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1
Nurmamadovna, Ishankulova Nasiba. "Coronary Heart Disease." American Journal of Medical Sciences and Pharmaceutical Research 03, no. 02 (February 28, 2021): 31–36. http://dx.doi.org/10.37547/tajmspr/volume03issue02-04.
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The article covers the etiology, pathogenesis, classification, diagnosis, clinical picture and treatment of coronary heart disease, provides a literature review. Cardiovascular disease (CVD) represents the leading cause of death among women as well as men. The number of deaths due to CVD in women are greater than in men. There are significant gender-related differences concerning CVD.
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Renaud, Serge, and Dominique Lanzmann-Petithory. "Coronary heart disease: dietary links and pathogenesis." Public Health Nutrition 4, no. 2b (April 2001): 459–74. http://dx.doi.org/10.1079/phn2001134.
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AbstractFor decades it has been postulated that the main environmental factor for coronary heart disease (CHD) was the intake of saturated fatty acids (SFA). Nevertheless, confirmation of the role of SFA in CHD through intervention trials has been disappointing. It was only when the diet was enriched in n-3 fatty acids that CHD was significantly prevented, especially cardiac death.In addition to n-3 fatty acids, many other foodstuffs or nutrients such as fibers, antioxidants, folic acid, calcium and even alcohol contribute to prevent CHD. Thus the relationship between diet and CHD morbidity and mortality appears to be much more complex than formerly suspected considering as key factors only SFA, linoleic acid, cholesterol and atherosclerosis. Some of the mechanisms are briefly described, but many additional nutrients (or non nutrients) may also play an important role in the pathogenesis of CHD.Finally, as a result of the most recent epidemiologic studies the ideal diet may comprise: 8% energy from SFA, 5% from polyunsaturated fatty acids with a ratio 5/1 of linoleic/alpha-linolenic acid+longer chains n-3, oleic acid as desired, large intake of cereals, vegetables, legumes and fruits, fish twice a week, cheese and yogurt as dairy products, rapeseed and olive oils as edible fat. Without side effects, such a diet can be highly palatable, easily enjoyed by many populations and may prevent effectively and rapidly (within a few weeks or months) CHD.
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Renaud, Serge, and Dominique Lanzmann-Petithory. "Dietary fats and coronary heart disease pathogenesis." Current Atherosclerosis Reports 4, no. 6 (November 2002): 419–24. http://dx.doi.org/10.1007/s11883-002-0045-z.
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OLIVEIRA, José Alberto Mello de. "HEART ANEURYSM IN CHAGAS' DISEASE." Revista do Instituto de Medicina Tropical de São Paulo 40, no. 5 (September 1998): 301–7. http://dx.doi.org/10.1590/s0036-46651998000500007.
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This prospective study on 41 autopsy collected human hearts concerns the "apical" lesion in Chagas' disease. Previous report did not show a correlation between lesion frequency and heart weight then discarding a vascular factor in its pathogenesis. The present paper involves other variables besides the heart weight to evaluate the relative coronary insufficiency. Distinct colored gel (green and red) injected through the capillary beds of both coronary arteries defined the extent of both vessels before separating the atria and removing the sub-epicardium fat. The Right Ventricle (RV) and Left Ventricle (LV) free walls furnished the RV/LV mass ratio. The myocardium mass colored green (right coronary artery - RC) and the whole Ventricular Weight (VW) determined the RC/VW mass ratio. The heart weight plus these mass ratios, graded and added, composed a score inversely proportional to the myocardium irrigation condition. It intended to be a more sensitive morphologic evaluation of the relative ischaemia to correlate to the apical lesion. This study showed a right deviation for the relative accumulated frequency of lesions plotted as a score function and a significant difference for higher scores in hearts with aneurysm. It suggests a ischaemic factor intervening in the apical lesion pathogenesis in Chagas' cardiopathy.
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OLIVER, M. "New horizons in the pathogenesis of coronary heart disease." European Journal of Clinical Investigation 22, no. 12 (December 1992): 761–63. http://dx.doi.org/10.1111/j.1365-2362.1992.tb01442.x.
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Kirichenko, A. A. "Coronary heart disease and inflammation." Clinical Medicine (Russian Journal) 96, no. 8 (December 20, 2018): 688–95. http://dx.doi.org/10.18821/0023-2149-2018-96-8-688-695.
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The increased content of inflammation markers in the blood is a significant prognostic sign of coronary events in persons with stable or asymptomatic course of coronary heart disease (CHD) and suggests that the inflammation underlying the destabilization of CHD has an independent character and is largely independent of the severity of stenotic lesions of coronary vessels. Activation of the local inflammatory process in the atherosclerotic plaque leads to the destruction of the fibrous capsule in combination with an increase in the activity of cellular and plasma factors of the coagulation system and inhibition of the fibrinolytic system. Cytomegalovirus, Chlamydia pneumoniae, pathogens of periodontal disease are nominated for the role of inducers of inflammatory reactions. The synergistic effect of several pathogens is reflected in the concept of burden of infection (“infectious burden”). Immuno-inflammatory rheumatic diseases are characterized by a high risk of cardiovascular complications. An important place in their prevention is an effective anti-inflammatory therapy: methotrexate, suppressing the formation of interleukin 1ft and tumor necrosis factor a, allows not only to modify the course of the disease, but also to reduce the risk of cardiovascular accidents. Chronic inflammation, as a key element of atherosclerosis pathogenesis, can be caused not only by infectious and immune factors, but also by metabolic factors. The activation of inflammasomes induced by cholesterol crystals in macrophages is an important link between cholesterol metabolism and inflammation in atherosclerotic plaques. Confirmation of the important pathogenetic role of inflammation is to reduce the risk of cardiovascular complications (CVD) on the background of anti-inflammatory therapy. In statin therapy, the decrease in The level of C-reactive protein (CRP) was significantly correlated with the suppression of atherosclerosis progression and a decrease in the risk of SSR, regardless of the degree of lowering the low-density lipoprotein cholesterol level. Taking colchicine in a low dose in patients with stable coronary artery disease, who received standard therapy, reduced the risk of acute coronary syndrome and sudden cardiac death. Secondary prevention of cardiovascular complications by human monoclonal antibodies to interleukin 1ft (kanakinumab) led to a decrease in the risk of SSR regardless of sex, Smoking, and lipid levels.
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Tennant, Christopher C., and Pauline M. Langeluddecke. "Psychological correlates of coronary heart disease." Psychological Medicine 15, no. 3 (August 1985): 581–88. http://dx.doi.org/10.1017/s0033291700031433.
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SynopsisThe Type A behaviour pattern and other measures of psychological traits and symptom states were assessed in 92 subjects (predominantly male) presenting for coronary angiography. These measures were correlated with three angiographic indices of coronary heart disease (CHD) severity and two clinical indices (angina and the duration of CHD). The only psychological measures associated with atherosclerosis (assessed by angiography) were indices of personality: Type A (the Jenkins Activity Survey), trait tension, trait anxiety and suppression of anger. It was concluded that these traits may have some role in the pathogenesis of coronary atherosclerosis. None of the measures of psychological symptoms showed a significant association with angiography indices. However, depressive symptoms and expressed hostility were associated with the severity of angina and duration of heart disease. It was concluded that these affects are the consequences of the physical disability of CHD.
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Sönmez, Hüseyin, Selma Süer, Turgut Ulutin, Emine Kökoglu, and Nergiz Uçişik. "The Relationship of Various Factors in the Pathogenesis of Atherosclerosis." Clinical and Applied Thrombosis/Hemostasis 4, no. 2 (April 1998): 105–10. http://dx.doi.org/10.1177/107602969800400205.
