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PubMed2000

Coronary calcification: assessment by intravascular ultrasound imaging.

The role of intralesional coronary calcification is not only an important prognostic factor with respect to interventions, but can be extremely important with respect to diagnostic classification of lesion subsets. Intravascular ultrasound details the relationship between plaque and vessel wall in real time throughout the coronary arterial tree. This provides the opportunity to exactly define not only the quantity but also the distribution of calcium within the vessel wall. This is particularly important from a diagnostic standpoint, as plaque-containing calcification can often lead to ambiguous or erroneous angiographic information. Being able to classify different plaque substructures with intravascular ultrasound can help not only to clarify the ambiguous angiogram but delineate the exact nature of luminal encroachment. From a treatment standpoint, the identification of calcification patterns, particularly those on the superficial intimal surface, can alert the operator to change the compliance prior to definitive therapy. High-speed rotational atherectomy is a technique that provides significant de-calcification in preparation for optimizing the stent geometry within such lesion subsets. Although electron beam computed tomography can accurately locate calcification patterns within the coronary tree in a non-invasive manner, it's often difficult to know the extent of calcification and the relationship to fibrofatty plaques. Intravascular ultrasound albeit invasive, provides the opportunity to delineate these plaque substructures and potentially identify lesion subsets that may have an important natural history in the development of coronary atherosclerosis.

Atherectomy, Coronary↗

PubMed2000

[Clinical significance of coronary calcifications in electron beam tomography].

Electron-beam computed tomography (EBCT) permits high-resolution imaging of the beating heart and the coronary arteries and visualization of coronary calcification. For clinical purposes, coronary calcification represents the formation of atherosclerotic plaques. EBCT provides for accurate quantification of calcification, which is itself related to the extent of coronary atherosclerosis in a linear fashion. Accordingly, EBCT has been shown to measure the extent of coronary atherosclerosis. Importantly, an EBCT scan negative for calcification has a high negative predictive value indicating the absence of obstructive coronary artery disease and an excellent short- to midterm prognosis. It appears that, in general, the amounts of calcification detected by EBCT can be used for prospective risk stratification in symptomatic and asymptomatic adults. However, data derived from unbiased populations are not available at present, and the role of calcification in predicting acute coronary syndromes remains debated. Longitudinal EBCT examinations have emerged as another area of substantial clinical interest. The clinical value of this method remains to be defined, in particular, in comparison with competing, established modalities.

Adult↗

PubMed2001

Regulation of vascular calcification in atherosclerosis.

Over a century ago it was recognized that the vessel wall is a predominant site for ectopic calcification which is a hallmark of clinically significant atherosclerotic lesions. Old observational studies, which characterized vascular calcification as osteogenesis, and recent identification of common molecular mechanisms in bone and vascular calcification have led to the new recognition that atherosclerotic calcification is an actively regulated process similar to osteogenesis and distinct from a metastatic passive mineralization. Since the atherosclerotic lesion is composed of a multitude of cells and inflammatory mediators, elucidation of the role of these components in induction and acceleration of calcification is of fundamental importance in better understanding its pathogenesis and identifying possible interventional targets. This article will focus on four important mediators of vascular calcification: 1) calcifying vascular cells, 2) oxidized lipids, 3) cytokines, and 4) leptin.

Arteriosclerosis↗

PubMed2001

The role of apoptosis in the initiation of vascular calcification.

The initiation sites for calcification in cartilage and bone are cellular products called matrix vesicles. Similar structures have been found in calcified arteries and recent studies suggest that these may be derived from apoptotic cells. It is well established that there is a link between cell death and calcification but the mechanism involved is not known. Since apoptotic cell death is known to occur in the vasculature, we set out to investigate the role of apoptosis in the initiation of vascular calcification. We used a human vascular calcification model in which postconfluent vascular smooth muscle cell (VSMC) cultures form nodules spontaneously and calcify after approximately 28 days. Our studies revealed that apoptosis occurred prior to the onset of calcification and that VSMC "blebs" or apoptotic bodies (ABs) could concentrate calcium in a crystallised form. These observations suggest that apoptosis is involved in the development of VSMC calcification and that VSMC-derived ABs have similarities with matrix vesicles.

