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PubMed1986

Patterns of calcific deposits in operatively excised stenotic or purely regurgitant aortic valves and their relation to mechanical stress.

Two hundred twenty-one aortic cusps from 96 patients who underwent aortic valve replacement were examined. Of all the cusps that showed any calcific deposits, 87% had calcific deposits in 1 of 2 specific patterns: a coaptation pattern, where calcific deposits occurred along the line of cusp coaptation, and a radial pattern, where calcific deposits occurred as spokes spread inward from the cusp attachment to the center of the cusp. This was true irrespective of the patients' sex or age, the type of disease, and the type of valve or the extent of calcific deposits. These patterns of calcific deposits relate to the area of maximal cusp flexion and, hence, maximal mechanical stress. It is therefore concluded that calcific deposits in aortic valve cusps occur in specific patterns in most cases, and that mechanical stress may be the initiating or accelerating factor in the calcification of these cusps.

Aged↗
PubMed1986

Pancreatic calcifications: no indicator of severe exocrine pancreatic insufficiency.

Pancreatic calcifications are believed to occur only in advanced stages of exocrine pancreatic insufficiency. This belief has been reevaluated by correlating the results of the secretin-pancreozymin test, fecal fat analysis, and the presence of pancreatic calcifications on plain abdominal x-rays in 79 patients with chronic pancreatitis. Exocrine pancreatic insufficiency was classified as slight, moderate, or severe according to the results of the function tests, and pancreatic calcifications were assessed semi-quantitatively (grades 1-3) by an independent examiner. The results showed that severe exocrine pancreatic insufficiency did occur even in the absence of calcifications. Calcifications were more frequently detected with increasing severity of exocrine pancreatic insufficiency. The qualitative demonstration of pancreatic calcification was, however, not an indicator of severe, decompensated exocrine pancreatic insufficiency (50% false-positive results). It is concluded that pancreatic calcification is not necessarily an indicator of severe exocrine pancreatic insufficiency, and vice versa. Comparison between the results of tests for endocrine pancreatic function and plain abdominal x-ray showed such similarity that it can also be concluded that pancreatic calcifications are no indication of abnormal endocrine function, and vice versa.

Calcinosis↗
PubMed1995

Prenatal diagnosis of liver calcifications.

OBJECTIVE: To report our experience with the prenatal diagnosis of hepatic calcification. METHODS: Routine ultrasonography was done in 24,600 consecutive pregnancies of 14-26 weeks' gestation. Detailed sonographic studies, amniocenteses, and chromosomal, bacteriologic, virologic, and serologic investigations were performed in each case with calcifications. RESULTS: Hepatic calcifications were diagnosed in 14 fetuses--an incidence of one in 1750--at gestational ages of 15-26 weeks. Twelve fetuses had one or two calcified foci, one fetus had four scattered foci, and one had diffuse calcification of the liver as well as peritoneal and intestinal calcifications. Three fetuses (21%) had associated severe malformations: two with trisomy 18 and one with dwarfism and hydronephrosis; these fetuses were aborted. One fetus with polyhydramnios and calcifications within the bowel died in utero; an autopsy was not allowed, but the external examination was normal. No case had serologic evidence of recent infection with Toxoplasma, rubella virus, cytomegalovirus, herpes simplex virus, or syphilis. Amniotic fluid (and neonatal urine where applicable) cultures for cytomegalovirus were negative. Ten fetuses were normal at birth, and nine of them were followed-up for a period of 4 months to 4.5 years. All were found to be healthy and thriving children. CONCLUSION: Our experience indicates that fetal hepatic calcification is not a rare ultrasonographic finding, and each fetus with such calcifications should be thoroughly evaluated for malformations, chromosomal anomalies, and viral infection. If the work-up is negative, subsequent neonatal outcome carries a good prognosis.

Calcinosis↗
PubMed1992

Coeliac disease, epilepsy, and cerebral calcifications. The Italian Working Group on Coeliac Disease and Epilepsy.

