Дисертації: "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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11

Du, Ying. "Ischemic and pharmacological preconditioning of rat myocardium : effects on ischemia-reperfusion injury /." View abstract or full-text, 2005. http://library.ust.hk/cgi/db/thesis.pl?BICH%202005%20DU.

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12

Фадєєва, Ганна Анатоліївна, Анна Анатольевна Фадеева, Hanna Anatoliivna Fadieieva, and М. Damodaran. "Amiodaron-induced thyroid dysfunction in patients with ischemic heart disease." Thesis, Sumy State University, 2017. http://essuir.sumdu.edu.ua/handle/123456789/64797.

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Amiodaron treatment is associated with thyroid dysfunction. Besides dyslipidemia, thyroid dysfunction can induce insulin resistance, hypertension, endothelial dysfunction and poor response to antiarrhythmic therapy. Study objectives: to determine prevalence of thyroid dysfunction among patients with ischemic heart disease (IHD) taking amiodarone in Sumy region.

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13

裴中 and Zhong Pei. "Neuroprotection of melatonin in ischemic stroke models." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31243526.

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14

Michallek, Florian [Verfasser]. "Fractal analysis of the ischemic transition region in chronic ischemic heart disease using Magnetic Resonance Imaging / Florian Michallek." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1127045822/34.

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15

Tapp, Dianne Marie Varin. "Exploring therapeutic conversations between nurses and families experiencing ischemic heart disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq24567.pdf.

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16

Groot, Monica Johanna Maria de. "The effect of lactate on the normoxic, ischemic and reperfused heart." [Maastricht : Maastricht : Rijksuniversiteit Limburg] ; University Library, Maastricht University [Host], 1992. http://arno.unimaas.nl/show.cgi?fid=5689.

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17

Badawi, Sally. "Characterization of dynamic molecular networks in control ischemic-reperfused mouse heart." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1158.

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Les maladies cardiovasculaires représentent un important problème de santé publique à travers le monde. Parmi ces pathologies, l’infarctus du myocarde (IM) a fait l’objet de nombreux essais visant à diminuer sa sévérité. Néanmoins peu ont remporté leur pari. Cet échec peut avoir plusieurs composantes parmi lesquelles la méconnaissance de la complexité des mécanismes moléculaires impliqués. Notre compréhension de l’IM a cependant été nettement améliorée grâce à des méthodes utilisées pendant les dernières décennies et qui consistaient à étudier séparément un nombre limité d’acteurs moléculaires impliqués dans un mécanisme simple et linéaire. Cependant, l’échec des essais cliniques basés sur ces approches réductionnistes ont montré leurs limites. L’émergence de la biologie des systèmes, ces dernières années, a stimulé les recherches visant à mieux intégrer et comprendre la nature complexe et stochastique des réseaux moléculaires et leur dynamique dans la progression des pathologies. L’objectif général de cette thèse a consisté en le développement et l’amélioration de méthode d’analyses et de combinaison des données spatio-temporelles issus d’expériences réalisées sur un modèle d’infarctus du myocarde chez la souris. L’objectif scientifique visait à caractériser les principaux signaux dynamiques au cours de la séquence d’ischémie-reperfusion. A cet effet, nous avons tout d’abord développé une chaîne de méthode utilisant la clarification d’organe et la microscopie de fluorescence permettant de quantifier, en 3 dimensions, la zone du myocarde soumise au choc oxydant lors de la reperfusion. Dans une seconde partie, nous avons développé une nouvelle chaîne analytique pour caractériser la dynamique d’expression des transcrits. Appliquée aux animaux contrôles (soumis à la chirurgie et l’anesthésie), nous mettrons, grâce à cette chaîne de méthode, le rôle majeur de la voie de l’interleukine 6 dans le développement de la réponse immunitaire et nous concluons ainsi sur la nécessité de réaliser une analyse dynamique du modèle expérimental pour caractériser sa réponse à l’échelle moléculaire et éviter toute surinterprétation de la réponse à l’IM
Cardiovascular diseases represent a major health burden worldwide. According to the World Health Organization, 17 million people are dying each year by heart diseases which account to 31% of total deaths globally. Among these diseases is myocardial infarction (MI). Several efforts have been made to decrease the associated mortality rates but unfortunately, only few has succeeded to date. This failure is contributed to several factors, among them is the misunderstanding of the mechanism responsible for the progression of the disease.Our understanding of the MI pathology has been greatly improved by the approaches that have been widely used in the previous decades, relying mainly on studying molecules/pathways separately. However, this knowledge was not enough to make a difference clinically. Therefore, deciphering the interconnections between molecules has become an urge for better understanding of the diseases’ progression. In this regard, the work in this doctoral thesis involves different aspects of the MI pathology. The general aim of this work is to improve the dynamic analytical approach using systems biology tools, where new mechanistic information is decoded. Firstly, in a 3D heart model, we propose a chain of methods using clarified mouse heart and fluorescence microscopy to molecularly characterize the area at risk in the myocardium of IR and cardioprotected mice based on its redox state. In addition, we aim to develop a new analytical approach using dynamical large-scale transcriptomic data for characterizing the dynamic transcripts expression. Applying this approach on a control mouse model (mice subjected to anesthesia and surgical interventions), we show that Il-6 is a major mediator of the activated inflammatory reaction. In conclusion, this analytical approach highlights the necessity of the sapatio-temporal analysis to characterize the molecular events occurring in response to MI