Apoptosis↗

PubMed1998

Evaluation of the Association Between Coronary Calcification Detected by Electron Beam Computed Tomography and Atherosclerosis of Extracranial Carotid Arteries In Vivo.

The aim of this study was to evaluate the association between carotid and coronary atherosclerosis and their diagnostic value for predicting angiographically significant coronary artery disease (CAD). We investigated 80 subjects (mean age 55 +/- 8 years) by electron beam computed tomography (EBT), the most sensitive technology for noninvasive detection of coronary calcification (a marker of coronary atherosclerosis); by carotid sonography; and by coronary angiography. Carotid ultrasound was performed with a 7.5 MHz Duplex probe, EBT was done with an EVOLUTION(R) scanner. In 47 subjects, coronary calcification as well as carotid atherosclerosis was present. Thirteen subjects showed isolated coronary calcification, 10 had isolated carotid atherosclerosis, and 10 showed neither coronary calcification nor carotid atheroscleroosis. The association between carotid atherosclerosis and CAD as well as the relationship between coronary calcification and CAD were statistically significant (p < 0.05), but the correlation between coronary calcification and CAD was higher than between carotid atherosclerosis and CAD (Pearson contingency coefficient: 0.34 vs 0.86). In subjects without carotid atherosclerosis, the mean area of coronary calcificiation was significantly (p < 0.01) lower (41 mm2) than in subjects with carotid atherosclerosis (113 mm2). For noninvasive detection of CAD, electron beam CT was superior to carotid sonography on sensitivity (95% vs 78%) and specificity (81% vs 48%). Former studies suggested that sonography of extracoronary vessels could aid in screening for CAD. In our study, the sonographic status of carotid arteries was associated with cardiovascular atherosclerosis but it did not allow us to make a judgment about the presence of CAD with sufficient reliability and it was inferior to electron beam CT as a noninvasive marker of CAD.

Journal Article↗

PubMed2004

The serum level of bone-specific alkaline phosphatase activity is associated with aortic calcification in osteoporosis patients.

It has been suggested that there are several possible linkages between vascular calcification and osteoporosis. In addition, the processes of vascular calcification may have a common etiology with bone formation. Thus, we hypothesized that the serum levels of bone metabolic markers would be different between osteoporosis patients with and without vascular calcification. In this study, we showed that the serum level of bone-specific alkaline phosphatase activity in osteoporosis patients with abdominal aortic calcification had a higher value than in those without the calcification. On the other hand, there were no significant differences in the urine levels of type I collagen cross-linked N-telopeptides (a bone resorption marker), or in the serum levels of intact osteocalcin, Ca, and P. Bone-specific alkaline phosphatase is the most important marker for osteoblast differentiation; furthermore, the serum level of its activity may reflect the process of calcification of the aorta in osteoporosis patients.

Aged↗

PubMed2005

Caseous calcification and liquefaction of the mitral annulus: a diagnostic confounder.

Caseous calcification of the mitral annulus is a rare form of periannular calcification that has a distinct appearance. It generally appears as a large spheric mass like calcification with a central echolucent area that may lead to diagnostic errors. Cardiac imagers should be familiar with this rare form of periannular calcification. We report the case of a 62-year-old woman in whom a suspicious spheric mass like calcification was detected with multislice computed tomography which was performed for coronary artery calcium scoring. Echocardiography displayed the typical findings of caseous calcification of the mitral annulus with central liquefaction.

Calcinosis↗

PubMed2004

Non-invasive assessment of coronary calcification.

