

Hill, John Stuart. "Genetic and environmental factors affecting the incidence of coronary artery disease in heterozygous familial hypercholesterolemia". Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/28810.

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Familial hypercholesterolemia (FH) is an autosomal dominant disorder in which the primary defect is a mutation in the LDL receptor. Heterozygous FH is among the most common inborn errors of metabolism and remains as the best example of an inherited defect causing premature coronary artery disease (CAD). This thesis describes the physical and biochemical characteristics of heterozygous FH in a large cohort consisting of 208 women and 156 men. The influence of both genetic and environmental factors on the clinical expression of FH were investigated to better understand the phenotypic variation within FH and thus improve the prediction and treatment of CAD in affected individuals. The general incidence of CAD in this population was lower compared to previous reports but the differences between the sexes were expected. It was shown that men had a much higher frequency of CAD (31%) compared to women (13%) despite having lower concentrations of total and LDL cholesterol. In addition, the average age of onset of coronary symptoms was delayed in females, 55 years compared to 48 years for males. A greater risk of developing CAD for men was associated with low levels of HDL cholesterol and a history of smoking. In women, however, CAD was associated with elevated triglyceride levels and the presence of hypertension. In order to efficiently assess the influence of the co-inheritance of the apolipoprotein E polymorphism in this large FH population, a novel apo E phenotyping procedure was developed. Phenotypes were determined directly from plasma which was neuraminidase treated, delipidated and focused in polyacrylamide minigels. The accuracy of this method was confirmed by making a comparison to the established procedure of phenotyping by isoelectric focusing of delipidated VLDL. The low cost, speed and simplicity of the minigel methodology provided ideal conditions to phenotype a large patient population. The frequencies of the ɛ2, ɛ3 and ɛ4 alleles of apolipoprotein E in 125 unrelated FH subjects did not differ significantly from the normal population. In addition, there was no apparent relationship between apo E4 and the concentration of any of the parameters in the plasma lipid profile. However, the presence of the E2 isoform was associated with significantly elevated triglycerides in both sexes. From this study, it is evident that the mutant FH gene exerts its effect within a system of interacting environmental and polygenic factors that are known to modify atherosclerotic risk. It has been established that the dissimilarity in the frequency of CAD between men and women is related to differences between the impact of known risk factors and the incidence of CAD. Therefore, the importance of the influence of these risk factors and the differences between men and women should be emphasized when treating and predicting the development of CAD in patients with FH.
Medicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate

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22

Jenneke, Cindy A. N. "The effect of dietary patterns on risk factors for CHD : a comparative study of students residing at the Adventist International Institute of Advanced Studies in the Philippines". Thesis, Link to online version, 2006. http://hdl.handle.net/10019/554.

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23

Loung, Le Anh. "Genetic variations in the interleukin-6(IL-6) gene : implication in coronary heart disease (CHD)". Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406589.

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24

Buri, Robert J. (Robert John). "The Role of Anger/Hostility on Physiological and Behavioral Risk Factors for Coronary Heart Disease". Thesis, University of North Texas, 1995. https://digital.library.unt.edu/ark:/67531/metadc278222/.

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The purpose of this study was to examine the role of anger/hostility on physiological and behavioral coronary heart disease risk factors. It was hypothesized that anger/hostility would contribute to the severity of CHD via consummatory behaviors such as smoking, poor diet, and excessive alcohol consumption. Some researchers suggest that negative consummatory behaviors play a direct causal role in CHD. The present study proposed that hostility predisposes an individual to these behaviors, and that these behaviors in turn, contribute to CHD. Further, it was proposed that some of the anger that exists in CHD patients may result from the individual being unable to participate in some of their previous consummatory behaviors after suffering a myocardial infarction. Also, it was hypothesized that the construct of anger/hostility would be differentially related to consummatory behaviors.

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25

Warner, Anke Sigrid. "The expression, regulation and effects of inducible nitric oxide synthase in hibernating myocardium". Title page, contents and summary only, 2002. http://web4.library.adelaide.edu.au/theses/09PH/09phw279.pdf.

