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At least 19 recordsLinked to original sources
PubMed1996

Medial arterial calcification, calcific aortic stenosis and mitral annular calcification in a diabetic patient with severe autonomic neuropathy.

Medial arterial calcification (Mönckeberg's arteriosclerosis) is well described in diabetic patients with autonomic neuropathy. There is also a high prevalence of diabetes mellitus among subjects with calcific aortic stenosis and mitral annular calcification. We describe a diabetic patient with autonomic neuropathy and extensive medial arterial calcification who also had calcification of the aortic valve and of the mitral valve annulus. We propose that autonomic neuropathy may play a role in calcification of these structures at the base of the heart.

Adult↗
PubMed1995

The diagnostic implication of falcine calcification on plain skull radiographs of patients with basal cell naevus syndrome and the incidence of falcine calcification in their relatives and two control groups.

The purpose of our study was to identify the incidence of falcine calcification shown on plain skull radiographs in people with basal cell naevus syndrome (BCNS) and in their relatives compared with a normal population. A population of people with BCNS and their relatives was identified on non-radiological grounds and the incidence of falcine calcification on skull radiographs in each of these two groups was compared with the incidence of falcine calcification in a control group of people and of a larger group who attended casualty departments. Falcine calcification was graded into dense, fine but definite, and faint. 85 people with BCNS had nearly 100% incidence of falcine calcification in adults. 83 first degree unaffected relatives showed no excess over "normal" incidence of falcine calcification. In the 970 casualty patients some falcine calcification was common (> 20%) in males over 30 and in females over 50 years of age. It occurred earlier and was more common in males than in females. Dense calcification occurred in 5-7% of females and males over 60 years of age. Dense calcification was rare (< 2%) under the age of 40 years. In conclusion, falcine calcification should be regarded as the fourth major feature and a very important diagnostic feature of BCNS. An adult labelled as a BCNS sufferer without falcine calcification probably has not got the syndrome. The genetic defect responsible for the metabolic defect resulting in dural calcification is probably the same as, or in close linkage disequilibrium to, that responsible for the major clinical features of the syndrome. The age and sex distribution of falcine calcification in a general hospital casualty population is described.

Adolescent↗
PubMed1979

Submitral calcification or sclerosis in elderly patients: M mode and two dimensional echocardiography in "mitral anulus calcification".

Submitral calcification or sclerosis was visualized with M mode echocardiography in 84 elderly patients, 35 of whom were also studied with two dimensional echocardiography. Posterior submitral calcification, commonly referred to as "mitral anulus calcification," was present in 82 patients and was located in the angle between the posterior mitral leaflet and left ventricular posterior wall, rather than in the mitral anulus proper. M mode scans from the left ventricle to the left atrium showed that posterior submitral calcification ended abruptly in 66 cases, and in these it became contiguous with the posterior atrioventricular junction (true mitral anulus) in only 14 instances, in 16 patients the posterior submitral calcification sloped anteriorly to merge with the posterior aortic root. Anterior submitral calcification was visualized in 12 patients, 10 of whom also had posterior submitral calcification. Anterior submitral calcification was usually located immediately anterior to the base of the anterior mitral cusp. In two cases, if appeared to arise in the region between the aortic and mitral rings; in one instance, it was located in the mid left ventricle, in the mitral chordal region. We suggest that the terms anterior and posterior submitral calcification are more appropriate than "mitral anulus calcification" because in most cases such calcific deposits do not appear to be located in or to arise from the true mitral anulus.

Age Factors↗
PubMed2002

The association between coronary calcification assessed by electron beam computed tomography and measures of extracoronary atherosclerosis: the Rotterdam Coronary Calcification Study.

OBJECTIVES: The present study was designed to examine the associations of coronary calcification assessed by electron beam computed tomography (CT) with measures of extracoronary atherosclerosis. BACKGROUND: Although measures of extracoronary atherosclerosis have been used to predict coronary events, it is not yet known to what extent those measures reflect coronary atherosclerosis. METHODS: The Rotterdam Coronary Calcification Study is a population-based study in subjects age 55 years and over. Participants of the study underwent an electron beam CT scan. Coronary calcification was quantified according to the Agatston calcium score. Measures of extracoronary atherosclerosis included common carotid intima media thickness (IMT), carotid plaques, ankle-arm index (AAI) and aortic calcification. We used the first 2,013 participants for the present analyses. Age-adjusted geometric mean calcium scores were computed for categories of extracoronary measures using analyses of variance. RESULTS: Graded associations with coronary calcification were found for the carotid and aortic measures. Associations were strongest for carotid plaques and aortic calcification; coronary calcification increased from the lowest category (no plaques) to the highest category 9-fold and 11-fold in men and 10-fold and 20-fold in women, respectively. A nonlinear association was found for AAI with an increase in coronary calcification only at lower levels of AAI. CONCLUSIONS: In this population-based study, graded associations were found between coronary calcification and common carotid IMT, carotid plaques and aortic calcification. A nonlinear association was found between coronary calcification and the AAI.

