Journal articles: 'Coronary heart disease – Genetic aspects'

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

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

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In this article elucidated the influence of allelic polymorphism of Gln27Glu of β2-adrenoceptors gene on patients that have coronary heart disease and obesity on the expansion and progression of congestive heart failure and left ventricular systolic dysfunction by surveying 222 patients. Presence of C allel of polymorphous locus Gln27Glu of β2-adrenoreceptors gene in patients with ischemic heart disease and concomitant obesity was associated with decreased risk of development of congestive heart failure (p < 0.05). The obtained data shown the absence of influence of polymorphous variants of β2-adrenoreceptors gene on progression of congestive heart failure in patients with ischemic heart disease and obesity (p > 0.05).

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Golukhova, Elena Z., Aygerim Z. Zholbaeva, Mari G. Arakelyan, Naida I. Bulaeva, and Michail M. Minashkin. "Genetic aspects of lone atrial fibrillation in patients without structural heart disease." Annals of the Russian academy of medical sciences 74, no. 4 (October 5, 2019): 245–52. http://dx.doi.org/10.15690/vramn1120.

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Background: Atrial fibrillation (AF) is the most common cardiac arrhythmia. Among patients with AF the subgroup posessing AF without traditional risk factors is differentiated. Such patients are commonly referred as having lone AF and comprise 1020% of all cases. A number of studies have demonstrated that the background of AF, and in particular lone AF, have a substantial genetic component. Aims: To evaluate the influence of gene polymorphism to the development of atrial fibrillation in patients without concomitant valvular pathology and coronary artery disease. Materials and methods: The study included 174 patients with atrial fibrillation and 124 controls without any cardiovascular pathology. All patients were divided into two subgroups: with lone AF (n=94) and with concomitant arterial hypertension (n=80). All patients underwent a complex of clinical, instrumental (ECG, echocardiography, computed tomography of the pulmonary veins) and laboratory tests (thyroid hormones, inflammatory markers, fibrosis), as well as genetic analysis (determination of single nucleotide polymorphisms described as AF risk factors in genes AGXT2, PDE4D, SLN, SCN5A, PITX2, PRRX1, ZFHX3, TBX5, CAV1 и HCN4). Results: For the rare polymorphisms rs12291814 (SLN) and rs137854601 (SCN5A) wasnt found anyone carrier of the minor allele (C and A, respectively). In the both patient subgroups the minor allele T of rs2200733 in PITX2 (OR=3.18, p0.0001), minor allele G of rs3903239 in PRRX1, and minor alleles A of 2 polymorphisms rs2106261 and rs7193343 in ZFHX3 gene were revealed as risk factor of AF (OR=2.96, p0.0001, OR=2.02, p=0.0045, OR=1.64, p=0.04, respectively). We also revealed significant difference between AF and control groups for rs3807989 in CAV1: homozygotic state of minor allele A has a protective effect on the development of arrhythmias (OR=0.39). Conclusions: We revealed the association between the polymorphisms in genes regulating transcription and the development of atrial fibrillation. These polymorphisms have already described but their frequencies have never investigated in Russian population. But the polymorphisms influence to gene functions stays unclear, although attempts to investigate relationship between genotype and gene expression have been made. When the relationship will be discovered it can help us to modify our approach in treatment to patients with atrial fibrillation.

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Golukhova, E. Z., O. I. Gromova, R. A. Shomahov, N. I. Bulaeva, and L. A. Bockeria. "Monogenec Arrhythmic Syndromes: From Molecular and Genetic Aspects to Bedside." Acta Naturae 8, no. 2 (June 15, 2016): 62–74. http://dx.doi.org/10.32607/20758251-2016-8-2-62-74.

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

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Islam, AKM Monwarul, AKM Mohibullah, and Timir Paul. "Cardiovascular Disease in Bangladesh: A Review." Bangladesh Heart Journal 31, no. 2 (April 28, 2017): 80–99. http://dx.doi.org/10.3329/bhj.v31i2.32379.

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

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Cavarretta, Elena, and Giacomo Frati. "MicroRNAs in Coronary Heart Disease: Ready to Enter the Clinical Arena?" BioMed Research International 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/2150763.

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Coronary artery disease (CAD) and its complication remain the leading cause of mortality in industrialized countries despite great advances in terms of diagnosis, prognosis, and treatment options. MicroRNAs (miRNAs), small noncoding RNAs, act as posttranscriptional gene expression modulators and have been implicated as key regulators in several physiological and pathological processes linked to CAD. Circulating miRNAs have been evaluated as promising novel biomarkers of CAD, acute coronary syndromes, and acute myocardial infarction, with prognostic implications. Several challenges related to technical aspects, miRNAs normalization, drugs interaction, and quality reporting of statistical multivariable analysis of the miRNAs observational studies remain unresolved. MicroRNA-based therapies in cardiovascular diseases are not ready yet for human trials but definitely appealing. Through this review we will provide clinicians with a concise overview of the pros and cons of microRNAs.