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18

Awad, Wael Ibrahim Issa. "Ischaemic preconditioning in the neonatal rat heart." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391636.

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19

Edström, Plüss Cathrine. "Effects of an expanded rehabilitation programme in patients with ischemic heart disease." Stockholm : Karolinska institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-707-8/.

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20

Rafatian, Ghazaleh. "Rejuvenation of Aged Heart Explant-Derived Cells for Repair of Ischemic Cardiomyopathy." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/38850.

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In autologous stem cell therapy, cell characteristics determine the potency of stem cells for regeneration. Aging and ischemia are two factors that are often neglected in pre-clinical tests for stem cell therapy. Here, we characterized cardiac explant-derived cells (EDCs) with a focus on distinguishing the effect of age and ischemia and then we looked for the effects of the combination of the two factors. We observed that ischemia worsens the age effect on EDCs. EDCs that were derived from aged mice with a history of myocardial infarction showed the highest number of senescent cells with dysregulation of the DNA repair system resulting in activation of cell cycle checkpoints. We over-expressed the anti-senescence Mybl2 transcription factor in EDCs from ischemic aged mice. The senescent state, paracrine profile and superoxide dismutase antioxidant enzyme activity improved in these cells. In vivo, we observed a boost in the potency of the Mybl2-modified EDCs, with an increase in short-term engraftment leading to improved heart function in infarcted mice. In general, Mybl2 over-expression rejuvenates senescent EDCs.

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21

Hamatani, Yasuhiro. "Incidence and predictors of ischemic stroke during hospitalization for congestive heart failure." Kyoto University, 2019. http://hdl.handle.net/2433/245292.

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22

Boslett, James J. "CD38 in the Heart: Effects of CD38 Activation on Post-Ischemic Injury." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1500293726035515.

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23

Shuper, V. A. "Clinical features of chronic obstructive pulmonary disease combined with ischemic heart disease." Thesis, БДМУ, 2017. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/17112.

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24

Bousette, Nicolas. "The role of urotensin-II in atherosclerosis and ischemic cardiomyopathy /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111848.

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Atherosclerosis, a vascular disease which may lead to coronary artery occlusion and consequent myocardial infarction is primarily caused by dyslipidemia. Ischemic cardiomyopathy due to atherosclerosis is the leading cause of morbidity and mortality in the western world today. Vasoactive factors are increasingly being recognized not only as contributors to atherosclerotic plaque formation, but also to cardiac function and remodeling following ischemic cardiac injury. Urotensin II (UII) is one such vasoactive factor. UII possesses a wide range of cardiovascular effects, from contraction of the rat aorta to complete cardiovascular collapse in cynomolgus monkeys. UII binds a seven transmembrane spanning G-protein coupled receptor termed UT. Expression of UII is significantly elevated in the hearts of patients with congestive heart failure (CHF). Recent reports have also shown increased plasma levels of the peptide in patients with CHF, and these levels correlated with the severity of the disease. This project was designed to investigate the role of UII and UT in both atherosclerosis and CHF. To this end, UII expression was evaluated both in a model of CHF in the rat, and in human atherosclerosis of the carotid arteries and aortae. Furthermore, the pathophysiological role of urotensin-I1 in CHF was investigated, with the use of a selective UII antagonist, SB-611812. Finally, genetically modified mice deficient in either ApoE, UT, or both genes, were evaluated to study the role of UII/UT signaling in a model of atherosclerosis. We found that UII and its receptor, UT, were both significantly elevated in a model of CHF induced by coronary artery ligation. UII antagonism significantly attenuated mortality, cardiac dysfunction, and hypertrophy. This was associated with a significant decrease in cardiac fibrosis. We next went on to demonstrate that UII and UT were significantly elevated in human atherosclerotic carotid arteries and aortae. Finally, we demonstrated that deletion of the UT gene in mice deficient for ApoE exacerbates atherosclerosis of the aorta. Furthermore, this was associated with significantly increased hyperlipidemia and organ hypertrophy as well as significantly reduced body mass, liver mass, and hepatic steatosis.
In conclusion we were the first to demonstrate a pathophysiological role for UII in cardiovascular diseases which may lead to a breakthrough in the management of CHF and may also give more insight into the pathogenesis of atherosclerosis.

