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1
Low, Wee Chuang Roger. "Molecular pathology of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) and hereditary multi-infarct dementia." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417546.
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Grau, Olivares Marta. "Neuropsychological and structural brain correlates of lacunar infarcts." Doctoral thesis, Universitat de Barcelona, 2008. http://hdl.handle.net/10803/2714.
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L’infart cerebral és la segona causa de mort, així com d’incapacitació a nivell mundial (Di Carlo et al.,2000), essent responsable de múltiples seqüeles físiques i cognitives, incloent la demència. L’infart cerebral es caracteritza per una simptomatologia neurològica focal i sobtada en consonància amb la localització topogràfica de la lesió cerebral, un cop s’han exclòs altres possibles causes. La demència vascular (DV) històricament s’ha basat en el model de demència multi-infart (Erkinjuntti et al.,2002), tot i que cada vegada hi ha una major evidència de que diferents patologies vasculars (malaltia vascular subcortical de petit vas o infarts llacunars), així com infarts corticals, poden contribuir a desenvolupar-la (Hachinski et al.,1974; Esiri et al.,1997; Rockwood et al.,1999; Erkinjuntti et al.,1999; Pohjasvaara et al.,2000; Ballard et al.,2000). L’objectiu d’aquesta recerca és l’estudi del perfil neuropsicològic i dels dèficits cognitius associats a la malaltia vascular cerebral de petit vas (infarts llacunars i lesions de la substància blanca), així com l’evolució d’aquests pacients després de 2 anys d’haver patit l’event vascular. Aquest tema mereix especial interès perque la malaltia vascular subcortical de petit vas és una de les causes més comunes de demència vascular (DV), i el fet de poder conèixer el seu estat prodròmic i poder previndre els principals factors de risc, ens podrien fer possible el desenvolupament d’estratègies preventives. Aquesta àrea d’estudi també mereix atenció perque s’han fet molts estudis sobre l’evolució i les seqüeles cognitives en els infarts isquèmics de gran vas, però no hi ha gaire evidència sobre l’efecte d’un primer ILL i l’evolució a llarg terme d’aquests pacients. Finalment, no hi ha estudis a la literatura sobre el perfil neuropsicològic de les diferents síndromes llacunars (segons Miller-Fisher) i la seva evolució a llarg terme.
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Luijckx, Gert-Jan Reinier. "Lacunar brain infarcts a clinical and pathogenetical study /." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1995. http://arno.unimaas.nl/show.cgi?fid=7285.
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Schmiedel, Janet, Georg Gahn, Rüdiger von Kummer, and Heinz Reichmann. "Cerebral Vasculitis with Multiple Infarcts Caused by Lyme Disease." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-135328.
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Schmiedel, Janet, Georg Gahn, Rüdiger von Kummer, and Heinz Reichmann. "Cerebral Vasculitis with Multiple Infarcts Caused by Lyme Disease." Karger, 2004. https://tud.qucosa.de/id/qucosa%3A27639.
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Marchbank, Gavin Clyde. "Posterior cerebral artery (PCA) infarcts and dreaming : a neuropsychological study." Master's thesis, University of Cape Town, 2013. http://hdl.handle.net/11427/14091.
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Recent case reports have shown that global loss of dreaming can result from medial occipitotemporal lesions. These findings have cast doubt on Solms's reformulation of Charcot-Wilbrand Syndrome (CWS) into two distinct disorders of dreaming, and caused substantial confusion in dream research as far as the neurological correlates of dreaming are concerned. This study attempted to confirm these case reports and determine whether there were any characteristics unique to the lesions among patients who had lost the ability to dream following damage to medial occipito-temporal cortex. Nine participants (three non-dreamers and six dreamers) who had suffered non-hemorrhagic infarction in the territory of the posterior cerebral artery were recruited in this study. Case histories and neuroradiological data were used to compare the lesion sites of non-dreamers with dreamers. It was confirmed that complete loss of dreaming could result from lesions in medial occipito-temporal cortex. It was found that non-dreamers always suffered bilateral cortical damage as opposed to dreamers who all suffered unilateral damage. The lesions in the non-dreamers tended to be more posterior than the dreamers. It was further speculated that concomitant damage to the thalamus or parietal areas played a role in the causation of heteromodal loss of dreaming. The implications of these findings were discussed in relation to CWS, Solms's dream system, and dream-function research. Finally, future directions were considered.
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Likens, Jacob Andrew. "The Pathophysiology of Chronic Stroke Infarcts| What Happens After Brain Tissue Dies?" Thesis, The University of Arizona, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10813111.
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<p> A stroke can occur when blood flow to a specific area of the brain is interrupted. There has been extensive research in both animal models and humans that has characterized the pathophysiology of the first few weeks following stroke. However, there has been far less research into the chronic stage of infarction. This is an important area for research because more than 10 million individuals worldwide suffer a stroke each year. Approximately one-third of these survivors develop dementia in the first year after their stroke. The cause behind this dementia is currently unclear, and there are no neuro-protective drugs that can improve recovery and provide cognitive protection in the chronic time period. Therefore, the chronic stage of stroke recovery is a promising target for future therapeutics for stroke-related dementia and, as will be shown later in the paper, Alzheimer’s disease as there are likely to be neurodegenerative processes that proceed for months following stroke. The goal of this thesis is to provide a review of what is currently known about the pathophysiology of chronic stroke infarcts (an area of brain tissue that has necrotized due to a blockage in an artery in the brain causing a lack of oxygen), explain why so little is known, and how we can learn more, and provide potential mechanistic links between the response to dead brain tissue and the development of dementia.</p><p>
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J?NCK, Fernanda. "A intoxica??o de bovinos por Pteridium (aquilinum) arachnoideum em Santa Catarina e a identifica??o das bact?rias envolvidas nos infartos do quadro agudo." Universidade Federal Rural do Rio de Janeiro, 2014. https://tede.ufrrj.br/jspui/handle/jspui/2306.
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Previous issue date: 2014-12-16<br>CAPES<br>Pteridium (aquilinum) arachnoideum is a cosmopolitan plant, responsible for heavy losses in cattle for heavy losses in almost all Brazil. This plant causes three clinical pictures: an acute disease, characterized by hemorrhages and fever, and two chronic diseases characterized by bladder tumors and carcinomas of the superior digestive tract. In Santa Catarina, in a retrospective study, the acute poisoning is the form that prevailed. Most of the cases ocurred in the autumn and the main clinical signs observed were fever and faeces with blood. The macroscopic lesions were widespread hemorrhages and infarcts mainly in lung, liver, intestine and lymphnodes, which were characterized by necrosis associated with groups of basophylic bact?ria, sometimes with formation of bubbles of gas. In the bone marrow there was rarefaction or absence of hematopoietic tissue. The experimental reproduction of the disease was realized in four cattle, two vaccinated against clostridioses and two not vaccinated. These cattle received doses of 20, 20, 14 and 10g/kg/day, and they died after 82, 94, 46 and 76 days, when they had ingested 149, 180, 71 and 75% of the plant in relation to their weight. The course of the clinical signs was 5, 4, 1 and 5 days, and at post-mortem examination the lesions found were hemorrhages of varied degrees and locations. Liver infarcts were found in bovines 2, 3 and 4, and in the intestine in all the cattle. The histological lesions were characterized by rarefaction and absence of hematopoietic tissue in the bone marrow, necrosis and bacterial aggregates in the liver, lung, intestine and lymphnodes. Histopathology did not reveal inflammatory reaction and if present the intensity was slight. Samples of organs with infarcts collected at necropsy, in the spontaneous and experimental intoxication, sown in Tarozzi medium, produced gas. Five samples caused death in mice after inoculation of the medium. At necropsy the carcasses had putrid smell, the subcutaneous tissue was red and there was edema and red liquid in the abdominal cavity. Two mice that were sacrificed presented inflammatory reaction in the place of the application, characterized by areas of adherence of the skin to the subcutaneous tissue and presence of abscesso, and four presented putrid smell at necropsy. The impression of of the liver capsula of the mice that died or got sick, revealed small Gram positive rods. Histopathology of the mice that died, revealed in the skeletal musculature of the thighs edema between the fibers with necrosis and eosinofilia of fibers and great amount of small basophylic rods, associated with slight inflammatory mononuclear infiltration and hemorrhage. In the skin also inflammatory filtrate was observed, with edema in the derma and great amount of small basophylics rods. The rest of the mice were sacrificed and no alterations were found. The identification by Chain reaction of Polimerase (PCR) of the liver of the mice that had died, in Tarozzi medium, resulted in Clostridium septicum.