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PubMed2000

Association of hostility with coronary artery calcification in young adults: the CARDIA study. Coronary Artery Risk Development in Young Adults.

CONTEXT: Psychosocial factors, including personality and character traits, may play a role in the development and expression of coronary artery disease. OBJECTIVE: To evaluate whether hostility, a previously reported predictor of clinical coronary artery disease, is associated with coronary calcification, which is a marker of subclinical atherosclerosis. DESIGN: Prospective cohort study. SETTING AND PARTICIPANTS: Volunteer subsample from Chicago, Ill, and Oakland, Calif, consisting of 374 white and black men and women, aged 18 to 30 years at baseline, who participated in the Coronary Artery Risk Development in Young Adults (CARDIA) study. Cook-Medley hostility assessment data were collected at baseline from 1985 to 1986 and at year 5 examinations from 1990 to 1992. After the 10-year examinations in the 1995-1996 year, electron-beam computed tomographic scans were performed. MAIN OUTCOME MEASURES: Presence of any detectable coronary artery calcification (coronary calcium score >0), and coronary artery calcium scores of 20 or higher. RESULTS: In logistic regression analysis adjusting for age, sex, race, and field center comparing those with hostility scores above and below the median of the distribution of the present sample, the odds ratio of having any coronary calcification was 2.57 (95% confidence interval, 1.31-5.22), and the odds ratio of having a calcium score of 20 or higher was 9.56 (95% confidence interval, 2.29-65.9) for calcium scores of 20 or higher. The associations with any coronary artery calcification persisted after adjusting for demographic, lifestyle, and physiological variables. Results using a cynical distrust subscale were somewhat weaker than for those using the global hostility score. Power was inadequate to perform sex- or race-specific analyses. CONCLUSION: These results suggest that a high hostility level may predispose young adults to coronary artery calcification. JAMA. 2000;283:2546-2551

Adult↗
PubMed1980

Cerebellar calcification on computerized tomography.

Cerebellar calcification on CT scan was observed in five patients over a two-year period. It was located bilaterally and symmetrically in the dentate nucleus in all 5 patients and inthe cerebellar vermis in one. Calcifications of the basal ganglia and cerebral cortex were associated in two cases each. Skull radiography did not reveal the cerebellar calcifications, and serum calcium levels were normal in all patients. None had symptoms or signs of cerebellar dysfunction, and they had a variety of different clinical diagnoses. Cerebellar calcification may be a form of benign intracerebral calcification.

Aged↗
PubMed1994

Physicochemical properties of calcific deposits isolated from porcine bioprosthetic heart valves removed from patients following 2-13 years function.

The purpose of this study was to characterize the physicochemical properties of calcific deposits that cause the failure of tissue-derived heart valve bioprostheses. This was done in an effort to understand the mechanism of pathologic biomineralization in the cardiovascular system and potentially prevent deterioration of bioprostheses. Calcific deposits taken from 10 failed bioprosthetic valves that had been implanted in patients for 2-13 years were characterized by chemical analysis, x-ray diffraction, FTIR spectroscopy, scanning electron microscopy, polarized light microscopy, and solubility measurements. The combined results identified the biomineral as an apatitic calcium phosphate salt with substantial incorporation of sodium, magnesium and carbonate. The average Ca/PO4 ratio for this "young" pathologic biomineral was approximately 1.3, considerably lower than approximately 1.7 found in mature atherosclerotic plaque biomineral and mature skeletal biomineral, both of which approximate hydroxyapatite in composition. Deproteinated calcific deposits from bioprostheses had thermodynamic solubilities comparable to those of both atherosclerotic plaque, typical pathologic biomineral and hydrolyzed octacalcium phosphate (OCP, Ca4H(PO4)3 x 2.5 H2O), a proposed precursor phase to biomineral apatite. This later finding, together with chemical composition and structural details of the bioprosthetic deposits themselves, supports a mechanism of cardiovascular calcification in which OCP plays a crucial role in the formation of the final apatitic phase. This suggests an approach toward prevention of bioprosthetic tissue calcification through control of the formation of the kinetically favored OCP precursor and/or its transformation into bioapatite.

