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Dissertations / Theses on the topic 'Coronary disease'
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1
Holt, Jim, and Gregg Mitchell. "Coronary Artery Disease KSA." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etsu-works/6457.
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Lee, Chi-hang, and 李志恆. "Microvascular obstruction following percutaneous coronary interventionfor coronary artery disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43278723.
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Lee, Chi-hang. "Microvascular obstruction following percutaneous coronary intervention for coronary artery disease." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43278723.
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Brouilette, Scott Wayne. "Telomeres and coronary heart disease." Thesis, University of Leicester, 2004. http://hdl.handle.net/2381/29899.
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Using mean telomere length as a marker of biological age, I show that: 1. Subjects with premature myocardial infarction (MI) have significantly shorter telomeres than age-sex matched, healthy, controls. The mean telomere length in MI subjects was similar to controls almost 11 years older. 2. Healthy young adult children of families with a strong history of premature MI have shorter telomeres than age matched children of families without such a history. 3. Shorter telomere lengths are associated with increase risk of subsequent CHD events in a prospective study. This analysis was carried out on samples collected in the West of Scotland Coronary Prevention Study (WOSCOPS). This randomised blinded trial was designated to examine the benefits of statin treatment on preventing CHD and showed a 30% reduction of events in those treated with pravastatin. Interestingly, my analysis showed that this benefit of statin is only seen in those subjects at higher risk of CHD based on their telomere length.;As the final part of the thesis I carried out a quantitative linkage trait (QTL) analysis in sib-pairs in an attempt to identify genetic loci regulating telomere length. I report the mapping of a major QTL on chromosome 12 that determines almost 50% of the inter-individual variation in mean telomere length.;These findings support a novel "telomere" hypothesis of CHD. They indicate that telomere biology is intimately linked to the genetic aetiology and pathogenesis of CHD. Specifically, the findings suggest that (i) those individuals born with shorter telomeres may be at increased risk of CHD (ii) rather than individual genes, a more global structural property of the genetic material may explain the familial basis of CHD (iii) variation in telomere length may explain, in part, the variable age of onset of CHD. The findings provide several new avenues for future research.
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Stancell-Smith, Gwendolyn Yvonne. "Women and Coronary Artery Disease." ScholarWorks, 2017. https://scholarworks.waldenu.edu/dissertations/3415.
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Heart disease, including coronary artery disease, affects approximately 42 million women in the United States. Many of those affected are not aware they have the condition. Contributing to the problem is the fact that women are more likely than men to be misdiagnosed and undertreated for heart disease. Morbidity and mortality are high in women affected by heart disease, making the problem important to address. The purpose of this project was to understand the coronary artery or heart disease risk and the treatment for the condition provided for 31 participants at a cardiology service in the Northeast U.S. The project question focused on understanding how coronary artery disease manifest in women and the gender differences in treatment for men and women. A descriptive case design was used by gathering data from patient risk profiles and treatments. Participants were males and females aged between 30 and 80. Qualitative data were obtained through cardiology staff interviews and existing literature. The data were subjected to a content analysis to identify emergent themes. Findings indicated that the women experienced different cardiac symptoms to men, and these differences translated to misdiagnosis and resulting treatment ineffectiveness. This project contributes to social change through raising awareness of the gender differences in heart disease presentation so that providers can recognize and treat the condition effectively.
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Starkhammar, Johansson Carin. "Periodontitis and coronary artery disease : Studies on the association between periodontitis and coronary artery disease." Doctoral thesis, Linköpings universitet, Kardiologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-86213.
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Periodontitis and coronary artery disease (CAD) are highly prevalent in Sweden’s population; both diseases have complicated pathogeneses and clinical manifestations due to immune-system triggered inflammation. Research in recent years reported that inflammation is a significant active participant in many chronic diseases. The literature described a CAD-periodontitis association, but underlying mechanisms are not fully understood. It is important to acquire knowledge about how periodontitis might influence CAD, which is one of the major causes of illness and death in western countries. Because periodontitis can be treated, this knowledge, when complemented with more knowledge about the CAD-periodontitis association, could lead to CAD prevention. The overall aim of studies reported in this thesis were to investigate the CAD-periodontitis association, and specifically, to: (i) compare periodontal conditions in patients with CAD and subjects without a history of CAD; (ii) study whether or not periodontal status influences outcomes in known CAD over an 8-year period; (iii) study whether or not concentrations and biological activity of hepatocyte growth factor (HGF) in serum from patients with severe CAD are different – depending on whether or not the subjects had periodontitis; and (iv) study concentrations and biological activity of hepatocyte growth factor in serum, saliva, and gingival crevicular fluid in healthy subjects with or without periodontitis. Here is a brief summary: In study I, 161 patients with CAD and 162 controls were compared regarding periodontal disease prevalence and severity. CAD patients had significant coronary stenosis and underwent percutaneous coronary intervention (PCI) or coronary artery by-pass grafts (CABG). Healthy controls were recruited from Sweden’s population database. Twenty-five per cent of the CAD patients had severe periodontitis, compared to 8% of the controls. In a multiple logistic regression analysis (controlled for age and smoking), severe periodontitis indicated an odds ratio of 5.74 (2.07–15.90) for CAD. Study II: Periodontal status was re-examined in 126 CAD patients and 121 controls from the initial sample after 8 years. Periodontal status at baseline was analysed and related to CAD endpoints (i.e., myocardial infarction, new PCI or CABG or death due to CAD) recorded from patients’ medical records and from the death index maintained by the National Board of Health and Welfare. The difference in periodontitis prevalence and severity between the two groups remained unchanged during the 8-year follow up. No significant differences were found regarding CAD