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PubMed1995

Distribution of calcification in the triangular fibrocartilage region in 181 patients with calcium pyrophosphate dihydrate crystal deposition disease.

PURPOSE: To investigate the occurrence of calcification around the triangular fibrocartilage complex in calcium pyrophosphate dihydrate (CPPD) crystal deposition disease. MATERIALS AND METHODS: The radiographs of 316 wrists in 181 patients with a definite or probable diagnosis of CPPD disease were reviewed to determine the occurrence of calcification in the inferior radioulnar joint cartilage, triangular fibrocartilage, lunotriquetral ligament, lunotriquetral cartilage, and triquetral cartilage. RESULTS: The distribution of calcification in the 316 wrists was as follows: inferior radioulnar joint cartilage, 87 wrists (28%), triangular fibrocartilage, 233 (74%); lunotriquetral ligament, 244 (77%); lunotriquetral cartilage, 167 (53%); and triquetral cartilage, 66 (21%). Forty-nine wrists had calcification in the lunotriquetral ligament or cartilage but not in the triangular fibrocartilage; 30 wrists had calcification in the triangular fibrocartilage but not in the lunotriquetral ligament or cartilage. This difference in prevalence was statistically significant (P = .0429). CONCLUSION: Radiologic diagnosis of CPPD crystal deposition disease in the wrist necessitates careful evaluation of the lunotriquetral ligament as well as the triangular fibrocartilage.

Aged↗
PubMed1996

Absence of coronary calcification on double-helical CT scans: predictor of angiographically normal coronary arteries in elderly women?

PURPOSE: To test the hypothesis that angiographically normal coronary arteries in elderly women are identifiable by the absence of coronary calcification on double-helical computed tomographic (CT) scans. MATERIALS AND METHODS: Forty-eight consecutive women (age range, 60-76 years) underwent coronary angiography for chest pain evaluation, as well as double-helical CT. Thirty women (mean age, 65 years +/- 5) had coronary artery disease (CAD), defined as any angiographic disease, and 18 women (mean age, 66 years +/- 4) had angiographically normal coronary arteries. RESULTS: Women with angiographically normal coronary arteries had lower coronary calcification scores than those of patients with CAD: 5.7 +/- 11 versus 580 +/- 634, respectively (P = .0004). Seven women with angiographically normal coronary arteries demonstrated mild coronary calcification (score < 50). Of the 11 women without coronary calcification, none had CAD. Thus, the absence of coronary calcification on double-helical CT scans in elderly women was predictive of angiographically normal coronary arteries with 61% sensitivity, 100% specificity, and 85% accuracy. CONCLUSION: Double-helical CT is an accurate, noninvasive modality for diagnosing angiographically normal coronary arteries in elderly symptomatic women.

Aged↗
PubMed2004

[Association between breast arterial calcifications and degree of control and severity of diabetes].

BACKGROUND AND OBJECTIVE: Our goal was to analyze the association between the presence of arterial calcifications detected on mammography and the degree of control and severity of diabetes. PATIENTS AND METHOD: We included all menopausal women with diabetes aged between 45 and 68 years from two health districts who participated in the breast cancer screening campaign of the region (n = 230). We reviewed their mammographies to evaluate the presence of arterial calcifications and thus associate these findings with factors determining the control and severity of diabetes (glycemia, glycosylated hemoglobin, micro- and macrovascular chronic complications) as obtained from the patients' medical records. RESULTS: The prevalence of breast arterial calcification was 40%. Patients with breast arterial calcifications had had diabetes for longer time and had more microvascular chronic complications. CONCLUSIONS: The presence of arterial calcifications detected on mammography in menopausal women with diabetes over 45 years of age is associated with microvascular chronic complications.

Aged↗
PubMedDate not supplied

Complete resorption of massive soft tissue calcification in a hemodialysis patient after parathyroidectomy.

Massive soft tissue calcification involving the abdomen of a dialysis patient is described. As the result of severe secondary hyperparathyroidism associated with intensive calcifications, the patient was disabled and confined to a wheelchair. Following parathyroidectomy, soft tissue calcifications resolved remarkably, symptoms were relieved and the patient was able to walk. Our patient presented an unusual site of soft tissue calcification in secondary hyperparathyroidism and showed an example of complete resorption of soft tissue calcification after parathyroidectomy.

