Changements hémostatiques du syndrome métabolique, de l'hypertension artérielle, et de l'insuffisance cardiaque : approches physiologique et physiopathologique

Abstract : Increasing life span has made heart failure (HF) a major issue for public health. The metabolic syndrome (MetS) and hypertension are two important factors which can lead to HF. Structural and cellular modification occurring in the arterial wall in the MetS, hypertension and HF may provoke hemostasis alterations that can worsen the clinical situation. We have shown in this work, hemostasis modifications in animal models of pathologies implicated in HF development. Hemostasis alterations were shown to precede functional modifications of the arterial wall and could favor HF development in Zucker rats. Spontaneously hypertensive rats showed an arterial wall hypercoagulability via smooth muscle cells. These results don't permit the implication of hypertension in the hypercoagulable state found in the Zucker rat. A mouse model with aldosterone receptor activation in the endothelium lead to a hypocoagulable state by increasing the protein C anticoagulant system via his receptor, the EPCR. Studying a human HF patient cohort permitted the measurement of cardiac function and of arterial stiffness parameters. This characterization is important to understand thrombosis events associated with HF in humans. The general conclusion of this work is that, in pathologies leading to HF, modification of hemostasis to a procoagulable state, implicates the arterial wall
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Jérémy Lagrange. Changements hémostatiques du syndrome métabolique, de l'hypertension artérielle, et de l'insuffisance cardiaque : approches physiologique et physiopathologique. Médecine humaine et pathologie. Université de Lorraine, 2013. Français. ⟨NNT : 2013LORR0160⟩. ⟨tel-01750341⟩

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