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Vascular Calcification

Vascular Calcification is the pathological deposition of calcium salts in the walls of blood vessels, which can occur in various cardiovascular diseases.
It is a complex process involving multiple cell types and signaling pathways.
Vascular calcification can lead to stiffening of the arteries, impaired blood flow, and an increased risk of cardiovascular events.
Understanding the mechanisms and finding effective interventions for vascular calcification is an important area of research in cardiovanscular medicine.

Most cited protocols related to «Vascular Calcification»

Details of materials and experimental procedures are in the Methods section in the Online Data Supplement.
The smooth muscle specific-Runx2 deficient mice were generated by crossing the Runx2 exon 8 floxed mice (Runx2f/f)25 (link) with the SM22α-Cre transgenic mice. Characterization of vascular calcification in vivo was performed with mice crossed into ApoE−/− background.
Publication 2012
ApoE protein, human Dietary Supplements Exons Mice, Laboratory Mice, Transgenic RUNX2 protein, human Smooth Muscles Vascular Calcification

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Publication 2017
Adult ARID1A protein, human Bones Calcium Cardiovascular System Chronic Kidney Disease-Mineral and Bone Disorder Conferences Diagnosis Grafts Phosphates System, Endocrine Vascular Calcification Vitamin D
In the current study, WWI (cm/√kg) was designed as an exposure variable, which was calculated as WC (cm) divided by the square root of weight (kg) (14 (link)). The anthropometry examinations were performed in the MEC by trained health technicians and monitored through direct observation, data reviews, and periodic expert examiner evaluations. The full procedure, including the protocols and quality control, was described at https://wwwn.cdc.gov/nchs/nhanes/ContinuousNhanes/Manuals.aspx?BeginYear=2013. Weight was measured to the nearest 0.1 kg using a digital weight scale. Each subject wore a standard MEC examination gown before weighting, then stood in the center of the digital scale with hands at sides and eyes looking straight forward. WC was measured using a retractable steel measuring tape. The iliac crests were palpated bilaterally and a horizontal line was drawn just above the uppermost lateral border of the right ilium. Then, the right midaxillary line was drawn. At the point where the two lines crossed, the measuring tape was positioned in the horizontal plane. Take the measurement to the nearest 0.1 cm at the end of the individual’s normal expiration.
The AAC score and severe AAC were designed as outcome variables. AAC was obtained from a lateral scan of the lumbar spine (vertebrae L1–L4) using DXA. The Kauppila score system was applied to quantify the AAC score. DXA scans were performed on eligible survey participants aged ≥ 40 years. Meeting any of the following criteria will be excluded: (1) self-report pregnancy and/or positive urine pregnancy test; (2) self-reported history of radiographic contrast material (barium) use in past 7°days; (3) self-reported weight over 450 pounds; (4) self-reported history of scoliosis with surgical rod implantation. A Kauppila score ≥ 6 was defined as severe AAC, which was recognized as severe vascular calcification according to previous studies (20 (link), 21 (link)).
Publication 2022
Barium Contrast Media Eye Fingers Iliac Crest Ilium Operative Surgical Procedures Ovum Implantation Physical Examination Pregnancy Pregnancy Tests Radionuclide Imaging Scoliosis Steel Tooth Root Urinalysis Urine Vascular Calcification Vertebra Vertebrae, Lumbar
Total hip was chosen as the main site for this analysis because hip BMD is a more robust marker of nonvertebral fracture risk than spine BMD,17, 18 and it is less affected by artifacts, such as coexisting vascular calcification or osteoarthritic changes that could influence the BMD measurement. Nonvertebral fractures (excluding those of the skull, face, mandible, metacarpals, fingers, or toes) confirmed by the central imaging vendor were included in the analysis. Pathologic nonvertebral fractures and those associated with severe trauma (defined as a fall from a height higher than a stool, chair, or the first rung of a ladder; or severe trauma other than a fall) were also excluded from the analysis.
The relationship between total hip T‐score and incidence of nonvertebral fractures and vertebral fractures through 10 years of denosumab therapy was analyzed post hoc, as follows: (1) a repeated‐measures model (fitting observed T‐scores against years on denosumab treatment at each BMD assessment, its quadratic term, and baseline T‐score with random intercept and slope for each subject) was used to estimate each subject's T‐score at specific time points during the entire follow‐up period; (2) Cox's proportional‐hazard model was fitted for time to first fracture with the corresponding estimated T‐score for the subject at the time of the fracture and its quadratic term as time‐dependent covariates; (3) the expected fracture risk during the entire follow‐up period was estimated for various T‐scores ranging from ‐3.0 to ‐0.5; and (4) the expected fracture risk at 1 year was extracted for each T‐score to depict the T‐score/fracture response curve. Baseline age (≥ 75 years versus < 75 years) and prior nonvertebral fracture status were evaluated separately as additional covariates in the Cox model. The significance of the reduction in 1‐year nonvertebral fracture risk between pairs of T‐scores that differed by an increment of 1.0 was assessed.
A sensitivity analysis of the relationship between total hip T‐score and incidence of nonvertebral fractures for the first 3 years of the FREEDOM trial (denosumab and placebo arms) was also conducted.
Baseline values are reported using descriptive statistics. Because the exact timing of vertebral fractures was generally unknown, the date of the spine X‐ray with confirmed vertebral fractures was used as a proxy for time to vertebral fracture.
The percentages of women with T‐scores of > ‐2.5, > ‐2.0, and > ‐1.5 at the total hip or femoral neck at baseline and over 10 years of denosumab treatment were determined. The percentages of women with baseline T‐scores of ≤ ‐2.5 at the total hip or femoral neck who attained a T‐score > ‐2.5, > ‐2.0, and > ‐1.5 over time were also determined. The influence of baseline T‐score on subsequent T‐score improvement at each follow‐up time point was also explored by grouping women based on baseline T‐score quartiles.
Publication 2019
Arm, Upper Bones, Metacarpal Cranium Denosumab Face Feces Fingers Fracture, Bone HIP1 protein, human Hypersensitivity Mandible Neck, Femur Pathological Fracture Placebos Spinal Fractures Toes Vascular Calcification Vertebral Column Woman Wounds and Injuries X-Rays, Diagnostic
This study is a double-blind, randomized placebo-controlled trial. Participants were recruited through a pre-existing diabetes cohort study (Utrecht participants only) (14 (link)), a Julius Center database of subjects who are interested in participating in studies, and via outpatient clinics of the University Medical Center Utrecht and Diakonessenhuis Utrecht. Participants who met the following criteria were included in the study: men and women aged >40 y with diagnosed type 2 diabetes and pre-existing CVD, because vascular calcification is highly prevalent in this patient group, and an estimated glomerular filtration rate (eGFR) >30. Exclusion criteria were vitamin K antagonist use, use of (multi)vitamins with vitamin K, unwillingness to stop vitamin K use before randomization, and known coagulation problems such as deep vein thrombosis. All participants gave written informed consent prior to participation. This trial was approved by the institutional review board of the University Medical Center Utrecht and registered at clinicaltrials.gov as as NCT02839044.
Publication 2019
Coagulation, Blood Deep Vein Thrombosis Diabetes Mellitus, Non-Insulin-Dependent Ethics Committees, Research Glomerular Filtration Rate Patients Placebos States, Prediabetic Vascular Calcification Vitamin K Woman