Aged↗
PubMed1988

[Intracranial physiological calcification on computed tomography (Part 1): Calcification of the pineal region].

Of intracranial physiological calcification, common calcification of pineal region, choroid plexus of lateral ventricles and of basal ganglia was examined based on the frequency of occurrence of age and sex and type of CT scanners. Consecutive cases of 2877 (1450 males and 1427 females) underwent plain CT scanning were studied. Pathological calcification was excluded from this study. Three types of CT scanners (SCN-200, Somatom 2 and TCT-10 A) were used. As a whole, calcification was shown in 67.7% in pineal region, 57.6% in choroid plexus of lateral ventricles and 7.5% in basal ganglia. First, we reported in detail the calcification of pineal region, in which calcification occurred most frequently. Calcification in pineal region had a close relation with age by increasing with aging. The youngest patient was 8 years old. There was a striking increase in number of patients aged from 10 to 39 years. There was a gradual increase in those aged over 40 years. Of patients aged from 70 to 79 years, calcification was found in 81.5%. The incidence was noted no changes in patients aged over 80 years. As for patients aged over 20 years, calcification was observed in 75.1% (82.6% males and 68.0% females). In patients aged from 20 to 79 years, the calcification was significantly higher in male than female. Although there was a different incidence of calcification examined by three types of CT scanners, it was not significant. There was no significant difference between thickness of 8 mm section and 10 mm.

Adolescent↗
PubMed1997

Cardiac valve calcification: characteristics of patients with calcification of the mitral annulus or aortic valve.

AIMS: To determine whether mitral annular calcification and aortic valve calcification, with or without stenosis, are expressions of atherosclerotic disease. METHODS: The incidence of atherosclerotic risk factors was analysed in patients with mitral annular calcification and aortic valve calcification and in control patients from a prospective echocardiographic database of 8160 consecutive patients; 657 patients (8%) were identified with mitral annular calcification and 815 (9%) with a calcified aortic valve, of whom 515 (6.3%) had stenosis with a minimal aortic valve gradient of 16 mm Hg. In these patients, cardiac and vascular risk factors were compared with 568 control patients using multiple logistic regression analysis. RESULTS: Age (odds ratio (OR) varying from 5.78 to 104, depending on age class), female sex (OR 1.75), hypertension (OR 2.38), diabetes mellitus (OR 2.85), and hypercholesterolaemia (OR 2.95) were strongly and significantly associated with aortic valve calcification without stenosis, as were age (OR varying from 8.82 to 67, depending on age class), female sex (OR 2.22), hypertension (OR 2.72), diabetes mellitus (OR 2.49), and hypercholesterolaemia (OR 2.86) with mitral annular calcification. Age (OR varying from 1.11 to 7.7), hypertension (OR 1.91), and hypercholesterolaemia (OR 2.55) were strongly and significantly associated with stenotic aortic valve calcification. CONCLUSIONS: Mitral annular calcification and stenotic or non-stenotic aortic valve calcification have a high incidence of atherosclerotic risk factors, suggesting they should be considered as manifestations of generalised atherosclerosis.

Adult↗
PubMed1988

[Intracranial physiological calcification on computed tomography (Part 2): Calcification in the choroid plexus of the lateral ventricles].

In this paper, we describe calcification in the choroid plexus of lateral ventricles with a discussion of the frequency of occurrence in categories of age, sex, and laterality, and its correlation with pineal calcification. The study was conducted on 2877 consecutive cases (1450 males and 1427 females) that had plain CT scanning. Three types of CT scanners (SCN-200, Somatom 2 and TCT-10 A) were used. This series included only calcification of the choroid plexus in the trigone of the lateral ventricles (glomus). Calcification was found in none of the cases aged under 9 years, 5.9% aged from 10 to 14 years and 17.4% aged from 15 to 19 years. The calcification rate strikingly increased with increasing age of the cases. It was 51.5% of cases between 30 and 39 years of age. After that, the increasing rate of calcification gradually decreased, however calcification was found in 74.4% of cases aged over 80 years. The calcification rate was 64.7% in our total series of cases aged over 20 years, 66.5% aged over 30 years and 70.7% aged over 50 years. The calcification rate of male cases was greater than that of females in the age group of over 15 years. However, there was a significant difference only in the cases ranging from 60 to 79 years of age. The initial incidence of male cases was found at the age of 12 years and that of females at the age of 16 years. There was no difference in calcification on right and left sides.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2002

Induction of calcification in rabbit aortas by high cholesterol diets: roles of calcifiable vesicles in dystrophic calcification.

