Risk Factor For Calcification Research Articles

Asymptomatic Coronary Artery Calcifications in Men with Systemic Lupus Erythematosus.

To determine whether the prevalence and extent of asymptomatic coronary artery atherosclerosis are increased in men with systemic lupus erythematosus (SLE) compared with age- and sex-matched controls, and to define the associated risk factors. Ninety-five patients with SLE (mean ± SD age, 34.7 ± 10.1 yrs) and 100 control subjects (age 34.8 ± 9.7 yrs) with no history of coronary artery disease were screened for coronary artery calcification using multidetector computed tomography. The extent of calcification was measured using the Agatston score. The frequency of risk factors for calcification was compared between patients and controls, and the relationship between clinical and immunological characteristics and the presence of coronary artery calcification was investigated. Coronary artery calcification was more frequent in patients than controls [18% vs 7%, respectively (OR 2.89, 95% CI 1.07-8.65)]. These factors were independently associated with the presence of calcifications: age (OR 1.12, 95% CI 1.04-1.20), SLE diagnosis (OR 3.38, 95% CI 1.07-10.64), diabetes mellitus (OR 6.88, 95% CI 1.50-31.62), Framingham risk score (OR 1.12, 95% CI 1.00-1.23), and glomerular filtration rate (OR 0.98, 95% CI 0.96-1.00). Among patients with SLE, coronary artery calcifications were observed starting at age 32 years, within 2.3 years of diagnosis. Increasing age (OR 1.18, 95% CI 1.06-1.31), Systemic Lupus International Collaborating Clinics score (OR 2.85, 95% CI 1.21-6.73), and cumulative dose of prednisone (OR 1.04, 95% CI 1.01-1.08) were independent risk factors. Men with SLE are at an increased risk of coronary artery calcifications than age- and sex-matched controls. Among patients with SLE, the increased risk is associated to older age, increasing chronic damage, and cumulative dose of corticosteroids.

INFLUENCE OF SECONDARY HYPERPARATHYROIDISM ON THE CALCIFICATION OF HEART VALVES IN PATIENTS WITH CHRONIC KIDNEY DISEASE VD STAGE

The aim of this work was to study the relationship of elevated levels of parathyroid hormone (PTH) with cardiovascular changes (calcification of the heart valves) and to identify possible risk factors of calcification in the group of patients receiving renal replacement therapy.
 Materials and methods. The study included 96 patients with ESRD: 1-st group receives the treatment of peritoneal dialysis (PD) (45 patients), 2-nd group haemodialysis (HD) (51 patients). In serum determined concentration of calcium, phosphorus, PTH. All patients underwent echocardiographic examination.
 Results. The prevalence of secondary hyperparathyroidism in PD-patients reached 72%, in HD-patients 83%. Calcification of heart valves in both groups occurred in patients with high PTH level (greater than 400 PG/ml). Patients in both groups were significantly more frequent in the combined mitrale-aortic calcification. Isolated mitral calcification was detected more often aortic. Predictors of progression of calcification of heart valves in patients on PD is the age, in patients on HD - level average BP and the duration of dialysis therapy.
 Conclusions. Echocardiological data and clinical and laboratory examination of patients with ESRD allowed us to estimate the prevalence and structure of mitrale-aortic calcification and its relationship with secondary hyperparathyroidism.

Superior mesenteric artery calcification is associated with cardiovascular risk factors, systemic calcified atherosclerosis, and increased mortality

