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PubMed2007

Effects of wall calcifications in patient-specific wall stress analyses of abdominal aortic aneurysms.

It is generally acknowledged that rupture of an abdominal aortic aneurysm (AAA) occurs when the stress acting on the wall over the cardiac cycle exceeds the strength of the wall. Peak wall stress computations appear to give a more accurate rupture risk assessment than AAA diameter, which is currently used for a diagnosis. Despite the numerous studies utilizing patient-specific wall stress modeling of AAAs, none investigated the effect of wall calcifications on wall stress. The objective of this study was to evaluate the influence of calcifications on patient-specific finite element stress computations. In addition, we assessed whether the effect of calcifications could be predicted directly from the CT-scans by relating the effect to the amount of calcification present in the AAA wall. For 6 AAAs, the location and extent of calcification was identified from CT-scans. A finite element model was created for each AAA and the areas of calcification were defined node-wise in the mesh of the model. Comparisons are made between maximum principal stress distributions, computed without calcifications and with calcifications with varying material properties. Peak stresses are determined from the stress results and related to a calcification index (CI), a quantification of the amount of calcification in the AAA wall. At calcification sites, local stresses increased, leading to a peak stress increase of 22% in the most severe case. Our results displayed a weak correlation between the CI and the increase in peak stress. Additionally, the results showed a marked influence of the calcification elastic modulus on computed stresses. Inclusion of calcifications in finite element analysis of AAAs resulted in a marked alteration of the stress distributions and should therefore be included in rupture risk assessment. The results also suggest that the location and shape of the calcified regions--not only the relative amount--are considerations that influence the effect on AAA wall stress. The dependency of the effect of the wall stress on the calcification elastic modulus points out the importance of determination of the material properties of calcified AAA wall.

Aorta, Abdominal↗
PubMed1995

Calcification of aortic valve detected incidentally on CT scans: prevalence and clinical significance.

OBJECTIVE: Aortic valve calcification that is visualized on chest radiographs is considered a marker for clinically significant aortic stenosis, but the clinical importance of this finding on CT is unknown. Accordingly, we studied the prevalence and clinical relevance of aortic valve calcification found incidentally on CT scans of the chest. MATERIALS AND METHODS: After comparing computer records of chest CTs and echocardiograms, we identified 109 patients who underwent both studies during a 2-year period. Two thoracic radiologists reviewed the CT scans to identify and quantify aortic valve calcification. The quantity of aortic valve calcification was graded on a scale of 1 to 3, with grade 3 indicating the most severe calcification. The prevalence of calcification was correlated with patient age and sex. The findings on CT were correlated with hemodynamic data from echocardiography. At echocardiography, a peak aortic valve gradient of greater than 25 mm Hg was defined as abnormal. RESULTS: Aortic valve calcification was noted on CT scans in 33 (30%) of the 109 patients. Aortic valve calcification shown by CT was significantly more common in patients more than 65 years old (p < .01). Five (15%) of 33 patients with aortic valve calcification shown by CT had abnormal aortic valve gradients at echocardiography. In contrast, none of 76 patients without aortic valve calcification shown by CT had abnormal aortic valve gradients (p < .01). All five patients with abnormal aortic valve gradients had moderate quantities of aortic valve calcification seen on CT scans. Two of the five were younger than 55 years old. CONCLUSION: Aortic valve calcification is a common finding on CT scans and is usually clinically insignificant. Nevertheless, some patients with aortic valve calcification on CT have aortic stenosis, particularly those younger than 55 years old and those with moderately dense aortic valve calcification shown by CT. These patients may benefit from hemodynamic assessment of the aortic valve by echocardiography.

Adult↗
PubMed1996

Calcium pyrophosphate dihydrate crystal deposition disease: frequency of tendon calcification about the knee.

