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PubMed2005

Ethnic differences in coronary calcification: the Multi-Ethnic Study of Atherosclerosis (MESA).

BACKGROUND: There is substantial evidence that coronary calcification, a marker for the presence and quantity of coronary atherosclerosis, is higher in US whites than blacks; however, there have been no large population-based studies comparing coronary calcification among US ethnic groups. METHODS AND RESULTS: Using computed tomography, we measured coronary calcification in 6814 white, black, Hispanic, and Chinese men and women aged 45 to 84 years with no clinical cardiovascular disease who participated in the Multi-Ethnic Study of Atherosclerosis (MESA). The prevalence of coronary calcification (Agatston score >0) in these 4 ethnic groups was 70.4%, 52.1%, 56.5%, and 59.2%, respectively, in men (P<0.001) and 44.6%, 36.5%, 34.9%, and 41.9%, respectively, (P<0.001) in women. After adjustment for age, education, lipids, body mass index, smoking, diabetes, hypertension, treatment for hypercholesterolemia, gender, and scanning center, compared with whites, the relative risks for having coronary calcification were 0.78 (95% CI 0.74 to 0.82) in blacks, 0.85 (95% CI 0.79 to 0.91) in Hispanics, and 0.92 (95% CI 0.85 to 0.99) in Chinese. After similar adjustments, the amount of coronary calcification among those with an Agatston score >0 was greatest among whites, followed by Chinese (77% that of whites; 95% CI 62% to 96%), Hispanics (74%; 95% CI 61% to 90%), and blacks (69%; 95% CI 59% to 80%). CONCLUSIONS: We observed ethnic differences in the presence and quantity of coronary calcification that were not explained by coronary risk factors. Identification of the mechanism underlying these differences would further our understanding of the pathophysiology of coronary calcification and its clinical significance. Data on the predictive value of coronary calcium in different ethnic groups are needed.

Black or African American↗
PubMed2000

A comparison of the Framingham risk index, coronary artery calcification, and culprit plaque morphology in sudden cardiac death.

BACKGROUND: Neither clinical prediction models nor noninvasive imaging tests that detect coronary artery calcification identify all patients who experience acute coronary events. Variations in culprit plaque morphology may account for these inaccuracies. METHODS AND RESULTS: We compared the 10-year Framingham risk index, histologic coronary calcification, and culprit plaque morphology in 79 consecutive adults with sudden cardiac death. There was a modest relationship between the Framingham risk index and the extent of histologic coronary calcification (r=0.35, P=0.002). Agreement in risk classification between the histologic calcification score and the Framingham risk index occurred in 50 of 79 cases (63.3%, P=0. 039). Either a focus of coronary artery calcification >/=40 micromol/L (62% of cases) or a Framingham risk index score >/= average risk for age (62% of cases) were present in 66 of 79 (83.5%) cases. Cases with plaque erosion (n=22) had significantly less coronary calcification (P=0.003) and lower Framingham risk index (P=0.001) scores than stable (n=27) or ruptured (n=30) plaques. Fourteen of 22 (63.6%) cases of plaque erosion were classified as low risk by both the Framingham risk index and the histologic calcification score. CONCLUSIONS: The prediction of sudden cardiac death using the Framingham risk index and the measurement of coronary calcification are distinct methods of assessing risk for sudden cardiac death. Excessive reliance on either method alone will produce errors in risk classification, particularly for patients at risk of plaque erosion, but their combination may be complementary.

Adult↗
PubMed1982

Calcification of porcine prosthetic heart valves: a radiographic and light microscopy study.