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Amendments inserted at back. "May 2002" Includes bibliographical references (leaves 237-290) Experiments described in this thesis address the potential role of inducible nitric oxide synthase (iNOS) in hibernating myocardium. Specifically it was sought to establish a cellular model of hibernating myocardium and investigate the expression, regulation and effects of iNOS in this model. Experiments were performed using primary cultures of neonatal rat ventricular myocytes.

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26

El, Rayess Mohamed Aghar. "Genetic variation in the PECAM-1 gene and its role in atherosclerosis and coronary heart disease". Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404401.

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27

Naqvi, Habib. "Coronary heart disease : Lay representations of genetics, genetic testing and the decision to pursue predictive genetic testing amongst South Asians". Thesis, University of the West of England, Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522563.

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Saleheen, Danish. "Genetic determinants of major lipids and myocardial infarction in Pakistan". Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609033.

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29

Pepe, Salvatore. "The influence of dietary fatty acids on cardiac function /". Title page, table of contents and abstract only, 1991. http://web4.library.adelaide.edu.au/theses/09PH/09php4201.pdf.

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30

Rajput-Williams, Jayshri. "Genetic variation at the apolipoprotein B gene and associations with coronary heart disease and its risk factors". Thesis, Queen Mary, University of London, 1996. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1681.

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Coronary heart disease (CED) is the major cause of mortality in Western societies. The main risk factors are plasma lipoprotein concentrations, smoking, blood pressure and family history. The effect of family history implies a genetic contribution to the aetiology, support for which has also come from twin, and other heritability studies. The genetic component of CHID may be studied by the candidate gene approach, whereby the genes of products most likely to be involved in the processes leading to CHD, and in its risk factors, are analysed. The plasma concentration of apolipoprotein (apo) B, the major protein component of low density lipoprotein (LDL), is positively correlated with the risk of developing CHD. In this research, the gene for apo B was analysed for restriction enzyme fragment length polymorphisms (RFLPs). A RFLP is caused by a sequence change in the DNA, and results in length variation in the fragments. RFLPs for apo B have been shown to be associated with CHD and the plasma concentrations of cholesterol, triglycerides and apo B in some population studies. However, other studies have failed to confirm these relations. The work described in this thesis was designed to overcome some of the problems which niay have produced these inconsistencies. A random sample of 300 men, aged 49-65 years, residing in South Wales was studied. RFLPs determined in these individuals were used to generate genotypes and haplotypes (arrangements of specific alleles on a single chromosome). Significant associations were found between some genotypes and some haplotypes with altered concentrations of plasma total cholesterol and LDL cholesterol and with risk of CHD and/or with obesity. Presence of Xbal site (X2X2 genotype) was significantly associated with higher concentrations of plasma LDL cholesterol (p=0.0 19). Absence of Mspl site (M 1) was associated with significantly elevated concentrations of plasma total and LDL cholesterol (p < 0.05) by both the techniques of genotype and haplotype analysis. EcoRl RFLP (absence of the site - El) was the minimum haplotype necessary to detect a significant association with decreased plasma cholesterol J Rajput- Williams Ph. D. Thesis Page 3 concentrations (p < 0.05). Genotypes generated from alleles defined by the Mspl-EcoRl RFLPs were associated with significant variation in serum cholesterol concentration (p < 0.03), showing a stratification of concentration with the highest being associated with loss of the Mspl site and the lowest with the presence of the EcoRl site. Both these RFLPs result in charged aminoacid alterations, and lie close to the LDL receptor binding domain of apo B. The minimum haplotype necessary for detection of apo B with CHD was Xbal-Mspl (p < 0.05). The minimum haplotype associated with obesity was the RFLP pair Pvull-Xbal (p < 0.05). Further examination for mutations of the CpG dinucleotide which may influence cholesterol metabolism was undertaken by screening around the putative LDL receptorbinding domain (RBD) of the apo B gene. One variant was detected for aminoacid residue 3500 (Arg,,,,, 4 Gln) mutation, and two variants for aminoacid residue 3611 which also corresponds to the MspI mutation (Arg,,, ,4 Gln).

