Relevant bibliographies by topics / Coronary heart disease – Genetic aspects

Academic literature on the topic 'Coronary heart disease – Genetic aspects'

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Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "Coronary heart disease – Genetic aspects"

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Cambien, François. "1.C.6 New genetic aspects of coronary heart disease." Atherosclerosis 134, no. 1-2 (October 1997): 6. http://dx.doi.org/10.1016/s0021-9150(97)88138-5.

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Kadykova, O. I. "GENETIC ASPECTS OF DEVELOPMENT AND PROGRESSION OF CONGESTIVE HEART FAILURE IN PATIENTS WITH ISCHEMIC HEART DISEASE AND OBESITY∗." Problems of Endocrine Pathology 57, no. 3 (August 23, 2016): 17–21. http://dx.doi.org/10.21856/j-pep.2016.3.02.

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In this article elucidated the influence of allelic polymorphism of Gln27Glu of β2-adrenoceptors gene on patients that have coronary heart disease and obesity on the expansion and progression of congestive heart failure and left ventricular systolic dysfunction by surveying 222 patients. Presence of C allel of polymorphous locus Gln27Glu of β2-adrenoreceptors gene in patients with ischemic heart disease and concomitant obesity was associated with decreased risk of development of congestive heart failure (p < 0.05). The obtained data shown the absence of influence of polymorphous variants of β2-adrenoreceptors gene on progression of congestive heart failure in patients with ischemic heart disease and obesity (p > 0.05).
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Golukhova, Elena Z., Aygerim Z. Zholbaeva, Mari G. Arakelyan, Naida I. Bulaeva, and Michail M. Minashkin. "Genetic aspects of lone atrial fibrillation in patients without structural heart disease." Annals of the Russian academy of medical sciences 74, no. 4 (October 5, 2019): 245–52. http://dx.doi.org/10.15690/vramn1120.

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Background: Atrial fibrillation (AF) is the most common cardiac arrhythmia. Among patients with AF the subgroup posessing AF without traditional risk factors is differentiated. Such patients are commonly referred as having lone AF and comprise 1020% of all cases. A number of studies have demonstrated that the background of AF, and in particular lone AF, have a substantial genetic component. Aims: To evaluate the influence of gene polymorphism to the development of atrial fibrillation in patients without concomitant valvular pathology and coronary artery disease. Materials and methods: The study included 174 patients with atrial fibrillation and 124 controls without any cardiovascular pathology. All patients were divided into two subgroups: with lone AF (n=94) and with concomitant arterial hypertension (n=80). All patients underwent a complex of clinical, instrumental (ECG, echocardiography, computed tomography of the pulmonary veins) and laboratory tests (thyroid hormones, inflammatory markers, fibrosis), as well as genetic analysis (determination of single nucleotide polymorphisms described as AF risk factors in genes AGXT2, PDE4D, SLN, SCN5A, PITX2, PRRX1, ZFHX3, TBX5, CAV1 и HCN4). Results: For the rare polymorphisms rs12291814 (SLN) and rs137854601 (SCN5A) wasnt found anyone carrier of the minor allele (C and A, respectively). In the both patient subgroups the minor allele T of rs2200733 in PITX2 (OR=3.18, p0.0001), minor allele G of rs3903239 in PRRX1, and minor alleles A of 2 polymorphisms rs2106261 and rs7193343 in ZFHX3 gene were revealed as risk factor of AF (OR=2.96, p0.0001, OR=2.02, p=0.0045, OR=1.64, p=0.04, respectively). We also revealed significant difference between AF and control groups for rs3807989 in CAV1: homozygotic state of minor allele A has a protective effect on the development of arrhythmias (OR=0.39). Conclusions: We revealed the association between the polymorphisms in genes regulating transcription and the development of atrial fibrillation. These polymorphisms have already described but their frequencies have never investigated in Russian population. But the polymorphisms influence to gene functions stays unclear, although attempts to investigate relationship between genotype and gene expression have been made. When the relationship will be discovered it can help us to modify our approach in treatment to patients with atrial fibrillation.
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Golukhova, E. Z., O. I. Gromova, R. A. Shomahov, N. I. Bulaeva, and L. A. Bockeria. "Monogenec Arrhythmic Syndromes: From Molecular and Genetic Aspects to Bedside." Acta Naturae 8, no. 2 (June 15, 2016): 62–74. http://dx.doi.org/10.32607/20758251-2016-8-2-62-74.