There have been anecdotal reports of an association between coeliac disease and epilepsy with cerebral calcifications that resemble those of the Sturge-Weber syndrome. A series of patients who had epilepsy with calcifications, in whom coeliac disease (CD) was incidentally observed, prompted us to study this association. 43 patients (15 male, age range 4.6-30.7 years) were selected from two series. 31 patients with cerebral calcifications of unexplained origin and epilepsy (series A) underwent intestinal biopsy. 12 patients with CD and epilepsy (series B) underwent computed tomography. Antibodies to gluten, folic acid serum concentrations, were measured, and HLA typing was done in most patients. 24 of the series A patients were identified as having CD on the basis of a flat intestinal mucosa (15/22 with a high concentration of serum antigluten), and 5 series B patients showed cerebral calcifications, giving a total of 29 cases with the combination of CD, epilepsy, and cerebral calcifications (CEC). In 27 of these CEC patients, calcifications were located in the parieto-occipital regions. Only 2 of the series A patients had gastrointestinal symptoms at the time of intestinal biopsy; most patients had recurrent diarrhoea, anaemia, and other symptoms suggestive of CD in the first 3 years of life. The epilepsy in CEC patients was poorly responsive to antiepileptic drugs. Gluten-free diet beneficially affected the course of epilepsy only when started soon after epilepsy onset. Cases of "atypical Sturge-Weber syndrome" (characterised by serpiginous cerebral calcifications and epilepsy without facial port-wine naevus) should be reviewed, and CD should be ruled out in all cases of epilepsy and cerebral calcifications of unexplained origin.

Adolescent↗
PubMed1992

Parkinson's disease and basal ganglia calcifications: prevalence and clinico-radiological correlations.

We reviewed computerized tomograms (CT) for basal ganglia and dentate nucleus calcifications in 79 patients with Parkinson's disease (PD), 54 patients with Alzheimer's disease (AD) and 109 controls aged 50 or more. When it was determined, no patient had disturbances in calcium metabolism. We found: (1) 30 subjects out of 242 (12.3%) with calcification located within the lenticular nucleus in 28. (2) Calcifications were unilateral in 11 and asymmetric in 11. (3) The prevalence of calcifications was 21.5% in PD, 9.2% in AD and 7.3% in controls and were significantly more severe in PD than in C and AD (P less than 0.02). (4) PD patients with calcifications were clinically indistinguishable from those without calcification. (5) Calcifications within the basal ganglia were not associated with a levodopa-resistance. We suggest the basal ganglia calcifications are more frequent in PD, but we cannot explain why, since post-synaptic lesions have never been showed in PD.

Aged↗
PubMed1994

Percutaneous mitral balloon valvotomy in patients with calcific mitral stenosis: immediate and long-term outcome.

OBJECTIVES: This study analyzed the immediate and long-term outcome of percutaneous balloon mitral valvotomy in patients with and without fluoroscopically visible mitral valve calcification. BACKGROUND: Mitral valve calcification has been shown to be an important factor in determining immediate and long-term outcome of patients undergoing surgical mitral commissurotomy. Patient selection has an important impact on the outcome of percutaneous balloon mitral valvotomy. METHODS: The immediate and long-term results of percutaneous balloon mitral valvotomy were compared in 155 patients with and 173 patients without mitral valve calcification. The patients with calcified valves were assigned to four groups according to severity of calcification. RESULTS: Patients with calcified mitral stenosis more frequently were in New York Heart Association functional class III or IV and more frequently had atrial fibrillation, previous surgical commissurotomy, echocardiographic score > 8, higher pulmonary artery and left atrial pressures, higher pulmonary vascular resistance and mean mitral valve gradient and lower cardiac output and smaller mitral valve area. Mitral valve area after valvotomy was significantly smaller in patients with calcified valves (1.8 +/- 0.06 vs. 2.1 +/- 0.06 cm2) and was > or = 1.5 cm2 in 65% of patients with and 83% of patients without calcified valves (p = 0.004). A successful outcome, defined as mitral valve area > 1.5 cm2 without significant mitral regurgitation and left to right shunting, was achieved in 52% of patients with and 69% of patients without uncalcified valves (p = 0.001). The success rate was 59%, 48%, 35% and 33% in subgroups with 1+, 2+, 3+ and 4+ calcification, respectively. The rates of significant left to right shunting and mitral regurgitation after valvuloplasty were similar in the two groups. Estimated survival rate (80% vs. 99%, respectively, p = 0.0001), survival rate without mitral valve replacement (67% vs. 93%, respectively, p < 0.00005) and event-free survival rate (63% vs. 88%, respectively, p < 0.00005) at 2 years were significantly better in the patients with uncalcified valves. Survival rate curves became progressively worse as the severity of calcification increased. CONCLUSIONS: These findings indicate that immediate and long-term results of mitral valvuloplasty are not as successful in patients with fluoroscopically visible mitral valve calcification as in those without calcification.