BackgroundAtherosclerosis is a major risk factor for morbidity and mortality. However, epidemiologic data are sparse regarding risk factors for superior mesenteric artery calcification (SMAC), the association between SMAC and disease in other arterial beds, or the independent contribution of SMAC to risk of mortality. The objective of this study was to test the hypothesis that presence and extent of SMAC are associated with cardiovascular disease (CVD) risk factors, calcification in other arterial beds, and both cardiovascular and all-cause mortality, independent of classic risk factors and calcification in other arterial beds. MethodsArterial calcification in the superior mesenteric artery, celiac trunk, coronaries, thoracic aorta, abdominal aorta, and iliac arteries was evaluated by computed tomography in adults with no known CVD. Multiple logistic regression models examined risk factor associations for SMAC and SMAC as a risk factor for calcification in other arterial beds. Cox models were used to examine the association between SMAC and mortality. ResultsThe average age of subjects was 56 years; 43.7% (1877/4300) were women, and 6.7% (290) had SMAC. Age (odds ratio [OR], 1.09; 95% confidence interval, 1.06-1.11), male sex (OR, 1.79; 95% CI, 1.08-3.03), dyslipidemia (OR, 1.38; 95% CI, 1.01-1.88), and any smoking (OR, 1.60; 95% CI, 1.20-2.14) were associated with SMAC presence. Notably, body mass index, body fat percentage, hypertension, diabetes, and family history of coronary heart disease were not significant risk factors for the presence of SMAC. SMAC presence was associated with calcification in all five other arterial beds (OR, 6.02; 95% CI, 3.76-9.66). During a median follow-up time of 9.4 years, there were 234 deaths, 76 of which were CVD related. SMAC extent (represented as per-unit increase in log [SMAC score + 1]; OR, 1.31; 95% CI, 1.01-1.71) was significantly associated with CVD mortality after full adjustment for risk factors and calcification in other arterial beds. SMAC presence (OR, 1.52; 95% CI, 1.10-2.12) and extent (OR, 1.25; 95% CI, 1.06-1.48) were also both significantly associated with all-cause mortality after full adjustment. ConclusionsSMAC is associated with specific CVD risk factors as well as with calcification in all other arterial beds. SMAC extent was significantly associated with incident cardiovascular mortality, whereas both SMAC presence and extent were significantly associated with all-cause mortality, even after adjustment for risk factors and calcification in other arterial beds. Further studies are needed to determine whether SMAC is simply a marker for advanced and systemic disease or whether it confers increased mortality risk through an independent mechanism.

Intraocular Lens Calcifications After (Triple-) Descemet Membrane Endothelial Keratoplasty

To identify incidence of and risk factors for calcifications of intraocular lenses (IOLs) after Descemet membrane endothelial keratoplasty (DMEK). Retrospective cohort study. Retrospective review of charts and slit-lamp images of 564 consecutive patients from the prospective Cologne DMEK database who underwent DMEK in pseudophakic eyes or DMEK in combination with cataract surgery (triple-DMEK) between September 3, 2013 and October 30, 2015 at the Department of Ophthalmology, University of Cologne. IOL calcifications after (triple-)DMEK occurred in 14 patients (2.5%). Visual acuities in affected and unaffected eyes were 0.33 ± 0.24 logMAR and 0.16 ± 0.01 logMAR after 3months (P < .001) as well as 0.28 ± 0.16 logMAR and 0.13 ± 0.08 logMAR (P < .001) after 6months, respectively. The proportions of triple-DMEK vs DMEK, the use of SF6 gas vs room air for anterior chamber tamponade, and the presence of hydrophilic vs hydrophobic acrylic IOLs were comparable in affected and unaffected eyes. Patients with IOL calcifications had higher rebubbling rates than patients without. Larger pupil diameters at the time of surgery showed a tendency to slightly larger areas of IOL calcifications. IOL calcifications after anterior chamber gas tamponade in DMEK lead to visual impairment and are associated with the number of rebubblings after DMEK. IOL calcifications also occur in hydrophobic acrylic IOLs.

Abstract P225: Calcification of the Splenic, Internal and External Iliac, and Breast Arteries and Risk of All-cause Mortality

