Search

The treatment of dyslipidemia exhibits wide variability in clinical practice and important limitations that make lipid-lowering goals more difficult to attain. Getting to know the management of these patients in clinical practice is key to understand the existing barriers and to define actions that contribute to achieving the therapeutic goals from the most recent Clinical Practice Guidelines.Observatory where the information gathered is based on routine clinical practice and the experience from the healthcare professionals involved in the treatment of dyslipidemia in Spain. The information is collected by health area through: (i) face-to-face meeting with three different medical specialties and (ii) quantitative information related to hypercholesterolemia patients' management (ad-hoc questionnaire). Information includes patients' profiles, assistance burden, guidelines and protocols used, goal attainment, limitations and opportunities in clinical practice.145 health areas are planned to be included, with the participation of up to 435 healthcare professionals from the 17 Autonomous Regions of Spain. Information collection will result in aggregated data from over four thousand patients.This observatory aims to understand how hypercholesterolemia is being treated in routine clinical practice in Spain. Even though the preliminary results show important improvement areas in the treatment of dyslipidemias, mechanisms to drive a change towards health outcomes optimization are also identified.

Objective Patients with RA present increased risk of cardiovascular (CV) disease compared with the general population. Moreover, CV risk factors that have a causal relationship with atherosclerosis do not seem to fully explain the accelerated process that they exhibit. We evaluated the association of a 10 microRNAs panel with surrogate markers of subclinical arteriosclerosis [carotid intima-media thickness (cIMT), carotid plaque presence (cPP), pulse wave velocity (PWV) and distensibility] in a cohort of RA patients. Material and methods A total of 199 patients with RA were included. Surrogate markers of arteriosclerosis were measured with My Lab 60 X-Vision sonographer. MicroRNAs were extracted from plasma and quantified with qPCR. Multivariate models and classification methods were performed. Results Multivariate models showed that microRNAs-24 (β = 15.48), 125a (β = 9.93), 132 (β = 11.52), 146 (β = 15.12), 191 (β = 13.25) and 223 (β = 13.30) were associated with cIMT globally. MicroRNA-24 [odds ratio (OR) = 0.41], 146 (OR = 0.36) and Let7a (OR = 0.23) were associated with cPP in men. Including the microRNAs in a partial least square discriminant analysis model properly classified men with and without cPP. MicroRNA-96 (β = –0.28) was associated with PWV in male patients. Finally, several miRNAs were also associated with cIMT, cPP and arterial stiffness in the high DAS28 group and in the earlier tertile groups of disease duration. Conclusion Plasmatic expression of microRNA-24, 96, 103, 125a, 132, 146, 191, 223 and Let7a were associated with surrogate markers of CV disease and could be predictors of CV risk in patients with RA.

Background: Patients with hypertension present a permanent state of low-grade inflammation, as the disease activates several pro-inflammatory cells and inflammatory pathways. Glycoproteins A, B, and F, determined by proton nuclear magnetic resonance, provide a highly sensitive method for determining a group of liver-derived pro-inflammatory proteins, and their role has not yet been explored in patients with hypertension. In this study, we evaluated the impact of plasma concentrations of these glycoproteins in patients with hypertension. Methods: This cross-sectional study involved 340 patients attending our vascular and metabolism medicine unit. Of them, 129 were normotensive and 211 were hypertensive. Standard biochemistry and carotid ultrasound measures were performed. Serum concentrations of glycoproteins A, B, and F were determined by proton nuclear magnetic resonance. Results: Hypertensive patients presented a higher prevalence of obesity, metabolic syndrome, and diabetes and higher glycoprotein A, B, and F concentrations. Glycoproteins A, B, and F were positively correlated with systolic and diastolic blood pressure. Multivariate logistic models showed that glycoproteins A, B, and F were associated with higher odds of being hypertensive. Machine learning methods corroborated the relationship between glycoproteins and high blood pressure. The higher prevalence of carotid plaques in patients with high blood pressure was partially mediated by glycoproteins A and F. Conclusions: Patients with hypertension present systemic, subclinical inflammation as assessed by liver-derived glycoprotein A, B, and F serum levels. These results support the effect of hypertension on the mechanisms of systemic inflammation. Hypertension-associated systemic inflammation plays a role in hypertension-associated vascular injury and probably in hypertension-induced damage to other organs.

