Готові списки джерел за темами / Ischemic pathology of heart

Добірка наукової літератури з теми "Ischemic pathology of heart"

Автор: Grafiati
Опубліковано: 30 травня 2022
Оновлено: 31 травня 2022

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Статті в журналах з теми "Ischemic pathology of heart"

1

Pulyaeva, I. S. "RESULTS OF INSPECTION AND TREATMENT OF PATIENTS WITH STENOSIS OF CAROTIDS IN COMBINATION WITH PATHOLOGIES OF OTHER SYSTEMS." Kharkiv Surgical School, no. 5-6 (December 25, 2019): 99–103. http://dx.doi.org/10.37699/2308-7005.5-6.2019.21.

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Summary. An aim of work is an analysis of results of inspection and treatment of patients with the hemodynamically meaningful defeat of carotids in combination with pathology of other organs and systems. Materials and methods. The results of treatment are analysed 187 patients with hemodynamically by meaningful stenosis of carotids in SI «Zaycev V.T. IGUS of NAMSU» from 2015 for 2018 on a background forthcoming surgical treatment of chronic ischemia of lower limbs, ischemic heart or pathology of gastrointestinal tract trouble. Patients are divided into 3 groups. The first group was made by patients with the chronic ischemia of lower limbs of 2-Д degree - 167 patients. 7 patients entered a group with pathology of gastrointestinal tract. 3 a group was made by 13 patients with ischemic heart trouble. Results and discussion. The direct results of operation we estimated complex on the basis of degree of change of clinical status and presence of postoperative complications. At 161 the patients of the first group in a postoperative period are not educed complications, for a 2th patient thrombosis of anastamosis and ischemic stroke, at 4th paresis of n. Hypoglossuss. In the second group for all operated patients concerning stenosis of carotid, complications were not in a postoperative period. For one patient with the cancer of stomach, that was not execute a reconstructive operation on a carotid an ischemic stroke developed in connection with bleeding. In 3 cases in a postoperative period observed symptomatology of stroke for patients operated concerning ischemic heart, carotid endarterectomia was not executed these patients. Conclusions. To the patients with general atherosclerosis and stroke in anamnesis it is necessary to conduct carotids screening. At hemodynamically meaningful stenosises patients with heart diseaseby and pathology of abdomen of must execute carotid endarterectomia of the first stage, that reduces the risk of ischemic stroke in a postoperative period at treatment of basic pathology.
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2

Iqbal, Sohail. "Cardiovascular Magnetic Resonance in Ischemic Heart Disease." European Journal of Medical and Health Sciences 3, no. 4 (July 5, 2021): 11–12. http://dx.doi.org/10.24018/ejmed.2021.3.4.927.

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Ischemic heart disease is one of the leading causes of death and disability, limiting individual’s quality of life. Cardiac magnetic resonance is radiation-free tool to image IHD patients and can depict inducible ischemia, extent and distribution of scar burden, associated complications like mitral regurgitation, thrombus, aneurysm formation, myocardial rupture, and any other incidental pathology. With increasing availability of the CMR there is an ever increasing need to interpret these images by non-imaging clinicians in order to manage patients more effectively. In this article, image interpretation for detection of ischemia, infarct and thrombus are discussed in simple easy to understand manner leaving behind intricate technical details which are of less important to the referring physicians.
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3

Frolov, M. A., N. A. Sakhovskaya, A. M. Frolov, and A. D. Pryamikov. "Feature of Ocular-Ischemic Syndrome in Patients with Cardiovascular Pathology. Literature Review." Ophthalmology in Russia 17, no. 2 (June 23, 2020): 188–94. http://dx.doi.org/10.18008/1816-5095-2020-2-188-194.