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In this study we investigated the levels of lipid parameters, fibronectin, tissue-type plasminogen activator and plasminogen activator inhibitor (t-PA-PAI-1) complex and si alidase in patients with coronary heart disease and a control group. Total cholesterol, triglyceride, low-density lipoprotein (LDL), and very-low-density lipoprotein (VLDL) cholesterol and lipoprotein Lp(a), levels in patients with coronary heart disease were found to be significantly higher than in the control group (p < .001). High-density lipoprotein (HDL) cholesterol levels in patient group were significantly lower than control group (p < .001). Plasma fibronectin and t-PA-PAI-1 complex levels in patients with coronary heart disease were found to be significantly higher than control group (p < .05 and p < .001, respectively). In addition, we found that serum sialidase levels in patients with coronary heart disease were significantly higher than in the control group (p < .001). The electrophoretic mobility of lipoproteins from patients with coronary heart dis ease was found to be greater than those from the control group. As a result Lp(a) may play an important role in the pathogen esis of atherosclerosis by causing foam cell formation because of interacting with LDL or fibronectin and by interfering with the fibrinolytic system because of binding to plasminogen re ceptors. In addition, modifications of Lp(a) (including desi alylation) may effect these events. Key words: Coronary heart disease—tPA-PAI-1 complex-Fibronectin-sialidase-Lipid parameters.
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Chazova, T. E., and G. A. Melnichenko. "Diabetes mellitus and coronary heart disease." Problems of Endocrinology 44, no. 1 (February 1, 1998): 54. http://dx.doi.org/10.14341/probl199844154-54.
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Atherosclerosis and related disorders of carbohydrate metabolism go beyond narrow cardiological problems and, in one way or another, are the subject of close attention of doctors of various specialties, including endocrinologists. In everyday practice, most endocrinologists leave the solution of issues related to hyperlipidemia “for later”, because, first, for many decades, full compensation for diabetes and hypothyroidism - conditions in which secondary hyperlipidemia is most common - was difficult ; secondly, there were no effective and safe means for treating hyperlipidemia, which made generations of doctors skeptical about the possibility of real correction of lipid metabolism disorders. Improving the methods for compensating for diabetes mellitus and the possibilities for treating hypothyroidism have brought clinicians to the problem of the need for additional therapy with lipid-lowering drugs, so the pathogenesis and treatment of hyperlipidemia are of great interest to them.
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Marin-Neto, José Antonio, Marcus V. Simões, Elias M. Ayres-Neto, J. Luiz Attab-Santos, L. Gallo Jr., Dalmo Souza Amorim, and Benedito Carlos Maciel. "Studies of the coronary circulation in Chagas' heart disease." Sao Paulo Medical Journal 113, no. 2 (April 1995): 826–34. http://dx.doi.org/10.1590/s1516-31801995000200014.
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Pathogenesis of chronic Chagas' heart disease may include various disturbances in the coronary circulation, that could be responsible for the myocardial lesions seen in human hearts and in experimental models of the disease. In this paper we critically reviewed the anatomical and functional abnormalities described in chronic chagasic patients, pertaining to the so-called vascular pathogenetic theory of Chagas' disease. The epicardial coronary arteries are usually free of significant obstructive disease in nonselected groups of chagasic patients examined at autopsy or by coronary angiography. However, chagasic patients who were studied after an episode of acute myocardial infarction, show the same patterns of atherosclerotic coronary artery disease seen in the general nonchagasic population. Studies of chagasic patients with angiographically normal coronary arteries, by several scintigraphy methods, revealed myocardial perfusion abnormalities which may be caused by the microcirculatory derangements described in animals experimentally infected with the T. cruzi. Since hypoperfusion has been detected in regions with normal or mildly impaired wall motion, it is likely that the microvascular disturbances precede and may be a causative mechanism for the subsequent myocardial damage. We speculate that hibernating ventricular areas may occur in chagasic patients, on the basis of the evidence gathered from these studies. Recent investigations of chronic patients with Chagas' disease and chest pain showed attenuation of the vasomotor responses to physiological and pharmacological stimuli, in the epicardial coronary arteries.
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Carpio, Carlos, Rodolfo Álvarez-Sala, and Francisco García-Río. "Epidemiological and Pathogenic Relationship between Sleep Apnea and Ischemic Heart Disease." Pulmonary Medicine 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/405827.
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Obstructive sleep apnea is recognized as having high prevalence and causing remarkable cardiovascular risk. Coronary artery disease has been associated with obstructive sleep apnea in many reports. The pathophysiology of coronary artery disease in obstructive sleep apnea patients probably includes the activation of multiple mechanisms, as the sympathetic activity, endothelial dysfunction, atherosclerosis, and systemic hypertension. Moreover, chronic intermittent hypoxia and oxidative stress have an important role in the pathogenesis of coronary disease and are also fundamental to the development of atherosclerosis and other comorbidities present in coronary artery diseases such as lipid metabolic disorders. Interestingly, the prognosis of patients with coronary artery disease has been associated with obstructive sleep apnea and the severity of sleep disordered breathing may have a direct relationship with the morbidity and mortality of patients with coronary diseases. Nevertheless, treatment with CPAP may have important effects, and recent reports have described the benefits of obstructive sleep apnea treatment on the recurrence of acute heart ischaemic events in patients with coronary artery disease.
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Yusupova, A. O., M. V. Kozhevnikova, Yu N. Belenkov, and E. V. Privalova. "Co-morbid pathology: coronary heart disease and gastroesophageal reflux disease." Clinical Medicine (Russian Journal) 95, no. 4 (June 6, 2017): 293–301. http://dx.doi.org/10.18821/0023-2149-2017-95-4-291-301.
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The article presents data of domestic and foreign authors illustrating current views of mechanisms underlying development, pathogenesis, and difficulties of differential diagnostics of coronary heart disease (CHD) concurrent with gastroesophageal reflux disease (GERD). High prevalence of both conditions and their common risk factors are responsible for frequent occurrence of co-morbidity. The available data suggest positive effect of treatment with proton pump inhibitors (decreased frequency of myocardial ischemia and heart arrhythmia). Co-morbidity of CHD and GERD requires long-term treatment and the use of safe medications having no adverse effects on the course of CHD.
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Lin, Jie, Jun Jiang, Ruifang Zhou, Xiaojie Li, and Jun Ye. "MicroRNA-451b participates in coronary heart disease by targeting VEGFA." Open Medicine 15, no. 1 (December 26, 2019): 1–7. http://dx.doi.org/10.1515/med-2020-0001.
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AbstractCoronary artery disease (CAD) is one of the main causes of hospitalization worldwide and has high morbidity. MicroRNAs (miRNAs) play an important role in the pathogenesis of cardiovascular diseases. miR-451 is a special miRNA that is involved in many cancers’ development. At present, there is no research about miR-451 in coronary heart disease. In this study, we aimed to identify the action mechanism of miR-451 in coronary heart disease and human umbilical vein endothelial cells (HUVECs). In this study, we found that miR-451 is up-regulated in the peripheral blood of patients with coronary heart disease. Moreover, TargetScan and dual-luciferase reporter gene assay results showed that VEGFA is a direct target gene of miR-451. C (CCK-8) and flow cytometry assay results showed that miR-451 mimic significantly inhibits cell proliferation and promotes apoptosis in HUVECs. Moreover, we found that the role of miR-451 in HUVECs is associated with the PI3K-Akt-mTOR pathway. Taken together, the data indicates that miR-451 might be a novel bio-marker for coronary heart disease.