endpoints during follow-up in relation to baseline periodontal status in the CAD-patient group. In study III, higher HGF serum concentrations (p<0.001) were found in CAD patients, compared to healthy blood donors, which reflects chronic inflammation. In CAD patients without periodontitis, HGF concentrations increased significantly 24 hours after PCI – in parallel with increased HGF biological activity. In CAD patients with periodontitis, only small fluctuations were seen in HGF values, i.e., concentration and biological activity. HGF biological activity was temporarily elevated after PCI but only in patients without periodontitis. Thus chronic inflammation related to periodontitis might reduce HGF biological activity. In study IV, HGF concentration and biological activity in saliva, in gingival crevicular fluid (GCF), and serum were compared between 30 generally healthy subjects with severe untreated periodontitis and 30 healthy subjects without periodontitis. Compared to periodontally healthy controls, periodontal patients showed higher HGF concentrations in saliva p<0.001, gingival crevicular fluid p<0.0001, and in serum p<0.001. HGF biological activity (measured as the binding affinity to its HSPG and c-MET receptors) was significantly reduced in saliva (p<0.0001) and GCF samples (p<0.0001 for HSPG and p<0.01 for c-MET) from periodontitis patients. The only significant difference in serum samples was an increases in c-MET binding three minutes after subgingival debridement in periodontitis patients (p<0.05), which might reflect that patients had active bursts of periodontitis. In conclusion, CAD patients more often showed severe periodontitis but there were no differences in CAD endpoints during the eight-year follow-up in relation to baseline periodontal status. Periodontitis seems to influence HGF concentration and biological activity in CAD patients, but studies on factors that cause lower HGF biological activity are necessary – to find out if periodontal treatment influences HGF biological activity. Healthy periodontitis patients had higher HGF concentrations locally and systemically, but biological activity was reduced. This might indicate that periodontitis can influence wound healing and tissue repair in other body parts.The ISBN 987‐91‐7519‐748‐7 is incorrect. Correct ISBN is 978‐91‐7519‐748‐7.
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Heiser, Claire Anne. "Personality predictors of coronary heart disease." Thesis, Virginia Polytechnic Institute and State University, 1985. http://hdl.handle.net/10919/50027.
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Fifty percent of the diagnosed cases of coronary heart disease in the United States are of unknown etiology. This study proposed that five personality traits— achievement, dominance, aggression, succorance and Critical Parent—differentiate individuals with coronary heart disease manifestations. The ultimate goal of this research was to formulate a predictive profile of at-risk individuals of developing coronary heart disease.
Cardiac rehabilitation units' participants from across the United States were recruited as subjects. Randomly selected cardiac rehabilitation units were sent an initial letter inquiring whether their staff would be willing to participate in the study by administering the instruments to their participants. Eight units from each of the 50 states were contacted. A total of fourteen units agreed to participate. One hundred sixty-nine subjects completed the Demographic Data Questionnaire and the Adjective Check List.
Five scale scores, representing the five personality differentials, were analyzed. Comparison of the male subject population (n=135) and the male normative population (n=198) revealed no significant differences in terms of the five traits. Comparison of diagnostic subgroups of the subject population also revealed no significant differences.
It was concluded that the subject population did not differ significantly from the normative population in terms of the five traits assess by the instrument used. The goal of a predictive profile was not realized due to this lack of findings.Master of Science
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Rose, Edward Leslie. "Coronary heart disease in patients with peripheral vascular disease." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.305544.
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Jensen, Jens. "On-line vectorcardiography during coronary angioplasty and unstable coronary artery disease /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4357-5/.
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Danesh, John. "Chronic infection and coronary heart disease." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326020.
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Ahmed, Nabeel. "Platelet reactivity in coronary artery disease." Thesis, Imperial College London, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.530480.
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Kounali, Daphne. "Early growth and coronary heart disease." Thesis, University of Southampton, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436926.
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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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Vollmer, Sandra Jeanne. "Diagonal earlobe creases and coronary artery disease." FIU Digital Commons, 1996. http://digitalcommons.fiu.edu/etd/3066.
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PURPOSE: The purpose of this study was to examine the relationship between the diagonal earlobe crease and the incidence of coronary artery disease.
PATIENTS AND METHODS: A descriptive, correlational, retrospective and concurrent approach was utilized in examining 61 patients, all with a cardiac catheterization within the last six months. All were examined for the presence of diagonal earlobe crease, presence of coronary artery disease, total blood cholesterol levels, age, sex, and past medical histories. Analyses included the Fischer's exact test, regression analysis, and multiple logistic regression analysis.
RESULTS: The mean age of all the subjects 70.3. Mean cholesterol level of all subjects= 199.68. A significant association between presence of earlobe creases and presence of coronary artery disease with P value <0.025. Gender (male) was the most predictive for the presence of CAD of the four covariates (including age, cholesterol, and ELC status), P<0.006. Earlobe status was the second most powerful predictor of CAD status, P=0.019. Neither age (P=0.40) nor cholesterol (P=0.16) were significant predictors of CAD status.
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Korte, Philippus Jacobus de. "Probability analysis in diagnosing coronary artery disease." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1993. http://arno.unimaas.nl/show.cgi?fid=5861.
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Bagés, Nuri. "Psychosocial risk factors and coronary heart disease." [Maastricht : Maastricht : Universiteit Maastricht] ; University Library, Maastricht University [Host], 2000. http://arno.unimaas.nl/show.cgi?fid=6899.
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Chandola, Tarani. "Social inequality in coronary heart disease outcomes." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285007.
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Schulz, Katharine I. "Coping strategies in coronary artery disease patients." Virtual Press, 1993. http://liblink.bsu.edu/uhtbin/catkey/862273.