To determine the incidence and extent of calcification of implanted glutaraldehyde-treated porcine prosthetic heart valves, 82 valves explanted from 73 patients were examined for calcium by radiography and light microscopy. At the time of valve implantation, the patients were 2 1/4-76 years old. The included 15 children (patients younger than 15 years of age, mean age at time of valve implantation 8.7 +/- 4.1 years) and 58 adults (patients older than 15 years, mean age at time of valve implantation 53.5 +/- 15.1 years). Valves explanted from children (average time implanted 4.6 +/- 1.7 years) included four aortic, five mitral, as well as six right ventricle-pulmonary artery conduits and one left ventricle-abdominal aorta conduit. Valves explanted from adults (average time implanted 3.2 +/- 2.5 years) included 32 aortic and 32 mitral, as well as one tricuspid valve and one valve from a right ventricle-pulmonary artery conduit. Calcification of explanted valves was graded from 0 to 4+ based on radiographs. All 16 valves from children were calcified, with grade 3+ or 4+ calcification in each of the aortic and mitral valves. In adult patients, calcification was present in 10 of 33 valves (30%) implanted for less than 3 years (average time implanted 1.0 year), in nine of 11 valves (82%) implanted for 3-5 years (average time implanted 3.7 years) and in 21 of 22 valves (96%) implanted for 5 years or longer (average time implanted 6.2 years). Analysis of variance demonstrated that calcification was strongly related to the duration that valves were implanted (p less than 0.001). Age at the time of valve implantation also had a strong effect (p less than 0.001) on the amount of valvular calcium. Valves from children showed the most calcification, and the amount did not change when valves were implanted in patients 30 years of age or older. Patient sex and valve position had no effect on the amount of calcification. Calcification occurred at each right- and left-heart valve position, most frequently at sites of commissural attachments.

Adolescent↗
PubMed1985

Inhibition by diphosphonate compounds of calcification of porcine bioprosthetic heart valve cusps implanted subcutaneously in rats.

Calcification limits the long-term success of heart valve bioprostheses fabricated from glutaraldehyde cross-linked porcine aortic valves. The pathophysiology of calcification of bioprostheses has been studied experimentally with subcutaneous implants of the valve cusps in rats; in this preparation, the accumulation of calcific deposits is biochemically and morphologically identical to that occurring in clinical specimens. The objective of the present study was to determine whether mineralization of bioprosthetic valve cusps (BC) subcutaneously implanted in 3-week-old male rats could be inhibited through the use of diphosphonate compounds. Ethanehydroxydiphosphonate (EHDP), administered by daily subcutaneous injection (25 mg/kg/24 hr) for 21 days inhibited calcification (BC Ca++ = 154.9 +/- 4.1), but caused somatic growth retardation and disruption of epiphyseal development. However, local administration of EHDP by osmotic pump (5 mg/kg/24 hr) implanted in direct contact with the cuspal tissue for 14 days prevented BC calcification (BC CA++ = 4.3 +/- 0.7) without adverse effects. Furthermore, EHDP given by osmotic pump had a prolonged effect on reducing calcification, as demonstrated by implants harvested 21 days (BC CA++ = 12.2 +/- 6.4) after the drug supply was exhausted. Finally, BC preincubated in aminopropanehydroxydiphosphonate for 24 hr before 21 day implantation underwent less calcification (CA++ = 24.2 +/- 7.4) than control valves (BC CA++ 126.6 +/- 7.5) with no adverse effects. We conclude that diphosphonates inhibit BC calcification, and that adverse effects of systemic therapy can be avoided by local administration.

Animals↗
PubMed1997

Active serum vitamin D levels are inversely correlated with coronary calcification.

BACKGROUND: Arterial calcification is a common feature of atherosclerosis, occurring in >90% of angiographically significant lesions. Recent evidence from this and other studies suggests that development of atherosclerotic calcification is similar to osteogenesis; thus, we undertook the current investigation on the potential role of osteoregulatory factors in arterial calcification. METHODS AND RESULTS: We studied two human populations (173 subjects) at high and moderate risk for coronary heart disease and assessed them for associations between vascular calcification and serum levels of the osteoregulatory molecules osteocalcin, parathyroid hormone, and 1alpha,25-dihydroxyvitamin D3 (1,25-vitamin D). Our results revealed that 1,25-vitamin D levels are inversely correlated with the extent of vascular calcification in both groups. No correlations were found between extent of calcification and levels of osteocalcin or parathyroid hormone. CONCLUSIONS: These data suggest a possible role for vitamin D in the development of vascular calcification. Vitamin D is also known to be important in bone mineralization; thus, 1,25-vitamin D may be one factor to explain the long observed association between osteoporosis and vascular calcification.

Adult↗
PubMed2007

Genome-wide linkage mapping for valve calcification susceptibility loci in hypertensive sibships: the Hypertension Genetic Epidemiology Network Study.