Background and aims Inflammation is a pathophysiological mechanism of atherosclerosis, and several mediators have been proposed as biomarkers. Acute-phase serum glycoproteins are upregulated in the liver during systemic inflammation. Because of their unique biochemical characteristics, they can be measured by 1H-NMR, and their role as subclinical inflammation markers is under clinical evaluation. We aimed to assess the clinical value of plasma glycoproteins in familial hypercholesterolemia (FH) patients. Methods We recruited 295 FH patients (75.6% with FH-associated genetic variants). At baseline, a full glycoprotein profile, glycoprotein A and B (GlycA and B) concentrations and their height and width ratios (H/W) were analysed by 1H-NMR. A carotid artery ultrasound study was performed at baseline and prospectively at the 5-year follow-up in 144 FH patients. Results At baseline, the GlycA and GlycB concentrations and their H/W ratios were correlated with lipid profile and adiposity parameters, with the correlation between the GlycA and triglyceride concentrations (r = 0.780; p Conclusions The concentrations of serum glycoproteins as assessed by 1H-NMR are robust markers of subclinical inflammation. In FH patients, they are increased in the presence of subclinical vascular damage and could be considered atherosclerosis risk markers in the long term.

Familial Hypercholesterolemia (FH) is an autosomal dominant disease with an estimated prevalence between 1/200-250. It is under-treated and underdiagnosed. Massive data screening can increase the detection of patients with FH.Study population: Residents in the health coverage area (N: 195.000 inhabitants) and with at least one determination of cholesterol linked to low-density lipoproteins (LDL-C) carried out between January 1, 2010 and December 30, 2019. The highest LDL-C values were selected.nephrotic syndrome, hypothyroidism, Hypothyroid treatment or triglycerides400 mg / dL. Seven algorithms suggestive of Familial Hypercholesterolemia Phenotype (HF-P) were analyzed, selecting the most efficient algorithm that could easily be translated into clinical practice.Based on 6.264.877 assistances and 288.475 patients, after applying the inclusion-exclusion criteria, 504.316 tests were included, corresponding to 106.382 adults and 10.50918 years. The selected algorithm presented a prevalence of 0.62%. 840 patients with HF-P were detected, 55.8% being women and 17818 years old, 9.3% had a history of cardiovascular disease (CVD) and 16.4% had died. 65% of the patients in primary prevention had LDL-C values130 mg / dL and 83% in secondary prevention values70mg / dL. A ratio of 7.64 (1-18) patients with HF-P per analytical requesting physician was obtained.Massive data screening and patient profiling are effective tools and easily applicable in clinical practice for the detection of patients with FH.

Bempedoic acid acts by inhibiting adenosine triphosphate-citrate lyase (ACL) and consequently cholesterol biosynthesis, leading to increased expression of LDL receptors and increasing low-density lipoproteins (LDL-C) plasma clearence. It is a prodrug for oral administration with intracellular activation. It is activatedin liver cells and to a lesser extent in kidney cells, being absent in adipose tissue and muscle cells. Therefore, unlike statins, its potential myotoxic effect is very limited. It has recently been approved as a lipid-lowering drug in combination with diet, with statins, or with other lipid-lowering drugs in patients with hypercholesterolaemia, mixed dyslipidaemia, statin intolerance, or when these are contraindicated. The marketing of bempedoic acid implies, in clinical practice, having a new family of lipid-lowering drugs.