Bioprosthesis↗
PubMed1994

Effect of 2-amino oleic acid exposure conditions on the inhibition of calcification of glutaraldehyde cross-linked porcine aortic valves.

Postimplant calcific degeneration is a frequent cause of clinical failures of glutaraldehyde cross-linked porcine bioprosthetic heart valves (BPHV). It was demonstrated previously that 2-amino oleic acid (AOA) used as a bioprosthesis treatment was highly effective in mitigating aortic valve cusp but not aortic wall calcification. Our main objective was to study the efficacy of various AOA exposure conditions for inhibiting calcification of both cusps and aortic wall tissues using rat subdermal implants. BPHV tissues were treated with a saturated AOA solution for different time intervals before experimental. Aortic wall AOA levels were consistently lower than that of the cusps after the same exposure times. The diffusion of calcium ion across both cusp and aortic wall tissues was evaluated, and the results demonstrated that there was an AOA exposure time-dependent retardation of calcium ion penetration for cusp but not aortic wall. An 8-month extraction study was performed to determine the stability of AOA binding. When Tween 80 was used as an extraction medium, cusp and aortic wall retained 12.9 and 48.7%, respectively, of their initial AOA levels. AOA inhibition of calcification in rat subdermal implants (60 days) was found to be exposure time-dependent with maximum treatment time (120 h), resulting in the lowest calcium levels (20.1 +/- 10.3 and 71.4 +/- 5.4 micrograms/mg of cusp and aortic wall, respectively) as compared with controls (219.1 +/- 6.8 and 104.9 +/- 8.5 micrograms/mg of cusp and aortic wall, respectively). The significance of AOA binding on BPHV tissue was determined by either blocking or reducing BPHV's (cusp and aortic wall) free aldehyde residues with lysine or NaBH4, respectively, before AOA treatment. For aortic cusps, the AOA contents after 72 h were 98.3 +/- 2.7, 34.2 +/- 3.6, and 54.1 +/- 3.0 nM/mg of tissue for AOA (control), lysine-pretreated (plus AOA) and NaBH4-pretreated (plus AOA) tissues, respectively. However, their calcium levels after 60 days of rat subdermal implant were all comparable (i.e., 48.1 +/- 6.2, 38.2 +/- 9.1, and 47.0 +/- 15.0 micrograms calcium per mg of tissue). Similar results were observed on BPHV aortic wall. It can thus be concluded that AOA inhibition of BPHV calcification is exposure time-dependent, but the efficacy of AOA for aortic wall is less than that noted for aortic cusps, perhaps because of lower AOA binding and differences in calcium diffusion kinetics.

Animals↗
PubMed2003

Prevention of polyurethane valve cusp calcification with covalently attached bisphosphonate diethylamino moieties.

OBJECTIVE: Calcification of polyurethane prosthetic valve leaflets causes a major functional impairment. Previously we showed that polyurethane heart valves modified with covalently linked bisphosphonate groups were resistant to calcification in vivo. However, we also found that the highly polar anionic bisphosphonate groups on the polyurethane surface attracted sodium counter ion adsorption, and thereby increased the elastomer's water absorption to 20% of total weight. In this study we address the increased water absorption by investigating the hypothesis that covalently attaching cationic diethylamino groups to the bisphosphonate-modified polyurethane will reduce water absorption. Thus we evaluated the mechanical and in vivo anticalcification properties of heart-valve leaflets composed of this modified polymer. METHODS: Diethylamino and bisphosphonate groups (DBP) were appended to the polyurethane Biospan's hard segment using previously published bromoalkylation methodology. Water absorption and biaxial mechanical and uniaxial failure testing were used to determine the mechanical properties of the DBP-modified polymer. Rat subdermal implants (60 days) and extended (150 days) single pulmonary leaflet replacements in juvenile sheep provided in vivo assessments of the bisphosphonate-modified polyurethane. RESULTS: The water absorption properties of the DBP-modified polymers and unmodified polyurethanes were 1.86 and 2.3 %, respectively. Biaxial mechanical tests showed the DBP-modified polymer was more compliant than the unmodified control material, but all polymeric material had similar uniaxial failure properties. In both rat subdermal and sheep circulatory implants, the DBP-modified polyurethane resisted calcification, as assessed by scanning electron microscopy, with complete calcification inhibition in prosthetic sheep valve leaflet replacements. CONCLUSION: DBP polyurethane possesses physical (water absorption) and biomechanical properties comparable to unmodified polyurethane and can resist intrinsic heart-valve leaflet calcification in blood-stream implants.

