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PubMed1985

The influence of dietary calcium on kidney calcification and renal function in rats fed high-phosphate diets.

This study was carried out to test the hypothesis that kidney calcification caused by high dietary phosphorus intake can be prevented by increasing the calcium content of the diet, because the latter reduces the intestinal P absorption. The investigation was conducted in rats fed semipurified diets with either a low (0.15%) or a high (1.20%) P content. Although dietary Ca supplementation (as CaCO3 or CaCl2) reduced the intestinal P absorption, it did not prevent kidney calcification induced by high dietary P. On the contrary, when CaCO3 was supplemented for 16 weeks, renal calcification increased, probably due to the alkaline nature of this salt. Both CaCO3 and CaCl2 in the high-P diets adversely influenced Mg use. This might explain the failure of these salts to prevent kidney calcification.

Animals↗
PubMed2005

Cocaine and coronary calcification in young adults: the Coronary Artery Risk Development in Young Adults (CARDIA) Study.

BACKGROUND: Cocaine use is associated with myocardial ischemia and infarction, but it is unclear whether this is only because of the acute effects of cocaine on heart rate, blood pressure, and vasomotor tone or whether accelerated atherosclerosis from long-term exposure to cocaine also contributes. METHODS: We sought to measure the association between cocaine exposure and coronary calcification, a marker for atherosclerosis, among participants in the CARDIA Study who received computed tomography scanning and answered questions about illicit drug use at the year 15 examination in 2000-2001. RESULTS: Among 3038 CARDIA participants (age 33-45 years, 55% women and 45% black), past cocaine exposure was reported by 35% and was more common among men, smokers, drinkers, and participants with less education. Powdered cocaine exposure was more common among whites, crack cocaine among blacks. Before adjustment, cocaine exposure was strongly associated with coronary calcification. After adjusting for age, sex, ethnicity, socioeconomic status, family history, and habits, however, these associations disappeared: adjusted odds ratios for coronary calcification were 0.9 (95% CI 0.6-1.3) for 1 to 10, 1.2 (95% CI 0.8-1.7) for 11 to 99, and 1.0 (95% CI 0.6-1.6) for > or =100 lifetime episodes of cocaine use, in comparison with none. Sex, tobacco, and alcohol use appeared to be primarily responsible for the confounding we observed in unadjusted models. CONCLUSION: We found no evidence of a causal relationship between long-term exposure to cocaine and coronary calcification and conclude that acute nonatherogenic mechanisms probably explain most cocaine-associated myocardial infarction.

Adult↗
PubMed2006

Cardiovascular morbidity and mortality in community-dwelling elderly individuals with calcification of the fibrous skeleton of the base of the heart and aortosclerosis (The Cardiovascular Health Study).

In the elderly, mitral annular calcification (MAC) and aortic valve sclerosis (AVS) are associated with increased cardiovascular morbidity and mortality. Aortic annular calcification (AAC) commonly occurs with MAC. However, the prognostic value of AAC, singly or in combination with MAC and AVS, for incident cardiovascular disease and mortality is unknown. From the Cardiovascular Health Study, we analyzed 3,782 participants (76 +/- 5 years of age, 60% women) who had an echocardiogram at the 1994 to 1995 examination and who were prospectively followed for an average of 6.6 years (range 0.01 to 8.5). All 3 calcification categories were associated with incident congestive heart failure (MAC: hazard ratio [HR] 1.71, 95% confidence interval [CI] 1.35 to 2.18, AAC: HR 1.62, 95% CI 1.28 to 2.06, and AVS: HR 1.50, 95% CI 1.19 to 1.89) and death. A stronger association with incident cardiovascular disease and mortality was observed with a larger number of calcification categories and with increased MAC severity. Moreover, in the participants with prevalent cardiovascular disease at echocardiographic examination (n = 1,054), MAC and AAC were still associated with cardiovascular mortality (MAC: HR 1.91, 95% CI 1.04 to 3.50; AAC: HR 2.11, 95% CI 1.16 to 3.85) even in fully adjusted models. In conclusion, MAC, AAC, and AVS are associated with a significant risk of incident congestive heart failure, cardiovascular and all-cause mortalities, and worse outcome in older patients with preexisting cardiovascular disease. Elderly patients with these findings represent a high-risk group and may require close medical attention.