Background and aims Familial hypercholesterolemia (FH) is a codominant autosomal disease characterized by a high risk of cardiovascular disease when not in lipid-lowering treatment. However, there is a large variability in the clinical presentation in heterozygous subjects (HeFH). Maternal hypercholesterolemia has been proposed as a cardiometabolic risk factor later in life. Whether this phenotype variability depends on the mother or father origin of hypercholesterolemia is unknown. The objective of this study was to analyze potential differences in anthropometry, superficial lipid deposits, comorbidities, and lipid concentrations depending on the parental origin of hypercholesterolemia within a large group of HeFH. Methods This is a cross-sectional observational, multicenter, nation-wide study in Spain. We recruited adults with HeFH to study clinical differences according to the parental origin. Data on HeFH patients were obtained from the Dyslipidemia Registry of the Spanish Atherosclerosis Society. Results HeFH patients were grouped in 1231 HeFH-mother-offspring aged 45.7 (16.3) years and 1174 HeFH-father-offspring aged 44.8 (16.7) years. We did not find any difference in lipid parameters (total cholesterol, triglycerides, LDLc, HDLc, and Lp(a)), nor in the comorbidities studied (cardiovascular disease prevalence, age of onset of cardiovascular disease, obesity, diabetes, and hypertension) between groups. Lipid-lowering treatment did not differ between groups. The prevalence of comorbidities did not show differences when they were studied by age groups. Conclusions Our research with a large group of subjects with HeFH shows that a potential maternal effect is not relevant in FH. However, due to the size of our sample, potential differences between genders cannot be completely ruled out. This implies that severe maternal hypercholesterolemia during pregnancy is not associated with additional risk in the FH affected offspring.

Resumen Introduccion y objetivos La menor prevalencia de diabetes mellitus tipo 2 (DM2) en pacientes con hipercolesterolemia familiar heterocigota (HFHe) podria explicar por que la DM2 no siempre se ha descrito como un predictor de enfermedad cardiovascular (ECV) en estos pacientes. El objetivo del presente estudio fue evaluar los aspectos clinicos y geneticos de pacientes con HFHe y DM2 del registro de dislipidemias de la Sociedad Espanola de Arteriosclerosis. Metodos Los pacientes con HFHe se clasificaron segun la presencia/ausencia de DM2. Se compararon las caracteristicas clinicas, bioquimicas y geneticas de ambos grupos. Resultados De los 2.301 casos de hipercolesterolemia primaria del registro, se incluyeron 1.724 casos con el diagnostico cierto o probable segun la Dutch Lipid Clinic Network para la hipercolesterolemia familiar. Los pacientes con HFHe y DM2 presentaron una tasa mas elevada de ECV y un perfil lipidico menos favorable, con niveles mas elevados de colesterol total (366,9 ± 86,7 mg/dl frente a 342,0 ± 74,7 mg/dl; diferencia media 24,894; IC95%, 5,840-43,949) y colesterol no-unido a lipoproteinas de alta densidad (316,9 ± 87,8 mg/dl frente a 286,4 ± 75,4 mg/dl; diferencia media 30,500; IC95%, 11,211-49,790). No se encontraron diferencias significativas entre los grupos con respecto al tipo de mutacion (p = 0,720). Despues de ajustar por los principales factores de riesgo, el analisis de regresion logistica confirmo una relacion entre la DM2 y la ECV (OR = 2,01; IC95%, 1,18-3,43; p = 0,010). Conclusiones Los pacientes con HFHe y DM2 presentan una tasa mas elevada de ECV y un perfil lipidico menos favorable, independientemente del tipo de mutacion. La diabetes mellitus es un factor asociado a la presencia de ECV en estos pacientes.