<br>Pteridium (aquilinum) arachnoideum ? planta cosmopolita, respons?vel por perdas vultuosas na cria??o de bovinos em quase todas as regi?es do Brasil. Esta planta ? respons?vel por causar tr?s quadros cl?nicos: um quadro agudo, caracterizado por hemorragias e febre, e dois quadros cr?nicos caracterizados por tumores de bexiga e do trato digest?rio superior. Em Santa Catarina, em estudo retrospectivo, a intoxica??o aguda ? a forma que prevaleceu sobre as demais. A maioria dos casos ocorreu no outono e os principais sinais cl?nicos observados foram febre e fezes com sangue. As les?es macrosc?picas encontradas foram hemorragias generalizadas e infartos principalmente em pulm?o, f?gado, intestino e linfonodo, os quais se caracterizavam por necrose associada a agregados bacterianos bas?filos, em alguns casos com forma??o de bolhas de g?s. Na medula ?ssea havia rarefa??o ou aus?ncia do tecido hematopo?tico. A reprodu??o experimental da doen?a foi realizada em quatro bovinos, dois vacinados contra clostridioses e dois n?o vacinados. Estes receberam doses de 20, 20, 14 e 10g/kg/dia de Pteridium (aquilinum) arachnoideum, e morreram com 82, 94, 46 dias e 76 dias, quando tinham ingerido 149, 180, 71 e 75% de planta em rela??o ao peso vivo. A evolu??o dos sinais cl?nicos foi de 5, 4, 1 e 5 dias, e, ? necropsia, as les?es consistiram de hemorragias em variados graus e localiza??es. Infartos de f?gado foram encontrados nos Bovinos 2, 3 e 4 e no intestino em todos os bovinos. As les?es histol?gicas se caracterizaram por rarefa??o e aus?ncia de tecido hematopo?tico na medula ?ssea, necrose e agregados bacterianos no f?gado, pulm?o, intestino e linfonodo. As les?es histol?gicas n?o revelaram rea??o inflamat?ria e quando presente, a intensidade era leve. Amostras de ?rg?os com infartos coletadas de necropsias nas intoxica??es espont?nea e experimental foram semeadas no meio de cultivo de Tarozzi e produziram g?s. Cinco amostras causaram a morte dos camundongos ap?s inocula??o do meio. ? necropsia desses camundongos verificou-se carca?as com cheiro p?trido, tecido subcut?neo avermelhado e com edema e l?quido avermelhado na cavidade abdominal. Dois camundongos que foram eutanasiados apresentaram rea??o inflamat?ria no local da aplica??o, caracterizada por ?reas de ader?ncia da pele com o tecido subcut?neo e abscessos; quatro exalavam cheiro p?trido na hora da realiza??o da necropsia. A impress?o da c?psula do f?gado dos camundongos que morreram e que ficaram doentes, revelou bastonetes Gram-positivos. ? histologia dos camundongos que morreram verificou-se na musculatura esquel?tica da regi?o da coxa, edema e hemorragia entre as fibras, necrose e eosinofilia de fibras e grande quantidade de bastonetes bas?filos, associado a infiltrado inflamat?rio mononuclear leve e hemorragia. Na pele tamb?m verificou-se, infiltrado inflamat?rio, com edema na derme e grande quantidade de bastonetes bas?filos. Os demais camundongos foram eutanasiados e n?o tiveram altera??es. A identifica??o por Rea??o em Cadeia de Polimerase (PCR) do meio de Tarozzi do f?gado dos camundongos que morreram foi detectado Clostridium septicum.
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Boon, Arthur Edwin. "Cardiac and vascular riskfactors in stroke the role of cardiac valve calcification and silent brain infarcts /." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1996. http://arno.unimaas.nl/show.cgi?fid=7392.
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Munro, N. A. R. "The control of saccadic and smooth pursuit eye movements in patients with lesions of the central nervous system." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319050.
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Nguyen, Thuy-Vi V., Jennifer B. Frye, Jacob C. Zbesko, et al. "Multiplex immunoassay characterization and species comparison of inflammation in acute and non-acute ischemic infarcts in human and mouse brain tissue." BIOMED CENTRAL LTD, 2016. http://hdl.handle.net/10150/622005.
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This study provides a parallel characterization of the cytokine and chemokine response to stroke in the human and mouse brain at different stages of infarct resolution. The study goal was to address the hypothesis that chronic inflammation may contribute to stroke-related dementia. We used C57BL/6 and BALB/c mice to control for strain related differences in the mouse immune response. Our data indicate that in both mouse strains, and humans, there is increased granulocyte macrophage colony-stimulating factor (GM-CSF), interleukin-6 (IL-6), interleukin-12 p70 (IL-12p70), interferon gamma-induced protein-10 (IP-10), keratinocyte chemoattractant/interleukin-8 (KC/IL-8), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1 alpha (MIP-1 alpha), macrophage inflammatory protein-1 beta (MIP-1 beta), regulated on activation, normal T cell expressed and secreted (RANTES), and Tumor necrosis factor-alpha (TNF-alpha) in the infarct core during the acute time period. Nevertheless, correlation and two-way ANOVA analyses reveal that despite this substantial overlap between species, there are still significant differences, particularly in the regulation of granulocyte colony-stimulating factor (G-CSF), which is increased in mice but not in humans. In the weeks after stroke, during the stage of liquefactive necrosis, there is significant resolution of the inflammatory response to stroke within the infarct. However, CD68+ macrophages remain present, and levels of IL-6 and MCP-1 remain chronically elevated in infarcts from both mice and humans. Furthermore, there is a chronic T cell response within the infarct in both species. This response is differentially polarized towards a T helper 1 (Th1) response in C57BL/6 mice, and a T helper 2 (Th2) response in BALB/c mice, suggesting that the chronic inflammatory response to stroke may follow a different trajectory in different patients. To control for the fact that the average age of the patients used in this study was 80 years, they were of both sexes, and many had suffered from multiple strokes, we also present findings that reveal how the chronic inflammatory response to stroke is impacted by age, sex, and multiple strokes in mice. Our data indicate that the chronic cytokine and chemokine response to stroke is not substantially altered in 18-month old compared to 3-month old C57BL/6 mice, although T cell infiltration is attenuated. We found a significant correlation in the chronic cytokine response to stroke in males and females. However, the chronic cytokine response to stroke was mildly exacerbated by a recurrent stroke in both C57BL/6 and BALB/c mice.
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Martin, Roswell James. "CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) : clinical features and approaches to genetic screening in the UK." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609947.
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Indja, Ben. "Subclinical brain injury after cardiac surgery." Thesis, University of Sydney, 2020. https://hdl.handle.net/2123/24086.
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Brain injury continues to be one of the most feared complications following cardiac procedures. While clinically overt cerebrovascular accidents are extremely well characterised and relatively rare under optimised conditions, at the other end of the spectrum, subclinical brain injury – which consists of post-operative cognitive dysfunction and silent brain infarcts (SBIs) – is poorly defined but of greater incidence. The lack of knowledge of subclinical brain injury is in large part due to lack of an objective means of measurement, meaning it is quantified using variable definitions and generally subjective clinical assessments. Structural magnetic resonance neuroimaging techniques are a potentially useful tool that can objectively characterise subclinical brain injury by providing a means to measure the neural network disruption that underlies even subtle cognitive and emotional deviations. The aim of this thesis was (i) to frame the true extent of the problem that is subclinical brain injury after cardiac surgery and (ii) to develop structural MRI techniques that might produce a biomarker to objectively measure neural network changes associated with subclinical brain injury.
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Sadauskienė, Eglė. "Papildomas adenozino vaidmuo mažinant infarkto dydį ir išsaugant kairiojo skilvelio funkciją pacientams, sergantiems ūminiu miokardo infarktu." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2011. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2011~D_20111102_110756-41335.
