A Self-Representation-Based Fuzzy SVM Model for Predicting Vascular Calcification of Hemodialysis Patients.

In end-stage renal disease (ESRD), vascular calcification risk factors are essential for the survival of hemodialysis patients. To effectively assess the level of vascular calcification, the machine learning algorithm can be used to predict the vascular calcification risk in ESRD patients. As the amount of collected data is unbalanced under different risk levels, it has an influence on the classification task. So, an effective fuzzy support vector machine based on self-representation (FSVM-SR) is proposed to predict vascular calcification risk in this work. In addition, our method is also compared with other conventional machine learning methods, and the results show that our method can better complete the classification task of the vascular calcification risk.

Osteoporosis y calcificación vascular: un escenario compartido / Osteoporosis and vascular calcification: A shared scenario

La osteoporosis es una enfermedad esquelética sistémica, caracterizada por baja masa ósea y deterioro en la microarquitectura del tejido óseo, que origina un aumento de la fragilidad ósea y, en consecuencia, mayor susceptibilidad a fracturas. Es la enfermedad metabólica ósea más frecuente en nuestra población, y las fracturas resultantes de la osteoporosis son cada vez más comunes. Por otro lado, la calcificación vascular es un factor de riesgo reconocido de morbimortalidad cardiovascular, que históricamente era considerada como un proceso pasivo y degenerativo. Sin embargo, en la actualidad se reconoce como un proceso activo que tiene características histopatológicas, de composición mineral y de mecanismos de iniciación y desarrollo propias de la formación del hueso. Paradójicamente, los pacientes con osteoporosis muestran con frecuencia calcificaciones vasculares. Tradicionalmente se han considerado como procesos independientes relacionados con la edad, aunque estudios epidemiológicos recientes han evidenciado que existe una estrecha relación entre la pérdida de masa ósea y la calcificación vascular, independiente de la edad. De hecho, ambas entidades comparten factores de riesgo y mecanismos fisiopatológicos. Entre ellos destacan la relación entre proteínas de origen óseo, como la osteopontina y la osteoprotegerina, con la patología vascular, y el sistema intercelular proteico RANK/RANKL/OPG y la vía de señalización Wnt. Los mecanismos vinculados en ambas patologías deben considerarse en las decisiones clínicas, dado que los tratamientos para la osteoporosis podrían tener efectos imprevistos en la calcificación vascular, y a la inversa. En definitiva, una mejor comprensión de la relación entre ambas entidades puede contribuir a plantear estrategias para disminuir la prevalencia creciente de calcificación vascular y osteoporosis en la población que envejece

Osteoporosis is a systemic skeletal disease, characterised by low bone mass and deterioration in the micro-architecture of bone tissue, which causes increased bone fragility and consequently greater susceptibility to fractures. It is the most frequent metabolic bone disease in our population, and fractures resulting from osteoporosis are becoming more common. Furthermore, vascular calcification is a recognised risk factor of cardiovascular morbidity and mortality that historically has been considered a passive and degenerative process. However, it is currently recognised as an active process, which has histopathological characteristics, mineral composition and initiation and development mechanisms characteristic of bone formation. Paradoxically, patients with osteoporosis frequently show vascular calcifications. Traditionally, they have been considered as independent processes related to age, although more recent epidemiological studies have shown that there is a close relationship between the loss of bone mass and vascular calcification, regardless of age. In fact, both conditions share risk factors and pathophysiological mechanisms. These include the relationship between proteins of bone origin, such as osteopontin and osteoprotegerin (OPG), with vascular pathology, and the intercellular protein system RANK/RANKL/OPG and the Wnt signalling pathway. The mechanisms linked in both pathologies should be considered in clinical decisions, given that treatments for osteoporosis could have unforeseen effects on vascular calcification, and viceversa. In short, a better understanding of the relationship between both entities can help in proposing strategies to reduce the increasing prevalence of vascular calcification and osteoporosis in the aging population

Chronic Total Occlusion Crossing Approach Based on Plaque Cap Morphology: The CTOP Classification.

