Publications by authors named "P Lacolley"
Inflammatory bowel disease (IBD) displays an increased venous and arterial thrombotic risk despite the common occurrence of intestinal bleeding. While some of the mechanisms leading to these thrombotic complications have been studied, other specific changes in the hemostasis profile of IBD patients have been less explored. One such example relates to von Willebrand factor (VWF) whose plasma levels have been reported to be modulated in IBD.
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- The text highlights the critical role of elastic properties in conductance arteries for maintaining proper blood flow and their dysfunction's link to aging and cardiovascular diseases.
- It reviews important factors contributing to arterial stiffness, focusing on vascular smooth muscle cell behavior and various biological mechanisms influencing this condition.
- The article emphasizes recent clinical studies that are reshaping treatment approaches for arterial stiffness, advocating for personalized strategies based on individual cardiovascular risks.
Aims: Although the risk of thrombosis is well documented for inflammatory bowel disease [IBD] patients, the underlying pathological mechanism seems to be different from other thrombotic conditions. Determining the factors responsible for the increased risk of thrombosis in IBD would help to improve the management of this frequent complication.
Methods: We studied the interplay between platelets, coagulation, and von Willebrand factor [VWF] in 193 IBD patients and in experimental models [acute and chronic] of colitis in wild-type and VWF-deficient mice.
Background: The effect of factor VIII (FVIII) or emicizumab on thrombin generation is usually assessed in assays using synthetic phospholipids. Here, we assessed thrombin generation at the surface of human arterial cells (aortic endothelial cells [hAECs] and aortic vascular smooth muscle cells [hVSMCs]).
Objectives: To explore the capacity of hAECs (resting or stimulated) and hVSMCs to support thrombin generation by FVIII or emicizumab.