[Calcareous or punctate chondroangiopathy].
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Blood Vessels↗
SEARCH · PubMed Health
Results for “Vascular Calcification”
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Calcifying subpopulation of bovine aortic smooth muscle cells is responsive to 17 beta-estradiol.
BACKGROUND: Arterial calcification, common in atherosclerosis, is associated with an increased risk of clinical events such as myocardial infarction. We previously identified a subpopulation of bovine aortic medial cells, calcifying vascular cells (CVCs), that have osteoblastic characteristics and form bone mineral in vitro in the form of calcified nodules. To assess whether estrogen modulates arterial calcification as well as bone calcification, we tested CVCs for estrogen receptors and for the effect of 17 beta-estradiol on formation of calcified nodules, calcium content, alkaline phosphatase activity, and osteocalcin concentration in the culture medium. METHODS AND RESULTS: Estrogen receptor immunoreactivity was identified in the cytoplasm and the perinuclear region of CVCs by immunocytochemistry. CVCs were treated with 17 beta-estradiol at concentrations of 0, 5, and 10 nmol/L. Twenty-one days of 17 beta-estradiol treatment resulted in a significantly increased number of calcified nodules, visualized by von Kossa staining, as well as increased calcium content of the cultures. Increases in alkaline phosphatase activity, a marker for early osteoblastic differentiation, and secreted osteocalcin, a marker for late osteoblastic differentiation, were enhanced in cells treated with 17 beta-estradiol compared with control cells. CONCLUSIONS: These results suggest that 17 beta-estradiol promotes osteoblastic differentiation and calcification in vascular cells and that estrogen may play a regulatory role in arterial calcification.
Alkaline Phosphatase↗
[Diffuse muscular calcification with subcutaneous cysts].
OBJECTIVE: Diffuse muscular calcification was rare myopathological change due to abnormal metabolism of calcium, which was mainly found in dermatomyositis and myositis ossificans progressiva. Here we reported a case of diffuse muscular calcification that clinically mimicked myositis ossificans progressiva. The disease might be a new type of congenital calcium metabolic disease. METHODS: A 15-year-old girl developed subcutaneous cysts in the wrist and ankle when she was 1 year old. At the age of 9, she developed recurrent fever with myalgia, fatigue and diffuse muscular calcification. It was difficult for her to squat, run or walk. Protuberance presented in the subcutaneous tissue of her trunk. Some nodules ruptured with outflow of chalky material. ESR, ENA, RF, CRP, PTH, CK were in normal limits. EMG was unremarkable. X-ray confirmed diffuse calcification in the muscle and subcutaneous tissues. Biceps muscle biopsy was performed. RESULTS: Numerous inflammatory cells infiltrated around vessels in the perimyosium with perifascicular muscle fiber atrophy and degeneration. Many RRF and SDH positive fibers were also observed. EM showed tubular reticular inclusions in vascular endothelium. CONCLUSION: Diffuse muscular calcification indicated existence of systemic calcium metabolic abnormality. As the clinical symptoms and distribution pattern of calcification were different from dermatomyositis with subcutaneous calcification and myositis ossificans progressiva, our case might be a new type of disease. The microvascular changes might result in the lesion of muscle fibers.
Adolescent↗
Genetic background of neurological disorders with basal ganglia calcification.
BACKGROUND: Bilateral basal ganglia calcifications (BGCs), if severe, are known hallmarks for idiopathic BGC disease (IBGC), but if milder, are often considered radiological findings of unknown significance. In previous studies, only a minority of patients with BGC had monogenic forms of IBGC. METHODS: We studied consecutive patients from a tertiary neurology clinic with bilateral BGCs of variable severity, and their families. We analyzed known IBGC genes, and an extended panel of genes linked to monogenic stroke and metabolic conditions. Clinical, radiological, and genetic data were collected, including vascular risk factors, cerebrovascular events, imaging findings (total calcification score, white matter hyperintensities, ischemic/hemorrhagic lesions), and relevant family history. RESULTS: Twenty-four families with BGCs and neurological symptoms were analyzed. Disease-causing variants were identified in 14 families (58.3%). Eight patients had IBGC (variants in SLC20A2, PDGFB, MYORG), 4 had mitochondrial disease (MT-TL1), and 2 had monogenic vascular conditions (GAL, MAP3K6). Three variants were novel. BGC severity was highest in IBGC cases, while vascular and mitochondrial cases had milder calcifications. White matter hyperintensities were seen in 94.7% of cases and correlated highly with the total calcification score. Clinical vascular events had occurred in 41.7% cases. No monogenic cause was found in 10 patients, although many of these showed clinical or radiological features suggestive of monogenic disease. CONCLUSIONS: Bilateral BGCs can occur in many neurogenetic disorders apart from IBGCs, and a broader genetic search increases the diagnostic yield. Patients with BGCs frequently had clinical cerebrovascular events, which emphasizes the role of cerebrovascular pathology in BGCs.
