Letteratura scientifica selezionata sul tema "Insuffisance cardiaque – Étiologie"
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Articoli di riviste sul tema "Insuffisance cardiaque – Étiologie":
Tounkara, Alhadji Ahmadou, Nouhoum Coulibaly, Idrissa Sissoko e Mahamane Kalil Maiga. "Problem of management of obstetrical renal insufficiency in the department of nephrology, CHU Point G". Batna Journal of Medical Sciences (BJMS) 3, n. 1 (29 giugno 2016): 32–34. http://dx.doi.org/10.48087/bjmsoa.2016.3106.
Parrot, A., G. Voiriot, A. Canellas, A. Gibelin, J. M. Nacacche, J. Cadranel e M. Fartoukh. "Hémorragies intra-alvéolaires". Médecine Intensive Réanimation 27, n. 4 (luglio 2018): 331–43. http://dx.doi.org/10.3166/rea-2018-0060.
Yayehd, K., T. Tcherou, W. D. Ziga, S. Pessinaba, Y. T. Abena, M. M. Matelbe, N. W. N'da, E. K. Togbossi, S. Baragou e F. Damorou. "Profil du patient africain porteur d’une cardiomyopathie dilatée dans un hôpital universitaire de Lomé". Journal de la Recherche Scientifique de l’Université de Lomé 26, n. 1 (18 aprile 2024): 81–89. http://dx.doi.org/10.4314/jrsul.v26i1.15.
Hess, OM. "Insuffisance cardiaque: définition, étiologies et classifications". Forum Médical Suisse ‒ Swiss Medical Forum, 26 novembre 2003. http://dx.doi.org/10.4414/fms.2003.05039.
Tesi sul tema "Insuffisance cardiaque – Étiologie":
Decoin, Raphaël. "Impact de la stéatohépatite non alcoolique sur le remodelage myocardique et sur les complications cardiovasculaires". Electronic Thesis or Diss., Université de Lille (2022-....), 2023. https://pepite-depot.univ-lille.fr/ToutIDP/EDBSL/2023/2023ULILS066.pdf.
Cardiac remodeling is a pathophysiological phenomenon during which the cardiac muscle undergoes structural alterations at both tissue and cellular levels, leading to functional changes. The clinical implications are diverse, including the development of atrial fibrillation and heart failure. Among the numerous risk factors identified, Non-Alcoholic Fatty Liver Diseases (NAFLD) have an emerging role. This liver disease, characterized by steatosis, inflammation, and fibrosis, is associated with the development of myocardial pathologies.In this study, we hypothesize that NAFLD specifically triggers characteristic cardiac remodeling at both histological and functional levels. To explore this hypothesis, we employ a translational approach using various cohorts from the Lille University Hospital, as well as a murine model of NAFLD. Three distinct objectives have been defined: 1) demonstrate an association between atrial remodeling and NAFLD in patients; 2) propose an early diagnostic method for cardiac remodeling; 3) propose mechanistic hypotheses for the liver-heart connection through a translational methodology. Firstly, we characterized atrial cardiac remodeling in a cohort of patients indicated for atrial fibrillation ablation. Among these patients, we observed a positive association between the progression of hepatic pathology (assessed through clinical-biological scores) and, on one hand, dilation and impaired contractility of the left atrium as estimated by echocardiography, and on the other hand, the presence of areas with low extracellular voltages. This remodeling profile was also linked to a poor prognosis of ablation. In a second cohort of patients scheduled for cardiac surgery (POMI-AF), we demonstrated greater fibrosis in the atrial myocardium of patients with a high-risk NAFLD-related fibrosis compared to those without NAFLD. Next, using the same POMI-AF cohort, we showed that quantifying myocardial fat (intracardiomyocytic lipid droplets) using VARPRO MRI sequence is a robust, reliable, and feasible analysis in NAFLD-affected patients. Lastly, in a murine model of NAFLD developed in the laboratory (high-fat, sucrose, and cholesterol diet for 24 weeks), we described the presence of cardiac remodeling. Mice subjected to the NAFLD-inducing diet developed diastolic dysfunction with preserved ejection fraction, assessed by echocardiography, in comparison to the control diet group. This loss of function was associated with concentric left ventricular hypertrophy. Histologically, this hypertrophy was explained by an increase in the cross-sectional diameter of cardiomyocytes, which was also associated with diffuse interstitial fibrosisstarting from a vascular point. These observations were more pronounced with higher hepatic involvement, reinforcing the initial hypothesis. Total ventricular mRNA sequencing revealed a significantly altered transcriptional profile in NAFLD-affected mice, indicating impaired energy metabolism and a profound immune signature. Subsequently, flow cytometry analysis of immune populations revealed macrophage and dendritic cell infiltration in the myocardium, similar to what is observed in NAFLD liver. This macrophage infiltration was also evident in human biopsies from patients with advanced NAFLD.In conclusion, we demonstrate that NAFLD-associated cardiac remodeling affects both the left atrium and the left ventricle. Additionally, we have shown that quantifying cardiac lipid droplet accumulation is feasible using MRI. Finally, the myeloid infiltration observed in the myocardium of NAFLD patients and in our murine model suggests a potential link between hepatic dysimmunity and cardiac remodeling
Badat, Rahfick. "Sclérodermie et insuffisance aortique : à propos d'un probable cas et revue de la littérature". Bordeaux 2, 2000. http://www.theses.fr/2000BOR2M075.