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Liesmaa, Inka, Antti Kuoppala, Naotaka Shiota, Jorma O. Kokkonen, Karam Kostner, Mikko Mäyränpää, Petri T. Kovanen, and Ken A. Lindstedt. "Increased expression of bradykinin type-1 receptors in endothelium of intramyocardial coronary vessels in human failing hearts." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 5 (May 2005): H2317—H2322. http://dx.doi.org/10.1152/ajpheart.00815.2004.
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In experimental animals, bradykinin type-1 receptors (BK-1Rs) are induced during inflammation and ischemia, and, by exerting either cardioprotective or cardiotoxic effects, they may contribute to the pathogenesis of heart failure. Nothing is known about the expression of BK-1Rs in human heart failure. Human heart tissue was obtained from excised hearts of patients undergoing cardiac transplantation ( n = 13), due to idiopathic dilated cardiomyopathy (IDC; n = 7) or to coronary heart disease (CHD; n = 6), and from normal hearts ( n = 6). The expression of BK-1Rs was analyzed by means of competitive RT-PCR, Western blot analysis, and immunohistochemistry. Expression of BK-1R mRNA was increased in both IDC (2.8-fold) and CHD (2.1-fold) hearts compared with normal hearts. The observed changes were verified at the protein level. Expression of BK-1Rs in failing hearts localized to the endothelium of intramyocardial coronary vessels and correlated with an increased expression of TNF-α in the vessel wall. Treatment of human coronary artery endothelial cells with TNF-α increases their BK-1R expression. These novel results show that BK-1Rs are induced in the endothelium of intramyocardial coronary vessels in failing human hearts and so may participate in the pathogenesis of heart failure.
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Strilchuk, L. M., O. O. Zimba, and I. B. Zhakun. "DECREASE IN SERUM BILIRUBIN AS AN UNFAVORABLE MARKER OF CARDIOVASCULAR DISORDERS." Eastern Ukrainian Medical Journal 8, no. 3 (2020): 268–75. http://dx.doi.org/10.21272/eumj.2020;8(3):268-275.
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Serum bilirubin, the end product of heme metabolism, is a routine biochemical parameter. Bilirubin is not a liver function parameter exclusively: its concentration correlates with ischemic heart disease (IHD) risk, estimated glomerular filtration rate, retinopathy or neuropathy in diabetes mellitus, atherosclerosis etc. The aim of this paper was to estimate the clinical value of bilirubin analysis according to literature data and own clinical observations in patients with IHD and acute and chronic rheumatologic diseases. Materials and methods. We conducted a literature overview in Pubmed database and domestic sources and also analyzed the standard examinaions of 515 patients: 353 patients with coronary heart disease (acute forms, coronary bypass grafting – 98; acute myocardial infarction, pharmacotherapy – 75; unstable angina pectoris – 101; stable angina pectoris – 79) and 162 rheumatologic patients (haemorrhagic vasculitis – 71; rheumatic fever – 57; chronic rheumatic heart disease with valvular defects – 34). Control group consisted of 22 patients with gastroduodenal zone diseases without helicobacter (esophagitis, gastritis, peptic ulcer). Results and discussion. It was revealed that in case of diseases with oxidative stress in their pathogenesis (acute forms of coronary heart disease, haemorrhagic vasculitis, rheumatic fever) bilirubin level was lower than in case of non-oxidative disorders (non-infectious esophagitis, gastritis, ulcer). Increase of inflammation potency was accompanied by bilirubin decrease. Correlation analysis showed that both bilirubin increase and decrease were unfavourable. Conclusions. Bilirubin concentration correlated with parameters of cytolysis, intoxication, anemia, inflammation, carbohydrate and lipid metabolism, heart structure. Bilirubin decrease associated with the increase of stenosis of coronary arteries (left, left circumflex and anterior interventricular) in a logarithmic way. Hypobilirubinemia (< 9.6 mkmol/L) significantly more often accompanied diseases with oxidative stress in pathogenesis, acute forms and more active systemic inflammation. Keywords total bilirubin, hypobilirubinemia, coronary heart disease, haemorrhagic vasculitis, rheumatic fever, chronic rheumatic heart disease.
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Zhao, Long, Ying Li, Di Wu, Tao Ma, Shu-Yue Xia, and Zhi Liu. "Cx37C1019T Polymorphism May Contribute to the Pathogenesis of Coronary Heart Disease." Genetic Testing and Molecular Biomarkers 18, no. 7 (July 2014): 497–504. http://dx.doi.org/10.1089/gtmb.2014.0034.
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Polyakova, E. A. "The role of soluble leptin receptor in the pathogenesis of coronary heart disease." Regional blood circulation and microcirculation 20, no. 3 (September 27, 2021): 34–45. http://dx.doi.org/10.24884/1682-6655-2021-20-3-34-45.
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Introduction. The participation of soluble leptin receptor (SLR) in the formation of hyperleptinemia and leptin resistance in patients with coronary artery disease (CAD) in combination with obesity is discussed. Aim. Study of the role of SLR in the pathogenesis of ischemic heart disease. Materials and methods. A cohort study of 744 patients was performed: 465 patients with CAD (56 years old, Q1=44; Q3=62), 270 patients without CAD (52 years old, Q1=44; Q3=56). Methods: EchoCG, heart computed tomography, coronary angiography. In the blood serum, the lipids, glucose, creatinine, uric acid, and c-reactive protein were assessed using a highly sensitive method (HF-CRP). Concentrations of SLR, leptin (LN), adiponectin (total and high molecular weight), fatty acid binding protein-4 (FABP-4) tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), serum insulin were determined by enzyme immunoassay. Results. The level of SLR in blood serum in men and women with CAD is lower than in men without CAD (p <0.001). In CAD patients, obesity was associated with a low SLR level in the blood serum and a high free LN index. At a serum SLR concentration of <7.5ng/ml in men with CAD, the incidence of obesity was higher simultaneously with signs of visceral obesity of the heart, the presence of atherosclerotic plaques in the common carotid arteries, high glycaemic levels, insulin, IL-6, and LN in serum, serum LN/adiponectin ratio and a high HOMA-IR index. Diabetes mellitus, visceral obesity, high levels of hs-CRP, TNF-α, FABP-4, serum insulin, and HOMA-IR index were more often detected in women with coronary artery disease with SLR <10.2 ng/ml. In men and women with CAD, there were no differences in SLR concentration depending on the extent of coronary atherosclerosis. Conclusion. An increase in the free LN index indicates the disruption of connections in the leptin-receptor system and reflects the mechanisms of compensation for overcoming the resistance of peripheral tissues to leptin, which is confirmed by a noticeable negative relationship between the levels of SLR and leptin in the serum of men with coronary artery disease. A low concentration of SLR in patients with CAD is associated with obesity, pro-atherogenic and pro-inflammatory markers of cardiovascular diseases.
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Perepech, N. B. "Acute coronary syndrome: pathogenesis, diagnosis, treatment, rehabilitation (Lecture 3)." CardioSomatics 7, no. 3-4 (December 15, 2016): 111–21. http://dx.doi.org/10.26442/cs45271.
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The lecture discusses methods of ensuring hemodynamic and neurohormonal unloading of the heart, current recommendations for the prevention of exacerbations of coronary heart disease in patients with myocardial infarction or unstable angina episode. Narrow organizational, diagnostic and therapeutic tasks that need to be addressed at the stage of hospital treatment of patients with acute coronary syndrome. Substantiates the principle of modular construction of individual rehabilitation programs, discussed methodological procedures of obtaining and analyzing the information necessary for the individualization of rehabilitation programs, as well as methods of physical, mental rehabilitation and disability assessment of patients after myocardial infarction.
