Informe de Bellagio sobre agricultura saludable, nutrición saludable, población saludable / Bellagio report on healthy agriculture, healthy nutrition, healthy people

El informe del Bellagio sobre Agricultura Saludable, Nutrición Saludable, Población Saludable es el resultado de la reunión mantenida en el Centro Bellagio de la Fundación Rockefeller en el Lago de Como en Italia, entre el 29 de Octubre y el 2 de Noviembre de 2012. La reunión basada en la ciencia, fue orientada hacia la política. Se discutió extensamente el papel y la cantidad de grasas saludables y perjudiciales, con atención al contenido relativo de los ácidos grasos omega-3 y omega-6, el azúcar, y particularmente la fructosa en los alimentos que pueden conllevar la epidemia de enfermedades no transmisibles (EnT) a través del mundo. El informe concluye que el consumo del azúcar, especialmente en forma de fructosa de alta energía utiizada en bebidas refrescantes, posee una amenaza muy importante de la salud, especialmente en niños, y la mayoría de las dietas, aunque con diferencias regionales, son deficientes en ácidos grasos omega-3 y demasiado altas en ácidos grasos omega-6. Las interacciones gen-nutriente en el crecimiento y desarrollo y en la prevención de la enfermedad son fundamentales para la salud, por lo que deberían establecerse a través de todo el mundo Centros regionales de Genética, Nutrición y Condición Física para la Salud. Los jefes de estado y gobierno deben priorizar dentro de sus nacionales de forma urgente la Nutrición, cuyo acceso a una dieta saludable debería considerarse un derecho humano y dirigir la responsabilidad para que la Nutrición tenga un lugar en los Ministerios de Salud, más que la agricultura de modo que los requerimientos de salud conduzcan a prioridades agrícolas, y no viceversa. La seguridad nutricional debería ser considerada como prioridad como lo es la seguridad alimentaria (AU)

The Bellagio Report on Healthy Agriculture, Healthy Nutrition, Healthy People is the result of the meeting held at the Rockefeller Foundation Bellagio Center in Lake Como, Italy, 29 October-2 November 2012. The meeting was science-based but policy-oriented. The role and amount of healthy and unhealthy fats, with attention to the relative content of omega-3 and omega-6 fatty acids, sugar, and particularly fructose in foods that may underlie the epidemics of non-communicable diseases (NCD's) worldwide were extensively discussed. The report concludes that sugar consumption, especially in the form of high energy fructose in soft drinks, poses a major and insidious health threat, especially in children, and most diets, although with regional differences, are deficient in omega-3 fatty acids and too high in omega-6 fatty acids. Gene-nutrient interactions in growth and development and in disease prevention are fundamental to health, therefore regional Centers on Genetics, Nutrition and Fitness for Health should be established worldwide. Heads of state and government must elevate, as a matter of urgency, Nutrition as a national priority, that access to a healthy diet should be considered a human right and that the lead responsibility for Nutrition should be placed in Ministries of Health rather than agriculture so that the health requirements drive agricultural priorities, not vice versa. Nutritional security should be given the same priority as food security (AU)

Atrial fibrillation and upper limb thromboembolectomy: a national cohort study.

BACKGROUND: The risk factors associated with, and the incidence of systemic embolism in patients with atrial fibrillation (AF) are poorly understood. OBJECTIVES: We studied the association between AF and upper limb thromboembolectomy involving brachial, ulnar or radial artery in a national cohort study that included all individuals aged 40-99 years with incident AF. METHODS: Data were retrieved from the Danish National Vascular Registry, the National Registry of Patients, the Danish Civil Registration System and Statistics Denmark. RESULTS: In total, 131,476 patients (68,042 men and 63,434 women) with AF without previous thromboembolectomy in the upper limb were registered. In the study cohort, 130 men underwent upper limb thromboembolectomy over 220,890 person-years of observation, whilst 275 women underwent thromboembolectomy over 197,777 patient-years. The incidence per 100,000 person-years was 58.9 (95% CI, 49.2-69.8) for men and 139.1 (95% CI, 123.1-156.5) for women. The relative risk of thromboembolectomy among patients with AF compared to the background population was 7.5 (95% CI, 6.3-8.9) for men, and 9.3 (95% CI, 8.3-10.5) for women. Women with AF had a relative thromboembolectomy risk of 1.8 (95% CI, 1.5-2.3) compared to men with AF. Among patients with AF, history of hypertension (HR 2.2-2.9), myocardial infarction (HR 2.9-3.9), heart failure (HR 1.6-1.9) and stroke (HR 2.2-3.8) were significantly associated with increased risk of thromboembolectomy in both men and women. CONCLUSIONS: AF substantially increases the risk of upper limb thromboembolectomy. This risk is higher with increasing age, female gender, and associated with hypertension, myocardial infarction, heart failure and stroke.

