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PubMed2003

Warfarin-induced tracheobronchial calcification.

Calcification of the trachea and proximal bronchi is a common, normal finding on chest radiographs in the elderly population, especially in women. More extensive airway calcification is also a rare manifestation of many pathologic conditions. The authors report a case of pathologic tracheobronchial calcification associated with long-term warfarin therapy. Chest radiographs showed prominent, diffuse calcification of the tracheobronchial tree. Computed tomography showed extensive calcification of the airway walls, extending from the trachea to the lung periphery.

Aged↗
PubMed1994

Morphologic changes in the pancreas detected by screening ultrasonography in a mass survey, with special reference to main duct dilatation, cyst formation, and calcification.

Subclinical morphologic changes in the pancreas detected by screening ultrasonography of 130,951 subjects were analyzed in relation to their incidence and background factors. Main pancreatic duct (MPD) dilatation, cystic lesion, and calcification were found in 644 (0.49%), 271 (0.21%) and 65 (0.05%) patients, respectively. The incidence of MPD dilatation and calcification was significantly higher in men (p < 0.0001), whereas cystic lesion was significantly more frequent in women (p < 0.01). Age-dependent increase in the incidence of MPD dilatation and cystic lesion was observed in both sexes whereas that of calcification was observed only in men. Further detailed examinations for 312 randomly selected patients with these findings revealed that 97% of MPD dilatation, 95% of cystic lesion, and 86% of calcification were correctly identified by ultrasonography. Finally, 18 (5.8%) patients with chronic pancreatitis, 16 (5.1%) with neoplastic cysts, 3 with mucin-producing tumors, and 3 with carcinomas (0.96%, respectively) were detected. On the other hand, in 84.0% of MPD dilatation, 87.4% of cystic lesion, and 50.0% of calcification, we could not attribute their etiology to any known pancreatic disease. It is indicated that aging and gender are major clinically related factors of these changes.

Adult↗
PubMed1991

Myocardial calcifications in neonates and infants: a unique tissue reaction.

The deposit of calcium salts into myocardial cells represents the process of dystrophic calcification. Once it causes alterations in cellular calcium hemostasis, it can initiate deleterious events leading to ischemic myocardial injury and cell death. Myocardial calcifications in infants are markedly different from those in adults; calcifications are significantly more frequent in cases of myocardial necrosis in the young, and can be demonstrated microscopically without removal of necrotic fibers and scar formation, which are the adult's usual stages of response to myocardial necrosis. Important functional and clinical implications in myocardial calcification, other than serving as a marker for necrosis, relate to accelerated myocardial calcification after cardiac surgery in infants.

Calcinosis↗
PubMed1993

Local calcification as a determinant of the outcome of excimer laser coronary angioplasty: an in vitro study.

BACKGROUND: Calcification influences the outcome of various angioplasty techniques in the treatment of coronary artery disease. During angioscopic in vitro studies, we observed that dissections and perforations not caused by vessel bending frequently occurred at the boundary areas of plaque and adjacent vessel wall. This study investigated whether this is related to the distribution of calcific deposits. METHODS: Postmortem excimer laser coronary angioplasty (308-nm XeCl) was performed in 51 stenotic coronary arteries. Twenty-three segments were further examined; these consisted of 11 perforations, six dissections, three segments with no ablative effect after the application of 20,000 laser impulses, and three successfully passed stenoses without complications. X-ray diffraction analysis and scanning electron microscopy were performed to detect calcium deposits and their spatial relationship to perforations and dissections. RESULTS: X-ray diffractions analysis detected calcifications in 21 of 23 specimens. Postmortem angiography revealed calcifications only on 11 of 23 segments. Three of 11 perforations were located at the plaque border, as were three of six dissections. In all six complications at the plaque border, x-ray diffraction analysis revealed that the plaque border was identical with a border of calcium deposits. Eight of 11 perforations and three of six dissections could be explained by axis divergence between the laser catheter and the vessel orientation. CONCLUSIONS: Contributing factors for perforations and dissections during excimer laser coronary angioplasty are axis divergence and the distribution of plaque calcification. More sensitive methods are needed to detect local vessel wall calcium in vivo.

Angioplasty, Balloon, Coronary↗
PubMed1999

Vascular calcification.

Vascular calcification is an active and modifiable process involved in many disease entities, including atherosclerosis, cardiac valve disease and calcific uremic arteriolopathy. It occurs with distinct characteristics at different sites in the vessel wall. The mechanism by which calcification is induced remains uncertain; the roles of bone matrix and extracellular matrix proteins, estrogen and vitamin D are being further defined in animal models and clinical trials. Some risk factors for calcific uremic arteriolopathy and cardiac valve calcification, both disproportionately affecting chronic hemodialysis patients, have been identified in observational studies.