It remains unclear whether genetic factors contribute to the susceptibility to valve calcification. Accordingly, echocardiograms and genotyping were performed in 1871 hypertensive siblings who participated in the Hypertension Genetic Epidemiology Network Study. Genome-wide affected sibpair nonparametric linkage analysis was conducted using the allele-sharing method implemented in the Merlin computer program. A total of 1014 sibships from 858 families were evaluated for aortic valve sclerosis or mitral annular calcification. Of these, 78 sibships from 68 families contained > or =2 affected siblings with > or =1 type of valve calcification (142 affected siblings). All 3 of the traits showed a modest degree of familial aggregation, with sibling recurrence risk (SD) and sibling recurrence risk ratio (95% CI) being 0.25 (0.035) and 2.31 (1.72 to 3.11) for aortic valve sclerosis, 0.25 (0.035) and 1.78 (1.36 to 2.33) for mitral annular calcification, and 0.31 (0.030) and 1.52 (1.24 to 1.85) for aortic valve sclerosis and mitral annular calcification, respectively. Affected sibpair linkage analysis revealed the highest logarithm of odds score (3.14) in chromosome 16 at 105.6 cM for aortic valve sclerosis. Other chromosomal regions with logarithm of odds score > or =1.9 were found in chromosomes 19 (2.88), 16 (2.63), 1 (2.12), and 2 (2.03) for aortic valve sclerosis and chromosome 13 (2.12) for any valve calcification. There was no logarithm of odds score > or =1.9 for mitral annular calcification. Our study shows strong linkage of aortic valve sclerosis to chromosome 16q22.1-q22.3 and suggestive linkage to chromosome 19p13.11-p11 and identifies several other promising genomic regions that may contain specific susceptibility loci for valve calcification.

Adult↗
PubMed2002

SB 242784, a selective inhibitor of the osteoclastic V-H+ATPase, inhibits arterial calcification in the rat.

The present experiments were carried out to further test the hypothesis that arterial calcification is linked to bone resorption by determining whether the selective inhibition of bone resorption with SB 242784, a specific inhibitor of the osteoclastic V-H+-ATPase, will inhibit arterial calcification. Treatment for 96 hours with toxic doses of vitamin D caused widespread calcification in the aorta and in the femoral, mesenteric, hepatic, renal, and carotid arteries, and treatment with SB 242784 completely prevented the vitamin D-induced calcification of each of these arteries at a dose of 40 mg/kg per day and significantly reduced calcification at a dose of 10 mg/kg per day. Treatment with vitamin D also caused extensive calcification in the lungs, tracheal cartilage, and kidneys, and treatment with SB 242784 prevented or reduced calcification at each of these sites. Measurement of serum levels of cross-linked N-telopeptides, a specific measure of bone resorption activity, showed that treatment with vitamin D alone produced the expected 2.4-fold increase in bone resorption activity and that concurrent treatment with the 40-mg dose of SB 242784 reduced bone resorption activity to below control levels. With the inclusion of the present results, there are now three types of bone resorption inhibitors (each with an entirely different mode of action on the osteoclast) that share the ability to potently inhibit arterial calcification in the rat, the V-H+-ATPase inhibitor SB 242784, the cytokine osteoprotegerin, and the amino bisphosphonates alendronate and ibandronate.

Animals↗
PubMed2006

Statins protect human aortic smooth muscle cells from inorganic phosphate-induced calcification by restoring Gas6-Axl survival pathway.

