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Valve Calcification (valve + calcification)
Selected AbstractsNatural and Prosthetic Heart Valve Calcification: Morphology and Chemical Composition CharacterizationARTIFICIAL ORGANS, Issue 4 2010Raquel F. Weska Abstract Calcification is the most common cause of damage and subsequent failure of heart valves. Although it is a common phenomenon, little is known about it, and less about the inorganic phase obtained from this type of calcification. This article describes the scanning electron microscopy (SEM)/energy dispersive X-ray spectroscopy and Ca K -edge X-ray absorption near edge structure (XANES) characterization performed in natural and bioprosthetic heart valves calcified in vivo (in comparison to in vitro-calcified valves). SEM micrographs indicated the presence of deposits of similar morphology, and XANES results indicate, at a molecular level, that the calcification mechanism of both types of valves are probably similar, resulting in formation of poorly crystalline hydroxyapatite deposits, with Ca/P ratios that increase with time, depending on the maturation state. These findings may contribute to the search for long-term efficient anticalcification treatments. [source] A Novel In Vitro Assessment of Tissue Valve Calcification by a Continuous Flow Type MethodARTIFICIAL ORGANS, Issue 2 2000Jong-Chul Park Abstract: A dynamic flow type testing to study calcification was self-designed to investigate calcification in bioprosthetic heart valves. The apparatus consists of a container into which leaflets from a porcine aortic valve are placed, a chamber that contains calcium solution, and a peristaltic pump that provides a continuous supply of the solution toward the container. Efficacy of the apparatus was compared with the conventional batch type calcification testing at 37°C through measuring the amount of calcium and phosphate deposited by inductively coupled plasma (ICP) and scanning electron microscope (SEM). After 14 days, calcium levels detected from the calcified deposit on leaflets were 470.4 ± 37.0 ,g/cm3 in the flow type testing whereas in the batch type testing levels were 81.0 ± 6.7 ,g/cm3. Though the calcium level on the leaflet increased as the exposure time to calcium solution increased in both testings, the rate and the tendency of calcification could be assessed very rapidly by flow type testing in comparison with batch type testing. [Ca]/[P] molar ratio decreased over time, and after 14 days, the ratio was close to 1.83 ± 0.18 in the flow type testing. The ratio could not be determined in the batch type testing because the deposit was too small to assess. The descending rate of [Ca]/[P] molar ratio demonstrates that deposited calcium-complex at the earliest stage may interact with inorganic phosphate ions to create a calcified deposit mineral precursor. This in vitro dynamic flow type calcification testing was a favorable tool for rapid investigation of calcification. [source] Impact of Valvular Calcification on the Diagnostic Accuracy of Transesophageal Echocardiography for the Detection of Congenital Aortic Valve MalformationECHOCARDIOGRAPHY, Issue 7 2007Akash Makkar M.D. Background: Degeneration of congenital bicuspid or unicuspid aortic valves can progress more rapidly than that of tricuspid valves, and an early diagnosis significantly impacts decision making and outcome. We hypothesized that the extent of valvular calcification would negatively influence the diagnostic accuracy of multiplane transesophageal echocardiography (TEE) for the diagnosis of congenital aortic valve disease. Methods: TEE was performed in 57 patients undergoing aortic valve replacement surgery for aortic stenosis (n = 46), pure regurgitation (n = 9), or significant regurgitation with less than severe aortic stenosis (n = 2). The degree of aortic valve calcification and the number of valve cusps were determined at surgery. Results: Surgical inspection confirmed 14 bicuspid and 43 tricuspid aortic valves. Sensitivity and specificity of TEE for the diagnosis of congenital aortic valve malformation was 93% (13/14) and 91% (39/43) (P = 0.0001), respectively. In patients with no or mild aortic valve calcification (n = 13), sensitivity and specificity of TEE for the diagnosis of congenitally malformed aortic valve was 100% (5/5) and 100% (8/8) (P = 0.001), respectively. In patients with moderate or marked aortic valve calcification (n = 44), sensitivity and specificity of TEE for the diagnosis of congenitally malformed aortic valve was 89% (8/9) and 89% (31/35) (P<0.0001), respectively. In this subgroup of 44 patients, there were four false-positive and one false-negative diagnoses due to valvular calcification. Conclusions: Although TEE is highly sensitive and specific for the detection of congenital aortic valve malformations, presence of moderate or marked calcification of the aortic valve may result in false positive and false negative diagnoses. [source] Hypercholesterolemia Association with Aortic Stenosis of Various EtiologiesJOURNAL OF CARDIAC SURGERY, Issue 2 2009Murat Bülent Rabu The aim of this study was to investigate the role of hypercholesterolemia in development of aortic valve calcification in different etiologies. Methods: The study included 988 patients with rheumatic, congenital, or degenerative aortic stenosis, who underwent aortic valve replacement at Ko,uyolu Heart and Research Hospital between 1985 and 2005. Effects of hypercholesterolemia and high low-density lipoprotein level on calcific aortic stenosis or massive aortic valve calcification were analyzed for each etiologic group. Results: Both univariate and multivariate analyses revealed that the high serum cholesterol level (>200 mg/dL) was related to massive aortic valve calcification in all patients (p = 0.003). Hypercholesterolemia was linked to calcific aortic stenosis and massive calcification in patients with degenerative etiology (p = 0.02 and p = 0.01, respectively) and it was related to massive calcification in patients with congenital bicuspid aorta (p = 0.02). Other independent risk factors for calcific aortic stenosis and massive calcification in the degenerative group were high low-density lipoprotein level (>130 mg/dL; p = 0.03 and p = 0.05, respectively) and high serum C-reactive protein level (p = 0.04 and p = 0.05, respectively). Conclusions: Hypercholesterolemia is related to increased risk of aortic valve calcification in patients with degenerative and congenital etiology. Preventive treatment of hypercholesterolemia could play an important role to decrease or inhibit development of aortic valve calcification. [source] Aortic sclerosis,a marker of coronary atherosclerosisCLINICAL CARDIOLOGY, Issue 12 2004Yogendra Prasad M.D. Abstract Aortic valve sclerosis is defined as calcification and thickening of a trileaflet aortic valve in the absence of obstruction of ventricular outflow. Its frequency increases with age, making it a major geriatric problem. Of adults aged> 65 years, 21,29% exhibit aortic valve sclerosis. Incidence of aortic sclerosis increases with age, male gender, smoking, hypertension, high lipoprotein (Lp) (a), high low-density lipoprotein (LDL), and diabetes mellitus. Aortic valves affected by aortic sclerosis contain a higher amount of oxidized LDL cholesterol and show increased expression of metalloproteinases. Clinically, it can be suspected in the presence of soft ejection systolic murmur at the aortic area, normal split of the second heart sound, and normal volume carotid pulse, but it can be best detected by echocardiography. Aortic sclerosis may be accompanied by mitral annulus calcification up to 50% of cases. It is associated with an increase of approximately 50% in the risk of death from cardiovascular causes and the risk of myocardial infarction. The mechanism by which aortic sclerosis contributes to or is associated with increased cardiovascular risk is not known. Aortic sclerosis is associated with systemic endothelial dysfunction, and a small percentage of cases may progress to aortic stenosis. Lowering of LDL cholesterol by 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors have been shown to decrease progression of aortic valve calcification. Aortic sclerosis is not a mere benign finding. Once diagnosis of aortic sclerosis has been made, it should be considered a potential marker of coexisting coronary disease. Aggressive management of modifiable risk factors, especially LDL cholesterol lowering, may slow progression of the disease. [source] | ||||||||||