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La cardiopatia arritmogènica de ventricle Esquerre (AVLC) és una afecció cardíaca que provoca el creixement del teixit fibrogras en aquest ventricle del cor. Aquesta malaltia pot arribar a provocar greus complicacions i inclús la mort sobtada de pacients joves. El coneixement d'aquesta malaltia és reduït, sobretot envers les seves afeccions als senyals electrocardiogràfics. La majoria de la informació que es coneix de la seva caracterització és sobre altres proves mèdiques, com la ressonància magnètica. En aquest projecte, una vegada es va portar a terme una investigació minuciosa sobre l'estat de l'art de la malaltia i els coneixements actuals, es va començar el desenvolupament del codi en Matlab. S'ha automatitzat el procés de detecció d'un llistat de biomarcadors mitjançant dos mètodes d'obtenció de marques: Single Lead (SL) i la Single Lead + Rule (SLR). Aquests biomarcadors són: el ritme cardíac, l'interval PR, el voltatge pic a pic, la duració del complex QRS, l'interval QT, l'interval QT corregit, l'àrea en valor absolut, l'energia i la potencia mitja del complex QRS. Posteriorment, s'hi ha elaborat dues anàlisis estadístiques, el codi del qual també ha estat automatitzat. En aquestes proves s'ha comparat els registre electrocardiogràfics de diferents grups amb la intenció de caracteritzar la malaltia. La primera anàlisi és una comparació entre registres d'un mateix pacient amb una diferència temporal entre els ECGs. El segon anàlisis elabora una comparació entre registre de dos grups de pacients amb diferents característiques. Els resultats mostren que els biomarcadors del voltatge pic a pic, l'àrea en valor absolut, l'energia i la potència del QRS mostren diferències significatives a major diferència de temps entre registres; disminuint el seu valor amb el temps. Per altra banda, els resultats de l'anàlisi intergrupal entre homes i dones, i hipertensos i no hipertensos; no mostren diferències significatives. La cardiopatía arritmogénica de ventrículo izquierdo (AVLC) es una afección cardíaca que provoca un crecimiento del tejido fibrograso en este ventrículo del corazón. Esta enfermedad puede llegar a provocar complicaciones graves o incluso muerte súbita en pacientes jóvenes. El conocimiento al respecto es reducido, sobretodo sobre su afección sobre las señales electrocardiográficas. La mayoría de la información se conoce sobre su caracterización en otras pruebas médicas, como la resonancia magnética. En este proyecto, una vez se llevó a cabo una investigación minuciosa sobre el estado del arte de la enfermedad y los conocimientos actuales, se empezó el desarrollo de código en Matlab. Se automatizó el proceso de detección de un listado de biomarcadores mediante dos métodos de detección de marcas: la Single Lead (SL) y la Single Lead + Rule (SLR). Estos biomarcadores son: el ritmo cardiaco, el intervalo PR, el voltaje pico a pico, la duración del complejo QRS, el intervalo QT, el intervalo QT corregido, el área en valor absoluto, la energía y la potencia media del complejo QRS. Posteriormente, se realizó dos análisis estadísticos, cuyo código también está automatizado. En estas pruebas se comparan registros electrocardiográficos de diferentes grupos con la intención de caracterizar la enfermedad. El primer análisis es una comparación entre registros de un mismo paciente con una diferencia temporal entre los ECGs. El segundo análisis efectúa una comparación entre registros de grupos de pacientes con diferentes características. Los resultados muestran que los biomarcadores del voltaje pico a pico, el área en valor absoluto, la energía y la potencia media del QRS, muestran diferencias significativas a mayor diferencia de tiempo entre registros; disminuyendo sus valores con el tiempo. Por otra banda, los resultados del análisis intergrupal entre hombres y mujeres, e hipertensos y no hipertensos no muestran diferencias significativas. Arrhythmogenic left ventricular cardiomyopathy (AVLC) is a heart condition that causes the growth of fibro-fatty tissue in this ventricle. This disease can lead to severe complications, even sudden death in young patients. And the knowledge about this illness is limited, especially in relation to electrocardiographs. Thus, most information about its characterization is about other medical tests, such as magnetic resonance imaging. Firstly, it was carried out a thorough investigation of the state of the art of the disease and current knowledge. Secondly, the code development in Matlab was started about the signal processing. The process of detecting a list of biomarkers was automated using two methods of tag detection: Single Lead (SL) and Single Lead + Rule (SLR). These biomarkers are: heart rate, PR interval, peak-to-peak voltage, QRS complex duration, QT interval, corrected QT interval, the absolute area, energy and mean QRS complex power. Subsequently, two statistical analyses have been performed, also with automated code. These tests compare electrocardiographic recordings from different groups with the intention of characterizing the disease. The first analysis is between recordings from the same patient with a time difference between ECGs. The second analysis is a comparison of recordings from groups of patients with different characteristics. The results show that the biomarkers of peak-to-peak voltage, absolute area, energy and the power of the QRS show significant differences with the increment of time; when their values gradually decrease. On the other hand, the results of the intergroup analysis between men and women, and hypertensives and non-hypertensives show no significant differences.

