Aortic Stenosis in Elderly : Determinant of Progression
Recruitment status was Recruiting
Aortic stenosis (AS) is AS is caused by calcium deposits in the aortic valve. Calcification is progressive and eventually leads to reduced leaflet motion with obstruction of the left ventricular outflow. The only treatment is surgery. There are evidences that AS is a regulated process with similarities to atherosclerosis but determinants of AS progression are unknown. The study aims at evaluating these determinants and more specifically the role of lipids, inflammation and platelet aggregation.
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
|Official Title:||Aortic Stenosis in Elderly : Determinant of Progression. COFRASA (French Cohort)|
|Study Start Date:||November 2006|
|Estimated Study Completion Date:||November 2012|
|Estimated Primary Completion Date:||November 2012 (Final data collection date for primary outcome measure)|
Aortic stenosis (AS) is the most common valvular disease and the second most common indication for cardiac surgery in Western countries. AS prevalence increases with age and with aging of the population, AS is a major public health problem. AS is due to calcium deposits within the aortic valve. Calcium deposit is progressive and eventually leads to reduced leaflet motion with obstruction of the left ventricular outflow. There is currently no effective medical therapy. Once the stenosis is severe and patients symptomatic, outcome is poor unless surgery (aortic valve replacement) is promptly performed. AS has long been considered as a passive and degenerative process. Recent data challenged this concept, showing that AS is an active and highly regulated process with some similarities to atherosclerosis. However, AS progression is highly variable from one individual to another and determinants of AS progression are poorly known. Their identification is crucial if we want to develop new medical strategies. The aims of the present study are to identify the determinants of AS progression and more specifically to evaluate the role of lipids, inflammation and platelet aggregation.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00338676
|Contact: David Messika-Zeitoun, MD||00 1 1 40 25 66 email@example.com|
|Paris, France, 75018|
|Contact: David Messika-Zeitoun, MD 00 1 40 25 66 01 firstname.lastname@example.org|
|Principal Investigator:||David Messika-Zeitoun, MD||Assistance Publique des Hopitaux de Paris|