Vascular calcification is clinically important in the development of cardiovascular disease. It is reported that hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (statins) inhibited vascular calcification in several clinical trials. However, the mechanism is poorly understood. Recently, it has been suggested that apoptosis is one of the important processes regulating vascular smooth muscle cell (VSMC) calcification. In this study, we investigated the effect of statins on VSMC calcification by testing their effect on apoptosis, focusing in particular on regulation of the survival pathway mediated by growth arrest-specific gene 6 (Gas6), a member of the vitamin K-dependent protein family, and its receptor, Axl. In human aortic smooth muscle cells (HASMC), statins significantly inhibited inorganic phosphate (Pi)-induced calcification in a concentration-dependent manner (reduced by 49% at 0.1 micromol/L atorvastatin). The inhibitory effect of statins was mediated by preventing apoptosis, which was increased by Pi in a concentration-dependent manner, and not by inhibiting sodium-dependent phosphate cotransporter (NPC) activity, another mechanism regulating HASMC calcification. Furthermore, the antiapoptotic effect of statins was dependent on restoration of Gas6, whose expression was downregulated by Pi. Restoration of Gas6 mRNA by statins was mediated by mRNA stabilization, and not by an increase in transcriptional activity. Suppression of Gas6 using small interfering RNA and the Axl-extracellular domain abolished the preventive effect of statins on Pi-induced apoptosis and calcification. These data demonstrate that statins protected HASMC from Pi-induced calcification by inhibiting apoptosis via restoration of the Gas6-Axl pathway.

Aorta↗
PubMed2005

Stroke attributable to a calcific embolus from the brachiocephalic trunk.

BACKGROUND AND PURPOSE: Calcific brain embolization is a rare event that is usually secondary to cardiac valve calcification. We present a case of stroke caused by embolization of calcific material from the brachiocephalic trunk, probably induced by radiotherapy. SUMMARY OF CASE: A 56-year-old right-handed female developed left-sided hemiparesis, hemihypesthesia, and sensory inattention. She had a history of right breast carcinoma that was excised 8 years previously followed by radiotherapy. She had no other history of note. Computed tomography of the head and magnetic resonance imaging confirmed a calcific embolus in right middle cerebral artery and an acute infarction in the corresponding territory. Plain chest radiography, carotid ultrasonography, transthoracic and transoesophageal echocardiography failed to demonstrate the source of calcific embolism. Computed tomography of the thorax revealed heavy calcification of the brachiocephalic trunk and the origin of the right common carotid artery. CONCLUSIONS: Undertaking a vigilant systematic search for the source in cases of calcific embolization is necessary. The aorta and its main branches are possible, yet unusual, sources of calcific emboli that merit investigation.

Atherosclerosis↗
PubMed2003

Compression-induced changes on physical structures and calcification of the aromatic polyether polyurethane composite.

It is generally accepted that stress causes calcification in both bio-prosthetic and polyurethane heart valves. However, simple uni-axially- and bi-axially-stretched samples did not yield a feasible model for the elaboration of the stress-induced calcification. In this study, heat compaction combined with the incorporation of polyethylene has been explored. Specimens of polyurethane were solution cast onto a porous bi-axially-drawn ultra-high-molecular-weight polyethylene film and then heat compacted under a pressure of 18 MPa at a chosen temperature for 1.5 h. The heat-compaction-induced calcification and physical changes of the polyurethane composite were evaluated using a 28-day in vitro calcification model and Attenuated Total Reflection-Fourier Transform-Infrared (ATR-FT-IR) spectroscopy. The calcification results indicated that heat-compaction-induced calcification was double that achieved without heat compaction. Heat-compacted polyurethane composite showed higher affinity to calcium ions than the non-heat compacted sample. The ATR-FT-IR results showed that the heat-compaction-induced physical changes include distortions of polymeric molecules and permanent changes of microstructures. The distortions of polymeric molecules could be deteriorated in contact with different media. The relaxation of the stressed structures of the polyether moiety might serve as a calcium trap and a heterogeneous nucleation site for calcification. The permanent changes of microstructures resulted from high distortions also served as affinity sites attracting calcification.

Biocompatible Materials↗
PubMedDate not supplied

The role of valvular and thoracic aortic calcifications in distinction between ischemic and nonischemic cardiomyopathy.

