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Valve repair in mitral regurgitation complicated by severe annulus calcification.

BACKGROUND: Valvuloplasty has significant advantages over valve replacement for mitral regurgitation, but the presence of severe calcification of the mitral valve apparatus has been thought to preclude successful valve reconstruction in general. The purpose of this report is to assess the results of valvuloplasty in patients with severe mitral regurgitation having extensive calcification extending from the mitral annulus to underlying myocardium and parts of the papillary muscles. METHODS: Thirty-seven adult patients with severe mitral regurgitation and calcification were operated on between April 1990 and January 1998. Twenty-six patients had degenerative disease, 4 had acute bacterial endocarditis, 6 had postrheumatic fever, and 1 patient had Marfan's disease. The valve repair comprised of en bloc decalcification with extensive leaflet debridement and reconstruction of the annulus. Autologous pericardium was used in patch-extended endocardial annuloplasty or leaflet repair. Valve competence was retained after correction of regurgitation by sliding atrioplasty, rotation paracommissural sliding plasty, cusp remodeling, or chordal repair. All patients required a prosthetic annuloplasty. RESULTS: Follow-up echocardiography at 47 months (range, 3 to 92 months) showed no or only trivial mitral regurgitation in 33 patients; 3 had grade I-II mitral regurgitation and 1 required valve replacement after 3 months. Freedom of reoperation at 1 and 5 years was 94.6%. At last examination, 33 patients were in New York Heart Association functional class I and 3 in class I-II; there has been no mortality and no thromboembolic events. CONCLUSIONS: Valvuloplasty can be safely and successfully carried out in patients suffering from regurgitation associated with severe calcification of the mitral apparatus. With encouraging beneficial midterm results, we suggest patients with calcified valves should not be excluded from mitral repair.

Adult↗

Effect of ethanol and ether in the prevention of calcification of bioprostheses.

BACKGROUND: Lipids play a significant role in the process of calcification of bioprostheses. We assessed whether lipid extraction by ethanol, ether, or a surfactant could mitigate calcification of glutaraldehyde-treated bioprostheses. METHODS: On 200 bovine pericardium samples pretreated with 0.6% glutaraldehyde, lipid extraction was carried out by ethanol, ether, or the tween 80 surfactant, and combinations thereof. The treated tissues were implanted subcutaneously in 50 juvenile rats for 4 and 6 months. Lipids were analyzed by Fourier transform infrared spectrophotometer and chromatography before implantation. Calcium content of implanted tissues was assessed by atomic absorption spectrometer. RESULTS: Ethanol, ether, or surfactant did mitigate calcification. The most efficient pretreatments were the combination of ethanol and surfactant (calcium content: 15.5+/-6.8 microg/mg dry tissue after 6 months implantation) or the combination of ethanol, ether, and surfactant (13.1+/-6.2 microg/mg dry tissue) when compared with surfactant alone (42.9+/-12.7 microg/mg dry tissue). CONCLUSIONS: Ethanol or the combination of ethanol and ether added to the currently used glutaraldehyde-surfactant treatment further mitigates calcification.

Animals↗

Mechanical stresses on closed cusps of porcine bioprosthetic valves: correlation with sites of calcification.

The purpose of this study was to (1) evaluate the magnitude and distribution of mechanical stresses on closed leaflets of porcine bioprosthetic valves (PBVs) by using a nonlinear, finite-element model, and (2) determine if a relationship exists between the magnitude of stresses at various sites on the leaflet and the incidence of calcification at those sites. Mechanical stresses were found to be highest near the commissures and lowest at the base of the leaflet. At a pressure of 100 mm Hg applied to the closed valve, the maximal principal normal stress was 160 kPa near the commissures, 140 kPa in the body of the leaflet, 70 kPa at the free margin, and 60 kPa near the base. Similarly, the maximal shear stress, at an applied pressure of 100 mm Hg, was 80 kPa near the commissures, 70 kPa in the body of the leaflet, 50 kPa at the free margin, and 40 kPa near the base. This distribution of mechanical stresses on the PBV leaflet coincided with the incidence of calcification of the various regions of the leaflet. Calcification was found most frequently near the commissures, less frequently in the body of the leaflet and free margin, and least frequently at the base. These observations suggest a possible causative relation between the magnitude of mechanical stresses and the site of calcification of PBV leaflets.