PURPOSE: To present the chronic total occlusion (CTO) crossing approach based on plaque cap morphology (CTOP) classification system and assess its ability to predict successful lesion crossing. METHODS: A retrospective analysis was conducted of imaging and procedure data from 114 consecutive symptomatic patients (mean age 69±11 years; 84 men) with claudication (Rutherford category 3) or critical limb ischemia (Rutherford category 4-6) who underwent endovascular interventions for 142 CTOs. CTO cap morphology was determined from a review of angiography and duplex ultrasonography and classified into 4 types (I, II, III, or IV) based on the concave or convex shape of the proximal and distal caps. RESULTS: Statistically significant differences among groups were found in patients with rest pain, lesion length, and severe calcification. CTOP type II CTOs were most common and type III lesions the least common. Type I CTOs were most likely to be crossed antegrade and had a lower incidence of severe calcification. Type IV lesions were more likely to be crossed retrograde from a tibiopedal approach. CTOP type IV was least likely to be crossed in an antegrade fashion. Access conversion, or need for an alternate access, was commonly seen in types II, III, and IV lesions. Distinctive predictors of access conversion were CTO types II and III, lesion length, and severe calcification. CONCLUSION: CTOP type I lesions were easiest to cross in antegrade fashion and type IV the most difficult. Lesion length >10 cm, severe calcification, and CTO types II, III, and IV benefited from the addition of retrograde tibiopedal access.

[Vascular calcifications in subjects with and without chronic renal failure: types, sites and risk factors].

Vascular calcifications worse outcomes in the general population and in patients on dialysis. We investigated 146 patients on chronic hemodialysis and 63 healthy controls with normal renal function under 65 years of age. All subjects underwent B-mode ultrasonography of common and internal carotid artery, abdominal aorta, common and superficial femoral artery and posterior tibial artery to assess the presence of intimal and medial calcifications. Intimal and media calcifications were present at the level of the carotid vessel, the abdominal aorta, the common femoral artery, the superficial femoral artery and the posterior tibial artery, respectively in 45%, 50%, 45%, 50%, 42% of patients on dialysis and in 5%, 15%, 24%, 5%, 2% of controls (p <0,01). On multivariate logistic analysis of regression, after adjustment for potential confounders, carotid intimal calcification, abdominal aortic calcification, medial calcification of the superficial femoral artery and posterior tibial artery calcification were associated with dialysis and with cardiovascular disease. Only intimal arterial calcification were associated with older age and smoking. Vascular calcifications are extremely common in middle-aged patients on chronic hemodialysis. Ultrasonography currently available in Nephrology, is a sensitive, reproducible, inexpensive imaging technique to identify arterial intimal and medial calcification in high-risk cardiovascular subjects.

Prevalence of factors related to vascular calcifications in patients with chronic kidney disease on dialysis.

The main aim of the study was to determine the prevalence of vascular calcifications in patients with chronic kidney disease on dialysis in our population assessed by X-ray. The secondary objectives were to determine the cardiovascular risk factors associated with the presence of vascular calcifications and to evaluate the complementary use of the echocardiogram in a cross-sectional, observational, multicentric study. We included patients with chronic kidney disease on dialysis, age =18 years with at least 3 months of renal replacement therapy in 8 dialysis centres in Argentina. The degree of vascular calcification was determined using Adragao and Kauppila scores. The presence of valvular calcifications was established through a trans-thoracic doppler echocardiogram. Univariate and multivariate analysis were undertaken, considering the degree of vascular calcification as the dependent variable; 443 adult patients were evaluated at 8 centres across 5 provinces in Argentina. The prevalence of vascular calcifications by the X-rays was 63%, while 73% presented calcifications in hands and pelvis, with an Adragao score > 3, and 60% presented calcifications in the abdominal aorta with a Kauppila score > 4. The prevalence of valvular calcifications: 28%. We have shown a higher rate of vascular calcifications with the use of plain X-rays when compared to the prevalence of valvular calcifications obtained with echocardiograms. In this regard, valvular calcifications were present particularly in those patients with a severe level of radiological vascular calcification.

