Academic literature on the topic 'Fibrose cardiaque'
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Journal articles on the topic "Fibrose cardiaque"
Samuel, Jane-Lise, and Claude Delcayre. "La fibrose cardiaque." Bulletin de l'Académie Nationale de Médecine 201, no. 4-6 (April 2017): 775–84. http://dx.doi.org/10.1016/s0001-4079(19)30460-1.
Full textCaudron, J., Y. Arous, J. Fares, V. Lefebvre, and J. N. Dacher. "Fibrose endomyocardique dans le cadre d’un syndrome hyperéosinophilique : apport de l’IRM cardiaque." Journal de Radiologie Diagnostique et Interventionnelle 93, no. 10 (October 2012): 838–40. http://dx.doi.org/10.1016/j.jradio.2011.07.023.
Full textFassnacht, F., F. Ackermann, T. Sene, I. Marroun, O. Bletry, and J. E. Kahn. "Transplantation cardiaque pour une fibrose endomyocardique liée à une leucémie chronique à éosinophiles." La Revue de Médecine Interne 34 (June 2013): A153. http://dx.doi.org/10.1016/j.revmed.2013.03.154.
Full textTerrier, B., A. Dechartres, H. Gouya, A. Régent, B. Dunogué, P. Cohen, A. Berezne, et al. "La fibrose myocardique microscopique évaluée par séquences mapping T1 en IRM cardiaque permet de prédire les événements cardiaques au cours de la sclérodermie systémique." La Revue de Médecine Interne 39 (December 2018): A43. http://dx.doi.org/10.1016/j.revmed.2018.10.285.
Full textJeanson, L., A. Fevet, M. P. Blanchard, A. D. Lajoix, B. Jover, and C. Desmetz. "Prévention de la fibrose cardiaque par un régime alimentaire pauvre en sel au cours du syndrome métabolique : implication de la transition endothélio-mésenchymateuse." Nutrition Clinique et Métabolisme 34, no. 1 (April 2020): 32–33. http://dx.doi.org/10.1016/j.nupar.2020.02.228.
Full textHumez, Sarah, Jean-Baptiste Gibier, Morgan Recher, Stéphane Leteurtre, Xavier Leroy, and Louise Devisme. "Le fibrome cardiaque : une cause rare de mort subite de l’enfant." Annales de Pathologie 35, no. 5 (October 2015): 445–48. http://dx.doi.org/10.1016/j.annpat.2015.05.004.
Full textDissertations / Theses on the topic "Fibrose cardiaque"
Eschalier, Romain. "Fibrose et insuffisance cardiaque." Thesis, Clermont-Ferrand 1, 2013. http://www.theses.fr/2013CLF1MM12/document.
Full textNo abstract available
Grimbert, Lucile. "Régulation du métabolisme énergétique cardiaque par l’AMP kinase : Implication dans l’insuffisance cardiaque et effet du sexe biologique." Thesis, Université Paris-Saclay (ComUE), 2019. http://www.theses.fr/2019SACLS430/document.
Full textAMPK is a metabolic sensor which phosphorylates a various number of substrates in order to maintain cellular energetic homeostasis. In the heart, a protective role of AMPK has been demonstrated in pathological models, nevertheless the tissue, the metabolic and the sexual specificity of those effects has not been fully investigated. Thus, we generated a mice model of AMPKalpha2 deletion, the major cardiac isoform, specifically induced in the heart and at adult age after tamoxifen injection. At basal condition, AMPKalpha2 deletion lead to a progressive systolic dysfunction of the left ventricle and to the development of fibrosis only in males. Sixteen weeks after the deletion induction, these alterations were associated to a decrease of the mitochondrial respiration initiated by complex I of the observed in these KO male mice respiratory chain which could be linked to a cardiolipin species remodeling and to an increase of complex I proportion which is not integrated in supercomplexes. These effects induced by AMPKalpha2 deletion were not observed in KO female mice; however the cardiac fibrosis and the cardiolipins remodeling were found in KO female mice with ovariectomy. These last results tend to confirm an involvement of AMPK in fibrosis regulation and membrane cardiolipin composition and highlight a sexual dimorphism which could be due to female hormones. Analysis of a similar study in a pathological model is ongoing in order to specify the AMPK cardioprotective effects
Vergaro, Giuseppe. "Galectin-3 and aldosterone profibrotic pathways in the failing heart." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC235.