Calcinosis↗
PubMed2005

Calcification of tissue heart valve substitutes: progress toward understanding and prevention.

Calcification plays a major role in the failure of bioprosthetic and other tissue heart valve substitutes. Tissue valve calcification is initiated primarily within residual cells that have been devitalized, usually by glutaraldehyde pretreatment. The mechanism involves reaction of calcium-containing extracellular fluid with membrane-associated phosphorus to yield calcium phosphate mineral deposits. Calcification is accelerated by young recipient age, valve factors such as glutaraldehyde fixation, and increased mechanical stress. Recent studies have suggested that pathologic calcification is regulated by inductive and inhibitory factors, similar to the physiologic mineralization of bone. The most promising preventive strategies have included binding of calcification inhibitors to glutaraldehyde fixed tissue, removal or modification of calcifiable components, modification of glutaraldehyde fixation, and use of tissue cross linking agents other than glutaraldehyde. This review summarizes current concepts in the pathophysiology of tissue valve calcification, including emerging concepts of endogenous regulation, progress toward prevention of calcification, and issues related to calcification of the aortic wall of stentless bioprosthetic valves.

Animals↗
PubMed2004

The amount of calcium-deficient hexagonal hydroxyapatite in aortic valves is influenced by gender and associated with genetic polymorphisms in patients with severe calcific aortic stenosis.

AIMS: The study evaluated the relationship between cardiovascular risk factors (CRF), gene polymorphism, calcification and fibrosis of stenotic aortic valves. METHODS AND RESULTS: The calcium content of 187 excised stenotic aortic valves was determined using atomic absorption spectroscopy. Hydroxyproline content was quantified. Left-heart catheterization was performed. CRF and genotypes of the interleukin 10, connective tissue growth factor (CTGF) and chemokine receptor 5 (CCR5) polymorphisms were assessed. Calcification consisted of Ca-deficient hexagonal hydroxyapatite, Ca(10 - x)(HPO4)x(PO4)(6 - x)(OH)(2 - x); with 0<or=x<or=1. Calcification (quintiles) was positively associated with the mean gradient across the aortic valve (44 +/- 14, 52 +/- 17, 54 +/- 16, 60 +/- 15, 68 +/- 19 mm Hg; p<0.001). Males (n=101) had a higher degree of calcification (26.1 +/- 8.9 vs 20.8 +/- 9.2 mass%; p<0.001), despite the same mean gradient across the aortic valve (56 +/- 17 vs 56 +/- 19 mm Hg; p=0.958). CRF were not, whereas interleukin 10 polymorphisms -1082, -819, and -592 were significantly associated with the degree of calcification. Furthermore, if certain allele carriers had additionally the rare CCR5 or CTGF allele the degree of calcification was higher. CONCLUSION: Calcification of stenotic aortic valves consists of Ca-deficient hexagonal hydroxyapatite. Gender and genetic polymorphisms have an impact on the degree of aortic valve calcification.

Aged↗
PubMed2005

Aortic calcification.

OBJECTIVES: Vascular calcification is a complicating factor observed in advanced atherosclerosis. This review summarises the present knowledge regarding abdominal aortic calcification. DESIGN: Literature review. METHODS: A literature review was carried using MEDLINE and PUBMED with the search terms 'abdominal', 'aortic' and 'calcification'. Articles were assessed for data regarding mechanisms, measurement, risk factors and outcomes of aortic calcification. RESULTS: Thirty relevant studies were identified. These demonstrated a positive correlation between abdominal aortic calcification and the following factors: older age, hypertension, and smoking. Further studies are required to critically assess other risk factors such as gender, diabetes mellitus and renal failure. Calcification of the abdominal aorta is associated with an increased risk of mortality, coronary heart disease and stroke. CONCLUSION: Aortic calcification predicts an increased incidence of cardiovascular events, however, the reasons for this association requires further investigation. Accurate measurement of aortic calcification is likely to be increasingly used to determine the risk of cardiovascular events.