Animals↗
PubMed2002

Phosphorus restriction and control of coronary calcification as assessed by electron beam tomography.

PURPOSE OF REVIEW: Patients suffering from end-stage renal disease and undergoing dialysis demonstrate extremely elevated cardiovascular morbidity and mortality rates. Though the prevalence of traditional risk factors is very high, the extent and severity of cardiovascular complications seem disproportionate to the underlying risk profile. RECENT FINDINGS: A growing body of evidence indicates that abnormalities of calcium and phosphorus metabolism may play an important role in the morbidity and mortality of end-stage renal disease patients. Calcification of several cardiovascular structures, a likely complication of hyperphosphatemia and excessive calcium load, is both highly prevalent and extensive in end-stage renal disease patients and carries a negative prognostic weight. The extent of calcification can be accurately quantified with noninvasive radiological techniques such as electron beam tomography. Utilizing electron beam tomography in patients undergoing dialysis it has been possible to demonstrate the rapid progression of cardiovascular calcification and to gauge the effect of treatment provided to slow such process. SUMMARY: The presence of deleterious cardiovascular calcification in end-stage renal disease can be diagnosed accurately and noninvasively with electron beam tomography. This technology also allows precise assessment of the effect of medical treatment for hyperphosphatemia on calcification of cardiovascular structures.

Calcinosis↗
PubMed2006

Chondral metaplasia in calcific insertional tendinopathy of the Achilles tendon.

OBJECTIVE: To ascertain whether tendon samples harvested from patients with calcific insertional Achilles tendinopathy showed features of failed healing response, and whether abnormal quantities of type II collagen had been produced in that area by these tenocytes. DESIGN: Comparative laboratory study. DESIGN: University teaching hospitals. PATIENTS: Tendon samples were harvested from eight otherwise healthy male individuals (average age 47.5+/-8.4 years, range 38 to 60) who were operated for calcific insertional Achilles tendinopathy and from nine male patients who died of cardiovascular events (mean age 63.1+/-10.9 years) while in hospital. INTERVENTIONS: Open surgery for calcific insertional Achilles tendinopathy. MAIN OUTCOME MEASURE: Semi-quantitative histochemical, immunohistochemical, and immunocytochemical methods to ascertain whether tendinopathic tendons were morphologically different from control tendons, and whether abnormal types of collagen were produced. RESULTS: Tenocytes from tendons from patients with calcific insertional Achilles tendinopathy exhibit chondral metaplasia, and produce abnormally high quantities of collagen type II and III. CONCLUSIONS: The altered production of collagen may be one reason for the histopathological alterations described in the present study. Areas of calcific insertional Achilles tendinopathy have been subjected to abnormal loads. These tendons may be less resistant to tensile forces. Further studies should investigate why some tendons undergo these changes.

Achilles Tendon↗
PubMed2006

Calcification of the gastric mucosa associated with tumor lysis syndrome in a child with non-Hodgkin lymphoma.

Tumor lysis syndrome (TLS) is an important complication associated with hematological malignancies leading to increased morbidity and mortality. Metastatic calcification due to calcium phosphate crystals precipitated in soft tissues is rarely encountered in TLS. We describe a child with non-Hodgkin lymphoma who had gastric mucosal calcification related to severe hyperphosphatemia due to TLS. Upper-gastrointestinal endoscopic examination performed because of abdominal complaints revealed diffuse mucosal white lesions in mucosa of the gastric antrum and corpus. Pathological examination of the mucosa of the gastric corpus showed marked calcification in the lamina propria. We suggest that calcification in mucosa of the gastric corpus may be seen in patients with TLS. We also suggest that gastric mucosal calcifications should be considered in patients with hematological malignancies from TLS.

Calcinosis↗
PubMedDate not supplied

A greater reduction in high-frequency heart rate variability to a psychological stressor is associated with subclinical coronary and aortic calcification in postmenopausal women.