Full textBackgroundGalectin-3 (Gal-3) is biologically linked to the process of inflammation and fibrosis in heart failure (HF). The renin-angiotensin-aldosterone system (RAAS) has been largely demonstrated to exert profibrotic, prohypertrophic and proinflammatory effects in the pathophysiology of HF. Further, there is initial experimental evidence that Gal-3 and RAAS may interplay in the development of cardiovascular damage in hypertensive models. However, such interaction has not been investigated in the setting of left ventricular (LV) dysfunction and HF. We aimed therefore to test the following hypotheses:1. Gal-3 participates in the mechanisms of aldosterone mediated cardiac fibrosis and tissue remodeling in a murine model of LV dysfunction;2. Gal-3 level is associated with the development of LV remodeling and fibrosis and can predict the effects of neurohormonal antagonism in patients with chronic HF due to non-ischemic dilated cardiomyopathy (NIDCM).Methods1. Adult male mice with cardiac-specific hyperaldosteronism (AS) underwent isoproterenol subcutaneous injections (200 mg/kg x 2/day over two days), to be then randomized to receive placebo, a Gal-3 inhibitor (modified citrus pectin, MCP), an aldosterone antagonist (potassium canrenoate), or MCP+canrenoate for 14 days.2. We enrolled 150 patients with a diagnosis of NIDCM. All patients underwent a comprehensive clinical and biohumoral evaluation, including Gal-3 assay, 2-D echocardiography, and a contrast-enhanced cardiac magnetic resonance (CMR) for the assessment of LV volumes and fibrosis by the late gadolinium enhancement (LGE) technique. A smaller cohort of 70 patients also received soluble suppression of tumorigenicity protein 2 (sST2) assay at baseline as well as a follow-up CMR after 24 months for the evaluation of LV reverse remodeling, defined as a >10 percentage units increase in LV ejection fraction or a >10% decrease in LV end-diastolic volume indexed.ResultsIsoproterenol induced a rapid and persistent decrease in LV systolic function which was markedly improved by treatment with either MCP or canrenoate. MCP and canrenoate also reduced cardiac hypertrophy and fibrosis and the expression of genes involved in fibrogenesis (Coll-1 and Coll-3) and macrophage infiltration (CD-68 and MCP-1). The combined use of antagonists of Gal-3 and aldosterone resulted in enhanced effects on cardiac hypertrophy, inflammation, and fibrosis, when compared to MCP or canrenoate alone. In our cohort of NIDCM patients, median Gal-3 value was 14.4 ng/mL; LGE was detected in 106. Patients with LGE had higher Gal-3 than those without (p=0.006). Among univariate predictors of LGE, Gal-3 maintained its predictive value at multivariate analysis, together with sex, hypertension, disease duration and right ventricular ejection fraction. At follow-up CMR, 35 patients showed reverse remodeling. Gal-3, but not sST2 resulted as an independent predictor of LV reverse remodeling at multivariate analysis.ConclusionGal-3 participates in mechanisms of aldosterone-mediated myocardial damage in murine model of HF. Likewise, in the clinical setting of NIDCM, Gal-3 seems to be associated with LV fibrosis and to the evolution of cardiac remodeling, possibly identifying the subset of patients with a more pronounced response to pharmacological neurohormonal antagonism
Moubarak, Majed. "Étude des effets du peptide natriurétique atrial sur les fibroblastes : implication physiopathologique dans le remodelage cardiaque." Thesis, Poitiers, 2014. http://www.theses.fr/2014POIT2312/document.