Most recents protocols related to «Vascular Calcification»

The Kolmogorov–Smirnov test was used to test for normal or Gaussian distribution, a condition not fulfilled by several variables. Therefore, non-parametric tests, such as Mann–Whitney’s U test and Kruskal–Wallis test and Spearman’s correlation analysis were used to analyze differences or correlations among non-parametric variables. When the variables subjected to analysis showed a normal distribution, Student’s t test, variance analysis and Pearson’s correlation analysis were used. Stepwise logistic regression analyses (dichotomizing the selected variables according to medians) were used to discern if a given result obtained in the univariate analyses was independent of confounding factors. Multiple linear regression analyses were also used to disclose the confounding effect of age (or other continuous variables) on significant results observed in the univariate analyses. In addition, the ability of sclerostin as a diagnostic marker of vascular damage and/or brain atrophy was also explored using ROC curves analysis. Considering that hypertension is a well-known factor involved in vascular damage, the sensitivity and specificity of sclerostin levels over the median in the diagnosis of vascular calcification or brain shrinkage (assessed by ROC curves) were tested both in the whole group and in the non-hypertensive group. All these analyses were performed with the SPSS program (Chicago, IL, USA).
The study protocol was approved by the local ethical committee of our Hospital (number 2017/50) and conforms to the ethical guidelines of the 1975 Declaration of Helsinki. All the patients gave their written informed consent.
Publication 2023
Atrophy Blood Vessel Brain Diagnosis High Blood Pressures Patients Student Vascular Calcification
We conducted a systematic review of the published literatures in electronic databases PubMed, Embase, Web of Science and Cochrane Library from their inceptions until 1 September 2022. The details of search strategies and results in mentioned databases are presented in Supplementary table 2. No restrictions to languages, regions and publication types were set. Two reviewers (Huang Linxi and Hu Junjie) independently screened article titles, abstracts and full texts to identify potential studies. The inclusion criteria were followed: (1) observational or cohort studies were eligible; (2) subjects were diagnosed with kidney stone or vascular calcification. Reviews, case reports, comments and duplicates were removed. The main flow-work was diagramed in Figure 1, and any disagreement in the procedure was resolved by discussion.
Publication 2023
cDNA Library Kidney Calculi Vascular Calcification
For the primary analysis, we categorized patients as aged ≥75 and <75 years. This threshold was chosen based on the known knowledge gaps in health status outcomes in adults ≥75 years, the underrepresentation of adults ≥75 years from prior CTO revascularization studies,10, 27 and studies demonstrating comparatively fewer adults aged 70 to 79 and ≥80 years being referred for CTO PCI.11 Continuous variables were summarized as means±SDs or medians (interquartile range), and categorical variables as counts (percentage). For descriptive purposes, continuous variables were compared between the 2 groups with the 2‐tailed t test or Wilcoxon Rank Sum test, and categorical variables were compared with χ2 analysis. As a supplementary analysis, we also compared differences in baseline characteristics, procedural characteristics, and health status outcomes among adults aged <65, 65 to 74, and ≥75 years using 1‐way ANOVA or the Kruskal–Wallis test for continuous variables and χ2 analysis for categorical variables.
We examined the association between age category (aged ≥75 and <75 years) and technical success using hierarchical modified Poisson regression with robust error variance to account for clustering of patients within sites.28 Covariates for model adjustment were determined a priori based on clinical experience, and included vessel treated, presence of a bypass graft to the CTO vessel, prior stenting of the CTO vessel, and each component of the Japan CTO score: presence of a blunt proximal cap, vessel calcification, vessel bending ≥45°, CTO length ≥20 mm, and whether the current procedure was a repeat attempt of a previously failed CTO PCI.
For the health status outcomes analysis, we excluded 37 of the 1000 patients enrolled in OPEN‐CTO with missing baseline health status or all 3 follow‐up health status assessments. Unadjusted health status outcomes were compared between adults ≥75 and <75 years at baseline, 1, 6, and 12‐months. Differences in health status between adults aged ≥75 years and adults <75 years were modeled using hierarchical multivariable linear regression with repeated measures, which allowed for better informing of the 12‐month estimate (the primary health status outcome of interest) using 1 and 6‐month estimates. Models were developed for SAQ Summary Score, SAQ Angina Frequency Score, SAQ Physical Limitations, SAQ QOL, and RDS. Each model included age and time as categorical effects, an age by time interaction, and adjusted for the corresponding baseline health status as a restricted cubic spline term. Each model was further adjusted for potential confounders based on clinical experience, including sex, diabetes, congestive heart failure, chronic lung disease, prior myocardial infarction, chronic kidney disease, and whether technical success was achieved. We also included a sex‐by‐age interaction, as sex‐related differences in cardiovascular risk profiles may lead to differential health status benefits in older women as compared with older men.29 In a sensitivity analysis, we repeated the above analysis adjusting for in‐hospital MACCE.