Determination of underlying etiology in patients with dilated and globally hypokinetic left ventricles may sometimes be difficult even after detailed history and complete clinical evaluation. Cardiac valvular and thoracic aortic calcifications have previously been reported to be used as a window to diffuse atherosclerosis of the vascular system. The authors prospectively examined the predictive value of mitral annular calcification (MAC), aortic valve calcification (AVC), and thoracic aortic calcification (TAC) in diagnosis of coronary artery disease as the underlying cause of diffuse left ventricular dilatation and systolic dysfunction. The study included 98 consecutive patients (male/female = 76/22, mean age = 58.9 +/- 10.7 years, range: 33 to 75 years) over the age of 30 years admitted to their clinics between October 1999 and December 2001 with signs and symptoms of congestive heart failure associated with documented cardiomegaly. Transthoracic echocardiography and coronary angiography were performed in all patients for the evaluation of valvular calcifications and coronary status. Although there was no significant difference between the groups with and without coronary artery stenosis (CAS), with regard to presence of MAC, patients with CAS tended to have MAC more frequently (12/61, 20% vs 4/37, 11%, p > 0.05). AVC and TAC were found to be significantly more frequent in patients with CAS compared to those without CAS (AVC, 35/61, 57% vs 4/37, 11%, p < 0.001 and TAC, 28/61, 46% vs 2/37, 5%, p < 0.001). While all 3 calcifications had sensitivity under 60%, and specificity and positive predictive value over 75% individually, the presence of any of them had a sensitivity of 80%, specificity of 86%, positive predictive value of 91%, and negative predictive value of 73%. Thus the presence of any of these calcifications distinguished patients with coronary artery disease with a sensitivity of 80% and specificity of 86%. The presence of aortic valvular valve and thoracic aortic calcifications seems to be associated with significant coronary arterial stenosis; however, with relatively low negative predictive values these cannot be used in clinical practice for diagnosis of underlying coronary artery disease in patients with dilated left ventricles and impaired systolic functions.

Aorta, Thoracic↗
PubMed1996

Brain calcification in patients with cerebral lupus.

Cerebral lupus (CL) is a common cause of morbidity and mortality in patients with SLE. The brain CTs of 27 consecutive adult patients with SLE and various neurological presentations were reviewed. The median age and duration of neurological symptoms at the time of the brain CT were 30 years (range = 14-51 years) and six days (range = 1 day-22 years), respectively. Eleven patients (41%) had normal CTs. The abnormalities in the remaining patients could be divided into six categories: (a) cerebral atrophy alone (two patients); (b) calcification alone (three patients); (c) infarct(s) alone (five patients); (d) cerebral atrophy and calcification (three patients); (e) cerebral atrophy and infarct(s) (one patient) and (f) cerebral atrophy, calcification and infarct(s) (two patients). Altogether eight patients (30%) (age range = 17-47 years) had intracerebral calcification: the globus pallidus was involved in all, putamen in two, head of the caudate nucleus in one, thalamus in one, centrum semiovale in two and cerebellum in three patients. Two patients had extensive calcifications of most of the basal ganglia, centrum semiovale and cerebellum. There was no relationship between the presence/degree of calcification and age of patients/duration or type of neurological presentation. The pathogenesis of cerebral calcification in CL is unknown. Cerebral lupus must now be included in the differential diagnosis of intracerebral calcification.

Adolescent↗
PubMed1997

The incidence of coronary artery calcification on standard thoracic CT scans.

Coronary artery calcification indicates the presence of atheromatous disease and can represent an area of severe stenosis. The absence of calcification does not correlate with the absence of coronary artery disease, but an incidental finding of calcification has important prognostic implications. The best method available at present is electron beam computed tomography (EBCT) but these are often dedicated units in specialist centres and currently this modality is not widely available in the UK. This is the first study to establish the age/sex frequency with which incidental coronary artery calcification is detected using standard CT scanning in a large population. The methods used are simple, reproducible and based on standard thoracic protocols. The presence of calcification is easily detected using readily available equipment. The reported incidence of calcification using EBCT, the most sensitive method available, was compared with standard CT detection rates. While standard CT underestimates the presence of calcification, the age/sex trends are very similar. Standard CT probably detects the most dense lesions, missing areas of mild calcification, recent studies having shown that these lesions are most likely to represent areas of stenosis. This study shows that, with very little change in current practice and on readily available equipment, it is possible to obtain important diagnostic information suggesting the presence of severe coronary artery disease.

Adult↗
PubMed2003

Calcification in coronary arteries as quantified by CT scans correlated with tobacco consumption in patients with inoperable non-small cell lung cancer treated with three-dimensional radiotherapy.