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Berezikova, Ye N., M. G. Pustovetova, S. N. Shilov, A. V. Yefremov, A. T. Teplyakov, I. D. Safronov, and Ye N. Samsonova. "Effects of caspase 8 gene polymorphism on the risks for development/course of chronic heart failure." Patologiya krovoobrashcheniya i kardiokhirurgiya 17, no. 2 (October 10, 2015): 45. http://dx.doi.org/10.21688/1681-3472-2013-4-45-49.

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The aim of the study was to identify genetic determinants of increased risks for heart failure severity. Clinical and genetic aspects of the effects of gene polymorphism caspase 8 (polymorphic loci -652(6N)I/D and D302H) on the risks for development and severity of chronic heart failure (CHF) in patients with coronary artery disease were investigated. 277 patients with CHF were studied (182 males and 95 females aged 45 to 65 years (mean age 59.27.7 years). Genotypes were identified by using RFLP analysis of PCR products. The control group included 136 people (mean age 53.64.8 years) who had no symptoms of cardiovascular disorders. The presence of del allele and genotype del/del polymorphic locus -652(6N)I/D gene caspase 8 was associated with an increased risk for heart failure, while the allele ins and genotype ins/ins were found to serve as protective factors. Allele ins and genotype ins/ins polymorphic locus -652(6N)I/D gene caspase 8 proved to be associated with protective effects on the course of CHF in patients with coronary artery disease, while allele del and genotype del/del could be considered as predictors of an unfavorable course of the disease. The analysis revealed no significant differences in the frequency distribution of genotypes and alleles of polymorphic loci D302H gene caspase 8 in patients with chronic heart failure and in the control group, as well as in the dependence on the functional class of heart failure. The definition of polymorphism -652(6N)I/D gene caspase 8 can be recommended for early prediction of risks and severity of heart failure.

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Groznova, O. S., I. M. Miklashevich, V. Yu Voinova, M. A. Shkolnikova, O. N. Tkacheva, E. N. Dudinskaya, and I. A. Kovalev. "Biomarkers of early cardiovascular aging." Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) 64, no. 4 (September 15, 2019): 11–18. http://dx.doi.org/10.21508/1027-4065-2019-64-4-11-18.

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Genetic aspects regulate the intensity and rate of aging (no toxic effects considered), their negative role depends on the pathogenicity of the mutation. The light variant of the genetic “defect” has no clinical signs which feature a certain known genetic syndrome, but it has the biochemical, immunological, vascular and other abnormalities leading to pathological aging. In the most severe case, e.g. progeria, pathological aging is the main phenotypic symptom that manifests already in childhood. The subject of the pathological aging research covers the whole range of intermediate states. The review focuses on aging in individuals without validated signs of disease: coronary heart disease, hypertension, diabetes or fasting hyperglycemia, hyperlipidemia, and others. The authors present the main searching directions of aging biomarkers (size and speed of telomere shortening, breaks in their terminal loops; expression of inflammatory proteins, synaptic interactions proteins and neurotrophic processes; mitochondrial biogenesis; endothelial dysfunction; DNA methylation activity).

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Khaw, Kay-Tee. "Epidemiological aspects of ageing." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 352, no. 1363 (December 29, 1997): 1829–35. http://dx.doi.org/10.1098/rstb.1997.0168.

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A major societal challenge is to improve quality of life and prevent or reduce disability and dependency in an ageing population. Increasing age is associated with increasing risk of disability and loss of independence, due to functional impairments such as loss of mobility, hearing and vision; a major issue must be how far disability can be prevented. Ageing is associated with loss of bone tissue, reduction in muscle mass, reduced respiratory function, decline in cognitive function, rise in blood pressure and macular degeneration which predispose to disabling conditions such as osteoporosis, heart disease, dementia and blindness. However, there are considerable variations in different communities in terms of the rate of age–related decline. Large geographic and secular variations in the age–adjusted incidence of major chronic diseases such as stroke, hip fracture, coronary heart disease, cancer, visual loss from cataract, glaucoma and macular degeneration suggest strong environmental determinants in diet, physical activity and smoking habit. The evidence suggests that a substantial proportion of chronic disabling conditions associated with ageing are preventable, or at least postponable and not an inevitable accompaniment of growing old. Postponement or prevention of these conditions may not only increase longevity, but, more importantly, reduce the period of illnesses such that the majority of older persons may live high–quality lives, free of disability, until very shortly before death. We need to understand better the factors influencing the onset of age–related disability in the population, so that we have appropriate strategies to maintain optimal health in an ageing population.

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Barton, Matthias, and Masashi Yanagisawa. "Endothelin: 30 Years From Discovery to Therapy." Hypertension 74, no. 6 (December 2019): 1232–65. http://dx.doi.org/10.1161/hypertensionaha.119.12105.

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

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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.

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Iakoubova, Olga, Carmen Tong, Joseph Catanese, Charles Rowland, May Luke, Maryann Tranquilli, and John Elefteriades. "KIF6 719Arg Genetic Variant and Risk for Thoracic Aortic Dissection." AORTA 04, no. 03 (June 2016): 83–90. http://dx.doi.org/10.12945/j.aorta.2016.16.003.

