The goal of this study is to describe the increase in plasma serotonin or 5-hydroxytryptamine (5-HT) in patient with increased severity of aortic stenosis and increased weight cardiac muscle.
Calcific aortic stenosis is the most frequent valve disease in adults. Without therapeutic strategy, this disease leads to heart failure and death. Surgical aortic valve replacement is now a well tolerated cardiac surgery leading to excellent outcomes. Until recently, calcific aortic stenosis was considered to be histopathologically degenerative or passive in origin. It is now recognized, however, as a complex cellular process with features of atherosclerosis. It has been observed that drugs may slow dawn the progression of aortic stenosis in observational studies. It has been suggested that serotonin, a monoamine neurotransmitter and a peripheral signal mediator, may be involved in the progression of aortic stenosis and also in its consequences on myocardium hypertrophy. In the blood, serotonin in mainly stored in platelets, which release serotonin involved in post-injury vasoconstriction, thrombus formation, fibrosis and atherogenesis. This study hypothesized those patients with aortic stenosis exhibit higher circulating serotonin levels than their counterparts without heart disease. In addition to circulating serotonin, its metabolite 5-HIAA will be systematically measured on all patients. This study would allow to determine the potential of plasma serotonin as a prognosis marker and perhaps suggest the discovery of new targets for treatment of aortic stenosis.
Study Type
INTERVENTIONAL
Allocation
NON_RANDOMIZED
Purpose
DIAGNOSTIC
Masking
NONE
Enrollment
52
transthoracic echocardiography, radial, and aortic arterial blood sampling
University Hospital
Toulouse, France
Measurements of 5-HT
Measurement of 5-HT were performed by high pressure liquid chromatography (HPLC)
Time frame: baseline
Measurements of acide 5-hydroxy-indol-acetic (5-HIAA)
Measurements of 5-HT monoamine oxidase (MAO)-A-dependent degradation product, 5-HIAA, were performed by HPLC
Time frame: Baseline
Arterial platelet activation
Arterial platelet activation was assessed by flow cytometry analysis of platelet surface expression of P-selectin and activated integrin GPIIb/IIIa
Time frame: Baseline
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