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The abrupt cessation of effective cardiac function that is generally due to heart rhythm disorders can cause sudden and unexpected death at any age and is referred to as a syndrome called sudden cardiac death (SCD). Annually, about 400,000 cases of SCD occur in the United States alone. Less than 5% of the resuscitation techniques are effective. The prevalence of SCD in a population rises with age according to the prevalence of coronary artery disease, which is the most common cause of sudden cardiac arrest. However, there is a peak in SCD incidence for the age below 5 years, which is equal to 17 cases per 100,000 of the population. This peak is due to congenital monogenic arrhythmic canalopathies. Despite their relative rarity, these cases are obviously the most tragic. The immediate causes, or mechanisms, of SCD are comprehensive. Generally, it is arrhythmic death due to ventricular tachyarrythmias - sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Bradyarrhythmias and pulseless electrical activity account for no more than 40% of all registered cardiac arrests, and they are more often the outcome of the abovementioned arrhythmias. Our current understanding of the mechanisms responsible for SCD has emerged from decades of basic science investigation into the normal electrophysiology of the heart, the molecular physiology of cardiac ion channels, the fundamental cellular and tissue events associated with cardiac arrhythmias, and the molecular genetics of monogenic disorders of the heart rhythm (for example, the long QT syndrome). This review presents an overview of the molecular and genetic basis of SCD in the long QT syndrome, Brugada syndrome, short QT syndrome, catecholaminergic polymorphic ventricular tachycardia and idiopathic ventricular fibrillation, and arrhythmogenic right ventricular dysplasia, and sudden cardiac death prevention strategies by modern techniques (including implantable cardioverter-defibrillator).
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Islam, AKM Monwarul, AKM Mohibullah, and Timir Paul. "Cardiovascular Disease in Bangladesh: A Review." Bangladesh Heart Journal 31, no. 2 (April 28, 2017): 80–99. http://dx.doi.org/10.3329/bhj.v31i2.32379.

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Like elsewhere, cardiovascular disease (CVD) is an increasingly important cause of morbidity and mortality in Bangladesh. Over the past few decades, because of epidemiological transition, the prevailing disease pattern in this country changed from predominantly communicable to predominantly non- communicable disease, CVD contributes to the latter a lot. Actually, CVD particularly coronary artery disease (CAD) is getting epidemic proportion day by day. Hypertension and heart failure are on the rise, whereas the prevalence of acute rheumatic fever is declining. However, despite some efforts, reliable data concerning various aspects of CVD is inadequate at present. The current prevalence of hypertension, CAD, rheumatic fever and rheumatic heart disease and stroke may be 20-25%, 4-6%, <1/1000, 0.3- 1.0% respectively. Besides conventional risk factors for different CVD, genetic predisposition and some novel issues like high salt intake, arsenicosis, hypovitaminosis D and air pollution may play important role in the aetiopathogenesis of CVD in this population. Formulation of appropriate policy and more emphasis on preventive strategy may help combat CVD in Bangladesh.Bangladesh Heart Journal 2016; 31(2) : 80-99
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Cavarretta, Elena, and Giacomo Frati. "MicroRNAs in Coronary Heart Disease: Ready to Enter the Clinical Arena?" BioMed Research International 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/2150763.