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31

Williams, Angela B. "Incidence and implications of atypical exercise blood pressure responses in adults without diagnosed coronary heart disease". Thesis, Virginia Tech, 1985. http://hdl.handle.net/10919/45657.

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Data were collected from the initial symptomâ limited maximal exercise tests of 161 patients without. diagnosed coronary heart disease (CHD). Subjects were grouped according to their systolic (SBP) and diastolic (DBP) blood pressure changes between the final two stages of exercise.
Master of Science

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32

Abbott, Janice Melodie. "Psychological, cardiovascular and haematological aspects of the Type A behaviour pattern in relation to coronary heart disease". Thesis, University of Central Lancashire, 1988. http://clok.uclan.ac.uk/20137/.

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The programme of work comprised two maj or aspects of enquiry. Firstly, the work aimed to identify specific situations which promote the Type A coping response. Secondly, the research aimed to investigate the biological mechanisms by which Type A behaviour may be translated into coronary heart disease. Specifically, the sympathetic adrenomedullary process operating via platelet and prostaglandin activity provided a major focus of the work. Type A's (defined by both the Bortner and Thurstone Scales) have been shown to perceive performance tasks as more threatening than Type B's. not only by their enhanced cardiovascular reactivity (heart rate and systolic blood pressure), but also by their superior word recall performance. Dyadic interactive situations, in which combinations of Type A's and Type B's work together on a task, and only one member of the dyad has response control, promote intriguing behavioural, and cardiovascular coping patterns. On a difficult task, Type A dyads (and dyads in which Type A's lacked response control) performed poorer than other dyadic combinations. Cardiovascularly, Type A's demonstrated the greater heart rate, systolic and diastolic pressure, and slower cardiovascular recovery, particularly, if they lacked control of responding, or were paired with another Type A. A long-term naturalistic study provided validity for the acute laboratory tasks. Behavioural, cardiovascular and haematological response patterns, and the timing of reactivity, differentiated Type A's from Type B's. Whilst preparing for and following final year examinations, Type A individuals demonstrated the greater elevations in heart rate, systolic and diastolic blood pressure, plasma adrenaline and noradrenaline. They also demonstrated the faster platelet aggregation (although percentage aggregation decreased similarly for both groups), together with the greater increase in the anticoagulant, antithrombin III. The complexity of these haenatological findings encouraged the examination of two prostaglandins which control platelet function (the coagulatory thromboxane A2 , and the anticoagulatory prostacyclin). Different response patterns emerged prior to, and following a mental arithmetic challenge. The task anticipation effect involved elevated heart rate, systolic and diastolic pressure, plasma adrenaline and prostacyclin. Type A's demonstrated the greater reactivity in all parameters. Following the task, a decrease in the percentage and speed of aggregation was recorded, together with an increase in plasma noradrenaline and thromboxane A 2 . At this stage, Type A's demonstrated the faster platelet aggregation, and the greater noradrenai.ine levels. The thromboxane/prostacyclin ratios, however, remained similar for both groups. The Type A psychobiological response pattern, characterised by the greater magnitude and duration of potentially pathological cardiovascular and hasnatological parameters, may exert profound effects on the development of atherosclerosis and the onset of clinical coronary events.

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33

吳湘舒 i Xiangshu Wu. "Illness perception and coping among older adults with coronary heart disease: a study at acute convalescentstage". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31243794.

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34

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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35

Esslinger, Krista. "Dietary outcomes of a school-based trial to reduce risk factors for coronary heart disease". Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31227.