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Tyrime analizuojama adenozino, kuriuo papildoma įprastinė reperfuzinė terapija (perkutaninė koronarinė intervencija), įtaka mažinant infarkto dydį ir išsaugant kairiojo skilvelio funkciją pacientams, sergantiems ūminiu miokardo infarktu. Tyrimo metu siekta įvertinti PKI ir stentavimo būdu atveriant priekinės nusileidžiančios šakos spindį, kurio okliuzija sąlygojo kairiojo skilvelio priekinės sienelės ūminį miokardo infarktą, papildomai naudojamo adenozino įtaką mažinant miokardo išeminį-reperfuzinį pažeidimą, lėtos ar nutrūkusios tėkmės fenomeno pasireiškimą ir išplitimą. Reperfuzinės terapijos (PKI naudojant adenoziną ir PKI be adenozino) rezultatų ypatumai ir skirtumai palyginti dviejose homogeniškose pagal kontrolinius kintamuosius pacientų grupėse. Pasitelkus naujausius neinvazinius vaizdinimo metodus (miokardo perfuzijos radionuklidinę kompiuterinę tomografiją, transtorakalinę doplerinę echokardiografiją, dobutamino krūvio echokardiografiją) nustatyta, kad adenozinas, gerindamas kraujo tėkmės atstatymą ne tik stambiosiose vainikinėse arterijose, bet ir mikrocirkuliacijos grandyje, užtikrindamas adekvačią bei efektyvią miokardo reperfuziją, išsaugo miokardo kontraktilinį bei koronarinės tėkmės rezervus ūminio miokardo infarkto metu, mažina galutinį infarkto dydį, gerina bendrosios ir segmentinės kairiojo skilvelio kontraktilinės funkcijos atsistatymą praėjus 5 mėn. po reperfuzinio miokardo infarkto gydymo.<br>Study evaluates adenosine, which is used as an adjunct to conventional reperfusion therapy (percutaneous coronary intervention, i.e. PCI), role in reducing the infarct size and preserving the left ventricular function in patients with acute myocardial infarction. During the study we examined patients with the left ventricular anterior wall acute myocardial infarction (AMI), when PCI and stenting were used for infarct-related artery (IRA) re-opening. Study evaluates influence of complementary use of adenosine in reducing the myocardial ischemic-reperfusion injury, the manifestation of slow-reflow or no-reflow phenomenon. The results of reperfusion therapy with adjunctive adenosine and without adenosine were analyzed in two homogeneous patient groups. By using new non-invasive imaging methods (single photon emission computer tomography, transthoracic Doppler echocardiography, dobutamine stress echocardiography) it was estimated, that adenosine preserves myocardial contractility and coronary flow reserve during the acute phase of myocardial infarction, reduces the final infarct size, improves the recovery of left ventricular global and segmental contractile function at five months follow-up. Those results are achieved due to adenosine impact on improving blood flow restoration not only in major coronary arteries, but also at microcirculatory level and ensuring of adequate and effective myocardial reperfusion.
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Bonnin, Vilaplana Marc. "SAHS en els infarts cerebrals: Topografies relacionades, presència de Cheyne-Stokes i eficàcia d'un tractament precoç." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/398954.
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Estudis recents han demostrat una elevada freqüència de trastorns respiratoris del son (TRS) en pacients amb ictus.
Presentem els tres articles que formen part de la tesi doctoral:
Sleep-related breathing disorders in acute lacunar stroke.
J Neurol. 2009 Dec; 256(12):2036-42
L’objectiu va ser examinar la presència de TRS en pacients amb un primer infart lacunar. Es van estudiar 68 pacients amb infart lacunar i es va realitzar una poligrafia respiratòria. Un total del 69% dels pacients tenia un IAH ≥ 10, i un 25% tenia un IAH ≥ 30. Un 20,6% dels pacients tenien respiració de CS.
La combinació de les variables tabaquisme o afectació topogràfica a càpsula interna o protuberància va ser significativament més freqüent en pacients amb un IAH ≥ 10 que amb un IAH < 10 (80,9% vs 57,1%; p=0,04). Per altra banda, la combinació de les variables tabaquisme i afectació de la càpsula interna o protuberància va ser més freqüent en els pacients amb un IAH ≥ 30 respecte als pacients amb un IAH < 30 (29,4% vs 3,9%; p=0,001).
L’anàlisi multivariant mostrava una relació significativa i independent entre l’IAH ≥ 10 i el tabaquisme o l’afectació neurològica a la càpsula interna o a la protuberància (OR = 3.17, 95% IC 1.02-9.79; p=0,045); i entre l’IAH ≥ 20
amb l’afectació de la càpsula interna o la protuberància en fumadors (OR = 9.25, 95% IC 1.05-81.70; p=0.045).
Els infarts lacunars amb afectació de la càpsula interna i la protuberància en pacients fumadors s’associen a una major incidència de TRS.
Cheyne-stokes respiration in patients with first-ever lacunar stroke.
Sleep Disord. 2012; 2012:257890
Aquest segon treball valora la presència de respiració de CS en pacients amb infart lacunar, determinant la seva freqüència en aquests pacients i identificant les variables associades a aquest patró de respiració en aquesta mostra.
L’estudi va incloure 68 pacients ingressats per un primer infart lacunar. Es va observar respiració de CS en 14 pacients (20,6%).
Els pacients amb respiració de CS en comparació amb aquells sense respiració de CS, van mostrar una mitjana de l’IAH significativament més alt (IAH 34,9, DE 21,7) vs (IAH 18,5, DE 14,4; p=0,001), així com de l’ IAC (IAC 13,1, DE 13,8) vs (IAC 1,8, DE 3,4; p=0,0001), i presentaven majors puntuacions de l’índex de Barthel i l’escala neurològica canadenca i més dies d’ingrés hospitalari.
Es va poder observar una tendència a una major probabilitat de respiració de CS en els infarts lacunars amb disfunció motora possiblement per una lesió a la via piramidal.
Early treatment of obstructive apnoea and stroke outcome: a randomised controlled trial.
Eur Respir J. 2011 May; 37(5):1128-36.
L'objectiu d’aquest assaig clínic, multicèntric, va ser avaluar l'impacte del tractament amb CPAP en pacients amb ictus isquèmic en un seguiment a 2 anys. Els pacients amb un IAH ≥ 20 van ser aleatoritzats per rebre tractament
convencional de l'accident cerebrovascular i afegint el tractament amb la CPAP o el tractament convencional sense CPAP (grup control) durant la fase aguda de l'ictus.
El percentatge de pacients amb millora neurològica 1 mes després de l’ictus va ser major en el grup CPAP (Rankin 90,9 vs 56,3%, p=0,01; Canadenca 88,2 vs 72,7%, p=0,05). El temps mitjà fins a l'aparició d'esdeveniments cardiovasculars va ser superior en el grup CPAP (14,9 vs 7,9 mesos; p=0.044), tot i que la supervivència lliure d'esdeveniments cardiovasculars als 24 mesos i la taxa de mortalitat cardiovascular va ser similar als dos grups.
L'ús precoç de la CPAP després d’un ictus sembla accelerar la recuperació neurològica i pot retardar l'aparició d’esdeveniments cardiovasculars, malgrat no es va observar una millora en la supervivència dels pacients.<br>Sleep-related breathing disorders in acute lacunar stroke.
J Neurol. 2009 Dec; 256(12):2036-42
The purpose was to examine the occurrence of sleep-related breathing disorders (SRBD) and variables related to SRBD in patients with acute lacunar stroke. A total of 69.1% of patients showed AHI ≥10, 44.1% AHI ≥20, and 25% AHI ≥30. Cheyne-Stokes respiration (CSR) was present in 20.6% of patients.
In the multivariate analysis, smoking or capsular or pontine topographies were associated with AHI ≥10 (OR=3.17, 95%(CI) 1.02–9.79; P=0.045). Lacunes in the internal capsule or the pons in smokers were associated with AHI ≥20 (OR=9.25, 95%(CI) 1.05–81.70; P=0.045).
Smoker patients with capsular or pontine acute lacunar stroke should be screened for SRDB.
Cheyne-stokes respiration in patients with first-ever lacunar stroke.
Sleep Disord. 2012; 2012:257890
The aim of this single-center prospective study was to assess the presence CSR and CSR-related variables in 68 consecutive patients with radiologically proven first-ever lacunar stroke. CSR was diagnosed in 14 patients (20.6%).
Patients with CSR as compared with those without CSR showed a significantly higher scores of the Barthel index and the Canadian Neurological scale as a measure of stroke severity, and longer hospital stay.
The presence of CSR was associated with a trend towards a higher functional stroke severity and worse prognosis.
Early treatment of obstructive apnoea and stroke outcome: a randomised controlled trial.
Eur Respir J. 2011 May; 37(5):1128-36.
The aim of the present study was to assess the impact of nCPAP in ischaemic stroke patients followed for 2 yrs. Stroke patients with an AHI ≥ 20 events/h were randomised to early nCPAP (n571; 3–6 days after stroke onset) or conventional treatment (n569).
The percentage of patients with neurological improvement 1 month after stroke was significantly higher in the nCPAP group. The mean time until the appearance of cardiovascular events was longer in the nCPAP group (14.9 versus 7.9 months; p=0.044), although cardiovascular event-free survival after 24 months was similar in both groups.
Early use of nCPAP seems to accelerate neurological recovery and to delay the appearance of cardiovascular events, although an improvement in patients survival was not shown.
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Olivot, Jean-Marc. "Thrombomoduline et infarctus cérébral." Paris 5, 2006. http://www.theses.fr/2006PA05P618.