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25

Falk, Melanie. "Evaluation of a novel model of cardiac ischemic preconditioning and role of ecto-5'-nucleotidase in ischemic preconditioning of the heart /." Tübingen, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000254316.

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26

Prosser, Hamish Charles Graydon. "Involvement of Novel Cardiac Peptides in Healthy and Ischemic Hearts." Thesis, University of Canterbury. Biological Sciences, 2009. http://hdl.handle.net/10092/2731.

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The role and functions of Urotensin II (UII), Urotensin II-related peptide (URP) and proangiotensin-12 (PA12) are currently ambiguous, either due their relatively new identification and isolation from their host species, or due to contrasting and conflicting reports observing the physiological and pathophysiological role of these spasmogens within the mammalian cardiovascular system. Accordingly, we sought to determine the true physiological functions of these peptides in both healthy and diseased states. The initial task was to reveal potential reasons for the contrasting responses to UII, and to define the role of UII within the isolated rat heart. UII and URP retain a highly conserved cyclic region, shown to be necessary in receptor binding and activation, with the high inter-species variance within the N-terminus reported to be of little importance. Our research revealed UII to be highly species-specific, stimulating potent, sustained vasodilation of the coronary arteries in response to the native form infused, while non-native UII peptides had either no effect, or caused significant vasoconstriction. UII-induced vasodilative effects were found to be mediated by nitric oxide and prostaglandin activity combined. Reviewing publications to date it was evident that many studies employed UII foreign to the host species, reporting potentially untrue effects, based on our findings. Recent studies have identified UII as a potent agent in developing and promoting atherosclerosis and coronary artery disease through UII-induced mitogenic activity and promoting foam cell formation. Hence, we observed the effect of infusing the native species of UII and URP into a model of cardiac ischemia-reperfusion. Both preconditioning the heart with UII or URP, or infusing UII or URP upon reperfusion caused significant coronary vasodilation following ischemia, and significantly attenuated ischemic-induced myocardial injury. These studies indicated elevating UII and URP provided a level of cardioprotection, not only when administered into healthy hearts prior to an ischemic event, but also in hearts having already undergone ischemia and the resultant endothelial damage. PA12 was the third peptide tested in the current thesis. Being newly identified and suggested to be a new component of the renin-angiotensin system (RAS) it was important to define the physiological role of PA12 upon the cardiovasculature, as the RAS is heavily associated with the development and progression of cardiovascular disease. Utilising the Langendorff isolated rat heart technique, PA12 was found to cause potent vasoconstriction of the coronary arteries, mediated by the angiotensin II type 1 receptor (AT₁R). Furthermore, using subjecting the perfusate samples to radioimmunoassay and RP-HPLC revealed PA12 was converted to AngII. Both PA12-induced vasoconstriction and generation of AngII were found to be dependent upon chymase activity, with inhibition of ACE1 having little effect. Myography was employed to further study the vascular response to PA12 throughout the rat arterial system from the common carotid to the femoral arteries. PA12-induced vasoconstriction displayed a potency gradient, with greatest constriction observed in vessels closest to the heart, with potency reduced and eventually lost further from the heart. PA12-induced vasoactivity was shown to be dependent upon both chymase and ACE1 activity, with ACE1 regulating PA12 activity with greater potency. The intracellular pathways stimulated in response to PA12 were defined using western blotting, with PA12 stimulating phosphorylation of ERK1/2, JNK, p38 and PKCα/β₁₁, but having no influence on PKCδ/θ. Stimulation of these pathways is consistent with the observed PA12-induced vasoconstriction, and also indicates that PA12 activation of AT₁R and the subsequent cytokines, could potentially stimulate hypertrophy, apoptosis, cell growth and differentiation, and inflammation, promoting cadiovascular remodelling and progressing atherosclerosis, hypertension and other vascular diseases if not sufficiently regulated. Taken together, these studies indicate PA12 may have a primary role within the local, tissue-based RAS, providing an alternate substrate to angiotensin I, while ACE1 is the primary regulatory enzyme within the circulation. Our findings also display the chymase-dependent PA12/AT₁R pathway as potential novel targets for pharmacological inhibition of RAS activity to ameliorate hypertension and maladaptive vascular remodelling.

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27

Schmidt, Christian Alexander Peter. "Stimulating angiogenesis into biomaterials through the delivery of growth factors." Doctoral thesis, University of Cape Town, 2007. http://hdl.handle.net/11427/26618.