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Williams, Simon Robert Pask. "The physique associated with coronary artery disease." Thesis, Open University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250507.
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Freitag, Daniel Franz. "Inflammatory pathways and coronary heart disease risk." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648461.
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Гордіна, Марина Андріївна, Марина Андреевна Гордина, and Maryna Andriivna Hordina. "Vitamin D deficiency and coronary heart disease." Thesis, Сумський державний університет, 2013. http://essuir.sumdu.edu.ua/handle/123456789/33551.
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Coronary heart disease (CHD) is the result of the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium with oxygen and nutrients. The WHO estimated that in 2002, 12.6% of deaths worldwide were from CHD.
When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/33551
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Roberts, Robert. "A genetic basis for coronary artery disease." Elsevier, 2015. http://hdl.handle.net/10150/623296.
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CAD and cancer account for over one-half of all deaths in the world. It is claimed that the 21st century is the last century for CAD. This is, in part, because CAD is preventable based on randomized, placebo-controlled clinical trials, which show modifying known risk factors such as cholesterol is associated consistently with 40–60% reduction in morbidity and mortality from CAD. Comprehensive prevention will require modifying genetic risk factors that are claimed to account for 40–60% of predisposition to CAD. The 21st century is meeting this challenge with over 50 genetic risk variants discovered and replicated in large genome-wide association studies involving over 200,000 cases and controls. Similarly, 157 genetic variants have been discovered that regulate plasma lipids including, LDL-C, HDL-C, triglycerides, and total cholesterol. A major finding from these studies is that only 15 of the 50 genetic variants for CAD act through known risk factors. Hence, the pathogenesis of CAD in addition to cholesterol and other known risk factors is due to various other factors, many of which remain unknown. Secondly, genes regulating the plasma triglyceride levels are strongly associated with the pathogenesis of CAD. Thirdly, Mendelian randomization studies show no protection from genes that increase plasma HDL cholesterol. This is contrary to current opinion. These genetic risk variants have provided new targets for the development of novel therapies to prevent CAD. Already a new and potent drug has been developed targeting PCSK9, which is in phase 3 clinical trials and shows great efficacy and safety for prevention of CAD. The 21st century is looking very bright for the prevention of CAD.
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Gadd, Malin. "Cardiovascular diseases in immigrants in Sweden /." Stockholm : Neurotec, Center for family and community medicine, Karolinska institutet, 2006. http://diss.kib.ki.se/2006/91-7140-627-1/.
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Thompson, Mary. "Coronary effects of endothelins." Thesis, University of Bath, 1995. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296580.
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Du, Ying. "Ischemic and pharmacological preconditioning of rat myocardium : effects on ischemia-reperfusion injury /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BICH%202005%20DU.
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Ho, Lai-yi Ada. "Does social support influence coronary heart disease prognosis? : a meta-analysis /." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/b39724116.
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Dorn, Karen LaVonne Toft. "Circulatory, hormonal, and metabolic effects of arbutamine compared to exercise in persons with known or suspected coronary artery disease /." This resource online, 1994. http://scholar.lib.vt.edu/theses/available/etd-06062008-164634/.
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Chaichana, Thanapong. "Haemodynamic evaluation of coronary artery plaques : prediction of coronary atherosclerosis and disease progression." Thesis, Curtin University, 2012. http://hdl.handle.net/20.500.11937/1233.
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Coronary artery disease is the leading cause of death in advanced countries. Coronary artery disease tends to develop at locations where disturbed flow patterns occur, such as the left coronary artery. Haemodynamic change is believed to play an important role in the pathogenesis of coronary artery disease. This study was conducted to analyse the haemodynamic variations in the left coronary artery, with normal and diseased conditions, based on idealised human left coronary artery models and realistic reconstructed left coronary geometries. Computational fluid dynamics analysis was performed, to replicate the actual physiological conditions that reflect the in vivo cardiac haemodynamics with high resolution CT images. The wall shear stress, wall shear stress gradient, velocity flow patterns, pressure gradient, wall pressure, wall pressure gradient, wall pressure stress gradient, were calculated though in idealised but near realistic left coronary geometries during the cardiac pulsatile cycles. This novel research was performed in four stages, with Stage 1 studying the correlation between bifurcation angle and subsequent haemodynamic effects; Stage 2 focused on the position of plaques in the left coronary artery and corresponding haemodynamic variations based on realistic models; Stage 3 investigated the impact of plaques on coronary side branches based on realistic models. Stage 4 analysed individual patients with the bifurcation stenosis based on CT images.Normal coronary artery geometries were generated to investigate the haemodynamic variations of various angulations of the left coronary artery, based on idealised and actual coronary artery models. Eight idealised left coronary artery models were generated, with inclusion of different coronary angulations, namely, 120°, 105°, 90°, 75°, 60°, 45°, 30° and 15°. Four realistic left coronary artery geometries were reconstructed, based on selected patient's data, with angulations ranging from wide angulations of 110° and 120° to narrow angulations of 73° and 58°. There were twelve left coronary artery models in total which consisted of left main stem, left anterior descending and left circumflex branches. Haemodynamic analysis showed that disturbed flow patterns were observed in both idealised and realistic left coronary geometries with wider angles. Wall pressure was found to reduce when the flow changed from the left main stem to the bifurcated locations. A low wall shear stress gradient was revealed at left main bifurcations in models with wide angulations. There is a direct correlation between coronary angulations and subsequent haemodynamic changes, based on realistic and idealised geometries.Diseased coronary