Aortic valve imaging with computed tomography: a review.
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The finding of aortic valve calcification is of clinical relevance. Thickening and calcification of the aortic valve ('aortic sclerosis') may progress over time to calcific aortic stenosis, and calcification of the aortic valve has prognostic importance even in the absence of valve obstruction. Aortic valve calcification may also have effects on the conduction system. There is progressive awareness of the need for an imaging technique that can accurately and reproducibly quantify calcification of native and prosthetic aortic valves. Through adaptation of techniques from electron beam computed tomography (CT) coronary calcium scoring, CT has been proposed as the appropriate imaging modality. Although originally described as a method of comparing the calcification of different aortic valve bioprostheses, the major role suggested for CT aortic valve calcium quantification is now in the field of preventive medicine. This has stemmed from the recognition that traditional vascular risk factors also have a role in the etiology of calcific aortic stenosis. Subsequently, the realization that pharmacological modification of lipid profiles may result in slowing of progression or even regression of aortic valve calcification has led to a need to quantify aortic valve calcification for follow up purposes. Echocardiography has been used to estimate aortic valve calcification in studies of the natural history of aortic stenosis, but it does not accurately quantify calcium. CT appears able to fulfil this requirement, though the technique is still relatively novel. This review examines the need for aortic valve calcium quantification and the evolution of imaging to the current status. Future directions and the promise of new helical CT technologies with respect to cardiac imaging are explored.Cite
Among various hypotheses proposed for pathological tissue calcification, recent evidence supports the possibility that self-replicating calcifying nanoparticles (CNPs) can contribute to such calcification. These CNPs have been detected and isolated from calcified human tissues, including blood vessels and kidney stones, and are referred to as nanobacteria. We evaluated calcific aortic valves for the presence of CNP. Calcific aortic valves were obtained from 75 patients undergoing surgical valve replacement. The control group was formed by eight aortic valves corresponding to patients with heart transplants. In the microbiology laboratory, valves were screened for CNP using a 4–6 weeks specific culture method. The culture for CNP was positive in 48 of the 75 valves with aortic stenosis (64.0%) in comparison with zero of eight (0%) for the control group (P = 0.0005). The observation of cultures by way of scanning electron microscopy highlighted the resemblance in size and morphology of CNP. Self-replicating calcific nanometer-scale particles, similar to those described as CNP from other calcific human tissues, can be cultured and visualized from calcific human aortic valves. This finding raises the question as to whether CNP contribute to the pathogenesis of the disease or whether they are only innocent bystanders.
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The finding of aortic valve calcification is of clinical relevance. Thickening and calcification of the aortic valve ('aortic sclerosis') may progress over time to calcific aortic stenosis, and calcification of the aortic valve has prognostic importance even in the absence of valve obstruction. Aortic valve calcification may also have effects on the conduction system. There is progressive awareness of the need for an imaging technique that can accurately and reproducibly quantify calcification of native and prosthetic aortic valves. Through adaptation of techniques from electron beam computed tomography (CT) coronary calcium scoring, CT has been proposed as the appropriate imaging modality. Although originally described as a method of comparing the calcification of different aortic valve bioprostheses, the major role suggested for CT aortic valve calcium quantification is now in the field of preventive medicine. This has stemmed from the recognition that traditional vascular risk factors also have a role in the etiology of calcific aortic stenosis. Subsequently, the realization that pharmacological modification of lipid profiles may result in slowing of progression or even regression of aortic valve calcification has led to a need to quantify aortic valve calcification for follow up purposes. Echocardiography has been used to estimate aortic valve calcification in studies of the natural history of aortic stenosis, but it does not accurately quantify calcium. CT appears able to fulfil this requirement, though the technique is still relatively novel. This review examines the need for aortic valve calcium quantification and the evolution of imaging to the current status. Future directions and the promise of new helical CT technologies with respect to cardiac imaging are explored.
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Dyslipidemia
Systolic hypertension
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Aortic stenosis (AS), an age-related disease characterized by narrowing and obstruction of the aortic valve opening, is often related to progressive valve calcification. Mechanisms of valvular calcification involve several pathways influenced by aging. Some of these pathways might be induced by short telomeres, one of the hallmarks of aging. Currently, however, the role of telomere length (TL) in the onset and progression of AS remains unclear. To shed light on the implication of telomere dynamics in aortic valve calcification and aortic stenosis, we measured TL in aortic valves from patients with and without AS. We found that non-calcified areas of stenotic valves display shorter telomeres than corresponding valve areas of non-stenotic valves. Furthermore, we observed that within a calcified valve, calcified areas exhibit shorter telomeres than non-calcified areas, whereas telomerase activity was not detected in any of those. In addition, study of TL distributions (TLD) showed that, beside mean TL, calcification is associated with changes in TLD shape. Finally, preliminary results of a transcriptomic analysis revealed that TL in aortic valves might be involved in the regulation of gene expression. These results suggest that short telomeres in aortic valves may contribute to the onset and development of AS. In addition, a further decrease of TL in calcified areas seems to be an after effect of the calcification process. These findings may have long-term ramifications that will potentially allow identification of individuals at high risk for aortic valve stenosis during the aging process. For a better understanding of the involvement of telomere length in aortic valve calcification further mechanistic studies are required.
