Готові списки джерел за темами / Coronary heart disease Molecular aspects

Добірка наукової літератури з теми "Coronary heart disease Molecular aspects"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 1 лютого 2022

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Статті в журналах з теми "Coronary heart disease Molecular aspects":

Pries, Axel R., Wolfgang M. Kuebler, and Helmut Habazettl. "Coronary Microcirculation in Ischemic Heart Disease." Current Pharmaceutical Design 24, no. 25 (November 8, 2018): 2893–99. http://dx.doi.org/10.2174/1381612824666180625142341.

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Background: Ischemic heart disease has long been considered to be exlusively caused by stenosis or occlusion. However, the coronary microcirculation too may play an important role in ischemic conditions. Also, the crucial role of microvessels in not only regulating blood flow on a local level but also mediating vascular permeability or inflammatory responses has been recognized. Objective: To review important physiological and pathophysiological mechanisms of coronary microcirculatory control with focus on heterogeneity of local perfusion, microvascular permeability and inflammation. Method: Selective research of the literature. Results: Heterogeneity is a characteristic of microvascular networks and affects structural and functional parameters such as vessel diameter, length, and connection pattern, flow velocity, wall shear stress, and oxygenation. Microvascular networks are optimized to meet the metabolic demand of all tissue compartments. This requires continuous vascular adaptation regulated by local hemodynamic and metabolic stimuli. Compromising this regulation results in functional arterio-venous shunting and tissue areas with either hyperperfusion or hypoxia in close proximity. In ischemia-reperfusion, increased microvascular permeability may aggravate tissue hypoxia by increasing extravascular pressure and seems to contribute to adverse myocardial remodeling. Transendothelial transport mechanisms and deterioration of the endothelial glycocalyx seem to be major contributors to tissue edema. Also in the context of ischemia-reperfusion, an inflammatory response mediated by venular endothelium expressing specific adhesion molecules contributes to tissue injury. However, anti-inflammatory therapies failed in clinical studies and a multi-targeted approach for cardiac protection is required. Conclusion: Disturbances of the coronary microcirculation are involved in different pathophysiological aspects of reperfusion injury.

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.

Santosa Putra, Iwan Cahyo, and William Kamarullah. "Diving deep into chelation therapy for coronary artery disease: a review." International Journal of Basic & Clinical Pharmacology 8, no. 12 (November 25, 2019): 2769. http://dx.doi.org/10.18203/2319-2003.ijbcp20195295.

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Chelation therapy is still a mainstay therapy when it comes to dealing with heavy metal intoxication. The ability of various chelators to bind metal and other chemical molecules led to the idea whether chelation therapy can be used as an alternative therapy to enchain calcium element that is known to be present in the atherosclerotic plaque. Various studies have been conducted, one of which is a large trial to assess chelation therapy study to show in case ethylenediaminetetraacetic acid (EDTA) chelator can be proven by evidence-based in managing coronary heart disease. Despite the favorable results that were found in many literature studies, the results of the study are still under debate in various aspects. To address this issue, we conducted a review article to discuss comprehensively the general description of EDTA as chelation therapy, various mechanisms that can explain the use of EDTA in the management of coronary heart disease, the pharmacokinetic aspects of EDTA chelation therapy, as well as describing various existing studies with a good level of evidence to review the effectiveness of these therapies against coronary artery disease.

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.

Malekmohammad, Khojasteh, Robert D. E. Sewell, and Mahmoud Rafieian-Kopaei. "Antioxidants and Atherosclerosis: Mechanistic Aspects." Biomolecules 9, no. 8 (July 25, 2019): 301. http://dx.doi.org/10.3390/biom9080301.