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lschemic disease in form of ischemic heart disease (IHD), ischemic stroke and peripheral arterial disease (PAD) due to atherosclerosis represents a massive clinical and economic burden to healthcare and is currently the number one cause of death in the world. Treatment modalities for peripheral arterial disease include bypass surgery involving autologous vein or synthetic materials such as ePTFE. Long term patency of small diameter vascular grafts used for infra-inguinal reconstructions, however, is below 50 % 5 years after implantation. Therefore, novel vascular graft concepts and materials are needed. The concept of transmural in vivo endothelialisation of vascular grafts holds great promise for increasing long term patency. To achieve complete luminal endothelial cell coverage and optimal integration of the porous synthetic graft material into the host tissue, transmural ingrowth of tissue and vasa vasorum might have to be facilitated. Since VEGF1ss and PDGF-BB are growth factors known to stimulate and consolidate angiogenesis, this PhD thesis hypothesized, that neovascularisation of porous polyurethane (PU) can be increased by delivery of vascular endothelial growth factor (VEGF1ss) and platelet derived growth factor (PDGF-BB). To prove this hypothesis, subcutaneous implantation of PU discs was established as a valid, reproducible, relatively simple and quantifiable neovascularisation model. Three different ways of growth factor delivery were investigated. The gene encoding for human VEGF15s was cloned into the genome of adeno associated viruses (AAV), which served as a vector for gene transduction of autologous wound healing cells in vivo using the "Gene Activated Matrix" approach. Genetically modified matrix embedded AAV-VEGF155 was loaded into porous PU and transduced autologous ingrowing wound cells. In contrast to the excellent transduction efficiency in myocytes, AA V showed a poor tropism for wound healing cells. The second approach to increase neovascularisation into porous PU was the surface modification of PU by covalent attachment of nitrous acid degraded heparin. Neovascularisation into the biomaterial was increased by 77 % after 10 days of subcutaneous implantation. Since certain angiogenic growth factors show a high affinity for heparin, additional loading of heparin surface modified PU with VEGF165 increased neovascularisation even further up to 115 % at 10 days compared to control. Dual growth factor delivery of VEGF 165 and PDGF-BB not only initiated increased vascularisation of porous PU, but also created a stable vascular network 2 months after implantation. In contrast, PU loaded with VEGF165 alone showed regression of total vascular area of 61 % compared to vascular area at 10 days. Thirdly, to study the effects of controlled, prolonged growth factor delivery, a "Neovascularisation Construct" was developed which was implanted subcutaneously in rats. The construct consisted of an osmotic mini pump and a tube of porous PU lined with ePTFE, into which a defined amount of VEGF16s was pumped for 10 days. After implantation, granulation tissue was growing into the pores of the PU and neovascular area was increased up to 265 % compared to PBS control. Furthermore, using different growth factor concentration, a dose dependency was shown. In addition, this thesis investigated the functional perfusion of the micro vascular network growing into PU by four different vascular quantification techniques. lntravital perfusion with biotinylated lycopersicon esculentum followed by microscopical analysis, vascular corrosion casting quantified by scanning electron microscopy as well as the novel micro-CT analysis of silicone rubber perfused vessels were compared to conventional immunhistochemical analysis of endothelial cells by CD31. Interestingly, PBS perfused "Neovascularisation Constructs" showed a relatively poor perfusion; therefore CD31 immunohistochemistry "overestimated" functional neovascularisation 3 fold. All perfusion techniques indicated a strong effect of VEGF 165 delivery on vessel perfusion (10 to 20 fold increases of vascular area and volume compared to PBS control). Micro-CT scanning was shown to be an excellent tool to study micro vascular networks in a three-dimensional fashion across the whole length of the sample in a limited amount of time and to provide reliable and reproducible data on vessel density, vascular volume, and connectivity. Since resolution is still limited today to about 10 μm using a commercially available bench top scanner, this new technology still needs to be complemented by immunohistochemistry and perfusion studies such as lectin perfusion and corrosion casting. In summary, the induction of neovascularisation was achieved by heparin surface modification alone, which was even increased through additional delivery of growth factors into the biomaterial PU. The development of a stable micro vascular network at 2 months was achieved and the functionality was shown using four different, independent techniques including the novel micro-CT scanning of neovascularisation into biomaterials. Towards the development of an in vivo, spontaneously and transmurally endothelialising vascular graft with superior long-term patency further investigations are necessary. As an initial step, increased spontaneous neovascularisation of the possible graft material polyurethane was achieved. Future steps are clearly indicated to study the translation of increased neovascularisation of the biomaterial polyurethane towards increased endothelialisation in a vascular graft model.

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28

MAEKAWA, Atsuo, Jong-Kook LEE, Keiko MIWA, Takashi NAGAYA, Yuichi UEDA, and Itsuo KODAMA. "Overexpression of Calpastatin Ameliorates Functional Recovery from Ischemic Injury in the Rat Heart." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2793.