Full textANP is a cardiac hormone released during heart failure and acts as a regulator of the extracellular matrix (ECM). Cardiac fibroblasts are responsible for the synthesis of ECM components and acquire under pathological conditions the capacity to differentiate into myofibroblasts, leading to cardiac fibrosis. Regulatory mechanisms involving ANP and its receptors (NPR) are poorly known and make the subject of our work. Ventricular fibroblasts were isolated from Wistar rat hearts and cultured to induce differentiation. The cultures were then subjected to various treatments involved in the ANP/NPR pathway. ANP decreases the proliferation rate, cell migration and collagen secretion. This effect was mimicked by 8-Br-cGMP. In addition, genomic and proteomic analysis confirmed the presence of the natriuretic receptor A and B in our cells. Furthermore, the expression of ten phosphodiesterases isoforms in the myofibroblasts was revealed by genomic screening. The non-selective inhibition of these phosphodiesterases causes a decrease in the proliferation and secretion of collagen. Finally, the intracellular concentrations of cAMP and cGMP were increased in the presence of ANP. In parallel, the characterization of ionic currents present in myofibroblasts revealed the absence of rapid sodium and potassium ATP-dependent currents. This study shows the role of the ANP/NPR/cGMP pathway in modulating fibroblast properties and exposes the complexity of the cell differentiation process during cardiac fibrogenesis
Bun, Sok-Sithikun. "Quantification non invasive de la fibrose cardiaque diffuse par imagerie de résonance magnétique et par cartographie endocavitaire." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0235/document.
Full textFibrosis represents the main substrate for cardiac arrhythmias, either atrial or ventricular. MRI has become a critical tool to not only diagnose the presence of cardiac fibrosis, but also provides important informations on the prognosis and the follow-up of patients with atrial fibrillation (AF), especially in its persistent type. The gold standard is the Late Gadolinium Enhancement, allowing to reveal localized regions of fibrosis. Our study reported a technique for non invasive quantification of interstitial diffuse ventricular fibrosis in diabetic mice (T2 measurement high field MRI at 11,75 T). This fibrosis was significantly correlated to the occurrence of ventricular arrhythmias in comparison with the control group. The next step was the transposition of this T2 measurement with MRI in the clinical setup of patients who undergo an AF ablation procedure. The second technique for atrial fibrosis assessment for patients suffering from AF is the invasive realization of left atrial voltage mapping. A new ultra-high definition system was used to quantify the fibrosis (dense scar) in regions with bipolar amplitude electrograms of less than 0,015 mV. This cutoff was far lower than the previously published definition of the dense scar in the literature (< 0,1 mV)
Tannous, Cynthia. "Rôle de la nicotinamide riboside kinase 2 dans le remodelage cardiaque pathologique." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066107/document.
Full textDilated cardiomyopathy (DCM) is a severe heart disease characterized by reduced ejection fraction, altered systolic function, extracellular matrix disorganization and metabolic defects. In different mice models of DCM, the expression of the nicotinamide riboside kinase 2 (Nmrk2) implicated in the synthesis of NAD, a major coenzyme in energy metabolism and a signaling molecule, is increased. NMRK2 is similar to the muscle integrin binding protein (MIBP) that binds to the integrin α7β1 heterodimer. The role of Nmrk2 in the heart is unknown. Young Nmrk2-KO mice develop a normal cardiac hypertrophic response to angiotensin-II exposure and transverse aorta constriction (TAC) but follow-up echocardiography until 8 weeks post-TAC and during aging from 5 to 24 months revealed a more severe decrease in the EF and the development of a DCM phenotype. RT-qPCR analysis of cardiac mRNAs showed an increase in the slow, cardiac, β myosin heavy chain isoform starting at 12 months. NMRK2 was not essential to maintain myocardial NAD levels in response to pro-hypertrophic treatments and in young adults. However Nmrk1 and Nampt expression level declined strongly with aging and Nmrk2-KO mice displayed a 50% reduction in myocardial NAD levels at 24 months. The α7β1 integrin complex was repressed at this age. Immunofluorescent analyses and electron microscopy revealed a defect in laminin deposition and enlarged intercellular space in the Nmrk2-KO heart. The Nmrk2 gene is required to preserve cardiac function and structure during aging and becomes indispensable for maintaining NAD at late age. Molecular characterization of compounds modulating this pathway could give future therapeutic prospect
Poinsignon-Clique, Hélène. "Mise en place d'une mesure quantitative du T1 en IRM cardiaque." Thesis, Université de Lorraine, 2012. http://www.theses.fr/2012LORR0363/document.