Introduction and objectives The lower prevalence of type 2 diabetes mellitus (T2DM) in patients with heterozygous familial hypercholesterolemia (HeFH) could explain why T2DM has not always been identified as an independent predictor of cardiovascular disease (CVD) in different familial hypercholesterolemia cohort studies . The aim of the present study was to evaluate clinical and genetic aspects of HeFH patients with T2DM in the dyslipidemia registry of the Spanish Arteriosclerosis Society. Methods HeFH patients were classified according to the presence or absence of T2DM. The clinical, biochemical and genetic characteristics of the 2 groups were compared. Results Of the 2301 patients with primary hypercholesterolemia included in the registry, 1724 with a probable or definite diagnosis according to the Dutch Lipid Clinic Network score were finally included. HeFH patients with T2DM had a higher rate of CVD and a less favorable lipid profile, with higher total cholesterol (366.9 ± 86.7 mg/dL vs 342.0 ± 74.7 mg/dL; mean difference 24.894; 95%CI, 5.840-43.949) and non–high-density lipoprotein cholesterol (316.9 ± 87.8 mg/dL vs 286.4 ± 75.4 mg/dL; mean difference 30.500; 95%CI, 11.211-49.790) levels. No significant differences were found between the groups concerning the specific type of HeFH-causing mutation (P = .720). After adjustment for major risk factors, logistic regression analysis confirmed a relationship between T2DM and the presence of CVD (OR, 2.01; 95%CI, 1.18-3.43; P = .010). Conclusions HeFH patients with T2DM have a higher rate of CVD and a less favorable lipid profile, regardless of genetic mutation type. In these patients, T2DM is associated with the presence of CVD.

Objetivo Describir las características clínicas, las razones del inicio de la terapia y los efectos del tratamiento en la fase inicial de disponibilidad de evolocumab en las unidades de lípidos/medicina interna de España. Métodos Estudio retrospectivo, observacional, a partir de las historias clínicas de pacientes consecutivos que iniciaron tratamiento con evolocumab (de febrero de 2016 a julio de 2017) en 20 unidades de medicina interna en España. Se revisaron las características demográficas y clínicas de los pacientes, el tratamiento hipolipemiante y la evolución de los perfiles lipídicos entre 12 semanas antes y 12 ± 4 semanas después del inicio de evolocumab. Resultados Se analizaron 136 pacientes: el 64,0% eran hombres, con edad media (desviación estándar, DE) de 56,6 (11,5) años. El 75,0% tenían hipercolesterolemia familiar (4 homocigotos), de los que el 51,0% habían sufrido al menos un evento cardiovascular. El 61,0% del total de pacientes presentaban enfermedad cardiovascular aterosclerótica (ECVA). Al inicio de evolocumab, el 61,0% de los pacientes tomaban estatinas de alta intensidad y el 60,3% estaban recibiendo ezetimiba. La media (DE) de los niveles de cLDL al inicio de evolocumab fue de 169,1 (56,6) mg/dl. En 46,4% de los pacientes el cLDL fue superior a 160 mg/dl y en el 26,5% ? 190 mg/dl. Durante el período de observación, evolocumab produjo reducciones significativas de cLDL del 55,7% (p < 0,0001), alcanzando unos valores medios de 74,3 mg/dl. En la semana 12 el 53,8% de los pacientes alcanzaron niveles de cLDL < 70 mg/dl y el 26,9% < 50 mg/dl. Conclusiones En las unidades de lípidos/medicina interna evolocumab se prescribió predominantemente en pacientes con hipercolesterolemia familiar con o sin ECVA. El uso inicial de evolocumab se ajustó a las pautas de la Sociedad Española de Arteriosclerosis (SEA) de 2016, estando las concentraciones de cLDL claramente por encima de los umbrales recomendados para inicio de tratamiento. El tratamiento con evolocumab en la práctica clínica redujo los niveles de cLDL en torno al 55%, cifra comparable a los ensayos clínicos, lo que permitió alcanzar los objetivos terapéuticos en la mayoría de los casos. Objective To describe the clinical characteristics, the reasons for initiating therapy, and the effects of treatment in the initial phase of evolocumab availability in lipid/internal medicine units in Spain. Methods Retrospective, observational study, based on the medical records of consecutive patients initiating treatment with evolocumab (from February 2016 to July 2017) in 20 internal medicine units in Spain. A review was made of the demographic and clinical characteristics of the patients, the lipid lowering treatment, and the evolution of the lipid profiles between 12 weeks pre-initiation and 12 ± 4 weeks post-initiation of evolocumab. Results A total of 136 patients were analysed, of whom 64.0% were men, and the mean age (standard deviation, SD) was 56.6 (11.5) years. The large majority (75%) had familial hypercholesterolaemia (4 homozygous), and 51.0% of them had suffered at least one cardiovascular event. Atherosclerotic cardiovascular disease (ASCVD) was present in 61% of all patients. At initiation of evolocumab, 61.0% of the patients were taking high-intensity statins, and 60.3% were receiving ezetimibe. The mean (and SD) of LDL-C levels at initiation of evolocumab was 169.1 (56.6) mg/dL. The LDL-C was greater than 160 mg/dL in 46.4% of patients, and ? 190 mg/dL in 26.5%. During the observation period, evolocumab produced significant reductions in LDL-C of 55.7% (P < .0001), achieving mean values of 74.3 mg/dL. At week 12, more than half (53.8%) of patients achieved LDL-C levels < 70 mg/dL, and 26.9% < 50 mg/dL. Conclusions In the lipid/internal medicine units, evolocumab was mainly prescribed in patients with familial hypercholesterolaemia, with or without ASCVD. The initial use of evolocumab was in accordance with the guidelines of the Spanish Society of Arteriosclerosis (SEA) of 2016, with LDL-C levels being well above the recommended thresholds for treatment initiation. Evolocumab treatment in clinical practice reduced LDL-C levels by about 55%, a similar reduction to that reported in clinical trials. Most patients achieved LDL-C goals.