Aged↗
PubMed2004

Regulatory role of endothelium in the expression of genes affecting arterial calcification.

Vascular calcification is a highly regulated process sharing features of bone mineralization. Since endothelium regulates many of the processes during atherogenesis, we monitored the expression of genes involved in calcification upon exposure of human coronary artery endothelial cells (HCAECs) to atherogenic stimuli. Genes studied were: core binding factor alpha-1 (Cbfa1/Runx2), a pivotal transcriptional regulator of osteogenesis; bone morphogenetic protein-2 (BMP2), an inducer of cartilage and bone; and matrix gla-protein (MGP), a potent inhibitor of calcification, which exerts its action by blocking BMP2. HCAECs were treated with oxidized-low density lipoprotein (ox-LDL, 80 microg/mL) or tumor necrosis factor-alpha (TNFalpha, 10 ng/mL), and the expression of Cbfa1, BMP2, and MGP was quantified by real-time PCR. Cbfa1 was expressed at low levels in untreated HCAECs, and its expression did not change with ox-LDL or TNFalpha treatment. The expression of BMP2 and MGP increased early after exposure to ox-LDL or TNFalpha (at 2-8 h), and the increase was not evident at 24 h. Ox-LDL exerted a stronger effect on MGP than on BMP2 expression. The effects of ox-LDL, but not TNFalpha, on MGP and BMP2 expression were inhibited by pretreatment of cells with an antibody directed at LOX-1, a lectin-like receptor for ox-LDL (10 microg/mL). Thus, the endothelium, when exposed to atherogenic stimuli, ox-LDL in particular, regulates the process of calcification by enhancing the expression of the bone inhibitory MGP, while the expression of Cbfa1 remains unchanged. Upregulation of BMP2 may represent a feedback upregulation in response to increase in MGP. The effect of ox-LDL appears to be mediated by LOX-1 activation.

Antibodies↗
PubMed2005

Morphological and topographic effects on calcification tendency of pHEMA hydrogels.

Poly(2-hydroxyethyl methacrylate) hydrogels were prepared in the presence of varying concentrations of water, or a co-monomer ethoxyethyl methacrylate at different strengths of crosslinking agent ethylene glycol dimethacrylate. Calcification tendency and its correlation with monomer mixture composition, topography and porosity of these materials were investigated. Scanning (SEM) and transmission electron microscopy (TEM) was used to study topography and porosity respectively. Calcification and calcium diffusion ability in to the hydrogels were investigated by light microscopy, SEM and energy dispersive analysis of X-rays (EDAX) after incubation of the materials in a metastable calcifying solution for 48 days. Polymer and solvent volume fractions were also studied to determine if a correlation existed between porosity and calcification. Most of the series of hydrogels showed surface irregularities. Internal structure showed evidence of a porous structure in one of the series. Calcification studies indicated diffusion of calcium ions in some of the series. The diffusion of calcium is limited to 30-40 microm in most calcified specimens. For hydrogels that exhibited substantial surface irregularities and micro channels, the infiltration of calcium up to 200 microm was observed. Attempts to detect porosity by electron microscopy failed in some of the hydrogels due to difficulty in sample processing and sectioning. However, collaboration of the results with different techniques used, indicated that surface defects are the major contributors to calcium deposition. Decrease in porosity reduces the amount of calcium deposits and infiltration with decreasing solvent volume fraction which is associated with crosslinking concentration and initial water content of the polymer.

Biocompatible Materials↗
PubMedDate not supplied

Toward cell therapy for vascular calcification: osteoclast-mediated demineralization of calcified elastin.

