[Fahr's disease; vascular intracerebral, idiopathic non-arteriosclerotic calcifications].
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Basal Ganglia Diseases↗
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Results for “Vascular Calcification”
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[MPS metabolic disorders of the vascular wall in vitamin D induced calcification].
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Animals↗
Heteroplastic calcification ulcers. Refractory ulcers in peripheral vascular diseases.
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Adipose Tissue↗
Elastin degradation and calcification in an abdominal aorta injury model: role of matrix metalloproteinases.
BACKGROUND: Elastin calcification is a widespread feature of vascular pathology, and circumstantial evidence exists for a correlation between elastin degradation and calcification. We hypothesized that matrix metalloproteinase (MMP)-mediated vascular remodeling plays a significant role in elastin calcification. METHODS AND RESULTS: In the present studies, we determined that short-term periadventitial treatment of the rat abdominal aorta with low concentrations of calcium chloride (CaCl2) induced chronic degeneration and calcification of vascular elastic fibers in the absence of aneurysm formation and inflammatory reactions. Furthermore, the rate of progression of calcification depended on the application method and concentration of CaCl2 applied periarterially. Initial calcium deposits, associated mainly with elastic fibers, were persistently accompanied by elastin degradation, disorganization of aortic extracellular matrix, and moderate levels of vascular cell apoptosis. Application of aluminum ions (known inhibitors of elastin degradation) before the CaCl2-mediated injury significantly reduced elastin calcification and abolished both extracellular matrix degradation and apoptosis. We also found that MMP-knockout mice were resistant to CaCl2-mediated aortic injury and did not develop elastin degeneration and calcification. CONCLUSIONS: Collectively, these data strongly indicate a correlation between MMP-mediated elastin degradation and vascular calcification.
Animals↗
Sonographic features of nonpalpable breast cancer: a study based on ultrasound-guided wire-localized surgical biopsies.
The purpose of this study is to investigate the correlation between surgicopathological findings and ultrasonic images of nonpalpable breast lesions. The study was composed of 220 nonpalpable breast lesions from 193 patients. The breast lesions were classified into soft tissue type (185 lesions) and calcification type (35 lesions). Of the 220 lesions, 62 (28%) were malignant. For soft tissue type lesions, the sonographic features of sound attenuation (p < 0.001) and irregular border (p < 0.001) were significantly associated with the malignant diagnosis. For soft tissue-type and calcification-type lesions, the presence of increased vascularity (p < 0.001) or calcification (p < 0.001) was significantly associated with the malignant diagnosis. Of the 164 breast lesions with corresponding mammograms, 37 of 74 mammographically identifiable lesions were pathologically malignant, as compared with 16 of 90 lesions with negative mammograms (p < 0.001). In our study, the more sensitive sonographic features for predicting malignancy were irregular border and increased vascularity (sensitivity 88% and 82%, respectively), whereas the features of sound attenuation and presence of calcifications were more specific (specificity 88% and 80%, respectively). In conclusion, ultrasound-guided wire localization of breast lesions is not only useful in assisting surgical biopsy, but the sonographic findings obtained by this procedure correlate with pathologic diagnosis.
Adolescent↗
Endothelial cells modulate osteogenesis in calcifying vascular cells.
The potential role of vascular endothelium in atherosclerotic calcification is unknown. Endothelial cells (EC) express bone morphogenetic proteins (BMP), and EC-conditioned medium is osteoinductive in marrow stromal cells. To test whether EC are osteoinductive in vascular cells, we used calcifying vascular cells (CVC) that form nodules and mineralize in vitro. We established a coculture model with EC grown opposite CVC on membranes coated with collagen I or collagen IV, both of which are expressed in atherosclerotic lesions. On collagen I, EC did not alter CVC nodule formation, calcification or expression of the osteogenic marker Cbfa1, the chondrogenic marker collagen IX or smooth muscle cell alpha-actin. However, on collagen IV, EC abolished nodule formation and calcification, and expression of cell markers decreased, suggesting dedifferentiation. Matrix GLA protein (MGP), also expressed in atherosclerotic lesions, was added to CVC in coculture. Unexpectedly, MGP enhanced Cbfa1 expression in CVC on both collagen I and IV. The enhancement was most apparent on collagen IV, where calcification also increased. However, MGP did not restore nodule formation on collagen IV, suggesting that nodule formation and cell differentiation are separate processes. The effect of EC on CVC calcification was suppressed by noggin, an inhibitor of BMP activity, and in part mimicked by replacement of EC by BMP-2. Our results support a role for endothelium in vascular calcification, modulated by collagens and MGP.