A P value of <0.05 was considered statistically significant. All statistical analyses were performed in SAS version 9.4 (SAS Institute, Cary, NC USA).
Publication 2023
Adult Angina Pectoris Blood Vessel Chronic Kidney Diseases Congestive Heart Failure Cuboid Bone Diabetes Mellitus Disease, Chronic Grafts Hypersensitivity Lung Lung Diseases Myocardial Infarction neuro-oncological ventral antigen 2, human Patients Physical Examination Vascular Calcification Woman
This study was a single-center retrospective observational study of 1691 consecutive patients undergoing deceased donor kidney transplantation between January 2006 and December 2015. We analyzed patient charts of all kidney transplant recipients to identify those patients with peripheral artery disease (PAD), diabetes mellitus, hypertension, history of coronary artery disease, and smoking. Other data, including clinical presentation, operative details, graft, and patient survival, were extracted from medical records.
All patients receiving renal transplants were assessed preoperatively according to an established protocol that included a complete assessment of their vascular status based on medical history and physical examination. When atherosclerosis of the aorta, iliac, or femoral arteries was suspected, ankle-brachial pressure index (ABI) was measured, and axial computed tomographic scan (CT) of abdomen and pelvis was performed in case the ankle-brachial pressure index measurement detected any abnormality. The ABI measurements were grouped into four categories: normal (0.90–1.39), mild disease (0.70–0.89), moderate disease (0.40–0.69), and severe disease (0–0.39). Additionally, we analyzed the type of PAD presentation (claudication, chronical limb ischemia, ulceration/gangrene) and the level of PAD (stenosis, occlusion). Consequently, the indication for vascular reconstruction was defined by the transplant team and was based on vascular calcification, considering the risk of technical obstacles for renal transplantation caused by significant occlusive lesions. Patients with diffuse aorto-iliac atherosclerosis, type-C or -D aorto-iliac disease according to the Trans-Atlantic Inter-Society Consensus Document (TASC), [11 (link)] were considered as candidates for pretransplant vascular bypass surgery. Symptomatic patients with TASC type-A or -B aorto-iliac disease were considered as candidates for pretransplant iliac artery angioplasty. Patch angioplasty was performed in selected patients with extensive calcified plaques or a small iliac artery. Patients with normal ABI and without pronounced calcification of the iliac arteries were not revascularized and excluded from the study. Also patients undergoing re-transplants, younger than 18 years and those with missing data were also excluded from the study.
We retrospectively analyzed patients with the necessity of vascular revascularization before kidney transplantation to protect the inflow to the renal graft and to optimizing blood supply to the extremities. Finally, data of 18 patients with vascular revascularization were available for complete analysis. The primary endpoint included patient survival and graft survival. The secondary endpoints evaluate perioperative and early postoperative complication rates after kidney transplantation.
All study procedures adhered to the Declaration of Helsinki and were approved by the Institutional Ethics Committee (18–8023-BO). All patients provided written informed consent for kidney transplantation.
Publication 2023
Abdomen Angioplasty Aorta Atherosclerosis Blood Vessel Calcinosis Coronary Artery Disease Dental Occlusion Diabetes Mellitus Donors Femoral Artery Gangrene Grafts Graft Survival High Blood Pressures Iliac Artery Ilium Indices, Ankle-Brachial Institutional Ethics Committees Ischemia Kidney Transplantation Patients Pelvis Peripheral Arterial Diseases Physical Examination Postoperative Complications Radionuclide Imaging Reconstructive Surgical Procedures Senile Plaques Stenosis Ulcer Vascular Calcification Vascular Surgical Procedures X-Ray Computed Tomography Youth
Statistical analysis was performed using the IBM Statistical Package for Social Sciences (SPSS) Statistics v26 for windows. The Shapiro–Wilk or the Kolmogorov–Smirnov tests were applied to examine the normality of the distribution for continuous variables. Data from normally distributed and non-normally distributed variables were expressed as Mean ± Standard Deviation and Median and Interquartile Range, respectively. Similarly, differences between groups were estimated using Student’s t test for independent samples or Mann–Whitney U test, respectively. Pearson’s and Spearman’s coefficients were used for the correlation between normally and non-normally distributed variables. Odds Ratio (OR) and Receiver Operating Characteristics (ROC) curves were applied to estimate the incidence of serum OPG levels in the presence of vascular calcifications. Multivariate analysis was performed to evaluate serum OPG levels and other independent parameters contributing to the presence of vascular calcifications. Finally, Cox regression analysis was performed to estimate the contribution of OPG serum levels to the progression of vascular calcifications 5 years after the enrollment of the patients. Values of p < 0.05 (two-tailed) were considered statistically significant for all comparisons.
Publication 2023
Disease Progression Patients Serum Student Vascular Calcification