Abdomen↗
PubMed1999

Murmurs associated with mitral annular calcification and aortic sclerosis.

BACKGROUND: Auscultation of patients with mitral annular calcification on echocardiography revealed a particular constellation of findings. OBJECTIVE: To test the hypothesis that a particular auscultatory constellation provides a high degree of certainty in diagnosing the combination of mitral annular calcification and aortic sclerosis so often found in the elderly. METHODS: Two groups of patients were studied to evaluate the particular auscultatory constellation under consideration which consisted of: (1) a harsh ejection systolic murmur heard from the 2nd right interspace to the cardiac apex and usually loudest between the 3rd left interspace and the apex; (2) the murmur radiates from the apex towards the left axilla and radiates poorly or not at all from the 2nd right interspace to the neck, and (3) the 2nd heart sound at the cardiac base is normal in intensity, and no ejection clicks are present. Group 1 consisted of patients with mitral annular calcification on echocardiographic examination, and group 2 consisted of patients in whom the particular constellation of auscultatory findings was present and who were then referred for echocardiographic assessment. RESULTS: The particular auscultatory constellation under investigation allowed the diagnosis of the presence of the combination of mitral annular calcification and aortic sclerosis with substantial accuracy. CONCLUSION: The findings in this exploratory study suggest that the pathologic combination of mitral annular calcification and aortic sclerosis can be diagnosed with a reasonably high degree of certainty in elderly patients, if the particular auscultatory configuration is identified.

Aged↗
PubMed2002

Novel insights into uremic vascular calcification: role of matrix Gla protein and alpha-2-Heremans Schmid glycoprotein/fetuin.

Cardiovascular mortality is markedly increased in the dialysis population when compared to non-uremic subjects. Vascular and valvular calcifications are most frequently found in dialysis patients at risk and are independent predictors of cardiovascular death in this population. Traditionally, the presence of hyperphosphatemia and an increased calcium x phosphate product was considered a major pathomechanistic condition leading to excessive vascular and soft-tissue calcifications in uremic subjects. Recent studies in knockout mice, however, revealed that deficiencies in calcium-regulatory proteins may also directly contribute to the development of extraosseus calcifications. alpha(2)-Heremans Schmid glycoprotein and matrix Gla protein are important inhibitors of calcification in vivo and there is novel evidence available that a deficiency in such proteins is involved in the pathogenesis of cardiovascular calcifications in dialysis patients.

Animals↗
PubMedDate not supplied

Kangaroo vs. porcine aortic valves: calcification potential after glutaraldehyde fixation.

The aim of this study was to evaluate and compare the calcification potential of kangaroo and porcine aortic valves after glutaraldehyde fixation at both low (0.6%) and high (2.0%) concentrations of glutaraldehyde in the rat subcutaneous model. To our knowledge this is the first report comparing the time-related, progressive calcification of these two species in the rat subcutaneous model. Twenty-two Sprague-Dawley rats were each implanted with two aortic valve leaflets (porcine and kangaroo) after fixation in 0.6% glutaraldehyde and two aortic valve leaflets (porcine and kangaroo) after fixation in 2% glutaraldehyde respectively. Animals were sacrificed after 24 h and thereafter weekly for up to 10 weeks after implantation. Calcium content was determined using inductively coupled plasma-mass spectrometry and confirmed histologically. Mean calcium content per milligram of tissue (dry weight) treated with 0.6 and 2% glutaraldehyde was 116.2 and 110.4 microg/mg tissue for kangaroo and 95.0 and 106.8 microg/mg tissue for porcine valves. Calcium content increased significantly over time (8.8 microg/mg tissue per week) and was not significantly different between groups. Regression analysis of calcification over time showed no significant difference in calcification of valves treated with 0.6 or 2% glutaraldehyde within and between the two species. Using the subcutaneous model, we did not detect a difference in calcification potential between kangaroo and porcine aortic valves treated with either high or low concentrations of glutaraldehyde.

Animals↗
PubMed1986

Pulmonary calcifications in children on dialysis.