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Atherosclerosis is a chronic inflammatory disease which is a major cause of coronary heart disease and stroke in humans. It is characterized by intimal plaques and cholesterol accumulation in arterial walls. The side effects of currently prescribed synthetic drugs and their high cost in the treatment of atherosclerosis has prompted the use of alternative herbal medicines, dietary supplements, and antioxidants associated with fewer adverse effects for the treatment of atherosclerosis. This article aims to present the activity mechanisms of antioxidants on atherosclerosis along with a review of the most prevalent medicinal plants employed against this multifactorial disease. The wide-ranging information in this review article was obtained from scientific databases including PubMed, Web of Science, Scopus, Science Direct and Google Scholar. Natural and synthetic antioxidants have a crucial role in the prevention and treatment of atherosclerosis through different mechanisms. These include: The inhibition of low density lipoprotein (LDL) oxidation, the reduction of reactive oxygen species (ROS) generation, the inhibition of cytokine secretion, the prevention of atherosclerotic plaque formation and platelet aggregation, the preclusion of mononuclear cell infiltration, the improvement of endothelial dysfunction and vasodilation, the augmentation of nitric oxide (NO) bioavailability, the modulation of the expression of adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) on endothelial cells, and the suppression of foam cell formation.

Simmonds, Steven J., Ilona Cuijpers, Stephane Heymans, and Elizabeth A. V. Jones. "Cellular and Molecular Differences between HFpEF and HFrEF: A Step Ahead in an Improved Pathological Understanding." Cells 9, no. 1 (January 18, 2020): 242. http://dx.doi.org/10.3390/cells9010242.

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Heart failure (HF) is the most rapidly growing cardiovascular health burden worldwide. HF can be classified into three groups based on the percentage of the ejection fraction (EF): heart failure with reduced EF (HFrEF), heart failure with mid-range—also called mildly reduced EF— (HFmrEF), and heart failure with preserved ejection fraction (HFpEF). HFmrEF can progress into either HFrEF or HFpEF, but its phenotype is dominated by coronary artery disease, as in HFrEF. HFrEF and HFpEF present with differences in both the development and progression of the disease secondary to changes at the cellular and molecular level. While recent medical advances have resulted in efficient and specific treatments for HFrEF, these treatments lack efficacy for HFpEF management. These differential response rates, coupled to increasing rates of HF, highlight the significant need to understand the unique pathogenesis of HFrEF and HFpEF. In this review, we summarize the differences in pathological development of HFrEF and HFpEF, focussing on disease-specific aspects of inflammation and endothelial function, cardiomyocyte hypertrophy and death, alterations in the giant spring titin, and fibrosis. We highlight the areas of difference between the two diseases with the aim of guiding research efforts for novel therapeutics in HFrEF and HFpEF.

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).

Bastos, Marcelo B., Maarten P. van Wiechen, and Nicolas M. Van Mieghem. "PulseCath iVAC2L: next-generation pulsatile mechanical circulatory support." Future Cardiology 16, no. 2 (March 2020): 103–12. http://dx.doi.org/10.2217/fca-2019-0060.

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Contemporary state of the art percutaneous coronary intervention techniques offer treatment strategies and solutions to an increasing number of patients with heart failure and complex coronary artery disease. Percutaneous mechanical circulatory support is intended to alleviate the mechanical and energetic workload imposed to a failing ventricle by reducing left ventricle pressures and volumes and potentially also increasing coronary blood flow. The PulseCath iVAC2L is a transaortic left ventricular assist device that applies a pneumatic driving system to produce pulsatile forward flow. Herein, the essential aspects regarding iVAC2L are discussed with focus on its mechanisms of action and the available clinical experience.

Ventegodt, Søren, Efrat Merrick, and Joav Merrick. "Clinical Holistic Medicine: The Dean Ornish Program (“Opening the Heart”) in Cardiovascular Disease." Scientific World JOURNAL 6 (2006): 1977–84. http://dx.doi.org/10.1100/tsw.2006.330.

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Dean Ornish of the Preventive Medicine Research Institute in Sausalito, California has created an intensive holistic treatment for coronary heart patients with improved diet (low fat, whole foods, plant based), exercise, stress management, and social support that has proven to be efficient. In this paper, we analyze the rationale behind his cure in relation to contemporary holistic medical theory. In spite of a complex treatment program, the principles seem to be simple and in accordance with holistic medical theories, like the Antonovsky concept of rehabilitating the sense of coherence and the life mission theory for holistic medicine. We believe there is a need for the allocation of resources for further research into the aspects of holistic health and its methods, where positive and significant results have been proven and reproduced at several sites.