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The dietary outcomes of a school-based heart health promotion program in a low-income, multiethnic, inner-city neighbourhood of Montreal, Canada, were investigated. Eight intervention schools and sixteen control schools participated in the project from 1993 to 1997. Twenty-four hour recall data, as well as data on anthropometric and sociodemographic characteristics, were collected from a subsample of all students in grades 4--6 (aged 9--12 years) at baseline (n = 498), after two years (n = 491), and after four years (n = 347). There were no significant differ in nutrient intakes between 1995 and 1997, so these data were combined for analyses. Compared to students in control schools, students exposed to the program had a significantly increased mean intake of vitamin C per 1000 kcal (4184 kJ) (p = 0.0013). Compared to students in designated intervention schools at baseline, mean make of vitamin C per 1000 kcal was significantly increased (p = 0.002) and mean folate intake was significantly domed (p = 0.0058) in exposed to the program. When the intervention group was restricted to only those students who had received 16 hours or more of program exposure (n = 113), there were no significant differences in any nutrient intakes when compared to control students or students in intervention schools at baseline. This program was unsuccessful in changing nutrient intakes of school-aged children, contributing further evidence that conscious dietary change is difficult to achieve by means of a school-based program with a reasonable number of curriculum hours.

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36

Coe, Ellen Moster. "The correlation between changes in conicity index and changes in other risk factors for coronary heart disease at baseline and after a six- month intervention program". Virtual Press, 1995. http://liblink.bsu.edu/uhtbin/catkey/941352.

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The emphasis of the study was to determine the degree of correlation between the Conicity Index and known risk factors for heart disease. Conicity Index was shown in one study to be a useful screening tool in assessing the relationship between body composition and risk for heart disease. This study was designed to provide nutrition education and teach lifestyle modification to fourteen Veteran's Affairs patients. Change in specific risk factors including Waist-to-Hip Ratio, Body Mass Index, serum lipid levels and dietary intakes were correlated with change in Conicity Index over the six month study. Results from the present study did not suggest that the Conicity Index would serve as an effective screening tool for the present population. Mean body weight, body mass index, hip circumference, cholesterol and triglyceride levels, total caloric and fat intake all decreased significantly as a result of the program. Through nutrition education, behavior modification and group support, the risk for heart disease was successfully modified in this population.
Department of Family and Consumer Sciences

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37

Bruce, Sharon Diane. "Development of rate related exercise-induced myocardial ischemia and risk of selected coronary diesease endpoints". Thesis, This resource online, 1993. http://scholar.lib.vt.edu/theses/available/etd-11102009-020132/.

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38

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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39

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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40

Lai, Josanna Yuk-Lin. "Is keeping in or letting out anger good for your heart?" Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30099.

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Given the presumed importance of cardiovascular reactivity and the role of anger in the development of hypertension and coronary heart disease, this study is the first to jointly examine three related areas (i.e. gender effects, anger direction preference, and opportunity/no opportunity to aggress following an anger Inducing situation). The present study tested the following hypotheses: a) that cardiovascular reactivity would vary as a function of subjects' gender and direction preference; b) that the rate of cardiovascular recovery would vary as a function of anger direction preference and opportunity/no opportunity to aggress; c) that the subjective feelings of anger after harassment would vary as a function of gender, anger direction preference, and opportunity/no opportunity to aggress; and d) that the evaluation of experimenter's competency and performance would vary as a function of anger preference. 56 females and 49 males executed a math task while being harassed for "poor performance". Next, they were randomly assigned to either write a negative evaluation of the frustrator or to copy a neutral paragraph and then to circle some letters in another paragraph. Heart rate and blood pressure were measured intermittently throughout. Subjects' preferred mode of anger expression (i.e. anger-in versus anger-out) had been previously assessed and cross validated by self as well as peer evaluations. Results indicated that gender was a better predictor than anger direction preference for cardiovascular reactivity to harassment. Complex patterns of recovery were detected with Intriguing sex differences. Results on male diastolic recovery were consistent with a matching hypothesis of anger direction preference but only for anger-out males. In addition, subjective anger for males was related to opportunity/no opportunity conditions, whereas females did not show such a relationship. Female anger-ln's showed quicker systolic recovery than anger-out's. Lastly, the evaluation of experimenter's competency and performance did not vary as a function of anger preference. Therapeutic implications of the findings within the context of anger control as well as trends for future research are discussed.
Arts, Faculty of
Psychology, Department of
Graduate

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41

Chan, Kin-wang, i 陳健宏. "Study of the in vivo role of TSPYL2 in transgenic mice". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B38225049.