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29

Berg, Kirsti. "Oxidative stress and the ischemic heart : A study in patients undergoing coronary revascularization." Doctoral thesis, Norwegian University of Science and Technology, Department of Circulation and Medical Imaging, 2004. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-389.

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The isoprostane 8-iso-PGF_2αproved to be a valuable marker of conditions associated with oxidative stress in all three clinical studies (I-III). Somewhat surprising, no significant correlation with myocardial reperfusion events was found. Only the duration of severe ischemia correlated positively in patients with AMI undergoing primary PCI (II). Thus the first aim of this thesis was partly fulfilled. A particular finding was that other conditions than myocardial ischemia-reperfusion such as interventional (I) and surgical (III) traumas contributed to an apparent oxidative stress in the patient groups. In parallel, pro- or antioxidant drug effects seemed to have influenced the release pattern of 8-iso-PGF_2α, underlining the versatility of this parameter of lipid peroxidation.

The second aim of the thesis, to establish a relationship between oxidative stress and myocardial injury, was not fulfilled. Thus the present studies I-III seem to refute the hypothesis of a major ROS-involvement in myocardial ischemia-reperfusion injuries as shown in animal experiments. Another interpretation is that an oxidation-injury relationship was masked in the more complex pathophysiology of a clinical setting. A further implication may be that 8-iso-PGF_2α behaved as a passive indicator of successful reperfusion rather than as an active indicator of severe and injury-inducing oxidative stress, reflecting the role as a ROS-imprint and not as an injury marker.

The third aim of the thesis, to try out potent antioxidants on a rational basis, did not materialize as the studies went on. However, in the course of time new mechanisms of cardioactive or adjunctive drugs were recognized. Thus both ASA and heparin are two candidates which may have had a major impact on the results in all three studies. Concerning ASA both positive effects of an acute booster dose (II) and negative effects of withdrawal (III) warrant further attention.

Although the study is limited by the low numbers of patients, it seems justified to suggest that the lack of success in translating principles of oxidative stress and antioxidant therapy from the experimental to the clinical stage of myocardial ischemia-reperfusion may now have found a more plausible explanation than hitherto proposed. Thus oxidative stress, if present, is a multifactorial process with complex interactions between pro- and antioxidant factors and with largely unrecognized protection by drugs in common use.

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30

Feng, Jun. "The mechanism of ischemic preconditionning in rat heart, implications of norepinephrine and bradykinin." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ32626.pdf.

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31

Verhoef, Bastiaan Abram Willem. "Elemental analysis of ischemic and reperfused rat heart tissue using the proton microprobe." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1997. http://arno.unimaas.nl/show.cgi?fid=5932.

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32

Nilsson, Staffan. "Chest pain and ischemic heart disease : Diagnosis and management in primary health care." Doctoral thesis, Linköping : Department of Medical and Health Sciences, Linköpings universitet, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-11390.

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33

La, Bonte Laura. "The Role of Complement in Ischemic Heart Disease in Type 2 Diabetes Mellitus." Diss., The University of Arizona, 2008. http://hdl.handle.net/10150/193747.

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The mechanisms responsible for the enhanced inflammatory response in type 2 diabetes (T2DM) and its contribution to the severe ischemia/reperfusion (I/R) injury observed in the T2DM heart are unclear. I/R is associated with an acute inflammatory response recognized by reactive oxidant production, complement activation, and leukocyte-endothelial cell adhesion, among others. Complement activation plays an important role in the inflammatory response and is involved in the manifestation of I/R injury in the non-diabetic heart, and is a potent chemoattractant for circulating neutrophils (PMNs). The purpose of this dissertation research was to test the hypothesis that the complement system, predominantly the lectin pathway, is a significant contributor to the excessive response of the Zucker Diabetic Fatty (ZDF), a rat model of T2DM, to myocardial I/R injury. Following 30min of coronary artery occlusion and 120min of reperfusion we measured C3 deposition, PMN accumulation, PMN CD11b expression, and ICAM-1 expression. We found significantly more C3 deposition, PMN accumulation, ICAM-1 and PMN CD11b expression in diabetic samples compared to non-diabetic samples. To elucidate a role for complement system activation, we treated animals with FUT-175, a broad complement inhibitor. In vivo, FUT-175 treatment significantly decreased complement deposition (66%), PMN accumulation (59%), and infarct size (55%) compared to untreated animals in both non-diabetic Sprague-Dawley and diabetic ZDF rats. To specifically examine the role of the lectin pathway, we selectively inhibited rat MBL-A prior to myocardial I/R in ZDF rats. Anti-MBL treatment significantly decreased infarct size, C3 deposition and PMN accumulation in the ZDF post-ischemic left ventricle (LV). Genomic analysis revealed that gene expression of the pro-inflammatory cytokines IL-6 and IL-1Î± was enhanced in the ZDF heart following reperfusion, and quantitative RT-PCR results confirmed IL-6 upregulation. We found significantly increased complement C5a receptor (CD88) expression on diabetic neutrophils prior to ischemia, suggesting that diabetic PMNs are "primed" to respond to complement activation. Taken together, these results provide evidence that 1) the ZDF rat is a good model for chronic inflammation in the setting of T2DM, 2) lectin pathway activation plays a significant role in the inflammatory response to I/R injury in the ZDF heart, and 3) anti-complement therapy may be particularly cardio-protective in T2DM.