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Background: Carriers of the 719Arg variant in KIF6, compared with noncarriers, have been reported to be at greater risk for coronary heart disease (CHD) in six prospective studies. Because CHD, thoracic aortic dissection, and nondissection thoracic aortic aneurysm share some risk factors and aspects of pathophysiology, we investigated whether carriers of the 719Arg variant also have greater odds of thoracic aortic dissection or nondissected thoracic aortic aneurysm than noncarriers. Methods: We genotyped 140 thoracic aortic dissection cases, 497 nondissection thoracic aortic aneurysm cases, and 275 disease-free controls collected in the United States, Hungary, and Greece and investigated the association between KIF6 719Arg carrier status and thoracic aortic dissection, and between KIF6 719Arg carrier status and nondissection thoracic aortic aneurysm, using logistic regression models adjusted for age, sex, hypertension, smoking, and country. Results: The odds of aortic dissection were two-fold greater in KIF6 719Arg carriers compared with noncarriers (odds ratio (OR) 2.14, 95% confidence interval (CI) 1.18-3.9). To account for the potential of concomitant CHD to confound the association between the KIF6 719Arg and thoracic aortic dissection, we repeated the analysis after removing subjects with concomitant CHD; the estimates for association of KIF6 719Arg carrier status remained essentially the same (OR 2.04, 95% CI 1.11-3.77). In contrast, KIF6 719Arg carrier status was not associated with risk for nondissection thoracic aortic aneurysm. Conclusions: We observed an association of the KIF6 719Arg genetic variant with thoracic aortic dissection in this multicenter case-control study. This association may enhance our management of patients with thoracic aortic disease.

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Hidirova, L. D., D. A. Yakhontov, S. A. Zenin, and V. N. Maximov. "Genetic markers of atrial fibrillation in patients with hypertension in combination with non-cardiac diseases." Patologiya krovoobrashcheniya i kardiokhirurgiya 23, no. 1 (July 9, 2019): 83. http://dx.doi.org/10.21688/1681-3472-2019-1-83.

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Letter to the editor:The world medical community has categorised atrial fibrillation (AF) as one of the three cardiovascular ‘epidemics of the 21st century’, along with chronic heart failure and diabetes mellitus [1]. In recent years, the prevalence of AF has increasing steadily. However, the exact cause for the increase in the incidence of AF cannot be explained only by the increase in life expectancy, prevalence of cardiac valve disease or prevalence of myocardial infarction [2].Although AF occurs in individuals with various manifestations of coronary heart disease, it is increasingly being diagnosed in patients with arterial hypertension without coronary heart disease [3]. AF causes serious cardiovascular complications; thus, a deep understanding of its pathogenetic aspects and a comprehensive study that considers comorbid pathologies for identifying the predictors of the development and progression of AF are required [4].Hereditary factors can play a significant role in the development of AF and hypertension; consequently, the worldwide practice of scientific research in basic medicine pays significant attention to the molecular genetics methods of analysis.This study aimed to evaluate the genetic determinants in patients with hypertension with AF progression accompanied by various extra-cardiac comorbid pathologies.This prospective cohort study included 167 patients with a paroxysmal and persistent form of AF and stage III hypertonic disease without coronary heart disease. The average age of the patients was 53.3 ± 7.1 years. DNA isolation from blood leucocytes was performed using phenol–chloroform extraction. The rs1378942 polymorphism of the CSK gene, the rs220073 polymorphism and the -174G/C polymorphism (rs1800795) of the IL6 gene were assessed using polymerase chain reaction-restriction fragment length polymorphism. The statistical hypotheses were considered significant at a critical level of p = 0.05, i.e. the difference was considered statistically significant at p < 0.05. The lower limit of evidentiary power was equal to 80%.This study reported associations between the rs1378942 polymorphism of the CSK gene, the rs1800795 polymorphism of the IL6 gene and the rs220073 polymorphism and the progression of AF in combination with the following associated diseases: hypertension, chronic obstructive pulmonary disease, hypothyroidism, type 2 diabetes mellitus and abdominal obesity. The relative risk of the progression of AF in carriers of the allele C was 1.94 times higher than that in carriers of the allele A [95% confidence interval (CI), 1.21–3.09]. Carriage of the AA genotype was conditionally protective against the progression of AF (relative risk, 0.41; 95% CI, 0.21–0.80; p = 0.010).Associations of the rs1378942 and rs1800795 polymorphisms with the risk of recurrence of AF in combination with certain diseases were also found. In addition, associations were identified between rs1378942 and glomerular filtration rate, systolic and diastolic blood pressure, left atrial wall thickness and glucose, high-density lipoprotein (HDL) cholesterol, triglyceride and creatinine levels; between rs220073 and levels of triglycerides, atherogenic index, creatinine, fibrinogen and the number of months before the development of relapse and between rs1800795 and HDL cholesterol, creatinine and galectin-3 levels and diastolic blood pressure.The secondary form of AF as a multi-factorial disease develops under the influence of many factors of both the external environment and hereditary nature. The complexity of the etio-pathogenesis of the disease makes it extremely difficult for researchers to identify the factors that play a leading role in the development of the pathological process. Currently, associative studies of AF with polymorphisms of >260 genes have been conducted, and genome-wide associative studies have been performed as well. The reproducibility of the results depends on several factors: age, sex, comorbidities, ethnicity, penetrance, expressiveness, pleiotropy, various epigenetic influences and many more.Despite the limitations of the sample, our study adds to the data material already available that can serve in the prognostic assessment of the development and progression of AF. Further studies will allow the development of a personalised algorithm for predicting the progression of AF in hypertension combined with extra-cardiac diseases. In this regard, further larger studies are necessary that involve other institutions and a larger sample of patients, which will make it possible to predict the progression of AF with the definition of additional molecular criteria for evaluating the effectiveness of pathogenetic therapy and the possibilities of targeted treatment. Funding: The study did not have sponsorship. Conflict of interest: Authors declare no conflict of interest.