Assessment of individual cardiovascular risk, distinguishing primary and secondary prevention, would improve the clinical management of the population with familial hypercholesterolemia. We aimed to develop and validate two risk functions to predict incident and recurrent atherosclerotic cardiovascular disease (ASCVD) in a primary care-based population with familial hypercholesterolemia phenotype (FHP), and to compare their predictive capacity with that of the SpAnish Familial hypErcHolEsterolemiA cohoRT (SAFEHEART) risk equation (SAFEHEART-RE).Data from the Catalan primary care system database (SIDIAP) of patients ≥18 years old with FHP in 2006-2013 were used to develop and validate two risk functions to predict incident and recurrent ASCVD. A validation dataset was also used to compare the model predictive capacity to that of SAFEHEART-RE.The new model (SIDIAP-FHP) included age, diabetes, smoking, sex (male), hypertension, and baseline low-density lipoprotein cholesterol in the primary prevention cohort and age, diabetes, smoking, and disease characteristics (progressive, recent, polyvascular, or included myocardial infarction) in the secondary prevention cohort. The models demonstrated a fair fit: C-Statistic: 0.71 (95%CI:0.68-0.75) in primary prevention and 0.65 (95%CI:0.60-0.70) in secondary prevention (higher than that of SAFEHEART-RE: 0.64 [95%CI:0.60-0.68] and 0.55 [95%CI:0.51-0.59], respectively; both p 0.01). The Brier scores obtained with the SIDIAP-FHP score were significantly lower than that obtained with SAFEHEART-RE in both the primary and secondary prevention cohorts.The SIDIAP-FHP score provides accurate ASCVD risk estimates for primary and secondary prevention in the FHP population, with better predictive capacity than that of SAFEHEART-RE in this general population, especially in persons with previous ASCVD.