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Vascular pathology of the vision organ is one of the leading causes of irreversible vision loss. Ocular ischemic syndrome is a serious condition that requires special attention to prevent adverse effects and outcomes. Today, this syndrome mainly occurs in the form of ischemic optic neuropathy and chronic ischemic retinopathy, which are based on damage caused by impaired perfusion in the pool of the ophthalmic artery. According to the data presented in foreign and domestic literature, there is an correlation between the ocular ischemic syndrome and the pathology of the cardiovascular system. Often, this pathology is accompanied by such diseases as: coronary heart disease, atherosclerosis, arterial hypertension, and diabetes mellitus. A number of studies have shown that an important risk factor for the development of vascular eye’s pathology is the combination of coronary heart disease with elevated total blood cholesterol and atherosclerosis in combination with arterial hypertension. Also, there are data indicating the association of the risk of ischemic opticopathy with the presence of cardiovascular diseases in patients, and vice versa, previously transferred opticopathy can be considered as predictors of cardiovascular pathology. Thus, prevention and treatment of this pathology is an interdisciplinary problem. The classical approach in the treatment of ocular ischemic syndrome today remains conservative therapy, which aims to reduce local ischemia and the effects of hypoxia. However, conservative treatment does not eliminate the main reason for the development of this condition; therefore, the search continues for new, more effective methods of preventing and treating this pathology. In recent years, data on high clinical efficacy in the treatment and prevention of ocular ischemic syndrome manifestations have appeared in the literature after surgery to restore the main blood flow at the level of the brachiocephalic arteries. A variety of cardiovascular diseases and various levels of its damage determine the approach to the treatment of this pathology. This literature review is devoted to the analysis of the causes of ocular ischemic syndrome, depending on the level of localization of the lesion of the cardiovascular system.
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4

Aretz, H. Thomas. "Nenstherscloerotic Ischemic Heart Disease." American Journal of Surgical Pathology 14, no. 4 (April 1990): 402. http://dx.doi.org/10.1097/00000478-199004000-00019.

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5

Morales, Azorides R. "Non-atherosclerotic ischemic heart disease." Human Pathology 21, no. 1 (January 1990): 124. http://dx.doi.org/10.1016/0046-8177(90)90091-i.

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6

Andonieva, N. M., E. A. Huts, М. Ya Dubovik, S. A. Olyanich, and L. V. Mykhailiuk. "CARDIOVASCULAR PATHOLOGY AS AN IMPORTANT SOCIAL PROBLEM IN PATIENTS WITH CKD." Experimental and Clinical Medicine 86, no. 1 (March 31, 2020): 58–64. http://dx.doi.org/10.35339/ekm.2020.86.01.08.

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A study of 114 patients who received renal replacement therapy by peritoneal dialysis, whose average age was (47.9±1.2) years, the duration of dialysis therapy - (53.0±2.3) months. EchoCG results with Doppler, bicycle ergometric loading ECG tests are analyzed in dynamics. Depending on the detected changes, patients were divided into five clinical groups. The first group included patients who suffered an acute myocardial infarction during the study. To the second - patients with stable angina. To the third - patients with painless myocardial ischemia. The fourth group included patients with ischemic dilated cardiomyopathy (IDCMP). Fifth - the comparison group, which included patients without signs of coronary heart disease. Patients were determined biochemical parameters of phosphorus-calcium, lipid metabolism, proinflammatory interleukins (TNF-a, IL-1ß, IL-8), C-reactive protein and CAA protein. It was found that cardiorenal syndrome in patients with chronic kidney disease on peritoneal dialysis leads to the progression of coronary heart disease. The formation of different clinical variants of coronary heart disease in such patients is multifactorial, initiated by impaired lipid metabolism with subsequent immunological changes in combination with the processes of remodeling of the left ventricular myocardium, calcification and fibrosis of the aorta, cardiac structures and heart valves. Proinflammatory interleukins TNF-a, IL-1ß, and C-reactive protein are most likely predictors of acute myocardial infarction, whereas IL-8 and acute inflammatory protein (serum amyloid) are associated with ischemic dilated cardiomyopathy, in patients with chronic kidney disease on peritoneal dialysis. Keywords: renocardial syndrome, renal replacement therapy, peritoneal dialysis, coronary heart disease, heart failure.
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7

Dzhaiani, N. A. "CANDESARTAN IN CARDIOLOGY PRACTICE." Medical Council, no. 7 (December 30, 2017): 12–16. http://dx.doi.org/10.21518/2079-701x-2017-7-12-16.