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Błyszczuk, Przemysław, and Zoltan Szekanecz. "Pathogenesis of ischaemic and non-ischaemic heart diseases in rheumatoid arthritis." RMD Open 6, no. 1 (January 2020): e001032. http://dx.doi.org/10.1136/rmdopen-2019-001032.
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Rheumatoid arthritis (RA) is characterised by a chronic inflammatory condition of the joints, but the comorbidities of RA predominantly contribute to the reduced lifespan associated with this disease. Clinical data indicate that cardiovascular disease is the major comorbidity associated with mortality in RA. In this review, we aimed to describe the pathogenesis of heart failure in RA. First, we emphasised the fundamental differences between ischaemic and non-ischaemic heart diseases and referred to their relevance in excessive cardiovascular-dependent mortality in RA. Second, we highlighted aspects of asymptomatic changes in cardiac tissue and in coronary blood vessels that are commonly found in patients with diagnosed RA. Third, we focused on high-grade systemic inflammation as a key trigger of ischaemic and non-ischaemic heart diseases in RA, and described the implication of conventional and biologic antirheumatic medications on the development and progression of heart disease. In particular, we discussed the roles of tumour necrosis factor-alpha (TNF-α) and anti-TNF-α therapies on the development and progression of ischaemic and non-ischaemic heart diseases in RA.
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Neznanov, N. G., S. N. Kozlova, G. E. Mazo, N. G. Shlyakhto, and B. I. Smirnov. "Comorbidity of depressive disorders and coronary heart disease: general aspects of pathogenesis." Zhurnal nevrologii i psikhiatrii im. S.S. Korsakova 115, no. 5 (2015): 20. http://dx.doi.org/10.17116/jnevro20151155120-26.
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Todd Miller, M., Carl J. Lavie, and Christopher J. White. "Impact of Obesity on the Pathogenesis and Prognosis of Coronary Heart Disease." Journal of the CardioMetabolic Syndrome 3, no. 3 (June 2008): 162–67. http://dx.doi.org/10.1111/j.1559-4572.2008.00004.x.
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Olson, Kari, Fawziah Marra, and Rubina Sunderji. "The Role of Chlamydia Pneumoniae in the Pathogenesis of Coronary Heart Disease." Journal of Pharmacy Technology 15, no. 5 (September 1999): 157–61. http://dx.doi.org/10.1177/875512259901500503.
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Kolesnikov, A. N., A. V. Dubovaya, and Yu V. Udovitchenko. "PARTICIPATION OF VITAMIN D IN PATHOGENESIS OF CARDIOVASCULAR DISEASES." Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) 63, no. 5 (November 20, 2018): 43–50. http://dx.doi.org/10.21508/1027-4065-2018-63-5-43-50.
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The article presents data of experimental and clinical studies devoted to the influence of vitamin D on the origin and progression of the cardiovascular diseases: arterial hypertension, atherosclerosis, coronary heart disease, cardiac rhythm disturbances. The results of the studies indicate that a pronounced deficiency of vitamin D is highly correlated with sudden cardiac death, cardiovascular catastrophes, and overall mortality. The decrease in vitamin D is followed by an increase in total cholesterol, low-density lipoproteins and triglycerides, an increase in the heart rate and the level of systolic blood pressure. The Meta-analyzes of randomized controlled trials demonstrated that the addition of vitamin D to treatment and rehabilitation measures of the patients with cardiovascular disease helps to reduce overall mortality.
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Sofogianni, Areti, Stelina Alkagiet, and Konstantinos Tziomalos. "Lipoprotein-associated Phospholipase A2 and Coronary Heart Disease." Current Pharmaceutical Design 24, no. 3 (April 13, 2018): 291–96. http://dx.doi.org/10.2174/1381612824666180111110550.
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In the last decades, the role of inflammation in the pathogenesis of atherosclerosis has been the topic of intense research. Several markers of inflammation have shown predictive value for first and recurrent coronary events in patients without and with established Coronary Heart Disease (CHD). Among these markers, lipoprotein- associated phospholipase A2 (Lp-PLA2) has recently received considerable attention. In the present review, the potential role of Lp-PLA2 as a marker of CHD risk and as a therapeutic target is discussed. Elevated Lp- PLA2 mass and activity appears to be associated with increased risk for CHD, both in the general population and in patients with established CHD. However, it is unclear whether the measurement of Lp-PLA2 improves risk discrimination when incorporated in models that include traditional cardiovascular risk factors. Moreover, the lack of effect on CHD events of darapladib, a potent, selective Lp-PLA2 inhibitor, in two large, randomized, placebo-controlled trials and the mostly negative findings of genetic association studies suggest that Lp-PLA2 is unlikely to represent a causal factor in atherogenesis. Therefore, it is doubtful whether Lp-PLA2 will constitute a therapeutic target for the prevention of CHD.
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Shmatova, E. N., and Yu I. Grinshtein. "Microvascular angina: pathogenesis, clinical picture, diagnosis and therapy tactics." Russian Medical Inquiry 4, no. 7 (2020): 425–30. http://dx.doi.org/10.32364/2587-6821-2020-4-7-425-430.
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The literature review presents current data on some mechanisms of development, clinical picture, diagnosis, and therapy tactics of microvascular angina (MA). The important role of microcirculatory pathology in the genesis of coronary heart disease is emphasized. Endothelial dysfunction and angiospasm have been shown to be the basis of MA. The article presents MA detection, including the presence of myocardial ischemia in the absence of obstructive coronary artery disease (coronary artery disease <50% or fractional flow reserve >0.80). It was noted that Holter monitoring was not informative for reliable diagnosis of myocardial ischemia, since the results of the study did not exclude or confirm the presence of coronary heart disease, including MA. Stress echocardiography and positron emission tomography were highly informative in the diagnosis of myocardial ischemia caused by microvascular pathology. The article also considers drug therapy tactics with the use of beta-adrenergic blocking agents and calcium channel blockers for patients with MA and the low efficacy of nitrates. The role of second-line drugs such as Nicorandil, Ranolazine, and Trimetazidine is discussed. The important role of statins and angiotensin-converting enzyme inhibitors, which have proven to be effective in the treatment of endothelial dysfunction, is emphasized. Disaggregants, like statins, are an important therapy component of MA.KEYWORDS: microvascular angina, endovascular dysfunction, diagnostics, therapy tactics.FOR CITATION: Shmatova E.N., Grinshtein Yu.I. Microvascular angina: pathogenesis, clinical picture, diagnosis and therapy tactics. Russian Medical Inquiry. 2020;4(7):425–430. DOI: 10.32364/2587-6821-2020-4-7-425-430.
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Podolskaya, A. A., A. S. Galyavich, E. V. Maikova, O. A. Kravtsova, and F. K. Alimova. "The role of antioxidant system genes in the formation of coronary heart disease clinical phenotypes." Kazan medical journal 94, no. 2 (April 15, 2013): 228–34. http://dx.doi.org/10.17816/kmj1594.