Humans↗
Changes in polyurethane calcification due to antibiotics.
To develop artificial materials for prolonged use in the vascular system, the complicated process of surface-induced calcification must be better understood. Calcification was examined on porous polyurethane incubated in metastable solutions of calcium phosphate, and the role of certain antibiotics in the medium was evaluated. It seems that certain aminoglycoside antibiotics can modify polyurethane surfaces and, subsequently, their mineralization process. In addition, these antibiotics may alter the calcium transport through polyurethanes. Therefore, it is conceivable that certain antibiotics can, in addition to producing their antibacterial effect, modulate surface calcium binding by changing the calcium mobilization and crystallization. Additional studies are needed to develop applications.
Aminoglycosides↗
Characteristics and performance of an immunosorbent assay for human matrix Gla-protein.
BACKGROUND: Matrix gammacarboxyglutamate (Gla)-protein (MGP) is a strong inhibitor of soft tissue calcification and is mainly produced by chondrocytes and vascular smooth muscle cells (VSMCs). MGP-deficient mice have extensive calcifications of cartilage and arteries leading to osteopenia, fractures and blood vessel ruptures. Promotor polymorphisms resulting in decreased expression levels were found to be associated with an increased risk for cardiovascular disease in humans. METHODS: Recently, an ELISA-based assay has become available with which MGP may be detected in the circulation. The principle of the test kit is that of a competitive immunoassay using a monoclonal antibody against MGP bound to the microtiter plate. RESULTS: Here, we report on a critical evaluation of this assay and its potential diagnostic utility in diseases associated with the degeneration of the arterial vessel wall and cartilage. The biochemical performance of the kit is satisfactory, and significant differences were found between a number of patient cohorts and the reference population. Serum MGP concentrations were significantly decreased in patients with angina pectoris and in various cartilage diseases. CONCLUSIONS: The assay allows comparison of groups and may become a suitable marker for risk assessment or diagnosis in cardiovascular disease and osteoarthritis.
Aging↗
Radiographic diagnosis of meningioma of the lateral ventricle. Review of 22 cases.
Review of 22 cases of meningioma indicates that this lesion occurs slightly more frequently on the left but without predilection for sex or age of the patient. The presenting symptoms were nonspecific. Plain radiographs of the skull sometimes demonstrated calcification in the tumor, but more often did not. Cerebral angiography frequently showed enlargement and displacement of the anterior choroidal artery on the side of the tumor; the lateral posterior choroidal artery on the side of the tumor was also enlarged and displaced in seven of nine patients who underwent vertebral arteriography. Pneumoencephalography accurately demonstrated the site and size of the lesion, as did radionuclide scanning if the lesion was vascular. Computerized tomographic (TC) scanning also determined the location and size of the tumors, as well as their mass effect and vascularity; CT scanning also demonstrated calcification that was not visible on the plain skull radiographs in two of six patients who underwent CT scanning and had calcification.
Adolescent↗
ARTERIAL CALCIFICATION IN INFANCY.
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Arteries↗
Evaluation of 18F-FDG uptake and arterial wall calcifications using 18F-FDG PET/CT.