Prevalence of factors related to vascular calcification in patients with chronic kidney disease on dialysis

The main aim of the study was to determine the prevalence of vascular calcifications in patients with chronic kidney disease on dialysis in our population assessed by X-ray. The secondary objectives were to determine the cardiovascular risk factors associated with the presence of vascular calcifications and to evaluate the complementary use of the echocardiogram in a cross-sectional, observational, multicentric study. We included patients with chronic kidney disease on dialysis, age =18 years with at least 3 months of renal replacement therapy in 8 dialysis centres in Argentina. The degree of vascular calcification was determined using Adragao and Kauppila scores. The presence of valvular calcifications was established through a trans-thoracic doppler echocardiogram. Univariate and multivariate analysis were undertaken, considering the degree of vascular calcification as the dependent variable; 443 adult patients were evaluated at 8 centres across 5 provinces in Argentina. The prevalence of vascular calcifications by the X-rays was 63%, while 73% presented calcifications in hands and pelvis, with an Adragao score >3, and 60% presented calcifications in the abdominal aorta with a Kauppila score >4. The prevalence of valvular calcifications: 28%. We have shown a higher rate of vascular calcifications with the use of plain X-rays when compared to the prevalence of valvular calcifications obtained with echocardiograms. In this regard, valvular calcifications were present particularly in those patients with a severe level of radiological vascular calcification.

El objetivo primario del estudio fue determinar la prevalencia de calcificaciones vasculares en pacientes con enfermedad renal crónica (ERC) en diálisis, a través de métodos accesibles y reproducibles. Como objetivo secundario: determinar los factores de riesgo cardiovascular asociados a la presencia de calcificaciones vasculares y evaluar la utilidad complementaria del ecocardiograma. Fue un estudio prospectivo, transversal y multicéntrico sobre pacientes prevalentes con ERC en diálisis. Se les realizaron radiografía de columna lumbar, de manos y panorámica de pelvis, para la determinación de las escalas de Adragao y Kauppila. La presencia de calcificaciones valvulares fue establecida por ecocardiograma doppler color transtorácico. Se obtuvieron los datos de 30 variables determinadas para el análisis uni y multivariado (regresión logística) de los factores de riesgo asociados. Se evaluaron 443 pacientes adultos de 8 centros de 5 provincias de la Argentina. La prevalencia de calcificaciones vasculares, determinada por las radiografías, fue 63%. La prevalencia de calcificaciones valvulares fue 28%. Las calcificaciones valvulares estuvieron presentes en aquellos pacientes con graves calcificaciones radiológicas. Las calcificaciones estuvieron asociadas a la edad (>55 años), sexo masculino, diabetes, tiempo de diálisis, tabaquismo y la presencia de enfermedad vascular periférica. Este es el estudio con mayor número de pacientes evaluados en Latinoamérica. Se encuentra alta prevalencia de calcificaciones vasculares en Argentina, fácilmente medibles con técnicas no invasivas como la radiografía simple, que resulta más sensible que el ecocardiograma. Ambos estudios deben ser utilizados de manera complementaria.

Performance of ultra-low-dose CT for the evaluation of coronary calcification: a direct comparison with coronary calcium score.

AIM: To evaluate the diagnostic performance of ultra-low-dose computed tomography (ULDCT) in comparison to standard coronary calcium score (CCS) acquisition for the evaluation of coronary artery calcification (CAC). MATERIALS AND METHODS: Standard CCS acquisition and ULDCT were performed in patients referred for coronary CT angiography for the evaluation of coronary artery disease. CAC in ULDCT was graded subjectively using a four-point scale (from 0, no calcification, to 3, severe calcification) for the complete study and for each individual coronary segment. The summation of all individual coronary segment scores generated an ULDCT total CAC score. ULDCT results were compared to standard Agatston score and sensitivity and specificity of ULDCT were calculated. RESULTS: CCS and ULDCT were performed in 74 patients, with a mean DLP of 77.7 mGy·cm (±12.1) and 9.3 mGy·cm (±0.6), respectively (p<0.001). Coronary calcification was detected in 47 patients (63.5%) in standard CCS acquisition (median Agatston score of 41; interquartile range [IQR]:0263), in comparison to 42 patients (56.8%) in ULDCT (p<0.001). The sensitivity and specificity of the ULDCT total CAC score ≥1 was 80.9% and 85.2%, respectively, with an accuracy of 82.4%. The area under the receiver operating characteristic curve for the presence of CAC was 0.87. CONCLUSION: ULDCT shows good sensitivity, specificity, and overall accuracy for the detection of coronary calcification with a markedly lower radiation dose in comparison to CCS. ULDCT is unlikely to miss coronary calcification in individuals with at least moderate calcium load (Agatston score >100).