Animals↗
PubMed2006

Fibronectin enhances in vitro vascular calcification by promoting osteoblastic differentiation of vascular smooth muscle cells via ERK pathway.

The process of vascular calcification presents several features similar to osteogenesis in which fibronectin (FN) acts as a regulator of osteoblastic differentiation and the ERK signal pathway is involved. In order to find whether FN promotes the osteoblastic differentiation of vascular smooth muscle cells (VSMCs) through the ERK signal pathway, we investigated the effect of FN on the calcification of VSMCs by using an in vitro cell model. VSMCs cultured in plates with FN (0-20 microg/cm2) coating were induced to calcify by 10 mM sodium beta-glycerophosphate (beta-GP). FN exacerbated VSMC calcification in a dose- and time-dependent manner, as indicated by the number of calcifying nodules per slide and the amount of calcium in the deposition. Data from RT-PCR and immunoblotting assay revealed that FN also enhanced the expression of several phenotypic markers of osteoblasts, including alkaline phosphatase (ALP) activity, osteocalcin (OC), and Osf2/Cbfa1, a key transcription factor in osteoblastic differentiation. Furthermore, a specific inhibitor for ERK, PD98059 (10 microM), significantly suppressed the effect of FN on calcification and phenotypic marker expression. These findings seem to suggest that FN enhanced vascular calcification by promoting the osteoblastic differentiation of VSMCs via ERK signal pathway.

Animals↗
PubMed2005

Severe fetal brain dysgenesis with focal calcification.

OBJECTIVE: To describe a fetal syndrome of abnormal brain development with intracranial calcification, identified in three successive pregnancies. METHODS: Clinical, imaging, and pathological descriptions, and pedigree assessment. RESULTS: All three affected pregnancies were terminated, following imaging diagnosis of brain abnormality. The most complete fetal study, from the third of these pregnancies, showed widespread foci of brain calcification not associated with inflammation, with extensive necrosis and calcification of periventricular white matter, but with sparing of thalamus and basal ganglia. The corticospinal tracts were severely hypoplastic. CONCLUSION: This condition appears to be a 'new' genetically determined, probably autosomal recessive disorder of severe early brain dysgenesis with focal calcification, resembling, but distinct from, certain other clinical genetic entities of which brain calcification is a part.

Abnormalities, Multiple↗
PubMed2001

Matrix Gla protein accumulates at the border of regions of calcification and normal tissue in the media of the arterial vessel wall.

Vitamin K-dependent matrix Gla protein (MGP) has been suggested to play a role in the inhibition of soft-tissue calcification. Here we report the expression of recombinant prokaryotic MGP as part of a fusion protein and the preparation of two antibodies that specifically recognize MGP. Monoclonal antibodies were raised against synthetic peptides homologous to the sequences 3-15 and 63-75 of human MGP. Both antibodies recognize recombinant and synthetic human MGP. Immunohistochemical analysis showed that MGP was associated with the extracellular matrix of noncalcified bone and with chondrocytes in cartilage. In the healthy human arterial vessel wall, MGP antigen was demonstrated in association with smooth muscle cells and elastic laminae of the tunica media and with the extracellular matrix of the adventitia. Colocalization with the elastic laminae was lost at sites of medial calcification; in both human and rat arteries, high amounts of MGP were found in the extracellular matrix at borders of intimal and medial calcification. Our data demonstrate the close association between MGP and calcification. It is suggested that undercarboxylated MGP is biologically inactive and that poor vascular vitamin K status may form a risk factor for vascular calcification.