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Coronary artery disease (CAD) and its complication remain the leading cause of mortality in industrialized countries despite great advances in terms of diagnosis, prognosis, and treatment options. MicroRNAs (miRNAs), small noncoding RNAs, act as posttranscriptional gene expression modulators and have been implicated as key regulators in several physiological and pathological processes linked to CAD. Circulating miRNAs have been evaluated as promising novel biomarkers of CAD, acute coronary syndromes, and acute myocardial infarction, with prognostic implications. Several challenges related to technical aspects, miRNAs normalization, drugs interaction, and quality reporting of statistical multivariable analysis of the miRNAs observational studies remain unresolved. MicroRNA-based therapies in cardiovascular diseases are not ready yet for human trials but definitely appealing. Through this review we will provide clinicians with a concise overview of the pros and cons of microRNAs.
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Berezikova, Ye N., M. G. Pustovetova, S. N. Shilov, A. V. Yefremov, A. T. Teplyakov, I. D. Safronov, and Ye N. Samsonova. "Effects of caspase 8 gene polymorphism on the risks for development/course of chronic heart failure." Patologiya krovoobrashcheniya i kardiokhirurgiya 17, no. 2 (October 10, 2015): 45. http://dx.doi.org/10.21688/1681-3472-2013-4-45-49.

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The aim of the study was to identify genetic determinants of increased risks for heart failure severity. Clinical and genetic aspects of the effects of gene polymorphism caspase 8 (polymorphic loci -652(6N)I/D and D302H) on the risks for development and severity of chronic heart failure (CHF) in patients with coronary artery disease were investigated. 277 patients with CHF were studied (182 males and 95 females aged 45 to 65 years (mean age 59.27.7 years). Genotypes were identified by using RFLP analysis of PCR products. The control group included 136 people (mean age 53.64.8 years) who had no symptoms of cardiovascular disorders. The presence of del allele and genotype del/del polymorphic locus -652(6N)I/D gene caspase 8 was associated with an increased risk for heart failure, while the allele ins and genotype ins/ins were found to serve as protective factors. Allele ins and genotype ins/ins polymorphic locus -652(6N)I/D gene caspase 8 proved to be associated with protective effects on the course of CHF in patients with coronary artery disease, while allele del and genotype del/del could be considered as predictors of an unfavorable course of the disease. The analysis revealed no significant differences in the frequency distribution of genotypes and alleles of polymorphic loci D302H gene caspase 8 in patients with chronic heart failure and in the control group, as well as in the dependence on the functional class of heart failure. The definition of polymorphism -652(6N)I/D gene caspase 8 can be recommended for early prediction of risks and severity of heart failure.
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Groznova, O. S., I. M. Miklashevich, V. Yu Voinova, M. A. Shkolnikova, O. N. Tkacheva, E. N. Dudinskaya, and I. A. Kovalev. "Biomarkers of early cardiovascular aging." Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) 64, no. 4 (September 15, 2019): 11–18. http://dx.doi.org/10.21508/1027-4065-2019-64-4-11-18.

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Genetic aspects regulate the intensity and rate of aging (no toxic effects considered), their negative role depends on the pathogenicity of the mutation. The light variant of the genetic “defect” has no clinical signs which feature a certain known genetic syndrome, but it has the biochemical, immunological, vascular and other abnormalities leading to pathological aging. In the most severe case, e.g. progeria, pathological aging is the main phenotypic symptom that manifests already in childhood. The subject of the pathological aging research covers the whole range of intermediate states. The review focuses on aging in individuals without validated signs of disease: coronary heart disease, hypertension, diabetes or fasting hyperglycemia, hyperlipidemia, and others. The authors present the main searching directions of aging biomarkers (size and speed of telomere shortening, breaks in their terminal loops; expression of inflammatory proteins, synaptic interactions proteins and neurotrophic processes; mitochondrial biogenesis; endothelial dysfunction; DNA methylation activity).
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Khaw, Kay-Tee. "Epidemiological aspects of ageing." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 352, no. 1363 (December 29, 1997): 1829–35. http://dx.doi.org/10.1098/rstb.1997.0168.