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42

何耀 i Yao He. "A case-control study on passive smoking and coronary heart disease in never-smoking women in Xi'an, China". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31235839.

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43

Zhian, Samaneh. "Molecular Genetic Analysis of CRELD1 in Patients with Heterotaxy Disorder". PDXScholar, 2011. https://pdxscholar.library.pdx.edu/open_access_etds/410.

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Heterotaxy refers to the abnormal arrangement of internal organs in relation to each other. Model organism studies have shown that functions of more than eighty genes are required for normal asymmetric left-right organ development. CRELD1 has been shown to be necessary for proper heart development and mutations in CRELD1 are known to increase risk of cardiac atrioventricular septal defects (AVSD). AVSD is the most common form of heart defect associated with heterotaxy, and we have previously shown that some individuals with heterotaxy-related AVSD have mutations in CRELD1. Therefore, we propose to examine the CRELD1 gene in a large sample of patients with heterotaxy syndrome. Our goal was to determine if mutations in CRELD1 are associated with other manifestations of heterotaxy or if they only coincide with AVSD. To achieve this aim, a sample size of 126 patients with heterotaxy collected by Dr. Belmont, Baylor college of Medicine, Texas, with approximately 66% of the heterotaxy population with different types of heart defects, were used for this study. Ten exons, promoter regions, and regulatory elements in the introns of CRELD1 gene were sequenced and analyzed. In this study three different heterozygous missense mutations in CRELD1 were identified in three unrelated individuals. These three individuals were diagnosed with different forms of heart defects in addition to AVSD. All three mutations were identified in highly conserved regions of CRELD1 possibly altering the CRELD1 properties. This demonstrates that mutations in CRELD1 may increase the susceptibility of AVSD in heterotaxy population. This information can help us to find factors effecting disease susceptibility in heterotaxy patients since the heart defects are a complex trait with incomplete penetrance.

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44

Harshfield, Eric Leigh. "Genomics of lipid metabolism : identification of genetic determinants of lipid metabolites and the effect of perturbations of lipid levels on coronary heart disease risk factors". Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/277818.

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Background: Coronary heart disease (CHD) is one of the leading causes of death worldwide, and global mortality rates are expected to continue to rise over the coming decades. In Pakistan in particular, chronic diseases are responsible for 50% of the total disease burden. Circulating lipids are strongly and linearly associated with risk of CHD; however, despite considerable efforts to demonstrate causality, available evidence is conflicting and insufficient. Study of the underlying metabolic pathways implicated in the association between lipids and CHD would help to disentangle and elucidate these complex relationships. Objectives: The primary objectives of this dissertation were to (1) identify the genetic determinants of lipid metabolites and (2) advance understanding of the effect of perturbations in lipid metabolite levels on CHD and its risk factors. Methods: Direct infusion high-resolution mass spectrometry was performed on 5662 participants from the Pakistan Risk of Myocardial Infarction Study to obtain signals for 444 known lipid metabolites. Correlations and associations of the lipids with smoking, physical activity, circulating biomarkers, and other CHD risk factors were assessed. Genome-wide analyses were conducted to analyse the association of each lipid with over 6.7 million imputed single nucleotide polymorphisms. Functional annotation and Gaussian Graphical Modelling were used to link the variants associated with each lipid to the most likely mediating gene, discern the underlying metabolic pathways, and provide a visual representation of the genetic determinants of human metabolism. Mendelian randomisation was also implemented to examine the causal effect of lipids on risk of CHD. Results: The lipids were highly correlated with each other and with levels of major circulating lipids, and they exhibited significant associations with several CHD risk factors. There were 254 lipids that had significant associations with one or more genetic variants and 355 associations between lipids and variants, with a total of 89 sentinel variants from 23 independent loci. The analyses described in this dissertation resulted in the discovery of four novel loci, identified novel relationships between genetic variants and lipids, and revealed new biological insights into lipid metabolism. Conclusion: Analyses of lipid metabolites in large epidemiological studies can contribute to enhanced understanding of mechanisms for CHD development and identification of novel causal pathways and new therapeutic targets.