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The most significant risk factor for the development of cardiovascular diseases such as myocardial infarction, ischemic heart disease, chronic heart failure, is arterial hypertension (AH). [1] AH also contributes to the development of cerebrovascular pathology (ischemic or hemorrhagic stroke, transient ischemic attack) and kidney diseases (chronic kidney disease).
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8

Majetschak, Matthias. "Regulation of the proteasome by ATP: implications for ischemic myocardial injury and donor heart preservation." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 3 (August 1, 2013): H267—H278. http://dx.doi.org/10.1152/ajpheart.00206.2012.

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Several lines of evidence suggest that proteasomes are involved in multiple aspects of myocardial physiology and pathology, including myocardial ischemia-reperfusion injury. It is well established that the 26S proteasome is an ATP-dependent enzyme and that ischemic heart disease is associated with changes in the ATP content of the cardiomyocyte. A functional link between the 26S proteasome, myocardial ATP concentrations, and ischemic cardiac injury, however, has been suggested only recently. This review discusses the currently available data on the pathophysiological role of the cardiac proteasome during ischemia and reperfusion in the context of the cellular ATP content. Depletion of the myocardial ATP content during ischemia appears to activate the 26S proteasome via direct regulatory effects of ATP on 26S proteasome stability and activity. This implies pathological degradation of target proteins by the proteasome and could provide a pathophysiological basis for beneficial effects of proteasome inhibitors in various models of myocardial ischemia. In contrast to that in the ischemic heart, reduced and impaired proteasome activity is detectable in the postischemic heart. The paradoxical findings that proteasome inhibitors showed beneficial effects when administered during reperfusion in some studies could be explained by their anti-inflammatory and immune suppressive actions, leading to reduction of leukocyte-mediated myocardial reperfusion injury. The direct regulatory effects of ATP on the 26S proteasome have implications for the understanding of the contribution of the 26S proteasome to the pathophysiology of the ischemic heart and its possible role as a therapeutic target.
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9

Rodríguez-Calvo, M. S., M. N. Tourret, L. Concheiro, J. I. Muñoz, and J. M. Suárez-Peñaranda. "Detection of Apoptosis in Ischemic Heart." American Journal of Forensic Medicine and Pathology 22, no. 3 (September 2001): 278–84. http://dx.doi.org/10.1097/00000433-200109000-00016.

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10

Kaplunova, V. Y., G. A. SHakaryants, M. V. Kozhevnikova, I. S. Ilgisonis, E. V. Privalova, N. V. Khabarova, Y. I. Naymann, Y. N. Belenkov, and V. A. Shakaryants. "Hypertrophic Cardiomyopathy and Ischemic Heart Disease. Variants of Combination Pathology." Kardiologiia 17, no. 12 (2017): 16–24. http://dx.doi.org/10.18087/cardio.2017.12.10062.

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Дисертації з теми "Ischemic pathology of heart"

1

Vos, Lynette Christine. "Growth factor expression and release in the ischemic heart." Scholarly Commons, 2004. https://scholarlycommons.pacific.edu/uop_etds/2665.