Animals↗
PubMed1997

Calcification potential of small intestinal submucosa in a rat subcutaneous model.

Glutaraldehyde treatment of collagen biomaterials promotes calcification, poor host-tissue incorporation, and ultimately mechanical failure of bioprotheses. Porcine small-intestinal submucosa (SIS) is a biomaterial which has been investigated for several applications including arterial and venous grafts and repair of tendon, ligament, body wall, and urinary bladder defects. The calcification potential of peracetic acid (PAA)-sterilized SIS was studied. Four test samples, (1) native (cleaned, untreated) SIS, (2) SIS sterilized with 0.1% PAA, (3) SIS treated with 0.25% glutaraldehyde for 20 min, and (4) commercially available glutaraldehyde-preserved porcine bioprosthetic heart valve cusp segments (GPV), were each implanted subcutaneously in each of 24 weanling rats. Six rats were euthanatized at 1, 2, 4, and 8 weeks. Evaluation of calcium concentration by atomic absorption spectroscopy and extent of mineralization and fibrosis by light microscopy were performed. Atomic absorption revealed no calcification in native or peracetic acid-treated SIS at any time point compared with preimplant calcium concentration. Statistically significant (P < 0.0001) calcification occurred in glutaraldehyde-treated materials (SIS and GPV) at each evaluation as compared to native and peracetic acid-treated samples. Histopathology indicated native and peracetic acid-treated SIS showed no implant mineralization (P < 0.0001) and little peri-implant fibrosis (P < 0.0001). Results suggested that native and peracetic acid-treated SIS have a low calcification potential and further study of this biomaterial is warranted.

Animals↗
PubMed1989

Promotion of calcification by imidazole and its suppression by diltiazem in the growth cartilage of rats with HEBP induced rickets.

The object of our experiments was to determine the effect of imidazole on the growth cartilage of rats with HEBP induced rickets. When HEBP (1-hydroxyethylidene-1, 1-bisphophonic acid) was given to young rats in large doses over a short period, rickets was consistently produced. We found that imidazole had a calcification promoting action in the growth plate cartilage where there had been an increase in thickness due to the inhibition of calcification. In an attempt to clarify the mechanism of accelerated calcification due to imidazole, the effects of diltiazem, a calcium antagonist, were observed; it was found to suppress the accelerated calcification. If diltiazem inhibits the entry of calcium ions into the cells of the growth cartilage, as it does in smooth muscle and myocardial cells, then our results indicate that intracellular concentrations of calcium may play an important role in the accelerated calcification due to imidazole.

Animals↗
PubMed1986

Intracranial calcification in paediatric computed tomography.

An analysis of the computed tomograms of 18000 children examined consecutively form the basis of an assessment of the diagnostic significance of intracranial calcification. The low incidence of physiological calcification in the pineal and choroid of about 2% up to the age of 8 years, but increasing 5-fold by the age of 15 years, is confirmed. Pathological calcification occurred in 1.6%, the commonest causes being neoplasms (43%), neuroectodermal syndromes (20%) and infections (12%). Diffuse basal ganglia calcification (15%) bore little relation to the diverse clinical symptomatology, and routine biochemical studies showed a disorder of metabolism to be present in only 6 cases. Calcification has not been previously noted in acute haemorrhagic leukoencephalitis, Pertussis or Cocksackie encephalitis, infantile neuraxonal dystrophy, Marinesco-Sjögren syndrome or in the basal ganglia in neurofibromatosis.

Acute Disease↗
PubMed1982

Meconium peritonitis, intraperitoneal calcifications and cystic fibrosis.

