View clinical trials related to Aortic Stenosis.
Filter by:Mutations in the SLC34A2 gene, that encodes the sodium phosphate co-transporter (NaPi-IIb), cause defect cell-uptake of phosphate, which leads to formation of calcium-phosphate concretions in the lungs as seen in Pulmonary Alveolar Microlithiasis (PAM). Extra pulmonary calcifications, including heart valve calcification, have previously been reported in patients with PAM. Calcific Aortic Valve Disease (CAVD) is a common disease in the elderly and is characterised by thickening and calcification of the aortic valve leaflets in the absence of rheumatic heart disease. CAVD is present in more than 25% of patients older than age 65 years and is associated with an increased risk of cardiovascular events. Currently, there is no effective therapy for the disease other than surgical aortic valve replacement. Both calcium and phosphate are the major components of calcific deposits in PAM and CAVD. Based on these preliminary findings, the investigators hypothesize that mutations in sodium phosphate co-transporters may play a role in both pulmonary and extra pulmonary calcifications. Two studies will be performed: 1. A retrospective cross-sectional study including patients with an age ≤ 65 years with CAVD from Denmark and Örebro, will be carried out. Genetic association analysis will be performed to investigate the incidence of common variants in five genes representing sodium phosphate co-transporters (SLC34A1, SLC34A2, SLC34A3, SLC20A1, SLC20A2) compared to healthy controls. Associated genes will subsequently be sequenced to identify possible causal mutations. 2. In a prospective study, aortic valve tissue will be collected from patients with AS undergoing surgical valve replacement. Molecular characterisation of the transporters will be conducted by determining the level of specific mRNA and protein by RT-PCR/qPCR, and Western Blotting, respectively. The localisation and visualisation will be investigated by immunostaining and confocal laser microscopy. Fibroblasts and endothelial cells will be isolated and grown in cultures with subsequent functional studies of the phosphate uptake.
TASS-2 (Tyrolean Aortic Stenosis Study-2) aims to characterize the clinical value of minimally elevated troponin T plasma levels both in patients with asymptomatic and symtomatic aortic stenosis.
The primary purpose of the LAA-CLOSURE trial is to assess the efficacy and safety of surgical closure of LAA in patients undergoing aortic valve replacement. This randomized, prospective, open-label international multicenter trial will enroll 1040 patients undergoing aortic valve replacement with CHA2DS2-VASC score ≥2 but without an indication for anticoagulation at the time of enrollment. Patients will be randomized in 1:1 fashion to standard therapy + surgical closure of LAA vs. standard therapy alone. The duration of the study is five years (plus additional 10 years).
There is a correlation between endothelial progenitor cells (stem cells) and stenosis of the aortic valve.
The objective is to observe trends in patient characteristics and outcomes after aortic or mitral transcatheter heart valve replacement over time.
Our main hypothesis on the present study is that new parameters such as risk-taking behavior, patients motivation, health related quality of life, new biomarkers and more precise echocardiography measures in addition to traditional parameters will improve pre-operative risk assessment in patients with AS and better guide patients and doctors in decision whether to operate or not.
The primary aim of the present study was to examine the haemodynamic changes in primary hypertension and secondary hypertension (renal diseases, endocrine diseases, obesity-associated hypertension) with a non-invasive haemodynamic measurement protocol utilizing radial pulse wave analysis and whole-body impedance cardiography in both supine position and during head-up tilt. For comparison, haemodynamics of subjects with chronic fatigue syndrome will also be recorded.
Intervention study focused on preventing the progression of aortic valve calcification. Vascular and cardiac calcifications are a marker of risk and poor outcome, especially the severe calcified aortic stenosis and coronary calcification. Its increasing prevalence is now a health problem. The knowledge and the therapeutic objective of this condition have changed in recent years and pathophysiological aspects at present, focus on atherosclerotic disease and inflammation. Several clinical trials have failed to demonstrate that statins or ACE inhibitors prevent the progression of cardiovascular calcification. Taking into account the new concepts of ectopic calcification and research results from our group, the most logical approach to prevent progression would be an early intervention and management of the calcification inhibiting agents such as phytate (inositol six-phosphate -- InsP6). Hypothesis: The phytate prevents or delays the progression of cardiovascular calcification. It is a clinical trial of intervention of oral phytate (InsP6) in patients with mild to moderate cardiovascular calcification (aortic valve and / or coronary arteries) compared with placebo over a period of 24 months. It is a prospective, randomized minimization of variables to ensure homogeneity of the groups. The primary analysis will be the time evolution of the extent of calcium in the aortic valve and coronary arteries made with CT. Secondary variables are the degree of progression of aortic stenosis and clinical events (death, stroke, angina, stroke and cancer of any type).
The purpose of the study is to determine whether the excretion of renal water- and salt-channels in the urine reflects the handling of water and salt in the kidneys, and whether the excretion can be used to monitor and/or predict the effects of treatment of certain heart or lung diseases.
Abundant evidence suggests that Angiotensin Converting Enzyme (ACE) inhibition potentially could reduce the hazardous effects of aortic stenosis and improve haemodynamics. The treatment seems safe even in patients with severe stenosis. There are however no randomised clinical trials that can confirm this hypothesis.