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Strath, Scott J. "The effect of a light-moderate versus hard exercise intensity on health and fitness benefits". Virtual Press, 1998. http://liblink.bsu.edu/uhtbin/catkey/1115726.

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The purpose of this study was to determine the effect of a light-moderate versus hard exercise intensity on health and fitness benefits in a previously sedentary population. Twenty-six subjects, 17 male (mean age 45 + 3 yrs), 9 female (mean age 48 + 3 yrs) with at least one coronary artery disease risk factor volunteered to participate in this study. Subjects underwent laboratory testing comprising of, resting heart rate and blood pressure, body composition, blood lipid analysis and aerobic capacity (V02 ), prior to and 22-32 weeks after participating > 2 days per week in the Adult Physical Fitness Program (APFP) at Ball State University. After an initial exercise prescription subjects self selected an exercise intensity between 40-80% of their maximal heart rate range (MHRR) at which to train. Subjects were then grouped into those who trained at < 60% (light-moderate) and those who trained at > 60% (hard) of their MHRR.Those that self selected a hard training intensity did show a significantly greater decrease in diastolic blood pressure than the light-moderate intensity group. Subjects received a main training effect with a mean decrease in systolic blood pressure (123 ± 2.8 to 119 ± 2.4 mmHg), diastolic blood pressure (78 ± 2.2 to 75 ± 1.7 mmHg), and mean increases for HDL-cholesterol (49 ± 2.5 to 53 ± 2.8 mg/dL), absolute functional capacity (2.676 +.162 to 2.843 +.169 L/min) and relative functional capacity (30.2 ± 1.5 to 32.8 + 1.8 ml/kg/min). In conclusion this study demonstrated health and fitness benefits when training at least 2 days per week with greater effects when training at a hard versus light-moderate intensity with regards to diastolic blood pressure.
School of Physical Education

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46

Ward, Clay Herold. "Psychological aspects and potential pathogenic processes of achievement striving associated with the Type A personality". Diss., Virginia Polytechnic Institute and State University, 1986. http://hdl.handle.net/10919/82607.

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The Type A personality has been associated with coronary heart disease and other psychosomatic illnesses. Previous investigators have suggested that a major stress-related feature of the Type A personality is "excessive" striving for achievement, even though ambition is often conceptualized as a positive aspect of personality. The purpose of the present dissertation was to examine whether there are psychological differences in how Type A individuals, compared to their Type B counterparts, approach and respond to an achievement situation, which, in addition to defining the Type A personality, have potential pathogenic health and personal adjustment implications. Three experiments are reported which examined self-directed behavior in an achievement situation where subjects were required to perform sequential general information tests. The results of Experiment I support the hypotheses that Type A individuals, compared to Type B individuals, adopt very high standards for performance, which increase the probability that they will not achieve their personal goals. The results of Experiment II expand on the findings of Experiment I by indicating that in addition to not achieving personal goals, Type A individuals, relative to Type B individuals, also tend to devalue their actual performance. Furthermore, failure to achieve personal goals was associated with increased self-report of psychological distress. The findings of Experiment III replicate previous results and further indicate that failure to achieve personal goals is associated with specific negative consequences of increased anger and decreased self-esteem. The results also indicate that Type A individuals compared to Type B individuals, tend to make internal attributions for failure, while at the same time, they take less personal credit for success. Finally, the results of Experiment III suggest that the Type A personality is related to general negative affective states, psychosomatic illness, and daily stress. Results of the three experiments indicate that there are important psychological characteristics of how Type A individuals approach and respond to an achievement situation, which appear to have pathogenic health and personal adjustment consequences. Recent reconceptualizations of the Type A personality have emphasized a trait-like dimension of hostility, characterized by cynicism, resentment, and suspiciousness toward others as the "toxic" component of the Type A personality. The present study urges that striving toward lofty goals, devaluation of performance, self-blame for failure without taking comparable self-credit for success, along with negative self-evaluation also be viewed as important unhealthy aspects of the Type A personality.
Ph. D.