Pulmonary calcifications are known to occur in patients with chronic renal failure. Recently, scintigrams with bone-seeking radionuclides have been used to detect subclinical pulmonary calcium deposits. We studied 18 children on maintenance dialysis without evidence of pulmonary calcification on chest X-ray. Four children (22.2%) had a positive technetium 99m hydroxymethylene diphosphate scan (group 1), and 14 children had a negative scan (group 2). Mean serum aluminum levels were 2.68 +/- 0.30 mumol/l (mean +/- SD) in group 1 as compared to 1.66 +/- 0.72 in group 2 (p less than 0.01). No significant difference was found between the groups with respect to serum levels of calcium, phosphorus, bicarbonate, magnesium and the calcium-phosphorus product as well as parathyroid hormone and vitamin D levels. The patients with pulmonary calcifications were on dialysis a significantly longer time than those of group 2 (62 +/- 15 versus 35.7 +/- 23 months; p less than 0.01). These data show that pulmonary calcification occurs with high frequency in children undergoing long-term dialysis. They seem to be related to high serum aluminum levels. We propose that pulmonary scintigrams with bone-seeking radionuclides be used routinely for the diagnosis and follow-up of uremic pulmonary calcification.

Adolescent↗
PubMed1987

Calcific aortic stenosis: a complication of chronic uraemia.

The incidence of aortic stenosis was studied in 174 consecutive patients aged less than 55 years at initiation of maintenance haemodialysis. Severe, calcific aortic stenosis developed in 6 patients a mean 9.7 years after starting haemodialysis (p = 0.0004 compared to population incidence). In 5 patients stenosis was due to severe premature calcification of a tricuspid aortic valve. Necropsy proven aortic valve calcification (with or without stenosis) was associated with an increased duration of haemodialysis, age greater than 35 years at starting dialysis and mitral annular calcification. There is an increased incidence of aortic stenosis in patients with chronic renal failure due to premature valvular calcification, which may be related to abnormal calcium and phosphate metabolism in uraemia.

Adult↗
PubMed2004

Matrix Gla protein is associated with coronary artery calcification as assessed by electron-beam computed tomography.

Matrix Gla protein (MGP) is an extracellular matrix protein with wide tissue distribution. It has been demonstrated that the expression of MGP is detected not only in the normal blood vessels but also calcified atherosclerotic plaques, and that MGP deficient mice develop extensive arterial calcification. MGP is thought to be a regulator of vascular calcification. A recent clinical study demonstrates the association between polymorphisms of the MGP gene and increased risk of myocardial infarction. However, there are no reports of the relationship between serum MGP levels and coronary artery calcification (CAC). We evaluated the severity of CAC using electron-beam computed tomography (EBCT), and measured serum MGP levels by enzyme-linked immunosorbent assay in 115 subjects with suspected coronary artery disease. CAC scores were correlated with traditional risk factors, such as age, gender, hyper-tension, diabetes, hyperlipidemia and smoking. The serum MGP levels were lower in patients with CAC than in those without CAC (p<0.001). As the severity of CAC increased, there was a significant decrease in serum MGP levels. Serum MGP levels (U/L) were 116.7 +/- 20.3, 104.9 +/- 19.2, 95.2 +/- 15.2 and 82.2 +/- 19.7, (medians 115.5, 105.0, 94.8, and 81.9) for the subjects with normal (CAC score=0), mild (CAC score=1 to 99), moderate (CAC score=100 to 400), and severe (CAC score >400) coronary calcification, respectively. We found that serum MGP levels are inversely correlated with the severity of CAC. These data suggest a possible role for MGP in the development of vascular calcification.

Aged↗
PubMed1994

Detection and quantitation of calcific atherosclerosis by ultrafast computed tomography in children and young adults with homozygous familial hypercholesterolemia.