Introduction: Prognostic consequences of and risk factors for coronary and aortic calcification are well known. Less is known about the consequences of and risk factors for calcification in other arteries. Hypothesis: We hypothesize that calcifications in the splenic, internal and external iliac, and breast arteries (in females) have different risk factor profiles, and that calcification in these beds is associated with mortality. Methods: We conducted a case cohort study from 5196 individuals who self-referred for whole body computed tomography (CT). We selected a random sub-cohort of 395 individuals. Our cases were 298 individuals who died during a median follow-up of 9.4 years. CT scans were scored for splenic, internal and external iliac, and, in females, breast artery calcification. The associations between risk factors and presence or absence of calcification in each vascular bed in the random sub-cohort was evaluated using logistic regression. Using both the sub-cohort and death cases, we used Prentice-weighted Cox proportional hazards models to assess associations of calcification in each bed with mortality. Results: Within the random sub-cohort, prevalence of calcification was 11.6% (46 of 395) in the splenic, 47.9% (187 of 390) in the internal iliac and 9.5% (37 of 390) in the external iliac arteries. Among the 163 women, 3.7% had breast artery calcification. In multivariable models, age (OR 1.62 [95%CI 1.04-2.54] per 10 years), diabetes (OR 5.80 [95%CI 1.37-24.61]), log-transformed abdominal aortic calcium (AAC) (OR 1.36 [95%CI 1.09-1.70]) and log-transformed CAC score (OR 1.38 [95%CI 1.13-1.68]) were independently associated with splenic artery calcification. Age (OR 1.60 [95%CI 1.09-2.33], male gender (OR 3.86 [95%CI 2.09-7.15]), AAC (OR 1.44 [95%CI 1.28-1.62]) and CAC score (OR 1.23 [95%CI 1.08-1.39]) were associated with internal iliac artery calcium. Smoking (current vs. never OR 9.87 [95%CI 2.24-43.61]) and AAC (OR 1.96 [95%CI 1.24-3.11]) were associated with external iliac artery calcium. For the breast arteries, numbers were too small to fit these multivariable models. Although calcification in the splenic, internal, and external iliac arteries were significantly associated with mortality in unadjusted models, these associations were attenuated and no longer statistically significant after adjusting for cardiovascular risk factors. Among women, breast artery calcification was associated with mortality independent of traditional CVD risk factors and a 0-5 score of the number of calcified vascular beds out of the carotids, coronaries, abdominal and thoracic aorta and common iliacs (HR 5.67 [95%CI 1.50-21.41]). Conclusions: Calcification in the splenic, internal and external iliac arteries was strongly associated with calcification in the abdominal aorta. In females, breast artery calcification was strongly and independently associated with mortality.

Correlation between coronary and valve calcification: Review of current evidence

&lt;p&gt;We carried out a review of the correlation between calcification of different arteries and valves and their risk factors to determine the extent of the association. We found a strong correlation between calcification presence, extent and progression between different arterial beds and the aortic valve, suggesting that calcification is a systemic diffuse disease, affecting the arterial tree as a whole. Despite this strong association, a comparison between coronary artery calcification (CAC) and calcification of other arteries may not be strictly valid, since only intimal calcification is seen in the coronary artery while other arteries may also contain medial calcification, with current scanning modalities being incapable of detecting the difference. Furthermore the pathogenesis of each type may be different.&lt;/p&gt;&lt;p&gt;Calcification seems to appear first in the coronary artery in younger adults but may be more prevalent in the aorta in the elderly, although the incidence is notably higher in the abdominal aorta among women. Mitral annulus calcification (MAC) occurs less frequently than aortic valve calcification (AVC) in asymptomatic subjects only. MAC is correlated with calcification of the aorta and advanced MAC is found with higher CAC but there is little relationship with AVC and calcification of other arterial beds. As with the coronary artery, in the aorta and aortic valve, calcium begets calcium. Although age, male gender and possibly systolic hypertension are most frequently associated with arterial calcification, there is little consistency for other conventional risk factors and MAC and&lt;/p&gt;&lt;p&gt;abdominal aortic calcification may be more prevalent among postmenopausal women. When the presence of CAC is factored in as a risk factor for calcification of the other arteries, multivariate analysis shows no additional significant risk factors except age.&lt;/p&gt;&lt;p&gt;Although AVC has been viewed as a cardiac manifestation of atherosclerosis, we found little evidence to suggest that this is also true of MAC.&lt;/p&gt;

Low arterial blood oxygenation is associated with calcification of the coronary arteries in patients with chronic obstructive pulmonary disease.

Cigarette smoking is a well-known major cause of both chronic obstructive pulmonary disease (COPD) and atherosclerosis. However, few studies have investigated the correlation between COPD and coronary atherosclerosis. We recruited 54 patients with stable COPD (51 men, 3 women) but without angina symptoms. Arterial blood gas analyses were performed, pulmonary function was assessed, and calcification of the coronary arteries was evaluated by computed tomography (CT). Calcification of the coronary arteries was noted in 25 patients. There were no significant differences in age, body mass index, respiratory function, and levels of low-density lipoprotein cholesterol, hemoglobin A1c, glucose, or C-reactive protein between patients with or without calcification of the coronary arteries. Arterial blood oxygenation was significantly lower in patients with calcification of the coronary arteries. On both univariate and multivariate analyses, low arterial blood oxygenation was an independent risk factor for calcification of the coronary arteries. In patients with COPD, low arterial blood oxygenation was strongly associated with calcification of the coronary arteries and may be a significant predictor of cardiovascular disease.