It has been shown that radiological manifestations of coronary artery sclerosis are an indirect measure of co-morbidity and predictive of survival. The aim of the present study is to evaluate the outcome and side effects after three-dimensional (3D) radiotherapy in patients with unresectable non-small cell lung cancer (NSCLC) stage I, II and IIIA, depending on coronary artery calcification, Karnofsky performance index (KI) and co-morbidity. Between 1993 and 1999, 89 patients with unresectable NSCLC were treated with 3D-radiotherapy. The median age was 66.6 years and median KI 80%. All patients had 3D-treatment planning, based on CT scans. The median total dose was 60 Gy in 2 Gy fractions five times a week. The mean follow-up period was 13.2 months and mean survival time 12.2 months. Significant prognostic factors for improved survival were KI and tumour stage. Patients with a KI<90% had a median survival of 6.5 months compared with 14 months, in patients with KI>/==" BORDER="0">90% (p<0.001). NSCLC stage I+II showed a significantly longer median survival than patients with NSCLC stage IIIA (16.5 months versus 7 months, p<0.004). A significant correlation was seen between pack-years and coronary artery calcification (p<0.05) and between age and marked coronary artery calcification. The incidence of calcification was 67% in smokers (>/==" BORDER="0">20 pack-years) and 43/58 in patients >60 years (p<0.007). Side effects, e.g. pneumonitis, did not correlate with coronary artery calcification but correlated with chronic obstructive lung disease in 19/89 patients. Conventional CT scans for 3D-treatment planning are able to detect coronary artery calcification. There is a significant correlation between age, KI, tobacco consumption and vascular calcification. Although there was a trend to worse overall survival, coronary artery calcification was not a significant predictor of progression-free and overall survival.

Adult↗
PubMed2004

Left ventricular hypertrophy is associated with arterial stiffness and vascular calcification in hemodialysis patients.

Left ventricular hypertrophy (LVH) is the most frequent cardiac abnormality in patients with end-stage renal disease (ESRD). Recent studies have shown that arterial stiffness is associated with mediacalcinosis in these patients. However, whether arterial stiffness and vascular calcification are associated with the LVH in patients with ESRD has not been well established. Forty-nine patients on chronic hemodialysis participated in this study. 1) To better understand the mechanism underlying the increased incidence of LVH, we studied the relation between LVH and each of arterial wall stiffness, aortic calcification, and numerous clinical parameters in 49 patients on chronic hemodialysis. 2) To evaluate the contribution of arterial stiffness and arterial calcification to LVH in hemodialysis patients, we performed the present clinical analysis on 49 patients on chronic hemodialysis. We used an automatic device to measure arterial pulse wave velocity (PWV) as an index of arterial wall stiffness. The aortic calcification index (ACI) was quantified morphometrically by CT scan. The left ventricular mass index (LVMI) was estimated by M-mode echocardiography. To understand the mechanism underlying the increased incidence of LVH, we examined the factors contributing to LVMI in these patients. The correlation between each of the study parameters and LVMI as an indicator of LVH was then examined. The LVMI value was correlated positively with PWV (r=0.439, p=0.0014), systolic blood pressure (r=0.421, p=0.0023), and ACI (r=0.467, p=0.0006). A stepwise linear regression analysis showed that PWV, systolic blood pressure, and ACI were independently associated with LVH in our subjects. These results suggest that LVH is associated with hypertension, increased arterial stiffness, and the extent of vascular calcification in hemodialysis patients, with vascular calcification being the most important contributor to the development of LVH. Alteration of pulsatile dynamics contributes to an increase in left ventricular load and thus is also related to the LVH in these patients. These results suggest that LVH is associated with hypertension, increased arterial stiffness, and the extent of vascular calcification in hemodialysis patients. Vascular calcification, which alters the pulsatile dynamics and thereby contributes to an increase in left ventricular load, is the most important contributor to the development of LVH in patients undergoing hemodialysis.

Aortic Diseases↗
PubMed2005

Cross-sectional association of kidney function with valvular and annular calcification: the Framingham heart study.