Age Factors↗
PubMed2006

Calcification of glutaraldehyde cross-linked collagen in bladder neck injections in children with incontinence: a long-term complication.

PURPOSE: We report the incidence of calcifications developing at the bladder neck/urethra in pediatric patients treated with glutaraldehyde cross-linked collagen for urinary incontinence. MATERIALS AND METHODS: We reviewed charts of patients treated with glutaraldehyde cross-linked collagen injections for urinary incontinence between 1994 and 1999. Etiology of incontinence, pertinent medical history, operative details and postoperative imaging were examined. RESULTS: Of 31 patients 4 (13%) had development of submucosal calcifications in the bladder neck/urethra. All 4 patients had received multiple injections of glutaraldehyde cross-linked collagen for incontinence secondary to neurogenic bladder. The calcifications were confirmed surgically. Pathology reports available for 2 of 4 patients showed chronic inflammation without dysplasia or malignant changes. Mean followup was significantly different between calcified and noncalcified cases (10.3 vs 7.2 years, p = 0.009), as was total volume of collagen injected (21 vs 12 cc, p = 0.012). Mean time to diagnosis of calcifications was 8.8 years (range 7 to 11) after first injection. A total of 24 patients without calcification underwent bladder imaging at a mean of 6.8 years (+/-2.2) after glutaraldehyde cross-linked collagen injection, which was not significantly different than the time to diagnosis (p = 0.089). The number of injections was not significantly different between the 2 groups (p = 0.426). CONCLUSIONS: Of our patients 13% had development of calcifications at the site of prior glutaraldehyde cross-linked collagen injections for incontinence. These calcifications were surrounded by chronic inflammation. Patients who have undergone glutaraldehyde cross-linked collagen injections may benefit from long-term followup with bladder imaging to detect and follow calcifications at prior injection sites.

Adolescent↗
PubMed1999

Calcification characteristics of porcine stentless valves in juvenile sheep.

OBJECTIVE: To compare calcification characteristics of two porcine stentless valves (Toronto SPV and Freestyle) with different designs, fixation and antimineralization techniques using a juvenile sheep model of valve implantation inside the circulation. METHODS: The stentless valves (n = 2 x 6) were implanted in juvenile sheep in the pulmonary artery as an interposition, while the circulation was maintained with a right ventricular assist device. The model was validated by the implantation of, clinically well-known, porcine (Hancock II) and pericardial (Pericarbon) valves. Half of the valves were explanted after 3 months, the rest after 6 months. Valves were examined macroscopically, by X-ray, light microscopy (HE, Masson, Von Giesson, Von Kossa, PTAH stains), and transmission electron microscopy. Quantitative determination of the calcium content of the cusps was performed with atomic absorption spectrometry. RESULTS: After 3 months, the Freestyle had an extensively calcified aortic wall, most prominent at the outflow side of the porcine valve. After 6 months, calcification increased transmurally, but the valve cusps were free of calcification, and the inflow side was only slightly calcified. The Toronto SPV valve also started to calcify at the inflow side of the valve after 3 months with increased calcification after 6 months. The base of the Toronto SPV valve cusps showed slight calcification after 6 months of implantation. CONCLUSIONS: The pattern of calcification of the porcine aortic wall differs between the two studied stentless valves, with calcification located predominantly at the outflow side in the Freestyle valve, but also at the inflow side in the Toronto SPV valve. The cusps of the Freestyle valve were less prone to calcification than those from the Toronto SPV valve.

Animals↗
PubMedDate not supplied

Change of calcifications after arthroscopic subacromial decompression.

Fifty patients were reviewed after arthroscopic subacromial decompression. Twenty-five had calcific deposits in the rotator cuff visible on x-ray evaluation. Each patient with calcification was matched with a patient without calcification who had a similar state of the rotator cuff, date of surgery, age, and sex. The calcific deposits were left untouched in all cases. No significant difference was found in the postoperative outcome between the patients in the two groups measured by the Constant score. Before surgery 7 (28%) patients had calcifications of < 5 mm, and 18 (72%) patients had calcifications that were > or = 5 mm. At a 2-year follow-up (n = 24) these figures were 20 (83%) and 4 (17%), respectively (p < 0.001). Postoperative x-ray evaluations revealed a disappearance or decrease in size of the calcific deposits in 19 (79%) of the patients. These results provide new information on the course of calcifying tendinitis, which may indicate that we can leave calcific deposits untouched within the rotator cuff when performing arthroscopic subacromial decompression.