Vascular theory of the formation of Randall plaques.

The relationship between calcium-based calculi and Randall plaques is well documented, but the role these plaques play in the early process of urinary stone formation remains unknown. The vascular hypothesis of Randall plaque formation has been proposed, and recent works support this concept. The renal papilla's vascular environment is subject to relative hypoxia, hyperosmolar surroundings, and turbulent blood flow. These factors together create an environment prone to vascular injury and may potentiate Randall plaque precipitation. Recent data support the similarity between the vascular calcification process itself and urinary stone formation. Furthermore, epidemiological studies have suggested an association between urinary stones, adverse cardiovascular events, and vascular calcification risk factors. The concept that an initial vascular insult precipitates a Randall plaque and subsequent urolithiasis is compelling and represents an area in need of continued research. This may lead to future novel treatment approaches to urolithiasis.

Risk Factor Analysis of Calcification in Aortic and Mitral Valves in Maintenance Peritoneal Dialysis Patients

Background/Aims: This study aimed to investigate potential risk factors for calcification in aortic and mitral valves in maintenance peritoneal dialysis (MPD) patients. Methods: We enrolled MPD patients who had undergone over 18 months of dialysis in our dialysis center, examined their cardiac valve calcification status by echocardiography, and recorded their biochemical data and dialysis-related indicators. These results were compared by logistic regression analyses to identify the risk factors associated with calcification in aortic and mitral valves. Results: Among the 117 enrolled MPD patients, 41 exhibited calcification in aortic or mitral valves, including 38 with aortic valve calcification (AVC) and 17 with mitral valve calcification (MVC); 14 of them had calcification in both aortic and mitral valves. Multivariate logistic regression analysis revealed that age (OR=1.965, p=0.01), diabetes history (OR=4.693, p=0.029), calcium-phosphorus product (OR=2.373, p=0.001) and prealbumin (OR=0.908, p=0.012) were independently related to AVC, whereas age (OR=3.179, p=0.023), calcium-phosphorus product (OR=6.512, p=0.001), prealbumin (OR=0.885, p=0.033), high-density lipoprotein (OR=19.540, p=0.011) and diabetes history (OR=6.948, p=0.038) were independently related to MVC. Conclusions The incidence of cardiac valve calcification in MPD patients is high, and the incidence of AVC is higher than MVC. Age, diabetes history, calcium-phosphorus product and hypo-prealbuminemia are independent risk factors for AVC, whereas age, calcium-phosphorus product and hypo-prealbuminemia are independent risk factors for MVC.

Cardiovascular risk assessment in children with chronic kidney disease

Chronic kidney disease (CKD) is a major factor contributing to cardiovascular (CV) morbidity and mortality with the highest risk in patients on dialysis. An estimation of CV risk is important not only to identify potential modifiable risk factors but also to evaluate the effect of treatments aimed to reduce the risk. Non-invasive methods of measuring vascular changes and circulating biomarkers are available to assess the presence and severity of cardiovascular damage. These include measures of structural (carotid intima-media thickness and coronary artery calcification score) and functional (aortic pulse wave velocity, 24-h ambulatory blood pressure monitoring, ambulatory arterial stiffness index, heart rate variability and flow-mediated dilatation) changes in the vessel wall. In addition, a number of circulating biomarkers of vascular damage and its progression have been studied. Many of these tests are well validated as surrogate markers of future cardiovascular events and death in adult CKD patients, but need technical adaptation, standardization and validation for use in children. With our current state of knowledge, these are best reserved for research studies and scarce clinical resources may be better utilized for preventative strategies to reduce the modifiable risk factors for calcification from early CKD stages.

CLINICAL STUDY OF OLD AGED PATIENTS WITH AORTIC VALVE CALCIFICATION

ObjectivesTo evaluate the incidence of aortic valve calcification, and the correlation with valve function and commonly encountered disease in the agedMethods996 patients underwent ultrasonic cardiograph (UCG) in our hospital were...

