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At least 1,621 records · Page 90Linked to original sources
PubMed1989

The mechanism of the obstruction in calcific aortic stenosis with bicuspid valve: a reason for failure of balloon aortic valvuloplasty in the elderly.

Percutaneous aortic balloon valvuloplasty failed to relieve the obstruction in 2 elderly patients with calcific aortic stenosis. Intraoperative and pathologic examination showed bicuspid aortic valve with symmetric cusps, straight and fibrotic cusp edges and fractured calcific nodules of the aortic valve. Failure of balloon valvuloplasty in these patients, in spite of successful fractures of calcific nodules, was due to inability to influence the spring-like action of the thickened edges of the valve which represents a specific additional cause of obstruction in calcific bicuspid aortic valve of the elderly.

Aged↗
PubMed1996

Free protein S deficiency in hemodialysis patients due to vascular calcifications?

Vascular calcifications are frequent in hemodialysis patients. Its incidence ranges from 25 to 67% depending of different series. Thirty hemodialysis patients were selected from a dialysis population of 150 patients. These 30 patients were divided into two groups: group I included 15 hemodialysis patients with severe secondary hyperparathyroidism and severe, roentgenographically visible diffuse vascular calcifications, and group II included 15 other hemodialysis patients with moderate hyperparathyroidism without radiographic evidence of arterial calcifications. The control group comprised 20 normal volunteers. In all patients, measurements of protein C activity, free protein S and intact parathyroid hormone (PTH) were performed. Statistical analysis showed that free protein S in the patients of group I had a tendency to be lower than in the patients of group II (p < 0.01) and the control group (p < 0.001). We did not find significant differences in free protein S between group II and control group patients nor a significant correlation between intact PTH and free protein S in groups I and II. Protein C activity was found to be in the normal range in both groups. Free protein S deficiency in patients of group I would suggest a synthesis defect by impaired endothelial cells-due to vascular calcifications (?). Free protein S deficiency could increase the risk of thrombotic complications in these patients.

Adult↗
PubMed2005

Calcification of advanced atherosclerotic lesions in the innominate arteries of ApoE-deficient mice: potential role of chondrocyte-like cells.

OBJECTIVE: Advanced atherosclerotic lesions in the innominate arteries of chow-fed apolipoprotein E-deficient mice become highly calcified with 100% frequency by 75 weeks of age. The time course, cell types, and mechanism(s) associated with calcification were investigated. METHODS AND RESULTS: The deposition of hydroxyapatite is preceded by the formation of fibro-fatty nodules that are populated by cells that morphologically resemble chondrocytes. These cells are spatially associated with small deposits of hydroxyapatite in animals between 45 and 60 weeks of age. Immunocytochemical analyses with antibodies recognizing known chondrocyte proteins show that these cells express the same proteins as chondrocytes within developing bone. Histological and electron microscopic analyses of lesions from animals between 45 and 60 weeks of age show that the chondrocyte-like cells are surrounded by dense connective tissue that stains positive for type II collagen. Nanocrystals of hydroxyapatite can be seen within matrix vesicles derived from the chondrocyte-like cells. In mice between 75 and 104 weeks of age, the lesions have significantly reduced cellularity and contain large calcium deposits. The few remaining chondrocyte-like cells are located adjacent to or within the large areas of calcification. CONCLUSIONS: Calcification of advanced lesions in chow-fed apolipoprotein E-deficient mice occurs reproducibly in mice between 45 and 75 weeks of age. The deposition of hydroxyapatite is mediated by chondrocytes, which suggests that the mechanism of calcification may in part recapitulate the process of endochondral bone formation.

Alkaline Phosphatase↗
PubMed1998

Fibronectin and collagen I matrixes promote calcification of vascular cells in vitro, whereas collagen IV matrix is inhibitory.