Aims A Markov model was adapted to assess the real-world cost-effectiveness of rivaroxaban, dabigatran and apixaban. Each of these non-vitamin K antagonist oral anticoagulants was compared with vitamin K antagonist for stroke prevention in patients with non-valvular atrial fibrillation in Spain. Methods All inputs were derived from real-world studies: baseline patient characteristics, clinical event rates, as well as persistence rates for the vitamin K antagonist treatment option. A meta-analysis of real-world studies provided treatment effect and persistence data for rivaroxaban, dabigatran and apixaban, each compared with vitamin K antagonist therapy. The model considered 3-month cycles over a lifetime horizon. The model outcomes included different costs, quality-adjusted life years and life-years gained. Sensitivity analyses were performed to test the robustness of the model. Results When compared with vitamin K antagonist, rivaroxaban incurred incremental costs of €77 and resulted in incremental quality-adjusted life years of 0.08. The incremental cost per quality-adjusted life year was €952. For the same comparison, the incremental cost per quality-adjusted life year for dabigatran was €4,612. Finally, compared with vitamin K antagonist, the incremental cost per quality-adjusted life year for apixaban was €32,015. The sensitivity analyses confirmed the robustness of the base case results. The probabilities to be cost-effective versus vitamin K antagonist were 94%, 86% and 35%, respectively, for rivaroxaban, dabigatran and apixaban, considering a willingness-to-pay threshold of €22,000 per quality-adjusted life year gained, based on a cost-effectiveness study of the Spanish National Health System. Conclusion These results suggest that rivaroxaban and dabigatran are cost-effective versus vitamin K antagonist for stroke prevention in non-valvular atrial fibrillation, from the Spanish National Health System perspective.

The mechanisms leading to cardiac remodeling in Marfan syndrome (MFS) are a matter of debate since it could be either due to structural dysfunction of the myocardial extracellular matrix or to increased afterload caused by the dilated aorta. We aim to characterize the presence of abnormal myocardial function in MFS and to investigate its potential association with increased afterload. Aorta, left ventricle (LV) and the postsystolic thickening (PST) were analyzed in echocardiography in Fbn1C1039G/+ mice and in patients with MFS in comparison with wild type (WT) mice and healthy humans. PST was more frequent in MFS than in WT mice (p

Developing children are particularly vulnerable to the effects of exposure to per- and polyfluoroalkyl substances (PFAS), a group of endocrine disrupting chemicals. We hypothesized that early life exposure to PFASs is associated with poor metabolic health in children. We studied the association between prenatal and postnatal PFASs mixture exposure and cardiometabolic health in children, and the role of inflammatory proteins. In 1,101 mothers-child pairs from the Human Early Life Exposome project, we measured the concentrations of PFAS in blood collected in pregnancy and at 8 years (range = 6-12 years). We applied Bayesian Kernel Machine regression (BKMR) to estimate the associations between exposure to PFAS mixture and the cardiometabolic factors as age and sex- specific z-scores of waist circumference (WC), systolic and diastolic blood pressures (BP), and concentrations of triglycerides (TG), high-density lipoprotein (HDL-C) and low-density lipoprotein (LDL-C) cholesterol. We measured thirty six inflammatory biomarkers in child plasma and examined the underlying role of inflammatory status for the exposure-outcome association by integrating the three panels into a network. Exposure to the PFAS mixture was positively associated with HDL-C and systolic BP, and negatively associated with WC, LDL-C and TG. When we examined the independent effects of the individual chemicals in the mixture, prenatal PFHxS was negatively associated with HDL-C and prenatal PFNA was positively associated with WC and these were opposing directions from the overall mixture. Further, the network consisted of five distinct communities connected with positive and negative correlations. The selected inflammatory biomarkers were positively, while the postnatal PFAS were negatively related with the included cardiometabolic factors, and only prenatal PFOA was positively related with the pro-inflammatory cytokine IL-1beta and WC. Our study supports that prenatal, rather than postnatal, PFAS exposure might contribute to an unfavorable lipidemic profile and adiposity in childhood. This work was supported by the Norwegian Research Council under the