Potential Utility of Multidetector Computed Tomography to Identify both Cardiac Embolic Sources and Coronary Artery Disease in Patients with Embolic Stroke.

OBJECTIVES: Our objective was to study the potential utility of multidetector computed tomography (MDCT) to identify both cardiac embolic sources and coronary artery disease (CAD) in embolic-stroke patients. METHODS: We performed MDCT for 184 patients with embolic stroke but without known CAD. Twenty-six patients had atrial fibrillation. We investigated the prevalence of the potential source of the embolism and the coronary characteristics. RESULTS: Overall, 64 potential embolic sources were detected in 59 patients (32.1%). Left atrial appendage thrombus, left ventricular thrombus and aortic atheroma were detected in 3.3, 0.5 and 15.8% of patients, respectively. Circulatory stasis and patent foramen ovale were detected in 8.7 and 6.5%, respectively. As for coronary calcium score, only 47 patients (25.5%) had a score of zero and 51 (27.7%) had a score of ≥ 400. Significant CAD was detected in 18 patients (9.8%). One hundred and thirty-seven (74.5%) had coronary plaques. The prevalence of positive remodeling, low-attenuation plaque, spotty calcification and a napkin-ring sign was 7.1, 1.6, 5.4 and 2.7%, respectively. Importantly, only 34 patients (13.0%) had no abnormalities detected by MDCT. CONCLUSIONS: Our results suggest that MDCT has potential to identify both cardiac embolic sources and CAD in patients with embolic stroke but without known CAD.

The clinical and cost burden of coronary calcification in a Medicare cohort: An economic model to address under-reporting and misclassification.

BACKGROUND: Coronary artery calcification (CAC) is a well-established risk factor for the occurrence of adverse ischemic events. However, the economic impact of the presence of CAC is unknown. OBJECTIVES: Through an economic model analysis, we sought to estimate the incremental impact of CAC on medical care costs and patient mortality for de novo percutaneous coronary intervention (PCI) patients in the 2012 cohort of the Medicare elderly (≥65) population. METHODS: This aggregate burden-of-illness study is incidence-based, focusing on cost and survival outcomes for an annual Medicare cohort based on the recently introduced ICD9 code for CAC. The cost analysis uses a one-year horizon, and the survival analysis considers lost life years and their economic value. RESULTS: For calendar year 2012, an estimated 200,945 index (de novo) PCI procedures were performed in this cohort. An estimated 16,000 Medicare beneficiaries (7.9%) were projected to have had severe CAC, generating an additional cost in the first year following their PCI of $3500, on average, or $56 million in total. In terms of mortality, the model projects that an additional 397 deaths would be attributable to severe CAC in 2012, resulting in 3770 lost life years, representing an estimated loss of about $377 million, when valuing lost life years at $100,000 each. CONCLUSIONS: These model-based CAC estimates, considering both moderate and severe CAC patients, suggest an annual burden of illness approaching $1.3 billion in this PCI cohort. The potential clinical and cost consequences of CAC warrant additional clinical and economic attention not only on PCI strategies for particular patients but also on reporting and coding to achieve better evidence-based decision-making.

[Pathophysiological mechanisms of vascular calcification]. / Mécanismes physiopathologiques impliqués dans le développement des calcifications vasculaires.

Vascular calcification (VC) is a degenerative pathology of the vessel wall. In the general population, VC appearance is associated with aging, but this pathology can also develop as a consequence of atherosclerosis, diabetes, inflammatory and chronic kidney disease. VC is strongly associated with increased risk of mortality and cardiovascular disease. Although VC has long been considered as the result of a passive precipitation of mineral, it is now well established that this pathology results from an active and highly regulated cellular process, which shares similarities with bone formation. This review summarizes our current knowledge on VC formation, and details the modalities of action of the main actors known to modulate this process.

[Vascular Calcification - Pathological Mechanism and Clinical Application - . Mechanisms of vascular calcification].