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A major societal challenge is to improve quality of life and prevent or reduce disability and dependency in an ageing population. Increasing age is associated with increasing risk of disability and loss of independence, due to functional impairments such as loss of mobility, hearing and vision; a major issue must be how far disability can be prevented. Ageing is associated with loss of bone tissue, reduction in muscle mass, reduced respiratory function, decline in cognitive function, rise in blood pressure and macular degeneration which predispose to disabling conditions such as osteoporosis, heart disease, dementia and blindness. However, there are considerable variations in different communities in terms of the rate of age–related decline. Large geographic and secular variations in the age–adjusted incidence of major chronic diseases such as stroke, hip fracture, coronary heart disease, cancer, visual loss from cataract, glaucoma and macular degeneration suggest strong environmental determinants in diet, physical activity and smoking habit. The evidence suggests that a substantial proportion of chronic disabling conditions associated with ageing are preventable, or at least postponable and not an inevitable accompaniment of growing old. Postponement or prevention of these conditions may not only increase longevity, but, more importantly, reduce the period of illnesses such that the majority of older persons may live high–quality lives, free of disability, until very shortly before death. We need to understand better the factors influencing the onset of age–related disability in the population, so that we have appropriate strategies to maintain optimal health in an ageing population.
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Barton, Matthias, and Masashi Yanagisawa. "Endothelin: 30 Years From Discovery to Therapy." Hypertension 74, no. 6 (December 2019): 1232–65. http://dx.doi.org/10.1161/hypertensionaha.119.12105.

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Discovered in 1987 as a potent endothelial cell–derived vasoconstrictor peptide, endothelin-1 (ET-1), the predominant member of the endothelin peptide family, is now recognized as a multifunctional peptide with cytokine-like activity contributing to almost all aspects of physiology and cell function. More than 30 000 scientific articles on endothelin were published over the past 3 decades, leading to the development and subsequent regulatory approval of a new class of therapeutics—the endothelin receptor antagonists (ERAs). This article reviews the history of the discovery of endothelin and its role in genetics, physiology, and disease. Here, we summarize the main clinical trials using ERAs and discuss the role of endothelin in cardiovascular diseases such as arterial hypertension, preecclampsia, coronary atherosclerosis, myocardial infarction in the absence of obstructive coronary artery disease (MINOCA) caused by spontaneous coronary artery dissection (SCAD), Takotsubo syndrome, and heart failure. We also discuss how endothelins contributes to diabetic kidney disease and focal segmental glomerulosclerosis, pulmonary arterial hypertension, as well as cancer, immune disorders, and allograft rejection (which all involve ET A autoantibodies), and neurological diseases. The application of ERAs, dual endothelin receptor/angiotensin receptor antagonists (DARAs), selective ET B agonists, novel biologics such as receptor-targeting antibodies, or immunization against ET A receptors holds the potential to slow the progression or even reverse chronic noncommunicable diseases. Future clinical studies will show whether targeting endothelin receptors can prevent or reduce disability from disease and improve clinical outcome, quality of life, and survival in patients.
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Dissertations / Theses on the topic "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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Books on the topic "Coronary heart disease – Genetic aspects"

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The Apoe gene diet: A breakthrough in lowering cholesterol, weight, and the risk of cardiovascular and Alzheimer's disease through knowledge of your body's genes. Santa Rosa, CA: Elite Books, 2007.

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McDonald, Pamela. Apo e gene diet. Livermore, CA: WingSpan Press, 2006.

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Goldbourt, Uri, Ulf de Faire, and Kåre Berg, eds. Genetic factors in coronary heart disease. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0.

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Mothers, babies and disease in later life. London: BMJ Pub. Group, 1994.

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Berg, Kare, Victor Bulyzhenkov, Yves Christen, and Pierre Corvol, eds. Genetic Approaches to Coronary Heart Disease and Hypertension. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76891-0.

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S, Leon Arthur, ed. Coronary heart disease: A behavorial perspective. Champaign, Ill: Research Press, 1992.

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Budnick, Herbert N. Heart to heart: A guide to the psychological aspects of heart disease. Santa Fe, NM: Health Press, 1991.

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Thompson, David R. Counselling the coronary patient and partner. Harrow: Scutari Press, 1990.

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Kris-Etherton, P. M. Trans fatty acids and coronary heart disease risk. Washington, D.C: ILSI Press, 1995.