geometry was used to study the haemodynamic changes surrounding the bifurcation plaques based on patient’s data. High resolution CT images of the coronary plaques were used to locate and generate the position of actual plaques, which was combined with the reconstructed left coronary disease geometry. Coronary plaques were replicated and located at the left main stem and the left anterior descending to produce at least 60% coronary stenosis. Computational fluid dynamic analysis was used to investigate the haemodynamic effects with and without the presence of coronary plaques. Our results revealed that the highest pressure gradients were observed in stenotic locations caused by the coronary plaques. Low flow velocity regions were found at post-stenotic locations in the left bifurcation, left anterior descending, and left circumflex. Wall shear stress at the plaque locations was similar between the non-Newtonian and Newtonian models, although more details were observed with non-Newtonian model. There is a direct correlation between coronary plaques and subsequent haemodynamic changes, based on the simulation of plaques in the realistic left coronary geometries.Coronary artery disease with their side branches was used to analyse the change of haemodynamic factors surrounding bifurcation plaques to characterise the effect of disturbed flow to their side branches. Coronary plaques were located at the left main bifurcation, which is composed of the left main stem and the left anterior descending to generate >50% narrowing of the coronary lumen. Haemodynamic parameters were compared in the left coronary artery models, with and without the presence of plaques. The analysis demonstrated that wall shear stress decreased while wall pressure stress gradient was increased in coronary side branches due to the presence of plaques. There is a direct relationship between coronary plaques and subsequent haemodynamic changes based on the bifurcation plaques located in the realistic coronary geometries.Patient-specific models with coronary disease were used to analyse the haemodynamic variations surrounding the stenotic locations. Three sample patients with left coronary artery disease were chosen based on CT data. Coronary plaques were shown at the left anterior descending and left circumflex branches with more than 50% lumen narrowing. Wall shear stress and blood flow changes in the left coronary artery disease were calculated during cardiac pulsatile cycles. Our results showed that wall shear stress was found to increase at the stenotic regions and decrease at pre- and post-plaque regions, while the disturbed flow regions was found at post-plaque location. There is a direct effect bifurcation plaque on the changes of blood flow and wall shear stress, based on the realistic coronary disease geometries.In summary, the results of this project show that coronary angulation is directly related to haemodynamic changes, resulting in the formation of atherosclerosis, leading to coronary artery disease. Presence of coronary plaques impacts the haemodynamic changes to both the left main coronary artery, and side branches. Computational fluid dynamic analysis of realistic normal and diseased coronary models improves our understanding of the pathogenesis of coronary artery disease. Further studies are needed to correlate the haemodynamic changes in the presence of plaques with clinical outcomes in patients with suspected coronary artery disease.
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Kunutsor, Setor Kwadzo. "Markers of liver dysfunction and risk of coronary heart disease." Thesis, University of Cambridge, 2014. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708216.
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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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Mehilli, Julinda. "Have women with coronary artery disease a higher risk than men after coronary stenting?" [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=965479668.
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Kumar, Nicky. "Progression of coronary artery disease in patients with end stage renal disease." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/11656.
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Coronary artery disease is highly prevalent in the end stage renal disease population. For the general population, there are guidelines for managing coronary artery disease, however there are no clear consensus guidelines for patients with end stage renal disease. Renal transplantation is superior to dialysis in terms of both patient survival and quality of life. A significant proportion of potential renal transplant candidates are at high risk of coronary artery disease; they need to be scrutinized and aggressively treated for risk factors in order to maintain the graft and survival benefit that has been created by organ donation. In addition, clinicians also need to consider the risk of cardiovascular disease for dialysis patients not undergoing transplantation. In terms of pathophysiological processes, there is growing evidence of a varied and significant effect of chemokines on cardiovascular disease; of particular interest are MCP-1, CCL15 and CCL18. There also exists established data demonstrating that the non-invasive investigation of measuring carotid intimal media thickness appears to be predictive of cardiovascular mortality in patients with end stage renal disease. Whilst coronary angiography is considered the gold standard investigation for diagnosing and treating coronary artery disease, it is an invasive procedure and therefore not without complication and is an expensive resource. This work examines the effect of elective coronary angiography on glomerular filtration rate in patients with advanced chronic kidney disease and has demonstrated that coronary angiography performed in a timely fashion did not accelerate the decline in renal function. In addition this work examines the cardiac survival of potential transplant patients undergoing coronary angiography and intervention and has demonstrated that a thorough approach to diagnosing and intervening on angiographically significant coronary artery disease was associated with a low incidence of cardiac mortality and morbidity. Finally, this work has demonstrated higher chemokine levels in patients with progressive coronary artery disease compared to patients without progressive coronary artery disease, and shows that a significant proportion of patients with normal coronary angiograms at initial screening have no evidence of angiographically progressive disease over a 3 year period. These results can be applied when performing cardiac risk stratification in an end stage renal failure population. In addition this work provides some evidence to support chemokines as appealing targets for novel therapies in the future.
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Nijm, Johnny. "Inflammation and cortisol response i coronary artery disease." Doctoral thesis, Linköpings universitet, Institutionen för medicin och hälsa, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-15978.