Aim Assessing the effect of statin therapy (ST) at hospital admission for COVID-19 on in-hospital mortality. Methods and results Retrospective observational study. Patients taking statins were 11 years older and had significantly more comorbidities than patients who were not taking statins. A genetic matching (GM) procedure was performed prior to analysis of the mortality risk. A Cox proportional hazards model was used for the cause-specific hazard (CSH) function, and a competing-risks Fine and Gray (FG) model was also used to study the direct effects of statins on risk. Data from reverse transcription-polymerase chain reaction-confirmed 2157 SARS-CoV-2-infected patients [1234 men, 923 women; age: 67 y/o (IQR 54–78)] admitted to the hospital were retrieved from the clinical records in anonymized manner. Three hundred and fifty-three deaths occurred. Five hundred and eighty-one patients were taking statins. Univariate test after GM showed a significantly lower mortality rate in patients on ST than the matched non-statin group (19.8% vs. 25.4%, χ2 with Yates continuity correction: P = 0.027). The mortality rate was even lower in patients (n = 336) who maintained their statin treatments during hospitalization compared with the GM non-statin group (17.4%; P = 0.045). The Cox model applied to the CSH function [HR = 0.58(CI: 0.39–0.89); P = 0.01] and the competing-risks FG model [HR = 0.60 (CI: 0.39–0.92); P = 0.02] suggest that statins are associated with reduced COVID-19-related mortality. Conclusions A lower SARS-CoV-2 infection-related mortality was observed in patients treated with ST prior to hospitalization. Statin therapy should not be discontinued due to the global concern of the pandemic or in patients hospitalized for COVID-19.

Purpose Low-density lipoprotein (LDL) cholesterol reduction by statin therapy is dose-dependent, varies among different statins, and has wide inter-individual variability. The present study aimed to compare mean LDL cholesterol reduction and its variability achieved with different doses of the three statins most frequently used in monotherapy or combined with ezetimibe in a real clinical setting. Methods Of 5620 cases with primary hypercholesterolemia on the Spanish Arteriosclerosis Society Registry, 1004 with non-familial hypercholesterolemia and complete information on drug therapy and lipid profile were included. Results The lowest mean percentage LDL cholesterol reduction was observed with simvastatin 10 mg (32.5 +/- 18.5%), while the highest mean percentage LDL reduction was obtained with rosuvastatin 40 mg (58.7 +/- 18.8%). As to combined treatment, the lowest and highest mean percentage LDL cholesterol reductions were obtained with simvastatin 10 mg combined with ezetimibe (50.6 +/- 24.6%) and rosuvastatin 40 mg combined with ezetimibe (71.6 +/- 11.1%), respectively. Factors associated with a suboptimal response were male sex, lower age, body mass index, and baseline LDL cholesterol levels. Combined treatment was associated with less variability in LDL cholesterol reduction (OR 0.603, p < 0.001). Conclusion In a real clinical setting, rosuvastatin was superior to the other statins in lowering LDL cholesterol, both as monotherapy or combined with ezetimibe. Factors associated with a suboptimal response in LDL cholesterol decline were male sex, age, body mass index, and baseline LDL cholesterol levels. Combined treatment was associated with less variability in LDL cholesterol improvement.

Clinical studies show that patients with high cardiovascular risk are still far from reaching the therapeutic objectives, especially of the levels of LDL cholesterol. If the management of these patients in specialized units differs from other scenarios is known.61 certified Lipid Units were selected in the Registry of Dyslipemias of the Spanish Arteriosclerosis Society for the collection of study data. The study included 3958 subjects18 years of age who met the criteria for hypercholesterolemia (LDL cholesterol ≥160 mg/dL or non-HDL cholesterol ≥190 mg/dL) without familial hypercholesterolemia. A total 1,665 subjects were studied with a mean follow-up time of 4.2 years.A total of 42 subjects had a cardiovascular event since their inclusion in the Registry, which represents 0.6%. There were no differences in the treatment used at follow-up, but 50% of the patients did not reach the therapeutic goals at the visit end of follow-up. An increase in the potency of the lipid-lowering treatment was observed, including PCSK9 inhibitors use in 16.7% of subjects with recurrences.