Valvular calcification is common in the setting of end-stage kidney disease and is associated with increased risks for cardiovascular disease events. It is unknown whether the prevalence of valvular calcification is increased in milder kidney disease after accounting for cardiovascular risk factors. Participants who attended the sixth examination of the Framingham Offspring Study (1995 to 1998) were eligible. Kidney function was estimated by GFR using the simplified Modification of Diet in Renal Disease Study equation. Mitral annular calcification (MAC), aortic sclerosis, and aortic annular calcification were assessed by two-dimensional echocardiography. Logistic regression was used to examine the odds of valvular calcification among participants with chronic kidney disease (CKD; GFR < 60 ml/min per 1.73 m(2)). A total of 3047 participants (52% women; mean age 59 +/- 10 yr) were available for analysis. CKD was present in 8.6% (n = 262) of the sample. Among participants with valve/annular calcification (n = 284; 9.3%), 20% had CKD, compared with 7% in patients without valvular calcification. After adjustment for age, gender, systolic and diastolic BP, hypertension treatment, total/HDL cholesterol, body mass index, diabetes, smoking status, and cardiovascular disease, participants with CKD had a 60% increased odds of MAC (odds ratio 1.6; 95% confidence interval 1.03 to 2.5). There was no significant association between CKD and either aortic sclerosis or aortic annular calcification (odds ratio 1.1 and 1.1, respectively). After age and gender adjustment, the combination of both CKD and MAC was associated with a three-fold increased risk for death compared with those with neither condition (P = 0.0004). In the community, CKD is associated with presence of MAC before the onset of ESRD. Further research is warranted to understand whether traditional and novel vascular risk factor burden, as well as metabolic derangements found in early kidney disease, can account for the CKD-MAC association.

Aged↗
PubMed2005

Reducing the burden of cardiovascular calcification in patients with chronic kidney disease.

Patients with chronic kidney disease (CKD) have a higher burden of atherosclerotic coronary artery disease compared with age- and gender-matched individuals with normal renal function. Cardiovascular calcification (CVC), a marker of atherosclerosis, is also more prevalent in these patients and is associated with serious clinical consequences. The pathogenesis of CVC is complex and includes factors that promote calcification and others that inhibit calcification. Thus, multiple therapeutic interventions should be used simultaneously to reduce the burden of calcification in patients with CKD. Thus far, interventional attempts have focused on curtailing the effects of factors that promote calcification such as management of known traditional factors for atherosclerotic coronary artery disease and on adopting specific approaches to normalize mineral metabolism, deliver adequate dialysis, and control serum cholesterol level. By contrast, interventions that may bolster the effects of inhibitors of calcification have not yet been studied well but are beginning to attract attention. Ideally, the goal of interventions is not only to slow or halt progression of calcification but also to reverse pre-existing calcification. Whether this goal is achievable is not currently known. This review examines the potential of various therapeutic interventions in reducing the CVC burden in patients with CKD. Moreover, the review is intended to stimulate more research in this area because the efficacy of these interventions has not been examined in controlled clinical trials.

Calcinosis↗
PubMed2004

The natural history of cervical disc calcification in children.

BACKGROUND: Calcification of cervical intervertebral discs is uncommon in children. The cases of approximately 200 children have been reported in the literature. The objective of the present study was to examine the natural history of this condition. METHODS: Seventeen consecutive children, ten boys and seven girls, with calcified cervical intervertebral discs were included in the study. The mean age at diagnosis was 7.7 years. Three children had had a fever, and two had a history of trauma. All of the children complained of neck pain except one who was asymptomatic and was identified by chance. On radiographs, the calcification was seen within the central part of the cervical intervertebral discs. All children had treatment of the symptoms, and they were then followed periodically until the disappearance of both the symptoms and the calcific deposits. RESULTS: The children were followed for a mean of five years, and all had a complete disappearance of both the symptoms and the calcification. None had recurrent symptoms or calcifications. The average time to resolution of the symptoms and the calcifications was 34.3 days (range, seventeen to 173 days) and fifteen months (range, three to sixty months), respectively. With the numbers available, factors such as age, level of disc calcification, severity of symptoms, and degree of spinal canal compromise were not related to the time of resolution. CONCLUSIONS: Cervical disc calcification in children is a self-limiting condition with an excellent prognosis. Even if clinical symptoms due to nerve-root or spinal cord compression are present, conservative therapy produces satisfactory results. Therefore, nerve-root or spinal cord compression by a calcified cervical disc should not be considered an absolute indication for surgical intervention.

Adolescent↗