MILJØFORSK-Miljøforskning for en grønn samfunnsomstilling call (project No. 268465-short name: "CATCHUP project"). The HELIX project is funded by the European Community's Seventh Framework Programme (FP7/2007–2013) under grant agreement no 308,333 – the HELIX project. The HELIX program is built on six existing cohorts that received previous funding. The Born in Bradford (BiB) study presents independent research commissioned by the National Institute for Health Research Collaboration for Applied Health Research and Care (NIHR CLAHRC) and the Programme Grants for Applied Research funding scheme (RP-PG-0407–10044). INMA data collections were supported by grants from the Instituto de Salud Carlos III, CIBERESP, and the Generalitat de Catalunya-CIRIT. KANC was funded by the grant of the Lithuanian Agency for Science Innovation and Technology (6–04-2014_31V-66). Dr. Maribel Casas received funding from Instituto de Salud Carlos III (Ministry of Economy and Competitiveness) (MS16/00128). Dr. Leda Chatzi was supported by NIH/NIHES R01 ES029944, R01ES030691, R01ES030364, R21 ES029681, R21 ES028903, and P30 ES007048-23. Dr. David Conti was supported by P01CA196569, R01CA140561, R01 ES016813, R01 ES029944, R01ES030691, R01ES030364. Dr. Nikos Stratakis was supported by NIH/NIHES R21 ES029681 and P30 ES007048-23, and NIH/NIDDK P30 DK048522-24. The CRG/UPF Proteomics Unit is part of the Spanish Infrastructure for Omics Technologies (ICTS OmicsTech) and it is a member of the ProteoRed PRB3 consortium which is supported by grant PT17/0019 of the PE I + D + i 2013–2016 from the Instituto de Salud Carlos III (ISCIII) and ERDF. ISGlobal affiliated researchers acknowledge support from the Spanish Ministry of Science, Innovation and Universities, “Centro de Excelencia Severo Ochoa 2013–2017”, SEV-2012–0208, and “Secretaria d’Universitats i Recerca del Departament d’Economia i Coneixement de la Generalitat de Catalunya” (2017SGR595)

El síndrome de Brugada es una patología cardiaca eléctrica primaria genéticamente determinada. Esta se caracteriza por alteraciones electrocardiográficas distintivas, en donde el paciente puede llegar a presentar muerte súbita cardiaca secundaria a taquicardia ventricular polimórfica/ fibrilación ventricular, afectando mayormente a personas en la cuarta década de la vida. Pese a la creciente información sobre el síndrome de Brugada, en la actualidad persisten controversias en los ámbitos como la base fisiopatológica o en el de estratificación de riesgo arrítmico en pacientes asintomáticos. El presente estudio se basa en la evaluación de la variabilidad de la frecuencia cardiaca (VFC) como método electrocardiográfico simple y no invasivo para evaluar el equilibrio simpatico-vagal, con el fin de detectar diferencias entre los periodos diurnos y nocturnos, diferencias entre hombres y mujeres que padecen del síndrome de Brugada y diferencias entre aquellos pacientes sintomáticos de los asintomáticos. La VFC implica el uso de métricas en el dominio del tiempo que se aplican de manera directa a la serie de tiempo de intervalos RR. La métrica más evidente es el promedio de los intervalos RR (𝑅����𝑅����̅̅̅̅). La desviación estándar de los intervalos NN (SDNN) reflejan la variación global dentro de la serie RR. Cuando se mide la VFC en un tiempo determinado, se utiliza como indicadores la raíz cuadrática media de las diferencias sucesivas de intervalos NN (RMSSD). En el análisis espectral de la VFC, se analizan los componentes HF Y LF, donde el HF, proviene de las arritmias sinusales respiratorias, que es cuando hay una oscilación de alta frecuencia entre 0.15 y 0.4 Hz, relacionada con las fases de respiración y mediada casi que por la actividad parasimpática del nódulo sinoauricular. El otro componente, se relaciona con la presión sanguínea, que es cuando hay una oscilación de baja frecuencia (LF) entre 0.04 y 0.15 Hz considerada de origen simpático y parasimpático. Al ser las oscilaciones poco pronunciadas y los picos en el espectro de potencia son indistinguibles, se cuantifica en su lugar la potencia en las bandas de frecuencia LF y HF. Un aumento en la potencia LF se asocia a un aumento de la actividad simpática y contrariamente un aumento en la potencia HF se asocia a un aumento de la actividad parasimpática y la relacion entre estas dos variables LF/HF, se utiliza como indicador del equilibrio autonómico. Los resultados obtenidos de los intervalos diurnos y nocturnos de 5 minutos de los registros de ECG de 24 horas de los 32 pacientes con Sindrome de Brugada, muestran valores más altos de la VFC durante la noche que durante el día, así como también una VFC más baja en pacientes sintomáticos en comparación con asintomáticos. También se ha podido observar un