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Hidirova, L. D., D. A. Yakhontov, S. A. Zenin, and V. N. Maximov. "Genetic markers of atrial fibrillation in patients with hypertension in combination with non-cardiac diseases." Patologiya krovoobrashcheniya i kardiokhirurgiya 23, no. 1 (July 9, 2019): 83. http://dx.doi.org/10.21688/1681-3472-2019-1-83-85.

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Letter to the editor:The world medical community has categorised atrial fibrillation (AF) as one of the three cardiovascular ‘epidemics of the 21st century’, along with chronic heart failure and diabetes mellitus [1]. In recent years, the prevalence of AF has increasing steadily. However, the exact cause for the increase in the incidence of AF cannot be explained only by the increase in life expectancy, prevalence of cardiac valve disease or prevalence of myocardial infarction [2].Although AF occurs in individuals with various manifestations of coronary heart disease, it is increasingly being diagnosed in patients with arterial hypertension without coronary heart disease [3]. AF causes serious cardiovascular complications; thus, a deep understanding of its pathogenetic aspects and a comprehensive study that considers comorbid pathologies for identifying the predictors of the development and progression of AF are required [4].Hereditary factors can play a significant role in the development of AF and hypertension; consequently, the worldwide practice of scientific research in basic medicine pays significant attention to the molecular genetics methods of analysis.This study aimed to evaluate the genetic determinants in patients with hypertension with AF progression accompanied by various extra-cardiac comorbid pathologies.This prospective cohort study included 167 patients with a paroxysmal and persistent form of AF and stage III hypertonic disease without coronary heart disease. The average age of the patients was 53.3 ± 7.1 years. DNA isolation from blood leucocytes was performed using phenol–chloroform extraction. The rs1378942 polymorphism of the CSK gene, the rs220073 polymorphism and the -174G/C polymorphism (rs1800795) of the IL6 gene were assessed using polymerase chain reaction-restriction fragment length polymorphism. The statistical hypotheses were considered significant at a critical level of p = 0.05, i.e. the difference was considered statistically significant at p < 0.05. The lower limit of evidentiary power was equal to 80%.This study reported associations between the rs1378942 polymorphism of the CSK gene, the rs1800795 polymorphism of the IL6 gene and the rs220073 polymorphism and the progression of AF in combination with the following associated diseases: hypertension, chronic obstructive pulmonary disease, hypothyroidism, type 2 diabetes mellitus and abdominal obesity. The relative risk of the progression of AF in carriers of the allele C was 1.94 times higher than that in carriers of the allele A [95% confidence interval (CI), 1.21–3.09]. Carriage of the AA genotype was conditionally protective against the progression of AF (relative risk, 0.41; 95% CI, 0.21–0.80; p = 0.010).Associations of the rs1378942 and rs1800795 polymorphisms with the risk of recurrence of AF in combination with certain diseases were also found. In addition, associations were identified between rs1378942 and glomerular filtration rate, systolic and diastolic blood pressure, left atrial wall thickness and glucose, high-density lipoprotein (HDL) cholesterol, triglyceride and creatinine levels; between rs220073 and levels of triglycerides, atherogenic index, creatinine, fibrinogen and the number of months before the development of relapse and between rs1800795 and HDL cholesterol, creatinine and galectin-3 levels and diastolic blood pressure.The secondary form of AF as a multi-factorial disease develops under the influence of many factors of both the external environment and hereditary nature. The complexity of the etio-pathogenesis of the disease makes it extremely difficult for researchers to identify the factors that play a leading role in the development of the pathological process. Currently, associative studies of AF with polymorphisms of >260 genes have been conducted, and genome-wide associative studies have been performed as well. The reproducibility of the results depends on several factors: age, sex, comorbidities, ethnicity, penetrance, expressiveness, pleiotropy, various epigenetic influences and many more.Despite the limitations of the sample, our study adds to the data material already available that can serve in the prognostic assessment of the development and progression of AF. Further studies will allow the development of a personalised algorithm for predicting the progression of AF in hypertension combined with extra-cardiac diseases. In this regard, further larger studies are necessary that involve other institutions and a larger sample of patients, which will make it possible to predict the progression of AF with the definition of additional molecular criteria for evaluating the effectiveness of pathogenetic therapy and the possibilities of targeted treatment. Funding: The study did not have sponsorship. Conflict of interest: Authors declare no conflict of interest.