Bioprosthesis↗

Calcific stenosis of the porcine heterograft.

We have encountered two cases of late calcification of the porcine heterograft. A patient in chronic renal failure died of sepsis and endocarditis fifteen months after replacement of the mitral and tricuspid valves. At postmortem examination, both heterograft valves exhibited severe calcification and thrombosis. A second patient with rheumatic heart disease and sickle cell disease underwent mitral valve replacement for severe regurgitation. Thirty months later, cardiac catheterization revealed prosthetic valve stenosis. The valve was replaced successfully, and the excised heterograft exhibited severe calcification with restriction of leaflet motion. Although calcification of the porcine heterograft is known to occur in patients with infection or disorders of calcium metabolism, dysfunction of the heterograft is rare in our experience.

Adolescent↗

Prevention of calcification in glutaraldehyde-treated porcine aortic and pulmonary valves.

BACKGROUND: The problem of calcification in porcine aortic (AVs) and pulmonary (PVs) valves and its relationship to glutaraldehyde (GA) is of current interest. We proposed an anticalcification treatment to develop noncalcifying porcine AVs and PVs. METHODS: Porcine AVs and PVs were cross-linked in GA. Partially degraded heparin was coupled to the GA-treated AVs and PVs through intermediate surface-bound substrate containing amino groups. Control AVs and PVs were cross-linked in 0.625% GA but had no heparin coupling. All specimens were implanted subdermally in 3-week-old rats for 5 months for calcification studies. RESULTS: Control AVs (Ca, 233.69 +/- 42.61 mg/g) and PVs (Ca, 181.48 +/- 4.06 mg/g) were severely calcified. Coupling of partially degraded heparin revealed complete prevention of calcification in GA-treated AVs (Ca, 0.73 +/- 0.27) and PVs (Ca, 1.125 +/- 0.22 mg/g) implanted subcutaneously in weanling rats for 5 months. CONCLUSIONS: The proposed anticalcification treatment is effective in preventing calcification of GA-treated AVs and PVs implanted subcutaneously in weanling rats for 5 months.

Animals↗

Does glutaraldehyde induce calcification of bioprosthetic tissues?

BACKGROUND: Glutaraldehyde has been said to be responsible in part for the calcification of glutaraldehyde-treated tissues after implantation in animals or humans. We investigated whether the origin of the tissue, autologous or heterologous, could have a more prominent role in the process of calcification. METHODS: Three-month-old sheep received sheep pericardial samples (n = 133) and human pericardial samples (n = 123) implanted subcutaneously. Samples were treated with 0.6% glutaraldehyde for 5, 10, or 20 minutes or 7 days and then rinsed thoroughly before implantation. Samples were then retrieved after 3 months. Calcium content was assessed by spectrophometry. RESULTS: The results show a low calcium content in the autologous group (mean 1.14+/-2.07) and a high calcium content in the heterologous group (mean 38.97+/-26). These results were the same regardless of the duration of the treatment. CONCLUSIONS: Glutaraldehyde treatment (0.6%) does not play a significant role in the calcification of glutaraldehyde-treated tissue regardless of the origin, autologous or heterologous, of the tissue. Glutaraldehyde-treated autologous tissues are associated with an incidence of calcification lower than heterologous tissues.

Analysis of Variance↗

Vascular calcification: expression patterns of the osteoblast-specific gene core binding factor alpha-1 and the protective factor matrix gla protein in human atherogenesis.