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Atherosclerosis is characterized by a chronic inflammation, involving autoimmune components, in the arterial wall. An increase in proinflammatory activity relative to anti-inflammatory activity is considered to cause a progression of the disease towards plaque instability and risk of atherothrombotic events, such as acute coronary syndrome (ACS). Cortisol, the end product of the hypothalamus-pituitary-adrenal (HPA) axis, is a powerful endogenous anti-inflammatory mediator. Disturbances in the HPA axis have been reported in chronic inflammatory/autoimmune diseases, like rheumatoid arthritis. The aim of this thesis was to study various markers of systemic inflammation in patients with acute and stable conditions of coronary artery disease (CAD) and relate these findings to the cortisol response. Both patients with ACS and patients with stable CAD had high levels of C-reactive protein (CRP), interleukin (IL)-6 and IL-1 receptor antagonist, compared with healthy controls. In addition, patients with stable CAD had significantly more neutrophil-platelet aggregates than controls, as a possible indicator of neutrophil activation. The cortisol response was determined in two different cohorts of CAD patients; one consisting of patients with a first-time myocardial infarction and one consisting of patients with long-term stable CAD. From the acute phase to 3 months, the patients with a myocardial infarction showed a higher 24-h cortisol secretion and a flattened diurnal slope caused by higher cortisol levels in the evening, as compared with healthy controls. The patients with long-term stable CAD showed similarly high levels of cortisol in the evening. The levels of evening cortisol were strongly correlated with CRP and IL-6. When exposed to acute physical or acute psychological stress at 3 months, the ACS patients showed a markedly blunted cortisol response compared with healthy controls. Following the stress tests, a significant increase in CRP was observed in the patients but not in the controls, indicating a failure of the HPA axis to compensate for stress-induced inflammation in CAD. In the ACS patients, the time course of matrix metalloproteinases (MMPs) and their tissue inhibitor TIMP-1 was determined during the 3 months follow-up. A major finding was that the MMP-9 and TIMP-1 levels remained significantly higher in the patients at all time points compared to the controls. MMP-9 and TIMP-1, but not MMP-2, MMP-3 or MMP-7, were related to inflammatory activity, as assessed by CRP and IL-6. MMP-9 and TIMP-1 showed significant correlation with evening cortisol, even after adjustment for CRP and IL-6, lending further support for a link between ´high´ flat cortisol rhythm and systemic inflammatory activity. The activation status of neutrophils in stable CAD was further examined by measuring the expression, affinity state and signalling capacity of b2-integrins and the innate production of reactive oxygen species (ROS). However, the neutrophils in patients were not more activated in vivo than were cells in healthy controls, neither were they more prone to activation ex vivo. The data rather indicated an impaired function of neutrophils in stable CAD. The neutrophils in CAD patients showed a significantly lower number of total glucocorticoid receptors (GRs) and a lower GRa:GRb ratio compared to healthy controls, indicating a chronic over activation of the HPA axis and, possibly, a state of glucocorticoid resistance. Moreover, the evening cortisol levels in patients were associated with an overexpression of annexin-1, the ´second messenger´ of glucocorticoid action. In contrast to neutrophils in controls, the neutrophils in patients also showed a hyper responsiveness to exogenous annexin-1 resulting in impaired neutrophil function. To conclude, clinically stable CAD was associated with a systemic inflammatory activity, involving a high MMP-9:TIMP-1 ratio and an increased inflammatory response to acute stress but not any activation of neutrophils. This inflammatory activity was associated with a dysregulated cortisol secretion, defined by a flat diurnal rhythm and a blunted cortisol response to stress. Although the clinical relevance remains to be verified, an intriguing hypothesis is that a hyporesponsive HPA axis favours the development towards plaque instability.On the day of the defence date the title of article III was: "A sustained elevation of serum matrix metalloproteinase-9 is associated with diurnal salivary cortisol in patients with acute myocardial infarction-a 3-month follow-up".
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Gorog, Diana Adrienne. "Influences on platelet function in coronary artery disease." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272333.
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Shaw, James A. (James Alexander) 1968. "Mechanisms of plaque stability in coronary artery disease." Monash University, Dept. of Medicine, 2001. http://arrow.monash.edu.au/hdl/1959.1/9016.
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Söderman, Eva. "Depression, coronary artery disease and change of lifestyle /." Stockholm : [Karolinska institutets bibl.], 2001. http://diss.kib.ki.se/2001/91-7349-089-x/.
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Nijm, Johnny. "Inflammation and cortisol response in coronary artery disease /." Linköping : Univ, 2007. http://www.bibl.liu.se/liupubl/disp/disp2007/med1037s.pdf.
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Guibert, Remy L. "Death certificate coding variation and coronary heart disease." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66229.
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Huff, Natasha Clare. "Coronary heart disease and the socio-economic environment." Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339634.
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Closa-LeoÌn, Trinidad. "Social support, cardiovascular reactivity, and coronary artery disease." Thesis, University of Birmingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433738.
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Roberts, Will. "Assessment of coronary artery disease by computed tomography." Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8708.