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Bambauer, Rolf, Carolin Bambauer, Boris Lehmann, Reinhard Latza, and Ralf Schiel. "LDL-Apheresis: Technical and Clinical Aspects." Scientific World Journal 2012 (2012): 1–19. http://dx.doi.org/10.1100/2012/314283.

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The prognosis of patients suffering from severe hyperlipidemia, sometimes combined with elevated lipoprotein (a) levels, and coronary heart disease refractory to diet and lipid-lowering drugs is poor. For such patients, regular treatment with low-density lipoprotein (LDL) apheresis is the therapeutic option. Today, there are five different LDL-apheresis systems available: cascade filtration or lipid filtration, immunoadsorption, heparin-induced LDL precipitation, dextran sulfate LDL adsorption, and the LDL hemoperfusion. There is a strong correlation between hyperlipidemia and atherosclerosis. Besides the elimination of other risk factors, in severe hyperlipidemia therapeutic strategies should focus on a drastic reduction of serum lipoproteins. Despite maximum conventional therapy with a combination of different kinds of lipid-lowering drugs, sometimes the goal of therapy cannot be reached. Hence, in such patients, treatment with LDL-apheresis is indicated. Technical and clinical aspects of these five different LDL-apheresis methods are shown here. There were no significant differences with respect to or concerning all cholesterols, or triglycerides observed. With respect to elevated lipoprotein (a) levels, however, the immunoadsorption method seems to be most effective. The different published data clearly demonstrate that treatment with LDL-apheresis in patients suffering from severe hyperlipidemia refractory to maximum conservative therapy is effective and safe in long-term application.

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Goetzl, Edward J., Markus Graeler, Mei-Chuan Huang, and Geetha Shankar. "Lysophospholipid Growth Factors and Their G Protein-Coupled Receptors in Immunity, Coronary Artery Disease, and Cancer." Scientific World JOURNAL 2 (2002): 324–38. http://dx.doi.org/10.1100/tsw.2002.124.

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The physiological lysophospholipids (LPLs), exemplified by lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P), are omnific mediators of normal cellular proliferation, survival, and functions. Although both LPA and S1P attain micromolar concentrations in many biological fluids, numerous aspects of their biosynthesis, transport, and metabolic degradation are unknown. Eight members of a new subfamily of G protein-coupled LPA/S1P receptors, originally termed Edg Rs, bind either LPA or S1P with high affinity and transduce a series of growth-related and/or cytoskeleton-based functional responses. The most critical areas of LPL biology and pathobiology are neural development and neurodegeneration, immunity, atherosclerosis and myocardial injury, and cancer. Data from analyses of T cells established two basic points: (1) the plasticity and adaptability of expression of LPA/S1P Rs by some cells as a function of activation, and (2) the role of opposing signals from two different receptors for the same ligand as a mechanism for fine control of effects of LPLs. In the heart, LPLs may promote coronary atherosclerosis, but are effectively cytoprotective for hypoxic cardiac myocytes and those exposed to oxygen free radicals. The findings of production of LPA by some types of tumor cells, overexpression of selected sets of LPA receptors by the same tumor cells, and augmentation of the effects of protein growth factors by LPA have suggested pathogenetic roles for the LPLs in cancer. The breadth of physiologic and pathologic activities of LPLs emphasizes the importance of developing bioavailable nonlipid agonists and antagonists of the LPA/S1P receptors for diverse therapeutic applications.

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Hui, Stanley Sai-chuen. "Current Perspectives on Health and Physical Activity in Hong Kong: A Review." Journal of Physical Activity and Health 1, no. 1 (January 2004): 56–70. http://dx.doi.org/10.1123/jpah.1.1.56.

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Promoting regular physical activity has been considered one of the most important aspects of preventive medicine in recent years. This is due to the fact that tremendous evidence has been found about the positive association between increasing physical activity and desirable health effects. Findings have been summarized in a number of review documents; however, most of these reviews emphasize findings retrieved from research conducted in Western countries. Few papers were found to summarize findings in physical activity and health of the Hong Kong Chinese population. Epidemiological studies revealed that there exists distinct diverse health status among different ethnic groups due to culture, beliefs, genetic makeup, health practices, and behaviors in these highly diverse groups. This chapter reviews what is known about the association between physical activity and health in the Chinese population of Hong Kong. Current health issues including coronary heart disease, obesity, diabetes, cancer, osteoporosis, and so on, that are specific to the Hong Kong situation are reviewed. Moreover, findings in physical activity participation levels of Hong Kong adults and children are introduced. Results indicate that the associations between physical activity and health found in the Chinese population of Hong Kong share similar trends as those reported in Western countries. Three quarters of Hong Kong children and adults are not physically active enough to achieve health benefits. The physical activity level for the Hong Kong Chinese population remains low. The need for promotional and intervention programs on physical activity participation is pressing.