Background Brief interventions (BI) for risky drinkers in primary healthcare have been demonstrated to be cost-effective but they are still poorly implemented. Digital BI seems to be a complementary strategy to overcome some barriers to implementation but there is a scarcity of studies in clinical environments. We present the results of a randomized controlled non-inferiority trial which tests the non-inferiority of facilitated access to a digital intervention (experimental condition) for risky drinkers against a face-to-face BI (control condition) provided by primary healthcare professionals. Method In a non-inferiority randomized controlled trial, unselected primary healthcare patients (≥ 18 years old) were given a brief introduction and asked to log on to the study website to fill in the 3-item version of the Alcohol Use Disorders Identification Test. Positively screened patients (4+ for women and 5+ for men) received further online assessment (AUDIT, socio-demographic characteristics and EQ-5D-5L) and were automatically randomized to either face-to-face or digital BI (1:1). The primary outcome was the proportion of patients classified as risky drinkers by the digitally administered AUDIT at month 3. A multiple imputation approach for the missing data was performed. Results Of the 4499 patients approached by 115 healthcare professionals, 1521 completed the AUDIT-C. Of the 368 positively screened patients, 320 agreed to participate and were randomized to either intervention. At month 3, there were more risky drinkers in the experimental group (59.8%) than in the control group (52%), which was similar to the distribution at baseline and less than the pre-specified margin of 10%. The difference was not significant when accounting for possible confounders. Conclusion Digital BI was not inferior to face-to-face BI, in line with previous findings and the a priori hypothesis. However, the low power of the final sample, due to the low recruitment and loss to follow-up, limits the interpretation of the findings. New approaches in this field are required to ensure the effective implementation of digital interventions in actual practice., Highlights • Early identification and Brief Intervention is a cost-effective approach to risky drinkers in primary healthcare. • In our trial, digital Brief Intervention was not inferior to face-to-face Brief Intervention. • Several barriers hinder the engagement with Digital Brief Interventions. • New approaches in this field are required to ensure the effective implementation of digital intervention in real practices.

Chylomicronemias are generally diagnosed genetically by genomic sequencing or screening for mutations in causal genes with a large phenotypic effect. This strategy has allowed to improve the characterization of these patients, but we still have 30% of the patients without a conclusive genetic diagnosis. This is why we hypothesize that by adding the epigenetic component we can improve the genetic diagnosis, and for this we have explored the degree of methylation in the DNA of hypertriglyceridemic patients.Blood cell DNA was obtained from 16 hypertriglyceridemic patients and from 16 age- and sex-matched control subjects. The degree of methylation in genome-wide DNA was determined using the Illumina® Infinium Methylation EPIC Array Analysis.We identified 31 differentially methylated cytosines by comparing the methylation patterns presented by hypertriglyceridemic patients vs. control subjects. The cg03636183 in the F2RL3 gene was 10% hypomethylated in hypertriglyceridemic patients, and has previously been associated with an increased cardiovascular risk. Cg13824500 is 10% hypomethylated in hypertriglyceridemic patients and is located in VTI1A, which is a limiting gene in the transit of chylomicrons in the enterocyte through the endoplasmic reticulum and the Golgi apparatus. Cg26468118 in the RAB20 gene (13% hypomethylated) and cg21560722 in the SBF2 gene (33% hypermethylated) are involved in the regulation of Golgi apparatus vesicles.Our results suggest that there are differentially methylated regions related to the formation of chylomicrons in hypertriglyceridemic patients.