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47

Hong, Ki-Ho. "The development of a normative reference standard for maximal oxygen con[s]umption using the Ball State University-Adult Physical Fitness Program cohort". Virtual Press, 2005. http://liblink.bsu.edu/uhtbin/catkey/1319542.

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Background: Normative values of VO2max have been developed or updated based on the estimated VO2max, but measured normative values of VO2max have not been developed yet. VO2max has been reported to relate to coronary heart disease (CHD) risk factors, yet most of the studies have used estimated VO2max to compare CHD risk factors. Therefore, the purpose of this study was to develop norms for VO2max from the Ball State University (BSU) Adult Physical Fitness Program cohort that represented percentiles based on the measured VO2max. In addition, this study evaluated the relationship between measured VO2max and six coronary heart disease (CHD) risk factors, which include Body Bass Index (BMI), high density lipoprotein cholesterol (HDL-C), glucose, triglyceride (TG), total cholesterol (TC) and resting blood pressure (BP).Methods: Subjects were healthy men (N=1,867) and women (N=1,253), ranging in age from 19 to 75 years, who completed the standard BSU Adult Physical Fitness Program quiet and exercise testing sessions between 1971 and 2000, with the graded exercise testing (GXT) conducted with one of the following protocols including modified walking, running, Balke, Bruce, and BSU/Bruce ramp. To be included, subjects had to achieve respiratory exchange ratio (RER) >1.0 during their exercise test.Results: All subjects were classified into ten group determined by deciles of VO2max for each decade of age for males and females respectively. A linear regression showed that VO2max decreased 10.1% per decade (0.44 mi.kg'•min'•yr') for men and 9.7% per decade (0.32 ml•kg-l.min-l.yr') for women. There was no significant difference in the rate of agerelated decline in VO2max per decade between men and women or between deciles of VO2max. Also, the percent of subjects with an exercise history code >5 (regularly participate in exercise at least 3 days per week) was higher in the higher VO2max deciles. In addition, five positive CHD risk factors were inversely related to VO2max, and one negative CHD risk factor was directly related to VO2max. As expected, the higher CRF groups had a more favorable CHD risk factor profile. Also, the mean of VO2max decreased with the greater number of CHD risk factors.Conclusion: This study developed normative values of the VO2max based on measured VO2max. VO2max was significantly correlated to CHD risk factors.
School of Physical Education, Sport, and Exercise Science

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Horner, Katrina E. "The effect of increasing physical activity on health benefits in sedentary women". Virtual Press, 1997. http://liblink.bsu.edu/uhtbin/catkey/1041902.

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The purpose of this study was to evaluate whether the current CDC/ACSM physical activity recommendation, ("30 minutes or more of accumulated moderate-intensity activity, most if not all, days of the week") would improve women's health through a reduction ofcoronary heart disease (CHD) risk factors. Twenty-one sedentary females (ages 49 ± 7 yrs.) with one or more CHD risk factors underwent baseline laboratory including: resting heart rate and blood pressure, resting electrocardiogram, body mass index, bioelectrical impedance, skinfold measures, waist-to-hip, blood lipid profile, and V02max. The VO2 was determined by an exercise treadmill test using the Ball State University Ramp protocol. The subjects were instructed on the CDC/ACSM recommendation, the physical activity survey, and given examples of moderate-intensity activity. The survey data was collected bimonthly over the six month period. The subjects reported participating in >_ 30 min. of moderate-intensity activity an average of 4 f 1 days/week with an average duration of 54 ± 26 min. On the remaining days, the subjects reported doing an average of 14 ± 6 minutes per day. Also, 90% of the women reported doing the activity in continuous bouts. Following the six month study period, the women were retested in the laboratory. Sixteen subjects completed the post-testing. The results of the sixteen women showed a significant improvements in HDL-cholesterol (51 ± 15 vs.56 ± 15 mmHg; p=<.05) and TC/HDL ratio (4.5 ± 1 vs.4.25 ± 1.3; p=<.05). There were no significant changes in the other risk factor variables examined or their V02,„.. It was concluded that the majority of previously sedentary, middle aged women can not meet the CDC/ACSM recommendations for daily activity and total energy expenditure. Additionally, it appears that when given the choice, these women choose to do activity in continuous time blocks versus breaking the daily activities into shorter time periods.
School of Physical Education