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Kumar, Shashank, and Abhay K. Pandey. "Chemistry and Biological Activities of Flavonoids: An Overview." Scientific World Journal 2013 (2013): 1–16. http://dx.doi.org/10.1155/2013/162750.

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There has been increasing interest in the research on flavonoids from plant sources because of their versatile health benefits reported in various epidemiological studies. Since flavonoids are directly associated with human dietary ingredients and health, there is need to evaluate structure and function relationship. The bioavailability, metabolism, and biological activity of flavonoids depend upon the configuration, total number of hydroxyl groups, and substitution of functional groups about their nuclear structure. Fruits and vegetables are the main dietary sources of flavonoids for humans, along with tea and wine. Most recent researches have focused on the health aspects of flavonoids for humans. Many flavonoids are shown to have antioxidative activity, free radical scavenging capacity, coronary heart disease prevention, hepatoprotective, anti-inflammatory, and anticancer activities, while some flavonoids exhibit potential antiviral activities. In plant systems, flavonoids help in combating oxidative stress and act as growth regulators. For pharmaceutical purposes cost-effective bulk production of different types of flavonoids has been made possible with the help of microbial biotechnology. This review highlights the structural features of flavonoids, their beneficial roles in human health, and significance in plants as well as their microbial production.

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Kringlen, E. "Psychosocial aspects of coronary heart disease." Acta Psychiatrica Scandinavica 74, no. 3 (September 1986): 225–37. http://dx.doi.org/10.1111/j.1600-0447.1986.tb06238.x.

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Seraganian, Peter. "Behavioural aspects of coronary heart disease." Canadian Psychology/Psychologie canadienne 26, no. 2 (April 1985): 113–20. http://dx.doi.org/10.1037/h0080026.

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Pakhomia, N. S., O. M. Uryasev, and Y. A. Panfilov. "Genetic aspects of ischemic heart disease." I.P.Pavlov Russian Medical Biological Herald 23, no. 4 (December 15, 2015): 126. http://dx.doi.org/10.17816/pavlovj20154126-132.

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22

WEISS, KENNETH M. "Genetic analysis of coronary heart disease." Journal of Heredity 76, no. 6 (November 1985): 481. http://dx.doi.org/10.1093/oxfordjournals.jhered.a110155.

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23

Breslow, Jan L. "Genetic markers for coronary heart disease." Clinical Cardiology 24, S2 (July 2001): 14–17. http://dx.doi.org/10.1002/clc.4960240706.

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Cohen, Jonathan C. "Genetic Approaches to Coronary Heart Disease." Journal of the American College of Cardiology 48, no. 9 (November 2006): A10—A14. http://dx.doi.org/10.1016/j.jacc.2006.06.046.

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Agewall, Stefan. "Some Aspects of Preventing Coronary Heart Disease." Angiology 63, no. 1 (May 8, 2011): 17–23. http://dx.doi.org/10.1177/0003319711407060.

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Coronary heart disease (CHD) is the leading cause of mortality in the industrialized world and that might also soon be the case in other parts of the world. There are several easily measured and potentially modifiable risk factors that account for a substantial proportion of the risk of CHD. The effect of risk factors interventions appears to be consistent in both genders, across different geographic regions, and by all ethnic groups, suggesting that approaches to prevention can be based on similar principles worldwide. Optimal target levels for serum cholesterol and blood pressure are not yet clear. Future risk CHD reduction will mainly be achieved by improved primary prevention.

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Keavney, Bernard. "Genetic epidemiological studies of coronary heart disease." International Journal of Epidemiology 31, no. 4 (August 2002): 730–36. http://dx.doi.org/10.1093/ije/31.4.730.

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Weiner, Kate, and Paul Martin. "A genetic future for coronary heart disease?" Sociology of Health & Illness 30, no. 3 (October 31, 2007): 380–95. http://dx.doi.org/10.1111/j.1467-9566.2007.01058.x.

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Keavney, Bernard. "Common Genetic Polymorphisms and Coronary Heart Disease." Seminars in Vascular Medicine 02, no. 3 (2002): 233–42. http://dx.doi.org/10.1055/s-2002-35391.

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Price, W. H., S. W. Morris, A. H. Kitchin, P. R. Wenham, P. R. S. Mckenzie, and P. M. Donald. "Genetic markers of familial coronary heart disease." Lancet 336, no. 8715 (September 1990): 629. http://dx.doi.org/10.1016/0140-6736(90)93425-o.

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Scott, C. D., and J. H. Dark. "Coronary artery disease after heart transplantation: clinical aspects." Heart 68, no. 9 (September 1, 1992): 255–56. http://dx.doi.org/10.1136/hrt.68.9.255.

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Srivastava, Deepak. "Developmental and genetic aspects of congenital heart disease." Current Opinion in Cardiology 14, no. 3 (May 1999): 263. http://dx.doi.org/10.1097/00001573-199905000-00011.