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La thrombomoduline (TM) est une glycoprotéine exprimée à la surface des cellules endothéliales (CE). La TM est le cofacteur de l'activation de la protéine C par la thrombine. La thrombine induit la prolifération des CE. Nous avons montré les extracellular regulated kinases 1&2 (ERK1 et 2) participaient au signal mitogène et que la liaison de la thrombine à la TM augmentait la durée de la translocation nucléaire de ERK1 et 2 induite par la thrombine. Nous avons montré dans l'étude cas témoin du profil Génétique de l'Infarctus Cérébral (GENIC), que l'élévation du taux de TM soluble (sTM) était associée avec une diminution du risque d'infarctus cérébral (IC) incident. Le suivi prospectif des cas a montré que le taux de sTM était associé avec une la mortalité des victimes d'un IC. Les 3 polymorphismes du gène de la TM (-1748G/C, -1208/-1209 delTT +1418 C/T) étaient déséquilibre de liaison. Ils n'influençaient pas les relations observées entre la sTM le risque et le pronostic de l'IC<br>Thrombomodulin (TM) is a glycoprotein found on endothelial cells (EC) surface. TM is the cofactor thrombin induced protein C activation. Thrombin induces EC proliferation. We found that extracellular regulated kinase 1&2 (ERK 1 et 2) are involved in mitogen signal and that thrombin binding to TM increased the duration of ERK1 and 2 nuclear translocation. We found among the subjects of the case control étude du profil Génétique de l'Infarctus Cérébral (GENIC) study, increased soluble (sTM) level is associated with a reduced risk of incident brain infarct (BI). The 5 years prospective follow up of cases found increased sTM level associated with the mortality of BI victims. Three TM gene polymorphisms (-1748G/C, -1208/-1209 delTT +1418 C/T) were tested. They were in linkage desequilibrium. They did not influence the relation observed between sTM, BI risk and prognosis
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Munsch, Fanny. "Pronostic après un infarctus cérébral : rôle de la localisation de la lésion." Thesis, Bordeaux, 2015. http://www.theses.fr/2015BORD0324/document.
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Dans ce travail de thèse, nous avons montré l'importance de l'imagerie, en sus de la clinique, et plus particulièrement de la localisation de la lésion ischémique, pour la prédiction de l'évolution d'un patient après un infarctus cérébral. Pour cela, nous avons utilisé une cohorte de 428 patients victimes d'un infarctus cérébral sus-tentoriel datant de 24 à 72 heures. Ces patients ont eu une évaluation clinique et un examen en imagerie par résonance magnétique à l'inclusion et ont été suivis à trois mois et à un an après l'ictus. À partir de cette cohorte, nous avons montré que la localisation précise de l'infarctus cérébral, définie à l'échelle du voxel avec la méthode Voxel-Based Lesion-Symptom Mapping, améliorait significativement le pronostic cognitif global évalué à trois mois après l'infarctus cérébral, et ce indépendamment des variables consensuelles comme la sévérité initiale, l'âge et le volume de la lésion. Par ailleurs, l'analyse de l'intégrité du faisceau cortico-spinal (CST) en tenseur de diffusion à la phase aigüe de l'infarctus cérébral a permis d'identifier un marqueur précoce de la dégénérescence wallérienne : le ratio du nombre de fibres initial (iFNR), défini comme le nombre de fibres du CST du côté ipsilatéral à l'infarctus cérébral normalisé par le nombre de fibres du CST du côté controlatéral. L'iFNR améliorait significativement la prédiction de la récupération motrice chez les patients ayant un déficit moteur initial sévère, alors que le score clinique initial seul ne le permettait pas<br>In this thesis works, we address the question of early outcome prediction after a cerebral infarct. In addition to clinical assessment, early MR Imaging of stroke location in eloquent regions and neuron fibers quantification improved the outcome prediction of cognitive functions and motor functions respectively. In that purpose, we used a large population of 428 patients with a supratentorial ischemic stroke between 24 and 72 hours after stroke onset. These patients were assessed with a magnetic resonance imaging and a clinical evaluation at baseline and were followed at three months and one year post-stroke. Using this stroke population, we demonstrated that an accurate stroke location, defined on a voxel basis with the Voxel-Based Lesion-Symptom Mapping method, significantly improved the prediction of global cognitive outcome assessed at three months post-stroke and was independent from classic predictors such as initial stroke severity, age and stroke volume. Furthermore, the analysis of corticospinal tract (CST) integrity using diffusion tensor imaging at the acute phase allowed to identify an early surrogate marker of wallerian degeneration : the initial fiber number ratio (iFNR) defined as the number of CST fibers from the ipsilateral side of stroke normalized by the number of CST fibers from the contralateral side. The iFNR significantly improved the prediction of motor recovery in stroke patients with an initial severe motor impairment, whereas initial clinical score alone could not
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Kaiser, Sylvie. "Infarctus du myocarde et météorologie." Montpellier 1, 1994. http://www.theses.fr/1994MON11147.
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Chillou, de Churet Christian de. "Potentiels tardifs et infarctus myocardique." Nancy 1, 1989. http://www.theses.fr/1989NAN11287.
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Salame, Boulos. "Myocardite et infarctus du myocarde." Université Louis Pasteur (Strasbourg) (1971-2008), 1991. http://www.theses.fr/1991STR1M175.
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LE, BLAN MANCHE CATHERINE. "Grossesse apres infarctus du myocarde." Lille 2, 1994. http://www.theses.fr/1994LIL2M109.
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Babin, Philippe. "Transport medicalise des infarctus du myocarde." Angers, 1989. http://www.theses.fr/1989ANGE1094.
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Godefroy, Olivier. "Les dysfonctionnements frontaux des infarctus laterostries." Lille 2, 1990. http://www.theses.fr/1990LIL2M226.
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Noichri, Yosri. "Stress oxydant et infarctus du Myocarde." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS479/document.
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L’infarctus du myocarde est l’une des principales causes de morbi-mortalité dans les pays développés, malgré l’amélioration enregistrée dans la prise en charge thérapeutique de cette urgence coronaire. Le stress oxydant est un facteur impliqué dans la physiopathologie de l’IDM. Notre étude a montré la diminution des capacités antioxydantes chez des patients hospitalisés pour un IDM aigu. Une partie de notre étude a été consacrée pour explorer le système Peroxyredoxine Thioredoxine. Il s’agit d’un système antioxydant majeur impliqué dans la régulation des voies d’apoptose. La connaissance des mécanismes moléculaires responsables des lésions myocardiques lors d’une ischémie, constitue l’une des avancées importantes dans la compréhension de la physiopathologie des syndromes coronaires aigus<br>Myocardial infarction is the leading cause of death in developed nations despite of recent advances in the management of this disease. Oxidative stress is involved in the physiopathology of Myocardial Infarction. Our study showed a decreased antioxidant activities in patients with Acute Myocardial Infarction. A part of the present study was designed to explore Peroxiredoxin Thioredoxin activity. It’s considered as a major antioxidant system and it control hydrogen peroxide levels which mediate the signal transduction, including apoptosis signal. Molecular mechanisms underlying the oxidative stress toxicity in cardiomyocytes have to be more elucidated and may help the evolving of therapeutic care strategies of coronary heart disease
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Grondin, Jean. "Infarctus par embolie de l'artère rénale." Bordeaux 2, 1994. http://www.theses.fr/1994BOR2M112.
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Santana, Eduardo Tadeu. "Caracterização da expressão gênica de vias de transdução do sinal no miocárdio remoto ao infarto induzido por ablação ventricular esquerda e oclusão da artéria coronária em ratos." Universidade Nove de Julho, 2015. http://bibliotecatede.uninove.br/handle/tede/1824.
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Previous issue date: 2015-12-18<br>The ligation of the anterior descending coronary artery is the most commonly used experimental model to induce myocardial infarction (MI) in rodents. A high mortality in the acute phase and the heterogeneity of the size of the MI obtained are drawbacks recognized in this model. In an attempt to solve the problem, our group recently developed a new MI experimental model which is based on application of myocardial ablation radio-frequency currents (AB-RF) that yielded MI with homogeneous sizes and significantly reduce acute mortality. In addition, cardiac structural and functional changes aroused by AB-RF were similar to those seen in animals with MI induced by coronary artery ligation. Herein, we evaluated modifications of gene expression that govern post-MI milieu in occlusion and ablation models. We analyzed 48 mRNA expressions of 9 different signal transduction pathways (signs of cell survival and metabolism, matrix extracellular, cell cycle, oxidative stress, apoptosis, calcium signaling, hypertrophy markers, angiogenesis and inflammation) in rat left ventricle 1 week after MI promoted by either coronary occlusion and AB-RF. Furthermore, high-throughput miRNA analysis was also assessed after either MI procedures. Interestingly, mRNA expression levels and miRNA expressions were similar in both models after MI, with few specificities in each model. This study reports for the first time the global changes in rat cardiac mRNA and miRNA contents after two different MI procedures and identifies key signaling regulators modulating the pathophysiology of these two models that might culminate in heart failure. Furthermore, these analyses would enhance our present knowledge regarding altered pathophysiology of these two different MI models.<br>A ligadura da artéria coronariana descendente anterior é o modelo experimental mais comumente usado para induzir o infarto do miocárdio (IM) em roedores. Entretanto, uma elevada taxa de mortalidade na fase aguda e a heterogeneidade do tamanho do IM obtidos são desvantagens reconhecidas neste modelo. Em uma tentativa de resolver o problema, o nosso grupo desenvolveu recentemente um novo modelo experimental de insuficiência cardíaca que se baseia na aplicação de correntes de radiofrequência ablação do miocárdio (AB-RF), produzindo IM com tamanhos homogêneos e com significativamente redução da mortalidade aguda. Além disso, alterações estruturais e funcionais do coração deste modelo foram semelhantes aos observados em animais com infarto induzido por ligação da artéria coronária. Aqui, nós avaliamos modificações da expressão de RNA mensageiro (RNAm) de genes após IM induzido por oclusão e ablação. Foram analisadas as expressões de 48 RNAm de 9 diferentes vias de transdução de sinal (sinais de sobrevivência celular e metabolismo, matriz extracelular, ciclo celular, estresse oxidativo, apoptose, sinalização de cálcio, marcadores de hipertrofia, angiogênese e inflamação) no ventrículo esquerdo de ratos uma semana após o IM promovido por oclusão coronária e AB-RF. Além disso, a análise de alto rendimento de miRNA também foi avaliada após ambos procedimentos de IM. Curiosamente, os níveis de expressão de RNAm e expressão de miRNA foram semelhantes em ambos os modelos após o IM, com algumas especificidades em cada modelo. Este estudo relata pela primeira vez as mudanças globais nos conteúdos de RNAm e miRNA após dois procedimentos de IM diferentes e identifica reguladores que podem modular a fisiopatologia desses dois modelos, culminando em insuficiência cardíaca.