Twelve cases of meconium peritonitis were retrospectively reviewed in this study. Five of these patients had cystic fibrosis. Of the patients with cystic fibrosis, intraperitoneal calcifications were present in three (60%) and two (40%) had none. All seven patients (100%) who had meconium peritonitis without cystic fibrosis had abdominal calcifications. These results indicate that the presence of intraperitoneal calcifications does not exclude the diagnosis of cystic fibrosis and that the absence of calcification favors cystic fibrosis. However, a review of the literature indicates the absence of calcification is merely of clue and not definitive as to the etiology of the meconium peritonitis.

Calcinosis↗
PubMed1976

Intracranial calcification mimicking the Sturge-Weber syndrome: a consequence of cerebral folic acid deficiency?

Cerebral cortical calcification identical to that of the Sturge-Weber syndrome was observed in two children. In one child the calcification appeared after intrathecal administration of methotrexate and skull irradiation because of leukemia involving the central nervous system. In the other child, who had coeliac disease and epilepsy, the calcification appeared after treatment with anticonvulsants. This treatment was also contributing to the development of profound megaloblastic anemia. The unspecificity of the Sturge-Weber calcification is stressed and the hypothesis is put forward that the calcification may be secondary to folic acid deficiency interfering with the matabolism in the central nervous system.

Angiomatosis↗
PubMed1994

MRI demonstration and CT correlation of the brain in patients with idiopathic intracerebral calcification.

Twenty-two patients aged 36-63 years were diagnosed as having Fahr's syndrome on the basis of the presence on CT of unexpected extensive calcification of the basal ganglia. Even when associated with calcification of other brain areas, the main diagnostic criterion remained basal ganglia calcification larger than 800 mm2. Normal values of parathormone, serum calcium and phosphorus excluded hypercalcaemia and hypoparathyroidism. Mitochondrial CNS disease was excluded clinically. MRI and repeated CT and neurological examination were performed in all of the patients. The patients were divided into two groups: neurologically asymptomatic (group 1) and neurologically symptomatic (group 2). T2-weighted sequences demonstrated hyperintense areas in all of the patients involving the white and the grey matter of the brain. In group 1 the hyperintense lesions were significantly smaller than in group 2. The neurological symptoms correlated better with the hyperintensities on T2-weighted MR images than with the calcification demonstrated on CT. Hyperintensities in T2-weighted MRI and the areas shown by CT to have calcification had different locations. In 15 patients with dementia, the white matter of the entire centrum semiovale was bilaterally hyperintense. In another 3 patients with hemiparesis, hyperintense areas in the internal capsule, contralateral to the side of hemiparesis, were demonstrated in the T2-weighted sequence. The hyperintense T2 signals may reflect a slowly progressive, metabolic or inflammatory process in the brain which subsequently calcifies and are probably responsible for the neurological deficit observed.

Adult↗
PubMed1991

Spontaneous regression of intervertebral disc calcifications in a child.

This article presents the case of a boy who complained of cervical and thoracic spine pain for the first time at the age of nine. Plain films of cervical and thoracic spine showed calcifications of intervertebral disc C4-C5, C5-C6, C6-C7 and D3-D4. The symptoms disappeared after conservative therapy. Plain films taken 16 months later showed spontaneous disappearance of all disc calcifications. This spontaneous regression of intervertebral disc calcifications in childhood has also been described in other cases reported in the medical literature. Except for the rare cases when disc calcifications are associated with disc herniation, the discovery of disc calcifications on a plain X-ray of a child corresponds to a benign abnormality.

Calcinosis↗
PubMed1988

Biochemical differences between dystrophic calcification of cross-linked collagen implants and mineralization during bone induction.