aumento del tono vagal nocturno. Sin embargo, no hubo diferencias significativas, en cuanto a sexo y sintomatología, debido a las limitaciones del estudio, debido a que había muy pocos participantes femeninos y sintomáticos. La síndrome de Brugada és una patologia cardíaca elèctrica primària genèticament determinada. Aquesta es caracteritza per alteracions electrocardiogràfiques distintives, on el pacient pot arribar a presentar mort sobtada cardíaca secundària a taquicàrdia ventricular polimòrfica / fibril·lació ventricular, afectant principalment a persones en la quarta dècada de la vida. Tot i la creixent informació sobre la síndrome de Brugada, en l'actualitat persisteixen controvèrsies en els àmbits com la base fisiopatològica o en el d'estratificació de risc arrítmic en pacients asimptomàtics. El present estudi es basa en l'avaluació de la variabilitat de la freqüència cardíaca (VFC) com a mètode electrocardiogràfic simple i no invasiu per avaluar l'equilibri simpàtic-vagal, per tal de detectar diferències entre els períodes diürns i nocturns, diferències entre homes i dones que pateixen de la síndrome de Brugada i diferències entre aquells pacients simptomàtics dels asimptomàtics. La VFC implica l'ús de mètriques en el domini de el temps que s'apliquen de manera directa a la sèrie de temps d'intervals RR. La mètrica més evident és la mitjana dels intervals RR ((𝑅��𝑅��̅̅̅̅) ).La desviació estàndard dels intervals NN (SDNN) reflecteixen la variació global dins de la sèrie RR. Quan es mesura la VFC en un temps determinat, s'utilitza com a indicadors l'arrel quadràtica mitjana de les diferències successives d'intervals NN (RMSSD). En l'anàlisi espectral de la VFC, s'analitzen els components HF I LF, on el HF, prové de les arítmies sinusals respiratòries, que és quan hi ha una oscil·lació d'alta freqüència entre 0.15 i 0.4 Hz, relacionada amb les fases de respiració i intervinguda gairebé que per l'activitat parasimpàtica de l'nòdul sinoauricular. L'altre component, es relaciona amb la pressió sanguínia, que és quan hi ha una oscil·lació de baixa freqüència (LF) entre 0.04 i 0.15 Hz considerada d'origen simpàtic i parasimpàtic. A l'ésser les oscil·lacions poc pronunciades i els pics en l'espectre de potència són indistingibles, es quantifica en el seu lloc la potència en les bandes de freqüència LF i HF. Un augment en la potència LF s'associa a un augment de l'activitat simpàtica i contràriament un augment en la potència HF s'associa a un augment de l'activitat parasimpàtica i la relació entre aquestes dues variables LF / HF, s'utilitza com a indicador de l'equilibri autonòmic . Els resultats obtinguts dels intervals diürns i nocturns de 5 minuts dels registres d'ECG de 24 hores dels 32 pacients amb Síndrome de Brugada, mostren valors més alts de la VFC durant la nit que durant el dia, així com també una VFC mes baixa en pacients simptomàtics en comparació amb asimptomàtics. També s'ha pogut observar un augment de el to vagal nocturn. No obstant això, no hi va haver diferències significatives, pel que fa a sexe i simptomatologia, a causa de les limitacions de l'estudi, pel fet que havien molt pocs participants femenins i simptomàtics. Brugada syndrome is a genetically determined primary electrical cardiac pathology. It is characterized by distinctive electrocardiographic alterations, in which the patient may present sudden cardiac death secondary to polymorphic ventricular tachycardia/ventricular fibrillation, affecting mostly people in the fourth decade of life. Despite the growing information on Brugada syndrome, controversies persist in areas such as the pathophysiological basis or arrhythmic risk stratification in asymptomatic patients. The present study is based on the evaluation of heart rate variability (HRV) as a simple, noninvasive electrocardiographic method to assess sympathovagal balance, in order to detect differences between daytime and nighttime periods, differences between men and women with Brugada syndrome, and differences between those patients who are symptomatic and those who are asymptomatic. HRV involves the use of time domain metrics that apply directly to the time series of RR intervals. The most obvious metric is the average of RR intervals ((𝑅�𝑅�̅̅̅̅) ). The standard deviation of NN intervals (SDNN) reflect the overall variation within the RR series. When measuring HRV at a given time, the root mean square root of successive NN interval differences (RMSSD). In the spectral analysis of HRV, the HF and LF components are analyzed, where HF comes from respiratory sinus arrhythmias, which is when there is a high frequency oscillation between 0.15 and 0.4 Hz, related to the respiratory phases and mediated almost exclusively by the parasympathetic