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PubMed2002

Carotid calcification on panoramic radiographs: an important marker for vascular risk.

OBJECTIVE: The objective of this study was to determine whether carotid calcifications are harbingers of future vascular events. STUDY DESIGN: Between 1986 and 2000, 71 patients were found to have carotid artery calcifications on routine panoramic films. Medical records were reviewed for vascular risk factors existing before and vascular end points subsequent to the radiographs. RESULTS: The mean age of our patients was 68 years. Sixty-one (86%) had preexisting vascular risk factors, 73% with multiple risk factors. Forty-one end points occurred in 29 patients. The average time to an end point was 2.7 years. The end points included myocardial infarction (8, 11%), stroke (5, 7%), death (11, 15%), revascularization procedures (8, 11%), transient ischemic attack (2, 3%), and angina (7, 10%). Twenty-three patients (34%) had major end points of myocardial infarction, stroke, or death. CONCLUSIONS: Carotid calcifications identified on panoramic radiographs are powerful markers for subsequent vascular events. Patients found to have carotid calcification on panoramic radiographs should be referred for cerebrovascular and cardiovascular evaluation and aggressive management of vascular risk factors.

Aged↗
PubMed1992

Calcification in marine molluscs: how costly is it?

Although crucial to our understanding of skeletal evolution in marine invertebrates, the cost of calcification has remained elusive for a simple reason: CaCO3 is an inorganic material. Its cost thus derives solely from the metabolic expenses of accumulating, transporting, and precipitating CaCO3 and cannot normally be separated from other metabolic costs. Traditionally, calcification cost has been ignored and total shell cost has been assumed to derive solely from skeletal organic matrix. The cost estimated here was permitted by the substantial natural variation in shell thickness in two rocky-shore gastropods (Nucella lamellosa and Nucella lapillus). In both the field and laboratory, data from three separate experiments revealed that groups of snails producing extra shell material under a particular set of experimental conditions also consumed extra food. The cost of calcification was estimated by computing the extra energy assimilated per unit extra shell produced at a common rate of tissue growth and then subtracting the cost of the organic matrix. At 1-2 J/mg of CaCO3, the calcification cost reported here is roughly 5% of that for the predominantly proteinaceous organic fraction of molluscan shells on a per-gram basis. This may explain why calcareous microstructures high in organic content have become less common evolutionarily.

Journal Article↗
PubMed2004

Lowering dietary phosphorus concentrations reduces kidney calcification, but does not adversely affect growth, mineral metabolism, and bone development in growing rabbits.

New Zealand White rabbits were used to investigate the influence of increasing dietary P concentrations on growth performance, mineral balance, kidney calcification and bone development. The minimum dietary P requirement of 0.22 % (National Research Council) is usually exceeded in commercial natural-ingredient chows, leading to undesirable kidney calcifications. In order to study the optimal dietary P level, rabbits were fed semi-purified diets with four different P levels (0.1, 0.2, 0.4, and 0.8 %; w/w) at a constant dietary Ca concentration (0.5 %) during an 8-week period. Body weight and growth were not influenced by the dietary P level. During two periods (days 20-23 and 48-51), faeces and urine were collected quantitatively for the analysis of Ca, Mg and P and balances were calculated. Increased dietary P intake caused increased urinary and faecal P excretion and P apparent absorption and retention. Faecal Ca excretion increased with higher dietary P levels, whereas urinary Ca excretion reacted inversely. The apparent absorption of Ca became reduced at higher dietary P concentrations, but Ca retention was unchanged. The response of Mg was in a similar direction to that of the Ca balance. Kidney mineral content increased with higher dietary P levels, indicating the presence of calcified deposits. Nephrocalcinosis became more severe in kidney cortex and medulla at increasing dietary P levels, as was confirmed by histological analysis. Femur bone length was not differentially influenced by dietary P. Bone density (g/cm(3)) of the femur diaphysis became significantly lower at the 0.8 % dietary P level as compared with the 0.2 % P group only. The bone Mg content was significantly increased on the 0.8 % P diet, both in the diaphysis and epiphysis. Plasma P concentration increased and plasma Ca decreased with higher dietary P levels, whereas plasma Mg levels were unaffected. The present study shows that the current recommended minimum dietary P level of 0.2 % for rabbits, as advised by the National Research Council in 1977, leads to a normal growth and bone development, but also causes some degree of kidney calcifications at a dietary Ca level of 0.5 %. As the dietary P level of 0.1 % virtually prevented kidney calcification and at the same time did not give evidence for any deleterious effects on growth and bone development, this indicates that the current recommended dietary P level for rabbits should be regarded as a maximum advisable concentration, and that a lower P level may be more optimal.