Upper-limb thrombo-embolectomy: national cohort study in Denmark.

OBJECTIVES: We investigated the incidence of thrombo-embolectomy in upper-limb and prognosis with respect to arm amputation, stroke and death. METHODS: We performed a national cohort study of individuals, aged 40-99 years, and undergoing first-time thrombo-embolectomy in the brachial, ulnar or radial artery in Denmark from 1990 to 2002. The data were retrieved from the National Vascular Registry and from the National Registry of Patients and the Civil Registration System. Patients were followed until 2006 to ascertain the occurrence of amputation and stroke and until 2007 with respect to death. RESULTS: In total, 1377 incident cases of thrombo-embolectomy were registered, comprising 504 (36.6%) males with a mean age of 72.0 (standard deviation (SD) 12.4) years and 873 (63.4%) females with a mean age of 77.2 (SD 11.7) years. Incidence was 3.3 (95% confidence interval (CI): 3.1-3.7) for males and 5.2 (95% CI: 4.9-5.6) for females per 100000 person-years. After thrombo-embolectomy, upper-limb amputation was performed in 11 (incidence 2.2%; 95% CI: 1.2-3.4) males and 31 (3.6%; 95% CI: 2.5-4.9) females. Age- and sex-specific risk of stroke was 2-16 times higher, and risk of death 3-11 times higher, than in the general population. CONCLUSIONS: Upper-limb thrombo-embolectomy is associated with an increased risk of limb amputation, stroke and death.

Cardiovascular outcomes and their relationships to lipoprotein components in patients with and without chronic kidney disease: results from the IDEAL trial.

OBJECTIVES: In Incremental Decrease in Endpoints through Aggressive Lipid-lowering (IDEAL), we compared cardiovascular outcomes in patients with and without chronic kidney disease (CKD) (estimated glomerular filtration rate <60 mL min(-1) 1.73 m(-2)) and analysed relationships between lipoprotein components (LC) and major coronary events (MCE) and other cardiovascular (CV) events. DESIGN: Exploratory analysis of CV endpoints in a randomized trial comparing high dose of atorvastatin to usual dose of simvastatin on MCE. SETTINGS: Patients with CKD were compared with the non-CKD patients. Cox regression models were used to study the relationships between on-treatment levels of LC and incident MCE. FINDINGS: Chronic kidney disease was strongly associated with cardiovascular end-points including total mortality. In patients with CKD, a significant benefit of high dose atorvastatin treatment was found for any CV events, stroke and peripheral artery disease, but not for MCE. However, all cardiovascular end-points except stroke and CV mortality were reduced in the non-CKD group. Differential changes in LC or relationships to LC could not explain the different treatment outcomes in MCE in the two groups. INTERPRETATION: Chronic kidney disease was a powerful risk factor for all cardiovascular end-points. The reason why the significant reductions achieved by high-dose statin treatment in most CV end-points in the non-CKD group were only in part matched by similar reductions in the CKD patients is not apparent. This difference did not result from differential changes in or relations to LC, but limited power may have increased the possibility of chance findings.

Nurse-coordinated multidisciplinary, family-based cardiovascular disease prevention programme (EUROACTION) for patients with coronary heart disease and asymptomatic individuals at high risk of cardiovascular disease: a paired, cluster-randomised controlled trial.