Animals↗
Medial arterial calcification mimicking temporal arteritis.
Medial arterial calcification, which has been increasingly recognized in end-stage renal disease (ESRD) patients, has been associated with acutely symptomatic vascular complications including calcific uremic arteriolopathy (calciphylaxis) and ischemic changes in the extremities. This report describes a 50-year-old ESRD patient on maintenance hemodialysis in whom medial arterial calcification developed with features mimicking the findings of temporal arteritis. He complained of persistent bilateral temporal area headaches with associated symptoms of blurred vision; pain in his shoulders, hips, and knees; and intermittent symptoms consistent with jaw claudication. He was not receiving calcium or vitamin D supplements. Superficial temporal arteries were dilated, tortuous, nodular, and tender to palpation. Ophthalmologic examination was unremarkable, except for the presence of peripapillary atrophy. Temporal artery biopsy results showed medial arterial calcification with mild inflammatory changes. No giant cells were identified. Additional long-term complications of medial arterial calcification have included the development of painful ischemic ulceration of the glans penis and extensive mitral annulus calcification detected by echocardiography. The findings in this patient show that clinical manifestations of medial artery calcification associated with ESRD can mimic those seen with other vascular diseases.
Arteriosclerosis↗
[Aortic valve stenosis: persistence of infective agents or noninfective inflammatory process?].
The probable risk factors leading to aortic valve calcification are not clearly defined. The cross-sectional study of 85 patients with vascular and valvular calcification was performed. Correlations between the immune tests and aortic stenosis severity were investigated. The predictors of aortic valve calcification were probably C-reactive protein and interleukin-6. The predictors of aortic stenosis progression were interleukin-8, antibodies of Chlamydia pneumoniae and cytomegalovirus, and dysregulation of complement's components. Implication of immune reactivity could influence aortic valve calcification.
Aged↗
Structural analysis of pulmonary vascular changes in a case of infantile calcifying arteriopathy.
In a well documented case of ACI, the pulmonary vessels were subjected to light microscopy, radiography, electron microscopy and X-ray microanalysis. The analysis of calcified foci in the walls of large and medium pulmonary arteries demonstrated a marked correlation between the deposits of calcium and phosphorus and the number of elastic fibers. The interpretation of our observations is in favour of a congenital defect of elastic fiber formation in the vascular walls, followed by calcification. Massive accumulation of calcium in the vascular walls was associated with tissue destruction, fragmentation of fibers and formation of irregular calcified foci which provoked a foreign-body reaction.
Arteries↗
Mechanism of intervertebral disc degeneration caused by nicotine in rabbits to explicate intervertebral disc disorders caused by smoking.
STUDY DESIGN: The effects of nicotine on intervertebral discs in rabbits were studied experimentally. OBJECTIVES: To investigate the effects of nicotine on the vascular buds in rabbits for elucidating the mechanism of nicotine-induced vertebral disc degeneration. BACKGROUND DATA: Several groups have suggested that cigarette smoking is associated with low back pain, but the exact mechanism is not yet fully understood. METHODS: The pump was filled with a diluted nicotine solution, then implanted under the skin of rabbits for 8 weeks. This model was designed to maintain blood nicotine concentration at approximately 110 ng/mL. Rabbits receiving physiologic saline were used as control animals. RESULTS: Nicotine treatment resulted in necrosis and hyalinization of the nucleus pulposus in all rabbits. The anulus fibrosus showed a disturbance of the pattern of overlapping laminae with and without clefts and separation. These resulted in changes indicative of stenosis of vascular buds and perivascular calcification. Nicotine treatment resulted in hypertrophy of vascular walls, necrotic changes in endothelial cells, and narrowing of the vascular lumen. Nicotine treatment resulted in delineation of vascular buds in the vicinity of the vertebral endplate and a reduction of their numbers. However, the control animals showed a dense vascular network. The number of vascular buds decreased in nicotine treatment. CONCLUSION: The authors believe that both reduction in the density of vascular buds and narrowing of the vascular lumen result in decreased oxygen tension, leading to decreased synthesis of proteoglycan and collagen, thus facilitating degeneration of the disc.
