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An overview of the mechanisms in vascular calcification during chronic kidney disease.
Voelkl, J, Cejka, D, Alesutan, I
Current opinion in nephrology and hypertension. 2019;(4):289-296
Abstract
PURPOSE OF REVIEW Chronic kidney disease (CKD) facilitates a unique environment to strongly accelerate vascular calcification - the pathological deposition of calcium-phosphate in the vasculature. These calcifications are associated with the excessive cardiovascular mortality of CKD patients. RECENT FINDINGS Vascular calcification is a multifaceted active process, mediated, at least partly, by vascular smooth muscle cells. These cells are able to transdifferentiate into cells with osteo/chondrogenic properties, which exert multiple effects to facilitate vascular tissue mineralization. As the understanding of the underlying pathophysiology increases, first therapeutic concepts begin to emerge. SUMMARY This brief review provides an overview on the so far known mechanisms involved in the initiation and progression of vascular calcification in CKD.
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Coronary artery calcium: A technical argument for a new scoring method.
Willemink, MJ, van der Werf, NR, Nieman, K, Greuter, MJW, Koweek, LM, Fleischmann, D
Journal of cardiovascular computed tomography. 2019;(6):347-352
Abstract
Coronary artery calcium (CAC) is a strong predictor for future cardiovascular events. Traditionally CAC has been quantified using the Agatston score, which was developed in the late 1980s for electron beam tomography (EBT). While EBT has been completely replaced by modern multiple-detector row CT technology, the traditional CAC scoring method by Agatston remains in use, although the literature indicates suboptimal reproducibility and subjects being incorrectly classified. The traditional Agatston scoring method counteracts the technical advances of CT technology, and prevents the use of thinner sections, obtained at lower tube voltage and overall decreased radiation exposure that has become available to other CT applications. Moreover, recent studies have shown that not only the total amount of CAC, but also its density and distribution in the coronary arterial tree may be of prognostic value. Acquisition and reconstruction techniques thus need to be adapted for modern CT technology and optimized for CAC quantification. In this review we describe the technical limitations of the Agatston score followed by our suggestions for developing a new and more robust CAC quantification method.
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Cardiovascular Risk Heterogeneity in Adults with Diabetes: Selective Use of Coronary Artery Calcium in Statin Use Decision-making.
Sarkar, S, Orimoloye, OA, Nass, CM, Blumenthal, RS, Martin, SS
Journal of general internal medicine. 2019;(11):2643-2647
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Abstract
Current American College of Cardiology/American Heart Association and American Diabetes Association guidelines recommend statin therapy for all patients with diabetes between the ages of 40 and 75, including those without cardiovascular disease (CVD). While diabetes is a major CVD risk factor, not all patients with diabetes have an equal risk of CVD. Thus, a more risk-based approach warrants consideration when recommending statin therapy for the primary prevention of CVD. Coronary artery calcium (CAC) is a noninvasive imaging modality that can help risk stratify patients with diabetes for future CVD events. CAC has been extensively studied in large cohorts such as the Multi-Ethnic Study of Atherosclerosis and found to outperform other novel risk stratification tools including carotid intima-media thickness. Moreover, a CAC score of 0 has been shown to be useful in downgrading the estimated risk of a CVD event in patients with diabetes and an intermediate Pooled Cohort Equation score. As clinicians weigh the recommendation for a lifelong therapy and the problem of statin nonadherence and patients weigh concerns about adverse effects of statins, the decision to initiate statin therapy in patients with diabetes is ideally a shared one between patients and providers, and CAC could facilitate this discussion.
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The "tangential calcium" sign.
Ponnatapura, J, Dyer, RB
Abdominal radiology (New York). 2019;(8):2933-2934
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Coronary Computed Tomography Angiography and Calcium Scoring.
DuBose, CO, Youngman, K, Barymon, D
Radiologic technology. 2019;(3):259CT-275CT
Abstract
Cardiovascular disease is the leading cause of death worldwide and describes many heart and vessel disorders. One of these disorders, coronary artery disease (CAD), occurs because of narrowed or blocked coronary arteries. Computed tomography (CT) is used to diagnose CAD because it displays coronary artery stenosis and calcified plaques in the coronary arteries. Coronary CT angiography visualizes coronary arteries for narrowing, and coronary artery calcium scoring visualizes calcium-containing plaques in the coronary arteries. Technological advancements have helped minimize radiation exposure associated with these examinations.
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Tissue Non-Specific Alkaline Phosphatase and Vascular Calcification: A Potential Therapeutic Target.
Azpiazu, D, Gonzalo, S, Villa-Bellosta, R
Current cardiology reviews. 2019;(2):91-95
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Abstract
Vascular calcification is a pathologic phenomenon consisting of calcium phosphate crystal deposition in the vascular walls. Vascular calcification has been found to be a risk factor for cardiovascular diseases, due to its correlation with cardiovascular events and mortality, and it has been associated with aging, diabetes, and chronic kidney disease. Studies of vascular calcification have focused on phosphate homeostasis, primarily on the important role of hyperphosphatemia. Moreover, vascular calcification has been associated with loss of plasma pyrophosphate, one of the main inhibitors of calcification, thus indicating the importance of the phosphate/pyrophosphate ratio. Extracellular pyrophosphate can be synthesized from extracellular ATP by ecto-nucleotide pyrophosphatase/ phosphodiesterase, whereas pyrophosphate is hydrolyzed to phosphate by tissuenonspecific alkaline phosphatase, contributing to the formation of hydroxyapatite crystals. Over the last decade, vascular calcification has been the subject of numerous reviews and studies, which have revealed new agents and activities that may aid in explaining the complex physiology of this condition. This review summarizes current knowledge about alkaline phosphatase and its role in the process of vascular calcification as a key regulator of the phosphate/pyrophosphate ratio.
