Disease relevance of Aortic Valve

• Long-term vasodilator therapy with nifedipine reduces or delays the need for aortic-valve replacement in asymptomatic patients with severe aortic regurgitation and normal left ventricular systolic function [1].
• Left ventricular hypertrophy (LVH) produced by aortic valve plication leads to increased myocardial cyclic GMP [2].
• Comparison of the cardiocirculatory effects of exercise and isoproterenol in children with pulmonary or aortic valve stenosis [3].
• The capability of radionuclide imaging to detect experimental aortic valve infective endocarditis was assessed with indium-111 (111In)-labeled blood cells [4].
• In rats with catheter-induced sterile aortic valve vegetations we studied the efficacy of single-dose amoxicillin and single-dose erythromycin prophylaxis for the prevention of bacterial endocarditis after extractions of periodontally diseased teeth [5].

High impact information on Aortic Valve

• In the patients with SLE, abnormalities included mitral valve leaflet thickening in six, aortic valve thickening in five, and mitral annular calcification in two [6].
• The only deaths among patients who had aortic valve replacement or repair of a ventricular septal defect occurred in those who had some serious complication before operation [7].
• The aorta and coronary ostia exhibited gross atheromata, and the aortic valve leaflets were thickened by cholesterol-laden macrophages [8].
• In order to determine the in vivo influx of plasma cholesterol into human aortic intimamedia tissue, specimens of the ascending aortic wall without visible atherosclerosis were obtained from patients undergoing aortic valve replacement [9].
• HMG CoA reductase inhibitor (statin) and aortic valve calcium [10].

Chemical compound and disease context of Aortic Valve

• After aortic valve replacement, aspirin provided a low rate of thromboembolism (0.8 +/- 0.2% per patient-year), not significantly different from warfarin or no treatment (2.9 +/- 1.6% and 1.5 +/- 0.6% per patient-year) (P = .07) [11].
• The aortic valves of animals fed a cholesterol-rich diet exhibit many characteristics in common with the early stages of aortic stenosis [12].
• For bioprosthetic heart valves, heparin is followed by oral anticoagulation as outlined for 3 months after mitral or aortic valve replacement and indefinitely after mitral valve replacement if there is atrial fibrillation or a very large left atrium; aspirin may be recommended indefinitely after aortic valve replacement [13].
• BACKGROUND: Calcium accumulation in the aortic valve is a hallmark of aortic sclerosis and aortic stenosis [14].
• SNV should be treated initially with prednisone and may also require the administration of cytotoxic agents, while aortitis and AI can be controlled with the administration of prednisone and surgical replacement of the aortic valve [15].

Biological context of Aortic Valve

• After aortic-valve replacement, 12 of the 16 patients (75 percent) in the digoxin group and all six patients in the nifedipine group who had had an abnormal left ventricular ejection fraction before surgery had a normal ejection fraction [1].
• OBJECTIVES: We sought to determine whether the cardiac renin-angiotensin system (RAS) is activated in human aortic valve disease depending on left ventricular function, and we analyzed the concomitant regulation of the extracellular matrix components [16].
• As TN-C is a multifunctional protein implicated in cell proliferation, migration and differentiation, we investigated the pattern of its expression in diseased human aortic valves [17].
• To assess the development of oxidative stress in cardiac ischemia/reperfusion, the resulting depletion of plasma ascorbate was monitored by electron spin resonance spectroscopic detection of ascorbyl free radical (AFR) in a homogeneous group of 12 patients undergoing aortic valve replacement [18].
• Acetylcholine-induced membrane potential changes in endothelial cells of rabbit aortic valve [19].

Anatomical context of Aortic Valve

• BACKGROUND: Calcification is a frequent cause of the clinical failures of glutaraldehyde-pretreated bioprosthetic heart valves (BPHV) fabricated from glutaraldehyde-cross-linked porcine aortic valves [20].
• BACKGROUND: Calcification of the cusps of bioprosthetic heart valves fabricated from either glutaraldehyde cross-linked porcine aortic valves or bovine pericardium frequently causes the clinical failure of these devices [21].
• Using endogenous radiolabeling, we found that all cell types except aortic valve endothelial cells synthesized and released into the culture media substantial quantities of fibronectin [22].
• To test the Ca2+ influx theory, cytosolic Ca2+ and Pi concentrations were assessed in glutaraldehyde-treated porcine aortic valve fibroblasts, and their relationship to a subsequent calcification was studied [23].
• METHODS: Cross-sectional area of the left and right coronary arteries was determined by quantitative coronary angiography in 52 patients: 12 control subjects and 40 patients (13 with hypertrophic cardiomyopathy, 12 with dilated cardiomyopathy and 15 with aortic valve disease) [24].

Associations of Aortic Valve with chemical compounds

• These findings indicate that heart failure in aortic valve disease is associated with low PCr, which could be due to loss of intracellular creatine [25].
• Because leaflet calcification occurs in areas of lipoprotein deposition, we hypothesised that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG COA) reductase inhibitors (statins) might slow aortic valve calcium (AVC) accumulation [10].
• Our investigations studied ethanol pretreatment of glutaraldehyde cross-linked porcine aortic valves as a new approach to prevent cuspal calcification [21].
• In other postoperative evaluations that included ergometric stress with isoproterenol and pacing, induced hemodynamic changes after aortic valve replacement were predictable and consistent with regard to both direction and magnitude, and they differed characteristically according to the type of stress used [26].
• Platelet survival time was measured (by the chromium-51 method) in 73 patients with aortic valve disease [27].

Gene context of Aortic Valve

• Immunohistochemistry for leukocytes, IL-1 beta and MMP-1 was performed on aortic valves with (n=6) and without (n=6) calcification obtained at valve replacement or autopsy [28].
• RESULTS: Fibrillin-1 content was reduced in bicuspid aortic valve aortas compared with that seen in tricuspid aortic valve aortas (P =.001), whereas the associated matrix components, elastin and collagen, were unchanged (P =.51 and P =.21) [29].
• RESULTS: beta-Actin expression in the aortic valve was significantly lower than in other valves [30].
• Mutations in NOTCH1 cause aortic valve disease [31].
• Human tricuspid aortic valves with and without calcific aortic stenosis were studied by immunohistochemistry for MMP-2, MMP-9 and TIMP-2 [32].

Analytical, diagnostic and therapeutic context of Aortic Valve

• Calcification limits the long-term success of heart valve bioprostheses fabricated from glutaraldehyde cross-linked porcine aortic valves [33].
• Our results suggest that the glutaraldehyde-fixed porcine heterograft warrants serious consideration when selecting a substitute aortic valve for man [34].
• In sheep aortic valve interstitial cell cultures 5-HT induced TGF-beta1 mRNA production and increased TGF-beta1 activity [35].
• Two patients with critical aortic stenosis (PSG greater than 165 mmHg), who exhibited a thick aortic valve on echocardiography with a relatively small aortic root and annulus, had a dramatic reduction in PSG [36].
• The myofibres in biopsies obtained from the left ventricle during cardiopulmonary bypass, in patients undergoing surgery for mitral and aortic valve replacement and the correction of atrial septal defect, contained inclusions thought to be type 1 cardiac colloid [37].

References