Ultrafast computed tomography (CT) is a new method for detecting calcific lesions in the coronary arteries. The ability of CT to detect and quantify coronary artery atherosclerosis in children and young adults at risk for malignant atherogenesis was evaluated. A total of 11 consecutive familial hypercholesterolemic (FH) homozygotes (3 to 37 years old) participated. Untreated total cholesterol concentrations were 488 to 1277 mg/dL (12.7 to 33.2 mmol/L). Angiography detected significant lesions in 7 of 11 patients. CT detected calcific atherosclerosis in all 9 of the patients older than 12 years of age, including all those with angina. CT was more sensitive in detecting aortic root and coronary ostial lesions, where atherosclerosis first appears in homozygous FH. The volume of calcification (in cubic millimeters) correlated with the severity and duration of the hypercholesterolemia (r = .62, P < .05) as well as with the presence of angina (P < .05). All patients with angina (7 of 7) had > 150 mm3 of calcified volume, whereas only 1 of 4 asymptomatic patients had a volume score > 150 mm3. We conclude that (1) coronary and aortic calcium phosphate deposits are common in young FH homozygotes; (2) these deposits are associated with the presence of angiographic stenoses, as has been seen in adults with coronary atherosclerosis; and (3) aortic calcific deposits are more common than calcific coronary lesions.

Adolescent↗
PubMed1999

Dexamethasone enhances In vitro vascular calcification by promoting osteoblastic differentiation of vascular smooth muscle cells.

Vascular calcification is often associated with atherosclerotic lesions. Moreover, the process of atherosclerotic calcification has several features similar to the mineralization of skeletal tissue. Therefore, we hypothesized that vascular smooth muscle cells might acquire osteoblastic characteristics during the development of atherosclerotic lesions. In the present study, we investigated the effect of dexamethasone (Dex), which is well known to be a potent stimulator of osteoblastic differentiation in vitro, on vascular calcification by using an in vitro calcification model. We demonstrated that Dex increased bovine vascular smooth muscle cell (BVSMC) calcification in a dose- and time-dependent manner. Dex also enhanced several phenotypic markers of osteoblasts, such as alkaline phosphatase activity, procollagen type I carboxy-terminal peptide production, and cAMP responses to parathyroid hormone in BVSMCs. We also examined the effects of Dex on human osteoblast-like (Saos-2) cells and compared its effects on BVSMCs and Saos-2 cells. The effects of Dex on alkaline phosphatase activity and the cAMP response to parathyroid hormone in BVSMCs were less prominent than those in Saos-2 cells. Interestingly, we detected that Osf2/Cbfa1, a key transcription factor in osteoblastic differentiation, was expressed in both BVSMCs and Saos-2 cells and that Dex increased the gene expression of both transcription factors. These findings suggest that Dex may enhance osteoblastic differentiation of BVSMCs in vitro.

Alkaline Phosphatase↗
PubMed2001

Natural history and topographic pattern of progression of coronary calcification in symptomatic patients: An electron-beam CT study.

Electron-beam CT may assess the progression of coronary atherosclerosis by visualizing changes in calcification. The present investigation analyzes (1) the rate of progression of calcification in symptomatic patients, (2) the topographic pattern, and (3) the influence of baseline plaque burden and risk factors. Progression of calcification during a mean (median) interval of 18 (15) months was measured in 102 symptomatic outpatients (aged 59+/-9 years, 80% male) with calcification. In 4 patient groups with a baseline total score (Agatston criteria) of 1 to 30, >30 to 100, >100 to 400, and >400, the median was 3.1, 26.1, 58.9, and 109.7, respectively, for absolute annual progression of the score (P<0.05) and 57%, 49%, 32%, and 15%, respectively, for relative progression (P<0.05). On the coronary segmental level, changes were largely restricted to typical predilection sites of coronary atherosclerosis. The presence of angiographically defined coronary narrowing influenced absolute, but not relative, progression. Of the risk factors, only low density lipoprotein cholesterol levels showed a trend, although not significant, for predicting progression. These data indicate that baseline plaque burden determines the rate of progression of calcification. This appears to be a coronary systemic process, reflecting the natural history of coronary atherosclerosis.

Aged↗
PubMed2003

Human aortic valve calcification is associated with an osteoblast phenotype.