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Fasnacht, Margrit S., and Edgar T. Jaeggi. "Fetal and Genetic Aspects of Congenital Heart Disease." Therapeutische Umschau 58, no. 2 (February 1, 2001): 70–75. http://dx.doi.org/10.1024/0040-5930.58.2.70.

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Die pränatale Kardiologie umfasst die intrauterine Diagnosestellung angeborener Herzfehler mittels zweidimensionaler Echokardiographie, die Diagnosestellung und eventuelle Therapie fötaler Herzrhythmusstörungen, die Beratung und Betreuung betroffener Eltern, das Planen der Geburt und die postpartale Betreuung in enger Zusammenarbeit mit Geburtshelfer und Neonatologen. Eine ausführliche pränatale kardiologische Abklärung ist aus zeitlichen und wirtschaftlichen Gründen Schwangerschaften mit erhöhtem Risiko für einen angeborenen Herzfehler oder bei Verdacht auf einen angeborenen Herzfehler beziehungsweise Rhythmusstörung vorbehalten. Da die meisten angeborenen Herzfehler bei Schwangerschaften ohne erhöhtes Risiko auftreten, ist ein Ultraschallscreening des fötalen Herzens im Rahmen der Routineultraschalluntersuchung empfehlenswert. Die Sensitivität dieser Untersuchung ist momentan noch unbefriedigend, obwohl die meisten schwerwiegenden angeborenen Herzfehler pränatal erfasst werden könnten. Wird pränatal ein angeborener Herzfehler diagnostiziert, ist eine weitere Abklärung hinsichtlich extrakardialer Missbildungen und Chromosomenanomalien indiziert. Auch muss der weitere Schwangerschaftsverlauf und die Geburt geplant werden. Insbesondere bei Vitien mit postpartal duktusabhängiger Lungen- oder Körperperfusion sollte unbedingt eine Entbindung an einem Zentrum mit Erfahrung im neonatalen Management von kritischen Herzfehlern erfolgen. Viele Herzfehler und Herzerkrankungen sind genetisch bedingt. Allgemein bekannt ist die Assoziation von Herzfehlern mit Trisomien (Trisomie 13, 18, 21). In den letzten Jahren konnten aber immer mehr molekulargenetische Veränderungen als Ursache für einen Herzfehler gefunden werden. Die bedeutungsvollste ist das Mikrodeletion 22q11 Syndrom (CATCH 22 Syndrom). Für viele andere Herzerkrankungen und Syndrome mit kardialer Beteiligung konnte eine genetische Ursache bewiesen werden. Das Wissen um genetische Ursachen angeborener Herzerkrankungen ist wichtig für die genetische Beratung, sowie die Betreuung der Patienten, da häufig zusätzliche extrakardiale Probleme vorliegen.

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Palmer, Sarah Jane. "New genetic tool for identifying coronary heart disease." British Journal of Cardiac Nursing 11, no. 11 (November 2, 2016): 567–68. http://dx.doi.org/10.12968/bjca.2016.11.11.567.

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Semaev, Sergey, and Elena Shakhtshneider. "Genetic Risk Score for Coronary Heart Disease: Review." Journal of Personalized Medicine 10, no. 4 (November 20, 2020): 239. http://dx.doi.org/10.3390/jpm10040239.

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The present review deals with the stages of creation, methods of calculation, and the use of a genetic risk score for coronary heart disease in various populations. The concept of risk factors is generally recognized on the basis of the results of epidemiological studies in the 20th century; according to this concept, the high prevalence of diseases of the circulatory system is due to lifestyle characteristics and associated risk factors. An important and relevant task for the healthcare system is to identify the population segments most susceptible to cardiovascular diseases (CVDs). The level of individual risk of an unfavorable cardiovascular prognosis is determined by genetic factors in addition to lifestyle factors.

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Muhlestein, Joseph B., and Jeffrey L. Anderson. "The 9p21.3 Genetic Region and Coronary Heart Disease." Journal of the American College of Cardiology 58, no. 4 (July 2011): 435–37. http://dx.doi.org/10.1016/j.jacc.2011.01.053.

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Bloch, Michael J. "Genetic risk scores and coronary heart disease risk." Journal of the American Society of Hypertension 9, no. 8 (August 2015): 580–81. http://dx.doi.org/10.1016/j.jash.2015.06.010.

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Kullo, Iftikhar J., and Keyue Ding. "Mechanisms of Disease: the genetic basis of coronary heart disease." Nature Clinical Practice Cardiovascular Medicine 4, no. 10 (October 2007): 558–69. http://dx.doi.org/10.1038/ncpcardio0982.

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Korzh, O. M. "CURRENT ASPECTS OF CORONARY HEART DISEASE DIAGNOSIS AND TREATMENT." International Medical Journal, no. 1 (March 5, 2020): 5–10. http://dx.doi.org/10.37436/2308-5274-2020-1-1.