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Computed Tomography Coronary Angiography (CTCA)is a technique for imaging coronary arteries with increasing indications in clinical cardiology. AIMS 1.Develop a heart rate (HR) lowering regime for CTCA and to measure its association with image quality. 2.Examine the diagnostic accuracy of 64 slice CTCA (CTCA64) in patients with known coronary artery disease (CAD). 3.Examine the diagnostic accuracy of CTCA64 for assessment of stent restenosis 4.Demonstrate utility of CTCA as an endpoint in assessment of novel diagnostic biomarkers of CAD. METHODS I developed a HR reducing strategy using metoprolol and assessed its effectiveness for improving CTCA64 image quality. The diagnostic value of CTCA in patients with suspected angina was evaluated by comparison with invasive coronary angiography. The diagnostic value of CTCA for quantifying stent restenosis was evaluated by comparison with intravascular ultrasound. The utility of CTCA for evaluating the diagnostic value of B-type natriuretic peptide (BNP) and high sensitivity cardiac troponin I (hs- TnI) was evaluated by blood sampling in patients with suspected angina who subsequently underwent CTCA. RESULTS 1.In 121 patients undergoing CTCA, 75 required rate control. This was achieved (rate ≤60 bpm) in 83% using a systematic regimen of oral and IV metoprolol (n=71) or verapamil (n=4). I demonstrated a significant relation between HR reduction and graded image quality (p<0.001). 2.80 patients underwent CTCA64 and invasive coronary angiography. 724 coronary arterial segments were available for analysis. The sensitivity and specificity of CTCA for significant luminal stenosis was 83.3% (95% CI 67.1-92.5%) and 96.7% (95% CI 95.1-97.9%), respectively, but the positive predictive value was only 63.5% (95% CI 50.4-75.3%). 3.80 patients with 125 stented segments underwent CTCA64 and invasive coronary angiography. Additional intravascular ult rasound (IVUS) examination of stented segments was performed in 48 patients. Using IVUS as the gold-standard for stent restenosis, CTCA and invasive coronary angiography had comparable diagnostic specificities for binary stent restenosis: 82.7% (95% confidence intervals 69.7- 91.84%)and 78.9% (95% confidence intervals 65.3-88.9%), respectively. Sensitivities were lower, particularly the sensitivity of CTCA which was only 11.8% (95% confidence intervals 1.5-36.4%) compared with 58.8% (95% confidence intervals 32.9-81.6%) for invasive coronary angiography. 4. In 93 patients with suspected angina CTCA64 provided a useful endpoint for assessing the diagnostic value of novel circulating biomarkers. BNP levels were higher in the 13 patients shown to have significant (≥50% stenosis) coronary artery disease compared with patients who had unobstructed coronary arteries (18.08pg/ml (IQR 22) vs 9.14pg/ml (IQR 12.62), p=0.024) and increased significantly with exercise, particularly in the group with anatomic coronary artery disease (2.73 ± 5.69 pg/ml vs 1.27±3.29 pg/ml, p=0.16). Conversely I found no association between hs-TnI and the presence of CAD. CONCLUSION Image quality of CTCA64 is enhanced by heart rate reduction below 60 bpm which can be achieved safely by a regimen of oral and intravenous metoprolol. Although CTCA64 is a useful non-invasive method for diagnosis of coronary artery disease, it has a low positive predictive value for identifying severe (≥50%) luminal stenosis which limits its clinical value. Its value for assessment of stent restenosis is even more limited but it finds useful application as an endpoint for diagnostic evaluation of novel biomarkers, allowing confirmation of an association between circulating BNP levels and stable coronary artery disease.
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Sensky, Penelope Ruth. "Cardiac magnetic resonance studies in coronary artery disease." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/29408.
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Johnman, Cathy. "Chronological and biological ageing in coronary artery disease." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6138/.
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Background: The elderly account for an increasing proportion of the population and have a high prevalence of coronary artery disease (CAD). Therefore, elderly patients represent an increasing proportion of those presenting for investigation and treatment of CAD. Management of CAD is undertaken to relieve the signs and symptoms of myocardial ischaemia, making quality of life (QoL) a critical consideration in clinical decision making. CAD is associated with both chronological and biological ageing processes. However, conflicting evidence exists as to whether leucocyte telomere length (LTL) is an appropriate biomarker of ageing in CAD. Methods: The thesis comprised four complementary studies. Firstly, secondary data analysis of the Scottish Coronary Revascularisation Register was used to undertake two retrospective cohort studies of patients attending for coronary angiography and percutaneous coronary revascularization. The aim was to compare case mix and outcomes of elderly versus younger patients. A prospective cohort study of 437 patients was then undertaken to assess QoL before, and three months after, PCI and to compare QoL changes in elderly versus younger patients. Finally a cross sectional study was used to investigate the association between LTL (T/S ratio -relative ratio of repeat to single copy number) measured using qPCR and CAD (presence and severity) in 1,846 patients attending a regional cardiovascular centre for coronary angiography. Results: The number and proportion of elderly patients undergoing coronary angiography increased from 669 (8.7%) in 2001 to 1,945 (16.8%) in 2010. Among the elderly (>= 75 years old), symptoms were more severe and disease more extensive compared to patients aged <75 years. Peri-procedural complications were infrequent irrespective of age: 2.0% of elderly patients suffered complications, compared with 1.6% of young patients (p<0.001). Thirty-day MACCE were more common in elderly compared with younger patients (2.0% vs 1.6%, p<0.001). Elderly patients with evidence of stenosis were less likely to proceed to revascularisation (adjusted OR 0.68, 95% CI 0.65–0.71, p<0.001) within one year of angiography, irrespective of disease severity. There was an increase in the number and percentage of PCIs undertaken in elderly patients, from 196 (8.7%) in 2000 to 752 (13.9%) in 2007. Compared with younger patients, the elderly were more likely to have multivessel disease, multiple comorbidity, and a history of myocardial infarction or coronary artery bypass grafting (χ2 tests, all p<0.001). The elderly had a higher risk of MACE within 30 days of PCI (4.5% versus 2.7%, χ2 test p<0.001) Following PCI, mean QoL improved in both elderly and younger patients. Elderly participants had higher baseline mental component score (MCS) but lower physical component score (PCS). After adjusting for baseline differences, QoL (both physical and mental components) in elderly patients improved as much as younger patients, following PCI (SF-12 v2 MCS 50.0(SD 10.4) to 53.0(SD 11.9) vs 46.7(SD 11.1) to 49.7(SD 11.1), p=0.652; and SF-12 v2 PCS 37.6(SD 10.1) to 41.9(SD 10.1) vs 39.7(SD 10.0) to 45.6(SD 10.8), p=0.373). An inverse relationship was found between LTL (T/S ratio) and age. No statistically significant difference was found in mean T/S ratio between those with and without CAD (0.87(SD 0.21) vs 0.89(SD 0.21), p=0.091), even after adjusting for baseline characteristics. In addition, there was no statistically significant difference in relative T/S length by severity of disease in those found to have stenosis on cardiac angiography: 0.875 (SD 0.211) vs 0.875 (SD 0.212) vs 0.860 (SD 0.203) vs 0.867 (SD 0.200), p=0.670. Conclusions: This thesis has demonstrated that, in Scotland, elderly patients account for an increasing number and proportion of diagnostic coronary angiograms and PCIs. However, the threshold for investigation and subsequent intervention appears to be higher among the elderly, even after adjusting for co-morbidities. While elderly patients have a higher risk of early complications than younger patients, their absolute risk is, nonetheless, low. This suggests that coronary angiography and PCI are safe procedures to perform in the elderly. Following PCI, the QoL of elderly patients improves at least as much as in younger patients. A recognized risk factor for CAD is chronological age, and there is increasing interest in whether biological age contributes to the development and progression of disease and can explain socioeconomic inequalities in health. However, the current thesis found no association between LTL and either the occurrence or severity of CAD, or its severity on cross-sectional study. While LTL is considered a useful biomarker of ageing, these findings suggest that LTL may not be as useful in CAD. Although findings suggest that coronary angiography and PCI are safe procedures in the elderly, results of this thesis suggest an age-based inequality in access to coronary artery investigation and intervention that is not explained by differences in demographic trends, levels of need, potential risk or potential benefit. These findings have significant implications for the delivery of cardiovascular clinical services to an increasing elderly population. Further investigation should be undertaken upstream of these studies, on patients referred for investigation rather than just those receiving it to determine the extent to which there are inequalities in referral threshold as well as procedure threshold. Further research is also required to identify those elderly patients who would most benefit from earlier investigation and management. There is also a need for longitudinal studies to assess the usefulness of LTL as a biomarker of ageing in CAD and to investigate whether LTL is associated with adverse outcomes in patients diagnosed with CAD.