OBJECTIVE: To delineate the prevalence of tendon and cartilage calcification as well as its possible predilection for age, sex, or side of involvement in calcium pyrophosphate dihydrate (CPPD) crystal deposition disease of the knee. METHODS: We reviewed 225 lateral knee radiographs from 138 patients (M/F: 85/52, 1 unspecified sex, mean age: 73 yrs) to document quadriceps and gastrocnemius tendon calcification. Chondrocalcinosis of the knee was evaluated on 275 knee radiographs (lateral and anteroposterior projection) from 153 patients (M/F: 97/55, 1 unspecified sex, mean age: 73 yrs) to determine the frequency of meniscal and hyaline cartilage calcification. RESULTS: Gastrocnemius tendon calcification was found in 28.4% of knees, which is significantly more common than quadriceps tendon calcification (8.4%). No significant age or laterality difference existed for calcification of either tendon. Quadriceps tendon calcification was more prevalent in men, but no sex difference was present for the gastrocnemius tendon. Calcification of either tendon never occurred without associated chondrocalcinosis. Meniscal calcification was significantly more prevalent than hyaline cartilage calcification; meniscal calcification also was significantly more frequent in men. Increased prevalence of calcification with age was observed in hyaline cartilage but not in the menisci. CONCLUSION: Gastrocnemius tendon calcification is not infrequent in CPPD crystal deposition disease of the knee; identification of such calcification may further delineate this extent of the disorder.

Adult↗
PubMed2004

Evidence for a serum factor that initiates the re-calcification of demineralized bone.

The present studies show for the first time that demineralized bone re-calcifies rapidly when incubated at 37 degrees C in rat serum: re-calcification can be demonstrated by Alizarin Red and von Kossa stains, by depletion of serum calcium, and by uptake of calcium and phosphate by bone matrix. Re-calcification is specific for the type I collagen matrix structures that were calcified in the original bone, with no evidence for calcification in periosteum or cartilage. Re-calcification ceases when the amount of calcium and phosphate introduced into the matrix is comparable to that present in the original bone prior to demineralization, and the re-calcified bone is palpably hard. Re-calcified bone mineral is comparable to the original bone mineral in calcium to phosphate ratio and in Fourier transform infrared and x-ray diffraction spectra. The serum activity responsible for re-calcification is sufficiently potent that the addition of only 1.5% serum to Dulbecco's modified Eagle's medium causes bone re-calcification. This putative serum calcification factor has an apparent molecular mass of 55-150 kDa and is inactivated by trypsin or chymotrypsin. The serum calcification factor must act on bone for 12 h before re-calcification can be detected by Alizarin Red or von Kossa staining and before the subsequent growth of calcification will occur in the absence of serum. The speed, matrix-type specificity, and extent of the serum-induced re-calcification of demineralized bone suggest that the serum calcification factor identified in these studies may participate in the normal calcification of bone.

Animals↗
PubMed2005

Increased arterial calcification in Paget's disease of bone.

When examining radiographs of patients with Paget's disease of bone (PD), we often observed calcification of the aorta and iliac or femoral arteries. The processes of extraosseous calcification or mineralization are very close to the mechanisms regulating mineralization of bone tissue. The aim of our study was to quantify the number, extent (length and thickness), and type (arteriosclerotic or medial arterial calcification) of vascular calcification in patients with Paget's disease and to compare them with those of controls, in order to discover whether PD is accompanied by increased calcification. Vascular calcification was quantified on the aorta, the iliac arteries, and their branches, the femoral, gluteal, and pelvic arteries of 42 patients with Paget's disease and 36 control subjects. Of the PD subjects, 52.4% had arteriosclerotic calcification versus 30.6% of controls (P = 0.05), and 38.6% of PD patients had medial arterial calcification versus 11.1% of controls (P = 0.05). The mean length of calcification was greater in PD patients: 1.93 +/- 2.85 cm versus 0.84 +/- 1.69 cm in controls (P = 0.04). The thickness of calcification was also greater in PD patients: 1.24 +/- 1.30 mm versus 0.56 +/- 0.94 mm (P = 0.01). Patients with Paget's disease more frequently had medial arterial or arteriosclerotic calcification than controls. These calcifications were longer and thicker. Our clinical study therefore confirms that abnormal vessel wall calcification and bone remodeling in Paget's disease are probably linked, although the mechanism of this relation is as yet unexplained.

Aged↗
PubMed2003

[Calcifications in temporal arteries -- their morphogenesis in comparison to physiological osteogenesis].