activity of the sinoatrial node. The other component, related to blood pressure, when there is a low frequency oscillation (LF) between 0.04 and 0.15 Hz considered to be of sympathetic and parasympathetic origin. As the oscillations are not very pronounced and the peaks in the power spectrum are indistinguishable, power in the LF and HF frequency bands is quantified instead. An increase in LF power is associated with an increase in sympathetic activity and conversely an increase in HF power is associated with an increase in parasympathetic activity and the ratio between these two variables, LF/HF used as an indicator of autonomic balance. The results obtained from the daytime and night time 5-minute intervals of the 24-hour ECG recordings of the 32 patients with Brugada Syndrome show higher HRV values during the night than during the day, as well as lower HRV in symptomatic patients compared to asymptomatic patients. Increased nocturnal vagal tone could also be observed. However, there were no significant differences, in terms of sex and symptomatology, due to the limitations of the study, because there were very few female and symptomatic participants.

During cardiac diseases many types of anatomical and functional remodeling of cardiac tissue can occur. In this work, we focus on two conditions: hypoxia and fibrosis, which are part of complex pathological modifications that take place in many cardiac diseases (hypertrophic cardiomyopathy, hypertensive heart disease, and recurrent myocardial infarction) and respiratory diseases (obstructive pulmonary disease, obstructive sleep apnea, and cystic fibrosis). Using computational models of cardiac electrophysiology, we evaluate if the interplay between hypoxia and fibrosis is sufficient to trigger cardiac arrhythmia. We study the mechanisms behind the generation of ectopic beats, an arrhythmic trigger also known as premature ventricular contractions (PVCs), in regions with high hypoxia and fibrosis. First, we modify an electrophysiological model of myocytes of the human left ventricle to include the effects of hypoxia. Second, diffuse fibrosis is modeled by randomly replacing cardiac myocytes by non-excitable and non-conducting cells. The Monte Carlo method is used to evaluate the probability of a region to generate ectopic beats with respect to different levels of hypoxia and fibrosis. In addition, we evaluate the minimum size of three-dimensional slabs needed to sustain reentries for different stimulation protocols. The observed mechanism behind the initiation of ectopic beats is unidirectional block, giving rise to sustained micro-reentries inside the region with diffuse fibrosis and hypoxia. In summary, our results suggest that hypoxia and fibrosis are sufficient for the creation of a focal region in the heart that generates PVCs. We acknowledge support from CAPES by the grant 88881.065002/2014-01 of the Brazilian program Science without borders, and from MINECO of Spain under the Ramon y Cajal program with the grant number RYC-2012-11265

DOI: 10.1016/j.ijcard.2016.04.184 Background/objectives The mechanisms underlying aortic dilation in bicuspid aortic valve (BAV) disease are unknown. Circulating endothelial microparticles (EMPs) have emerged as biomarkers of endothelial damage. We sought to evaluate the relationships among EMPs, BAV disease, and aortic dilation. Methods Four evaluations were used. Circulating EMPs (PECAM+, E-selectin+) were compared between BAV patients and tricuspid aortic valve (TAV) control subjects. The variables related to circulating EMPs were investigated in BAV patients. Circulating EMP levels were compared between BAV and TAV patients with a dilated aorta. Finally, circulating EMPs in BAV patients were evaluated over time with respect to aortic valve surgery (AVS) or aortic surgery. Results We observed higher levels of circulating PECAM+ EMPs in the BAV patients than in the control subjects (3.98 ± 0.2 vs. 2.39 ± 0.4 per log PECAM+ EMPs/μl, p = 0.001). Aortic dilation was the most significant variable that correlated with the PECAM+ EMP levels in the BAV patients (β = 0.321, p = 0.008). The BAV patients with aortic dilation exhibited higher PECAM+ EMP levels than the TAV patients with dilated aortas, and this correlation was independent of aortic valve function. We observed a drastic decrease in the circulating PECAM+ EMPs following AVS and aortic root replacement (4.27 ± 0.6 and 1.75 ± 0.3 per log PECAM+ EMPs/μl, p = 0.002). Conclusion The observed pattern of higher circulating PECAM+ EMP levels links BAV disease to endothelial damage and aortic dilation. Circulating PECAM+ EMPs were identified as a biological variable related to aortic dilation in patients with BAV disease.