Mechanisms and treatment of extraosseous calcification in chronic kidney disease

Strong and unidirectional associations exist between the severity of cardiovascular calcifications and mortality in patients with advanced chronic kidney disease. In the past 10 years, a wealth of experimental and clinical information has been published on the key pathophysiological events that contribute to the development and progression of vascular and soft-tissue calcifications. These processes involve a sensitive balance of calcification inhibition, induction and removal. The traditional view of regarding secondary hyperparathyroidism and elevated calcium × phosphate product as the pivotal risk factors for calcification has been challenged by data demonstrating a role for other, more subtle and complex pathomechanisms. These mechanisms include the loss of endogenous calcification inhibitors, deficient clearance of calcified debris, effects of vitamin K and vitamin D, and the action of calcification inducers as in osteogenic transdifferentiation. In this Review, we describe our current knowledge of the factors involved in the passive and active regulation of extraosseous calcification processes, with an assessment of their importance as targets for future diagnostic and therapeutic interventions.

Comparison of Coronary Artery Calcification and Some Coronary Artery Calcification Risk Factors in Patients on Haemodialysis and in Patients with Type 2 Diabetes

Patients on haemodialysis (HD) and patients with type 2 diabetes are at high-risk for coronary artery calcification (CAC). The coronary artery calcium score (CACS), quantified by computed tomography, cannot be completely explained by traditional cardiovascular disease risk factors. CAC was measured in 45 non-diabetic chronic kidney disease patients on HD and in 45 matched type 2 diabetes patients without diabetic nephropathy. Serum calcium, phosphate, 25-hydroxyvitamin D (25[OH]D), alkaline phosphatase, intact parathyroid hormone (iPTH), fetuin-A, high-sensitivity C-reactive protein (hsCRP), albumin, homocysteine, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides and femoral neck bone mineral density were also measured. No differences were observed in patient distribution across the CACS risk categories between the two groups. Significant differences were observed in serum calcium, phosphate, 25(OH)D, alkaline phosphatase, iPTH, fetuin-A, hsCRP, homocysteine and triglycerides between the two patient groups. Further research into the diverse, numerous and often interlinked factors that influence CAC in different groups of patients is warranted.

Association of Serum Phosphate and Related Factors in ESRD-Related Vascular Calcification.

Vascular calcification is common in ESRD patients and is important in increasing mortality from cardiovascular complications in these patients. Hyperphosphatemia related to chronic kidney disease is increasingly known as major stimulus for vascular calcification. Hyperphosphatemia and vascular calcification become popular discussion among nephrologist environment more than five decades, and many researches have been evolved. Risk factors for calcification are nowadays focused for the therapeutic prevention of vascular calcification with the hope of reducing cardiovascular complications.

Association of fetuin-A and cardiac calcification and inflammation levels in hemodialysis patients

Background. Vascular calcification is commonly found in chronic kidney disease (CKD) patients and it is one of the predictors of cardiovascular death. Recently, several studies have demonstrated that low fetuin-A levels are associated with mortality in uremic patients. Objectives. To investigate the importance of non-traditional risk factors of calcification including fetuin-A, IL-6 and high sensitivity CRP (hsCRP) in hemodialysis patients and their relationship to the extent of cardiac calcification by means of multislice computed tomography (MSCT), and echocardiography. Patients and methods. The study was conducted on 70 hemodialysis patients as well as 20 healthy control subjects. All patients were subjected to MSCT for evaluation of calcium score in the coronary arteries as well as echocardiography for detecting valvular calcification. In addition, the patients were sampled for evaluation of inflammatory markers such as hsCRP and IL-6 and also fetuin-A. Results. Mean serum fetuin-A was significantly lower in hemodialysis patients than controls subjects. By dividing the patients into tertiles of serum fetuin-A, a significant association between low levels of fetuin-A and high calcium score and valvular calcification were found. Multiple regression analysis showed that calcium scoring and IL-6 were the most independent risk factors for serum fetuin-A levels. Conclusion. Serum fetuin-A showed important association with coronary, valvular calcification and inflammation in hemodialysis patients. Assessment of both cardiac calcification and serum levels of fetuin-A may be of value to identify those subjects at higher risk of development and progression of vascular lesion and may be a novel therapeutic approach.

Is Valvular Calcification a Part of the Missing Link between Residual Kidney Function and Cardiac Hypertrophy in Peritoneal Dialysis Patients?

