A 64 years old male was submitted to the surgical substitution of a deteriorated biological aortic valve prosthesis with a new Hancock II biological prosthesis. The implantation was not followed by an anticoagulation or antiaggregation therapy. Two months later he was checked at our Institution because he complained symptoms and developed echocardiographic indexes suggestive of an aortic prosthesis obstruction by a clot. Both symptoms and the echocardiographic indexes of prosthesis obstruction faded away after giving warfarin; they arose again when the anticoagulation therapy was stopped and was replaced by aspirin. The following permanent use of warfarin normalized both clinic and echocardiographic aspects. The present case report underlines the utility of early controls after a biological prosthesis, yet aortic, implantation, when it is not followed by an anticoagulant therapy, also in subjects free from thrombosis high risk factors.
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http://dx.doi.org/10.4081/monaldi.2014.43 | DOI Listing |
J Transl Int Med
February 2024
Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University; NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Peking University; Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China.
Background And Objective: Hemodynamic changes that lead to increased blood pressure represent the main drivers of organ damage in hypertension. Prolonged increases to blood pressure can lead to vascular remodeling, which also affects vascular hemodynamics during the pathogenesis of hypertension. Exercise is beneficial for relieving hypertension, however the mechanistic link between exercise training and how it influences hemodynamics in the context of hypertension is not well understood.
View Article and Find Full Text PDFCell Discov
January 2025
Key Laboratory of Organ Regeneration and Reconstruction, State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Hematopoietic stem and progenitor cells (HSPCs) are critical for the treatment of blood diseases in clinic. However, the limited source of HSPCs severely hinders their clinical application. In the embryo, hematopoietic stem cells (HSCs) arise from hemogenic endothelial (HE) cells lining the major arteries in vivo.
View Article and Find Full Text PDFPLoS Biol
January 2025
Cardiovascular Institute and Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Definitive hematopoietic stem and progenitor cells (HSPCs) arise from a small number of hemogenic endothelial cells (HECs) within the developing embryo. Understanding the origin and ontogeny of HSPCs is of considerable interest and potential therapeutic value. It has been proposed that the murine placenta contains HECs that differentiate into HSPCs.
View Article and Find Full Text PDFElife
January 2025
Instituto Gulbenkian de Ciência, Rua da Quinta Grande, Oeiras, Portugal.
During the trunk to tail transition the mammalian embryo builds the outlets for the intestinal and urogenital tracts, lays down the primordia for the hindlimb and external genitalia, and switches from the epiblast/primitive streak (PS) to the tail bud as the driver of axial extension. Genetic and molecular data indicate that Tgfbr1 is a key regulator of the trunk to tail transition. Tgfbr1 has been shown to control the switch of the neuromesodermal competent cells from the epiblast to the chordoneural hinge to generate the tail bud.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
January 2025
Vascular Biology Center and Department of Medicine, Medical College of Georgia at Augusta University, Augusta, GA USA.
The contribution of sex hormones to cardiovascular disease, including arterial stiffness, is established; however, the role of sex chromosome interaction with sex hormones, particularly in women, is lagging. Arterial structural stiffness depends on the intrinsic properties and transmural wall geometry that comprise a network of cells and extracellular matrix (ECM) proteins expressed in a sex-dependent manner. In this study, we used four-core genotype (FCG) mice to determine the relative contribution of sex hormones versus sex chromosomes or their interaction with arterial structural stiffness.
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