Ectopic calcification of diseased tissues or around prosthetic implants can lead to serious disability. Therefore, calcification of implants of glutaraldehyde-cross-linked collagenous tissues and reconstituted collagen was compared with mineralization induced by demineralized bone matrix (DBM). Whereas implants of DBM accumulated large amounts of calcium and a bone-specific gamma-carboxyglutamic acid protein (BGP or osteocalcin) following implantation in both young and older rats, implants of cross-linked pericardium calcified with only traces of BGP. Glutaraldehyde-cross-linked DBM failed to calcify after implantation in 8-month-old rats for 2-16 weeks. Implants of cross-linked type I collagen exhibited small calcific deposits 2 weeks postimplantation but calcium content eventually dropped to levels equal to those of soft tissues as the implants were resorbed. The calcium content of DBM implanted in 1- and 8-month-old rats reached comparable levels after 4 weeks, but the BGP content was approximately twice as high in the younger animals than in the older ones. Glutaraldehyde-cross-linked implants of DBM, tendon, and cartilage calcified significantly in young but not in old animals. This form of dystrophic calcification was associated with only trace amounts of BGP. Alkaline phosphatase activity was high in implants of DBM and undetectable in implants of cross-linked collagenous tissues. These results show that implants of glutaraldehyde-cross-linked collagenous tissues and reconstituted collagen calcify to different extents depending upon their origin and the age of the host, and that the mechanism of dystrophic calcification differs significantly from the process of mineralization associated with bone induction as reflected by alkaline phosphatase activity and BGP accumulation.

Alkaline Phosphatase↗
PubMed2005

Coronary artery and abdominal aortic calcification are associated with cardiovascular disease in type 2 diabetes.

AIMS/HYPOTHESIS: The goals of this study were to determine whether coronary calcium is associated with the presence of clinical cardiovascular disease in individuals with type 2 diabetes and if the measurement of abdominal aortic calcium may have an independent or added benefit as a surrogate marker for clinical vascular disease. METHODS: A cross-sectional study of subjects with type 2 diabetes enrolled in seven medical centres in the USA participating in a Veterans Affairs Cooperative Study of glycaemic control. Enrolled subjects included 309 veterans over 40 years of age with type 2 diabetes, with or without stable cardiovascular disease, who had inadequate glycaemic control (HbA(1)c>7.5%) on oral agents and/or insulin. The study assessed lifestyle behaviours, standard cardiovascular risk factors and coronary artery and abdominal aorta calcification by electron beam computed tomography. RESULTS: Subjects with coronary artery or abdominal aorta calcification present had a strikingly higher prevalence of peripheral artery disease, coronary artery disease and all combined cardiovascular disease. Prevalence of each condition increased from 5- to 13-fold with increasing quintiles of coronary artery calcification and from 2- to 3-fold with increasing abdominal aorta calcification. These associations persisted after adjustment for lifestyle behaviours and standard cardiovascular risk factors. CONCLUSIONS/INTERPRETATION: These results support the notion that vascular calcium in type 2 diabetes provides additional information beyond that of standard risk factors in identifying the presence of cardiovascular disease. Subclinical measures of atherosclerosis such as arterial calcification may help more precisely stratify these individuals and alert healthcare providers to those individuals who have particularly accelerated atherosclerosis.

Aged↗
PubMed2005

Symptomatic calcification of the medial collateral ligament of the knee joint: a report about five cases.

Symptomatic calcifications of the rotator cuff tendons is well-known pathologic condition. However, pathologic calcifications may involve other structures of the locomotor system as well. We report about five patients (age 52-66 years) with a painful calcification at the proximal part of the medial collateral ligament of the knee joint. All five patients presented with load-dependent pain pretending meniscus symptoms, but manual valgus stress provoked severe pain at the medial side of the knee. Conventional X-ray examination showed a dense rounded deposit at the proximal part of the medial collateral ligament. Initially all patients were treated conservatively by needling and infiltration with a local anaesthetic. Open resection of the deposit was performed in four patients after unsuccessful conservative treatment. Postoperatively all patients were immediately free of pain. After a mean follow-up of 6 years (patient 1-4) (range=2.5-9.5 years), all patients were still free of pain. Histological evaluation of biopsies obtained during surgery showed nodular deposition of calcium at the collagen fibres, vascular proliferations and inflammative changes. Soft tissue calcifications have to be considered as a rare differential diagnosis in patients presenting with medial knee joint pain. Open resection reduces symptoms immediately. The histological changes seen were comparable to that reported about pathological tendon calcifications of the shoulder. Therefore, both conditions might be of the same aetiology.

Aged↗