Electron-beam tomography (EBT) and multi-detector computed tomography (MDCT) enable the noninvasive assessment of coronary calcification. The amount of coronary calcification, as detected by EBT, has a close relation with the amount of coronary atherosclerosis, which is the substrate for the occurrence of myocardial infarction and sudden cardiac death. Calcification of the coronary arteries can be seen as a cumulative measure of life-time exposure to cardiovascular risk factors. Several studies have shown that the amount of coronary calcification is associated with the risk of coronary heart disease. Therefore, coronary calcification is a promising method for non-invasive detection of asymptomatic subjects at high risk of developing coronary heart disease. Whether measurement of coronary calcification also increases the predictive power of coronary events based on cardiovascular risk factors is topic of current research.

Age Factors↗

PubMed1983

Mechanism of calcification of porcine bioprosthetic aortic valve cusps: role of T-lymphocytes.

Calcification of glutaraldehyde-preserved porcine aortic valve bioprosthetic cusps limits their success as cardiac valve substitutes. Subcutaneous implants of porcine bioprostheses in rats and rabbits have provided a convenient experimental tool to study this calcification process. Previous clinical research has suggested that the host's immune response to the porcine xenograft tissue may contribute to the calcific degeneration. To investigate the possible contribution of the immune response, porcine bioprosthetic cusps implanted subcutaneously in congenitally athymic (nude) BALBc mice and normal controls were analyzed biochemically and histologically after retrieval at 21 days. Calcification was comparable in implants retrieved from athymic (calcium 95.5 +/- 24.5 micrograms/mg) and normal mice (calcium 102.3 +/- 4.66 micrograms/mg). Explants from nude mice demonstrated fewer adherent cells than those from normal animals, but the morphologic characteristics of the calcification were the same in both groups, with dystrophic mineralization of the spongiosa predominating. Thus, normal T-lymphocyte function is not necessary for porcine bioprosthetic calcification, and immunologic processes do not contribute to this process.

Animals↗

PubMed1989

Geographic variation in the incidence of myocardial calcification associated with acute myocardial infarction.

There is reason to believe that calcium influx into heart muscle during acute myocardial infarction (AMI) can aggravate myocyte injury. Furthermore, the degree of such influx might correlate with the occurrence of microscopic myocyte calcification observed at autopsy. We have searched for evidence of myocyte calcification in hearts of patients found to have AMI at autopsy at the Veterans Administration Medical Center in Salt Lake City (SLCVA), a region with a low myocardial infection death rate, and at the George Washington University Medical Center in Washington, DC (GWUMC), a region with a high myocardial infection death rate. Of 23 consecutive cases examined under "blind" conditions at the GWUMC in which AMI was found, there were 15 instances of cardiac myocyte calcification observed in von Kossa-stained sections. Not a single example of myocyte calcification was found in 23 comparable cases at the SLCVA. The basis of this difference in myocyte calcification is unknown, but may be related to the fact that the Salt Lake City drinking water contains a higher level of magnesium, which is known to protect against soft tissue calcification, than does that of Washington, DC. This may be the basis for the apparent protection that dietary magnesium exerts against myocardial infarction death.

Black People↗

PubMed1981

Epididymal calcification in genital filariasis.

Although calcification of the epididymis has been described occasionally in the histologic sections of sperm granuloma, epididymal tuberculosis, and filarial funiculoepididymitis, it has not been demonstrated radiologically. Two cases of epididymal calcification due to long-standing genital filariasis are presented. Both the patients presented with chronic bilateral funiculoepididymitis, and in one secondary sterility also developed due to destruction and calcification of both the epididymides. Calcification of the epididymis in filariasis appears to be due to calcification of the dead adult filarial worm. Radiologic demonstration of this calcification would help to differentiate various types of funiculoepididymitis.

Adult↗

PubMed1990

Prevention of calcification of glutaraldehyde pretreated bovine pericardium through controlled release polymeric implants: studies of Fe3+, Al3+, protamine sulphate and levamisole.