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Frewen, Sharon H. "The design and evaluation of a short-term group psychotherapy model for survivors of a first myocardial infarction". Thesis, Rhodes University, 2005. http://hdl.handle.net/10962/d1015041.

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There is extensive evidence that the rehabilitation of individuals with coronary heart disease needs to include psychological components to complement the exercise and dietary recommendations that are normally provided. However, psychological aspects have not been integrated into medical care in South Africa to any significant degree. Psychological interventions overseas have included the modification of the Type A behaviour pattern, stress management, cognitive restructuring, relaxation techniques, improved communication skills, the identification and expression of emotions, and emotional support. The aim of the present study was to design a short-term group intervention which incorporated these aspects and which included an exploration of the mind-body experience post infarct. In addition, the intervention aimed to increase participants' awareness of the compensatory dynamics of the Type A behaviour pattern. The intervention was tailored to South African conditions and was evaluated by means of a multiple case study design. The intervention was delivered to a group of nine coronary heart disease patients which included six survivors of myocardial infarction, the remaining participants having undergone a by-pass operation. Data included weekly feedback sheets evaluating each session, repeated measures on the Profile of Mood States, the Jenkins Activity Survey, a Spouse Rating Scale and extensive qualitative data on each participant including tape recordings of each session and data collected from a series of interviews before, during and after the programme. The feedback sheets and recordings of the sessions were used as a basis for recommendations for revising the content and structure of the programme for future use. Case narratives were written for three of the participants and provided an in-depth look at how and why individual changes did or did not occur in response to the intervention. In addition, the case narratives revealed the role played by the compensatory dynamics of the Type A behaviour pattern in complicating rehabilitation for survivors of myocardial infarction. Two participants were offered a series of individual sessions at 18-month follow-up and the material from these sessions was also used to aid in the interpretation of the data. The content of the 18-month follow-up sessions provided evidence for the importance of conducting a developmental analysis of the origins of low self-esteem and insecurity that maintain and drive the Type A behaviour pattern. In these sessions, this analysis provided the basis for a brief focused psychodynamic psychotherapy that facilitated marked changes that had not been achieved in the 12-week structured group intervention. It is recommended that future research investigate the use of brief psychodynamic psychotherapy on an individual basis as a complement to a group intervention focusing on psycho-education, building social support and management of problematic emotions in everyday situations.

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Harper, Christopher Scott. "Family-Supportive Supervisory Behaviors as a Moderator of the Relationship between Job Strain and Workers' Blood Pressure". PDXScholar, 2011. https://pdxscholar.library.pdx.edu/open_access_etds/198.

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Cardiovascular disease is one of the leading causes of death in industrialized nations. Research indicates that job strain may be significantly related to cardiovascular disease in employees with little to no social support. Using the JDC-S model developed by Karasek (1979) and elaborated upon by Johnson and Hall (1988), the family-supportive supervisory behaviors (FSSB) measure created by Hammer et al., (2009), and the blood pressure wrist monitor device Omron317T, this study examined FSSB as a moderator of the relationship between job strain, job demands, job control and workers' blood pressure on work and non-work days. Sixty-nine grocery store workers from a Midwest grocery store chain participated in this study, fifty-six of which were included in the analyses. Though none of the interactions were significant at the .05 level, results indicate that FSSB is significantly related to a number of blood pressure readings at the grand centered mean of job strain, job control, and job demands.

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