UNLABELLED: Glucose metabolic activity expressed as (18)F-FDG uptake may be increased in active atherosclerotic plaque. Calcium depositions are often increased in mature atherosclerotic plaque. The purpose of the present study was to assess the patterns of vascular-wall (18)F-FDG uptake and CT calcifications using combined PET/CT. METHODS: One hundred twenty-two consecutive patients over the age of 50 (47 women and 75 men; mean age, 66 +/- 9 y) undergoing whole-body (18)F-FDG PET/CT for tumor assessment were retrospectively evaluated. PET, CT, and PET/CT slices were generated for review. Abnormal vascular findings in major arteries in the chest and abdomen were categorized as PET positive (PET+), PET negative (PET-), CT positive (CT+), or CT negative (CT-). The topographic relationship between increased vascular-wall (18)F-FDG uptake on PET and the presence of calcifications on CT was assessed on PET/CT fused images, with abnormal sites further classified as PET+/CT+, PET+/CT-, or PET-/CT+. The presence of CT calcifications and increased vascular-wall (18)F-FDG uptake was correlated with age, sex, presence of cardiovascular risk factors, and cardiovascular disease. RESULTS: Abnormal findings were identified at 349 sites. CT calcifications (CT+) were observed at 320 sites (92%) of 100 patients (82%), more commonly in men (P < 0.03), in older patients (P < 0.0001), in patients with hypertension (P < 0.003) or hyperlipidemia (P < 0.04), and in smokers (P < 0.008). Increased vascular-wall (18)F-FDG uptake (PET+) was observed at 52 sites (15%) of 38 patients (31%), more commonly in men (P < 0.02), in older patients (P < 0.0001), and in patients with hypertension (P < 0.02), and was borderline in patients with cardiovascular disease (P = 0.057). PET+ and CT+ findings correlated in 12 patients, a PET+/CT- pattern was found in 18 patients, and 8 patients had increased vascular-wall (18)F-FDG uptake in sites with and without calcifications (PET+/CT+, CT-). Twenty-two patients (18%) had a PET-/CT- pattern. CONCLUSION: Hybrid PET/CT can be used to identify and to correctly localize vascular-wall (18)F-FDG activity. Increased vascular-wall (18)F-FDG activity was found in 15% of sites and CT calcifications were noted in 92% of sites, with congruent findings in 7%. The clinical significance of the relationship between vascular-wall (18)F-FDG uptake and CT calcifications needs to be assessed by further prospective studies with long-term follow up.
Adult↗
Metastatic calcification of the cardiac conduction system with heart block: an under-reported entity in chronic renal failure patients.
Systemic metastatic calcification is a common complication of chronic renal failure. Cardiac involvement is particularly ominous, especially when the cardiac conduction system is affected. Conduction defects, arrhythmias, and sudden death have all been reported with conduction system calcification; however, these are relatively under-reported or unrecognized causes of cardiac morbidity and mortality. We describe a 40-year-old man with Von Hippel-Lindau disease who had been maintained on hemodialysis for two years following bilateral nephrectomies for renal cell carcinoma. The patient presented with symptomatic complete heart block that had progressed from Mobitz type I atrioventricular block. Two months later, while being internally paced, the patient died unexpectedly after a complicated hospital admission. Postmortem revealed extensive vascular, myocardial, and conduction system calcification. Conduction system calcification may cause sudden death in chronic renal failure patients during hospital admission, or unexpectedly while the patient is in the community. Knowledge of this condition is necessary to detect it, as the conduction system is not routinely examined. A routine abbreviated conduction system examination is warranted for patients with systemic metastatic calcification, especially if they have sudden death or a known history of heart block.
Adult↗
Maintenance of silastic-teflon shunts for intermitten haemodialysis.
The occurrence of infection in the tissues surrounding external arteriovenous shunts was studied and die important relationship of pyogenic infection to clotting was confirmed. The local application of fusidic add tulle and lanolin greatly reduced the occurrence of both infection and clotting and the need for cannula replacement.Urokinase used for declotting shunts when standard procedures had failed, restored blood flow whether dotting was related to infection or to local vascular factors. This treatment is not advised when clotting is associated with a local abscess, as it may make cannula replacement necessary. Severe local vascular factors, such as metastatic calcification, Raynaud's phenomenon, and venous stenosis, may lead to poor blood flow, so that despite clot lysis elective cannula replacement or the creation of a subcutaneous arteriovenous fistula is required.
Abscess↗
1,25-Dihydroxyvitamin D3 stimulates vascular smooth muscle cell proliferation through a VEGF-mediated pathway.