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Genetic predisposition alongside with environmental factors play a major role in the pathogenesis of coronary heart disease, causing the deregulation of various biochemical processes leading to the disease onset. Antioxidant system deregulation, marked mainly by lipid peroxidation products and a number of enzymes, is known to be one of the risk factors for coronary heart disease. A genetic defect might lead to a change in enzyme activity and inhibition of antioxidant protection. However, the pathogenic factors and antioxidant system deregulation mechanisms in different clinical courses of coronary heart disease are not studied enough as phenotypic expression of genetic polymorphism is largely dependent on the gene pool and the living conditions of a particular population, explaining the controversial data on the association of polymorphisms candidate genes with the risk of coronary heart disease. Currently, the role of genes encoding antioxidant system enzymes in predisposition to coronary heart disease development is not sufficiently studied, and research results are contradictory. The review summarizes the current data on the antioxidant system genes (superoxide dismutase enzymes, glutathione peroxidase and catalase) genetic polymorphisms association with the risk of coronary heart disease (as an acute myocardial infarction, angina рectoris).
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Oslopov, V. N., Y. V. Oslopova, and D. V. Borisov. "Cardiac syndrome X. the possible role of Na+-Li+-countertransport activity and other pathophysiological mechanisms in pathogenesis." Kazan medical journal 94, no. 3 (June 15, 2013): 355–61. http://dx.doi.org/10.17816/kmj2184.
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There are numerous pathophysiological mechanisms unequally responsible for the cardiac syndrome X development. The most important is endothelium and smooth muscle cells dysfunction that can intensify vasoconstriction and depress both endothelium-dependant and endothelium-independent vasodilatation, finally leading to coronary micro vascular dysfunction as the basis of the cardiac syndrome X pathogenesis. Together with other possible mechanisms of pathogenesis, studying the importance of increased cell membrane Na+-Li+-countertransport activity seems promising. If was found that a significant number of patients with cardiac syndrome X have increased Na+-Li+-countertransport activity, which is an in vitro marker of Na+-H+-antiporter. Therefore, it is important to measure Na+-Li+-countertransport speed in patients with coronary heart disease, because its high levels increases the chance for cardiac syndrome X, which is a coronary heart disease with no anatomic signs of coronary arteries involvement.
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S.M. Koval, I.O. Snigurska, V.V. Bozhko, and D.K. Miloslavsky. "The problem of hypertensive heart disease regression in patients with arterial hypertension." HYPERTENSION 13, no. 6 (November 1, 2020): 28–34. http://dx.doi.org/10.22141/2224-1485.13.6.2020.223078.
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The review presents data from the domestic and foreign literature on the prevalence, pathogenesis, modern methods of verification of hypertensive heart disease (left ventricular hypertrophy) in patients with arterial hypertension and conditions associated with it: coronary heart disease, atrial fibrillation, metabolic syndrome, diabetes mellitus. Methods of non-drug and drug correction of hypertensive heart disease, as well as factors that prevent the reverse regression of hypertrophied myocardium are considered.
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Mazurov, V. I., S. V. Stolov, I. B. Belyaeva, and E. A. Trofimov. "THE PARTICIPATION OF IMMUNE AND INFLAMMATORY MECHANISMSIN THE PATHOGENESIS OF CORONARY ATHEROSCLEROSIS." HERALD of North-Western State Medical University named after I.I. Mechnikov 7, no. 4 (December 15, 2015): 13–23. http://dx.doi.org/10.17816/mechnikov20157413-23.
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It was revealed that in development of a coronary atherosclerosis, participate the immune-mediated mechanisms. In blood of patients with coronary atherosclerosis the maintenance of the basic classes cytokines (IL-1 β, IL-2, IL-6, IL-8, TNF-a) were increased. Development of acute coronary insufficiency is accompanied by additional increase of levels of the data cytokines. The accessory of the cytokine activity to a coronary atherosclerosis was confirmed at studying the maintenance mRNA cytokines in a vascular wall. Thus in a zone atheromatous (aorta) it was synthesized mainly mRNA IL-2, while in a zone lipomatosis (a beam radial artery) it is formed nonspecific immune reaction with development of the mRNA IL-1 and IL-6. For patients with rheumatoid arthritis typically more active defeat of a coronary arteries, in comparison with healthy persons. Chronic immune-mediated process in frameworks of the autoimmune pathology can serve a trigger for accelerated development ischemic heart disease. The General immune-inflammatory mechanisms which participate in pathogenesis of the ischemic heart disease and rheumatoid arthritis, allow to spend the certain parallels between atherosclerotic process and autoimmune pathology.
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Bugger, Heiko, and E. Dale Abel. "Molecular mechanisms for myocardial mitochondrial dysfunction in the metabolic syndrome." Clinical Science 114, no. 3 (January 8, 2008): 195–210. http://dx.doi.org/10.1042/cs20070166.
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The metabolic syndrome represents a cluster of abnormalities, including obesity, insulin resistance, dyslipidaemia and Type 2 diabetes, that increases the risk of developing cardiovascular diseases, such as coronary artery disease and heart failure. The heart failure risk is increased even after adjusting for coronary artery disease and hypertension, and evidence is emerging that changes in cardiac energy metabolism might contribute to the development of contractile dysfunction. Recent findings suggest that myocardial mitochondrial dysfunction may play an important role in the pathogenesis of cardiac contractile dysfunction in obesity, insulin resistance and Type 2 diabetes. This review will discuss potential molecular mechanisms for these mitochondrial abnormalities.
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Gautam, Mani Prasad, Samir Gautam, Usha Ghimire, Sogunuru Guruprasad, Rabin Bhattacharya, and Gangapatnam Subramanyam. "Endothelial dysfunction and the role of hypertension in Nepalese subjects with major coronary risk factors." Nepalese Heart Journal 13, no. 1 (February 12, 2016): 13–18. http://dx.doi.org/10.3126/njh.v13i1.14539.
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Background and Aims: Hypertension is one of the major coronary heart disease risk factors. Endothelial dysfunction is thought to be the preclinical vascular changes in the pathogenesis of atherosclerosis and it its major manifestation; coronary heart disease. This study was designed to assess the endothelial function in subjects with major coronary risk factors including hypertension.Methods: The study was conducted in a tertiary referral centre in Central Nepal. A cross-sectional study was conducted on the cohort of 100 subjects with at least one out of six major coronary heart disease risk factors. JNC 7 criteria were used to define hypertension. Brachial artery flow-mediated dilation was measured using high-resolution ultrasound. Endothelial dysfunction was defined as flow-mediated dilation value <9.99%. The association between endothelial dysfunction and hypertension was assessed by univariate and multivariate analysis.Results: Out of 100 subjects with coronary risk factors (mean age 46.75±9.95 years, mean number of risk factors 2.81± 1.17), 65% subjects were hypertensive and 35% were non-hypertensive. Hypertension as a risk factor was evident in 80.39% and 48.98% subjects with abnormal and normal endothelial response respectively (p = 0.001). In addition, 63.08% and 28.57% subjects with and without hypertension had endothelial dysfunction respectively (p=0.01). Hypertension was the only coronary risk factor associated with endothelial dysfunction in a multivariate model (p=0.04).Conclusion: Hypertension was strongly associated with endothelial dysfunction and it could be the best predictor of endothelial dysfunction and subsequent coronary heart disease in coronary heart diseases risk factor cohorts.Nepalese Heart Journal 2016; 13(1): 13-18
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Skotnikov, A. S., E. A. Algiyan, and Zh M. Sizova. "A patient with atrial fibrillation and comorbidities in clinical practice." Russian Journal of Cardiology 25, no. 11 (December 5, 2020): 4178. http://dx.doi.org/10.15829/29/1560-4071-2020-4178.