BACKGROUND: Calcific aortic stenosis is the third most common cardiovascular disease in the United States. We hypothesized that the mechanism for aortic valve calcification is similar to skeletal bone formation and that this process is mediated by an osteoblast-like phenotype. METHODS AND RESULTS: To test this hypothesis, we examined calcified human aortic valves replaced at surgery (n=22) and normal human valves (n=20) removed at time of cardiac transplantation. Contact microradiography and micro-computerized tomography were used to assess the 2-dimensional and 3-dimensional extent of mineralization. Mineralization borders were identified with von Kossa and Goldner's stains. Electron microscopy and energy-dispersive spectroscopy were performed for identification of bone ultrastructure and CaPO4 composition. To analyze for the osteoblast and bone markers, reverse transcriptase-polymerase chain reaction was performed on calcified versus normal human valves for osteopontin, bone sialoprotein, osteocalcin, alkaline phosphatase, and the osteoblast-specific transcription factor Cbfa1. Microradiography and micro-computerized tomography confirmed the presence of calcification in the valve. Special stains for hydroxyapatite and CaPO4 were positive in calcification margins. Electron microscopy identified mineralization, whereas energy-dispersive spectroscopy confirmed the presence of elemental CaPO4. Reverse transcriptase-polymerase chain reaction revealed increased mRNA levels of osteopontin, bone sialoprotein, osteocalcin, and Cbfa1 in the calcified valves. There was no change in alkaline phosphatase mRNA level but an increase in the protein expression in the diseased valves. CONCLUSIONS: These findings support the concept that aortic valve calcification is not a random degenerative process but an active regulated process associated with an osteoblast-like phenotype.

Aortic Valve↗
PubMed2003

Association of serum antibodies to heat-shock protein 65 with coronary calcification levels: suggestion of pathogen-triggered autoimmunity in early atherosclerosis.

BACKGROUND: Previous studies demonstrated an association between antibodies to mycobacterial heat-shock protein 65 (mHSP65) and carotid artery thickening. We examined whether mHSP65 antibodies are associated with levels of coronary calcification that appear to reflect preclinical coronary artery disease (CAD). METHODS AND RESULTS: Serum specimens from 201 healthy asymptomatic subjects (52% male; mean age, 56.6 years) undergoing electron-beam computed tomographic imaging were used to measure levels of mHSP65 and human HSP60 antibodies and antibodies to several infectious pathogens. We found that 84% of the study subjects had anti-mHSP65 IgG antibodies. Mean titers of mHSP65 antibodies were higher (1:394 versus 1:267, P=0.012) in individuals with than in those without elevated levels of coronary calcium (calcium score > or =150). Increasing titers of mHSP65 antibodies were significantly associated, in a dose-response manner, with elevated levels of coronary calcification. Individuals with the highest titers of mHSP65 antibodies (> or =1:800) had an adjusted odds ratio (OR) of 14.3 for having elevated coronary calcium (P=0.004). Association of mHSP65 antibodies with elevated coronary calcification levels was independent of CAD risk factors after multivariate adjustment (P=0.037). Interestingly, mHSP65 antibody titers were correlated with Helicobacter pylori infection (P=0.004), which maintained significance after adjustment for CAD risk factors and seropositivities to other pathogens (adjusted OR, 3.1; 95% CI, 1.4 to 6.6). No association was found between antibodies to human HSP60 and levels of coronary calcification. CONCLUSIONS: Antibodies to mHSP65 are associated with elevated levels of coronary calcification and correlated with H pylori infection, suggesting that pathogen-triggered autoimmunity plays a role in early atherosclerosis.

Adult↗
PubMed1999

Medial localization of mineralization-regulating proteins in association with Mönckeberg's sclerosis: evidence for smooth muscle cell-mediated vascular calcification.