Atherosclerosis is a complex process characterized by an increase in the wall thickness owing to the accumulation of cells and extracellular matrix between the endothelium and the smooth muscle cell wall. This process is associated with different pathologies and it is accelerated in patients with chronic renal failure. In these patients, decreased synthesis of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) leads to secondary complications, like hyperparathyroidism, and treatment with 1,25(OH)(2)D(3) is a common practice. The effect of 1,25(OH)(2)D(3) on vascular smooth muscle cells (VSMCs) calcification has been widely studied, but the role of 1,25(OH)(2)D(3) on VSMC proliferation remains obscure. We have analyzed the effects of 1,25(OH)(2)D(3) in the proliferation of VSMC. We found that 1,25(OH)(2)D(3) (5-100 nM) induces a dose-dependent increase in VSMC proliferation in quiescent cells and in cells stimulated to grow. This increase in proliferation is achieved by shortening the G1 phase. The effect of 1,25(OH)(2)D(3) on VSMC proliferation is mediated by an increase of the expression of vascular endothelial growth factor A (VEGF), as the inhibition of VEGF activity totally blunted the 1,25(OH)(2) D(3)-induced VSMC proliferation. We found this increase in proliferation in vitro, ex vivo in aortic rings incubated with 1,25(OH)(2)D(3), and in vivo in animals with a model of chronic renal failure (5/6 nephrectomy) treated with 1,25(OH)(2)D(3) (1 mug/kg three times a week for 8 weeks). Thus, we conclude that 1,25(OH)(2)D(3) induces increases in VSMC proliferation through an increase on VEGF expression.
Actins↗
Vascular failure: A new clinical entity for vascular disease.
Atherosclerosis is characterized by the response of the vessel wall to chronic multifactorial injury leading to the formation of atheromatous or fibrous plaques. Endothelial dysfunction represents an initial stage of atherosclerosis. In addition to endothelial dysfunction, smooth muscle dysfunction, metabolic abnormalities of the vessel wall including inflammation, oxidative stress and alterations of neurohormonal balance occur in various stages of atherosclerosis. We now propose a new clinical entity 'vascular failure', defined as the integration of all of these vascular abnormalities. Vascular failure is not an anatomical disease, but rather a comprehensive syndrome of abnormal vascular function. Vascular failure extends from risk factors to established atherosclerotic disease with arterial stenosis, and further to calcification of the vessel wall or serious vascular events that may be caused by plaque rupture and thromboembolic occlusion. We propose aggressive intervention to modify various risk factors, applying to this integrated new entity, vascular failure.
Atherosclerosis↗
[The current concepts of the pathogenesis of Mönckeberg-type arteriosclerosis].
On the basis of experimental researches the circuit of pathogenesis of Mönckeberg's arteriosclerosis--one of the most widespread types of arteriosclerosis is offered. The most important mechanisms realized during development of this pathological process, following: 1) actions of the injuring factor cause necrobiotic change of vascular wall cells; 2) activation of proteolytic enzymes, disturbance of balance between proteinases and their natural inhibitors results in destruction of extracellular matrix fibers and excessive stimulation by products limited proteolysis of vascular wall cell; 3) infringements of intracellular ion homeostasis at the expense of the mentioned below factors exhaust energy systems (last in case of metabolic poison action can be primary are damaged); 4) infringements in system of blood, in particular, in calcium homeostasis, blood coagulation, lipid spectrum promote additional damage of vascular wall cells; 5) dystrophic and metastatic calcification of media; 6) development "unspecific mesenchymal reaction", including fibrosis and sclerosis, in damage zone of vascular wall.
Animals↗
Haemodynamic and tubular renal dysfunction in rats with sustained arterial calcinosis.
1. In humans, two of the principal characteristics of vascular ageing are arterial wall calcification and decreased arterial distensibility, which induce organ damage. To amplify arterial calcium accumulation in laboratory animals, it is necessary to use an overdose of vitamin D(3). 2. The aim of the present study was to assess the impact of arterial calcium overload on renal function. 3. Adult male Wistar rats were randomly divided into two groups: control and treated rats. Treated rats were injected 10 days before the experiment with a single dose of vitamin D(3) (300 000 IU/kg, i.m.). 4. Treated rats showed a decrease in renal blood flow and glomerular filtration rate. Tubular parameters were not modified under basal conditions. In contrast, a statistically significant increase in the fractional excretion of Na, K, Ca and H(2)O were observed in treated rats after the acute increment of sodium distal delivery, suggesting that the reabsorptive capacity of the thick ascending limb may be altered in treated rats. 5. Thus, Na(+)/K(+)-ATPase activity was evaluated in homogenates from renal cortex and medulla. Rats with arterial calcinosis presented a diminished activity of Na(+)/K(+)-ATPase in medulla homogenates. 6. An increment in the abundance of the Na-K-2Cl cotransporter (NKCC2) was observed in renal medulla homogenates from treated rats. It is suggested that this may compensate for the inefficiency of Na(+)/K(+)-ATPase under basal conditions but, in the presence of acute distal sodium overload, the increment in NKCC2 abundance may not be sufficient to compensate for the decrease in Na(+)/K(+)-ATPase activity. 7. In summary, in our experimental model of arterial calcinosis, renal function is impaired, presenting a vascular compromise and altered function of the medullar thick ascending limb that becomes evident in the presence of acute high distal sodium delivery.