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The angiogenic and cardioprotective effects of basic fibroblast growth factor (FGF-2) and vascular endothelial growth factor (VEGF) in the ischemic myocardium have been studied, but expression and release of endogenous FGF-2 and VEGF during myocardial ischemia are poorly understood. In addition, nitric oxide synthase isoforms eNOS and iNOS may play a role in myocardial ischemia. The purpose of this study was to investigate the release of FGF-2 and expression of FGF-2, VEGF, eNOS, and iNOS in the normal and ischemic heart. In Phase I, serum FGF-2 levels in patients undergoing treadmill stress test were measured to investigate correlation between serum FGF-2 levels and presence of ischemic heart disease. The study found that serum FGF-2 in ischemia-positive and ischemia-negative patients was not significantly elevated after treadmill stress test, and serum FGF-2 levels did not differ significantly between ischemia-positive and ischemia-negative patients. In Phase II, FGF-2 levels in coronary effluent from isolated perfused rabbit hearts subjected to low-flow ischemia was measured. Results suggest that FGF-2 is released into the coronary effluent of isolated perfused hearts over time and that this release may be elevated in ischemic (50% flow) hearts. Furthermore, the present study indicates that FGF-2 is released immediately after surgical isolation and instrumentation of the isolated heart. A linear model was developed to describe the release of FGF-2 from the isolated heart as a function of the coronary flow rate Q : [special characters omitted]where t = time and Q = 1 and 3.01 for normal and 50% flow rates respectively. In Phase III, effect of acute low-flow ischemia on FGF-2, VEGF, eNOS, and iNOS mRNA expression was measured in isolated perfused hearts using RT/PCR. Preliminary results indicate that FGF-2, VEGF, and iNOS mRNA expression is upregulated and eNOS expression is decreased in ischemic hearts suggesting that these growth factors play a role in short-term response of the myocardium to ischemia. The results of this study suggest that FGF-2, VEGF, and iNOS mRNA expression are increased, eNOS expression is decreased, and FGF-2 is released in response to low-flow ischemia in the isolated perfused heart.
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2

Vagnozzi, Ronald J. "Cardiac Troponin I-interacting Kinase (TNNI3K/CARK) Adversely Regulates Injury, Cell Death and Oxidative Stress in the Ischemic Heart." Thesis, Thomas Jefferson University, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3617188.

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Ischemic heart disease impacts millions worldwide and can progress to heart failure. Percutaneous coronary intervention (PCI) is first-line therapy for patients presenting with an acute ischemic event or acute coronary syndrome (ACS). However, PCI can also worsen cardiomyocyte death, cardiac dysfunction and adverse remodeling via reperfusion injury, largely an oxidative stress-mediated insult. Novel alternative therapies for ACS have proven elusive, with no new classes of agents in years. We investigated cardiac troponin I-interacting kinase (TNNI3K), a cardiomyocyte-specific kinase, as a potential modulator of ischemia/reperfusion (I/R) injury and chronic left ventricular (LV remodeling). We found TNNI3K enhances production of mitochondrial reactive oxygen species (mROS) and induces mitochondrial dysfunction, thus increasing cardiomyocyte death and I/R injury. Moreover, TNNI3K-mediated injury is largely dependent on p38 MAPK activation. We developed a series of small-molecule TNNI3K inhibitors that reduce mitochondrial-derived superoxide generation, p38 activation, and infarct size when delivered at reperfusion to mimic ACS intervention. Moreover, although TNNI3K inhibition does not modulate the adverse remodeling that occurs after a non-reperfused myocardial infarction (MI), TNNI3K inhibition preserves cardiac function and limits chronic adverse remodeling in a model of MI with reperfusion. Taken together, TNNI3K plays an adverse role in the cardiomyocyte response to I/R, in part by driving mROS production and augmenting p38-mediated cell death specifically via reperfusion injury. Our findings reveal a previously unexplored role for TNNI3K in regulating the oxidative stress response in the heart, and support the potential for TNNI3K as a novel therapeutic target for ACS.

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3

Straczek, Céline. "Epidémiologie des cardiopathies ischémiques du sujet âgé non institutionnalisé-Etude des Trois Cités." Phd thesis, Université Paris Sud - Paris XI, 2011. http://tel.archives-ouvertes.fr/tel-00670145.

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L'objectif est de tester les associations de marqueurs inflammatoires et lipidiques avec la survenue de cardiopathies ischémiques chez la personne âgée non institutionnalisée. Les analyses sont menées dans une étude cas cohorte dans le cadre de l'étude des 3 Cités. Elle inclut 199 sujets ayant développé un premier évènement coronaire sur 4 ans de suivi et 1086 sujets sans antécédents cardiovasculaires (sous cohorte). Un premier travail suggère que la protéine C-réactive (CRP-US) est un marqueur de risque indépendant des évènements coronaires (risque relatif standardisé du log de la CRP-US=1,27 ; IC95%=1,08-1,64) mais n'améliore pas la prédiction du risque coronaire. Le second travail démontre une hétérogénéité dans l'association des lipides classiques et des apolipoprotéines avec les évènements coronaires selon la prise et la nature du traitement hypolipémiant à l'inclusion. Le troisième travail indique que les apolipoprotéines AI et B100 mais pas le non-HDL cholestérol améliorent significativement la prédiction du risque coronaire sur la base d'indice de reclassification.
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4

Sartipy, Ulrik. "Left ventricular reconstruction in ischemic heart disease /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-028-2/.