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This article focuses on the etiology and pathogenesis of nonvalvular atrial fibrillation in patients with comorbidities such as coronary artery disease, heart failure, type 2 diabetes, and chronic kidney disease. The authors discuss the interconnection of atrial fibrillation and these diseases, and also note the need for protection of such patients (prevention of cardioembolic stroke and other systemic embolism, reduction of coronary risk, improvement of prognosis, slowing the progression of renal dysfunction, increasing medical adherence, etc.) by adequate antithrombotic therapy that does not lose effectiveness and/or safety in presence of multiple diseases and polypharmacy.
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Popovic-Pejicic, Snjezana, Ljiljana Todorovic-Djilas, and Pavle Pantelinac. "The role of autonomic cardiovascular neuropathy in pathogenesis of ischemic heart disease in patients with diabetes mellitus." Medical review 59, no. 3-4 (2006): 118–23. http://dx.doi.org/10.2298/mpns0604118p.
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Introduction. Diabetes is strongly associated with macrovascular complications, among which ischemic heart disease is the major cause of mortality. Autonomic neuropathy increases the risk of complications, which calls for an early diagnosis. The aim of this study was to determine both presence and extent of cardiac autonomic neuropathy, in regard to the type of diabetes mellitus, as well as its correlation with coronary disease and major cardiovascular risk factors. Material and methods. We have examined 90 subjects, classified into three groups, with 30 patients each: those with type 1 diabetes, type 2 diabetes and control group of healthy subjects. All patients underwent cardiovascular tests (Valsalva maneuver, deep breathing test, response to standing, blood pressure response to standing sustained, handgrip test), electrocardiogram, treadmill exercise test and filled out a questionnaire referring to major cardiovascular risk factors: smoking, obesity, hypertension, and dyslipidemia. Results. Our results showed that cardiovascular autonomic neuropathy was more frequent in type 2 diabetes, manifesting as autonomic neuropathy. In patients with autonomic neuropathy, regardless of the type of diabetes, the treadmill test was positive, i.e. strongly correlating with coronary disease. In regard to coronary disease risk factors, the most frequent correlation was found for obesity and hypertension. Discussion Cardiovascular autonomic neuropathy is considered to be the principal cause of arteriosclerosis and coronary disease. Our results showed that the occurrence of cardiovascular autonomic neuropathy increases the risk of coronary disease due to dysfunction of autonomic nervous system. Conclusions. Cardiovascular autonomic neuropathy is a common complication of diabetes that significantly correlates with coronary disease. Early diagnosis of cardiovascular autonomic neuropathy points to increased cardiovascular risk, providing a basis for preventive and therapeutic measures. .
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Neurauter, Gabriele, Barbara Wirleitner, Katharina Schroecksnadel, Harald Schennach, and Dietmar Fuchs. "Wine and Grape Juice Modulate Interferon-y-induced Neopterin Production and Tryptophan Degradation in Human PBMC." Pteridines 15, no. 1 (February 2004): 1–9. http://dx.doi.org/10.1515/pteridines.2004.15.1.1.
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Abstract Population-based studies suggest moderate and regular consumption of alcoholic beverages and especially of red wine to reduce morbidity and mortality from coronary heart disease. These beverages may interfere with immune activation cascades crucial in the pathogenesis of coronary heart diseases. Neopterin concentrations in human body tluids were found to increase in the course of coronary heart disease indicating the activity of the atherogenetic process. In this study, human peripheral blood mononuclear cells (PBMC) stimulated with mitogens phytohaemagglutinin and concanavalin A were exposed to red and white wines, to ethanol and to grape juice as a non-alcoholic control in vitro. Neopterin production and tryptophan degradation were measured in supcrnalants. Both biochemical effects are induced by Th 1-type cytokine interferon-y and allow monitoring of immune actnation. In stimulated PBMC increased production of neopterin and degradation of tryptophan was observed Red and white wines, as well as grape juice inhibited these stimulation-induced effects, higher concentrations being more cffective. Ethanol had comparably small if any effect, Red and white wines as well as grape juice down regulate cytokine-mediated effects in PBMC. Most likely, antioxidant ingredients of wine and grape juice such as resveratrol are capable of interfering with immunologic pathways which appear to be of relevance, e g.. in the pathogenesis of cardiovascular disease.
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Nonka, T. G., A. N. Repin, and T. N. Sergienko. "The effect of mood disorders on the course of coronary heart disease: a modern model of pathogenesis of depression, pathophysiological and behavioral patterns." CardioSomatics 5, no. 3-4 (December 15, 2014): 5–8. http://dx.doi.org/10.26442/cs45098.
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The prevalence of depressive disorders at the population level is from 2,5 to 10% among patients with coronary heart disease - 20%. The presence of depressive disorders in patients with coronary artery disease leads to hypersympathicotonia decrease vagal activity, endothelial dysfunction and blood coagulation system, weighing down the disease. The most significant theories of pathophysiological mechanism of increased mortality in patients with cardiovascular disease in combination with mood disorders are increased thrombus formation and disturbance of the autonomic regulation of heart rhythm.
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Detweiler, D. K. "Spontaneous and Induced Arterial Disease in the Dog: Pathology and Pathogenesis." Toxicologic Pathology 17, no. 1_part_2 (January 1989): 94–108. http://dx.doi.org/10.1177/019262338901700105.
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The spontaneous arterial diseases of the dog relevant to safety assessment studies of drugs are the extramural coronary arteritis of Hartman, intramural coronary arteriosclerosis (with amyloid deposition) occurring in older dogs with cardiac disability, intramural arteriosclerosis without amyloid deposition in the left ventricle of dogs with congenital subaortic stenosis or in the right ventricle in dogs with severe pulmonic stenosis, and necrotizing polyarteritis (nodosa). Experimentally induced lesions include right atrial necrosis and arteritis produced by minoxidil and theobromine, extramural coronary arteritis produced by positive inotropic/vasodilator drugs, intramural coronary arteriosclerosis associated with decreased peripheral resistance and tachycardia induced by hypotensive drugs (including antihypertensive and positive inotropic/vasodilator agents), and intramural arteriosclerosis associated with rapid ventricular pacing. The pathogenesis of none of these lesions is known. The left ventricular subendocardial and papillary muscle intramural coronary arterial lesions are associated with hyperdynamic activity and, in the case of drugs and subaortic stenosis, the possibility of lowered perfusion pressure and tachycardia. This has led to the supposition that these are ischemic lesions, but the evidence available either does not support or refutes that conclusion since subendocardial coronary flow and perfusion pressure are adequate with pacing tachycardia and in toxicity trials. Necrotizing polyarteritis appears to be an immune mediated disease that may appear in genetically prone beagles when they are placed under the stresses of experimental manipulation and/or a new environment. Since the right atrial minoxidil lesion can also be produced by theobromine in dogs and minoxidil can cause a left atrial lesion in swine, it is neither species nor drug specific. Its cause, however, escapes us. There appears to be little in common between the extramural coronary artery Hartman lesion and that caused by positive inotropic/vasodilator drugs. Left ventricular subendocardial and papillary muscle intramural coronary arterial lesions induced by ventricular pacing at 250 beats/min for 2 months are generally similar to those seen in toxicity trials with peripheral vasodilator drugs that induce tachycardia in electrocardiograms exceeding 200 beats/min, although in acute pacing experiments subendocardial perfusion is adequate at these heart rates. Coronary artery autoregulation may be compromised or so destabilized by the drugs that episodes of underperfusion can account for these lesions. Studies to date have been largely descriptive rather than investigational. In reviewing the literature on drug induced arterial lesions, it is clear that information that might add to our understanding is frequently not available. Some measures not commonly used in toxicity trials that could improve the data base when vascular lesions are induced include: Holter monitoring; adequate blood pressure monitoring; and at necropsy coronary perfusion fixation, quantitation of the amount of intramural coronary disease, and fluorescent or hemotoxylin basic fuchsin picric acid stains to identify recent myocardial necrosis. The feasibility of including echocardiographic estimates of cardiac function during toxicity trials should be examined.