Animals↗
PubMedDate not supplied

Etiology of pleural calcification: a study of Quebec chrysotile asbestos miners and millers.

A review of 15,689 chest radiographs of Quebec chrysotile miners and millers, representing the latest film prior to November 1, 1966, for all such persons ever x-rayed, identified 206 men with pleural calcification. Of these, 198 had worked in the Thetford Mines area, 6 at Asbestos, and 2 at St. Remi de Tingwick; 2.5%, 0.08%, and 1% of the films from these areas, respectively. A series of case-control studies revealed that pleural calcification was concentrated in men employed at a small group of mines in Thetford Mines and occurred more often among miners and maintenance personnel than among millers. Calcification was not related to past history of illness or injury, place of residence, or employment in other industries. The distribution of pleural calcification in this Quebec industry suggests that it is related to some characteristic of airborne dust or mineral closely associated with the chrysotile that is encountered during mining in Thetford Mines but not in other mining areas. Possible minerals include mica, talc, and breunnerite.

Adult↗
PubMed1988

Tissue calcification and alkaline phosphatase activity in uraemic rats.

The activity and localization of alkaline phosphatase activity (AP) in aorta and heart, and the incidence of calcifications in aorta, heart and kidney as well as cardial fibrosis were studied in uraemic rats treated with 1,25-dihydroxycholecalciferol (1,25-DCHH) and Nifedipine. 1,25-DHCC treatment elevated the serum Ca x P product and aggravated the development of renal and aortic calcifications and cardial fibrosis. Nifedipine did not protect against calcifications, but decreased the incidence of cardial fibrosis. The activity of AP was increased in the thoracic aorta in uraemia independent of 1,25-DHCC or Nifedipine treatment or presence of calcification. No changes of the AP activity were found in the heart.

Alkaline Phosphatase↗
PubMed2004

Breast arterial calcifications as an indicator of systemic vascular disease.

PURPOSE: To evaluate the association between mammographically detected arterial calcifications and systemic vascular disease. MATERIAL AND METHODS: The medical records of 77 women who had either breast arterial calcifications or underwent surgery for carotid stenosis, abdominal aortic aneurysm, or femoropopliteal bypass (study groups A and B) were evaluated and compared with 33 women without breast arterial calcifications (group C). Patients in both arms of the study underwent additional vascular tests or mammography. RESULTS: Currently available data indicate that there is a statistically significant correlation between the presence of arterial calcifications on the mammogram and atheromatosis of the carotid or femoral arteries. CONCLUSION: Screening mammograms might be useful in the detection of women at risk for systemic vascular disease.

Adult↗
PubMed1982

Phosphate depletion therapy in two ectopic calcification syndromes.