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5

Henareh, Loghman. "Impaired glucose tolerance in ischemic heart disease /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-445-7/.

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6

Ibrahim, Esha. "Angiogenesis and Myogenesis in a Chronic Ischemic Heart." Digital Commons @ East Tennessee State University, 2005. https://dc.etsu.edu/etd/1058.

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Miniswine underwent procedures to evaluate treating chronic ischemia with the implantation of autologous satellite cells and laser transmyocardial revascularization (TMR). The objective was to combine two therapies to restore cardiac function. This experiment involved three surgical procedures: (1) placing a constrictor on the coronary artery; (2) producing channels and implanting cells; (3) obtaining samples. The swine were divided into groups: Group 1, Ischemia; Group 2, Ischemia + Laser TMR; Group 3, Ischemia + Laser TMR+ Cells; Group 4, Ischemia + Cells. Sonomicrometry and Millar pressure transducers were used to determine contractility, left ventricular pressure, and pressure-volume loops. There were no significant differences (p<0.05)among the hemodynamic data except for Group 4, which produced significantly lower output values. Morphological evaluation revealed a significantly reduced scar area in Group 3. Although there was a significant difference in scar area, the phenomena behind this improvement as compared to the unimproved hemodynamic function is not understood.
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7

Moreira, Felismina Teixeira Coelho. "Fast screening for diagnostic of heart ischemic episodes." Doctoral thesis, Faculdade de Ciências e Tecnologia, 2013. http://hdl.handle.net/10362/11318.

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Dissertação para obtenção do Grau de Doutor em Química Sustentável
Cardiovascular diseases (CVD) are top-killer chronic diseases, accounting for al-most half of the European deaths in 2010 (Eurostat data). Most recent statistics in Portuguese territory confirm this scenario, with cardiovascular diseases killing about 11 persons per 100000 inhabitants. Reducing these numbers is urgent and requires early, quick and efficient diagnostic of the specific heart condition. Thus, the main goal of this proposal is to develop a low cost sensing-devices based on newly synthesized sensory biomaterials for screening cardiac bi-omarkers in point-of-care. These were applied to screen the conventional bi-omarkers of clinical interest, all peptides in nature. These include troponin T (TnT), creatine kinase isoenzyme (CK-MB) and myoglobin (Myo). This was achieved by means of novel and low cost biosensing materials that were designed to display good selectivity to each biomarker, assembled on nanostructured sens-ing units and tested on serum samples. The design of novel biosensing materials consisted on synthesizing plastic antibodies by means of novel molecular im-printing (MI) and enzymatic approaches. Nanostructured sensing units were as-sembled by modifying the surface of standard conductive materials with the pre-viously indicated biomaterials. Standard conductive supports selected for this purpose were carbon and gold. Overall, it is expected that the emerging biosensing materials and platforms out coming from this project may contribute for the development of new non-inva-sive or minimally invasive methods with clinical application in the early screen-ing of chronic diseases and fast-screening in point-of-care (POC) of acute events.
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8

Moore, Lynne. "Psychological stress and the incidence of ischemic heart disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0006/MQ33720.pdf.

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9

Vargas-Pinto, Pedro Alexis. "Atrial Structure and Function in Non-ischemic Heart Failure." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1353975728.

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10

Bachuk-Ponych, N. V. "Adjuvant therapy of meteosensivity patients with ischemic heart disease." Thesis, БДМУ, 2022. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/19560.

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Книги з теми "Ischemic pathology of heart"

1

International, Symposium on Molsidomine (1984 Düsseldorf Germany). Ischemic heart disease and heart failure: Advances in treatment with molsidomine. Munich ; Baltimore: Urban & Schwarzenberg, 1986.