Vascular calcification is an independent risk factor for the development of cardiovascular disease and is classified into two types based on the site of calcification : intimal atherosclerotic calcification and Mönckeberg's medial calcification. Matrix vesicles released from macrophages and vascular smooth muscle cells (VSMC) during apoptosis play a pivotal role in formation of fine granular calcification, while osteogenic differentiation of VSMC contributes to progression of advanced calcification. Recent noninvasive imaging studies of atherosclerotic calcification provide robust evidence that inflammation precedes active calcification, leading to establish the inflammation-dependent calcification paradigm. On the other hand, elastin degradation by increased elastolytic activities and disturbance of regulatory systems of extracellular pyrophosphate metabolism play an important role in development of Mönckeberg's medial calcification.

[Vascular Calcification - Pathological Mechanism and Clinical Application - . The significance of arterial calcification in unstable plaques].

Plaque rupture or erosion with subsequent thrombus formation is the principal mechanism underlying the sudden onset of acute coronary syndromes. Plaque inflammation and increased oxidative stress play important roles in the pathogenesis of plaque destabilization. Macrophages, T lymphocytes, and neutrophils are the dominant types of inflammatory cells at human coronary unstable plaques, such as ruptured plaques or eroded plaques. Calcification is a common finding in human atherosclerotic lesions, and arterial calcification is generally classified into calcification within an atherosclerotic plaque, and Mönckeberg's medial calcific sclerosis characterized by calcific deposits within the media of small and medium-sized muscular arteries. It has been reported that a spotty pattern of calcification is associated with coronary unstable ruptured plaques in patients with acute myocardial infarction. Patients undergoing hemodialysis (HD) have a high prevalence of arterial calcification and cardiovascular events. We recently demonstrated that plasma oxidized low density lipoprotein (LDL) levels significantly increased after a single HD session. This HD session-related increase in plasma oxidized LDL levels could contribute to the progression and acceleration of atherosclerosis and arterial calcification, leading to the development of cardiovascular events in HD patients.

Prevalence of severe subclinical coronary artery disease on cardiac CT and MRI in patients with extra-cardiac arterial disease.

OBJECTIVE: Patients with extra-cardiac arterial disease (ECAD) are at high risk of coronary artery disease (CAD). Prevalence of silent, significant CAD in patients with stenotic or aneurysmal ECAD was examined. Early detection and treatment may reduce CAD mortality in this high-risk group. MATERIALS AND METHODS: ECAD patients without cardiac complaints underwent computed tomography (CT) for calcium scoring, coronary CT angiography (cCTA) if calcium score was 1,000 or under, and adenosine perfusion magnetic resonance imaging (APMR) if there was no left main stenosis. Significant CAD was defined as calcium score over 1,000, cCTA-detected coronary stenosis of at least 50% lumen diameter, and/or APMR-detected inducible myocardial ischemia. In cases of left main stenosis (or equivalent) or myocardial ischemia, patients were referred to a cardiologist. RESULTS: The prevalence of significant CAD was 56.8% (95% CI 47.5 to 66.0). One-hundred and eleven patients were included. Eighty-four patients (76%) had stenotic ECAD, and 27 (24%) had aneurysmal disease. In patients with stenotic ECAD, significant coronary stenosis was present in 32 (38%) and inducible ischemia in eight (12%). Corresponding results in aneurysmal ECAD were eight (30%) and two (11%), respectively (p for difference >.05). Sixteen (19%) patients with stenotic and six (22%) with aneurysmal ECAD were referred to a cardiologist, with subsequent cardiac intervention in seven (44%) and three (50%), respectively (both p >.05). CONCLUSIONS: Patients with stenotic or aneurysmal ECAD have a high prevalence of silent, significant CAD.

Not all porcelain is the same: classification of circular aortic calcifications (porcelain aorta) according to the impact on therapeutic approach.

Severe aortic calcification, also known as "porcelain aorta," has a major impact on patient outcome. Its presence also influences the choice of procedure depending on where it is located. However, to date there is no clear definition on how this term should be employed, being often used as an exclusion criteria for conventional surgery where aortic clamping and/or cannulation is required.We here suggest a classification of the "porcelain aorta" regarding its location and how it influences particular therapeutic options. Therefore, making more clear what procedures would represent an increased risk for the patient and which are more suitable when discussed in a "Heart Team."Type I implies localization of a circumferential calcification in the ascending aorta. Type IA represents the calcified aorta with no possibility of clamping and Type IB represents the calcified aorta with possible clamping. Type II addresses the calcification of the descending aorta including or not the aortic arch.