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Trindade, Daniel de Castro. "Influ?ncia do sistema renina-angiotensina perif?rico e central no desenvolvimento de insufici?ncia card?aca em ratos." Universidade Federal Rural do Rio de Janeiro, 2008. https://tede.ufrrj.br/jspui/handle/tede/895.
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Previous issue date: 2009-02-28<br>The myocardial infarction was induced in rats by the permanent occlusion of left coronary artery in two different parts. In the first, infarcted rats were treated (CAPoral, 2g/L water) or not (INF) with oral captopril immediately after infarct and the whole experiment (21 days). In the second part, the infarcted rats were treated with captopril (CAPicv, 2 ?L 25 mg/mL/ 12-12 hours) or saline (SAL) intracerebroventricular (icv) during five consecutive days. The functional assessments were performed by electro (ECG) and echocardiogram before and after the experiment. The behavior study of water or hypertonic saline ingestion was performed in individual metabolic cages during the whole period of icv injections. The post-mortem assessment was performed in the end of each part. The ECG recorded from INF, CAPoral, SAL and CAPicv showed similar and indicative values of large myocardial infarction: decrease of QRS index amplitude, presence of Q wave in D1 and rightward deviation of the QRS axis. The main differences in the end of the treatment between INF and CAPoral groups were the prevention of P wave increase and attenuation in rightward deviation of the QRS axis in CAPoral. In the second part, there were no significant differences in ECG exam between infarcted groups. The ECO performed in the first part showed attenuation of the left atrial and ventricular dilatation, ejection fraction improvement and normalization of left ventricular filling only in CAPoral group. In the second part, ECO also showed that captopril treatment induced significative attenuation of left ventricular dilatation and improvement of ventricular filling similarly as captopril treatment by oral route. The study of fluids ingestion showed that CAPicv group exhibited less water ingestion if compared to SAL group. The hypertonic saline ingestion was not different between SAL and CAPicv groups. CAPoral group exhibited smaller scar tissue if compared to INF group. On the other hand, CAPicv group showed similar infarcted area to SAL group in histological study.<br>O infarto do mioc?rdio foi induzido em ratos pela oclus?o permanente da art?ria coron?ria esquerda em duas diferentes etapas. Na primeira, os ratos infartados foram tratados (CAPoral, 2g/L ?gua) ou n?o (INF) com captopril por via oral imediatamente ap?s o infarto e durante todo per?odo do experimento (21 dias). Na segunda etapa, os ratos infartados foram tratados com captopril (CAPicv, 2 ?L 25mg/mL/ 12-12 horas) ou salina (SAL) intracerebroventricular (icv) durante cinco dias consecutivos. As avalia??es funcionais foram realizadas por eletrocardiograma (ECG) e ecocardiografia (ECO) antes e ao final do experimento. O estudo comportamental de ingest?o de ?gua ou salina hipert?nica foi realizado em gaiolas metab?licas individuais durante todo per?odo de inje??es icv. A avalia??o post-mortem foi realizada no final de cada etapa. Os ECGs dos grupos INF, CAPoral, SAL e CAPicv apresentaram valores similares e indicativos de presen?a de infarto extenso do mioc?rdio como: diminui??o da amplitude do ?ndice QRS, presen?a de onda Q em D1 e desvio do vetor QRS para direita. As principais diferen?as ao final do tratamento entre os grupos INF e CAPoral foram a preven??o do aumento da onda P no grupo CAPoral e a atenua??o do desvio do vetor QRS para direita. Em rela??o aos animais da segunda etapa, n?o houve diferen?as significativas entre os grupos. No ECO realizado na primeira etapa, o grupo CAPoral mostrou atenua??o das dilata??es do ?trio e ventr?culo esquerdos, melhora na fra??o de eje??o e normaliza??o do padr?o de enchimento ventricular analisados pela t?cnica de Doppler. Na segunda etapa, o ECO mostrou que o tratamento com captopril promoveu redu??o significativa da dilata??o do ventr?culo esquerdo e melhora do enchimento ventricular. O estudo da ingest?o de fluidos mostrou que o grupo CAPicv apresentou menor ingest?o de ?gua quando comparado ao grupo SAL. O consumo de salina hipert?nica n?o foi significativamente diferente entre os grupos SAL e CAPicv. O grupo CAPoral apresentou menor tamanho de infarto quando comparado ao grupo INF, o que n?o foi observado no grupo CAPicv, que apresentou tamanho de infarto similar ao grupo SAL no estudo histol?gico.
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COLIN, REMY. "Infarctus du myocarde sans stenose coronaire significative." Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20828.
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VIGUE, ODILE. "Tachycardie ventriculaire post-infarctus et territoire coronarien." Aix-Marseille 2, 1992. http://www.theses.fr/1992AIX20801.
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BOUTTEN, BRIGITTE. "Demence thalamique par infarctus thalamique paramedian bilateral." Lille 2, 1988. http://www.theses.fr/1988LIL2M144.
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Nussbaum, Jeannette. "Embryonic stem cells for myocardial infarct repair /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/6312.
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Béjot, Yannick. "Infarctus cérébral et plasticité : focus sur le BDNF." Phd thesis, Université de Bourgogne, 2011. http://tel.archives-ouvertes.fr/tel-00939908.
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La récupération fonctionnelle des patients victimes d'un accident vasculaire cérébral (AVC) ischémique est largement sous-tendue par les propriétés plastiques du cerveau et plus précisément par sa capacité à remodeler les réseaux de neurones épargnés par l'infarctus. Les études réalisées sur différents modèles animaux d'infarctus cérébral s'accordent à montrer que ces changements plastiques sont induits par le BDNF (Brain-Derived Neurotrophic Factor). Aussi, augmenter les taux cérébraux de BDNF est considéré comme une stratégie thérapeutique prometteuse de réduction des déficiences post-AVC. Dans ce contexte, notre travail avait 2 objectifs : 1) chez le rat, identifier les cellules impliquées dans la surproduction de BDNF et évaluer la pertinence de la mesure des taux circulants de BDNF pour estimer les taux de BDNF présents dans le cerveau, 2) chez le patient victime d'un infarctus cérébral, étudier l'efficacité de la fluoxétine sur la récupération motrice à 3 mois, la fluoxétine étant un inhibiteur spécifique de la recapture de la sérotonine commercialisé comme antidépresseur et capable non seulement d'augmenter la production cérébrale de BDNF mais aussi de stimuler la plasticité post-lésionnelle.Les études précliniques ont été réalisées chez le rat soumis à l'embolisation unilatérale du cerveau par un nombre variable de microsphères (en carbone et calibrées à 50 µm) afin de reproduire le large panel de souffrance cérébrale rencontré en clinique. Le BDNF a été mesuré dans le cerveau et dans le sang (plasma et sérum par technique ELISA) avant et après (4, 24h et 8j) embolisation. Nos résultats montrent :- que la production de BDNF est plus intense et plus durable dans l'hémisphère embolisé que dans l'hémisphère non embolisé et que cette production est indépendante du degré d'embolisation, marqueur indirect de la souffrance cérébrale. - que les cellules non-neuronales deviennent une source non négligeable de BDNF en cas d'ischémie, notamment les cellules endothéliales et microgliales avant 24h et les astrocytes au temps 8j.- que les taux circulants et cérébraux de BDNF ne sont pas corrélés mais qu'il existe une corrélation entre le BDNF plasmatique mesuré au temps 4h et le degré d'embolisation.L'étude clinique correspond à un essai randomisé contrôlé en double aveugle comparant la fluoxétine (20mg/j, voie orale, pendant 3 mois et débutée entre 5 et 10j après les premiers symptômes) au placebo chez des patients présentant un déficit moteur modéré à sévère sur l'échelle motrice de Fugl-Meyer (n=59 dans chaque groupe). Nos résultats montrent que l'amélioration de la fonction motrice est meilleure sous fluoxétine que placebo. En conclusion, notre travail montre l'intérêt des médicaments capables d'augmenter le BDNF et la plasticité post-lésionnelle pour améliorer le pronostic clinique de l'AVC et identifie pour la première fois les cellules endothéliales cérébrales comme une cible potentielle de ces médicaments. Il remet également en cause l'idée largement répandue selon laquelle les taux circulants de BDNF varient dans le même sens que les taux cérébraux.