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2

K, Shah Prediman, and De Feyter Pim J, eds. Ischemic heart disease. London: Manson, 2007.

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3

Mochizuki, Seibu, Nobuakira Takeda, Makoto Nagano, and Naranjan S. Dhalla, eds. The Ischemic Heart. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/b102183.

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4

Roncella, Adriana, and Christian Pristipino, eds. Psychotherapy for Ischemic Heart Disease. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33214-7.

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5

Mueller, Xavier M. Lasers for Ischemic Heart Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56798-8.

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6

Wiviott, Stephen D., ed. Antiplatelet Therapy In Ischemic Heart Disease. Oxford, UK: Wiley-Blackwell, 2008. http://dx.doi.org/10.1002/9781444303339.

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Dumitrescu, Silviu Ionel, Ion C. Ţintoiu, and Malcolm John Underwood, eds. Right Heart Pathology. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73764-5.

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8

Lerman, Bruce B. Topics in arrhythmias and ischemic heart disease. New York: Demos Medical Pub., 2010.

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9

Van Der Vusse, Ger J., ed. Lipid Metabolism in Normoxic and Ischemic Heart. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-1611-4.

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10

Delgado, Reynolds, ed. Interventional Treatment of Advanced Ischemic Heart Disease. London: Springer London, 2009. http://dx.doi.org/10.1007/978-1-84800-395-8.

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Частини книг з теми "Ischemic pathology of heart"

1

Michaud, Katarzyna. "Ischemic Heart Disease." In Cardiac Pathology, 117–31. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-4471-2407-8_7.

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2

Vlodaver, Zeev, Richard W. Asinger, and John R. Lesser. "Pathology of Ischemic Heart Disease." In Congestive Heart Failure and Cardiac Transplantation, 59–79. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-44577-9_4.

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3

Antman, Elliott M., and John D. Rutherford. "Pathogenesis and Pathology of Ischemic Heart Disease Syndromes." In Coronary Care Medicine, 1–18. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2303-7_1.

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4

Rakusan, Karel, Nicholas Cicutti, and Tomas Sladek. "Ischemic Heart." In Advances in Experimental Medicine and Biology, 457–61. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0333-6_58.

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Driessen, Ann. "Ischemic Colitis." In Encyclopedia of Pathology, 426–31. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-40560-5_1441.

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Baldaia, Helena. "Ischemic Gastritis." In Encyclopedia of Pathology, 432–33. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-40560-5_1615.

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Padala, Santosh K., Mandeep S. Sidhu, and William E. Boden. "Stable Ischemic Heart Disease Stable Ischemic Heart Disease." In PanVascular Medicine, 2109–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-37078-6_70.

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Kireyev, Dmitriy, and Judy Hung. "Ischemic Heart Disease." In In Clinical Practice, 145–49. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-21458-0_12.

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Sakata, Yasuhiko, and Hiroaki Shimokawa. "Ischemic Heart Disease." In Interdisciplinary Concepts in Cardiovascular Health, 1–17. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-01074-8_1.

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10

Nuovo, Jim. "Ischemic Heart Disease." In Fundamentals of Family Medicine, 252–81. New York, NY: Springer New York, 1996. http://dx.doi.org/10.1007/978-1-4757-2535-3_12.

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Тези доповідей конференцій з теми "Ischemic pathology of heart"