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Belenkov, Yu N., O. A. Tsvetkova, E. V. Privalova, G. V. An, I. S. Ilgisonis, and O. O. Voronkova. "Comorbidity of Chronic Obstructive Pulmonary Disease and Cardiovascular Diseases: Place of Therapy with Modern β-Adrenoblockers." Kardiologiia 59, no. 6 (June 27, 2019): 48–55. http://dx.doi.org/10.18087/cardio.2019.6.n458.
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Chronic obstructive pulmonary disease (COPD) is the fourth largest cause of worldwide mortality. Presence of comorbidities is registered in 96% of COPD patients. The most important of these are cardiovascular diseases (coronary artery disease, arterial hypertension, chronic heart failure), which contribute to COPD patients’ mortality in every third case. COPD and cardiovascular diseases have common risk factors and pathogenesis mechanisms. Cardioselective beta-blockers reduce morbidity risk and frequency of COPD exacerbation, are effective and safe in treatment of COPD patients.
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Czyżewska, Emilia. "Amyloidoses – pathogenesis, classification, diagnosis." Diagnostyka Laboratoryjna 56, no. 4 (July 9, 2021): 1–13. http://dx.doi.org/10.5604/01.3001.0015.0266.
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Amyloidoses – also known as amyloidosis or betafibrillosis – a diverse group of diseases in which amorphous protein with a changed conformational structure is deposited extracellularly, leading to the failure of many organs. The basic classifications of amyloidoses take into account: the type of precursor protein, the division into generalized (systemic) amyloidoses, in which amyloid deposits accumulate in many organs, vessel walls and connective tissue (e.g. AL amyloidosis) and local (localized) amyloidoses – limited to only one organ (e.g. corneal amyloidosis) as well as congenital and acquired diseases. Symptoms of amyloidosis are non-specific and not very characteristic, moreover, their severity depends on the type of disease and organ involvement. The diagnosis of amyloidosis should be considered in patients with heart failure without coronary artery disease, with neuropathy, or proteinuria or hepatomegaly of unclear origin. Diagnosis of amyloidosis is based on the evaluation of tissue biopsy samples and the presence of abnormal proteins, i.e. amyloid, or on the fibrillary evaluation confirmation of the filamentous nature of amyloid deposits using electron microscopy. The next step is differential diagnosis and amyloid differential identification, which is based on immunohistochemical and immunofluorescence studies using labeled antibodies. The "gold standard" used in typing amyloidosis and identifying an amyloidogenic protein is mass spectrometry. Laboratory tests are used to assess organ involvement, which is the basis of the prognostic classification.
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Halliday, Anne. "2. The Horizons in the Pathogenesis of Coronary Heart Disease - London, June 22nd 1992." Nutrition Bulletin 17, no. 3 (September 1992): 229–32. http://dx.doi.org/10.1111/j.1467-3010.1992.tb00148.x.
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Jian-lin, M., L. Jin, and Z. Jin-wen. "The pathogenesis significance of changes of glycoprotein, platelet aggregation test and coronary heart disease." Heart 97, Suppl 3 (October 1, 2011): A192. http://dx.doi.org/10.1136/heartjnl-2011-300867.559.
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TASHKENBAEVA, Eleonora, Dilshod TOGAEV, Farzona KADIROVA, and Shukhrat ZIYADULLAEV. "Modern ideas about the role of hyperuricemia in the pathogenesis of coronary heart disease." Journal of biomedicine and practice 2, no. 1 (February 2, 2018): 47–54. http://dx.doi.org/10.26739/2181-9297-2018-2-8.
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Khukhlina, O. S., O. B. Kuzminska, T. M. Danylyshyn, O. Ye Grinyuk, and V. V. Kropyva. "ROLE OF OXIDATIVE STRESS IN PATHOGENESIS AND PROGRESSION OF NON-ALCOHOLIC STEATOHEPATITIS IN PATIENTS WITH CONCOMITANT CORONARY HEART DISEASE." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 18, no. 4 (December 20, 2018): 76–79. http://dx.doi.org/10.31718/2077-1096.18.4.76.
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The aim of the study: to investigate the state of the system of oxidant-antioxidant homeostasis in patients with NASH and comorbid coronary heart disease. Material and methods. We examined 86 patients with NASH, including 30 patients with NASH and obesity of I-II degree (group 1) and 56 patients with NASH and comorbid coronary heart disease (stable angina pectoris I-II) (group 2). The control group consisted of 30 healthy individuals of the comparable age. The average age of patients was 56,6 ± 5,74 years. Results. An essential pathogenetic factor for the onset and progression of NASH in the presence of comorbid coronary heart disease is the intensification of the processes of free radical lipids oxidation that determines the degree of activity of the pathological process in the liver: the accumulation of intermediate (isolated double bonds, diene conjugates, ketodiens and conjugated trienes) and terminal (malonic aldehyde of plasma and erythrocytes) products of lipid peroxidation against the background of disintegration of the system of antioxidant protection (reduction of the content of glutathione reduced in erythrocytes, compensatory growth of catalase activity). Insufficiency and disintegration in the system of antioxidant protection is one of the main factors resulting in the increase in metabolic intoxication, while preserving of glutathione in a reduced form is necessary to prevent the inactivation of a number of enzymes, protecting the hepatocyte membranes from the effects of oxidants. The oxidation of reduced glutathione leads to decrease in the intensity of glycolysis, lowered synthesis of ATP and decline in the energy potential of hepatocytes and cardiomyocytes that is particularly undesirable for the comorbidity of NASH and coronary heart disease.
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Rėkus, Algirdas, and Gediminas Jaruševičius. "BRIEF SUMMARY OF PATHOGENESIS, DIAGNOSIS AND MANAGEMENT OF SPONTANEOUS CORONARY ARTERY DISSECTION." Health Sciences 30, no. 3 (2020): 136–40. http://dx.doi.org/10.35988/sm-hs.2020.084.
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Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome (ACS). It was first described 80 years ago. Pathogenetic mechanisms are most likely to be associated with intimas tear or bleeding vasa-vasorum, which resulting in intramural haemorrhage. SCAD typically occurs in young women who do not have coronary heart disease risk factors and who have acute coronary syndrome. Half of all SCAD presents with ST – elevation myocardial infarction (STEMI), while the rest with non – ST – elevation myocardial infarction (NSTEMI). The gold standard method for diagnosis is interventional coronary artery angiography. After the acute ischemic onset syndrome, most patients have a stable, benign clinical course, and eventually experience spontaneous vessel wall healing. Therefore, conservative treatment (a watchful strategy) is recommended as the initial treatment. For the majority of cases as interventional and surgical treatment in most cases seems to be suboptimal. In this extremely complex situation, several novel and attractive coronary interventions have been proposed. The risk factors, pathogenesis theories, diagnosis, management, prognosis of SCAD will be summarized in this review.
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Frick, Barbara, Vera Rudzite, Katharina Schröcksnadel, Uldis Kalnins, Andrejs Erglis, Karlis Trusinskis, and Dietmar Fuchs. "Homocysteine, Β Vitamins and Immune Activation in Coronary Heart Disease." Pteridines 14, no. 3 (August 2003): 82–87. http://dx.doi.org/10.1515/pteridines.2003.14.3.82.