OBJECTIVE: Vascular calcification, traditionally regarded as a dystrophic process, has recently been interpreted as a bone-like biologically regulated phenomenon. Because temporal arteries which also contain calcifications are easily available from biopsies of older individuals with suspected giant cell arteritis, we studied the morphogenesis of this calcification in comparison with the development of fetal bone. MATERIAL AND METHODS: Formaldehyde fixed arteries were processed in paraffin sections and investigated by light-, transmission-, and scanning electron microscopy. The atomic composition of the calcifications was estimated by X-ray microanalysis. Fetal bone, also fixed with formaldehyde, was investigated using identical methods. RESULTS: Early calcifications are often present as focal or diffuse granular mediacalcinosis. With increasing age, calcified granules appear in association with the internal elastic membranes and progress to sheet-like calcifications. Ultrastructurally calcospherites, not rarely exhibiting the Liesegang phenomenon, are the hallmark of early calcifications. In advanced sheet-like calcification calcospherites could be detected as components of the calcified lumps. Calcospherites also appear in endochondral calcification, but are absent in calcified osteoid. The ultrastructure of calcospherites in provisional endochondral ossification differs from that in vascular calcification. Instead of corpuscles as with the Liesegang phenomenon, radial clusters of needle-like crystals resembling apatite are present. While calcospherites of the tunica media often contain a high amount of magnesium, calcified sheets as well as bone exhibited in contrast a low magnesium content. CONCLUSIONS: It is concluded that, comparable to granular mediacalcinosis of the aorta, development of calcified arteriosclerotic plaques, and Mönckeberg's disease, calcification of small muscular temporal arteries is also initially a calcospherite-dependent process. It is generally accepted that these calcified corpuscles represent remnants of calcified necrotic or apoptotic cells. In the phase of confluence with the appearance of sheet-like calcification, a low bone-like magnesium content that differs from the high amount in the isolated medial calcospherites was measured. This finding, together with the observation that calcified sheets contain calcospherites, supports the hypothesis that vascular calcification in general is different from bone formation and has to be regarded as a biphasic process initiated by the appearance of calcospherites and followed by a secondary calcifying phase with the formation of bone-like apatite that leads to rock hard lumps of calcified vessels.

Adult↗
PubMed2003

Calcification resistance with aluminum-ethanol treated porcine aortic valve bioprostheses in juvenile sheep.

BACKGROUND: Calcification of glutaraldehyde fixed bioprosthetic heart valve replacements frequently leads to the clinical failure of these devices. Previous research by our group has demonstrated that ethanol pretreatment prevents bioprosthetic cusp calcification, but not aortic wall calcification. We have also shown that aluminum chloride pretreatment prevents bioprosthetic aortic wall calcification. This study evaluated the combined use of aluminum and ethanol to prevent both bioprosthetic porcine aortic valve cusp and aortic wall calcification in rat subcutaneous implants, and the juvenile sheep mitral valve replacement model. METHODS: Glutaraldehyde fixed cusps and aortic wall samples were pretreated sequentially first with aluminum chloride (AlCl3) followed by ethanol pretreatment. These samples were then implanted subdermally in rats with explants at 21 and 63 days. Stent mounted bioprostheses were prepared either sequentially as previously described or differentially with AlCl3 exposure restricted to the aortic wall followed by ethanol pretreatment. Mitral valve replacements were carried out in juvenile sheep with elective retrievals at 90 days. RESULTS: Rat subdermal explants demonstrated that sequential exposure to AlCl3 and ethanol completely inhibited bioprosthetic cusp and aortic wall calcification compared with controls. However the sheep results were markedly different. The differential sheep explant group exhibited very low levels of cusp and wall calcium. The glutaraldehyde group exhibited little cusp calcification, but prominent aortic wall calcification. All sheep in the two groups previously described lived to term without evidence of valvular dysfunction. In contrast, animals in the sequential group exhibited increased levels of cusp calcification. None of the animals in this group survived to term. Pathologic analysis of the valves in the sequential group determined that valve failure was caused by calcification and stenosis of the aortic cusps. CONCLUSIONS: The results clearly demonstrate that a combination of aluminum and ethanol reduced aortic wall calcification and prevented cuspal calcification. Furthermore, this study demonstrates that exclusion of aluminum from the cusp eliminated the cuspal calcification seen when aluminum and ethanol treatments were administered in a sequential manner.