OBJECTIVE: Reduced cardiac parasympathetic activity, as indicated by a reduced level of clinic or ambulatory high-frequency heart rate variability (HF-HRV), is associated with an increased risk for atherosclerosis and coronary artery disease. We tested whether the reduction in HF-HRV to a psychological stressor relative to a baseline level is also associated with subclinical coronary or aortic atherosclerosis, as assessed by calcification in these vascular regions. METHOD: Spectral estimates of 0.15 to 0.40 Hz HF-HRV were obtained from 94 postmenopausal women (61-69 years) who engaged in a 3-minute speech-preparation stressor after a 6-minute resting baseline. A median of 282 days later, electron beam tomography (EBT) was used to measure the extent of coronary and aortic calcification. RESULTS: In univariate analyses, a greater reduction in HF-HRV from baseline to speech preparation was associated with having more extensive calcification in the coronary arteries (rho = -0.29, p = .03) and in the aorta (rho = -0.22, p = .06). In multivariate analyses that controlled for age, education level, smoking status, hormone therapy use, fasting glucose, high-density lipoproteins, baseline HF-HRV, and the stressor-induced change in respiration rate, a greater stressor-induced reduction in HF-HRV was associated with more calcification in the coronary arteries (B = -1.21, p < .05), and it was marginally associated with more calcification in the aorta (B = -0.92, p = .09). CONCLUSION: In postmenopausal women, a greater reduction in cardiac parasympathetic activity to a psychological stressor from baseline may be an independent correlate of subclinical atherosclerosis, particularly in the coronary arteries.

Aged↗
PubMed2006

Quantification of aortic valve calcification using multislice spiral computed tomography: comparison with atomic absorption spectroscopy.

OBJECTIVES: Multislice spiral computed tomography (MSCT) allows the in vivo detection of valvular calcification. The aim of this study was to validate the quantification of aortic valve calcification (AVC) by MSCT with in vitro measurements by atomic absorption spectroscopy. METHODS: In 18 patients with severe aortic stenosis, 16 detector row MSCT (SOMATOM Sensation 16, Siemens, Forchheim, Germany with scan parameters as follows: 420 milliseconds tube rotation time, 12 x 0.75 mm collimation, tube voltage 120 KV) was performed before aortic valve replacement. Images were reconstructed at 60% of the RR interval with an effective slice thickness of 3 mm and a reconstruction increment of 2 mm. AVC was assessed using Agatston AVC score, mass AVC score, and volumetric AVC score. After valve replacement, the calcium content of the excised human stenotic aortic valves was determined in vitro using atomic absorption spectroscopy. RESULTS: The mean Agatston AVC score was 3,842 +/- 1,790, the mean volumetric AVC score was 3,061 +/- 1,406, and mass AVC score was 888 +/- 492 as quantified by MSCT. Atomic absorption spectroscopy showed a mean true calcification mass (Ca5(PO4)3OH) of 19 +/- 8 mass%. There was a significant correlation between in vivo AVC scores determined by MSCT and in vitro mean true calcification mass (r = 0.74, P = 0.0004 for mass AVC score, r = 0.79, P = 0.0001 for volumetric AVC score and r = 0.80, P = 0.0001 for Agatston AVC score) determined by atomic absorption spectroscopy. Linear regression analysis showed a significant association between the degree of hydroxyapatite (given in mass%) in the aortic valve and the degree of AVC (R = 0.74, F = 19.6, P = 0.0004 for mass AVC score, R = 0.80, F = 29.3, P = 0.0001 for Agatston AVC score and R = 0.79, F = 27.3, P = 0.0001 for volumetric AVC score) assessed by MSCT. CONCLUSION: MSCT allows accurate in vivo quantification of aortic valve calcifications.

Aged↗
PubMed2007

Vitamin D and vascular calcification.

PURPOSE OF REVIEW: Vascular calcification is frequently found in patients with osteoporosis, atherosclerosis and chronic kidney disease, leading to high morbidity and mortality rates. The effects of vitamin D excess and deficiency on vascular calcification are reviewed in this article. RECENT FINDINGS: There is evidence from experimental studies that mediacalcinosis induced by vitamin D excess is an active and reversible process. Vitamin D excess, however, is rarely seen in the general human population. Experimental data also demonstrate that physiologic vitamin D actions include the inhibition of processes that are important for intimal and medial artery calcification such as pro-inflammatory cytokine release, adhesion molecule release, and proliferation and migration of vascular smooth muscle cells. In uremic rats, low levels of the vitamin D hormone calcitriol are associated with massive vascular and soft tissue calcifications. Whereas retrospective studies already indicate a beneficial effect of active vitamin D on mortality rates in chronic kidney disease, little is yet known about the effect of vitamin D deficiency on cardiovascular morbidity and mortality in the general population. SUMMARY: Available data indicate that vitamin D exerts a biphasic 'dose response' curve on vascular calcification with deleterious consequences not only of vitamin D excess but also of vitamin D deficiency.