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Introduction: The association between aortic valve calcification (AVC) and mean gradient (MG) is different between bicuspid (BAV) and tricuspid (TAV) aortic valve stenosis (AS), especially in young...
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The study aim was to evaluate the relationship between serum calcium levels and the degree of calcification found in stenotic aortic valves.Using atomic absorption spectroscopy, the hydroxyapatite content of 228 excised human stenotic aortic valves was determined and expressed as a percentage of valve mass. Left heart catheterization preceded valve replacement. In addition, serum levels of calcium and creatinine were determined before native calcific aortic valve excision.Valves from male patients contained more hydroxyapatite than those of female patients (26 +/- 9 versus 22 +/- 9 mass%; p < 0.001). Patients presenting with lower serum calcium levels showed a slight trend towards higher levels of valve calcification (r = -0.15, p = 0.026), but this association appeared only within the subgroup of male patients. Male patients with lowest serum calcium levels displayed greatest valvular hydroxyapatite deposition (1st calcium tertiary: 29.5 +/- 8.9 mass% versus 2nd calcium tertiary 26.4 +/- 7.8 mass% versus 3rd calcium tertiary 21.4 +/- 8.9 mass%; n = 122; p = 0.001; r = -0.25; p = 0.006). This association was even more distinct in male patients with normal serum creatinine levels. Furthermore, serum calcium was inversely and significantly associated with serum C-reactive protein in male patients (r = - 0.34; p < 0.001).Serum calcium levels appear to be inversely related to valve calcification in patients with severe calcific aortic stenosis (AS). This finding indicates the importance of systemic calcium metabolism in calcific AS, independent of manifest disorders of calcium metabolism or renal function. Interestingly, this association was evident only in male patients, suggesting a gender-dependent pathogenesis.
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Objective To explore the relationship between the aortic valve calcification(AVC) and coronary artery disease(CAD). Methods Six hundred and fifty-three patients underwent transthoracic echocardiography and coronary arteriography at the same time were analyzed retro-spectively in the study. All patients were divided into two groups: normal control group and aortic valve calcification group(left valve calcification, right valve calcification, multiple aortic valve calcification), comparison of the incidence of coronary artery disease between aortic valve calcification group and normal control group. Analysis of the correlation between single aortic valve calcification and coronary artery stenosis. Results The incidence of coronary artery disease aortic in AVC group was markedly higher than in normal control group. There was no obvious correlation between single aortic valve calcification and the same side coronary artery stenosis. Conclusion Patients with aortic valve calcification have a higher incidence of coronary artery disease, aortic valve calcification can be used as a reference index of noninvasive assessment of coronary artery disease.
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Raman microimaging was applied to study the biochemical composition in the aortic valves obtained from patients with calcific aortic stenosis. This progressive disease affects an increasing number of elderly patients with hyperlipidemia and hypercholesterolemia. Lipid accumulation in the tissue is associated with pathogenesis and progression of cardiac valve calcification. This is in line with our finding that lipid deposits, predominantly composed of cholesterol and its esters, are frequently co-localized with calcium salt deposits, even at an early stage of their development. Overall changes in the biochemical composition of the tissue upon pathology progression are less obvious. Globally, although the cholesterol level rises, the relative lipid-to-protein content decreases. The results broaden the knowledge of biochemical alterations in dysfunctional human aortic valves and may be helpful in designing lipid lowering therapies.
Raman microspectroscopy
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Calcified aortic valves were detected in 109 patients studied in hospital by an echocardiographic method (2D- and M-scanning). It was found that, unlike rheumatism, calcification starting in the aortic annulus and semilunar bases might result in formation of degenerative (non-inflammatory) calcific aortic stenosis. The latter differs from rheumatic aortic stenosis in commissural fusions. The authors defined clinical and echocardiographic differentially diagnostic criteria for degenerative (non-inflammatory) and rheumatic (inflammatory) calcific aortic stenosis. They also discussed pathogenetic aspects of aortic valve calcification and problems of terminology.
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