Aluminum Chloride↗
PubMed2003

Cardiac valve calcification as an important predictor for all-cause mortality and cardiovascular mortality in long-term peritoneal dialysis patients: a prospective study.

Calcification complications are frequent among long-term dialysis patients. However, the prognostic implication of cardiac valve calcification in this population is not known. This study aimed to determine if cardiac valve calcification predicts mortality in long-term dialysis patients. Baseline echocardiography was performed in 192 patients (mean +/- SD age, 55 +/- 12 yr) on continuous ambulatory peritoneal dialysis (mean +/- SD duration of dialysis, 39 +/- 31 mo) to screen for calcification of the aortic valve, mitral valve, or both. Valvular calcification was present in 62 patients. During the mean follow-up of 17.9 mo (range, 0.6 to 33.9 mo), 46 deaths (50% of cardiovascular causes) were observed. Overall 1-yr survival was 70% and 93% for patients with and without valvular calcification (P < 0.0001, log-rank test). Cardiovascular mortality was 22% and 3% for patients with and without valvular calcification (P < 0.0001). Multivariable Cox regression analysis showed that cardiac valve calcification was predictive of an increased all-cause mortality (hazard ratio [HR], 2.50; 95% CI, 1.32 to 4.76; P = 0.005) and cardiovascular death (HR 5.39; 95% CI, 2.16 to 13.48; P = 0.0003) independent of age, male gender, dialysis duration, C-reactive protein, diabetes, and atherosclerotic vascular disease. Eighty-nine percent of patients with both valvular calcification and atherosclerotic vascular disease, 23% of patients with valvular calcification only, 21% of patients with atherosclerotic vascular disease only, and 13% of patients with neither complication died at 1-yr (P < 0.0005). The cardiovascular death rate was 85% for patients with both complications, 13% for patients with valvular calcification only, 14% for patients with atherosclerotic vascular disease only, and 5% for those with neither complication (P < 0.0005). The number of calcified valves was associated with all-cause mortality (P < 0.0005) and cardiovascular death (P < 0.0005). One-year all-cause mortality was 57% for patients with both aortic and mitral valves calcified, 40% for those with either valve calcified, and 15% for those with neither valve calcified. In conclusion, cardiac valve calcification is a powerful predictor for mortality and cardiovascular deaths in long-term dialysis patients. Valvular calcification by itself has similar prognostic importance as the presence of atherosclerotic vascular disease. Its coexistence with other atherosclerotic complications indicates more severe disease and has the worst outcome.

Aged↗
PubMed2005

Arteriosclerosis, vascular calcifications and cardiovascular disease in uremia.

PURPOSE OF REVIEW: Arterial calcification in chronic kidney disease (CKD) is associated with increased cardiovascular risk. The mechanisms responsible for arterial calcification include alterations of mineral metabolism and expression of mineral-regulating proteins. RECENT FINDINGS: Arterial calcification is similar to bone formation, involving differentiation of vascular smooth muscle cells (VSMCs) into phenotypically distinct osteoblast-like cells. Elevated phosphate and/or calcium trigger a concentration-dependent increase of calcium precipitates in VSMC in vitro. The calcification is initiated by VSMC release of membrane-bound matrix vesicles and formation of apoptotic bodies. The presence of serum prevents these changes, indicating the presence of calcification inhibitors. Arterial calcification occurs in two sites: the tunica intima and tunica media. Intimal calcification is a marker of atherosclerotic disease and is associated with arterial stenotic lesions. Medial calcification influences outcome by promoting arterial stiffening whose principal consequences are left-ventricular hypertrophy and altered coronary perfusion. Aortic stiffness is an independent predictor of all-cause and cardiovascular mortality in CKD patients. Age, duration of dialysis, smoking and diabetes are risk factors for the development of arterial calcification in end-stage renal disease. Oversuppression of parathyroid hormone and low bone turnover potentiate the development of arterial calcification. SUMMARY: Arterial disease in CKD patients is characterized by extensive calcification. Evidence has accumulated pointing to the active and regulated nature of the calcification process. Elevated phosphate and calcium may stimulate sodium-dependent phosphate cotransport involving osteoblast-like changes in cellular gene expression. Arterial calcification is responsible for stiffening of the arteries with increased left-ventricular afterload and abnormal coronary perfusion as the principal clinical consequences.

