Aims: We aimed to validate a new scoring system based on extent of cardiac damage for risk stratification in patients undergoing transcatheter aortic valve replacement (TAVR) in a real-world cohort and to examine the addition of baseline albumin in risk assessment.
Methods And Results: We investigated 2608 patients undergoing TAVR. Subjects were divided into five groups based on their echocardiography findings.
Background: In contrast to surgical aortic valve replacement, left ventricle (LV) hypertrophy (LVH) had not been clearly associated with mortality following transcatheter aortic valve replacement (TAVR).
Methods: We performed a retrospective analysis of patients enrolled in the Israeli multicenter TAVR registry for whom preprocedural LV mass index (LVMI) data were available. Patients were divided into categories according to LVMI: normal LVMI and mild, moderate, and severe LVH.
Increased inflammatory response after aortic valve replacement is linked to higher postprocedural mortality. The aim of the present analysis was to assess the impact of baseline statin therapy on procedural outcomes and mortality after transcatheter aortic valve implantation (TAVI). We performed a retrospective analysis on patients who underwent TAVI stratified to 3 statin therapy groups: high-intensity statin (HIS), low-medium intensity statins, and no statin.
View Article and Find Full Text PDFCatheter Cardiovasc Interv
July 2019
Objective: To compare procedural outcomes of transcatheter aortic valve implantation (TAVI) patients who were implanted with older versus newer generation valves.
Background: The current evidence base for improved safety of the newer commercially available TAVI valves is limited.
Methods: A retrospective analysis of the Israeli multicenter TAVI registry was performed.
Type 1 diabetes (T1D) is an autoimmune disease where pancreatic β-cells are destroyed by islet-infiltrating T cells. Although a role for β-cell defects has been suspected, β-cell abnormalities are difficult to demonstrate. We show a β-cell DNA damage response (DDR), presented by activation of the 53BP1 protein and accumulation of p53, in biopsy and autopsy material from patients with recently diagnosed T1D as well as a rat model of human T1D.
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