Vascular calcification is a frequent component of atherosclerosis, yet the pathological mechanisms that regulate its formation are poorly understood. Calcification of the vessel wall may represent a process by which cells that normally exhibit a smooth muscle phenotype differentiate into cells that exhibit an osteoblast-like phenotype. One of the determinants of cellular phenotype is extracellular matrix; thus, we undertook the current study to evaluate the influence of extracellular matrix on calcification of vascular cells in vitro. Cell lines derived from bovine aortic media were divided into 1 of 3 groups: those that did not mineralize, those that mineralized slowly, or those that mineralized rapidly. When slowly mineralizing cells were plated onto matrix produced by rapidly mineralizing cells, the time required for mineralization decreased from 33+/-3.0 days to 7.8+/-1.3 days. Matrix produced by rapidly mineralizing cells was found to contain 3 times the amount of collagen I and fibronectin but 70% less collagen IV than nonmineralizing clones. When slowly mineralizing cells were cultured on purified collagen I or fibronectin, mineralized nodule formation, calcium incorporation, von Kossa staining, and alkaline phosphatase activity increased. In contrast, culturing slowly mineralizing cells on purified collagen IV inhibited these mineralization parameters. Furthermore, blocking antibodies to alpha5 integrins significantly inhibited the fibronectin-mediated increases in alkaline phosphatase activity, indicating that integrin-based signaling may be involved. These data suggest that matrix composition can regulate development of arterial calcification and that a subpopulation of vascular cells preferentially produces positively regulating matrix components.

Alkaline Phosphatase↗
PubMed1999

Noncollagenous bone matrix proteins, calcification, and thrombosis in carotid artery atherosclerosis.

Advanced atherosclerosis is often associated with dystrophic calcification, which may contribute to plaque rupture and thrombosis. In this work, the localization and association of the noncollagenous bone matrix proteins osteonectin, osteopontin, and osteocalcin with calcification, lipoproteins, thrombus/hemorrhage (T/H), and matrix metalloproteinases (MMPs) in human carotid arteries from endarterectomy samples have been determined. According to the recent American Heart Association classification, 6 of the advanced lesions studied were type V (fibroatheroma) and 16 type VI (complicated). Osteonectin, osteocalcin, and osteopontin were identified by monoclonal antibodies IIIA(3)A(8), G12, and MPIIIB10(1) and antiserum LF-123. Apolipoprotein (apo) AI, B, and E; lipoprotein(a); fibrinogen; fibrin; fragment D/D-dimer; MMP-2 (gelatinase A); and MMP-3 (stromelysin-1) were identified with previously characterized antibodies. Calcium phosphate deposits (von Kossa's stain) were present in 82% of samples (3 type V and 15 type VI). Osteonectin was localized in endothelial cells, SMCs, and macrophages and was associated with calcium deposits in 33% of type V and 88% of type VI lesions. Osteopontin was distributed similarly to osteonectin and was associated with calcium deposits in 50% of type V and 94% of type VI lesions. Osteocalcin was localized in large calcified areas only (in 17% of type V and 38% of type VI lesions). ApoB colocalized with cholesterol crystals and calcium deposits. Lipoprotein(a) was localized in the intima, subintima, and plaque shoulder. Fibrin (T/H) colocalized with bone matrix proteins in 33% of type V and 69% of type VI lesions. MMP-3 was cytoplasmic in most cells and colocalized with calcium and fibrin deposits. MMP-2 was less often associated with calcification. The results of this study show that osteonectin, osteopontin, and osteocalcin colocalized with calcium deposits with apoB, fibrin, and MMP-3 in advanced, symptomatic carotid lesions. These data suggest that the occurrence of T/H might contribute to dystrophic arterial calcification in the progression and complications of atherosclerosis.

Arteriosclerosis↗
PubMed2002

Evidence for heritability of abdominal aortic calcific deposits in the Framingham Heart Study.

BACKGROUND: Atherosclerosis is a systemic disease that underlies clinical cardiovascular disease. The radiographic finding of abdominal aortic calcific deposits is an indicator of the presence of aortic atherosclerosis and an independent predictor of cardiovascular disease events. Little is known about the heritability of aortic calcification. METHODS AND RESULTS: Original Framingham Heart Study cohort participants (2151) in 1109 extended pedigrees had a lateral lumbar radiograph. The presence and severity of abdominal aortic calcific (AAC) deposits at the levels of the first through fourth lumbar vertebrae was graded by a previously validated rating scale. Correlation coefficients were calculated in pairs of siblings, parent-offspring, and spouses. Age-, sex-, and multivariable-adjusted correlation coefficients for AAC were 0.52 for parent-offspring pairs and 0.20 for sibling pairs. In contrast, the multivariable-adjusted correlation for AAC in spouse pairs was -0.02. Using variance component methods implemented in SOLAR, the estimated heritability for age-, sex-, and multivariable-adjusted AAC was 0.49 (P<0.001). Thirty-one percent of the overall variance in AAC deposits was due to measured covariates, and 49% to heritable factors. CONCLUSIONS: In our large, population-based sample, heritable factors play a role in the presence and extent of abdominal aortic calcification. Thus, a substantial proportion of the variation in AAC is due to additive effects of genes, which have yet to be characterized. Measures of aortic atherosclerosis may provide heritable quantitative phenotypes for the genetic dissection of the complex condition of atherosclerosis in human populations.