Animals↗
PubMed2005

The frequency and determinants of calcification in intracranial arteries in Chinese patients who underwent computed tomography examinations.

BACKGROUND: Intracranial artery calcification is common but the prevalence and determinants are not well established. We aim to describe the prevalence and location of calcification in intracranial arteries according to brain multi-detector-row computed tomography (MDCT) images, and to investigate its correlation with potential risk factors. METHODS: We studied consecutive men and women referred for brain CT in December 2004. All patients received a questionnaire regarding their medical history related to atherosclerosis, including traditional risk factors of atherosclerosis, serum chemistry values and inflammatory markers. All CT examinations were done with a 16-slice MDCT and the severity of intracranial artery calcification was categorized. RESULTS: Four hundred and ninety patients aged 1.4-101 years (62.92+/-19.04; mean+/-SD) were included in our study. There were 340 patients (69.4%) who had intracranial artery calcification. The highest prevalence of intracranial artery calcification was seen in the internal carotid artery (60%), followed by vertebral artery (20%), middle cerebral artery (5%) and basilar artery (5%). Patients with calcification were significantly older than those without calcification (p<0.001). A significantly higher prevalence of calcification was present among patients with hypertension (p<0.001), diabetes (p<0.001), renal failure (p<0.05), atrial fibrillation (p<0.05), smoking (p<0.05), hyperlipidemia (p<0.001), ischemic heart disease (p<0.05) and ischemic stroke (p<0.001). Mean values of serum phosphate, serum urea and CRP level were also significantly higher in patients with intracranial artery calcification (p<0.05, respectively), and there was a trend that patients with intracranial calcification had a higher white blood cell count (p=0.070). Stepwise multiple logistic regression showed age (RR=2.795 per 10 years), a history of ischemic stroke (RR=3.915), and white blood cell count (RR=1.107) to be independently associated with intracranial artery calcification. CONCLUSIONS: Calcification of the intracranial arteries is associated with age, history of ischemic stroke and white blood cell count. Further prospective studies to investigate the clinical significance of intracranial artery calcification are needed.

Adolescent↗
PubMed2006

Relationship between aortic valve calcification and aortic atherosclerosis: a transoesophageal echocardiography study.

INTRODUCTION: Clinical and laboratory data provide an increasing amount of information regarding the common aetiopathogenetic background of acquired heart defects with calcification and arterial atherosclerosis. AIM: To evaluate the relationship between presence and severity of calcifications of the aortic semilunar valves and the intensity of atherosclerotic lesions in the aorta and aortic stiffness (AS). METHODS: The study group comprised 80 subjects (49 males and 31 females) aged 72.2 (+/-8.0) years with an aortic valve defect found on echocardiography. Patients were divided into two subgroups depending on the severity of valvular disease. Subgroup I comprised 42 patients with small valvular lesions (0--absence of calcification of the valve, or +--trivial valvular calcifications, possible to find on detailed evaluation of the valve). Subgroup II consisted of 38 patients with intense calcifications (++--large, easily found valve calcifications, +++--massive calcifications affecting leaflet mobility). All patients underwent transoesophageal echocardiography to evaluate atherosclerotic lesions in the aorta. The assessment included the following: location of the lesions in the aorta, intimal thickness, presence of calcifications and mobile parts of plaques and possible associated thrombi. Aortic stiffness was also measured using the formula: AS=log (SBP/DBP)/Ao(max)-Ao(min)/Ao(min). RESULTS: Atherosclerotic plaques were more frequent in patients with more prominent calcifications of the aortic valve (19 vs 10 patients, p <0.05). Intimal thickness was larger in patients with more pronounced valve calcifications (3.9+/-0.8 mm vs 2.2+0.6 mm, p <0.05). Presence of calcifications in the aortic wall was also more frequent in patients from group II, as they were found in 10 subjects compared to only 3 cases in group I. Mobile plaque parts were observed in 3 patients from group II; also thrombi were found in 3 individuals from this group. Patients with more prominent calcifications of the aortic valve had decreased aortic wall elasticity (AS 5.5+/-1.2 cm vs 3.4+/-0.9 cm, p <0.05). CONCLUSIONS: Severity of aortic valve calcification indicates simultaneous changes in the thoracic aorta. Stiffness of the aortic wall is greater in patients with a more pronounced defect of the aortic valve. Prevalence of atherosclerosis risk factors is increased in patients with aortic valve defect, enhanced atherosclerosis and rigidity of the aorta. Defect of the aortic valve and increased aortic rigidity may be different manifestations of atherosclerosis.