BACKGROUND: Our aim was to investigate whether a nurse-coordinated multidisciplinary, family-based preventive cardiology programme could improve standards of preventive care in routine clinical practice. METHODS: In a matched, cluster-randomised, controlled trial in eight European countries, six pairs of hospitals and six pairs of general practices were assigned to an intervention programme (INT) or usual care (UC) for patients with coronary heart disease or those at high risk of developing cardiovascular disease. The primary endpoints-measured at 1 year-were family-based lifestyle change; management of blood pressure, lipids, and blood glucose to target concentrations; and prescription of cardioprotective drugs. Analysis was by intention to treat. The trial is registered as ISRCTN 71715857. FINDINGS: 1589 and 1499 patients with coronary heart disease in hospitals and 1189 and 1128 at high risk were assigned to INT and UC, respectively. In patients with coronary heart disease who smoked in the month before the event, 136 (58%) in the INT and 154 (47%) in the UC groups did not smoke 1 year afterwards (difference in change 10.4%, 95% CI -0.3 to 21.2, p=0.06). Reduced consumption of saturated fat (196 [55%] vs 168 [40%]; 17.3%, 6.4 to 28.2, p=0.009), and increased consumption of fruit and vegetables (680 [72%] vs 349 [35%]; 37.3%, 18.1 to 56.5, p=0.004), and oily fish (156 [17%] vs 81 [8%]; 8.9%, 0.3 to 17.5, p=0.04) at 1 year were greatest in the INT group. High-risk individuals and partners showed changes only for fruit and vegetables (p=0.005). Blood-pressure target of less than 140/90 mm Hg was attained by both coronary (615 [65%] vs 547 [55%]; 10.4%, 0.6 to 20.2, p=0.04) and high-risk (586 [58%] vs 407 [41%]; 16.9%, 2.0 to 31.8, p=0.03) patients in the INT groups. Achievement of total cholesterol of less than 5 mmol/L did not differ between groups, but in high-risk patients the difference in change from baseline to 1 year was 12.7% (2.4 to 23.0, p=0.02) in favour of INT. In the hospital group, prescriptions for statins were higher in the INT group (810 [86%] vs 794 [80%]; 6.0%, -0.5 to 11.5, p=0.04). In general practices in the intervention groups, angiotensin-converting enzyme inhibitors (297 [29%] INT vs 196 [20%] UC; 8.5%, 1.8 to 15.2, p=0.02) and statins (381 [37%] INT vs 232 [22%] UC; 14.6%, 2.5 to 26.7, p=0.03) were more frequently prescribed. INTERPRETATION: To achieve the potential for cardiovascular prevention, we need local preventive cardiology programmes adapted to individual countries, which are accessible by all hospitals and general practices caring for coronary and high-risk patients.

[Familial hypercholesterolemia in St. Petersburg: diversity of mutations argues against a strong founder effect].

Examination of low-density lipoprotein (LDL) receptor, its promoter, and major exon-intron boundaries from a sample of patients with familial hypercholesterolemia (FH) from 74 probands of St. Petersburg revealed 34 mutations and 8 widely spread polymorphisms at this locus. Only four mutations were considered silent, while the other 30 are likely associated with familial hypercholesterolemia (FH). Mutations in the LDL receptor gene, inducing the disease, were identified in 41 (55%) out of 74 families with FH. Mutation R3500Q in apolipoprotein B (APOB) gene was not detected in all probands. Therefore in the families lacking mutations hypercholesterolemia was induced by mutations in the introns of the LDL receptor gene or by other genetic factors. Nineteen mutations causing disease progression were described in St. Petersburg for the first time, while 18 of them are specific for Russia. Among Ashkenazi Jews, major mutation G197del was detected in 30% (7 out of 22) of patients with FH. In the Slavic population of St. Petersburg, no major mutations were detected. Only five mutations were identified in two families, while 24 were found in isolated families. These data are indicative of the lack of a strong founder effect for FH in the St. Petersburg population.

Danish singles have a twofold risk of acute coronary syndrome: data from a cohort of 138 290 persons.