Residual renal function (RRF) predicts survival and shows an important inverse relation with cardiac hypertrophy in peritoneal dialysis (PD) patients. We hypothesized that valvular calcification and the calcification milieu may be part of the process linking loss of RRF and cardiac hypertrophy. A cross-sectional study was conducted by performing two-dimensional echocardiography on 230 PD patients to assess valvular calcification and left ventricular (LV) mass and collecting 24-h urine for estimation of RRF. Patients having valvular calcification had lower RRF than those without. Patients with no RRF showed higher calcium-phosphorus product (Ca x P) and C-reactive protein (CRP). Using multiple logistic regression analysis, every 1-ml/min per 1.73 m(2) increase in residual GFR was associated with a 28% reduction in the risk for valvular calcification. The association was lost after additional adjustment for Ca x P and CRP. Using multiple linear regression analysis, loss of RRF showed significant association with increased LV mass index, but this association was lost after additional adjustment for CRP, Ca x P, and valvular calcification. Patients with all three calcification risk factors, namely inflammation, high CaxP, and no RRF, showed the highest prevalence of valvular calcification and had the most severe cardiac hypertrophy. The association among loss of RRF, valvular calcification, and cardiac hypertrophy was closely linked to increased inflammation and high Ca x P in PD patients. These data suggest that valvular calcification and the calcification milieu are part of the processes linking loss of RRF and worsening cardiac hypertrophy in PD.

Hypercholesterolemia Association with Aortic Stenosis of Various Etiologies

Hypercholesterolemia has been found to be associated with aortic valve stenosis and to resemble the inflammatory process of atherosclerosis in many studies. The aim of this study was to investigate the role of hypercholesterolemia in development of aortic valve calcification in different etiologies. The study included 988 patients with rheumatic, congenital, or degenerative aortic stenosis, who underwent aortic valve replacement at Koşuyolu Heart and Research Hospital between 1985 and 2005. Effects of hypercholesterolemia and high low-density lipoprotein level on calcific aortic stenosis or massive aortic valve calcification were analyzed for each etiologic group. Both univariate and multivariate analyses revealed that the high serum cholesterol level (>200 mg/dL) was related to massive aortic valve calcification in all patients (p = 0.003). Hypercholesterolemia was linked to calcific aortic stenosis and massive calcification in patients with degenerative etiology (p = 0.02 and p = 0.01, respectively) and it was related to massive calcification in patients with congenital bicuspid aorta (p = 0.02). Other independent risk factors for calcific aortic stenosis and massive calcification in the degenerative group were high low-density lipoprotein level (>130 mg/dL; p = 0.03 and p = 0.05, respectively) and high serum C-reactive protein level (p = 0.04 and p = 0.05, respectively). Hypercholesterolemia is related to increased risk of aortic valve calcification in patients with degenerative and congenital etiology. Preventive treatment of hypercholesterolemia could play an important role to decrease or inhibit development of aortic valve calcification.

Short Sleep Duration and Incident Coronary Artery Calcification

Coronary artery calcification is a subclinical predictor of coronary heart disease. Recent studies have found that sleep duration is correlated with established risk factors for calcification including glucose regulation, blood pressure, sex, age, education, and body mass index. To determine whether objective and subjective measures of sleep duration and quality are associated with incidence of calcification over 5 years and whether calcification risk factors mediate the association. Observational cohort of home monitoring in a healthy middle-aged population of 495 participants from the Coronary Artery Risk Development in Young Adults (CARDIA) cohort Chicago site (black and white men and women aged 35-47 years at year 15 of the study in 2000-2001 with follow-up data at year 20 in 2005-2006). Potential confounders (age, sex, race, education, apnea risk, smoking status) and mediators (lipids, blood pressure, body mass index, diabetes, inflammatory markers, alcohol consumption, depression, hostility, self-reported medical conditions) were measured at both baseline and follow-up. Sleep metrics (wrist actigraphy measured duration and fragmentation, daytime sleepiness, overall quality, self-reported duration) were examined for association with incident calcification. Participants had no detectable calcification at baseline. Coronary artery calcification was measured by computed tomography in 2000-2001 and 2005-2006 and incidence of new calcification over that time was the primary outcome. Five-year calcification incidence was 12.3% (n = 61). Longer measured sleep duration was significantly associated with reduced calcification incidence (adjusted odds ratio, 0.67 per hour [95% confidence interval, 0.49-0.91 per hour]; P = .01). No potential mediators appreciably altered the magnitude or significance of sleep (adjusted odds ratio estimates ranged from 0.64 to 0.68 per sleep hour; maximum P = .02). Alternative sleep metrics were not significantly associated with calcification. Longer measured sleep is associated with lower calcification incidence independent of examined potential mediators and confounders.