Aorta, Abdominal↗
PubMed2002

Influence of lipid-lowering therapy on the progression of coronary artery calcification: a prospective evaluation.

BACKGROUND: Coronary calcification measured by fast computed tomography techniques is a surrogate marker of coronary atherosclerotic plaque burden. In a cohort study, we prospectively investigated whether lipid-lowering therapy with a cholesterol synthesis enzyme inhibitor reduces the progression of coronary calcification. METHODS AND RESULTS: In 66 patients with coronary calcifications in electron beam tomography (EBT), LDL cholesterol >130 mg/dL, and no lipid-lowering treatment, the EBT scan was repeated after a mean interval of 14 months and treatment with cerivastatin was initiated (0.3 mg/d). After 12 months of treatment, a third EBT scan was performed. Coronary calcifications were quantified using a volumetric score. Cerivastatin therapy lowered the mean LDL cholesterol level from 164+/-30 to 107+/-21 mg/dL. The median calcified volume was 155 mm3 (range, 15 to 1849) at baseline, 201 mm3 (19 to 2486) after 14 months without treatment, and 203 mm3 (15 to 2569) after 12 months of cerivastatin treatment. The median annualized absolute increase in coronary calcium was 25 mm3 during the untreated versus 11 mm3 during the treatment period (P=0.01). The median annual relative increase in coronary calcium was 25% during the untreated versus 8.8% during the treatment period (P<0.0001). In 32 patients with an LDL cholesterol level <100 mg/dL under treatment, the median relative change was 27% during the untreated versus -3.4% during the treatment period (P=0.0001). CONCLUSIONS: Treatment with the cholesterol synthesis enzyme inhibitor cerivastatin significantly reduces coronary calcium progression in patients with LDL cholesterol >130 mg/dL.

Adult↗
PubMed2003

Association between apolipoprotein E alleles and calcific valvular heart disease.

BACKGROUND: Studies on apolipoprotein E (apoE) alleles have reported an increased risk of coronary heart disease in patients with the apoE4 allele. Given the risk factor and histological similarities between coronary and calcific valvular heart disease (aortic stenosis [AS] and mitral annular calcification [MAC]), we postulated that apoE alleles might be associated with the development of these valvular lesions. METHODS AND RESULTS: We evaluated the association between apoE alleles and calcific valvular lesions in 802 patients undergoing transthoracic echocardiography using logistic regression analyses. No difference was noted in genotype distribution (P=0.59) or prevalence of apoE4 between those with or without MAC (30% versus 27%, respectively; P=0.57). Compared with patients without AS, the genotype distribution of patients with AS differed significantly (P=0.03), with increasing prevalences of the apoE 4 allele (27% in those without versus 40% in those with AS; P=0.01). In multivariate analyses adjusting for age, gender, low-density lipoprotein cholesterol levels, and coronary artery disease, increasing age and the apoE4 allele were significant independent predictors of AS (odds ratio, 1.94; 95% confidence interval, 1.01 to 3.71; P=0.046), whereas the apoE4 allele was not predictive of MAC. CONCLUSIONS: These findings support extension of the importance of the apoE4 allele beyond atherosclerosis and Alzheimer's disease to calcific AS.

Aged↗
PubMed2000

Tumor necrosis factor-alpha promotes in vitro calcification of vascular cells via the cAMP pathway.