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Magnesium and calciprotein particles in vascular calcification: the good cop and the bad cop.
Zeper, LW, de Baaij, JHF
Current opinion in nephrology and hypertension. 2019;(4):368-374
Abstract
PURPOSE OF REVIEW Vascular calcification is a major contributor to increased cardiovascular mortality in chronic kidney disease (CKD). Recently, calciprotein particles (CPP) were identified to drive the calcification process. CPP may explain the effects of high phosphate on vascular calcification. Magnesium is a promising novel therapeutic approach to halt vascular calcification, because it inhibits CPP maturation and is associated with reduced cardiovascular mortality in CKD. We aim to examine the current evidence for the role of CPP in the calcification process and to explain how magnesium prevents calcification. RECENT FINDINGS A recent meta-analysis concluded that reducing high phosphate levels in CKD patients does not associate with lowering cardiovascular mortality. Inhibition of CPP formation prevents phosphate-induced calcification in vitro. Consequently, delaying CPP formation and maturation may be a clinical approach to reduce calcification. Magnesium inhibits CPP maturation and vascular calcification. Clinical pilot studies suggest that magnesium is a promising intervention strategy against calcification in CKD patients. SUMMARY CPP induce vascular calcification and are modulated by serum phosphate and magnesium concentrations. Magnesium is a strong inhibitor of CPP maturation and therefore, a promising therapeutic approach to reduce vascular calcification in CKD. Currently, several studies are being performed to determine the clinical outcomes of magnesium supplementation in CKD.
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Extracellular vesicles in vascular calcification.
Yang, W, Zou, B, Hou, Y, Yan, W, Chen, T, Qu, S
Clinica chimica acta; international journal of clinical chemistry. 2019;:118-122
Abstract
Vascular calcification is associated with adverse cardiovascular events that increase the risk of cardiovascular death. Unfortunately, the pathogenesis of vascular calcification is complex and incompletely understood. As important intercellular signaling molecules, the role of extracellular vesicles (EVs) in vascular calcification has attracted wide attention in recent years. This review will briefly describe the role of EVs (mainly including exosomes and microvesicles) in the process of vascular wall calcification focusing on the specific mechanisms of smooth muscle cell (SMC) differentiation and calcium-phosphorus balance to illustrate the relationship between EVs and vascular calcification. It is likely that EVs may be prognostic markers in some cardiovascular diseases and have potential therapeutic potential.
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Role of Vascular Smooth Muscle Cell Phenotypic Switching and Calcification in Aortic Aneurysm Formation.
Petsophonsakul, P, Furmanik, M, Forsythe, R, Dweck, M, Schurink, GW, Natour, E, Reutelingsperger, C, Jacobs, M, Mees, B, Schurgers, L
Arteriosclerosis, thrombosis, and vascular biology. 2019;(7):1351-1368
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Abstract
Aortic aneurysm is a vascular disease whereby the ECM (extracellular matrix) of a blood vessel degenerates, leading to dilation and eventually vessel wall rupture. Recently, it was shown that calcification of the vessel wall is involved in both the initiation and progression of aneurysms. Changes in aortic wall structure that lead to aneurysm formation and vascular calcification are actively mediated by vascular smooth muscle cells. Vascular smooth muscle cells in a healthy vessel wall are termed contractile as they maintain vascular tone and remain quiescent. However, in pathological conditions they can dedifferentiate into a synthetic phenotype, whereby they secrete extracellular vesicles, proliferate, and migrate to repair injury. This process is called phenotypic switching and is often the first step in vascular pathology. Additionally, healthy vascular smooth muscle cells synthesize VKDPs (vitamin K-dependent proteins), which are involved in inhibition of vascular calcification. The metabolism of these proteins is known to be disrupted in vascular pathologies. In this review, we summarize the current literature on vascular smooth muscle cell phenotypic switching and vascular calcification in relation to aneurysm. Moreover, we address the role of vitamin K and VKDPs that are involved in vascular calcification and aneurysm. Visual Overview- An online visual overview is available for this article.
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Coronary risk assessment using traditional risk factors with CT coronary artery calcium scoring in clinical practice.
Kerut, EK, Hall, ME, Turner, MC, McMullan, MR
Echocardiography (Mount Kisco, N.Y.). 2018;(8):1216-1222
Abstract
As coronary artery calcium (CAC) is atherosclerosis and not just a marker of cardiovascular (CV) disease, measurement of a patient's coronary artery calcium score (CACS) is a strong predictor of risk. Clinically performed in asymptomatic patients, the CACS, along with several CV risk factors, namely age, sex, ethnicity, diabetes, tobacco use, family history, cholesterol level, blood pressure, and use of cholesterol or hypertensive medications, provide a predictive model of 10 year risk for CV events. A smartphone "App" makes this quick to obtain and use. This helps the clinician in making recommendations for both lifestyle changes and statin therapy. Those patients in which the most benefit occur from measurement of a CACS are those at an intermediate CV risk. Measurement of the CACS has become an integral part of the clinician's assessment of a patient's CV risk and for guiding preventative therapies.