Calcification is the principal cause of the clinical failure of bioprosthetic heart valves fabricated from glutaraldehyde pretreated porcine aortic valves or bovine pericardium. The present study investigated controlled-release implants for prevention of the calcification of glutaraldehyde pretreated bovine pericardium in a rat subdermal model. Either Al3+ and Fe3+ (inhibitors of the growth and dissolution rate of hydroxyapatite crystals), levamisole (alkaline phosphatase inhibitor) or protamine sulphate (charge modifier) were individually incorporated into various polymeric carriers (either silicone rubber, polyurethane or silicone rubber-polyurethane copolymer). Polymeric implants were evaluated for in vitro release kinetics, which revealed that sustained drug release was obtained from 21 d to more than 90 d from various drug matrices. In vivo efficacy was studied by co-implanting the polymeric delivery systems with glutaraldehyde pretreated bovine pericardium for 21 d using a subdermal rat model; glutaraldehyde pretreated bovine pericardium calcium levels were quantitated by atomic absorption spectroscopy in the explanted tissues. Fe3+ and Al3+ polymeric implants were the most effective for inhibiting deposition of calcium mineral. Al3+ demonstrated 82% inhibition of calcification compared to controls and Fe3+ resulted in 80% inhibition of calcification. Specific histologic staining methods showed that Fe3+ and Al3+ were localized within the devitalized cells of the explanted glutaraldehyde pretreated bovine pericardium. No adverse effects on somatic growth or recipient bone morphology were noted following controlled-release drug administration. Controlled release of protamine sulphate or levamisole did not significantly inhibit glutaraldehyde pretreated bovine pericardium calcification. It is concluded that regional controlled release of Fe3+ or Al3+ inhibits glutaraldehyde pretreated bovine pericardium calcification in the rat subdermal model without adverse effects.

Aluminum↗

PubMed1984

Computed tomography of calcification and ossification of posterior longitudinal ligament of the spine.

Calcification of the posterior longitudinal ligament occurs in about 3% of adults in Japan, and in about 0.7% of hospitalized adults with spinal symptoms in the United States. The condition may be asymptomatic, however, in patients with a stenotic spinal canal or when the calcification is large, it may cause compression of the spinal cord and myelopathy. The radiographic diagnosis is made when a band of calcification is noted in the spinal canal directly posterior to the vertebral bodies. Lateral tomograms of the spine are helpful for detection and measurement of the exact thickness of the calcification. Computed tomography is particularly helpful because it reveals the thickness and the extent of lateral extension of the calcification, as well as the size of the spinal canal and the extent of its narrowing by the calcification. Seventeen patients evaluated by computed tomography are reported.

Aged↗

PubMed1986

Calcific degeneration of pericardial valvular xenografts implanted subcutaneously in rats.

Tissue valve dystrophic calcification, resulting in hemodynamic regurgitation and/or stenosis, is the most serious complication when bioprosthetic heart valves are concerned. The objective of this investigation was to define morphologically the sequential development of calcific deposits in pericardial tissue cusps of unimplanted cardiac bioprostheses implanted subcutaneously in rats. Small samples of pericardium were implanted subcutaneously in the dorsal area of young rats weighing 60-80 g. The animals were selected randomly and sacrificed at days 1, 2, 7, 14 and 28 after implantation. The specimens were retrieved and studied morphologically. Calcific deposits were seen grossly as small punctate white masses from day 7 after implantation, progressively becoming more extensive. The light and electron microscopic studies showed that: calcific deposits occurred as early as 24 hours after implantation, the calcific degenerative process was progressive with time, and the mineralization was diffuse, although irregular in degree. The ultrastructural findings revealed that cytoplasmic organelles (mitochondria in particular) and plasma membrane of connective tissue cells appear to serve as initial sites of the process of calcification, which then progresses in the interfibrillar spaces, adjacent to collagen fibrils and elastic fibers.