Ectopic calcification may be a complication of a wide variety of pathologic conditions. Subcutaneous calcification frequently results in restriction of motion at joints in addition to cosmetic deformity. Parenchymal tissue calcification may result in decreased organ function. Dietary phosphate restriction and total body phosphate depletion with aluminum containing antacids were used in an attempt to decrease the deposition of subcutaneous calcium phosphate which occurs with two separate syndromes. Two subjects with hyperphosphatemic tumoral calcinosis were studied by metabolic balance, by long-term clinical evaluation, and routine laboratory and radiographic techniques before and after 1 year of phosphate depletion. One patient with a newly described syndrome--normocalcemic, hypercalciuric, subcutaneous calcification--was similarly studied. The etiology of this disorder is unknown. No consistent clinically significant evidence of regression of the lesions was noted in either syndrome, although one patient with tumoral calcinosis did demonstrate some regression of his lesions. It is not clear if this response failure was due to the intrinsic nature of the diseases or to failure of patient compliance secondary to a relatively unpalatable diet.

Adolescent↗
PubMed2005

Cardiac valve calcifications and left ventricular hypertrophy in hemodialysis patients.

Cardiac valve calcification (VC) is a common finding in end-stage renal disease patients. It was shown recently that VC is an independent predictor for all-cause and cardiovascular mortality in peritoneal dialysis patients. In hemodialysis (HD) patients, VC was associated with all-cause and cardiovascular mortality, but after adjusting for other cardiovascular risk factors and complications, as well as left ventricular mass index (LVMI), it lost significance. The aim of the study was to assess the relationship between VC and left ventricular hypertrophy in hemodialysis patients. Echocardiographic examination with mitral and aortic valves assessment and LVMI calculation was performed in 65 HD patients ages 49+/-12, with duration of HD therapy 38+/-32 months. VC were found in 32 of 65 patients (49%)-Group VC(+), mitral valve calcifications (MVC) in 10, aortic valve calcifications (AVC) in 9, and both valves calcifications (MVC+AVC) in 13 patients. Patients with VC were older, on HD therapy were longer, had higher systolic and pulse pressure, and had higher LVMI. Patients with both VCs had the highest LVMI. No significant differences were found with respect to Ca, P, PTH, and mean Ca x P product, but the incidence of Ca x P product above 4.43 mmol2/L2 was higher in VC(+) compared with those without VCs. VC coexists with left ventricular hypertrophy, particularly when both valves are calcified. Even short-lasting incidents of increased Ca x P product may lead to cardiac VC.

Adult↗
PubMed2000

Influence of glutaraldehyde fixation on the detection of SLA-I and II antigens and calcification tendency in porcine cardiac tissue.

OBJECTIVE: Immunological effects have been addressed as key factors for the long-term results of biological porcine aortic prostheses. In this study we investigated the influence of glutaraldehyde fixation on the expression of SLA (swine leucocyte antigens) and the calcification of porcine cardiac tissue. DESIGN: Deparaffinized sections obtained from porcine aortic tissue were fixed in a buffered glutaraldehyde solution for 1, 2, 3, 24 and 72 hours, respectively, and finally immunostained with monoclonal anti-SLA class I antibody 2.27-3a and anti-SLA-II antibody MSA3. Sixteen samples from fixed porcine cardiac tissue and, for comparison, 8 samples from leaflets of Toronto-SPV and Freestyle valves were implanted subcutaneously in 10 Wistar rats for 12 weeks and their calcium content was measured by atomic absorption spectrophotometry. RESULTS: SLA-I epitopes were no longer detectable using anti-SLA-I antibodies after fixation for 3 h. The SLA-II antigens remained detectable after longer fixation period. Short-time fixation resulted in marked calcification of the porcine cardiac tissue and to destruction of the SLA-I epitopes, whereas, even after longer fixation time, the epitopes of the SLA-II antigen remain unaffected. CONCLUSION: Chelate formation due to glutaraldehyde treatment provides protection against calcification. Short-time fixed porcine cardiac tissue has a tendency towards a greater degree of calcification than longer fixation periods. Based on the present results, it is pointless to set the length of fixation to switch off the immunogenicity.

Animals↗
PubMedDate not supplied

Idiopathic arterial calcification and unexpected infant death.