Atherosclerotic calcification may weaken the aorta wall and thereby lead to rupture of the vessel. The mechanism whereby aortas undergo calcification remains unclear. Previous reports in this laboratory showed that, after 2 months of cholesterol-supplemental feeding, an increase in calcifiability of membrane vesicles isolated from rabbit aortas precedes substantial arterial calcification. Further, the mineral was deposited by isolated calcifiable vesicles as an amorphous phase similar to minerals in human aortas at an early stage of atherosclerosis. In the current study, atherosclerotic calcification was induced by exposing rabbits to a 1% cholesterol-rich diet for 3 or 6 months. After 3 months of dietary interventions, atherosclerotic lesions were fully developed. Fatty streaks were evident in areas proximal to the heart and became less frequent in the distal areas. However, calcification was not yet identifiable histologically or by using Fourier transform spectroscopy (FT-IR). After 6 months of high cholesterol treatment, aortas were partially calcified. Histochemical staining for mineral revealed that calcification appeared to occur predominantly in the intimal areas immediately adjacent to the media. Fourier Transform Imaging analysis demonstrated that the mineral deposited in atherosclerotic rabbit aortas was a hydroxyapatite-like phase. To determine whether aorta vesicles play a role in mineral formation in aortas, vesicles were isolated from calcified aortas and then their calcifiability was compared to that in normal vesicles. Interestingly, during the course of vesicle isolation, we found that calcifiable vesicles with much higher calcifiability than normal vesicles could be readily isolated from atherosclerotic aortas simply by suspending minced tissues in PBS. The characteristics of the calcification process and the enzymatic contents of isolated vesicles were similar to those obtained using collagenase digestion. Correlatively, mineral deposited by calcifiable vesicles isolated from the calcified aortas was also of hydroxyapatite-like phases. Altogether, these observations indicate that (1) aortic calcification is a later event during atherogenesis, (2) calcifiable vesicles are loosely bound to the matrices of the lesions as the result of the disease process and (3) similarities in the mineral phases between those in aortas and by vesicles during atherogenesis further support the role of calcifiable vesicles in dystrophic calcification.

Animals↗
PubMed1997

Parathyroid hormone-related peptide as a local regulator of vascular calcification. Its inhibitory action on in vitro calcification by bovine vascular smooth muscle cells.

In the present study, we investigated the role of parathyroid hormone-related peptide (PTHrP) in vascular calcification by using an in vitro calcification model. We demonstrated that the expression of PTHrP decreased in the progression of bovine vascular smooth muscle cell (BVSMC) calcification and that inhibition of calcification by etidronate (EHDP) and levamisole restored PTHrP secretion, suggesting that the expression of PTHrP is associated with calcification. PTHrP (1-34) and PTH (1-34) dose-dependently inhibited BVSMC calcification. Protein kinase A (PKA) and protein kinase C (PKC) inhibitors completely blocked the inhibitory effect of PTHrP, suggesting that both PKA and PKC may be involved in its signaling pathway. Moreover, PTHrP inhibited alkaline phosphatase (ALP) activity, implying that the impact on ALP may contribute to its action on calcification. Furthermore, the PTHrP antagonist, PTHrP (7-34), dose-dependently increased calcium deposition by BVSMC. Interestingly, PTHrP production by BVSMC dramatically increased in the presence of EHDP, and PTHrP (7-34) partially antagonized the inhibitory effect of EHDP on BVSMC calcification. These results suggest that PTHrP may regulate vascular calcification as an autocrine/paracrine factor.

Alkaline Phosphatase↗
PubMed2002

Stroke is associated with coronary calcification as detected by electron-beam CT: the Rotterdam Coronary Calcification Study.