Animals↗

PubMed1992

Osteoporosis and calcification of the aorta.

In an age-stratified random sample of 200 Rochester, Minnesota women, the prevalence of aortic calcification rose with aging, as did the prevalence of vertebral fractures, while bone mass fell. The statistically significant positive association of aortic calcification with vertebral fractures and the negative associations with bone mass at six skeletal sites were mainly accounted for by age. After age-adjustment, the only association remaining was a negative one between calcified aortic plaques and bone mineral density (BMD) of the lumbar spine (P < 0.05). Aortic calcification was not associated with any measures of calcium metabolism, after adjusting for age, except for a slight negative association between linear aortic calcifications and 25(OH) vitamin D levels (P < 0.05). BMD values of the lumbar spine were somewhat greater than predicted for age in women with severe aortic calcification, but similar findings were seen at other skeletal sites and none of the differences was statistically significant. While overestimation of bone mass was generally minimal, severe aortic calcification may distort lumbar spine assessments in a minority of postmenopausal women.

Adult↗

PubMed1995

The vascular calcification-cutaneous necrosis syndrome.

BACKGROUND: Although medial calcification of larger elastic arteries in chronic kidney failure and with advancing age is relatively common, calcification of the cutaneous vascular system is rare. OBJECTIVE: Our purpose was to describe three patients with the vascular calcification-cutaneous necrosis syndrome and review the cause, clinical and pathologic features, and treatment of this syndrome. METHODS: We describe three patients with ischemic necrotic ulcers and underlying cutaneous vascular calcification. The clinical setting was abnormal calcium metabolism from either chronic kidney failure or excessive vitamin D intake. RESULTS: The clinical findings in all patients consisted of multiple tender livedoid nodules and ulcerative plaques on the thighs and legs, which developed in the setting of abnormal calcium metabolism from either chronic kidney failure or excessive vitamin D intake. Histologic study demonstrated vascular calcification. Although this syndrome usually has a chronic course with significant morbidity and mortality, subtotal parathyroidectomy followed by kidney transplantation resulted in complete resolution in one of our patients. CONCLUSION: The clinical and histopathologic findings in the vascular calcification-cutaneous necrosis syndrome are unique. The pathogenesis is likely multifactorial. Treatment for the skin lesions is largely supportive.

Adult↗

PubMed1977

CT evidence of grey matter calcification secondary to radiation therapy.

There are four previously reported cases of post-irradiation calcification in the basal ganglia as demonstrated on the conventional skull roentgenograms. We have described two additional cases with grey matter calcification, which were demonstrated 10 and 14 yr after radiation therapy for an optic glioma and a medulloblastoma, respectively. The calcification was clearly demonstrated on CT scan, although it was not apparent on the skull roentgenogram. The extract pathogenesis of this condition is not clear. It appears, however, to be related to radiation vasculitis of the small vessels of the brain with resultant hyalinization and calcification. A long-term follow up study would be necessary to evaluate the significance and implication of post-irradiation calcification of the grey matter. CT is the most sensitive method of demonstrating the intracranial calcification in vivo.

Basal Ganglia↗

PubMed2004

Vascular smooth muscle cells and calcification in atherosclerosis.

Vascular calcification is a prominent feature of atherosclerosis but the mechanisms underlying vascular calcification are still obscure. Since bone-associated proteins such as osteonectin, osteocalcin, and matrix Gla protein have been detected in calcified vascular tissues, calcification has been considered to be an organized, regulated process similar to mineralization in bone tissue. Vascular smooth muscle cells (VSMCs) are currently considered to be responsible for the formation of vascular calcifications. Apoptosis of VSMCs appears to be a key factor in this process, while other factors including cell-cell interactions (macrophages and VSMCs), lipids, and plasma inorganic phosphate levels modulate the calcification process. The focus of this review is on the role of VSMCs in the development of calcifications in atherosclerotic plaques.

Apoptosis↗