Full textT1 mapping is a useful quantitative MR technique for cardiac tissue characterization. Several studies have shown that T1 measurements are correlated with fibrosis, which is observed in cardiac diseases such as cardiomyopathy or myocardial infarction. However, cardiac T1 mapping remains challenging, mainly because of long acquisition times and interference from cardiac and respiratory motions. T1 quantification on the human myocardium is generally performed on breath-hold with 2D specific sequences. Unfortunately these sequences are scanner specific and poorly available for clinical use. To overcome these limitations, we propose a new method based on a 3D clinical sequence. This technique, using a variable flip angle approach that integrates B1 correction, was adapted in cardiac imaging. Phantom tests were used to select the optimal parameters and to show the method reproducibility. Then, the method was validated with a volunteer study using double synchronization (cardiac and respiratory). Moreover, a reconstruction method integrating physiological signals of motion was also used to perform T1 quantification in free breathing and to reduce the total acquisition time. The myocardial T1 values on volunteers ranged between 1289 ± 66 ms and 1376 ± 43 ms, which was in good agreement with previously published works. These studies allow the use of T1 mapping in patients with better characterization of pathologies and a better adaptation to therapeutic strategies
Biquand, Ariane. "De la caractérisation de la cardiomyopathie dilatée à la modulation à visée thérapeutique des voies de signalisation impliquées dans le phénotype cardiaque de myopathies d’origine génétique." Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASE004.
Full textDilated cardiomyopathy (DCM) is the most common form of heart disease associated with genetic myopathies. It is characterized by myocardial hypokinesia and dilation of the heart chambers, which are linked to significant cardiac remodeling with cardiomyocyte damage and fibrosis. DCM is currently the leading cause of heart failure and heart transplantation. Among the myopathies, titin and dystrophin deficiencies are 2 of the most frequent forms associated with cardiac damage. Titin is a giant protein that plays a crucial role in the integrity of the sarcomere and passive muscle tension, especially in the heart. Dystrophin, encoded by DMD, is a structural protein of the sarcolemma, essential for maintaining the architecture and integrity of muscle fibers during muscle contraction. Mutations in DMD leads to Duchenne muscular dystrophy. The objective of this study was from the characterization of 2 models carrying mutations in the 2 genes of interest, to define modified molecular pathways which could be targeted by therapeutic approaches. Characterization of the skeletal muscle and heart of the titin model was made on morphological, functional and molecular levels. The characterization highlights a cardiac phenotype of DCM with decrease in systolic function and dilation of the left ventricle associated with fibrotic tissue. The dystrophin model was already characterized in the literature. The evaluation of the cardiac transcriptome by RNA sequencing in the 2 models allowed identification of common molecular cascades implicated in heart failure. Finally, the effect of modulating these pathways on the cardiac phenotype of the titin model, the most severe, was evaluated by pharmacological inhibitors and by gene transfer vectors targeting highly dysregulated genes. The modulation of these pathways allowed the decrease of some DCM parameters in the model. These modulations will now be carried out on the dystrophin model in order to define if these approaches can be generalized and therefore represent a target for generic approaches of dilated cardiomyopathy
Robert, Valérie. "Developpement de la fibrose cardiaque au cours de l'hypertension arterielle et du vieillissement chez le rat." Clermont-Ferrand 2, 1995. http://www.theses.fr/1995CLF21698.
Full textPrud'homme, Mathilde. "Rôle de galectine-3 dans la dysfonction cardiaque après agression rénale aiguë." Thesis, Sorbonne Paris Cité, 2018. https://theses.md.univ-paris-diderot.fr/PRUDHOMME_Mathilde_2_20180316.pdf.
