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Purpose: The effect of intravenous glutamate infusion on myocardial diastolic function and overall hemodynamics were studied in patients undergoing elective aortic valve replacement with severe aortic stenosis and associated left ventricular hypertrophy .
Methods: 25 patients will be included in this double-blind randomized placebo-controlled study. Glutamate was administered intravenously immediately after aortic cross-clamp release. The patients receive either a low dose of 30mg kg-1 h-1 (LG-group) or high dose of 60 mg kg-1 h-1 (HG-group) or placebo (P-group) at a rate of 3.3ml kg-1h-1 for 2h. Transesophageal echocardiography (TEE) is used to measure diastolic and systolic ventricular function before sternotomy (T0), and 2h (T2), 3h (T3) and 6h (T4) after release of cross clamp. Additionally routine hemodynamic parameters are measured intraoperatively.
Allocation: Randomized, Control: Placebo Control, Endpoint Classification: Pharmacokinetics/Dynamics Study, Intervention Model: Parallel Assignment, Primary Purpose: Treatment
Hypertrophy, Left Ventricular
LG-group, HG-group, Placebo-group
Clin. Dept. of Cardiothoracic and Vascular Anaesthesia & Intensive Medicine, Medical University of Vienna, Vienna General Hospit
Medical University of Vienna
Published on BioPortfolio: 2014-08-27T03:12:55-0400
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A form of CARDIAC MUSCLE disease, characterized by left and/or right ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR; HYPERTROPHY, RIGHT VENTRICULAR), frequent asymmetrical involvement of the HEART SEPTUM, and normal or reduced left ventricular volume. Risk factors include HYPERTENSION; AORTIC STENOSIS; and gene MUTATION; (FAMILIAL HYPERTROPHIC CARDIOMYOPATHY).
Absence of the orifice between the RIGHT ATRIUM and RIGHT VENTRICLE, with the presence of an atrial defect through which all the systemic venous return reaches the left heart. As a result, there is left ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR) because the right ventricle is absent or not functional.
Enlargement of the LEFT VENTRICLE of the heart. This increase in ventricular mass is attributed to sustained abnormal pressure or volume loads and is a contributor to cardiovascular morbidity and mortality.
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