Animals↗
Changes in amount of ADM mRNA and RAMP2 mRNA in calcified vascular smooth muscle cells.
This work was aimed to explore the changes and significance of adrenomedullin (ADM) mRNA and receptor activity modifying protein 2 (RAMP2) mRNA in calcified vascular smooth muscle cells (VSMCs). Calcification of cultured rat VSMCs was produced by incubation with beta-glycerophosphate. Content of ADM released by VSMCs was measured by radioimmunoassay (RIA). The amount of ADM mRNA and RAMP2 mRNA was determined by competitive quantitative RT-PCR. The intracellular calcium content, alkaline phosphatases activity and cellular (45)Ca(2+)-uptake were determined. The results showed that the content of calcium, (45)Ca(2+)-uptake and alkaline phosphatases activity in calcified VSMCs were increased by 118%, 174% and seven-fold (all P<0.01), respectively, compared with control VSMCs. Content of ADM in medium was increased by 99% (P<0.01). Furthermore, it was found that the amount of ADM mRNA and RAMP2 mRNA in calcified cells was elevated by 78 and 56% (all P<0.05), respectively, compared with control. The elevated levels of RAMP2 mRNA were in positive correlation with ADM mRNA (r=0.76, P<0.05) in calcified VSMCs. In conclusion, calcified VSMCs generated an increased amount of ADM, and up-regulated gene expressions of ADM and RAMP2.
Adrenomedullin↗
Structural requirements for stabilization of vascular elastin by polyphenolic tannins.
Elastin-associated degeneration and calcification are potential causes of long-term failure of glutaraldehyde (Glut) fixed tissue bioprostheses used in cardiovascular surgery. This vulnerability may be attributed to the inability of Glut to cross-link and adequately protect vascular elastin from enzymatic attack. Tannic acid (TA), a poly galloyl glucose (Glc), is compatible with Glut fixation, binds to vascular elastin, improves resistance to degradation and reduces in vivo calcification. While these results provided evidence of a beneficial interaction between elastin and TA, the nature and mechanisms of these interactions are unclear; moreover, TA-elastin binding exhibits a partial instability after long-term interaction with vascular elastin which could contribute to issues of implant toxicity. In present studies, we used resistance to elastase, mechanical properties, and cell viability assays to evaluate the elastin-stabilizing potential and cytotoxicity of TA derivatives and individual TA components such as acetylated TA (AcTA), pentagalloylglucose (PGG), free gallic acid (Gall) and Glc. Our comparative study demonstrates that polyphenolic hydroxyl groups are the main structural groups essential to the interaction between TA and elastin. Furthermore, we show that PGG, the core structure of TA, possesses the same unique elastin-stabilizing qualities of TA, yet it is much less cytotoxic than TA and thus could be potentially useful as an elastin-stabilizing agent for cardiovascular bioprostheses.
Animals↗
Histology and ultrastructure of the carotid sinus in experimental hypertension.
Histological studies including electron microscopy were performed on the carotid sinuses of dogs with renal hypertension of 17 to 82 days duration or hypertension of two years secondary to aortic coarctation. Physiological abnormalities in the baroreceptors including resetting had been demonstrated before death. Histologically there were no qualitative or quantitative differences in the intrasinus nerve fibers of the hypertensive animals compared tp controls with normal blood pressures, and there was no evidence that baroreceptor degeneration occurred as a consequence of the hypertension. Structural lesions confined to the intima were evident in the sinus walls of some of the renal hypertensive animals whereas the dogs with coarctation showed more advanced sinus wall changes including medial calcification and enlargement of the vascular lumen.
Animals↗