This is the fourth update of the therapeutic planning tables. These tables are a simple desktop tool, to help in determining the most appropriate oral cholesterol-lowering therapy for patient. This can either be with monotherapy or combination therapy (statins plus ezetimibe), taking into account the patient LDL cholesterol (LDL-C) and the therapeutic objective to be achieved. These therapeutic indications are based on 2 fundamental principles: the causality of LDL-C, and that the effect of cardiovascular protection depends on the decrease in LDL-C. It is based on a colour code that indicates the drugs that have the necessary power to meet the therapeutic objectives of the patient. We provide some recommendations on the strategy to follow to implement the most effective treatment. It is assessed up to what levels a decrease in LDL-C can be expected by adding a PCSK9 inhibitor.

Resumen Se presenta la cuarta actualizacion de las tablas de planificacion terapeutica. Esta tabla es una sencilla herramienta de sobremesa que permite determinar la terapia hipocolesterolemiante oral mas apropiada para su paciente, bien con monoterapia, bien con terapia combinada (estatinas mas ezetimiba), teniendo en cuenta su colesterol ligado a lipoproteinas de baja densidad (c-LDL) de partida y el objetivo terapeutico a alcanzar. Estas indicaciones terapeuticas se basan en 2 principios fundamentales: la causalidad del c-LDL y que el efecto de proteccion cardiovascular depende del descenso del c-LDL. Se han disenado como un codigo de colores que senala los farmacos que tienen la potencia necesaria para llevar a su paciente a objetivos terapeuticos. Se establecen unas recomendaciones sobre la estrategia a seguir para implementar el tratamiento mas eficaz. Tambien se muestra hasta que niveles podemos esperar un descenso de c-LDL al anadir un inhibidor de PCSK9.

One of the main goals of the Spanish Society of Arteriosclerosis is to contribute to a wider and greater knowledge of vascular disease, its prevention and treatment. Cardiovascular diseases are the leading cause of death in our country and also lead to a high degree of disability and health expenditure. Arteriosclerosis is a multifactorial disease, this is why its prevention requires a global approach that takes into account the different risk factors with which it is associated. Thus, this document summarizes the current level of knowledge and integrates recommendations and procedures to be followed for patients with established cardiovascular disease or high vascular risk. Specifically, this document reviews the main symptoms and signs to be evaluated during the clinical visit, the laboratory and imaging procedures to be routinely requested or those in special situations. It also includes the estimation of vascular risk, the diagnostic criteria of the different entities that are cardiovascular risk factors, and presents general and specific recommendations for the treatment of the different cardiovascular risk factors and their final objectives. Finally, the document includes aspects that are not often mentioned in the literature, such as the organisation of a vascular risk consultation.

Introduction and objectives PCSK9 inhibitors (PCSK9i) are safe and effective lipid-lowering drugs . Their main limitation is their high cost. The aim of this study was to estimate the number of patients eligible for treatment with PCSK9i according to distinct published criteria. Methods Data were obtained from the Information System for the Development of Research in Primary Care. Included patients were equal to or older than 18 years and had at least 1 low-density lipoprotein cholesterol measurement recorded between 2006 and 2014 (n = 2 500 907). An indication for treatment with PCSK9i was assigned according to the following guidelines: National Health System, Spanish Society of Arteriosclerosis , Spanish Society of Cardiology, National Institute for Health and Care Excellence, and the European Society of Cardiology/European Atherosclerosis Society Task Force. Lipid-lowering treatment was defined as optimized if it reduced low-density lipoprotein levels by ≥ 50% and adherence was > 80%. Results Among the Spanish population aged 18 years or older, the number of possible candidates to receive PCSK9i in an optimal lipid-lowering treatment scenario ranged from 0.1% to 1.7%, depending on the guideline considered. The subgroup of patients with the highest proportion of potential candidates consisted of patients with familial hypercholesterolemia , and the subgroup with the highest absolute number consisted of patients in secondary cardiovascular prevention. Conclusions The number of candidates to receive PCSK9i in conditions of real-world clinical practice is high and varies widely depending on the recommendations of distinct scientific societies.