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Abstract Moderate hyperhomocysteinemia is associated with an increased risk of coronary heart disease (CHD). An inverse relationship usually exists between homocysteine and folate concentrations, and folate supplementation is often able to lower homocysteine concentrations. Thus, insufficient dietary intake of folate and/or vitamin B12 is considered to be responsible for the development of hyperhomocysteinemia. Inflammation and immune activation appear also to be important in the pathogenesis of CHD and may influence availability of folate. Blood concentrations of homocysteine, Β vitamins and neopterin were examined in 35 patients with CHD verified by coronary angiography, (2 1 patients with one-artery disease, 9 with two- or three-artery disease, 5 with restenosis). Compared to 30 healthy controls, a significant proportion of patients presented with increased homocysteine concentrations. Hyperhomocysteinemia coincided with lower folate and also with higher neopterin concentrations indicating immune system activation. In addition, correlations existed between neopterin and homocysteine (r = 0.472, ρ < 0.01) and folate (r = -0.370, ρ = 0.01). We conclude that higher homocysteine is not only associated with lower circulating folate but also with higher neopterin. Immune activation could be involved to cause an increased demand for folate resulting in hyperhomocysteinemia even when dietary folate intake is within the recommended range.
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Shalnev, V. I. "ACUTE CORONARY SYNDROME: A SEA CHANGE IN OUR UNDERSTANDING OF PATHOGENESIS AND WAY OF TREATMENT? (PART I)." EMERGENCY MEDICAL CARE 20, no. 2 (June 4, 2019): 67–73. http://dx.doi.org/10.24884/2072-6716-2019-20-2-67-73.
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The article highlights the hypothesis of the inflammatory pathways in pathogenesis of atherothrombosis and the conception of residual inflammatory risk in coronary heart disease patients. Modern approach to the correction of inflammatory risk by immune-modulating therapy in acute coronary syndrome setting is discussed. The results of most significant randomized clinical trials dedicated to this problem are also highlighted.
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Shalnev, V. I. "ACUTE CORONARY SYNDROME: A SEA CHANGE IN OUR UNDERSTANDING OF PATHOGENESIS AND WAY OF TREATMENT? (PART II)." EMERGENCY MEDICAL CARE 20, no. 3 (December 22, 2019): 62–67. http://dx.doi.org/10.24884/2072-6716-2019-0-3-62-67.
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The second part of review highlights the role of residual lipid and thrombotic risks in coronary heart disease patients and possible ways of its correction. The results of randomized clinical trials dedicated to the efficacy of new class of hypolipidemic drug (PCSK‑9 inhibitors) in acute coronary syndrome setting are discussed. Recently published new guidelines of European Society of Cardiology on acute coronary syndrome management are also highlighted.
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Sarkar, Amrita, and Khadija Rafiq. "Humoral Immunity in Heart Failure." Cardiovascular & Hematological Disorders-Drug Targets 19, no. 1 (January 28, 2019): 14–18. http://dx.doi.org/10.2174/1871529x18666180518101527.
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Cardiovascular Disease (CVD) is a class of diseases that involve disorders of heart and blood vessels, including hypertension, coronary heart disease, cerebrovascular disease, peripheral vascular disease, which finally lead to Heart Failure (HF). There are several treatments available all over the world, but still, CVD and heart failure became the number one problem causing death every year worldwide. Both experimental and clinical studies have shown a role for inflammation in the pathogenesis of heart failure. This seems related to an imbalance between pro-inflammatory and anti-inflammatory cytokines. Cardiac inflammation is a major pathophysiological mechanism operating in the failing heart, regardless of HF aetiology. Disturbances of the cellular and humoral immune system are frequently observed in heart failure. This review describes how B-cells play a specific role in the heart failure states. There is an urgent need to identify novel therapeutic targets and develop advanced therapeutic strategies to combat the syndrome of HF. Understanding and describing the elements of the humoral immunity function are essential and may suggest potential new treatment strategies.
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Kakorin, S. V., I. A. Averkova, and A. M. Mkrtumyan. "Hypoglycemic therapy in patients with type 2 diabetes and chronic heart failure." CardioSomatics 5, no. 1 (March 15, 2014): 33–40. http://dx.doi.org/10.26442/cs45071.
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The article presents a literature review of prevalence, prognosis and treatment of overt tactics of chronic heart failure (CHF) in patients with type 2 diabetes mellitus (T2DM). Application of modern pharmacological preparations and instrumental treatment of cardiovascular disease (CVD) increases life expectancy and improves the quality of life of patients with CHF as with normal carbohydrate metabolism (UO), and with type 2 diabetes. However, the risk of cardiovascular mortality (CAS) in patients with type 2 diabetes, compared to having a normal carbohydrate metabolism remains unchanged.Insulin resistance (IR) and compensatory hyperinsulinemia (GI) play a key role in the pathogenesis of type 2 diabetes. Ongoing research in the twentieth century of coronary heart disease (CHD) and heart failure in patients with type 2 diabetes revealed adverse effects of sulfonylurea medications on the metabolic processes in the myocardium and increased risk of death in patients with severe coronary artery disease. In comparison with sulfonylurea drugs, metformin and insulin not only reduces the risk of cardiovascular disease, but also can prevent or delay the development of type 2 diabetes in individuals with impaired glucose tolerance (IGT) and impaired fasting glucose. Metformin acts on the key link of pathogenesis - insulin resistance, affecting the lower incidence of cardiovascular diseases, the development of chronic disease and mortality compared with insulin and sulfonylurea drugs. However, in patients with chronic heart failure is contraindicated the use of thiazolidinediones and metformin is limited tothe severity of CHF I-II FC NYNA. With effective treatment of chronic heart failure by cardiologists in patients with type 2 diabetes, affecting therapy with insulin resistance should be mandatory.
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Saranchina, Yu V., S. V. Dutova, O. Yu Kilina, N. V. Khanarin, and T. S. Kulakova. "The role of neutrophils in the pathogenesis of atherosclerosis." Cardiovascular Therapy and Prevention 17, no. 6 (December 20, 2018): 110–16. http://dx.doi.org/10.15829/1728-8800-2018-6-110-116.
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Atherosclerosis (AS) is one of the causes of cardiovascular disease. The formation of atherosclerotic lesions of the arteries is a long process, and clinical symptoms appear already at the stage of atherosclerotic plaque (ASB), which prevents blood flow and can cause coronary heart disease, as well as acute coronary syndrome. The study of atherosclerosis mechanisms at the subclinical level is relevant. This article provides a summary of current data on the structure and functions of neutrophils (NF) in physiological processes. Particular attention is paid to the participation of neutrophils in the damage and formation of vascular endothelial dysfunction. Discusses several mechanisms of involvement of neutrophils in atherogenesis: the production of reactive oxygen species, which cause direct endothelial damage; the synthesis of cytokines that trigger the migration of leukocytes in inflammation; the formation of protein complexes with cholesterol, contributing to their deposition in the vessels, and neutrophil traps, triggering destructive-alterative reactions.
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Shalina, Maria A. "Metabolic syndrome in older women." Journal of obstetrics and women's diseases 68, no. 3 (July 8, 2019): 81–88. http://dx.doi.org/10.17816/jowd68381-88.
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This paper presents the current literature data on the pathogenesis of metabolic disorders in menopause. The association of metabolic syndrome with a high risk of coronary heart disease, hypertension, diabetes, and insulin resistance is of great medical and social importance. It emphasizes the need for early diagnosis of metabolic syndrome in older women and optimization of therapeutic and preventive measures. The article highlights the role of pathogenetic, multi-component therapy, including menopausal hormone one, in the treatment of metabolic disorders in menopause.