Two infants who died unexpectedly and who were found at autopsy to have idiopathic arterial calcification are presented. The first infant died within hours of the sudden onset of shortness of breath. The second infant died suddenly and unexpectedly in hospital where he was being treated for presumed sepsis and cardiac failure. Neither infant had significant past or family histories. Autopsy examination in both infants demonstrated widespread fibrointimal proliferation of elastic and muscular arteries with characteristic calcification of the internal elastic laminae. Kidneys and parathyroid glands were normal. Death in case 1 was attributed to extensive myocardial ischemic damage with right coronary artery ostial stenosis due to idiopathic arterial calcification. Death in case 2 was attributed to saddle pulmonary thromboembolism arising from a right atrial thrombus associated with cardiac failure secondary to idiopathic arterial calcification. These cases demonstrate the variable presentations, causes of death, and autopsy findings that may occur in this uncommon condition.

Arteries↗
PubMed2000

Osteoprotegerin reverses osteoporosis by inhibiting endosteal osteoclasts and prevents vascular calcification by blocking a process resembling osteoclastogenesis.

High systemic levels of osteoprotegerin (OPG) in OPG transgenic mice cause osteopetrosis with normal tooth eruption and bone elongation and inhibit the development and activity of endosteal, but not periosteal, osteoclasts. We demonstrate that both intravenous injection of recombinant OPG protein and transgenic overexpression of OPG in OPG(-/-) mice effectively rescue the osteoporotic bone phenotype observed in OPG-deficient mice. However, intravenous injection of recombinant OPG over a 4-wk period could not reverse the arterial calcification observed in OPG(-/-) mice. In contrast, transgenic OPG delivered from mid-gestation through adulthood does prevent the formation of arterial calcification in OPG(-/-) mice. Although OPG is normally expressed in arteries, OPG ligand (OPGL) and receptor activator of NF-kappaB (RANK) are not detected in the arterial walls of wild-type adult mice. Interestingly, OPGL and RANK transcripts are detected in the calcified arteries of OPG(-/-) mice. Furthermore, RANK transcript expression coincides with the presence of multinuclear osteoclast-like cells. These findings indicate that the OPG/OPGL/RANK signaling pathway may play an important role in both pathological and physiological calcification processes. Such findings may also explain the observed high clinical incidence of vascular calcification in the osteoporotic patient population.

Acid Phosphatase↗
PubMed1990

Automatic computer detection of clustered calcifications in digital mammograms.

The automatic detection of clusters of calcifications in digital mammograms has been investigated using image analysis techniques. The calcifications were segmented from the background of normal breast structure in the mammogram using a local area thresholding process. This procedure also identified other breast structures and the digital image properties of all segmented objects were analysed to extract clusters of calcifications. Seventy five clinical mammograms were digitised. These were divided into training and test sets of 25 and 50 films respectively. The results for the test set of 50 complete clinical mammograms show that the computer system achieves a 25/25 true positive film classification (i.e. those containing clusters of calcifications) with false positive clusters detected in 4/50 films. There were no false negative film classifications.

Algorithms↗
PubMed2005

Alcohol consumption, binge drinking, and early coronary calcification: findings from the Coronary Artery Risk Development in Young Adults (CARDIA) Study.

It is unclear to what extent the apparently beneficial cardiovascular effects of moderate alcohol consumption are mediated by protection against atherosclerosis. Alcohol consumption, coronary heart disease risk factors, and coronary calcification (a marker of atherosclerosis) were measured during 15 years of follow-up in the Coronary Artery Risk Development in Young Adults (CARDIA) Study (1985-2001). Among 3,037 participants aged 33-45 years after follow-up (55% women, 45% Black), the prevalence of coronary calcification was 8% for consumption of 0 drinks/week (n = 1,435), 9% for 1-6 drinks/week (n = 1,023), 13% for 7-13 drinks/week (n = 341), and 19% for > or = 14 drinks/week (n = 238) (p < 0.001 for trend). Calcification was also more common among binge drinkers (odds ratio = 2.1, 95% confidence interval: 1.6, 2.7). These associations persisted after adjustment for potential confounders (age, gender/ethnicity, income, physical activity, family history, body mass index, smoking) and intermediary factors (lipids, blood pressure, glucose, C-reactive protein, and fibrinogen). Stratification showed the dose-response relation most clearly in Black men; only heavier alcohol consumption (> or = 14 drinks/week) was associated with coronary calcification in other race/sex subgroups. These surprising findings suggest the presence of proatherogenic effects of alcohol in young adults, especially Black men, which may counterbalance high density lipoprotein cholesterol elevation and other possible benefits of alcohol consumption.