BACKGROUND: Calcification of the media of peripheral arteries is referred to as Mönckeberg's sclerosis (MS) and occurs commonly in aged and diabetic individuals. Its pathogenesis is unknown, but its presence predicts risk of cardiovascular events and leg amputation in diabetic patients. Several studies have documented expression of bone-associated genes in association with intimal atherosclerotic calcification, leading to the suggestion that vascular calcification may be a regulated process with similarities to developmental osteogenesis. Therefore, we examined gene expression in vessels with MS to determine whether there was evidence for a regulated calcification process in the vessel media. METHODS AND RESULTS: In situ hybridization, immunohistochemistry, and semiquantitative reverse-transcription polymerase chain reaction were used to examine the expression of mineralization-regulating proteins in human peripheral arteries with and without MS. MS occurred in direct apposition to medial vascular smooth muscle cells (VSMCs) in the absence of macrophages or lipid. These VSMCs expressed the smooth muscle-specific gene SM22alpha and high levels of matrix Gla protein but little osteopontin mRNA. Compared with normal vessels, vessels with MS globally expressed lower levels of matrix Gla protein and osteonectin, whereas alkaline phosphatase, bone sialoprotein, bone Gla protein, and collagen II, all indicators of osteogenesis/chondrogenesis, were upregulated. Furthermore, VSMCs derived from MS lesions exhibited osteoblastic properties and mineralized in vitro. CONCLUSIONS: These data indicate that medial calcification in MS lesions is an active process potentially orchestrated by phenotypically modified VSMCs.

Adult↗
PubMed1991

Effect of calcification on in vivo mechanical response of rabbit arteries to balloon dilation.

BACKGROUND: Atherosclerosis has been associated with loss of artery wall distensibility in human cadavers and in experimental animal models, giving it the lay term "hardening of the arteries." METHODS AND RESULTS: To assess the effect of calcification on arterial distensibility, balloon pressure and volume were recorded during dilation of calcified aortas in Watanabe heritable hyperlipidemic (WHHL) rabbits in vivo. Calcification was induced by dietary supplements of cholesterol, vitamin D2, and calcium. Balloon pressure, volume, and time signals were acquired at high frequency with controls for temperature and balloon inflation rate. Resistance to balloon dilation was minimal in control rabbit aortas (delta Vmax = 5.0 +/- 3.5 microliters) and in excised nonatherosclerotic human coronary arteries, and it was small in aortas from cholesterol-fed rabbits (12.3 +/- 8 microliters), even when lipid levels were markedly elevated by a high cholesterol diet (611 +/- 347 mg/dl). With dietary cholesterol, vitamin D2, and calcium supplements, WHHL rabbits developed mild hypercalcemia (15 +/- 1.9 mg/dl), hypercholesterolemia (1,100 +/- 633 mg/dl), moderate-to-marked aortic calcification, and high resistance to balloon dilation (38 +/- 27) comparable to that seen in angioplasty patients. CONCLUSIONS: It is concluded that experimentally induced calcification decreases the distensibility of the rabbit aorta in vivo and that it yields to balloon dilation by plastic deformation closely resembling that seen in balloon angioplasty of human coronary arteries. These findings suggest that calcification contributes to arterial "hardening" associated with atherosclerosis.

Animals↗
PubMed1997

Prevention of bioprosthetic heart valve calcification by ethanol preincubation. Efficacy and mechanisms.

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. Our investigations studied ethanol pretreatment of glutaraldehyde cross-linked porcine aortic valves as a new approach to prevent cuspal calcification. The hypothesis governing this approach holds that ethanol pretreatment inhibits calcification resulting from protein structural alterations and lipid extraction. METHODS AND RESULTS: Results demonstrated complete inhibition of calcification of glutaraldehyde-pretreated porcine bioprosthetic aortic valve cusps by 80.0% ethanol in rat subdermal implants (60-day ethanol-pretreated calcium level, 1.87 +/- 0.29 micrograms/mg tissue compared with control calcium level, 236.00 +/- 6.10 micrograms/mg tissue) and in sheep mitral valve replacements (ethanol-pretreated calcium level, 5.22 +/- 2.94 micrograms/mg tissue; control calcium level, 32.50 +/- 11.50 micrograms/mg tissue). The mechanism of ethanol inhibition may be explained by several observations: ethanol pretreatment resulted in an irreversible alteration in the amide I band noted in the infrared spectra for both purified type I collagen and glutaraldehyde cross-linked porcine aortic leaflets. Ethanol pretreatment also resulted in nearly complete extraction of leaflet cholesterol and phospholipid. CONCLUSIONS: Ethanol pretreatment of glutaraldehyde cross-linked porcine aortic valve bioprostheses represents a highly efficacious and mechanistically based approach and may prevent calcific bioprosthetic heart valve failure.

Animals↗