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BERTHELON, DIDIER. "Meningite a pneumocoque et infarctus cerebelleux chez l'enfant." Lyon 1, 1990. http://www.theses.fr/1990LYO1M167.
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GUERIOT, CLAUDE. "Les infarctus cerebraux jonctionnels : analyse de 53 observations." Aix-Marseille 2, 1988. http://www.theses.fr/1988AIX20378.
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Castro, González Lidia. "Estudio de las subunidades reguladas por SUR1 (Kir6.2 y TRPM4) en las contusiones cerebrales traumáticas y la isquemia cerebral focal. Desarrollo de un modelo animal de infarto maligno en cerdo." Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/668009.
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El traumatismo craneoencefálico (TCE) tiene un gran impacto socio-económico y sanitario en todo el mundo, y es una de las principales causas de mortalidad y discapacidad entre la población adulta menor de 40 años. El infarto cerebral maligno, es un tipo de infarto cerebral isquémico, que tiene una mortalidad de alrededor del 80%, y su incidencia aumenta con la edad del paciente. Ambas patologías se caracterizan porque su evolución puede provocar graves desequilibrios iónicos a nivel de las neuronas y de las células gliales, con el consecuente arrastre osmótico de agua y la formación de edema citotóxico. El edema puede evolucionar provocando un efecto de masa que causa la compresión, deformación y herniación de las estructuras cerebrales, pudiendo provocar la muerte del paciente, debido entre otras cosas al aumento de la presión intracraneal (PIC). Los TCEs y los infartos malignos se abordan siguiendo las mismas estrategias de tratamiento, que pasan por el seguimiento de la evolución de la lesión, la monitorización multimodal del paciente, y en último caso su intervención quirúrgica.
Entender los procesos implicados en la patofisiología del TCE y del infarto, es esencial para su correcto tratamiento. Muchos de los estudios actuales, dirigen su atención a los mecanismos implicados en la formación del edema citotóxico inicial, y en concreto al estudio de un nuevo canal iónico involucrado en su progresión. Este canal está formado por una subunidad reguladora que recibe el nombre de receptor de sulfonilurea 1 (SUR1) y una subunidad formadora de poro, el receptor de potencial transitorio de la melastatina 4 (TRPM4). Juntos constituyen el canal SUR1-TRPM4, que ha demostrado estar sobre-expresado en pacientes y modelos animales de TCE e infarto cerebral, entre otras patologías. El bloqueo de este canal con fármacos como la glibenclamida (un inhibidor de sulfonilureas), ha demostrado mejorar el pronóstico neurológico en modelos animales de roedores y estudios clínicos con pacientes. La subunidad reguladora SUR1, además de asociarse con TRPM4, también regula la apertura de canales de potasio dependientes de adenosín trifosfato (ATP)(KATPs), entre los que se encuentra el canal iónico rectificador de entrada de potasio 6.2 (Kir6.2). El canal SUR1-Kir6.2 ha sido estudiado ampliamente en células del páncreas y cardiomiocitos, entre otros. Sin embargo, la expresión de este canal no ha sido estudiada en profundidad a nivel cerebral en humanos. Este canal acopla el metabolismo de la célula a la actividad eléctrica, mediante la regulación del flujo de K+ a través de la membrana celular. Se considera que tiene una función neuroprotectora, induciendo la hiperpolarización celular durante episodios de hipoxia y/o isquemia.
Lo que esta tesis pretende es, en primer lugar, el desarrollo de un nuevo modelo animal de isquemia regional en cerdo común, que sea estable y reproducible. Este modelo permitirá una mejor comprensión de los procesos isquémicos que tienen lugar en pacientes que han sufrido un infarto cerebral maligno, para poder extrapolarlos en un segundo paso a las lesiones cerebrales traumáticas. El uso de modelos animales es esencial para conseguir una mejor comprensión de los mecanismos implicados en cualquier patología, así como para poder desarrollar nuevas estrategias protectoras contra esta. En segundo lugar, se pretende profundizar en el estudio de los canales regulados por SUR1, en concreto Kir6.2, el menos estudiado a nivel del SNC en humanos hasta la fecha. Para ello, se estudió su expresión en tejido pericontusional cerebral de humanos con la pretensión de conocer mejor su función en este tipo de patologías.<br>Traumatic brain injury (TBI) has a great socio-economic and sanitary impact in the whole world and is one of the leading causes of mortality and disability in adult population with less than 40 years. Malignant cerebral infarction is a type of ischemic cerebral infarct that has an elevated mortality of around 80%, and its incidence increases with the age of the patient. The evolution of both pathologies can lead to severe ionic disarrangements in neurons and glial cells, osmotic water displacement and cytotoxic edema formation. Edema can evolve causing a mass effect that leads to compression, deformation and herniation of the cerebral structures that can result in patient’s death, due to the increase of the intracranial pressure (ICP), among other causes. TBIs and malignant infarcts are treated following the same strategies, which are the monitoring of lesion evolution, multimodal monitoring of the patient and as a last resort, surgical intervention.
Understanding the processes involved in the pathophysiology of the TBI and cerebral infarct, is essential for their correct treatment. Many of the current studies, focus their attention on the mechanisms involved in the formation of the initial cytotoxic edema and specially, in the study of a new ionic channel that is related to the progression of the edema. This channel is constituted by a regulator subunit named sulfonylurea receptor 1 (SUR1) and a pore forming subunit called transient receptor potential melastatin 4 (TRPM4). Both subunits together form the channel SUR1-TRPM4 that is overexpressed in patients and in animal models of TBI and cerebral infarct, among other pathologies. The blockage of this channel with drugs like glibenclamide (an inhibitor of sulfonylureas), has demonstrated to improve neurological outcome in rodent animal models and also in clinical assays with patients. Regulator subunit SUR1 is not only associated to TRPM4, but also regulates the opening of adenosine phosphate (ATP)-sensitive potassium channels (KATPs), which include the inwardly rectifier potassium ion channel 6.2 (Kir6.2). The channel SUR1-Kir6.2 has been well studied in pancreatic and cardiac cells, among others. However, the expression of this channel has not been deeply studied in the human brain. This channel couples cell metabolism to electric activity, regulating the K+ flux through the cell membrane. It is considered that it has a neuroprotective function, inducing the cell hyperpolarization during hypoxic and/or ischemic episodes.
The aim of this doctoral thesis is, first of all, the development of a new animal model of regional ischemia in common pig, stable and reproducible. This model will allow a better understanding of the ischemic processes that occur in patients with a malignant cerebral infarction, to extrapolate it in second place to traumatic brain lesions. The use of animal models is essential to achieve a better understanding of the mechanisms involved in any pathology, and to develop new treatment strategies. The aim of the second part of this thesis was to study in detail the channels regulated by SUR1, and especially Kir6.2 channel, the less studied in human brain to the date. For this purpose, Kir6.2 expression was studied in human pericontusional brain tissue, with the aim to achieve a better understanding of its function in this kind of pathologies.
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Rosendahl, Lene. "Infarct size and myocardial function : A methodological study." Doctoral thesis, Linköpings universitet, Klinisk fysiologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-53943.