BACKGROUND: Elastin-oriented vascular calcification is a clinically significant feature, which involves formation of ectopic bone-like structures. Taking advantage of the similarities between arterial calcification and bone regulation, our hypothesis was that therapeutic approaches for limitation of vascular calcification could be developed using site-specific delivery of autologous osteoclasts. In the present paper, we tested the hypothesis that bone-marrow-derived osteoclasts have the ability to demineralize calcified elastin, without significant alterations in elastin integrity. METHODS: Active, multinucleated osteoclasts were obtained by in vitro maturation of rat bone-marrow-derived progenitor cells in the presence of vitamin D(3) and retinoic acid. Cell phenotype was validated by staining for tartrate-resistant acid phosphatase, formation of resorption pits on hydroxyapatite-coated disks, and RT-PCR for identification of cathepsin K gene expression. Calcified aortic elastin was seeded with osteoclasts and calcium, and phosphorous levels were monitored in gels and culture media to detect demineralization of elastin. Soluble elastin peptides were also monitored in culture media for elastin degradation. For in vivo experiments, pure aortic elastin was coimplanted with allogenic osteoclasts subdermally into rats, and the degree of elastin calcification and degradation was evaluated using mineral analysis and desmosine quantitation. RESULTS: Bone-marrow-derived osteoclasts reduced mineral content of calcified elastin in vitro by 80%. Moreover, in vivo implantation of allogenic osteoclasts in the vicinity of calcifying elastin limited elastin mineralization by almost 50%, in the absence of detectable elastin degradation. CONCLUSIONS: Osteoclasts have the ability to demineralize calcified elastin, without significant alterations in elastin integrity.

Animals↗
PubMed2005

Gender and age differences in the prevalence of coronary artery calcification in 953 Chinese subjects.

BACKGROUND: To investigate gender and age differences in coronary artery calcium (CAC) as determined by electron beam computed tomography (EBCT) in a Chinese population. METHODS: Consecutive patients undergoing EBCT were subdivided into groups based on gender and decades of life. They were further subdivided into three groups with respect to symptoms of coronary artery disease: typical, atypical and asymptomatic. Total calcium score was calculated for each patient and means calculated for each subgroup. Groups were then compared with respect to age, gender and symptoms. RESULTS: During the study period, 953 patients (736 men and 217 female) aged 17-86 years (mean 55+/-11 years) underwent EBCT. The prevalence of CAC increased significantly with increasing age. The mean total calcium score also increased with increasing age in males and females of each symptom subgroup. The prevalence of coronary artery calcification was significantly higher in males than females until age in excess of 69 years (p<0.05). The prevalence of coronary artery calcification and mean calcium scores were significantly different between each symptom subgroup (p<0.001) with higher scores and prevalence in patients with typical symptoms of coronary disease. CONCLUSIONS: There is an increase in the prevalence of coronary artery calcification with age in Chinese subjects. Male subjects are more likely than female subjects to have detectable coronary calcification up until an age in excess of 69 years. Patients under the age of 70 years, with typical symptoms of coronary artery disease have a higher prevalence and mean calcium score than those with atypical or no symptoms.

Adolescent↗
PubMed2003

Plaque blush, branch location, and calcification are angiographic predictors of progression of mild to moderate coronary stenoses.

BACKGROUND: Angiographic predictors of plaque progression are weak and few: length, irregular surface, turbulence, low shear, and (in some studies) eccentricity and calcification. Having noted plaques that briefly retained dye after angiography, we interpreted these as plaques with a fissured surface or neovascularization and hypothesized that progression would be predicted by "plaque blush." METHODS: Plaques (<50% diameter stenosis) in 68 pairs of angiograms, 5.6 +/- 4.8 months apart, were reviewed by 2 blinded observers. The presence of plaque blush, calcification, clot (mobile defect), eccentricity, and a branch point location were compared between progressing (> or =20% stenosis increase) and nonprogressing plaques. RESULTS: Sixteen lesions in 15 patients progressed from 29% +/- 13% to 68% +/- 14% over a period of 8.1 +/- 7.9 months. Patients with and without progression were similar in sex, age, congestive heart disease risk factors, medications, interval between angiograms, clinical presentation, and initial stenosis severity. By logistic regression, plaque blush (BL) (P =.002), calcification (CA) (P =.024), and a branch (BR) point location (P =.001) predicted plaque progression. The odds ratio for plaque progression (ORp) was calculated as ORp = e(2.5 x BL + 1.8 x CA + 2.6 x BR). Using an ORp of 1/3, the model has 81% sensitivity and 77% specificity. A second analysis in which each progressive lesion was compared with proximal and distal lesions and with one in a different coronary artery yielded similar results. CONCLUSIONS: In mild to moderate coronary stenoses, studied retrospectively, plaque blush (a new sign) and a branch point location were strong predictors of plaque progression, whereas calcification was a weak predictor of progression.

Calcinosis↗
PubMed2000

Late results of percutaneous mitral commissurotomy for calcific mitral stenosis.