Adult↗
PubMed2006

Statin therapy of calcific aortic stenosis: hype or hope?

Calcific aortic stenosis, with a prevalence of 3-9%, is the most frequent heart valve disease and the main cause for valve replacement in patients over 60 years of age. Once thought to be caused by a passive calcium precipitate within the aortic valve leaflets, there is now increasing evidence that development and progression of calcific aortic valve disease may be triggered by underlying genetic and cardiovascular risk factors, and is regulated by an active cellular process involving inflammatory pathways. Targeted drug therapy to prevent the progression of calcific aortic valve disease should ideally be based on the knowledge of risk factors and the molecular pathogenesis of the disease. Conflicting data exists on the potency of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (i.e. statins) to influence both risk factors and inflammatory pathways by lowering lipid levels and exerting anti-inflammatory properties, respectively. In this review, various aspects of the molecular pathogenesis of calcific aortic stenosis will be summarized and connected with recent experimental and clinical studies that address the potential benefit of the targeted drug therapy by statins in order to prevent the progression of the disease.

Aortic Valve Stenosis↗
PubMed1978

Valvular calcification in the elderly: possible pathogenic factors.

Calcification of the mitral ring and of the aortic valve cusps was studied in an unselected autopsy series of 219 patients over 60, dying in a department of geriatric medicine. Possible correlations with age, sex, heart size, systolic and diastolic blood pressures, bone density and serum calcium, phosphate and alkaline phosphatase were examined. There were no significant findings for aortic valve calcification though there was a weak association with advanced age. Mitral ring calcification was significantly associated with higher age, female sex and with increased heart weight after correction for body size. These findings suggest that mechanical factors, rather than changes in mineral metabolism, are implicated in the development of mitral ring calcification.

Age Factors↗
PubMed2005

Two year comparison of sevelamer and calcium carbonate effects on cardiovascular calcification and bone density.

BACKGROUND: Calcium-based phosphate binders may induce tissue calcification, and little is known about their effects on bone density. We compared the effects of a calcium with a non-calcium phosphate binder on both arterial calcification and bone density measured by computed tomography. METHODS: Seventy-two adult haemodialysis patients were randomized to treatment with calcium carbonate (CC) or sevelamer (SEV) for 2 years. Electron beam CT scans were performed at baseline and at 6, 12 and 24 months. Serum phosphorus, calcium, calcium x phosphorus product and intact parathyroid hormone (iPTH) were measured and other routine laboratory tests were also carried out. RESULTS: The average calcium x phosphorus product was similar in the two treatment groups. However, patients receiving CC had significantly lower average iPTH (P<0.01), were more likely to have hypercalcaemic episodes (P = 0.03) and had significantly greater increases in coronary artery (CC median 484, P<0.0001, SEV median 37, P = 0.3118, between-group P = 0.0178) and aortic (CC median 610, P = 0.0003, SEV median 0, P = 0.5966, between-group P = 0.0039) calcification scores. The CC group also had a significant decrease in trabecular bone density (CC median -6%, P = 0.0049, SEV median +3%, P = 0.0296, between-group P = 0.0025). However, there was no significant difference in cortical bone density between the two groups. CONCLUSIONS: This 2 year study shows that calcium carbonate use is continuously associated with progressive arterial calcification in haemodialysis patients. In addition, it suggests that it is also associated with decreased trabecular bone density. However, this latter finding requires confirmation by a study specifically devoted to this issue.