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Bolton, Jennifer Lynn. "Candidate genotypes in prediction of coronary heart disease." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/15877.
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Introduction There has been much discussion on personalised medicine; however use of genotype in risk prediction for coronary heart disease (CHD) has not resulted in appreciable improvements over non-genetic risk factors. The primary aim was to determine whether candidate single nucleotide polymorphisms (SNPs) identified from genome-wide association studies improved prediction of CHD over conventional risk factors (CRF). The secondary aim was to determine whether the use of apolipoproteins or lipoprotein(a) improved risk prediction of CHD. Methods Analyses used the Edinburgh Heart Disease Prevention Study (EHDPS), with 1592 men aged 30-59 and follow-up after 20 years; and the Edinburgh Artery Study (EAS), with 1592 men and women aged 54-75 and 15 years of follow-up. Candidate SNPs were identified by systematic literature reviews. CHD status was evaluated as severe (myocardial infarction or coronary revascularisation), and any (severe CHD, angina or non-specified ischaemic heart disease). Cox proportional hazards models were used to evaluate addition of candidate SNPs or lipids to models containing CRF. Results A group of genome-wide significant SNPs resulted in a non-significant improvement in C-index for severe CHD (0.038, p=0.082), and a significant improvement in C-index for any CHD (0.042, p=0.016); the associated net reclassification improvements (NRI) were 20.5% and 18.7%, respectively. Regression trees identified SNPs that were predictive of the remaining variance after adjusting for CRF; this resulted in a significant improvement in C-index for any CHD (0.031, p=0.008). The NRI were 11.0% and 9.6% for severe and any CHD, respectively. When compared with HDL cholesterol/total cholesterol, apolipoprotein AI/total cholesterol yielded a NRI of 3.3% for severe CHD. Lipoprotein(a) improved prediction of severe CHD, with a non-significant improvement in C-index (0.020, p=0.087), and NRI of 11.8%. Conclusion The results of this study indicate that a well selected group of candidate SNPs can improve risk prediction for CHD over-and-above CRF. The inclusion of lipoprotein(a), along with CRF, appeared to improve prediction of severe CHD, but not any CHD.
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Hartmann, Katherine Louise Seal Hartmann. "Addressing the Missing Heritability of Coronary Artery Disease." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1471544354.
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Wilson, Andrew. "Ethnicity, coronary heart disease risk and platelet aggregation." Thesis, The University of Sydney, 1996. https://hdl.handle.net/2123/27600.
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Objectives:
Part A. To analyse existing risk-factor studies in the population of Sydney for differences in established risk factors, particularly smoking, blood pressure and blood lipids, between Southern-European-born migrants and Australian-born subjects.
Part B. To examine a sample of Southern-European and Australia-born men without current CHD, of similar socio-economic background to:
i. Compare factors relating to haemostasis and coagulation which have been reported as predictive of CHD risk, especially platelet aggregability, fibrinogen and Factor VIIc levels.
ii. Compare other measures of haemostasis and coagulation which have been reported as varying among ethnic groups.
iii. Examine the determinants of platelet aggregability, especially the nutrient content of their usual diet.
iv. Examine the relations among established risk factor for CHD and measures of platelet aggregability.
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Morris, Paul. "Computational fluid dynamics modelling of coronary artery disease." Thesis, University of Sheffield, 2015. http://etheses.whiterose.ac.uk/11772/.