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34

Slunga, Lisbeth. "Serum lipoprotein(a) in relation to ischemic heart disease and associated risk factors." Doctoral thesis, Umeå universitet, Klinisk kemi, 1993. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-101298.

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Lipoprotein(a) (Lp(a)) consists of an LDL-like particle and the specific protein apo(a), which is very similar to plasminogen. Apo(a) contains repeated kringle structures and a serine protease domain, which cannot be activated by t-PA. Lp(a) is considered to be a predictor for atherosclerotic disease. It has been found incorporated in atherosclerotic plaques and inhibits in vitro fibrinolysis. Lp(a) was determined in 1527 randomly selected individuals participating in the Northern Sweden WHO-MONICA project. A weak but significant relation between Lp(a) and increasing age was found. Menopausal status was the strongest independent predictor of Lp(a) level in women. Fibrinogen was independently related to Lp(a) in both sexes. Only a minor fraction of Lp(a) variance could be explained for in a multiple regression model, which is in agreement with the contention that Lp(a) is highly genetically determined. Lp(a) was determined in 1571 patients investigated with coronary angiography because of suspected severe coronary artery disease (CAD). Patients with proven CAD at elective angiography had significantly higher Lp(a) than patients without significant CAD or healthy controls. Lp(a) was found to be an independent discriminator of CAD in both sexes. HLA-DR genotype 13 or 17 was found more frequently in 30 male patients with angiographic CAD at young age (< 50 years) than in 30 age matched controls. These genotypes were common in patients with high Lp(a) levels, which indicates that Lp(a) may be related to immunological processes. The reaction of Lp(a) was investigated in 32 patients with acute myocardial infarction (AMI). Lp(a) increased during the first week, but the response was comparatively weak. Individual Lp(a) responses were heterogeneous and no correlations to infarct size or changes in the acute phase proteins were found. In a randomized cross-over study on 36 hypercholesterolaemic patients treated with simvastatin/placebo during 12+12 weeks Lp(a) did not change significantly, but patients with high Lp(a) levels at baseline tended to develop further increased Lp(a). To conclude, Lp(a) was found to be an independent predictor of angiographic CAD in both men and women. Lp(a) levels are primarily genetically determined and only a small fraction of Lp(a) variance could be explained by other factors in this study. Lp(a) may be related to HLA DR types and immunological processes involved in atherosclerotic disease. Lp(a) increased slightly during the first week of AMI, but was not related to changes in the acute-phase proteins. The effective LDL-lowering agent simvastatin did not influence Lp(a) significantly.

Diss. (sammanfattning) Umeå : Umeå universitet, 1993, härtill 5 uppsatser.

digitalisering@umu

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35

Buccini, Stephanie M. "Cardiogenic differentiation of induced pluripotent stem cells for regeneration of the ischemic heart." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1382373160.

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36

Johnson, Paula Denise 1959. "Spontaneous congenital heart malformations in the Sprague-Dawley rat." Thesis, The University of Arizona, 1992. http://hdl.handle.net/10150/278074.

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The spontaneous rate of congenital cardiac defects in the commonly used Sprague-Dawley rat has not been extensively researched. The incidence of general congenital defects has been studied thoroughly and reported as very low incidence in this rat. Teratology studies using mammalian models are of increasing importance as the number of environmental contaminants increases. It is essential to know if the spontaneous congenital cardiac defect rate of this most common mammalian model in order to plan statistically appropriate research protocols. Using a thorough and detailed method of evaluating the structure of the Sprague-Dawley fetal rat heart, 624 fetal rat hearts were examined at term, just prior of delivery. The overall incidence of spontaneous congenital cardiac defects is 2.3%. This is similar to the incidence in man and thus enhances the suitability of the Sprague-Dawley rat as a small mammalian model for research into cardiac teratogenesis.

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37

Pandey, Raghav. "MicroRNA Mediated Proliferation of Adult Cardiomyocytes to Regenerate Ischemic Myocardium." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1505124343198575.