BACKGROUND: Vascular calcification is an ectopic calcification that commonly occurs in atherosclerosis. Because tumor necrosis factor-alpha (TNF-alpha), a pleiotropic cytokine found in atherosclerotic lesions, is also a regulator of bone formation, we investigated the role of TNF-alpha in in vitro vascular calcification. METHODS AND RESULTS: A cloned subpopulation of bovine aortic smooth muscle cells previously shown capable of osteoblastic differentiation was treated with TNF-alpha, and osteoblastic differentiation and mineralization were assessed. Treatment of vascular cells with TNF-alpha for 3 days induced an osteoblast-like morphology. It also enhanced both activity and mRNA expression of alkaline phosphatase, an early marker of osteoblastic differentiation. Continuous treatment with TNF-alpha for 10 days enhanced matrix mineralization as measured by radiolabeled calcium incorporation in the matrix. Pretreatment of cells with a protein kinase A-specific inhibitor, KT5720, attenuated cell morphology, the alkaline phosphatase activity, and mineralization induced by TNF-alpha. Consistent with this, the intracellular cAMP level was elevated after TNF-alpha treatment. Electrophoretic mobility shift assay demonstrated that TNF-alpha enhanced DNA binding of osteoblast specific factor (Osf2), AP1, and CREB, transcription factors that are important for osteoblastic differentiation. CONCLUSIONS: These results suggest that TNF-alpha enhances in vitro vascular calcification by promoting osteoblastic differentiation of vascular cells through the cAMP pathway.

Alkaline Phosphatase↗
PubMed1985

Digital subtraction fluoroscopy: a new method of detecting coronary calcifications with improved sensitivity for the prediction of coronary disease.

The association between calcification of the coronary arteries and coronary artery narrowing is well established. However, fluoroscopic visualization of coronary calcifications has been insufficiently sensitive to be useful as a screening test. Since digitization of radiographic images permits the subtraction of noncardiac structures from moving cardiac structures, such subtraction might increase the sensitivity of coronary fluoroscopy. To determine whether coronary calcifications were better visualized with digital subtraction fluoroscopy than with conventional fluoroscopy, we taped diseased human coronary arteries to a pulsating water balloon inside the thorax of a dog cadaver and studied this model with both fluoroscopic techniques. Calcific atherosclerotic plaques were more easily identified with digital subtraction fluoroscopy than with conventional fluoroscopy. We tested the method clinically by submitting 191 subjects without history or electrocardiographic evidence of previous myocardial infarction who were referred for coronary arteriography to both fluoroscopic studies. For at least one, at least two, and three calcified coronary arteries, digital fluoroscopy was more sensitive (92%, 66%, and 40%) than conventional fluoroscopy (63%, 21%, and 2%) (all p less than .001) for the prediction of significant coronary obstructions (greater than 50%). Although digital fluoroscopy was less specific than conventional fluoroscopy (digital: 65%, 89%, and 97%; conventional: 81%, 98%, and 100%) (all but last, p less than .01), receiver operating curve analysis revealed a significantly larger area under the curve, indicating higher accuracy for the digital technique (p = .03). Digital subtraction fluoroscopy was more accurate in younger than in older patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1994

Mechanism of efficacy of 2-amino oleic acid for inhibition of calcification of glutaraldehyde-pretreated porcine bioprosthetic heart valves.

BACKGROUND: Calcification is a frequent cause of the clinical failures of glutaraldehyde-pretreated bioprosthetic heart valves (BPHV) fabricated from glutaraldehyde-cross-linked porcine aortic valves. 2-Amino oleic acid (AOA) has been shown in previous in vivo studies to be a promising anticalcification agent. Our objective was to investigate the mechanism of calcification inhibition mediated by AOA pretreatment of porcine aortic valve bioprostheses. METHODS AND RESULTS: BPHV tissues were treated with an AOA solution for 72 hours before experimentation. The diffusion of AOA across both cusp and aortic wall was evaluated. The lag time for AOA to diffuse across the aortic wall was prolonged compared with that of the cusp. An extraction study was performed to determine the stability of AOA binding; the results indicated that the binding was relatively stable regardless of solvent extraction conditions. The interaction between ionic calcium and AOA on treated tissue also was investigated by evaluating the patterns of calcium diffusion across both treated and untreated tissues. The results showed that AOA significantly reduced the diffusion of calcium. AOA inhibition of aortic valve calcification (calcium level, 5.5 +/- 3.0 mg/g of tissue compared with control; calcium level, 91.2 +/- 19.5 mg/g of tissue) but not aortic wall (calcium level, 158.7 +/- 10.3 mg/g of tissue compared with control; calcium level, 157.5 +/- 7.9 mg/g of tissue) was demonstrated on representative specimens from valves implanted in left ventricular apicoaortic shunts explanted after 150 days. CONCLUSIONS: AOA covalently binds to glutaraldehyde-pretreated bioprosthetic heart valve tissue, presumably as the result of an aldehyde-amino reaction. Covalently bound AOA diminishes Ca2+ diffusion compared with non-AOA-pretreated bioprosthetic tissues. This may explain in part the anticalcification mechanism of AOA. Furthermore, AOA inhibits calcification of porcine BPHV cusps in the circulation.