Animals↗
[Embolization of an arteriovenous fistula in the posterior fossa: report of a case].
We report a case of posterior fossa arteriovenous fistula with a possible arterial aneurysm. The patient was a 15-year-old female. She was transferred to us because of a sudden onset of dyspnea, severe headaches, and loss of consciousness. The CT scan found an abnormal vascular lesion in the posterior fossa. Calcification was noted in the wall of the largest abnormal vascular structure. The angiogram showed a focal aneurysmal dilatation of the hemispheric branch of the right posterior inferior cerebellar artery, followed by an arteriovenous fistula, which drained to the right transverse sinus. Embolization was performed by implanting a detachable balloon into the proximal end of the aneurysm. These abnormal vascular structures disappeared completely on the angiogram after the embolization. CT scan one week after embolization showed increased density in these abnormal vascular structures, with no enhancement after contrast, indicating thrombosis or the formation of a blood clot in their lumen. The CT half a year after embolization showed reduction in size and a low density change in the largest vascular structure with calcification in the wall. All other abnormal vascular structures disappeared. An angiogram half a year after the embolization confirmed no recurrence of the aneurysm or arteriovenous fistula.
Adolescent↗
Cardiovascular disease in uremic patients on hemodialysis.
In conclusion, patients on chronic maintenance dialysis have an increased incidence of death from cardiovascular disease. Hypertension plays a major role, and these patients must be carefully monitored for complete control of blood pressure. Adequacy of ultrafiltration to maintain normal extracellular volume is an essential part of the dialytic treatment. Hypertensive patients should be screened for excessive renin secretion because of its possible role in unresponsive hypertension in patients on dialysis. Nephrectomy should be used when necessary, where dialysis and antihypertensive medication have not adequately controlled blood pressure. Patients must be monitored for the presence of pericardial disease to avoid subsequent pericardial effusion and the development of constrictive pericarditis with its adverse effect on myocardial function. When constrictive pericarditis is present, it obviously should be relieved by appropriate surgery. Efforts should be made to minimize cardiac output in hemodialysis patients. Whether or not routine transfusions to maintain a higher hematocrit are indicated is a question that cannot yet be answered. However, patients with marginal cardiovascular function who are accepted on hemodialysis and must have an arteriovenous shunt should be supported in any manner to minimize an increase in cardiac output. Early and aggressive treatment of known episodes of sepsis is important in the elimination of valvular endocarditis in this patient population. Perhaps one of the finer indicators of adequacy of hemodialysis will be K rate and peak immunoreactive insulin levels. Continued abnormality of these parameters may contribute to cardiovascular disease. Clearly, further study of the effect of abnormal carbohydrate metabolism on lipid metabolism is in order. Serum triglyceride, serum cholesterol and lipid electrophoretic pattern should be followed to evaluate the beneficial effects of drug therapy and changes in dialytic technique on the development of cardiovascular disease. Careful monitoring of calcium, phosphorus, bone films and parathyroid hormone levels is indicated to assess parathyroid status. The use of aluminum binders and parathyroidectomy to prevent vascular and myocardial calcification is important in the therapy of these patients. The use of cardiac catheterization, coronary artery arteriography, and possibly cardiac vascular repair, should be considered in the chronic hemodialysis patient with coronary artery disease if he is otherwise well. Adequacy of hemodialysis perhaps can be evaluated through its effect on all of the above parameters. Whether or not changes in artificial kidney treatments can correct the final vascular disease remains to be seen.
Antigens↗
The effects of various diphosphonates on a rat model of cardiac calciphylaxis.