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Mogadam, Michael. Choosing foods for a healthy heart. Yonkers, N.Y: Consumer Reports Books, 1993.

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Book chapters on the topic "Coronary heart disease – Genetic aspects"

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Erdmann, Jeanette, and Maria Loreto Muñoz Venegas. "The Genetics of Coronary Heart Disease." In Genetic Causes of Cardiac Disease, 141–68. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27371-2_4.

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Lemmer, Björn, and Klaus Witte. "Chronopharmacological aspects of coronary heart disease." In Developments in Cardiovascular Medicine, 295–308. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-1577-0_19.

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Dhawan, Jatinder. "Coronary Heart Disease and Related Diseases." In Genetic Disorders of the Indian Subcontinent, 447–66. Dordrecht: Springer Netherlands, 2004. http://dx.doi.org/10.1007/978-1-4020-2231-9_22.

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Goldbourt, Uri. "Genetic Variation and Nutrition." In Genetic factors in coronary heart disease, 397–408. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_28.

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Schonfeld, Gustav, and Elaine S. Krul. "Genetic Defects in Lipoprotein Metabolism." In Genetic factors in coronary heart disease, 239–66. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_16.

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Arcavi, Lidia. "Genetic variation and cardiac pharmacotherapy." In Genetic factors in coronary heart disease, 409–24. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_29.

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Rao, D. C., and George P. Vogler. "Assessing Genetic and Cultural Heritabilities." In Genetic factors in coronary heart disease, 71–81. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_5.

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Milewicz, Dianna M. "Genetic Aspects of Congenital Heart Disease." In Cardiovascular Medicine, 2599–605. London: Springer London, 2007. http://dx.doi.org/10.1007/978-1-84628-715-2_127.

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Shiomi, Masashi, and Yoshio Watanabe. "Rabbit Models in Genetic Research in Atherosclerosis." In Genetic factors in coronary heart disease, 115–24. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_8.

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Austin, Melissa A. "Low Density Lipoprotein Subclass Phenotypes." In Genetic factors in coronary heart disease, 105–13. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1130-0_7.

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Conference papers on the topic "Coronary heart disease – Genetic aspects"

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Murthy, H. S. Niranjana, and M. Meenakshi. "Dimensionality reduction using neuro-genetic approach for early prediction of coronary heart disease." In 2014 International Conference on Circuits, Communication, Control and Computing (I4C). IEEE, 2014. http://dx.doi.org/10.1109/cimca.2014.7057817.

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Uzbekova, Nelly, Sergey Kityan, and Nodira Badalbaeva. "USE OF PLETHYSMOGRAPHY IN THE ASSESSMENT OF THE ARTERIAL WALL IN PERSONS WITH CORONARY HEART DISEASE." In THEORETICAL AND PRACTICAL ASPECTS OF MODERN SCIENTIFIC RESEARCH. European Scientific Platform, 2021. http://dx.doi.org/10.36074/logos-30.04.2021.v2.43.

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Falk, E. A. "UNSTABLE ANGINA PECTORIS: PATHOLOGIC ASPECTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643711.