Adult↗
PubMed1997

Spontaneous calcification of arteries and cartilage in mice lacking matrix GLA protein.

Calcification of the extracellular matrix (ECM) can be physiological or pathological. Physiological calcification occurs in bone when the soft ECM is converted into a rigid material capable of sustaining mechanical force; pathological calcification can occur in arteries and cartilage and other soft tissues. No molecular determinant regulating ECM calcification has yet been identified. A candidate molecule is matrix GLA protein (Mgp), a mineral-binding ECM protein synthesized by vascular smooth-muscle cells and chondrocytes, two cell types that produce an uncalcified ECM. Mice that lack Mgp develop to term but die within two months as a result of arterial calcification which leads to blood-vessel rupture. Chondrocytes that elaborate a typical cartilage matrix can be seen in the affected arteries. Mgp-deficient mice additionally exhibit inappropriate calcification of various cartilages, including the growth plate, which eventually leads to short stature, osteopenia and fractures. These results indicate that ECM calcification must be actively inhibited in soft tissues. To our knowledge, Mgp is the first inhibitor of calcification of arteries and cartilage to be characterized in vivo.

Animals↗
PubMed2002

Case-control study of calcification of the hepatic artery in chronic hemodialysis patients: comparison with the abdominal aorta and splenic artery.

BACKGROUND AND AIMS: Studies of the hepatic artery are scarce. We have observed that hepatic artery calcification is very uncommon in patients with hyperparathyroidism that expedites calcification. METHODS: Plain abdominal CT was studied in 221 patients on chronic hemodialysis. Control consisted of 442 sex- and age-matched patients with other diseases. Calcification was graded as a percentage of the entire wall circumference for the aorta, and as a percentage of the entire length of the hepatic and splenic arteries from the celiac trunk to the hilum of each organ. RESULTS: Aortic calcification was seen in 79.2% of male dialysis patients, 22.1% of controls, 74.1% of female dialysis patients and 17.3% of controls (P < 0.0001). Hepatic artery calcification was seen in only 13 dialysis patients. The degree of calcification of the abdominal aorta was correlated with the length of hemodialysis period (P = 0.008), but not with serum calcium, serum phosphate or their product. Although serum parathormone levels were not correlated with calcification, seven of eight dialysis patients with hepatic artery calcification had very high parathormone levels. CONCLUSIONS: The hepatic artery is far less frequently calcified than are the abdominal aorta and splenic artery. This may be a teleologic phenomenon of the liver.

Adult↗
PubMed1999

Factors associated with calcification of the abdominal aorta in hemodialysis patients.

BACKGROUND: Cardiovascular and cerebrovascular injury caused by arteriosclerosis has been the major cause of the death in hemodialysis (HD) patients. We quantitatively analyzed and evaluated the severity of abdominal aortic calcification in HD patients in comparison to risk factors for arteriosclerosis. METHODS: One hundred thirty-seven HD patients were examined. Using image analysis software, areas of the calcified abdominal aorta were quantitatively analyzed on plain computerized tomography images. Other factors such as blood pressure (BP), lipid levels, and calcium (Ca) x phosphorus (Pi) value were also analyzed. RESULTS: Patients with a higher one-year average of systolic BP showed a higher severity of abdominal aortic calcification. That is, the severity of abdominal aortic calcification in patients with a one-year systolic BP average above 160 mm Hg was 31.5 +/- 13.6%, and this severity was significantly higher than that in patients with a one-year systolic BP average of less than 120 mm Hg (8.0 +/- 7.7%, P < 0.01). The severity of abdominal aortic calcification in patients demonstrating risk values of ectopic calcification, that is serum Ca x Pi > or = 60 (mg/dl), on more than 4 of 24 measurements within one year (25.8 +/- 13.6%) was significantly higher than the severity of aortic calcification in patients demonstrating this value less than four times in one year (P < 0.05). There was no correlation between levels of low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride, lipoprotein(a), and severity of abdominal aortic calcification. CONCLUSIONS: Systolic BP levels and the product of serum Ca and Pi were related to the severity of abdominal aortic calcification in HD patients. These observations suggested that BP control, as well as control of serum Ca and Pi levels, was important in preventing the progression of abdominal aortic arteriosclerosis.