Aged↗
PubMed2000

Effects of lectins on calcification by vesicles isolated from aortas of cholesterol-fed rabbits.

Advanced vascular calcification in atherosclerosis weakens arterial walls, thereby imposing a serious rupturing effect. However, the mechanism of dystrophic calcification remains unknown. Although accumulating morphological and biochemical evidence reveals a role for calcifiable vesicles in plaque calcification, the mechanism of vesicle-mediated calcification has not been fully explored. To study whether vesicles' membrane components, such as carbohydrates, may have a role in vesicle-mediated calcification, the effect of sugar-binding lectins on calcification was investigated. Atherosclerosis was developed by feeding rabbits with a diet supplemented with 0.5% cholesterol and 2% peanut oil for 4 months. Calcifiable vesicles were then isolated from thoracic aortas by collagenase digestion. The histological examination of aortas with hematoxylin counter-staining indicated abnormal formation of large plaques enriched with macrophage-derived foam cells. Fourier transform spectroscopy revealed mild calcification in aortas indicating that advanced stages of heavy calcification have yet to be reached. However, vesicles isolated from the aortas were capable of calcification in the presence of physiological levels of Ca(2+), Pi, and ATP. Thus, at this stage of atherosclerosis, aortas may start to produce calcifiable vesicles, but at a level insufficient for substantial formation of mineral in aortas. The assessments by FT-IR analysis and Alizarin red staining indicated that concanavalin A (Con A) substantially increased mineral formation by isolated vesicles. Con A also exerted a marked stimulatory effect on (45)Ca and (32)Pi deposition in a dose-dependent fashion with a half-maximal effect at 6-10 microg/ml. Either alpha-methylmannoside or alpha-methylglucoside, but not mannitol, at 10 mM abolished the stimulation. Con A stimulation was abolished after Con A was removed from calcifying media, suggesting that covalent binding may not be involved in the effect. Galactosides appear to also be implicated in (45)Ca and (32)Pi deposition since Abrus precartorius agglutinin, which specifically binds galactosides, enhanced the deposition. Neither wheat-germ agglutinin that binds N-acetylglucoside nor N-acetylgalactoside-specific Helix pomatia agglutinin was effective, suggesting that the acetylated forms of carbohydrate moieties are either absent in vesicles or may not be involved in calcification. None of these lectins exerted an effect on ATPase. Thus, the effects of lectins appeared to be mediated through interactions with carbohydrate moieties of calcifiable vesicles. Whether stimulation of vesicle-calcification by lectins is of pathological significance in atherosclerotic calcification requires further investigation.

Animals↗
PubMed2005

Dual-energy digital mammography for calcification imaging: scatter and nonuniformity corrections.

Mammographic images of small calcifications, which are often the earliest signs of breast cancer, can be obscured by overlapping fibroglandular tissue. We have developed and implemented a dual-energy digital mammography (DEDM) technique for calcification imaging under full-field imaging conditions using a commercially available aSi:H/CsI:Tl flat-panel based digital mammography system. The low- and high-energy images were combined using a nonlinear mapping function to cancel the tissue structures and generate the dual-energy (DE) calcification images. The total entrance-skin exposure and mean-glandular dose from the low- and high-energy images were constrained so that they were similar to screening-examination levels. To evaluate the DE calcification image, we designed a phantom using calcium carbonate crystals to simulate calcifications of various sizes (212-425 microm) overlaid with breast-tissue-equivalent material 5 cm thick with a continuously varying glandular-tissue ratio from 0% to 100%. We report on the effects of scatter radiation and nonuniformity in x-ray intensity and detector response on the DE calcification images. The nonuniformity was corrected by normalizing the low- and high-energy images with full-field reference images. Correction of scatter in the low- and high-energy images significantly reduced the background signal in the DE calcification image. Under the current implementation of DEDM, utilizing the mammography system and dose level tested, calcifications in the 300-355 microm size range were clearly visible in DE calcification images. Calcification threshold sizes decreased to the 250-280 microm size range when the visibility criteria were lowered to barely visible. Calcifications smaller than approximately 250 microm were usually not visible in most cases. The visibility of calcifications with our DEDM imaging technique was limited by quantum noise, not system noise.