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Abstract:
Unstable angina pectoris represents a common and important manifestation of acute ischemic heart disease encompassing the broad spectrum of clinical syndromes between stable effort angina and acute myocardial infarction. This group of patientsisfar from uniform concerning underlying pathogenetic mechanisms and prognosis, but generally the risk of infarction or deathis increased during the unstable period. Most patients are presenting with new or worsening effort angina or angina at rest,and especially patients with rest anginaassociated with transient ECG changes seem to constitute a high risk subgroup. Transient reductions in coronary blood flow,rather than increases in myocardial oxygen demand, seem to play the major role in rest angina, indicating an underlying 'dynamic' coronary stenosis.Furthermore, unstable angina seems to beagood clinicalmarker for actively progressing coronary-artery disease.Pathologically, a rapidly evolving coronary-artery lesion represented by a disrupted atherosclerotic plaque with variable degree of plaque hemorrhage and luminalthrombosis usually is present in patientscoming to autopsy after a period of rest angina. The thrombus at the rupture site may be mural and limited (just sealing therupture) or occlusive depending on the degree of preexisting atherosclerotic stenosis. An occlusive thrombus is seldom seen over ruptured plaques causing less tha15% stenosis (histologic area stenosis), but is found with increasing frequency when stenosis severety increases beyond 15%.Most occlusive thrombi have a layered structure with thrombus material of differing age indicating an episodic growth by repeated mural deposits. Aggregated platelets usually can be identified in the mostrecent part of the thrombus, while older parts are more homogeneous due to fibrin infiltration/stabilization. Additionally,microemboli and microinfarcts are frequently found in the myocardium downstream tocoronary thrombi. So, the period of unstable angina preceding a fatal heart attackseems to be characterized by an ongoing thrombotic process in a major coronary artery where recurrent mural thrombus formation alternates with intermittent thrombus fragmentation and peripheral embolization. Such a dynamic thrombosis (with or without a concomitant focal vasospastic phenomenon) at the site of an unstable (ruptured) atherosclerotic lesion obviously may lead to the other clearly thrombus-related acute ischemic events: myocardial infarction or sudden death.Clinical studies using coronary angiography and coronary angioscopy during the acute phase of unstable angina have revealed a high frequency of ulcerated (unstable) atherothrombotic lesion in arteries responsible for the acute ischemia. Furthermore, episodic platelet activation (usually associated with chest pain) has recently been demonstrated in patients with unstable angina.The mechanism underlying pain/ischemia(predominantly spasm?) and the rapid plaque progression (plaque hemorr.hage/luminal thrombosis?) during unstable angina maydiffer. Accordingly, therapy directed against a possible spasm (nitrates, calcium antagonists) usually relieves pain effectively without having any documented effect on infarction/survival, while antithr-ombotic therapy (aspirin, heparin) clearlyimproves the prognosis without apparent antianginal effect. Therefore, with the objective not only of relieving pain but also of improving the prognosis, more attention should be paid to the potentially fatal thrombotic process that apparently isgoing on in a major coronary artery of many patients with unstable angina.
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Denisova, Tatyana P., Lidia I. Malinova, and Igor A. Malinov. "Physical and mathematical aspects of blood-glucose- and insulin-level kinetics in patients with coronary heart disease and high risk of its development." In Saratov Fall Meeting 2000, edited by Valery V. Tuchin. SPIE, 2001. http://dx.doi.org/10.1117/12.431540.

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Vengrenyuk, Yuliya, Theodore J. Kaplan, Luis Cardoso, Gwendalyn J. Randolph, and Sheldon Weinbaum. "Biomechanical Modeling of Atherosclerotic Lesions in ApoE Deficient Mice." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206571.

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Cardiovascular disease remains the principal killer in the western world despite major advances in treatment of its patients [1]. It is generally accepted that sudden rupture of vulnerable plaque followed by thrombus formation underlies most cases of myocardial infarction and is responsible for more than a half of 500,000 coronary heart disease deaths every year. Although histopathological analysis of postmortem specimens have provided important data on histological features of ruptured human plaques, there is an urgent need for good representative animal models of plaque rupture. Over the last decade and a half, genetically engineered mice have been widely used to study the pathogenesis and potential treatment of atherosclerotic lesions, as well as genetic, hormonal and environmental influences on development of atherosclerosis. Though many of the features of plaque development and progression that occur in human plaques are similarly observed in murine plaques, these mouse models have long been regarded as poor models to study plaque rupture because the aortic sinus lesions seldom show any signs of fibrous cap disruption. Several recent studies reported potentially unstable atherosclerotic lesions in older apoE-deficient mice in another anatomic site, the proximal part of the brachiocephalic artery (BCA) [2, 3]. The unusual stability of aortic lesions compared to the BCA lesions in ApoE knockout mice is an unexplained paradox in developing a mouse model of plaque rupture. In this paper, we use histology based finite element analysis to evaluate peak circumferential stresses in aortic and BCA lesions from high fat fed ApoE KO mice.
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