BACKGROUND AND PURPOSE: Coronary calcification as detected by electron-beam CT measures the atherosclerotic plaque burden and has been reported to predict coronary events. Because atherosclerosis is a generalized process, coronary calcification may also be associated with manifest atherosclerotic disease at other sites of the vascular tree. We examined whether coronary calcification as detected by electron-beam CT is related to the presence of stroke. METHODS: From 1997 onward, subjects were invited to participate in the prospective Rotterdam Coronary Calcification Study and undergo electron-beam CT to detect coronary calcification. The study was embedded in the population-based Rotterdam Study. Calcifications were quantified in a calcium score according to Agatston's method. Calcium scores were available for 2013 subjects (mean age [SD], 71 [5.7] years). Fifty subjects had experienced stroke before scanning. RESULTS: Subjects were 2 times more likely to have experienced stroke when their calcium score was between 101 and 500 (odds ratio [OR], 2.1; 95% CI, 0.9 to 4.7) and 3 times more likely when their calcium score was above 500 (OR, 3.3; 95% CI, 1.5 to 7.2), compared with subjects in the lowest calcium score category (0 to 100). Additional adjustment for cardiovascular risk factors did not materially alter the risk estimates. CONCLUSIONS: In this population-based study, a markedly graded association was found between coronary calcification and stroke. The results suggest that coronary calcification as detected by electron-beam CT may be useful to identify subjects at high risk of stroke.

Aged↗
PubMed2003

Mobile components associated with rapidly developing mitral annulus calcification in patients with chronic renal failure: review of mobile elements associated with mitral annulus calcification.

Mitral annulus calcification may directly cause cerebrovascular accidents by serving as a source of calcific or thrombotic emboli. This hypothesis has been supported by recent reports of mobile components associated with mitral annulus calcification detected by echocardiography. Cardiovascular calcifications, including mitral annulus calcification, are common in end-stage renal disease and may develop and progress over a short period of time. We report two patients with mobile components associated with mitral annulus calcification and end-stage renal disease. Serial echocardiography documented that the mitral annulus calcification in these two patients had developed rapidly. Follow-up echocardiography in one patient demonstrated resolution of the mobile elements.

Calcinosis↗
PubMed2003

Parallels between arterial and cartilage calcification: what understanding artery calcification can teach us about chondrocalcinosis.

The pathogenesis of arterial calcification and chondrocalcinosis has become concurrently illuminated in recent years. For example, both processes occur in chronic inflammation-mediated degenerative diseases associated with aging (including atherosclerosis and osteoarthritis). Both processes are also modulated by altered gene expression by resident cells and by the release of mineralization-competent cell fragments (matrix vesicles and apoptotic bodies). Among the variety of genetic diseases associated with artery calcification are disorders that also promote cartilage calcification and/or dysregulated bone formation. Our discussion highlights that pathologic arterial and articular cartilage calcification both can be owing to genetic deficiencies of calcification inhibitors such as the inorganic pyrophosphate-generating ectoenzyme PC-1/nucleotide pyrophosphatase phosphodiesterase 1. Conversely, pathologic arterial and articular cartilage calcification also can primarily arise as a consequence of active processes driven by inflammatory cytokines and by disordered calcium and inorganic phosphate homeostasis. As discussed in this review, recent developments in the pathogenesis of arterial calcification provide valuable information pertinent to potential future advances in controlling chondrocalcinosis.

Animals↗
PubMed2001

Control of serum phosphorus: implications for coronary artery calcification and calcific uremic arteriolopathy (calciphylaxis).

There is mounting evidence that elevated serum phosphorus is an important cardiovascular risk factor in patients with end stage renal disease. Recent work has shown that vascular smooth muscle cells have the ability to undergo osteoblastic differentiation and produce an environment conducive to mineralization. Serum phosphorus is an important stimulator of this process and the adverse cardiovascular effects of hyperphosphatemia are most likely mediated via its ability to enhance the development of vascular calcification. Arterial calcification, whether it is intimal or medial in location, is a strong independent risk factor for cardiovascular morbidity and mortality. Both coronary artery calcification and calciphylaxis are prototypical examples of arterial calcification that have been associated with poor phosphate control. Furthermore, several investigators have recently suggested that the prescription of large doses of calcium to achieve phosphate control may augment, rather than diminish, the risk of vascular calcification. This is more likely to be true in the presence of low turnover bone disease, a diagnosis difficult to make with routine laboratory testing. A brief review of the molecular biology of vascular calcification supports the concept that warfarin administration may exacerbate the calcific process, particularly in the setting of hyperphosphatemia, as has been reported in patients with calciphylaxis. Recognizing the consequences of poor phosphate control, it is time to adopt strict target levels that aim to normalize serum phosphorus levels. The available evidence supports that this control should not be achieved through the use of supraphysiologic doses of supplemental calcium.