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38

Hinken, Aaron C. "Effects of ischemic metabolites and chronic exercise on cardiac myocyte function." Diss., Columbia, Mo. : University of Missouri-Columbia, 2005. http://hdl.handle.net/10355/4150.

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Thesis (Ph. D.)--University of Missouri-Columbia, 2005.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "May, 2005" Includes bibliographical references.

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39

Moustacalis, Estes. "Personality and emotional factors and quality of life in individuals with ischemic heart disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ54675.pdf.

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40

Rubilis, Aigars. "T-vector and T-loop morphology analysis of ventricular repolarization in ischemic heart diseases /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-443-3/.

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41

Detzer, Julia [Verfasser]. "Reg3beta restricts the spatiotemporal accumulation of neutrophil granulocytes within the ischemic heart / Julia Detzer." Gießen : Universitätsbibliothek, 2021. http://d-nb.info/1224970721/34.

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42

Wu, Joe. "HIF-1α in the Heart: Provision of Ischemic Cardioprotection and Remodeling of Nucleotide Metabolism". Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etd/2450.

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In our studies we found that stabilized expression of HIF-1α in heart led to better recovery of function and less tissue death after 30 minutes of global ischemia, via mechanisms that preserve the mitochondrial polarization. Our group previously showed that HIF-1α conferred ischemic tolerance by allowing cardiomyocytes to use fumarate as an alternative terminal electron acceptor to sustain anaerobic mitochondrial polarization. The source of fumarate was identified as the purine nucleotide cycle (PNC). Here we discovered that HIF-1α upregulates AMP deaminase 2 (AMPD2), the entry point to the PNC. The combination of glycolysis and the PNC may protect the heart's nucleotide resources. We subsequently examined the effects that HIF-1α exerts on nucleotide metabolism in the ischemic heart. We found that HIF-1α expression reduces adenosine accumulation in the ischemic heart. As ATP is depleted during ischemia, AMP accumulates. Our results suggest that AMP metabolism is shunted towards AMPD2 rather than the adenosine producing 5'-nucleotidase pathway. Subsequently, we treated hearts with the PNC inhibitor hadacidin followed by 30 minutes of global ischemia. Inclusion of hadacidin reduced ATP and adenylate energy charge in the hearts. These findings allow us to propose that activity of the PNC prevents the F0F1 ATP synthase from consuming glycolytic ATP in order to maintain mitochondrial polarization during ischemia. Thus, the PNC provides ATP sparing effects and preserves the energy charge in the ischemic heart. The fact that ATP and adenylate energy charge is better preserved during the initial 20 minutes of ischemia in HIF-1α expressing hearts is supportive of our observation that HIF-1α upregulates the PNC. HIF-1α also upregulates adenosine deaminase, which degrades adenosine. The limitation of adenosine accumulation may help HIF-1α expressing hearts avoid toxicity due to chronic adenosine exposure. Finally, we found that HIF-1α induces the expression of the nucleotide salvage enzyme hypoxanthine phosphoribosyl transferase (HPRT). Upon reperfusion HPRT serves to reincorporate the nucleotide degradation product, hypoxanthine, into the adenylate pool and may prevent the production of reactive oxygen species. Collectively, HIF-1α robustly protects the heart from ischemic stress and it upregulates several pathways whose cardioprotective role may extend beyond the remodeling of nucleotide metabolism.

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43

Nishizawa, Junichiro. "Reperfusion causes significant activation of heat shock transcription factor 1 in ischemic rat heart." Kyoto University, 1997. http://hdl.handle.net/2433/202145.

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44

Langner, Neima. "Cardiac risk factor management in the offspring of patients with premature ischemic heart disease." Thesis, University of Ottawa (Canada), 1993. http://hdl.handle.net/10393/6819.

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Objective. To determine the prevalence of cardiac risk factors in offspring of patients with premature ischemic heart disease, their awareness of these risk factors, and to find out what proportion of offspring have had risk factor assessment including cholesterol screening and what proportion have adopted risk factor reducing strategies. Main results. The median age of the offspring was 20 years (range 2-39). Among the late adolescent and young adult progeny 37% were smokers, 31% were overweight and 30% exercised less than three times per week. Although 78% had been examined by a physician in the preceding three years, only 97 (44%) reported having had a blood cholesterol measurement performed during that time and only five of the 97 actually knew their cholesterol levels. Fifty-seven percent of the males had had a blood pressure measurement in the previous year. Although all respondents were aware that eating fatty food could contribute to heart disease and cholesterol elevation, few (13%) recognized the role of heredity as a causal factor for heart disease and only 22% reported that they would know how to lower their blood cholesterol. Conclusions. The low rates of cardiovascular risk factor assessment and management identified in this survey represent missed opportunities for primary prevention. (Abstract shortened by UMI.)