Full textThe type 3 Cardio-Renal Syndrome (CRS-3) refers to an Acute Heart Failure (AHF) secondary to an Acute Kidney Injury (AKI). The pathophysiology of CRS-3 is complex and still poorly understood. The aim of this thesis is to highlight the role of Galectin-3 (Gal-3), a protein involved in inflammation, fibrosis and cardiac remodeling, in a mouse model of CRS-3.Prior to work involving the kidney, we found that Gal-3 was a key effector of cardiac remodeling in response to acute isoprenaline stress (Vergaro et al., 2014).In a murine model of renal ischemia/reperfusion (RIR) with contralateral nephrectomy we have shown that RIR induces transient renal dysfunction (peak of creatinine and urea at 24 hours post-RIR and return to normal at 72h) and an early rise (at 6h) in the amount of plasmatic pro-inflammatory cytokines. At the cardiac level, there was an increase in biomarkers of aggression (BNP and QSOX1-mRNAs) and inflammation (CD68, MCP1 and Galectin-3-mRNA) in the 72 hours following the surgery. At a later time, 28 days, renal IR induced inflammation and cardiac fibrosis and led to cardiac dysfunction (-10% of the shortening fraction). To determine the role of Gal-3 in this model, WT mice were treated with MCP (Modified Citrus Pectin, a Gal-3 inhibitor) before (J-3) or after (J+1) surgery, and Gal-3 KO mice were also used. The pharmacological inhibition of Gal-3 (MCP) or genetic, prevented the increase of plasmatic pro-inflammatory cytokines, the onset of cardiac fibrosis and cardiac dysfunction at day 28 post-RIR. In order to validate results obtained in the first model and to dissociate the cardiac effects of renal dysfunction, we performed the same analyzes in another model of renal injury that does not induce renal dysfunction. This model consists of an unilateral ureteral occlusion (UUO). The results obtained confirm the model of CRS-3, with the appearance at D28 post-UUO of cardiac fibrosis and dysfunction. Gal-3 seemed as equally involved as in the first model because its inhibition by MCP prevented heart damage.Subsequently, WT and Gal-3 KO mice were subjected to bone marrow transplantation. The WT mice were grafted with Gal-3 KO bone marrow (BM) and vice versa (WTKO BM and KOWT BM). The chimeric mice obtained did not express (WTKO BM) or express (KOWT BM) Gal-3 only in bone marrow-derived cells. These results show that in WTKO BM, with a specific Gal-3 deletion in bone marrow-derived cells, RIR did not induce fibrosis or cardiac dysfunction at D28.The overall results highlight the emergence of acute cardiac injury in response to an acute kidney injury leading at long term to cardiac dysfunction. These effects are prevented in Gal-3 KO mice or MCP treated mice. These results show that Galectin-3, and specifically Gal-3 from bone marrow derived-cells (probably macrophages), has a key role in cardiac damage after renal aggression
Book chapters on the topic "Fibrose cardiaque"
Cohen, Frédéric, Nicolas Amabile, Philippe Dory-Lautrec, Guillaume Louis, Arthur Varoquaux, Vincent Vidal, Jean-Michel Bartoli, Jean-Yves Gaubert, Guy Moulin, and Alexis Jacquier. "Thrombus et fibrose endomyocardique." In Collection de la Société française d’imagerie cardiaque et vasculaire, 59–61. Paris: Springer Paris, 2009. http://dx.doi.org/10.1007/978-2-287-99695-5_12.
Full textStephan, Eric, and Philippe Douek. "Fibrome intramyocardique." In Collection de la Société française d’imagerie cardiaque et vasculaire, 85–89. Paris: Springer Paris, 2009. http://dx.doi.org/10.1007/978-2-287-99695-5_18.
Full textBoyer, L., E. Dumousset, N. Mazet, A. Ravel, A. Alfidja Lankoande, and P. Chabrot. "Embolisation utérine pour fibromes." In Collection de la Société française d’imagerie cardiaque et vasculaire, 315–31. Paris: Springer Paris, 2012. http://dx.doi.org/10.1007/978-2-287-99170-7_19.
Full textConference papers on the topic "Fibrose cardiaque"
Lafont, J., J. H. Catherine, M. Lejeune, U. Ordioni, R. Lan, and F. Campana. "Manifestations buccales de la sclérose tubéreuse de Bourneville." In 66ème Congrès de la SFCO. Les Ulis, France: EDP Sciences, 2020. http://dx.doi.org/10.1051/sfco/20206603014.
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