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The size of a myocardial infarction (MI) and the concurrent effect on left ventricular (LV) function are essential for decisions regarding patient care and treatment. Images produced with the late gadolinium enhancement (LGE) technique visualize the scar with high spatial resolution. The general aim of this thesis was to study methods to assess scar size in chronic MI, primarily with the use of LGE, and to relate area‐at‐risk and LV function to scar size. Myocardial perfusion single photon emission computed tomography (MPS) is a well established technique for the assessment of MI size. Our study showed that there is a fairly good agreement between MPS and LGE in the determination of scar size. Wall motion score index (WMSI) correlated moderately with both infarct size and infarct extent determined with LGE. Manual delineation of myocardium and scar is time consuming and subjective and there is a need for help in objective assessment. We showed that the semi‐automatic computer software, Segment, reduced the evaluation time ≥50% with maintained clinical accuracy. The segmented scar sequence ‐ inversion recovery fast gradient echo, IR_FGRE, is a well documented sequence for scar determination, however, the sequence requires regular heart rhythm and breath holding for good imaging. We showed that a single shot scar sequence ‐ steady state free precession, SS_SSFP ‐ acquired under free breathing in patients with ongoing atrial fibrillation, had significantly better image quality than IR_FGRE. The scar size and the error of determination were equal for both sequences and the examination time was shorter with SS_SSFP. In an acute MI it is essential to know the myocardial area‐at‐risk. WMSI is clinically the most common way of assessing LV function, but is highly subjective. Tissue Doppler imaging with strain measurements is considered objective and quantitative in assessing both global and regional LV function compared to WMSI. Our results showed that WMSI is superior to strain for the detection of scar with transmurality ≥50% in patients with acute MI. Also WMSI correlated better than strain on all levels (global, regional, segmental) with final scar size determined with LGE. LGE images visualize myocardial scar much more distinctly than any other modality. This new technique needs clinical validation but promises intense competition with existing modalities such as myocardial scintigraphy and echocardiography. However, in individual patient care all modalities should be used according to their own advantages and limitation.
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Flynn, Erin Patricia. "Experimental infarct mitigation with hyperoxia at normobaric pressure." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0020/MQ55207.pdf.
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Fredenrich, Alexandre. "Infarctus du myocarde et troubles de la tolerance glucidique." Nice, 1988. http://www.theses.fr/1988NICE6050.
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Turpin, Béatrice. "Les infarctus pulmonaires pseudotumoraux : a propos de 5 observations." Lille 2, 1993. http://www.theses.fr/1993LIL2M050.
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SMADJA, DANIELE. "Potentiels tardifs : etude retrospective sur 213 coronariens avec infarctus." Lille 2, 1988. http://www.theses.fr/1988LIL2M382.
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LUCCHINI, PIERRE. "Les infarctus laterobulbaires : correlations clinico-irm, etiologie et pronostic." Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20857.
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Karam, Nicole. "Infarctus du myocarde et mort subite : approche en population." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066331/document.
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La mort subite est un problème majeur de santé publique. Plus de 75% des morts subites sont d'origine coronaire et la mort subite est le principal mode de décès des infarctus du myocarde (IDM). Une analyse des similitudes et associations entre les deux est nécessaire. Les IDM survenant en heures non ouvrables ont une mortalité accrue. Par une analyse des données du registre francilien du Centre d'Expertise Mort Subite, nous avons constaté une surmortalité en dehors des heures ouvrables suite à une prise en charge initiale moins optimale, la prise en charge médicalisée n’étant pas influencée par l'horaire. Il devient clair que les efforts devraient se focaliser sur la prise en charge très précoce de la mort subite pour améliorer son pronostic.La deuxième partie a visé à identifier, parmi les IDM, ceux à risque de mort subite préhospitalière, afin d’anticiper sa survenue. A partir du registre e-MUST des IDM en Ile-de-France, nous avons identifié 5 facteurs associés à un risque accru de mort subite pré-hospitalière (âge jeune, absence de diabète et d'obésité, dyspnée, délai court entre le début de douleur et l'appel des secours). Nous avons ainsi créé et validé en interne et externe, un score de risque de mort subite<br>It becomes clear that efforts should focus on early SCA management. The second part therefore aimed on identifying, among STEMI patients, those at risk of pre-hospital SCA, to plan early SCA management before it occurs. In the e-MUST registry for STEMI in the Greater Paris Area, we identified 5 simple predictors of pre-hospital SCA (young age, absence of obesity, absence of diabetes mellitus, shortness of breath, and short delay between pain onset and call to emergency medical services) that we used to build an SCA prediction score that we validated internally and externally. The first minutes after SCA are the main determinants of its prognosis and should ideally be planned before its occurrence. Anticipation of SCA in STEMI, the main cause of SCA, is feasible, allowing to tailor STEMI management accordingly. Even though the generalizability of this strategy to other causes of SCA remains to be demonstrated, a promising path for decreasing SCA burden can be foreseen
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Martin, Bertrand. "Deficits en proteine c ou s et infarctus cerebraux." Amiens, 1993. http://www.theses.fr/1993AMIEM016.
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FROISSARD, ERIC. "Infarctus renal par embolie : a propos de trois cas." Lille 2, 1990. http://www.theses.fr/1990LIL2M340.
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Vilar, Bergua Andrea. "Utilidad de los biomarcadores en el diagnóstico de la enfermedad cerebrovascular silente." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/386549.
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Hoy en día, las enfermedades cerebrovasculares tienen un impacto muy importante en la sociedad en países desarrollados, en el nuestro, son una causa muy frecuente de hospitalización, muerte y discapacidad. Además, el envejecimiento de la población conlleva un incremento en la incidencia de estas enfermedades, así como del coste sanitario asociado.
Desde hace años, sabemos que los infartos cerebrales pueden darse en ausencia de síntomas acompañantes sugestivos de ictus y en ese caso, hablamos de infartos cerebrales silentes o encubiertos, que en conjunto son cinco veces más frecuentes que el ictus clínico. La mayoría de ellos son infartos lacunares y suceden en el contexto de una enfermedad de pequeño vaso cerebral (EPVC), por lo que coexisten con otros marcadores radiológicos, tales como las lesiones de la sustancia blanca, microsangrados o espacios perivasculares dilatados. El estudio de la enfermedad de pequeño vaso cerebral en estas etapas iniciales o pre-sintomáticas podría contribuir al mejor conocimiento de los mecanismos que conducen a la enfermedad y así facilitar el desarrollo de medidas preventivas eficaces para reducir la incidencia de las mismas y de sus complicaciones (riesgo de ictus futuros y demencia).
En esta Tesis Doctoral hemos realizado una revisión bibliográfica que ha puesto de manifiesto que el número de estudios centrados en el uso de biomarcadores para la detección temprana de los signos de EPVC mediante la identificación de las lesiones cerebrales silentes o subclínicas se ha incrementado en los últimos años. Sin embargo, hasta la fecha no se ha conseguido establecer la capacidad diagnostica de los biomarcadores o su papel en la discriminación de las lesiones silentes junto a factores clínicos, que puedan justificar su utilidad clínica.
Los estudios previos tienen como limitaciones la heterogeneidad en las definiciones utilizadas de las lesiones de la enfermedad de pequeño vaso cerebral, la falta de replicación de los resultados en cohortes independientes y la inclusión de marcadores candidatos individuales en la mayor parte de casos. Por otra parte, se precisan estudios longitudinales para evaluar la progresión de las lesiones y su relación con los biomarcadores.
En esta tesis doctoral se recogen resultados del estudio de biomarcadores en una población hipertensa de entre 50 y 70 años de edad, sin antecedentes de ictus o demencia previos. Se trata de un sustrato adecuado para el estudio del inicio de la enfermedad de pequeño vaso puesto que la hipertensión es un factor de riesgo vascular establecido. Hemos seleccionado biomarcadores novedosos en el campo pero prometedores por su actividad biológica (fosfolipasa A2 ligada a lipoproteínas, NT-proBNP, perfil de N-glicosilación en suero, cociente albumina-creatinina en orina), como candidatos para la predicción de lesiones identificadas en la resonancia magnética cerebral (infartos cerebrales silentes, lesiones de la sustancia blanca y otros marcadores). Hemos analizado las lesiones definidas en la resonancia magnética por separado, y en conjunto, como un escenario más fisiológico de la enfermedad, mediante la aplicación de una escala de enfermedad de pequeño vaso cerebral ya descrita previamente. Se han aplicado criterios estadísticos para valorar la utilidad de los biomarcadores junto con variables clínicas de obtención en la práctica clínica habitual.
El estudio de estos y otros biomarcadores, en el contexto de la enfermedad de pequeño vaso cerebral, además de facilitar el diagnóstico, puede proporcionar información de los mecanismos subyacentes en esta etapa pre-clínica, y podrían ser útiles como dianas terapéuticas o para monitorizar la progresión de la enfermedad.<br>Nowadays cerebrovascular diseases have a major social impact; they are a commonly associated with increased rates of hospitalization, morbidity and mortality. Furthermore, it is expected that ageing will increases the incidence of cerebrovascular diseases and their associated healthcare costs.
Cerebral infarcts occurring without stroke-like symptoms are known as silent or covert cerebral infarcts; they are five times more common than symptomatic stroke. Most of them are lacunar infarcts and they appear associated with other imaging markers of cerebral small vessel disease, as white matter hyperintensities, microbleeds or dilated perivascular spaces. Research on cerebral small vessel disease pre-clinical or pre-symptomatic stages may potentially improve the knowledge of the leading and involved disease pathways, and the development of prevention approaches aimed to reduce their incidence and associated complications (such as stroke and dementia).