Algorithms↗
PubMed1995

Apoptosis and calcification.

Calcification in necrosis has long been known. Of the tissue components, the cells are most vulnerable. Nevertheless, little attention has been paid to the role of cell death in calcification. This review attempts to update the mechanism of calcification with an emphasis on the role of apoptosis in calcification. A brief review on the basic sciences relevant to calcification is followed by a discussion of abnormal Ca2+ and Pi homeostasis in cell injury and apoptosis. Concomitant increases in Ca2+ and Pi in blebs (and matrix vesicles) formed by apoptotic and/or necrotic cells are apparently the primary mechanism of calcification. In addition, membranous cellular degradation products (CDP) resulting from cell disintegration in toto frequently serve as the nidus of calcification. Published data on physiological calcification are compared with findings in various dystrophic calcinoses. This led to the conclusion that apoptosis most likely underlies the mechanism of both physiological and pathological calcifications. It is concluded that calcification is an important function of apoptosis. The mechanism of calcification by CDP and morphology of the resultant calcific deposits are complex.

Adenosine Triphosphate↗
PubMed2005

Coronary and aortic calcification in women with a history of major depression.

BACKGROUND: Although depression is a well-documented risk factor for clinical heart disease, its association with subclinical atherosclerosis is unclear. We hypothesized that middle-aged women with a history of recurrent major depression would show evidence of atherosclerosis. METHODS: Coronary and aortic calcification was measured by electron beam tomography in 58 African American and 152 white healthy middle-aged women. Women were administered the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition and a self-report measure of current depressive symptoms. RESULTS: Coronary calcification was found in 103 women (49%) and aorta calcification in 144 women (54%); high calcification scores were set at approximately 75% of the sample distribution (ie, at >/=10 for the coronary calcium score [n = 49 women] and at >100 for the aorta calcium score [n = 53 women]). Women with a history of recurrent major depression (n = 53) were more likely to have any coronary calcification or calcification in the high category at either site compared with women with a history of a single episode of depression or no depression. After stepwise forward adjustment for cardiovascular risk factors and sociodemographic characteristics, a history of recurrent major depression, compared with a single episode or no history, was associated with odds ratios (ORs) of 2.46 (95% confidence interval [CI], 1.06-5.67) for any coronary calcification, 2.71 (95% CI, 1.08-6.81) for high coronary calcification, and 3.39 (95% CI, 1.34-8.63) for high aortic calcification. Further adjustments for waist-hip ratio reduced the association between history of recurrent depression and any calcification (OR, 2.24; 95% CI, 0.94-5.32) and high calcification (OR, 2.31; 95% CI, 0.89-5.99). CONCLUSIONS: In this sample of asymptomatic middle-aged women without known coronary disease, recurrent major depression was independently associated with coronary and aortic calcification. Waist-hip ratio in part mediated the association. Our findings suggest that recurrent major depression may be a risk factor for early atherosclerosis in women.

Adult↗
PubMed2006

Role of fibroblast growth factor-23 in peripheral vascular calcification in non-diabetic and diabetic hemodialysis patients.