Shi, Qi, Kuo Gao, Huihui Zhao, Juan Wang, Xing Zhai, Peng Lu, Jianxin Chen, and Wei Wang. "Phenomics Research on Coronary Heart Disease Based on Human Phenotype Ontology." BioMed Research International 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/240284.

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The characteristics of holistic, dynamics, complexity, and spatial and temporal features enable “Omics” and theories of TCM to interlink with each other. HPO, namely, “characterization,” can be understood as a sorting and generalization of the manifestations shown by people with diseases on the basis of the phenomics. Syndrome is the overall “manifestation” of human body pathological and physiological changes expressed by four diagnostic methods’ information. The four diagnostic methods’ data could be the most objective and direct manifestations of human body under morbid conditions. In this aspect, it is consistent with the connation of “characterization.” Meanwhile, the four diagnostic methods’ data also equip us with features of characterization in HPO. In our study, we compared 107 pieces of four diagnostic methods’ information with the “characterization database” to further analyze data of four diagnostic methods’ characterization in accordance with the common characteristics of four diagnostic methods’ information and characterization and integrated 107 pieces of four diagnostic methods’ data to relevant items in HPO and finished the expansion of characterization information in HPO.

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Дисертації з теми "Coronary heart disease Molecular aspects":

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Книги з теми "Coronary heart disease Molecular aspects":

Vlodaver, Zeev. Coronary Heart Disease: Clinical, Pathological, Imaging, and Molecular Profiles. Boston, MA: Springer US, 2012.

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Smith, Timothy W. 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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Mangiapane, E. H. Diet, lipoproteins and coronary heart disease: A biochemical perspective. Nottingham: Nottingham University Press, 1998.

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International Berzelius Symposium (4th 1984 Stockholm, Sweden). Diet and prevention of coronary heart disease and cancer. Edited by Hallgren Bo 1919- and Svenska läkaresällskapet. New York: Raven Press, 1986.

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Pinckney, Neal. Healthy heart handbook: How to prevent and reverse heart disease ... Makaha, Hawaii: Healing Heart Foundation, 1994.

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Friedman, Meyer. Treating type A behavior and your heart. New York: Fawcett Crest, 1985.

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Частини книг з теми "Coronary heart disease Molecular aspects":

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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Galton, David J. "Molecular Genetics of Coronary Heart Disease." In Advances in Experimental Medicine and Biology, 95–105. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0733-4_13.

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Assmann, G., A. von Eckardstein, and H. Funke. "Apolipoproteins, Reverse Cholesterol Transport and Coronary Heart Disease." In Cellular and Molecular Biology of Atherosclerosis, 159–66. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-1909-8_15.

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Heusch, Gerd, and B. D. Guth. "New aspects on the pathophysiology of coronary heart disease." In Treatment with Gallopamil, 65–84. Heidelberg: Steinkopff, 1989. http://dx.doi.org/10.1007/978-3-642-85376-0_7.

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Patsch, J. R., and G. Miesenboeck. "High-Density Lipoprotein Cholesterol, Triglycerides and Coronary Heart Disease." In Cellular and Molecular Biology of Atherosclerosis, 153–57. London: Springer London, 1992. http://dx.doi.org/10.1007/978-1-4471-1909-8_14.

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Soubrier, F., X. Jeunemaître, B. Rigat, F. Cambien, and P. Corvol. "Molecular Genetics and Familial Arterial Hypertension." In Genetic Approaches to Coronary Heart Disease and Hypertension, 27–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76891-0_4.

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Calabresi, Laura, and Guido Francheschini. "Genetic LCAT Deficiency: Molecular Diagnosis, Plasma Lipids, and Atherosclerosis." In High Density Lipoproteins, Dyslipidemia, and Coronary Heart Disease, 89–93. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1059-2_11.

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Berg, Kåre. "Genetics of Coronary Heart Disease and its Risk Factors." In Ciba Foundation Symposium 130 - Molecular Approaches to Human Polygenic Disease, 14–33. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470513507.ch3.

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ter Keurs, Henk E. D. J. "Macroscopic and Microscopic Aspects of Cardiac Dysfunction in Congestive Heart Failure." In Molecular Defects in Cardiovascular Disease, 95–107. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-7130-2_8.