1

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

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Анотація:
Unstable angina pectoris represents a common and important manifestation of acute ischemic heart disease encompassing the broad spectrum of clinical syndromes between stable effort angina and acute myocardial infarction. This group of patientsisfar from uniform concerning underlying pathogenetic mechanisms and prognosis, but generally the risk of infarction or deathis increased during the unstable period. Most patients are presenting with new or worsening effort angina or angina at rest,and especially patients with rest anginaassociated with transient ECG changes seem to constitute a high risk subgroup. Transient reductions in coronary blood flow,rather than increases in myocardial oxygen demand, seem to play the major role in rest angina, indicating an underlying 'dynamic' coronary stenosis.Furthermore, unstable angina seems to beagood clinicalmarker for actively progressing coronary-artery disease.Pathologically, a rapidly evolving coronary-artery lesion represented by a disrupted atherosclerotic plaque with variable degree of plaque hemorrhage and luminalthrombosis usually is present in patientscoming to autopsy after a period of rest angina. The thrombus at the rupture site may be mural and limited (just sealing therupture) or occlusive depending on the degree of preexisting atherosclerotic stenosis. An occlusive thrombus is seldom seen over ruptured plaques causing less tha15% stenosis (histologic area stenosis), but is found with increasing frequency when stenosis severety increases beyond 15%.Most occlusive thrombi have a layered structure with thrombus material of differing age indicating an episodic growth by repeated mural deposits. Aggregated platelets usually can be identified in the mostrecent part of the thrombus, while older parts are more homogeneous due to fibrin infiltration/stabilization. Additionally,microemboli and microinfarcts are frequently found in the myocardium downstream tocoronary thrombi. So, the period of unstable angina preceding a fatal heart attackseems to be characterized by an ongoing thrombotic process in a major coronary artery where recurrent mural thrombus formation alternates with intermittent thrombus fragmentation and peripheral embolization. Such a dynamic thrombosis (with or without a concomitant focal vasospastic phenomenon) at the site of an unstable (ruptured) atherosclerotic lesion obviously may lead to the other clearly thrombus-related acute ischemic events: myocardial infarction or sudden death.Clinical studies using coronary angiography and coronary angioscopy during the acute phase of unstable angina have revealed a high frequency of ulcerated (unstable) atherothrombotic lesion in arteries responsible for the acute ischemia. Furthermore, episodic platelet activation (usually associated with chest pain) has recently been demonstrated in patients with unstable angina.The mechanism underlying pain/ischemia(predominantly spasm?) and the rapid plaque progression (plaque hemorr.hage/luminal thrombosis?) during unstable angina maydiffer. Accordingly, therapy directed against a possible spasm (nitrates, calcium antagonists) usually relieves pain effectively without having any documented effect on infarction/survival, while antithr-ombotic therapy (aspirin, heparin) clearlyimproves the prognosis without apparent antianginal effect. Therefore, with the objective not only of relieving pain but also of improving the prognosis, more attention should be paid to the potentially fatal thrombotic process that apparently isgoing on in a major coronary artery of many patients with unstable angina.
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2

Walsh, Peter W., Craig S. McLachlan, Leigh Ladd, Arie Blitz, R. Mark Gillies, Brett Hambly, Ryan Ocsan, and Glenn Edwards. "Echocardiography Evaluation of a Novel Stable Ovine Heart Failure Model Suitable for Cardiovascular Device Testing." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53824.

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Numerous large animal models of chronic cardiac ischemia have been developed to explore either pathological mechanisms and or device interventions in developed heart failure models. Traditionally chronic heart failure in large animal models such as sheep or pigs has been induced by either coronary ligation with or without reperfusion. Coronary ligation is often attempted in the open chest surgical model or more recently in the closed chest animal via angiography [1]. Both techniques can be challenging and also induce high mortality with the risk of myocardial stunning and resultant shock and or lethal arrhythmias. There is also difficulty in developing stable heart failure across cases where infarct sizes can be variable. One strategy to over come this variability has been via rapid ventricular pacing, however inducing heart failure does not induce sustained heart failure in many cases if the pacing is switched off, and additionally pacing does not induce some of the underlying pathology seen in the development of heart failure [1].
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3

Xiao Jie, B. Rodriguez, and N. Trayanova. "The Ischemic Heart: What Causes Ectopic Beating?" In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1616168.

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4

Ulbikas, J., A. Čenys, D. Žemaitytė, and G. Varoneckas. "Correlations in heart beat data as quantitative characterization of heart pathology." In Chaotic, fractal, and nonlinear signal processing. AIP, 1996. http://dx.doi.org/10.1063/1.51004.