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More about "Vascular Calcification"

Vascular calcification, also known as arterial calcification or vessel hardening, is a complex pathological process characterized by the deposition of calcium salts within the walls of blood vessels.
This condition can occur in various cardiovascular diseases, including atherosclerosis, chronic kidney disease, and diabetes.
The pathogenesis of vascular calcification involves multiple cell types, signaling pathways, and environmental factors.
One key factor in vascular calcification is the role of Vitamin D3, which can promote the mineralization of vascular smooth muscle cells.
Additionally, Glycerophosphate, a common dietary supplement, has been linked to the acceleration of calcification in in vitro studies.
Imaging techniques, such as the SOMATOM Force CT scanner, can be used to detect and quantify vascular calcification, while statistical software like SAS 9.4 can be employed for data analysis.
Nicotine, a component of tobacco products, has been shown to contribute to the development of vascular calcification, highlighting the importance of lifestyle factors in this condition.
The IntelliSpace Portal, a medical imaging and analysis platform, can assist in the visualization and assessment of vascular calcification.
In cell culture studies, the use of DMEM (Dulbecco's Modified Eagle Medium) and GraphPad Prism 7 software for data analysis have been common.
The MEG-01 cell line, derived from human megakaryoblastic leukemia, has been utilized as a model for investigating the cellular mechanisms underlying vascular calcification.
Interventions to prevent or treat vascular calcification are an active area of research in cardiovascular medicine.
Alkamuls EL-620, a surfactant, has been explored for its potential to inhibit the formation of calcium deposits in vascular tissues.
Understanding the complex interplay of these factors is crucial for developing effective strategies to manage and mitigate the impact of vascular calcification on cardiovascular health.