DOI: 10.1016/j.ijcard.2016.04.184 Background/objectives The mechanisms underlying aortic dilation in bicuspid aortic valve (BAV) disease are unknown. Circulating endothelial microparticles (EMPs) have emerged as biomarkers of endothelial damage. We sought to evaluate the relationships among EMPs, BAV disease, and aortic dilation. Methods Four evaluations were used. Circulating EMPs (PECAM+, E-selectin+) were compared between BAV patients and tricuspid aortic valve (TAV) control subjects. The variables related to circulating EMPs were investigated in BAV patients. Circulating EMP levels were compared between BAV and TAV patients with a dilated aorta. Finally, circulating EMPs in BAV patients were evaluated over time with respect to aortic valve surgery (AVS) or aortic surgery. Results We observed higher levels of circulating PECAM+ EMPs in the BAV patients than in the control subjects (3.98 ± 0.2 vs. 2.39 ± 0.4 per log PECAM+ EMPs/μl, p = 0.001). Aortic dilation was the most significant variable that correlated with the PECAM+ EMP levels in the BAV patients (β = 0.321, p = 0.008). The BAV patients with aortic dilation exhibited higher PECAM+ EMP levels than the TAV patients with dilated aortas, and this correlation was independent of aortic valve function. We observed a drastic decrease in the circulating PECAM+ EMPs following AVS and aortic root replacement (4.27 ± 0.6 and 1.75 ± 0.3 per log PECAM+ EMPs/μl, p = 0.002). Conclusion The observed pattern of higher circulating PECAM+ EMP levels links BAV disease to endothelial damage and aortic dilation. Circulating PECAM+ EMPs were identified as a biological variable related to aortic dilation in patients with BAV disease.

Background No comparisons have been made of scales estimating cardiovascular mortality and overall cardiovascular morbidity and mortality. The study objectives were to assess the agreement between the Framingham-D'Agostino cardiovascular risk (CVR) scale and the chart currently recommended in Europe (SCORE) with regard to identification of patients with high CVR, and to describe the discrepancies between them and the attendant implications for the treatment of hypertension and hyperlipidaemia. Methods A total of 474 hypertensive patients aged 40–65 years monitored in primary care were enrolled into the study. CVR was assessed using the Framingham-D'Agostino scale, which estimates the overall cardiovascular morbidity and mortality risk, and the SCORE chart, which estimates the cardiovascular mortality risk. Cardiovascular risk was considered to be high for values ≥ 20% and ≥ 5% according to the Framingham-D'Agostino and SCORE charts respectively. Kappa statistics was estimated for agreement in classification of patients with high CVR. The therapeutic recommendations in the 2007 European Guidelines on Cardiovascular Disease Prevention were followed. Results Mean patient age was 54.1 (SD 7.3), and 58.4% were males. A high CVR was found in 17.5% using the SCORE chart (25.3% males, 6.6% females) and in 32.7% using the D'Agostino method (56.9% males, 12,7% females). Kappa coefficient was 0.52, and increased to 0.68 when the high CVR threshold was established at 29% according to D'Agostino. Hypertensive patients with high SCORE and non-high D'Agostino (1.7%) were characterized by an older age, diabetes, and a lower atherogenic index, while the opposite situation (16.9%) was associated to males, hyperlipidaemia, and a higher atherogenic index. Variables with a greater weight in discrepancies were sex and smoking. A 32.0% according to SCORE and 33.5% according to D'Agostino would be candidates to receive antihypertensive treatment, and 15.8% and 27.3% respectively to receive lipid-lowering treatment. Conclusion A moderate to high agreement was found. SCORE may underestimate risk in males with an unfavourable lipid profile, and D'Agostino in diabetics with a lower atherogenic risk. Use of the D'Agostino scale implies treating more patients with lipid-lowering and antihypertensive drugs as compared to SCORE.