The aim of this study was to assess late results of percutaneous mitral commissurotomy (PMC) in calcific mitral stenosis and to identify predictors to improve patient selection. We analyzed 422 patients who underwent PMC for calcific mitral stenosis. The extent of calcium was graded from 1 to 4 by fluoroscopy: 227 patients (53%) were graded 1, 125 (30%) graded 2, 55 graded 3 (13%), and 15 graded 4 (4%). The procedure failed in 15 patients, used a single balloon in 11, a double balloon in 126, and the Inoue balloon in 270. In-hospital mortality was 1.2%. Good immediate results (valve area >/=1.5 cm(2) without mitral regurgitation >2/4), were obtained in 321 patients (76%). Multivariate analysis identified 5 predictors of good immediate results: a younger age (p = 0.0004), a lesser degree of stenosis (p = 0.0005), a smaller extent of calcium (p = 0.04), the use of the Inoue balloon (p = 0.015), and a larger effective balloon dilating area (p = 0.006). Good functional results, defined as survival with no further intervention and in New York Heart Association class I or II, were 36 +/- 4% at 8 years. The predictors of good functional results after good immediate results were a younger age (p = 0.04), a lower pre-PMC New York Heart Association class (p <0.0001), sinus rhythm (p = 0.0006), a smaller extent of calcium (p = 0.02), and a lower gradient after PMC (p <0.0001). Despite a frequent deterioration on follow-up after PMC for calcific mitral stenosis, the predictive analysis suggests that PMC may be useful in deferring surgery in selected patients with mild to moderate calcific deposits, who have otherwise favorable characteristics.

Aged↗
PubMed1980

Calcification in porcine xenograft valves in children.

Calcification developed in the degenerating collagen of the cusps of three porcine xenograft heart valves implanted in children for less than 4 years. The morphologic features and effects of this calcification are presented. Calcification of porcine xenografts seems to occur more frequently and at an earlier stage after insertion in children than in adults. Host factors, possibly related to calcium homeostasis, may promote calcification; hence, these valves may not be appropriate for use in children.

Adolescent↗
PubMed1983

Clinical and echocardiographic characteristics of patients with mitral anular calcification. Comparison with age- and sex-matched control subjects.

The clinical and echocardiographic features of 104 patients (53 women and 51 men) with mitral anular calcification (MAC) were compared with those of 121 age- and sex-matched control subjects (62 women and 59 men) without MAC. The incidence of coronary artery disease, rheumatic heart disease, systemic hypertension, and diabetes mellitus was similar in both groups. Patients with MAC had a greater incidence of cardiomegaly (p less than 0.001), cardiac conduction defects (p less than 0.001), and aortic outflow tract murmurs (p less than 0.005) than did control patients. Patients with MAC and without aortic root calcification had a higher incidence (p less than 0.001) of conduction defects than did patients with aortic root calcification without MAC. Control patients with and without aortic root calcification had a similar incidence of conduction defects. A higher incidence of atrioventricular block (p less than 0.025) and bundle branch block or left anterior hemiblock or intraventricular conduction defect (p less than 0.05) was present in anterior MAC than in posterior MAC. In conclusion, patients with MAC have a higher incidence of cardiomegaly, cardiac conduction defects, and aortic outflow tract murmurs than a control group.

Age Factors↗
PubMed1996

Relation of cholesterol-year score to severity of calcific atherosclerosis and tissue deposition in homozygous familial hypercholesterolemia.

The high concentrations of low-density lipoprotein cholesterol in plasma lead to accelerated atherosclerosis in patients homozygous for familial hypercholesterolemia (FH). We addressed the hypothesis that lipid deposition in the arterial vasculature and in nonvascular tissues in these patients correlates with both the duration and severity of their hypercholesterolemia. The severity of calcific atherosclerosis was defined by calcification scores and a calcified volume determined by electron beam tomography. The extent of tendinous xanthomatosis was quantitated by computed tomography. A cholesterol-year score was calculated based on the age and the yearly mean serum cholesterol concentration of each patient. Seventeen patients homozygous for FH were followed up. The average total cholesterol concentration in the study group was 780 +/- 231 mg/dl (20.2 mmol/L), and the cholesterol-year scores ranged from 2,172 mg-year/dl (56 mmol-year/L) to 32,260 mg-year/dl (834 mmol-year/L). Achilles tendon width (r=0.86) and cross-sectional area (r=0.81; both p <0.001) were best correlated with the cholesterol-year score. In addition, the coronary (r=0.61; p<0.05), ostial (r=0.45; p<0.05), and total (r= 0.77; p<0.001) calcification atherosclerosis scores all were best correlated with the cholesterol-year score. Calcific atherosclerosis was not observed in these patients until the cholesterol-year score exceeded 10,000 mg-year/dl (260 mmol-year/L). These findings establish a direct association of cholesterol-year with extravascular lipid deposition in tissues of patients with FH. The cholesterol-year score may be useful in defining the risk of atherosclerosis in patients with more common forms of hypercholesterolemia.