Seven diphosphonate analogs were treated for their effects on myocardial and cardiovascular degeneration and calcification in an experimental model of cardiac calciphylaxis. A single oral dose of dihydrotachysterol (DHT) administered to rats induced myocardial and vascular degeneration, focal myocarditis and vasculitis, and myocardial and vascular mineralization. The results demonstrated a considerable variation among the various diphosphonates in their ability to block the pathological changes observed in this model. Ethane-1-hydroxy-1,1-diphosphonate (EHDP) was the most effective diphosphonate in reducing myocardial and vascular degeneration and calcification, whereas diphosphonates such as ethane-1-amino-1,1-diphosphonate (EADP) and hydroxymethylene diphosphonate (HMDP) had little or no effect compared to saline controls. For those diphosphonates which were effective, e.g., EHDP, the tissue-protective effects were observed whether the rats were treated with drug prior to the administration of DHT, or whether drug treatment commenced after DHT administration. The results are discussed in terms of the known biological properties of the diphosphonate drugs.
Animals↗
Effects of plaque composition on vascular remodelling after angioplasty in the MultiVitamins and Probucol (MVP) trial.
BACKGROUND: The antioxidant probucol reduced coronary restenosis in the MultiVitamins and Probucol (MVP) trial by improving vascular remodelling. Whether calcification limits the extent of adaptive vessel enlargement is not known. OBJECTIVE: To determine whether plaque composition at the dilated site affects probucol-induced vascular remodelling after angioplasty. PATIENTS AND METHODS: Beginning 30 days before percutaneous transluminal coronary angioplasty (PTCA), 317 patients received either probucol, vitamins, probucol and vitamins, or placebo. Patients were then treated for six months after PTCA. Intravascular ultrasound (IVUS) was performed post-PTCA and at follow-up in 94 patients (111 segments). The cross-section for serial analysis was the one at the angioplasty site with the smallest lumen area at follow-up. Quantitative analysis consisted of measurements of lumen area and external elastic membrane (EEM) area. The selected cross-section was also divided into five regions according to the type of plaque present (calcific, fibrotic, hypoechoic, fibrohypoechoic or normal). Plaque characterization scores (PCS) (PCS for arc, area, inner perimeter and outer perimeter) were calculated using weighting factors. RESULTS: There were no interactions between potential PCS covariates and probucol main effect on changes in lumenal, EEM and wall area. There were no significant PCS covariates in the model for change in EEM as they were all removed using a backward stepwise procedure. The last potential covariate (area PCS) had a significance level of P=0.48. In contrast, probucol significantly influenced the change in EEM over time (P=0.003). CONCLUSION: Plaque composition at the dilated site does not appear to influence probucol-induced vascular remodelling after angioplasty.
Angioplasty, Balloon, Coronary↗
Neuroimaging findings (ultrasonography, CT, MRI) in 3 infants with congenital rubella syndrome.
Neuroimaging observations of three infants with congenital rubella syndrome are reported. We have observed congenital rubella syndrome lesions in the subependymal area, the basal ganglia and the deep white matter. Cranial ultrasonography defines subependymal cysts, calcification and possible vascular changes in the basal ganglia while MRI is the most sensitive to minor atrophic changes and white matter lesions. Although CT defines calcification, it is less sensitive than MRI to white matter changes and does not demonstrate subependymal cysts.
Female↗
Matrix GLA protein and BMP-2 regulate osteoinduction in calcifying vascular cells.
Expression of matrix GLA protein (MGP), an alleged calcification inhibitor, is increased in calcified arteries. We used calcifying vascular cells (CVC) that form calcified nodules in vitro to clarify the importance of MGP in vascular cell calcification and differentiation. Unexpectedly, MGP dose-dependently increased calcification in CVC. It also increased expression of the osteogenic marker Cbfal, while decreasing expression of the smooth muscle marker alpha-actin as assessed by immunoblotting. Bone morphogenetic protein-2 (BMP-2), a known osteoinductive factor also increased calcification and osteogenic differentiation in CVC. We hypothesized that the effect of MGP was linked to that of BMP-2 since previous studies show that MGP modulates BMP-2 activity. Therefore, we compared the effect of MGP at different levels of exogenous BMP-2. Results showed that high BMP-2 levels significantly increased the stimulatory effect of low levels of MGP. A relative inhibition of calcification was observed at intermediate levels of MGP and a trend towards renewed stimulation at high levels of MGP. Thus, addition of MGP either promoted or inhibited calcification, depending on the relative amounts of BMP-2 and MGP. This was confirmed in human CVC with different relative expression of BMP-2 and MGP. Calcification in CVC with high relative expression of BMP-2 was inhibited by MGP, while calcification in CVC with low relative expression of BMP-2 was stimulated by MGP. MGP and BMP-2 both accelerated nodule formation, but had opposite effects on nodule size; MGP decreased while BMP-2 increased nodule size. The effect of BMP-2 may partly be explained by a BMP-2 induced decrease in MGP expression. Together, our results suggest that the effect of MGP on calcification and osteogenic differentiation is determined by availability of BMP-2.