Prevalence and Associations of Coronary Artery Calcification in Patients With Stages 3 to 5 CKD Without Cardiovascular Disease

Patients with chronic kidney disease (CKD) have a high prevalence of coronary artery calcification, suggesting that CKD itself is a risk factor for its occurrence. Existing studies are confounded by the inclusion of patients who may not have CKD by means of diagnostic criteria and by failing to account for existing cardiovascular disease. Cross-sectional study. 119 patients with CKD stages 3 to 5 (excluding dialysis) without known cardiovascular disease receiving care at a single center in Kingston, Ontario, Canada. Glomerular filtration rate was estimated (eGFR) by using the 4-variable Modification of Diet in Renal Disease Study equation. Traditional and nontraditional coronary artery calcification risk factors were defined a priori. Coronary artery calcification was measured by means of multislice computed tomographic scan. Mean and median coronary artery calcification scores were 566.5 +/- 1,108 and 111 (interquartile range, 2 to 631.5), respectively. A total of 32.8% of patients showed little calcification (score, 0 to 10). Calcification correlated with age (r = 0.44; P < 0.001), body mass index (r = 0.28; P = 0.002), high-density lipoprotein cholesterol level (r = -0.23; P = 0.01), diabetes mellitus (r = 0.23; P = 0.01), and cardiovascular risk score (r = 0.35; P < 0.001). By means of multivariable linear regression controlling for eGFR and diabetes mellitus, age (beta = 0.05; 95% confidence interval, 0.03 to 0.06; P < 0.001), body mass index (beta = 0.04; 95% confidence interval, 0.02 to 0.07; P = 0.001), and serum calcium level (beta = 0.9; 95% confidence interval, 0.15 to 1.6; P = 0.02), were risk factors for coronary artery calcification. Inadequate sample size and uncontrolled confounding are possible limitations, but are unlikely to have changed the main study findings. In this study, traditional cardiovascular disease risk factors and serum calcium level were associated with coronary artery calcification. No association was shown with eGFR. Studies exploring protective mechanisms against coronary artery calcification are needed.

Fetuin-A, Valve Calcification, and Diabetes

In the current issue of Circulation , Ix et al demonstrate an inverse correlation between mitral and aortic valve calcification and serum fetuin-A levels in a cross-sectional study of 970 patients with coronary artery disease and without renal disease.1 Increased serum fetuin was significantly associated with diabetes mellitus, hypertriglyceridemia, serum albumin, and body mass index, with a weaker association with serum C-reactive protein, low-density lipoprotein cholesterol, and serum calcium. The link between aortic stenosis and fetuin held only in those without diabetes.1 The data highlight the complex interactions of fetuin with inflammation, insulin resistance, and tissue calcification. Furthermore, the results, though intriguing, underscore our lack of understanding of the cellular mechanisms of calcification in diverse pathological substrates, such as the degenerating aortic leaflet and mitral annulus. Article p 2533 Fetuin is a member of the cystatin superfamily of cysteine protease inhibitors, originally discovered as the major component of fetal bovine serum. It is a carrier for growth factors, binds to and inactivates transforming growth factor (TGF)–β and bone morphogenic protein, and is a major component of mineralized bone.2 Fetuin-A is also an acute-phase glycoprotein, produced in adults primarily in the liver, and is a powerful circulating inhibitor of hydroxyapatite formation. Mice that lack fetuin-A exhibit extensive soft-tissue calcification, which is accelerated on a mineral-rich diet, which suggests that fetuin-A acts to inhibit calcification systemically.3 In addition to its effects on mineralization, fetuin-A inhibits insulin receptor autophosphorylation and tyrosine kinase activity in vitro and in vivo. Fetuin-null knockout mice demonstrate improved insulin sensitivity and resistance to diet-induced obesity, and it has been postulated that the absence of fetuin in mice may contribute to the improvement of insulin sensitivity associated with aging.4 Clinically, serum fetuin-A is decreased in patients with moderate to severe chronic kidney disease, especially …