Animals↗
PubMed2001

Inhibition of bioprosthesis calcification due to synergistic effect of Fe/Mg ions to polyethylene glycol grafted bovine pericardium.

Calcification has limited the durability of bioprosthetic heart valves fabricated from glutaraldehyde pretreated porcine aortic valves or bovine pericardium (BP). The present study describes calcium antagonistic effect of polyethylene glycol grafted bovine pericardium (PEG-GABP) with Fe2+/Mg2+ delivery from a co-matrix system in rat subcutaneous model. Retrieved samples were biochemically evaluated for calcification and alkaline phosphate (AP) activity. Scanning electron micrographs of 21-day explants had shown excessive calcification with glutaraldehyde treated BP (control). However, the PEG grafting and Fe/Mg release had substantially inhibited the deposition of calcium on BP. The extractable alkaline phosphatase activity was also reduced with PEG grafting and metal ion release to BP. The extractable AP had shown peak activity at 72 h [for GATBP--250.5 +/- 1.2 nm pnp/mg protein/min enzyme activity (unit), PEG-GABP--165.2 +/- 16.6 units], but markedly reduced after 21 days (22.1 +/- 1.8 and 12.0 +/- 1.5 units, respectively). The initial high levels may be due to tissue injury via surgery, which mitigated with time. It is assumed that ferric ions may slow down or retard the calcification process by the inhibition of proper formation of hydroxy apatite while magnesium ions disrupt the growth of these crystals by replacing Ca2+. In addition it maybe hypothesized that these metal ions may inhibit the key element alkaline phosphatase, which acts as the substrate for mineralization. Hence, it is conceivable that a combination therapy via surface grafting of PEG and local delivery of low levels of ferric and magnesium ions may prevent the bioprosthesis associated calcification.

Alkaline Phosphatase↗
PubMedDate not supplied

Mitral annulus calcification with a mobile component as a possible source of embolism.

Mitral annulus calcification has been associated with embolic events, but the precise pathophysiology has not been elucidated. The authors describe four patients who experienced embolic events whose transesophageal echocardiograms showed a mitral annulus calcification, with a mobile component that exhibited the same echogenicity as the calcification. Three patients had no other conditions known to be associated with embolism. On follow-up transesophageal echocardiography, the mobile component of the mitral annulus calcification had disappeared in three patients. These findings support the hypothesis that mitral annulus calcification not only is associated with but also is possibly a direct cause of embolic events in some patients.

Aged↗
PubMed1980

Basal ganglia calcification in postoperative hypoparathyroidism.

The presence of bilateral basal ganglia calcification was sought in nine patients with post-operative and two patients with primary hypoparathyroidism, using computerized axial tomography (CAT) and plain skull radiographs. Calcification was detected with CAT in seven patients; five with post-operative and both with primary hypoparathyroidism, but in only one was it demonstrable on plain X-ray films. The presence of calcification appeared to be related to the duration of the disease and possibly the degree of control of serum calcium. Six of the seven patients with cerebral calcification also had cataracts. The incidence of basal ganglia calcification in hypoparathyroidism is probably much greater than previously recognized, especially in post-operative hypoparathyroidism.

Adult↗
PubMed2006

Vascular calcification and renal osteodystrophy relationship in chronic kidney disease.

Cardiovascular disease and stroke account for 60-70% of all deaths in patients with end-stage renal disease (ESRD), at a risk that is 10-20-fold the age- and sex-matched general population. There is also increased coronary artery calcification and increased cardiovascular mortality in chronic kidney disease (CKD) and dialysis patients compared with the general population. Bone is similarly abnormal in CKD. There is an increased incidence of low bone mass and fractures in dialysis patients compared with the general population. Furthermore, a hip fracture in a dialysis patient is associated with a doubling of the mortality observed in nondialysis patients with a hip fracture. These two problems may be linked, as cross-sectional studies have demonstrated an inverse relationship between osteoporosis and coronary artery calcification in the general population and in ESRD patients. In vitro and ex vivo, there is clear evidence that vascular calcification is an active cell-mediated process, made worse by disorders of mineral metabolism. Many factors known to be associated with cardiovascular disease in CKD patients can directly increase calcification in vitro. In addition, in CKD, there are many mechanisms by which bone may adversely affect vascular calcification including disorders of bone remodelling, altered secretion of parathyroid hormone (PTH), hyperphosphatemia, hypercalcaemia, use of calcium based binders, and excessive vitamin D therapy. The coexistence of vascular risk factors and abnormal bone represent a double threat to the well being of patients with CKD.