Animals↗
An update on vitamin D as related to nephrology practice: 2003.
In this article, an up-to-date consideration of vitamin D therapeutics in nephrology is reviewed. The condition of vitamin D insufficiency is defined as the level of serum 25(OH)vitamin D at which vitamin D2 or D3 supplementation leads to a reduction of levels of parathyroid hormone (PTH). The risks of such vitamin D insufficiency in the normal population and likely risks in individuals with chronic kidney disease (CKD) stages 3 and 4 are reviewed. The potential for its safe treatment and prevention using moderate supplements of vitamin D2 or vitamin D3 are outlined. The role of altered "vitamin D nutrition" in leading to the observed greater incidence of secondary hyperparathyroidism in African Americans with ESRD compared to other racial groups is considered. The actions of active vitamin D sterols to augment intestinal absorption of both calcium and phosphorus, the effect to reduce levels of PTH, and to be a factor contributing to the rising incidence of low bone turnover (adynamic bone) are discussed. Growing evidence for contributions of elevated levels of serum calcium, serum phosphorus, and the calcium x phosphorus product as factors contributing to vascular and cardiac calcification in ESRD patients are cited. Questions are raised about whether the current practice of vitamin D usage in ESRD patients might be a contributing factor to such vascular abnormalities. The economic factors that likely affect the usage of intravenous vitamin D sterols in the United States are reviewed. It is recommended that potential adverse vascular effects of vitamin D sterols related to the increments of serum Ca and P be carefully evaluated.
Chronic Kidney Disease-Mineral and Bone Disorder↗
Arterial osteoprotegerin: increased amounts in diabetes and modifiable synthesis from vascular smooth muscle cells by insulin and TNF-alpha.
AIMS/HYPOTHESIS: Extracellular matrix modifications and linear medial calcifications are elements of diabetic macroangiopathy. We hypothesised that the bone-related protein osteoprotegerin (OPG) may occur in altered amounts in the arterial wall in diabetes, putatively associated with altered synthesis from vascular cells. METHODS: The amount of OPG in the thoracic aorta, obtained at autopsy from 21 diabetic and 42 sex- and age-matched controls, was measured in tissue extracts by an ELISA. The production of OPG was estimated in conditioned media by an ELISA, and OPG mRNA was estimated by RT-PCR in vascular cells grown in vitro. RESULTS: The content of OPG was increased in tunica media samples from diabetic individuals. No differences between diabetic and non-diabetic subjects were observed in tunica intima. Human vascular smooth muscle cells (HVSMCs) produced approximately 30 times more OPG than human umbilical vein endothelial cells. The OPG production into the medium decreased dose- and time-dependently after insulin treatment (maximal effect approximately 60% of control) in HVSMCs, whereas TNF-alpha supplement gave rise to increased OPG synthesis in a time- and dose-dependent manner (maximal effect approximately 200% of control). Similar effects on OPG mRNA expression were observed. Addition of growth hormone (10 ng/ml) or extra glucose (25 mmol/l) to the growth medium had no effect. CONCLUSIONS/INTERPRETATION: Increased OPG concentrations in the arterial wall in diabetes may be part of generalised matrix alterations, putatively related to the development of vascular calcifications. Altered arterial OPG content may be a consequence of the effects of hormones and cytokines, like insulin and TNF-alpha.
Aorta, Thoracic↗