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5

Pugazhenthi, D., and V. Meenakshi. "Detection of Ischemic Heart Diseases from Medical Images." In 2016 International Conference on Micro-Electronics and Telecommunication Engineering (ICMETE). IEEE, 2016. http://dx.doi.org/10.1109/icmete.2016.97.

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6

Kumar, D., M. E. Rehman, B. Hooks, and V. Rayasam. "Pulmonary Sequestration Masking Symptoms of Ischemic Heart Disease." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3563.

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Bondareva, Erika, Jing Han, William Bradlow, and Cecilia Mascolo. "Segmentation-free Heart Pathology Detection Using Deep Learning." In 2021 43rd Annual International Conference of the IEEE Engineering in Medicine & Biology Society (EMBC). IEEE, 2021. http://dx.doi.org/10.1109/embc46164.2021.9630203.

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8

Chen, Mingzhe, and Yongzhen Zhang. "Applications of laser in ischemic heart disease in China." In International Symposium on Biomedical Optics, edited by Qingming Luo, Britton Chance, Lihong V. Wang, and Steven L. Jacques. SPIE, 1999. http://dx.doi.org/10.1117/12.364350.

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Vashakmadze, Nato, Leyla Namazova-Baranova, Tatiana Privalova, Anastasia Rykunova, Natalya Zhurkova, and Elena Komarova. "P44 Heart pathology in patients with syndrome maroto-lamy." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.399.

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10

Raihan, M., Parichay Kumar Mandal, Muhammad Muinul Islam, Tanvir Hossain, Promila Ghosh, Shakil Ahmed Shaj, Abdullah Anik, Mubtasim Rafid Chowdhury, Saikat Mondal, and Arun More. "Risk Prediction of Ischemic Heart Disease Using Artificial Neural Network." In 2019 International Conference on Electrical, Computer and Communication Engineering (ECCE). IEEE, 2019. http://dx.doi.org/10.1109/ecace.2019.8679362.

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Звіти організацій з теми "Ischemic pathology of heart"

1

Pleszkoch, Mark G., Hilda B. Klasky, Aneel Advani, Edmon Begoli, Aileen Boone, and Stephan D. Fihn. Game Theoretic Approach for Understanding and Modeling Clinical Pathways (Stable Ischemic Heart Disease). Office of Scientific and Technical Information (OSTI), October 2018. http://dx.doi.org/10.2172/1513403.

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2

Clapp, N. E., L. M. Hively, and R. E. Stickney. Heart pathology determination from electrocardiogram signals by application of deterministic chaos mathematics. CRADA final report. Office of Scientific and Technical Information (OSTI), March 1999. http://dx.doi.org/10.2172/325739.

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3

Akzhigitova, D. Z., and S. S. Spitsina. Prevalence of rhythm disturbances and conduction of the heart in the structure of ischemic disease in rheumatoid arthritis. Actual problems of experimental and clinical medicine: Materials 77th International Scientific and Practical Conference of Young Scientists and students, 2019. http://dx.doi.org/10.18411/akzhigitova-d-z.

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4

Li, Peng, Na jia, Bing Liu, and Qing He. Effect of cardiac shock wave therapy on adverse cardiovascular event for patients with coronary artery disease: an updated systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, January 2022. http://dx.doi.org/10.37766/inplasy2022.1.0103.

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Review question / Objective: We have previously demonstrated that cardiac shock wave therapy (CSWT) effectively improves myocardial perfusion in patients with coronary artery disease (CAD). In this study, we want to address whether CSWT could decrease the risk of adverse cardiovascular events in CAD patients unsuitable for revascularization. Eligibility criteria: Trials are considered eligible if they meet these criteria: (1) patients included are diagnosed as refractory angina or ischemic heart failure; (2) the study i a randomized controlled trial (RCT) or a prospective cohort study; (3) intervention consisted of CSWT; (4) patients in the control group are treated with optimal medical therapy, (5)the primary outcome of interest Is rate of MACE. Exclusion criteria were (1) patients with acute myocardial infarction, (2) repeated CSWT, (3) with coronary artery revascularization, (4) without primary outcome, (5) retrospective study, and (6)duplicated data.
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