Age Factors↗
PubMedDate not supplied

[Mineral analysis of roentgenologically defined calcifications in patients with chronic calcifying tendinitis of the rotator cuff].

AIM: Extracorporeal shockwave application (ESWA) is in clinical use to promote disintegration of symptomatic calcifications of the rotator cuff of the shoulder. However, disintegration of roentgenologically comparable calcifications of the rotator cuff is not always successfull. It is known from urologic stone lithotripsy that the susceptibility for disintegration of stone-like concrements depends on their mineral content. Therefore, in the present investigation the relative contents of calcium and phosphorus in rotator cuff calcifications were determined. METHOD: 39 surgically removed rotator cuff calcifications were analyzed by means of atomic emission spectrometry. RESULTS: The relative content of calcium of the rotator cuff calcifications was found to be 22.3 % +/- 5.7 % (mean +/- SD; 6.8 % - 32.4 %), that of phosphorus as 10.5 % +/- 2.4 % (2.7 % - 14.4 %). The data neither depend on the gender of the patients nor on their age at the time point of surgical removal of the rotator cuff calcifications. CONCLUSION: Roentgenologically comparable calcifications of the rotator cuff demonstrated distinct individual differences concerning the relative contents of calcium and phosphorus. The present results may serve as the first indication that the susceptibility of rotator cuff calcifications for disintegration may depend on their relative contents of calcium and phosphorus.

Adult↗
PubMed1986

[Incidence of pineal calcification in the first 18 years of life].

There are sparse or contradictory data on frequency and pathological significance of pineal calcifications in childhood. This is particularly so for children younger than 6 years of age. We therefore looked for pineal gland calcifications in 1044 consecutive a.p. and lateral skull films. Pineal calcification was diagnosed, if accepted by both authors, and if the calcified spot fitted into at least 2 of 4 localisation methods. 80 patients with pineal calcifications were detected using this method. In 40 of these patients CCT confirmed the calcification. The frequency of pineal calcification was 3% in the first 12 months of life rising gradually to 7.1% in children of 10 years of age. From 10 years onwards, there is a marked increase of frequency of calcifications of the pineal gland up to 33% in the group of children of 18 years of age. In contrast to some statements in literature, pineal calcifications seem to be physiological in a limited percentage even below the age of 6 years.

Adolescent↗
PubMed1998

Cardiac valve calcification in haemodialysis patients: role of calcium-phosphate metabolism.

BACKGROUND: Cardiac valve calcification (VC) has been detected with increased frequency in haemodialysis (HD) patients, making it necessary to determine the potential pathogenic factors in uraemic patients. METHODS: A total of 92 chronic HD patients (39 female, 53 male) and 92 age and gender-matched nondialysis control subjects were evaluated by echocardiography and a severity score for VC was determined. Calcium phosphate metabolism was evaluated at the beginning of haemodialysis. RESULTS: We found a greater prevalence of VC in dialysis patients than in normal patients (mitral annulus 44.5% vs 10%, P = 0.02; aortic annulus 52% vs 4.3%, P = 0.01). HD patients with mitral calcification were found to be older than patients without calcification, were on long-term renal replacement therapy, had longer duration of predialysis arterial hypertension, had greater values of the highest value of mean calcium phosphate product in 6 successive months (CaxP) and the highest absolute value of calcium-phosphate product (CaxPmax). We also found a positive correlation between calcification score, age, and CaxP. No correlation was found between actual VC and arterial hypertension or parathyroid hormone. Multiple stepwise regression analysis selected age and CaxP as the most predictive parameters for mitral calcification (r = 0.47). Mitral calcification was associated more frequently with rhythm and cardiac conduction defects, valvular insufficiency and with peripheral vascular calcification. Aortic calcification was correlated with age (r = 0.42) and longer duration of predialysis arterial hypertension. CONCLUSION: Our study confirmed an increased prevalence of VC in HD patients and selected age and calcium phosphate product as the most predictive parameters. These findings support careful monitoring of calcium metabolism beginning at the early stages of end-stage renal failure to reduce the risk of heart disease.

Aged↗