Adult↗
PubMed2005

Severe hyperparathyroidism with bone abnormalities and metastatic calcification in rats with adenine-induced uraemia.

BACKGROUND: Marked parathyroid hyperplasia with bone diseases and vascular calcification are unsolved issues in dialysis patients. In this study, we made azotemic model rats by adenine feeding and analyzed the development and progression of the abnormalities. METHODS: Renal failure was induced in 8-week-old male Wistar rats by feeding 0.75% adenine-containing diet for 6 weeks. Serum parameters, parathyroid hyperplasia, bone changes and metastatic calcification were examined at 2, 4 and 6 weeks. RESULTS: Progressive increase of serum creatinine and inorganic phosphate, and decreased levels of serum calcium and 1,25(OH)2D3 were confirmed. Markedly enlarged parathyroid glands and extremely high PTH levels were observed in all adenine-fed rats compared with the control (PTH: 199.3+/-58.0 vs 10.5+/-3.0 pmol/l, P<0.01, respectively, at 6 weeks). In cortical bone of the femur, the morphometric parameters showed increased bone resorption with increased fibrosis, whereas in the trabecular bone, bone resorption decreased and bone volume increased with a larger amount of osteoid compared with the control. Metastatic calcification in aorta, coronary artery and other soft tissues were also found in adenine-fed rats. CONCLUSIONS: Uraemic rats made by adenine diet developed severe abnormalities of calcium metabolism in a relatively short period and therefore they may serve as a useful model for the analysis of parathyroid hyperplasia and vascular calcification in chronic renal failure.

Adenine↗
PubMed2006

Measurement of vascular calcification using CT fistulograms.

BACKGROUND: Vascular calcification (VC), precipitated by calcium and phosphate imbalance, is a major contributor to cardiovascular disease (CVD) in chronic kidney disease (CKD). Electron-beam computed tomography (EBCT) quantitatively assesses coronary artery calcification (CAC), with VC scores predictive of atherosclerosis and cardiac events in the general and CKD population. EBCT is not readily available but spiral CT can also provide quantitative assessment of the extent of VC. CT fistulograms can be used as initial investigation for arterio-venous fistula (AVF) problems in haemodialysis (HD). The images obtained include thoracic aorta, brachio-cephalic, subclavian and common carotid arteries which allow assessment of the extent of VC in these vessels. No study to date has combined the CT fistulogram with concurrent determination of VC. METHODS: We hypothesize that a single investigation for AVF management may also provide information on VC. We retrospectively analysed CT fistulograms on 28 HD patients determining VC scores (in Hounsfield units) in AVF, subclavian and carotid arteries and aorta. We correlated these scores with patient demographics, serum markers of mineral metabolism (time averaged for the period 6 months prior to CT) and calcium-based phosphate binders. RESULTS: Patients (60.7% male) had a median age of 59 years and 46.4% were diabetic. The mean duration of dialysis was 17.5 months. CT fistulograms showed predominantly aortic (75% of patients) and subclavian (75%) calcifications, with only 21.4% having carotid VC and minimal VC at the level of AVF. Median VC scores were 619.8 (0-1481.4) for aorta and 521.7 (0-1139.6) for subclavian (scores of >400 indicate severe atherosclerotic disease), but there was no significant correlation with serum markers or duration of HD. Increasing age correlated significantly with greater VC in aortic (R = 0.53, P = 0.003) and subclavian (R = 0.40, P = 0.03) vessels, as well as with the number of VC sites involved. CAC was present in most patients (89.3%) but CAC scores were not able to be determined because of cardiac movement. CONCLUSION: Concurrent determination of the degree of calcification in certain vessels may be possible from CT studies assessing AVF structure. VC scores provided by CT fistulograms could contribute to HD patient CVD risk assessment but studies with larger patient numbers are required to determine their relevance.

Adult↗