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Inagaki, Tadakatsu, Hirotsugu Tsuchimochi, James T. Pearson, Daryl O. Schwenke, Keiji Umetani, Mikiyasu Shirai, and Yoshikazu Nakaoka. "Impaired Right Coronary Vasodilator Function in Pulmonary Hypertensive Rats Assessed by In Vivo Synchrotron Microangiography." In Molecular Mechanism of Congenital Heart Disease and Pulmonary Hypertension, 193–95. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1185-1_25.

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Тези доповідей конференцій з теми "Coronary heart disease Molecular aspects":

Tao, Weiye, Laiyou Wang, Guohua Cheng, Jun Liu, and Langping Tang. "Mechanism of Sini Decoction on Coronary Heart Disease in Molecular Level." In 2nd International Conference on Computer and Information Applications (ICCIA 2012). Paris, France: Atlantis Press, 2012. http://dx.doi.org/10.2991/iccia.2012.144.

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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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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.

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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Zhang, Song, John A. Crow, Robert C. Cooper, Ronald M. McLaughlin, Shane Burgess, Ali Borazjani, and Jun Liao. "Detection of Myocardial Fiber Disruption in Artificial Lesions With 3D DT-MRI Tract Models." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193121.

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In the United States, it is estimated that in 2008 approximately 1.2 million people will suffer a new or recurrent myocardial infarction. In 2005, the latest full year for which statistics are available, 16 million Americans (7.3% of the population) had some form of coronary heart disease. Loss of myocardium as a result of myocardial infarction increases wall stress locally and globally and triggers adaptive responses at the molecular, cellular, and tissue levels. These adaptive responses can lead to left ventricular dilation and congestive heart failure. Accurate non-invasive evaluation of myocardial structural degeneration (damage) and left ventricular remodeling following an infarct would have both prognostic and therapeutic value clinically.

Poniewierski, M., M. Barthels, and H. Poliwoda. "THE SAFETY AND EFFICACY OF A LOW MOLECULAR WEIGHT HEPARIN (FRAGMIN) IN THE PREVENTION OF DEEP VEIN THROMBOSIS IN MEDICAL PATIENTS: A RANDOMIZED DOUBLE-BLIND TRIAL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643224.

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The safety and efficacy of 2500 anti-Factor Xa U of a low molecular weight heparin (Kabi 2165, Fragmin) subcutaneously once a day, and 5000 IU of standard unfractionated Heparin (KabiVitrum, Stockholm) subcutaneously twice daily as thromboprophylaxis was compared in 200 medical patients in a randomized double blind trial. According to the risk of DVT the patients were stratified before randomization in a high and low risk group. The high risk group consisted of 100 patients mainly with malignant diseases and/or previous history of thromboembolism, the low risk group of 100 patients with mainly myocardial infarction and/or coronary heart disease. The prophylaxis was given for seven to ten days. In 192 consecutive patients the clinical status and thermographic screening for DVT (leg temperature profiles, DeVeTherm) were daily evaluated. In two cases of suspected DVT and one case of suspected PE, the following phlebography or pulmonary scintigraphy were found to be negative. In the high risk group, one patient treated with Fragmin having a central venous catheter developed on day 10 symptoms of an arm vein thrombosis. There were no bleeding complications observed in either of the two treatment groups. Two patients with trombocytopenia (25.000 and 22.000/pl) due to chemotherapy and underlying malignant disease were successfully treated with Fragmin without developing any bleeding complications. In eight patients during Fragmin prophylaxis invasive diagnostic methods as heart catheterization, gastroscopy, bronchoscopy or spinal puncture were performed without noticing any bleeding events. 2500 anti-Factor Xa U of Fragmin gave plasma levels by anti-Factor Xa assay (S-2222, Kabi) of mean 0,1 U/ml when blood was sampled three to four hours after the subcutaneus application. There was no accumulation during the treatment periode observed.This study suggests that 2500 anti-Factor Xa U of Fragmin once daily is as safe and effective as 5000 IU of standard heparin twice daily in these medical patients. Especially in patients who need prophylaxis for a long time eg. with malignant disease, the once daily injection is welcomed.