Animals↗
PubMed2005

Regulation of vascular calcification: roles of phosphate and osteopontin.

Vascular calcification is prevalent in aging as well as a number of pathological conditions, and it is now recognized as a strong predictor of cardiovascular events in the general population as well as diabetic and end-stage renal disease patients. Vascular calcification is a highly regulated process involving inductive and inhibitory mechanisms. This article focuses on two molecules, phosphate and osteopontin, that have been implicated in the induction or inhibition of vascular calcification, respectively. Elevated phosphate is of interest because hyperphosphatemia is recognized as a major nonconventional risk factor for cardiovascular disease mortality in end-stage renal disease patients. Studies to date suggest that elevated phosphate stimulates smooth muscle cell phenotypic transition and mineralization via the activity of a sodium-dependent phosphate cotransporter. Osteopontin, however, appears to block vascular calcification most likely by preventing calcium phosphate crystal growth and inducing cellular mineral resorption.

Animals↗
PubMed2005

Proinflammatory activation of macrophages by basic calcium phosphate crystals via protein kinase C and MAP kinase pathways: a vicious cycle of inflammation and arterial calcification?

Basic calcium phosphate (BCP) crystal deposition underlies the development of arterial calcification. Inflammatory macrophages colocalize with BCP deposits in developing atherosclerotic lesions and in vitro can promote calcification through the release of TNF alpha. Here we have investigated whether BCP crystals can elicit a proinflammatory response from monocyte-macrophages. BCP microcrystals were internalized into vacuoles of human monocyte-derived macrophages in vitro. This was associated with secretion of proinflammatory cytokines (TNFalpha, IL-1beta and IL-8) capable of activating cultured endothelial cells and promoting capture of flowing leukocytes under shear flow. Critical roles for PKC, ERK1/2, JNK, but not p38 intracellular signaling pathways were identified in the secretion of TNF alpha, with activation of ERK1/2 but not JNK being dependent on upstream activation of PKC. Using confocal microscopy and adenoviral transfection approaches, we determined a specific role for the PKC-alpha isozyme. The response of macrophages to BCP crystals suggests that pathological calcification is not merely a passive consequence of chronic inflammatory disease but may lead to a positive feed-back loop of calcification and inflammation driving disease progression.

Arteries↗
PubMed2005

Thyroid hormone targets matrix Gla protein gene associated with vascular smooth muscle calcification.

Thyroid hormones have marked cardiovascular effects in vivo. However, their direct effects on vascular smooth muscle cells have been unclear. Because thyroid hormones play critical roles in bone remodeling, we hypothesized that they are also associated with vascular smooth muscle calcification, one of the pathological features of vascular sclerosis. To test this hypothesis, we examined the effects of 3',3,5-triiodo-L-thyronine (T3) on the expression of calcification-associated genes in rat aortic smooth muscle cells (RAOSMCs). Quantitative RT-PCRs revealed that a physiological concentration of T3 (15 pmol/L free T3) increased mRNA level of matrix Gla protein (MGP), which acts as a potent inhibitor of vascular calcification in vivo, by 3-fold in RAOSMCs, as well as in cultured human coronary artery smooth muscle cells. In RAOSMCs transiently transfected with a luciferase reporter gene driven by the MGP promoter, T3 significantly stimulated luciferase activity. In addition, RNA interference against thyroid hormone receptor-alpha gene diminished the effect of T3 on MGP expression. Aortic smooth muscle tissues from methimazole-induced hypothyroid rats (400 mg/L drinking water; 4 weeks) also showed a 68% decrease in the MGP mRNA level, as well as a 33% increase in calcium content compared with that from the control euthyroid animals, whereas hyperthyroidism (0.2 mg T3/kg IP; 10 days) upregulated MGP mRNA by 4.5-fold and reduced calcium content by 11%. Our findings suggest that a physiological concentration of thyroid hormone directly facilitates MGP gene expression in smooth muscle cells via thyroid hormone nuclear receptors, leading to prevention of vascular calcification in vivo.

Animals↗
PubMed1997

New treatments using alginate in order to reduce the calcification of bovine bioprosthetic heart valve tissue.