INTRODUCTION: Fibroblast growth factor (FGF) 23 is a recently identified circulating factor that regulates phosphate (Pi) metabolism. Since the derangement of Pi control is an important risk factor for vascular calcification, we investigated the importance of plasma FGF-23 in the development of vascular calcification in the aorta and peripheral artery in hemodialysis patients with and without diabetes mellitus (DM). METHODS: Male hemodialysis patients with DM (n=32) and without DM (n=56) were examined. Plasma samples were obtained before the start of dialysis sessions, and the FGF-23 levels were determined by enzyme-linked immunosorbent assay. Roentgenography of the aorta and hand artery was performed, and visible vascular calcification was evaluated by one examiner, who was blinded to the patient characteristics. RESULTS: In the 56 non-DM hemodialysis patients, vascular calcification was found in the hand artery in 5 patients (8.9%) and in the aorta in 23 patients (41.1%). These levels were significantly lower (p<0.05) than in the 32 DM patients, of whom, 19 (59.4%) and 21 (65.6%) had vascular calcification of the hand artery and aorta, respectively. Multiple regression analyses performed separately in the non-DM and DM patients showed that the plasma FGF-23 level, CaxPi product, and body weight are independent factors significantly associated with hand-artery calcification and that diastolic blood pressure is associated with aorta calcification in non-DM patients. In DM patients, the plasma FGF-23 level and hemodialysis duration emerged as independent factors associated with hand-artery calcification and diastolic blood pressure was associated with aorta calcification. The independent association of the plasma FGF-23 level with hand-artery calcification was retained in both non-DM and DM patients when adjusted for the CaxPi product. CONCLUSION: Our findings show that the plasma FGF-23 level is an independent factor negatively associated with peripheral vascular calcification in the hand artery, but not in the aorta, in both male non-DM and DM hemodialysis patients, even when adjusted for the CaxPi product. This study raises the possibility that the plasma FGF-23 level may provide a reliable marker for Moenckeberg's medial calcification in male hemodialysis patients, independent of its regulatory effect on Pi metabolism.

Adult↗
PubMed1997

[Heterotopic (extraosseous) calcification (calcinosis). Etiology, pathogenesis and clinical importance].

Heterotopic tissue calcification represents a pathological event which goes along with active extra- and intracellular metabolic processes. The heterotopic calcification is not the manifestation of tissue ageing. Aetiologically, metastatic calcification, dystrophic calcification and genetic-hereditary calcification are distinguished. Two pathogenetic mechanisms play a role during the heterotopic calcification. The intracellular calcification is based upon the function of mitochondria as regulator of the calcium concentration and as "lime-catcher". The extracellular calcification is initiated by membraneous organelles--so-called matrix vesicles. The further steps are the production of hydroxylapatite crystals which are eliminated from the matrix vesicles in the extracellular spaces. Special types of heterotopic calcification are hypercalcaemias (tumour-associated hypercalcaemias, primary and tertiary hyperparathyroidism, drug-induced hypercalcaemias), tumoral calcinosis, intratumoral calcifications, calcifications of different organs (lung, heart, vessels, joints, ligaments, skin or kidney). Some calcifications of organs show partly overlapping aetiological factors and pathogenetic mechanisms.

Aging↗
PubMed2000

Mechanism of atherosclerotic calcification.

Calcification is almost invariably associated with atherosclerotic plaque lesions. Recent data suggest that plaque calcification is an active, regulated process similar to osteogenesis. In order to clarify the mechanism of plaque calcification, we developed an in vitro model of vascular calcification by utilizing bovine vascular smooth muscle cells (BVSMCs). This model is useful in that diffuse and massive calcification can be induced within 2 weeks and thereby biochemical analyses of vascular calcification can be performed. We have analyzed several aspects of vascular calcification by using this model and demonstrated as follows: 1) in vitro calcification of BVSMCs is regulated by calciotropic hormones and BVSMCs are equipped with a unique autocrine and/or paracrine system regulating calcium metabolism. 2) Sodium-dependent phosphate cotransport plays a crucial role in BVSMC calcification as well as in mineralization of skeletal tissues. 3) BVSMCs acquire osteoblastic phenotype under certain conditions. Finally, we discuss the roles of macrophages in the development of atherosclerotic calcification. Interferon-gamma (IFN-gamma) induces gene expression of 25-hydrovitamin D-1 alpha-hydroxylase (1 alpha OHase) and its activity in macrophages. Since 1 alpha OHase can locally convert 25-hydroxyvitamin D into 1 alpha, 25-dihydroxyvitamin D (1,25(OH)2D), an active metabolite of vitamin D, it is suggested that local production of 1,25(OH)2D by macrophages may promote atherosclerotic calcification. Moreover, macrophages may be involved in the phenotypic changes of vascular smooth muscle cells (VSMCs) to acquire calcifying capacity. Therefore, the phenotypic changes of VSMCs in atherosclerotic plaque may contribute to the development of atherosclerotic calcification.

Animals↗