OBJECTIVE: Increasing evidence suggests that vascular calcification is a regulated process. We studied the vascular expression pattern of a key factor in mineralization and a counteracting, protective factor. Based on the phenotype of null mice, Core binding factor alpha-1 (Cbfa-1) plays a pivotal role in bone formation, whereas Matrix Gla Protein (MGP) is a potent inhibitor of vascular calcification. METHODS: We investigated the expression of MGP and Cbfa-1 in cultured, human monocytic cells, endothelial cells and smooth muscle cells (SMC), as well as in normal and atherosclerotic vessel specimens. RESULTS: In cultured cells MGP is expressed in endothelial cells and SMC, whereas Cbfa-1 mRNA is predominantly present in macrophages and to a lesser extent in SMC. In the normal vessel wall MGP expression is high at the luminal side and declines toward the center of the media, whereas Cbfa-1 is absent. Moderate, diffuse calcification of the aorta media was observed only in those regions where MGP is low or absent. In atherosclerotic lesions MGP is expressed in endothelial cells and SMC that form fibrous caps, but is never present in macrophages. Cbfa-1 is synthesized in regions without MGP, it is associated with calcified areas and Cbfa-1 may be considered a marker for osteoprogenitor-like cells in the vessel wall. CONCLUSIONS: Our observations on MGP expression confirm and extend published data and are consistent with a protective function of MGP. Cbfa-1 expression is absent in normal medial SMC and co-localizes with neointimal macrophages and focal calcifications.

Arteriosclerosis↗

Patterns of breast calcification in patients on renal dialysis.

Patients on renal dialysis are prone to form areas of metastatic calcification in soft tissues. In this study we have analysed the mammograms of 16 women on renal dialysis and compared them with a control group of 32 women attending for routine mammographic screening. We found a significant increase in vascular and parenchymal calcifications in the women on renal dialysis. Ductal calcifications were no more prevalent in the patients on dialysis, and in no case did the calcification simulate malignancy.

Breast Diseases↗

Computer-assisted analysis of mammographic clustered calcifications.

A total of 127 biopsy-proven clustered mammographic calcifications were diagnosed and evaluated using multiple parameters. The results were subjected to computer analysis. The number of calcifications/cm2 was the most important parameter. Less than 10 calcifications/cm2 resulted in an 82% chance of being benign while 10 or more calcifications/cm2 had a 44% chance of being malignant. The average distance between the calcifications in the cluster was also significant, with a 92% chance of being benign if greater than 1 mm and a 52% chance of being malignant if less than 1 mm. The remaining parameters did not yield statistically significant results, but there were trends which suggest that less than 10 clustered calcifications that are regular in size and shape and orderly in appearance tend to be benign while disorderly clusters tend to be malignant. In order to decrease the number of false positive biopsies and improve the cost-effectiveness of screening mammography, radiologists should consider 6-month follow-up mammography as a reasonable alternative for clustered calcifications that appear benign.

Breast↗

Calcific tendinitis of the gluteus maximus tendon with abnormalities of cortical bone.

Calcific tendinitis of the gluteus maximus tendon is unusual and only eight cases associated with erosions of cortical bone have been reported. We present three further cases which demonstrate variation in appearances of the amorphous calcification in the tendon and cortical erosions on plain radiographs. Isotope bone scans show focal increased activity and computed tomography (CT) clearly demonstrates erosion of cortical bone and calcification within the tendon insertion of gluteus maximus. Follow-up examinations in two cases demonstrated resolution of the changes. We believe this series demonstrates the radiological features and natural history of a common condition occurring at an unusual site. Its recognition is important in order to avoid unnecessary surgical intervention. Resolution of the calcification and cortical erosions has not been previously described.

Adult↗

Advances in micro-calcification clusters detection in mammography.

A new mixed feature multistage false positive (FP) reduction method for micro-calcification clusters (MCCs) detection has been developed for improving the FP reduction performance. Eleven features were extracted from both spatial and morphology domains in order to describe MCCs from different perspectives. These features are grouped into three categories: gray-level description, shape description and clusters description. Two feature sets that focus on describing MCCs on every single calcification and on clustered calcifications, respectively, were combined with a back-propagation (BP) neural network with Kalman filter to obtain the best performance of FP reduction. First, nine of the eleven gray-level description and shape description features were employed with BP neural network to eliminate all the obvious FP calcifications in the image. Second, the remaining MCCs were classified into several clusters by a widely used criterion in clinical practice and then two cluster description features were added to the first feature set to eliminate the FP clusters from the remaining MCCs. The performance results of this approach were obtained using an image database of 67 real-patients mammogram images in H. Lee Moffitt Cancer Center imaging program. The proposed method successfully reduced the FP to 3.15/image, while the detection sensitivity or true positive rate improved to 97%.