Bone Remodeling↗
PubMed2006

Molecular mechanisms mediating vascular calcification: role of matrix Gla protein.

Patients with chronic kidney disease (CKD) have a higher incidence of vascular calcification and a greatly increased risk of cardiovascular death. The mechanisms involved in the accelerated vascular calcification observed in CKD have recently become clearer, leading to the hypothesis that a lack of natural inhibitors of calcification may trigger calcium deposition. One of these inhibitory factors, matrix Gla protein (MGP), is the focus of the present review. MGP, originally isolated from bone, is a vitamin K-dependent protein that is also highly expressed by vascular smooth muscle cells. MGP has been confirmed as a calcification-inhibitor in numerous studies; however, its mechanism of action is not completely understood. It potentially acts in several ways to regulate calcium deposition including: (i) binding calcium ions and crystals; (ii) antagonizing bone morphogenetic protein and altering cell differentiation; (iii) binding to extracellular matrix components; and (iv) regulating apoptosis. Its expression is regulated by several factors including retinoic acid, vitamin D and extracellular calcium ions, and a reduced form of vitamin K (KH2) is important in maintaining MGP in an active form. Therefore, strategies aimed at increasing its expression and activity may be beneficial in tipping the balance in favour of inhibition of calcification in CKD.

Calcinosis↗
PubMed2004

Vascular calcification: a stiff challenge for the nephrologist: does preventing bone disease cause arterial disease?

There has been an explosion of interest in vascular calcification in the last 5 years. Four key "germinal" findings have fallen onto very fertile soil. First, on the background of an increasing cardiovascular disease burden it has been found that at least cross-sectionally, and in a limited fashion prospectively, achieved dialysis plasma phosphate levels are linked to all-cause and cardiovascular mortality. Second, there are increasing reports of calcific uremic arteriolopathy in Australia and the United States. Third, we know know that the mechanical properties of the carotid artery, and the aorta, have a profound influence on survival for dialysis patients. Vascular calcification itself (as assessed by x-ray films and ultrasound) has been linked to aortic stiffness. Fourth, increasing numbers of studies are showing extremely extensive coronary artery calcification (CAC) in dialysis patients, even at a young age. From these apparently unlinked observations the following assertion has been posited-that in the widespread (over) use of calcium-containing oral phosphate binders (OPB) to prevent uremic osteodystrophy in our dialysis population we have unwittingly accelerated widespread uremic vasculopathy and thereby contributed to premature cardiovascular mortality. It is the purpose of this article to discuss vascular calcification (and particularly CAC) in dialysis patients as we understand it today. We will review the published series, with special reference to the Sevelamer Treat to Goal trial and also discuss the new Kidney Disease Outcome Quality Initiative (K-DOQI) guidelines on the use of phosphate binders in chronic kidney disease.

Bone Diseases↗
PubMed1996

Efficacy of the chitosan posttreatment in calcification prevention of the glutaraldehyde-treated porcine aortic noncoronary cusp implanted in the right ventricular outflow tract in dogs.

Calcific tissue failure results in poor performance of the bioprosthetic heart valve. Chitosan post-treatment has been shown to be effective in calcification prevention of the glutaraldehyde-treated bovine pericardium when implanted subdermally in rats for 12 weeks. The present study investigated the effectiveness of the chitosan posttreatment in prevention of calcification of the glutaraldehyde-treated porcine aortic noncoronary cusp 5 months after implantation in the right ventricular outflow tract (RVOT) in mongrel dogs. Either 0.625% glutaraldehyde-treated (Group 1, n = 6) or glutaraldehyde-chitosan-treated (Group 2, n = 6) porcine aortic noncoronary cusp with the aortic wall was sewn to the RVOT. Gross histological observations showed moderate calcification of the glutaraldehyde-treated cusps, but no calcification was noticed in the glutaraldehyde-chitosan-treated grafts at 5 months. This was confirmed by results of quantitative analyses for calcium in half of each explanted cusp with aortic wall. The calcium content of the 0.625% glutaraldehyde-treated cusps (Ca, 40.6 +/- 24.9 mg/g dry wt) was significantly (p < 0.01) higher than that of glutaraldehyde-chitosan-treated cusps (Ca, 1.3 +/- 0.29 mg/g dry wt). These findings suggest that chitosan post-treatment is effective in complete calcium mitigation of the glutaraldehyde-treated porcine aortic noncoronary cusps implanted in the RVOT in dogs.

Animals↗