Achilles Tendon↗
PubMed1997

Prognostic significance of coronary calcific deposits in asymptomatic high-risk subjects.

PURPOSE: To determine the predictive value of coronary calcifications for coronary heart disease events in high-risk, asymptomatic adults: PATIENTS AND METHODS: A prospective cohort study of 1,461 high-risk, asymptomatic subjects were followed for 55 months with a 98% success rate. Coronary risk factor assessment and cardiac fluoroscopy with digital subtraction enhancement were performed to determine the number of calcified coronary arteries. RESULTS: Fifty-eight percent of this cohort (852 subjects) had fluoroscopically detectable coronary calcification: 437 (30%) had calcium in one, 253 (17%) in two, and 162 (11%) in all three coronary vessels. There were 90 (6%) deaths, 35 (39%) attributable to coronary heart disease, and 43 (3%) nonfatal myocardial infarctions. Subjects with calcification in more than one major coronary artery were 2.2 times more likely to suffer coronary death or nonfatal infarction (P = 0.001) than were subjects with one or no calcified arteries. Multivariable logistic regression analysis showed that only the number of calcified arteries, age, total cholesterol, history of diabetes, and left ventricular hypertrophy by electrocardiogram were associated independently with the incidence of coronary death or infarction in these subjects. CONCLUSIONS: Coronary calcification predicts coronary heart disease death or infarction in high-risk asymptomatic adults as well as do standard risk factors.

Adult↗
PubMed2002

Capsular calcification of alloplastic orbital implants.

PURPOSE: To report calcification of the capsule surrounding alloplastic orbital implants and postulate this calcification as a possible cause of poor implant motility. DESIGN: Interventional case reports. METHODS: Two patients with alloplastic spherical implants after enucleation presented with poor implant motility. Both patients underwent orbital implant exchange with a quasi-integrated porous polyethylene orbital implant. RESULTS: During removal of the original alloplastic orbital implant, a hard, thick shell adherent to the surrounding orbital tissues was encountered. After complete excision of the shell, microscopic evaluation confirmed a dense, fibrous capsule with calcification. No evidence of inflammation or malignancy was associated with either capsule. Postoperatively, both patients had significant improvement in motility of their new orbital implant. CONCLUSIONS: Although calcification of the fibrous capsule surrounding alloplastic orbital implants is an unusual finding, it may result in poor implant motility. Capsule excision and implant exchange may significantly improve the motility of the orbital implant.

Calcinosis↗
PubMed1998

Choroidal calcification in Bartter syndrome.

PURPOSE: Bartter syndrome is characterized by hyperplasia of the renal juxtaglomerular apparatus, hyperaldosteronism, and hypokalemic alkalosis. We report a case of Bartter syndrome associated with normal serum calcium levels and posterior choroidal calcification. METHODS: Case report. A 59-year-old man with bilateral cataract and Bartter syndrome underwent a complete ophthalmic examination, including standardized echography before and after cataract surgery. RESULTS: Before cataract surgery, echography identified small, hyperreflective, multifocal, bilateral choroidal lesions with posterior shadowing. After surgery, these lesions appeared as yellow-white, barely elevated plaques with smooth edges and were diagnosed as choroidal calcification. CONCLUSIONS: Choroidal calcification may occur in patients with Bartter syndrome. This condition should be added to the differential diagnosis of posterior segment calcification.

Bartter Syndrome↗
PubMed2001

Matrix metalloproteinase-2 is associated with tenascin-C in calcific aortic stenosis.