Algorithms↗

Calcification of intervertebral discs in childhood.

Over 75 cases of intervertebral disc calcification in childhood have been reported, but the illness is seldom considered in the differential diagnosis of back pain inchildren. This paper reports two children who required surgery for intervertebral disc calcification. The histologic changes, which have not been described previously, include an amorphous calcification within the nucleus pulposus without any inflammatory reaction. The etiology of disc calcification remains unknown, but it can be differentiated both clinically and pathologically from other causes of calcified intervertebral discs and from spondylarthritis.

Biopsy↗

Cartilaginous metaplasia and calcification in aortic allograft is associated with transforming growth factor beta 1 expression.

BACKGROUND: Calcification of homografts and vascular conduits is poorly understood. Mechanisms leading to calcification were studied in a rat model of aortic allografts. METHODS: Rat aortas from Lew1W (RT1(u)) were transplanted into Lew1A (RT1(a)). Animals were killed at 30 days and 180 days, and aortic grafts were removed and analyzed for histologic and immunohistologic studies. RESULTS: Intimal surface increased progressively over 6 months and was the site of important modifications. Intimal cellular population changed from a leukocyte (CD45, OX1-OX30)- and macrophage (CD68, ED-1)-based population at 30 days to predominantly alpha-smooth muscle actin-expressing cells at 180 days. At 180 days, allografts were characterized by an abundant extracellular matrix composed of collagen and elastic fibers associated with extensive calcification (von Kossa staining) located in the intima and media. Osteoblastic activity was present in calcified lesion as shown by alkaline phosphatase activity. At 180 days, numerous chondrocytes (protein S100-positive and alpha-smooth muscle actin-negative) were present focally in the media. However, double immunostaining revealed that a cellular population within the media with a chondrocyte-like morphology was alpha-smooth muscle actin-positive and S100-negative. Active form of transforming growth factor beta1 was expressed from 30 to 80 days in the medial and intimal layers. CONCLUSIONS: These observations suggest that alpha-smooth muscle actin-positive cells within aortic allografts are eventually transformed to a chondrocyte-like structure, leading to vascular cartilaginous metaplasia associated with the expression of transforming growth factor beta1 and could be a potential pathway leading to extensive vascular wall calcification in allografts through endochondral ossification.

Animals↗

Ureteropelvic junction obstruction with renal pelvic calcification: a case report.

Calcification in the wall of the renal pelvis is rare. We report on a 65-year-old man with hydronephrosis secondary to ureteropelvic junction obstruction with renal pelvic calcification. Calcium deposit was found in the wall of the severely dilated renal pelvis. Pathological examination revealed a damaged and hyalinized fibrous renal pelvic wall and serum calcium level was normal. Thus, we speculated that this calcification was dystrophic. Chronic extensive dilatation with intermittent hemorrhage of the renal pelvic wall may have caused this dystrophic renal pelvic calcification.

Aged↗

Renal calcification in the first year of life.

The introduction of renal ultrasound technology has shown renal calcification to be more common in infancy than was previously believed. Understanding the role of inhibitors and promoters in crystal formation helps elucidate the pathophysiology of nephrocalcinosis. Identification of the presence or absence of hypercalcemia and hypercalciuria is an effective way to direct the diagnostic work-up of infants with nephrocalcinosis. The sonographic image of renal calcification resolves spontaneously in many infants. Whether microscopic nephrocalcinosis persists below the threshold of ultrasonographic detection is unknown. Renal calcification can be associated with persistent renal function abnormalities if hypercalciuria continues, such as in VLBW infants who receive long-term furosemide therapy after discharge from the hospital. Renal calcification may also progress to renal failure, such as in infants with primary hyperoxaluria, owing to the persistence of hyperoxaluria, a potent promoter of calcium crystal formation.