In this Thesis, we have performed a bibliographic literature review, and found that the number of studies regarding biomarker usefulness in the early detection of small vessel disease by identification of silent or subclinical cerebral lesions have increased for the last years. However, the use of biomarkers with diagnostic purposes to detect silent brain lesions has not been already established, so clinical their usefulness is still not justified.
Previous studies limitations are heterogeneity regarding cerebral small vessel disease lesions definitions, the lack of replication in independent cohorts and the use of individual candidate biomarkers. Also longitudinal studies are needed to evaluate lesions progression and biomarkers associations.
In this Thesis we also included biomarker study results, based on a hypertensive stroke and dementia-free population, 50-70 years old. This is a suitable population for the study of the onset of the disease, since hypertension is an established vascular risk factor.
Magnetic resonance imaging-defined lesions where analyzed individually, and then combined in a previously described cerebral small vessel disease score being the latter a more physiologic condition.
Statistic criteria were applied to evaluate the usefulness of the clinical models including the selected biomarkers, in the clinical practice.
Small vessel disease biomarkers study can improve diagnosis of silent brain cerebrovascular lesions and also provide information regarding preclinical stage leading pathways. They can be useful as therapeutic and disease progression monitoring targets.
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Lahosa, Marie-Line Aguilar. "Infarctus du myocarde, thrombolyses en phase aigue͏̈ par streptokinase intra-veineuse : expérience du Centre hospitalier de Béziers, janvier-juin 1987." Montpellier 1, 1988. http://www.theses.fr/1988MON11022.
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Génelot, Sylvie. "L'évolution de l'infarctus du myocarde récent au centre hospitalier général de Bagnols-sur-Cèze : étude prospective à propos de 110cas." Montpellier 1, 1989. http://www.theses.fr/1989MON11063.
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Faure, Erick. "Logistique pour une meilleure prise en charge des malades atteints d'infarctus du myocarde à la phase aigüe." Saint-Etienne, 1988. http://www.theses.fr/1988STET6040.
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Caldentey, Adrover Guillem R. "Paper del sistema GAS6-TAM en el remodelat ventricular post infart agut de miocardi." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/663844.
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La reparació cardíaca postinfart agut de miocardi és un procés actiu on la inflamació i la esferocitosi de cèl·lules apoptòtiques són factors clau. La inflamació és molt variable entre individus i una resposta excessiva pot tenir conseqüències catastròfiques a nivell tissular. El sistema proteínic de lligam-receptor GAS6-TAM intervé en la modulació de la resposta inflamatòria i la esferocitosi, i s´ha relacionat amb la fibrosi en diverses patologies.
En aquest treball es mesuren els nivells plasmàtics de GAS6 i del receptor AXL (forma part dels receptors TAM) en la fase aguda i als 6 mesos, en 227 pacients amb infart amb elevació del segment ST sotmesos a angioplàstia primària, i es comparen amb una població control. S´avalua la relació entre aquests marcadors i la presència d´insuficiència cardíaca, remodelat ventricular i fibrosi miocàrdica remota, mesurada mitjançant el càlcul del volum extracel·lular (VEC) per ressonància magnètica en la fase aguda i als 6 mesos.
Hem detectat un augment progressiu dels valors de sAXL (part soluble de AXL) des de la fase aguda fins als 6 mesos postinfart, fet que suggereix una activació del sistema GAS6-TAM en el moment de l´infart agut, que es manté durant tot el procés de cicatrització. A més, aquest augment en els nivells de sAXL és més pronunciat en pacients que presenten insuficiència cardíaca, sense que hi hagi correlació amb els nivells de pèptid natriurètic atrial, marcadors de necrosi miocàrdica ni els paràmetres de disfunció ventricular esquerra. Els valors de sAXL són més alts en els pacients que desenvolupen remodelat ventricular advers (augment >20% en el diàmetre telediastòlic del ventricle esquerre entre la ressonància inicial i als 6 mesos) i es correlacionen també amb la fibrosi miocàrdica difusa (mesurada en els segments miocàrdics no infartats).
Donats els resultats obtinguts, és raonable pensar que el sistema GAS6-TAM intervingui en processos d´inflamació i reparació miocàrdica a llarg termini.
El fet que els nivells de AXL circulant en la fase aguda de l´infart es correlacionin amb el remodelat advers durant el seguiment i amb la fibrosi miocàrdica difusa, fan plantejar que la detecció precoç d´aquesta proteïna pugui ser útil com a marcador pronòstic. Al ser un marcador independent de la determinació de BNP o el tamany de l´infart, ajudaria a identificar aquells potencials casos on valdria la pena intensificar la supressió del sistema renina-angiotensina-aldosterona o del sistema simpàtic durant els mesos posteriors a l´esdeveniment coronari. El fet que els nivells de sAXL siguin més alts en pacients amb insuficiència cardíaca, confirma l´important paper que juga aquest sistema en la inflamació crònica i el seu potencial valor pronòstic.
Per altra banda, s´han evidenciat menors nivells plasmàtics del lligam GAS6 en la fase aguda en els pacients amb infart en comparació al grup control. Aquests nivells augmenten durant els 6 mesos posteriors, arribant a valors comparables amb els controls sans. Aquest fet fa pensar que els menors nivells de GAS6 plasmàtic estarien associats a un major risc d´esdeveniments aguts, i podria utilizar-se com un marcador de risc, podent-se intensificar el control dels factors de risc cardiovascular i el tractament amb estatines en aquells pacients amb nivells més baixos.
El sistema GAS6-TAM podria intervenir en una nova via molecular relacionada amb la inflamació tissular i vascular i la insuficiència cardíaca.<br>During the acute phase of an ST-segment elevation myocardial infarction (STEMI), necrotic myocytes are progressively replaced by fibrotic tissue by an active and complex process involving multiple cell types. Inflammation is highly variable across individuals and an excessive response can have catastrophic consequences. The GAS6-TAM system (ligand-receptor) play an important role in inflammation regulation and efferocytosis after cardiac injury.
In the present work, plasmatic GAS6 and AXL (TAM receptor) levels were measured in the acute phase and at 6 months after STEMI in 227 patients treated with primary percutaneous coronary intervention and are compared with a control group.
A progressive increase in plasma AXL levels were found after STEMI suggesting that GAS6–TAM activation is triggered at the moment of the acute event and remains activated during the healing period. Patients who presented heart failure and cardiac remodeling had higher AXL values. Plasma AXL levels also correlated with the extracellular volume (ECV) measured by T1 mapping in the remote myocardium. It is reasonable to speculate whether the GAS6–TAM system, and particularly AXL, may be involved in myocardial repair processes at long-term. This contribution may be independent of other biomarkers as natriuretic peptides or troponin, more related to the necrotic extension.
These results suggest that early monitoring of plasma AXL levels after STEMI could be useful as a prognostic marker to identify those patients in whom a more aggressive renin-angiotensin-aldosterone system suppression and beta-blocker titration could be necessary.
On the other hand, lower GAS6 (ligand) levels were detected in the acute phase after STEMI compared to a control group, probably reflecting a higher risk for cardiovascular events. These levels increased after 6 months being comparable to the control group. Low plasma GAS6 levels could be used as a cardiovascular risk marker and could help to identify those patients in whom a more aggressive statin treatment deserve consideration.
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Burford, Evans J. "Myocyte Derived Cardiac Spheroids for Post Infarct Cardiac Regeneration." Digital WPI, 2014. https://digitalcommons.wpi.edu/etd-theses/145.
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Research has shown that autologous progenitor-like cardiac spheroids, when delivered to an infarcted heart, are able to restore mechanical function. These spheroids are made by isolating and expanding autologous cardiac progenitor cells. Though these results are promising, the process for creating cardiac spheroids is inefficient and time consuming, requiring a large amount of cardiac tissue. For every 10,000 cardiac myocytes in the heart there is only one cardiac progenitor cell; requiring a large amount of initial tissue. This clinical limitation could be overcome if cardiac myocytes, which are more abundant than cardiac progenitor cells, could be used to make cardiac spheroids. Research has shown that mesenchymal stem cells when co-cultured with adult cardiac myocytes cause the cardiac myocytes to behave like a progenitor cell. We found that, when co-cultured with mesenchymal stem cells, cardiac mycoytes could be made to form cardiac spheroid bodies. This was done by isolating adult myocytes from rat hearts and co-culturing them with human mesenchymal stem cells. After two weeks, cultures were observed to form spheroid bodies and the number of spheroids formed were compared to a pure myocyte control. Cardiac specific staining confirmed that the spheroids were made from the myocytes. It was also found that the mesenchymal stem cells, when co-cultured in the same well with the myocytes, form significantly more spheroids than myocytes treated with stem cell conditioned media. Further, no other cell type present in the co-cultures are able to create spheroid bodies when co-cultured with mycoytes or stem cells. The ability to create cardiac spheroid like bodies from adult myocytes offers a way to overcome the limitations of the time needed and the large quantity of autologous cardiac tissue required to currently make these types of bodies.