We previously showed that the expression of tenascin (TN-C), an extracellular matrix glycoprotein found in developing bone and atherosclerotic plaque, and matrix metalloproteinase-2 (MMP-2) are coordinated and interdependent in cultured vascular smooth muscle cells. In this study, we hypothesized that TN-C and MMP-2 are mechanistically involved in the pathobiology of calcific aortic stenosis. Human calcific aortic stenosis cusps demonstrated immunohistochemically prominent deposition of TN-C, MMP-2, and alkaline phosphatase activity, as well as MMP-2 gelatinolytic activity. Although far lesser amounts of TN-C were noted in several of the grossly non-calcified valve cusps, MMP-2 and AP were never detected. Further, when aortic valve interstitial cells (both sheep and human) were cultivated on collagen supplemented with TN-C, both MMP-2 mRNA expression and MMP-2 gelatinolytic activity (both pro and active forms), were up-regulated compared to control. These observations support the view that accumulation of first TN-C and then MMP-2 are associated with progression of calcification. The residual presence of these proteins in severe calcifications is indicative of their involvement in the pathogenesis.

Animals↗
PubMed2005

Triglycidylamine crosslinking of porcine aortic valve cusps or bovine pericardium results in improved biocompatibility, biomechanics, and calcification resistance: chemical and biological mechanisms.

We investigated a novel polyepoxide crosslinker that was hypothesized to confer both material stabilization and calcification resistance when used to prepare bioprosthetic heart valves. Triglycidylamine (TGA) was synthesized via reacting epichlorhydrin and NH(3). TGA was used to crosslink porcine aortic cusps, bovine pericardium, and type I collagen. Control materials were crosslinked with glutaraldehyde (Glut). TGA-pretreated materials had shrink temperatures comparable to Glut fixation. However, TGA crosslinking conferred significantly greater collagenase resistance than Glut pretreatment, and significantly improved biomechanical compliance. Sheep aortic valve interstitial cells grown on TGA-pretreated collagen did not calcify, whereas sheep aortic valve interstitial cells grown on control substrates calcified extensively. Rat subdermal implants (porcine aortic cusps/bovine pericardium) pretreated with TGA demonstrated significantly less calcification than Glut pretreated implants. Investigations of extracellular matrix proteins associated with calcification, matrix metalloproteinases (MMPs) 2 and 9, tenascin-C, and osteopontin, revealed that MMP-9 and tenascin-C demonstrated reduced expression both in vitro and in vivo with TGA crosslinking compared to controls, whereas osteopontin and MMP-2 expression were not affected. TGA pretreatment of heterograft biomaterials results in improved stability compared to Glut, confers biomechanical properties superior to Glut crosslinking, and demonstrates significant calcification resistance.

Animals↗
PubMed2004

A locus on chromosome 7 determines dramatic up-regulation of osteopontin in dystrophic cardiac calcification in mice.

Calcification of necrotic tissue is frequently observed in chronic inflammation and atherosclerosis. A similar response of myocardium to injury, referred to as dystrophic cardiac calcinosis (DCC), occurs in certain inbred strains of mice. We now examined a putative inhibitor of calcification, osteopontin, in DCC after transdiaphragmal myocardial freeze-thaw injury. Strong osteopontin expression was found co-localizing with calcification in DCC-susceptible strain C3H/HeNCrlBr, which exhibited low osteopontin plasma concentrations otherwise. Osteopontin mRNA induction was 20-fold higher than in resistant strain C57BL/6NCrlBr, which exhibited fibrous lesions without calcification and little osteopontin expression. Sequence analysis identified several polymorphisms in calcium-binding and phosphorylation sites in osteopontin cDNA. Their potential relevance for DCC was tested in congenic mice, which shared the osteopontin locus with C57BL/6NCrlBr, but retained a chromosomal segment from C3H/HeNCrlBr on proximal chromosome 7. These mice exhibited strong osteopontin expression and DCC comparable to C3H/HeNCrlBr suggesting that a trans-activator of osteopontin transcription residing on chromosome 7 and not the osteopontin gene on chromosome 5 was responsible for the genetic differences in osteopontin expression. A known osteopontin activator encoded by a gene on chromosome 7 is the transforming growth factor-beta1, which was more induced (3.5x) in C3H/HeNCrlBr than in C57BL/6NCrlBr mice.

Animals↗