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Among the cardiovascular diseases associated with atherosclerosis, chronic coronary heart disease, including angina, is the most common form. It is the myocardium lesion that develops as a result of an imbalance between the coronary circulation and metabolic needs of heart muscle. The presence of angina symptoms often indicates a pronounced narrowing of one or more coronary arteries, but also occurs in non−obstructive arterial impairment and even in normal coronary arteries. Factors of functional damage to the coronary arteries are spasm, temporary platelet aggregation and intravascular thrombosis. Today there are opportunities not only to use the therapy with proven effectiveness, aimed at reducing the risk of complications, including fatal, but also to treat angina (ischemia), which improves the patient's life quality. The drug protocol includes the ones with a proven positive effect on this disease prognosis, which are mandatory if there are no direct contraindications to use, as well as a large group of antianginal or anti−ischemic drugs. The choice of a particular drug or its combinations with other drugs is carried out in accordance with generally accepted recommendations: taking into account the individual approach, the severity of angina, hemodynamic parameters (heart rate and blood pressure, presence of comorbid conditions). If drug therapy is ineffective, the option of coronary myocardial revascularization (percutaneous coronary angioplasty or coronary artery bypass grafting) is considered. Due to the high mortality and morbidity rates of coronary heart disease worldwide, one of the priorities of practical health care is the prevention of diseases caused by atherosclerosis. Key words: coronary heart disease, angina, family physician, prognosis, drug therapy.

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39

Hegele, Robert. "Genetic prediction of coronary heart disease: Lessons from Canada." Scandinavian Journal of Clinical and Laboratory Investigation 59 (1999): 153–67. http://dx.doi.org/10.3109/00365519909168339.

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Agah, Ramtin, and Eric J. Topol. "Genetic testing for coronary heart disease: the approaching frontier." Expert Review of Molecular Diagnostics 2, no. 5 (September 2002): 448–60. http://dx.doi.org/10.1586/14737159.2.5.448.

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Dhokley, Waheeda, Tahreem Ansari, Naeema Fazlani, and Heena Mohd.Hafeez. "New Improved Genetic Algorithm for Coronary Heart Disease Prediction." International Journal of Computer Applications 136, no. 5 (February 17, 2016): 34–37. http://dx.doi.org/10.5120/ijca2016908419.

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42

Cambien, Frangois. "Insight into the Genetic Epidemiology of Coronary Heart Disease." Annals of Medicine 28, no. 5 (January 1996): 465–70. http://dx.doi.org/10.3109/07853899608999109.

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Vaarhorst, Anika A. M., Yingchang Lu, Bastiaan T. Heijmans, Martijn E. T. Dollé, Stefan Böhringer, Hein Putter, Sandra Imholz, et al. "Literature-Based Genetic Risk Scores for Coronary Heart Disease." Circulation: Cardiovascular Genetics 5, no. 2 (April 2012): 202–9. http://dx.doi.org/10.1161/circgenetics.111.960708.

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Hegele, Robert A. "Genetic prediction of coronary heart disease: Lessons from Canada." Scandinavian Journal of Clinical and Laboratory Investigation 59, sup230 (January 1999): 153–67. http://dx.doi.org/10.1080/00365519909168339.

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Ganna, Andrea, Patrik K. E. Magnusson, Nancy L. Pedersen, Ulf de Faire, Marie Reilly, Johan Ärnlöv, Johan Sundström, Anders Hamsten, and Erik Ingelsson. "Multilocus Genetic Risk Scores for Coronary Heart Disease Prediction." Arteriosclerosis, Thrombosis, and Vascular Biology 33, no. 9 (September 2013): 2267–72. http://dx.doi.org/10.1161/atvbaha.113.301218.

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46

Seo, David, and Pascal J. Goldschmidt-Clermont. "Cardiovascular Genetic Medicine: The Genetics of Coronary Heart Disease." Journal of Cardiovascular Translational Research 1, no. 2 (May 23, 2008): 166–70. http://dx.doi.org/10.1007/s12265-008-9034-0.

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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.

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JIANG, Ting-Ting, Xing CHEN, Ting-Ting LI, Feng-Guo ZHANG, Yi XIE, Jian-Ning ZHANG, Jie PENG, Tian-Jiao LIU, Gang CHEN, and Yuan GUO. "Genetic scanning on chromosome 8 loci for coronary heart disease." Hereditas (Beijing) 34, no. 8 (August 28, 2012): 1043–49. http://dx.doi.org/10.3724/sp.j.1005.2012.01043.

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Previato, L., F. Sandrelli, S. Stefanato, A. Codemo, R. Razzolini, I. Cortella, S. Martini, C. Gabelli, and G. Crepaldi. "Genetic risk factors in coronary heart disease (CHD) and restenosis." Atherosclerosis 151, no. 1 (July 2000): 108. http://dx.doi.org/10.1016/s0021-9150(00)80488-8.

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Qi, Lu, Layla Parast, Tianxi Cai, Christine Powers, Ernest V. Gervino, Thomas H. Hauser, Frank B. Hu, and Alessandro Doria. "Genetic Susceptibility to Coronary Heart Disease in Type 2 Diabetes." Journal of the American College of Cardiology 58, no. 25 (December 2011): 2675–82. http://dx.doi.org/10.1016/j.jacc.2011.08.054.

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

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