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45

Hjelmström, Anna. "Use of electronic cigarettes among patients with ischemic heart disease at Örebro University hospital." Thesis, Örebro universitet, Institutionen för medicinska vetenskaper, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-48461.

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46

Husarchuk, A. G. "Peculiarities of cardiac injury in patients with ischemic heart disease on rheumatoid arthritis background." Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18050.

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47

Yasynska, E. Ts. "The role and place of ischemic heart disease as a cause of temporary disability." Thesis, БДМУ, 2017. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/12162.

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48

Grytsiuk, M. I. "Mortality structure and rate due to ischemic heart disease among residents of Chernivtsi region." Thesis, БДМУ, 2017. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/12159.

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49

Mäkikallio, A. (Anne). "Cardiovascular autonomic and hormonal dysregulation in ischemic stroke with an emphasis on survival." Doctoral thesis, University of Oulu, 2005. http://urn.fi/urn:isbn:9514278526.

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Abstract Ischemic stroke is associated with cardiovascular autonomic nervous system (ANS) disturbances, including reduced heart rate (HR) variability and acute phase neurohumoral activation with elevated stress hormone levels. The impact of HR variability and neurohumoral factors such as natriuretic peptides on the long-term survival of patients with ischemic stroke has not been studied previously. This study was designed to evaluate cardiovascular autonomic regulation in ischemic stroke patients by assessing HR dynamics and various neurohumoral factors. The values of the assessed variables in predicting mortality were evaluated. HR variability assessments were performed in the acute phase of ischemic stroke and for a general elderly population. Various neurohumoral factors were also assessed in the acute phase of stroke. After follow-up, the survival of the subjects was assessed and the prognostic values of the measured factors were evaluated. Stroke patients were found to have cardiovascular autonomic and hormonal disturbances manifested as reduced traditional time and frequency domain measures of HR variability, altered long-term HR dynamics and elevated levels of natriuretic peptides in the acute phase. Altered long-term HR dynamics in the acute phase of stroke predicted long-term mortality after stroke and cerebrovascular mortality in the general elderly population. Neuroendocrine activation involving elevated natriuretic peptide values that were associated with high cortisol and catecholamine levels was observed in the acute phase of ischemic stroke. Neurohumoral disturbance was prognostically unfavourable. The most powerful predictors of poststroke mortality were altered long-term HR dynamics and elevated levels of natriuretic peptides and cortisol, which predicted mortality independently of the conventional risk factors in multivariate analysis. Prognostically unfavourable cardiovascular autonomic dysfunction with disturbances in the long-term behaviour of HR dynamics was found to be related to ischemic stroke. Neurohormonal activation with elevated natriuretic peptide and cortisol levels in the acute phase predicts long-term mortality after ischemic stroke.

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50

Chen, Yinhong. "The effects of murine AIDS and ethanol consumption on the severity of myocardial ischemic injury." Diss., The University of Arizona, 2001. http://hdl.handle.net/10150/289750.

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Cardiovascular complications are prevalent in patients with AIDS. Cardiovascular complications, particularly ischemia-reperfusion injury, may be severe in AIDS patients. The pathology underlying cardiovascular complications in AIDS patients is unclear. Perhaps interplay of several pathologic factors amplifies the response to ischemia. Murine retrovirus (LP-BM5) induced murine AIDS is the best model of human AIDS research because LP-BM5 causes similar immune changes. Ethanol consumption has the advantage and disadvantage to health. The aim of this study was to determine if chronic ethanol consumption influences pathological changes caused by murine AIDS, specifically in cardiovascular complications, and if vitamin E supplementation could attenuate cardiovascular injury by murine AIDS. In our present study, we found that retrovirus infection enhanced neutrophil CD11b expression and ROS production, increased platelet CD62p and platelet microparticle formation, exaggerated coronary permeability to macromolecules and caused a severe myocardial ischemia-reperfusion injury. Chronic ethanol consumption down-regulated neutrophil CD11b expression, but neutrophil ROS production, platelet CD62p expression and platelet microparticle formation were enhanced. Chronic moderate ethanol consumption improved coronary microcirculation and attenuated ischemia-reperfusion injury. Our results indicate that neutrophil and platelet adhesion molecule expression increases in murine AIDS. Neutrophil and platelet-mediated severe ischemia-reperfusion injury may contribute to increased incidence of cardiomyopathy in AIDS. The cardiovascular protective effects of moderate ethanol consumption may be related to modulation of neutrophil CD11b expression and improve coronary microcirculation. However, chronic ethanol consumption did not preserve myocardial damage by retrovirus infection. In this study, we also demonstrated that vitamin E attenuated AIDS-induced myocardial injury. Vitamin E may be a therapeutic adjuvant agent for preventing and treatment AIDS-induced cardiovascular diseases.

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