[Arterial heterogeneity]. / Artériopathie et hétérogénéité artérielle.

More and more clinical observations and trials support the concept of heterogeneity of atheroma according to the arterial bed. In a pilot study named "Étude Comparative des Lésions Athéromateuses" (ECLA), we have shown that carotid and femoral plaques possess different characteristics. Carotid arteries display increased lipid content compared to femoral arteries whereas femoral arteries are more prone to calcify and to develop osteoid metaplasia. These observations should lead the researcher and the clinician to look at the cellular and molecular mechanisms governing the heterogeneity of atheromas. At last, a better understanding of the characteristics of plaques should help us to determine plaque stability, to prevent cardiovascular events and to choose the best medical, endovascular or surgical option.

St George's Vascular Institute Protocol: an accurate and reproducible methodology to enable comprehensive characterization of infrarenal abdominal aortic aneurysm morphology in clinical and research applications.

PURPOSE: To define the reproducibility of a protocol for the analysis of infrarenal abdominal aortic aneurysm (AAA) morphology for clinical and research purposes. METHODS: A protocol for the comprehensive assessment of preoperative AAA morphology based on formal systematic review and expert opinion featured 114 morphological parameters (maximum and minimum diameters, cross-sectional areas, vessel lengths, volumes, angulation, and calcification and tortuosity indices) in each of 3 regions: the neck, sac, and access vessels. To validate the protocol, 4 observers measured these variables on the preoperative computed tomographic angiograms from 50 patients (45 men; mean age 75 years, range 52-89) scheduled for endovascular aneurysm repair using software for 3-dimensional image reconstruction. One observer performed repeated measurements. The intra- and interobserver variabilities were calculated for all parameters; measurement time for all 114 features was recorded. RESULTS: Aortoiliac diameter, length, volume, area, and tortuosity index measurements showed good inter/intraobserver agreement. Aortic neck and aortoiliac angle measurements displayed high intra/interobserver repeatability coefficients (28%-43% and 29%-61%, respectively). Calcification measurements had the highest variability within and between observers: 39%-65% and 44%-96%, respectively. The measurement protocol was completed in a mean 105 minutes (range 55-420). CONCLUSION: Accurate 3-dimensional analysis of AAA morphology can be performed reliably within a reasonable time. Measurements that relied on consistent anatomical landmarks were most reproducible. Assessment of angulation and calcification required a number of subjective judgments, increasing the potential for variation. Automated methods are likely to be more suitable for certain measurements.

Calcificación vascular: tipos y mecanismos / Vascular calcification: types and mechanisms

Clásicamente se consideraba que la calcificación vascular era un proceso pasivo y degenerativo que frecuentemente ocurría con la edad avanzada, aterosclerosis, varias alteraciones metabólicas (como diabetes mellitus y estados finales de enfermedad renal) y en raras enfermedades genéticas. Sin embargo, desde hace algunos años, la calcificación vascular es considerada como un proceso activo y regulado de manera semejante a la mineralización y metabolismo del hueso, en el se encuentran implicadas diversas proteínas óseas. Resultados recientes cuestionan la clásica separación de la calcificación vascular en calcificación de la íntima y calcificación de la media, al menos en arterias de capacitancia. Mecanismos procalcificantes y anticalcificantes desempeñan un papel activo en la deposición de calcio en las células vasculares, por lo que su estudio se ha convertido en un área muy activa de investigación. La identificación de dianas terapéuticas que puedan enlentecer o incluso revertir la calcificación vascular podría suponer un avance muy importante en las estrategias terapéuticas para los pacientes afectados de enfermedades renales (AU)

Vascular calcification has traditionally been considered to be a passive process that was associated with advanced age, atherosclerosis, uncommon genetic diseases and some metabolic alterations such as diabetes mellitus and end–stage kidney failure. However, in the last years, vascular calcification has been proven to be an active and regulated process, similar to bone mineralisation, in which different bone–related proteins are involved. Recent results question the classic classification of vascular calcification into intimal and medial calcification, at least in capacitance arteries. Pro and anti–calcifying mechanisms play an active role in calcium deposition in vascular cells, making this area an active focus of research. The identification of therapeutic targets which can slow down the progression or even reverse vascular calcification could be an important step forward in the treatment of patients with chronic kidney disease (AU)