Calcification limits the functional lifetime of cardiac valve substitutes fabricated from glutaraldehyde preserved bovine pericardium. Host factors, mainly younger age, and implant factors, mainly glutaraldehyde cross-linking, are implicated in the calcification process. Glutaraldehyde cross-linking is believed to activate the potential sites in the tissues for biocalcification. In the present work, we investigated the possibility of using alginate azide (AA) instead of glutaraldehyde for the preservation of pericardial tissues in order to enhance the durability of bioprosthetic heart valves. Grafting with poly(GMA-BA) copolymer to the alginate azide cross-linked pericardial (AACPC) tissue was carried out to obtain better stability, strength, and anticalcification properties. The strength property and thermal stability of the AA cross-linked tissues were studied. Calcification studies in rat subdermal models reveal that AA cross-linking reduces the calcification to negligible levels. After 30 days implantation, the calcium content was found to be 10.4 +/- 1.2 and 6.1 +/- 0.3 micrograms mg-1 for untreated AACPC and polymer grafted AACPC, respectively, compared to a value of 100 +/- 1.2 micrograms mg-1 calcium recorded for control glutaraldehyde cross-linked pericardial (GCPC) tissues.

Alginates↗
PubMed1994

High expression of genes for calcification-regulating proteins in human atherosclerotic plaques.

Calcification is common in atheromatous plaques and may contribute to plaque rupture and subsequent thrombosis. However, little is known about the mechanisms which regulate the calcification process. Using in situ hybridization and immunohistochemistry we show that two bone-associated proteins, osteopontin (OP) and matrix Gla protein (MGP), are highly expressed in human atheromatous plaques. High levels of OP mRNA and protein were found in association with necrotic lipid cores and areas of calcification. The predominant cell type in these areas was the macrophage-derived foam cell, although some smooth muscle cells could also be identified. MGP was expressed uniformly by smooth muscle cells in the normal media and at high levels in parts of the atheromatous intima. Highest levels of this matrix-associated protein were found in lipid-rich areas of the plaque. The pattern of expression of these two genes contrasted markedly with that of calponin and SM22 alpha, genes expressed predominantly by differentiated smooth muscle cells and whose expression was generally confined to the media of the vessel. The postulated function of OP and MGP as regulators of calcification in bone and the high levels and colocalization of both in atheromatous plaques suggest they have an important role in plaque pathogenesis and stability.

Arteriosclerosis↗
PubMed2001

Association between mitral annular calcification and carotid atheroma.

Carotid artery atherosclerosis is a strong predictor of stroke and represents a potential source of cerebral emboli. The aim of this study was to investigate whether an association exists between mitral annular calcification and carotid atheroma. In addition, the characteristics of carotid atheromas were compared between patients with and without mitral annular calcification. The authors found that there was a significant association between the presence of mitral annular calcification and carotid atheroma. Mitral annular calcification in the elderly may be a form of atherosclerosis.

Aged↗
PubMed1992

Detection of coronary artery calcification by X-ray computed tomography and its significance: a new CT scoring technique.

In order to study the utility of X-ray computed tomography (CT) for the evaluation of coronary stenosis, the authors developed a scoring system for calcification seen through CT and compared the results with coronary angiographic (CAG) findings (Friesinger's scoring system). Their study included 143 patients (angina pectoris 53, myocardial infarction 44, control 46) who received both CT and CAG. Judkins method was selected for CAG, and stenosis greater than or equal to 75% was defined as significant. Horizontal slices of CT from ascending aorta to cardiac apex at 1 cm intervals were imaged without contrast enhancement. CT scoring system was as follows: no calcification = 0, the length of calcification less than 1 cm = 1, 1-2 cm = 2, more than 2 cm = 3 points. They then totaled the separate scores of all the slices for each coronary artery. Sensitivity, specificity, and predictive value of CT against coronary stenosis were good (79%, 80%, 69%, respectively). The correlation between CT and CAG scores was significant (r = 0.644, p less than 0.01). For all coronary arteries, no correlation was found between the CAG and CT findings for patients less than forty-five years of age. However, from 45 years of age upward, the results were significant. Until now, to the best of their knowledge, no satisfactory system to define the severity of coronary calcification has existed. Density cannot be used, because values are dependent on the area of the region of interest used. They demonstrated the considerable potential usefulness of CT in predicting the presence of coronary stenosis and analyzing its severity.

Calcinosis↗