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Background Coronary artery disease (CAD) is the leading cause of death in the world. Physiological lesion assessment with indices such as fractional flow reserve (FFR) is now accepted as the invasive gold-standard for diagnosing the significance of CAD and for guiding treatment. Patients undergoing percutaneous coronary intervention (PCI) guided by FFR have better clinical outcomes than those undergoing standard assessment. Furthermore, FFR-guided PCI is associated with decreased stent implantation and reduced long-term cost. Only a minority of patients undergoing invasive coronary angiography are currently afforded these benefits due to a number of procedure, operator, and economic related factors. There may be additional benefits from combined pressure and flow measurement. There is therefore a need for a technology that delivers the benefits of physiological lesion assessment without the factors which limit use of the invasive technique. Hypothesis Computational fluid dynamics (CFD) modelling based upon invasive coronary angiographic images (ICA) can characterise and predict intracoronary physiology. Aims (i) To develop a CFD-based model capable of simulating and predicting clinically relevant intracoronary physiology and (ii) validate model performance using clinical data from patients with CAD. Methods A workflow, based upon 3-D CFD modelling, capable of predicting intracoronary pressure and ‘virtual’ FFR from ICA, was developed. The model was validated against in vivo clinical measurements in 35 unique arterial datasets. The model predicted physiological lesion significance with 97% overall accuracy. Computation was prolonged (>24hrs). Two novel methods for solving the 3-D CFD were therefore developed. These methods enabled accurate computation of results in clinically tractable timescales (<5mins), at least equivalent to invasive measurement. The critical influence of system boundary conditions was explored, characterised, and quantified. A novel approach to patient-specific tuning of the outlet boundary conditions was developed and evaluated. The workflow was adapted to compute the pressure-flow relationship from measured pressure boundary conditions within a fully patient-specific in silico model. Results were validated within a novel experimental flow circuit incorporating patient-specific 3-D printed coronary arterial phantom models. Conclusions It is possible to compute clinically relevant intracoronary physiology (pressure or flow) from ICA. Results can be generated in clinically tractable timescales. The CFD model can be tuned to individual patient characteristics. The developed tools may be commercially desirable. Prior to full clinical translation, the model must be evaluated in a clinical trial.
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Bose, Jolly. "Percutaneous transluminal coronary angioplasty (PTCA) in the treatment of coronary artery disease in Hong Kong : procedural success, complications and long-term follow-up /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2084282X.
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Leong, Yuk-yan Pauline, and 梁玉恩. "The effectiveness of exercise-based cardiac rehabilitation program for secondary prevention of coronary heart disease : a systematic review." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193828.
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Objective: To examine the effect of exercise-based cardiac rehabilitation program for secondary prevention of coronary heart disease on cardiac-related mortality, recurrent cardiovascular event and quality of life.
Methods: All studies published between 1990 and 2013 in PubMed, and from 1980 to 2013 in EMBASE, which evaluated the effectiveness of exercise-based cardiac rehabilitation program for coronary heart disease. Using the specific keywords “Cardiac rehabilitation”, “Coronary heart disease” OR “Ischemic heart disease” [MeSH], “Exercise” OR “Physical activities” AND “Quality of life” OR “Mortality” AND Cardiovascular events” were searched. A total of 7randomized controlled trials out of 5,051articles from PubMed and 117 articles from EMBASE were included in this systematic review. The primary outcome measures used in the included seven studies were HRQOL, restenosis, cardiac event, cardiac related mortality. Similar demographic and clinical characteristics of the subjects between the intervention and the control groups were recorded. The studies were from five countries. The average age of the subjects in the seven studies was 61years, the average half of them have history of myocardial infarction. Though there were discrepancies among the results generated in the included studies, the potential benefits of exercise-based cardiac rehabilitation could be seen.
Results: Compared with the non-exercise-based cardiac rehabilitation, patients allocated to the exercise-based cardiac rehabilitation program had greater improvement in HRQOL and reduction of cardiac events. The result of reducing restenosis was inconsistent. The cardiac related mortality is not significant difference between exercise-based and non-exercise-based cardiac rehabilitation.published_or_final_version
Public Health
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Master of Public Health
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Taraboanta, Catalin. "Impact of family history of premature coronary disease on carotid ultrasound and coronary calcium findings." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/721.
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First degree relatives (FDRs) of subjects with early onset of coronary heart disease (CHD) have higher risk of developing cardiovascular disease. We verified early CHD by angiography in the index patients and extensively phenotyped their FDRs to investigate the relationship of traditional and non-traditional cardiovascular risk factors to carotid ultrasound and coronary calcium scoring findings.
B-mode carotid ultrasound was used to assess the combined intima-media thickness and plaque burden in 111 FDRs. The biochemical and anthropometrical characteristics of the FDRs were compared with those of healthy controls matched for sex, age, ethnicity and BMI. Odds ratios indicate that FDRs are more likely to have positive carotid ultrasound findings compared to controls; 2.23 (95% CI 1.14 – 4.37) for intima-media thickness and 2.3 (95% CI 1.22 - 4.35) for average total thickness. In multivariate analysis positive carotid ultrasound findings were higher in FDRs independent of age, gender, total cholesterol over HDL-c ratio, systolic blood pressure and smoking but not homocysteine which had higher values in FDRs compared to controls. In conclusion FDRs of patients with angiographically confirmed CHD have higher burden of subclinical atherosclerosis even when considered in the context of traditional risk factors.
Coronary artery calcium scoring (CAC), assessed by 64-slice multi-detector computed tomography (MDCT), was used to assess burden of subclinical atherosclerosis in 57 FDRs compared to controls. FDRs have a two-fold increase in risk of having CAC positive findings; odds ratios for the 75th percentile was 1.96 (95%CI 1.04 – 3.67, p<0.05) while for the 90th percentile odds ratio was 2.59 (95% 1.232 – 5.473, p<0.05). In summary, the risk of significant CAC findings, measured by 64-slice MDCT, is two-fold higher in FDRs than controls. These findings correlate highly with carotid ultrasound findings in the same cohort. Different thresholds for CAC may be appropriate when assessing male versus female FDRs.
Together increased carotid ultrasound findings and CAC scoring results in FDRs of patients with validated early onset of CHD suggest these imaging techniques as potentially useful tools in cardiovascular risk assessment that will go above and beyond the current diagnostic algorithms.