Arterioles↗
PubMed2000

Apoptosis regulates human vascular calcification in vitro: evidence for initiation of vascular calcification by apoptotic bodies.

The mechanisms involved in the initiation of vascular calcification are not known, but matrix vesicles, the nucleation sites for calcium crystal formation in bone, are likely candidates, because similar structures have been found in calcified arteries. The regulation of matrix vesicle production is poorly understood but is thought to be associated with apoptotic cell death. In the present study, we investigated the role of apoptosis in vascular calcification. We report that apoptosis occurs in a human vascular calcification model in which postconfluent vascular smooth muscle cell (VSMC) cultures form nodules spontaneously and calcify after approximately 28 days. Apoptosis occurred before the onset of calcification in VSMC nodules and was detected by several methods, including nuclear morphology, the TUNEL technique, and external display of phosphatidyl serine. Inhibition of apoptosis with the caspase inhibitor ZVAD.fmk reduced calcification in nodules by approximately 40%, as measured by the cresolphthalein method and alizarin red staining. In addition, when apoptosis was stimulated in nodular cultures with anti-Fas IgM, there was a 10-fold increase in calcification. Furthermore, incubation of VSMC-derived apoptotic bodies with (45)Ca demonstrated that, like matrix vesicles, they can concentrate calcium. These observations provide evidence that apoptosis precedes VSMC calcification and that apoptotic bodies derived from VSMCs may act as nucleating structures for calcium crystal formation.

Amino Acid Chloromethyl Ketones↗
PubMed1995

Aorto-pulmonary calcification: an unusual manifestation of idiopathic calcification of infancy evident antenatally.

BACKGROUND: Idiopathic arterial calcification of infancy represents a clinical spectrum involving calcification of large and medium-sized blood vessels with an unknown etiology. Its complications include severe systemic hypertension and cardiomyopathy. CASE: A twin infant with a variant of idiopathic arterial calcification was diagnosed antenatally by the detection of hyperechogenicity of the proximal aorta and central pulmonary vessels. The calcification was apparently isolated to these vessels and was associated with polyhydramnios and hypertrophic cardiomyopathy. CONCLUSION: Because antenatal diagnosis is possible, we suggest that there should be a high index of suspicion for idiopathic arterial calcification when there is sonographic hyperechogenicity of vessel walls, evidence of polyhydramnios, cardiomyopathy, or a family history of idiopathic arterial calcification.

Adult↗
PubMed2002

Coronary calcification detected by electron-beam computed tomography and myocardial infarction. The Rotterdam Coronary Calcification Study.

AIMS: Available data are insufficient to determine the relation between coronary calcification and coronary events in the general population. We cross-sectionally examined the association between coronary calcification and myocardial infarction in the prospective Rotterdam Coronary Calcification Study. METHODS AND RESULTS: From 1997 onwards, subjects were invited for electron-beam computed tomography scanning to detect coronary calcification. The study was embedded in the population-based Rotterdam Study. Calcifications were quantified in a calcium score according to Agatston's method. Calcium scores were available for 2,013 participants with a mean age of 71 years (standard deviation, 5.7 years). A history of myocardial infarction prior to scanning was present in 229 subjects. Compared to subjects in the lowest calcium score category (0-100), the age-adjusted odds ratio for myocardial infarction in subjects in the highest calcium score category (above 2,000) was 7.7 (95% confidence interval, 4.1-14.5) for men, and 6.7 (95% confidence interval, 2.4-19.1) for women. Additional adjustment for cardiovascular risk factors only slightly altered the estimates. The association was observed across all age subgroups, i.e. also in subjects of 70 years and older. CONCLUSION: A strong and graded association was found between coronary calcification and myocardial infarction. The association remained at high ages.

Calcinosis↗
PubMed1991

[The demonstration of calcifications in magnetic resonance tomography (MRT). The effect of different parameters on the MRT imaging of cerebral calcifications].

The effect of various factors on the demonstration of calcified lesions was studied in 131 areas of calcification which had been demonstrated by CT. By means of MRI (SE 400/30 or GE315/14, 90 degrees and SE 1600/30 + 70; 0.5T) 117 of the 131 calcified lesions (89%) produced a signal difference. Of these 117 lesions, 80 (61%) were recognised as calcification by MRI. Large areas of calcification (more than 5 mm) and high density calcification (more than 100 Hu) were recognised significantly more often than small or low density calcifications. T2-weighted images demonstrated calcification more often than other sequences. With conventional pulse sequences, calcified lesions were frequently recognised as abnormalities on MRI, but their recognition as calcified lesions is unreliable.

Brain↗