Calcinosis↗

Aortic calcification as a predictor of cardiovascular mortality.

Since aortic calcification is seen on X-rays of the prelumbar region in many patients, its relation with cardiovascular disease (CVD) was investigated in a prospective study in The Netherlands. X-rays were taken of 1359 men and 1598 women, in 1975-78. In the subsequent 9 years, 50 men and 33 women died from CVD. The prevalence of aortic calcification was about 10% in middle-aged subjects and rose with age to a maximum of 45% in men and 75% in women. Aortic calcification was associated with a six-fold increased risk of CVD death in men aged 45 years, independent of major CVD risk factors. For each year of age over 45, risk associated with the presence of aortic calcification declined by 6%. Death rates in middle-aged women were too small for risk analysis. These results suggest that atherosclerosis in other than coronary or cerebral vessels may have predictive relevance for CVD death: its diagnosis indicates intervention on present CVD risk factors.

Aged↗

Heparin coupling in inhibition of calcification of vascular bioprostheses.

Inhibitory effect of heparin coupling on calcification of bioprosthetic vascular grafts of different origin was studied. Heparin-bonded (Hep) and 0.625% glutaraldehyde-cross-linked (GA) segments of porcine thoracic aorta (AO), pulmonary artery (PA), jugular vein (JV) and rabbit aorta (RA) were implanted subcutaneously in weanling rats for 5 months. Heparin bonding is ineffective in prevention of calcification of JV (Hep: Ca, 159 +/- 32.26 mg g-1; GA: Ca, 193.55 +/- 17.81; p = 0.075) and RA (Hep: Ca, 150.17 +/- 14.78; GA: Ca, 192.12 +/- 26.61; p = 0.015). Calcium content of heparin-coupled PA and AO was significantly less when compared with their GA-treated counterparts. Calcification inhibition was achieved to a greater extent in heparin-bonded PA (Hep: Ca = 22.62 +/- 5.72, GA: Ca = 115.99 +/- 21.91, p < 0.0001) than in the AO coupled to heparin (Hep: Ca = 63.77 +/- 22.75, GA: Ca = 150.40 +/- 35.21, p < 0.0001). Elastin fibers were the predominant site of calcification in all explanted vascular grafts. Heparin-bonded porcine pulmonary artery is seemed to be the best among all vascular bioprostheses in this study.

Animals↗

Calcification mimicking manganese-induced increased signal intensities in T1-weighted MR images in a patient taking herbal medicine: case report.

Characteristic high signal intensities confined to the globus pallidus on T1-weighted magnetic resonance image (MRI) can be observed in manganese (Mn)-exposed workers, however, these high signals should be differentiated from those due to other causes such as fat, hemoglobin breakdown products, melanoma, neurofibromatosis, and calcification. A 39-year-old woman was admitted with mutism and involuntary movements which had developed the day before. She had ingested two packs of liquid herbal medicine containing 0.53 mg of Mn daily for 4 months prior to visiting our hospital. Her MRI showed high signals, confined mainly to the globus pallidus on T1-weighted images. Follow-up brain MRI at an interval of 11 months showed no interval change. Brain computed tomography (CT) at the time of the second MRI showed symmetric calcification on both globus pallidus. Blood levels of liver function tests, calcium, phosphorus, and parathyroid hormone were within normal ranges. The increased signals, which were first presumed to be induced by Mn, were concluded to be due to calcification based on the following reasons. First, follow-up brain MRI at an interval of 11 months did not show any interval change. Second, the ingested amount of 1.06 mg Mn daily for 4 months is even less than that added to mineral supplements for adults. Third, Mn-induced high signals in T1-weighted MRI do not show any abnormal findings in brain CT. The present case report suggests that brain CT should be performed to rule out symmetric calcification on basal ganglia in patients showing increased signals in T1-weighted MRI, but who do not have a significant exposure history to Mn. The present report also showed that the amount of 1.06 mg Mn daily ingested for 4 months did not cause the high signal in brain MRI.

Adult↗