STUDY OBJECTIVE: Atherosclerosis of the coronary and other arteries is an important health problem in virtually all countries of the world, and thus there is a persisting need for the development of preventive programmes including population risk group identification. The aim of the study was to identify sociodemographic population risk indicators of an initial episode of acute coronary syndrome (ACS), including unstable angina pectoris (UAP), myocardial infarction (MI), and sudden cardiac death (SCD). DESIGN: Cohort study of 138 290 residents of the municipality of Aarhus, Denmark, aged 30-69 years. Information on population members' individual age, sex, social background, and eventual death was obtained from Danish Population Registers. SETTING: University hospital. PATIENTS: The study prospectively identified 646 victims of ACS from 1 April 2000 to 31 March 2002. MAIN RESULTS: Based on multiple logistic regression, age and single living were found to be positively associated with incident ACS in both sexes. Women >60 years living alone and men >50 years living alone were at especially high risk. They constituted only 5.4% and 7.7% of the source population, respectively, but they accounted for 34.3% and 62.4% of ACS patients dying within 30 days. CONCLUSIONS: Single living is associated with an increased risk of ACS. Thus, risk groups identified by use of information on their age and family structure may be targets for future more focused and cost effective preventive strategies. In Western populations, such high risk groups will constitute comparatively limited parts of the population, and in Denmark they are easily identifiable in routine population registers.

Apo B versus cholesterol in estimating cardiovascular risk and in guiding therapy: report of the thirty-person/ten-country panel.

There is abundant evidence that the risk of atherosclerotic vascular disease is directly related to plasma cholesterol levels. Accordingly, all of the national and transnational screening and therapeutic guidelines are based on total or LDL cholesterol. This presumes that cholesterol is the most important lipoprotein-related proatherogenic risk variable. On the contrary, risk appears to be more directly related to the number of circulating atherogenic particles that contact and enter the arterial wall than to the measured concentration of cholesterol in these lipoprotein fractions. Each of the atherogenic lipoprotein particles contains a single molecule of apolipoprotein (apo) B and therefore the concentration of apo B provides a direct measure of the number of circulating atherogenic lipoproteins. Evidence from fundamental, epidemiological and clinical trial studies indicates that apo B is superior to any of the cholesterol indices to recognize those at increased risk of vascular disease and to judge the adequacy of lipid-lowering therapy. On the basis of this evidence, we believe that apo B should be included in all guidelines as an indicator of cardiovascular risk. In addition, the present target adopted by the Canadian guideline groups of an apo B <90 mg dL(-1) in high-risk patients should be reassessed in the light of the new clinical trial results and a new ultra-low target of <80 mg dL(-1) be considered. The evidence also indicates that the apo B/apo A-I ratio is superior to any of the conventional cholesterol ratios in patients without symptomatic vascular disease or diabetes to evaluate the lipoprotein-related risk of vascular disease.

Guía Europea de Prevención Cardiovascular en la Práctica Clínica (y II) / Spanish adaptation of the European Guidelines on Cardiovascular Prevention (and II)

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Methods for detecting coronary disease: epidemiology and clinical management.

The epidemic of atherosclerotic disease in wealthy countries had probably begun by 1900. Although a few physicians understood how atherosclerosis/thrombosis of the coronary arteries caused angina pectoris and myocardial infarction, the medical community did not accept that relationship until the 1920s. In wealthy countries, the epidemic peaked in mid-century, and it is now advancing in poor countries and in countries becoming affluent. Two recent developments in methods for disease detection, however, will profoundly affect not only our understanding of the epidemic of atherosclerotic disease, but also our management of patients. A redefinition of the clinical diagnosis of myocardial infarction, a well-used but imperfect measure of the epidemic, was published in September 2000. Criteria employed for about 50 years have now been replaced by criteria based on sensitive biochemical markers of necrosis of as little as 1 g of myocardium, accompanied by chest discomfort or electrocardiographic (ECG) changes, or following coronary artery intervention. The new criteria, adopted by the major societies of cardiology in Europe and the United States, is likely to increase the apparent incidence and prevalence of coronary heart disease (CHD). In the beginning of the twentieth century, diagnosis of CHD required an autopsy. In the end it was carried out by angiography as well, but it could not be applied to large proportions of the population. That has now been changed by new, non-invasive methods of computer tomography (CT) and magnetic resonance imaging (MRI), and patients, however, asymptomatic, will expect treatment for a disease that physicians have detected. Coronary artery disease (CAD) will be to CHD what occult cancer is to cancer.

LDL receptor mutation genotype and vascular disease phenotype in heterozygous familial hypercholesterolaemia.

Patients with homozygous familial hypercholesterolaemia (FH) caused by receptor-negative, low-density lipoprotein (LDL) receptor gene mutations have higher concentrations of LDL-cholesterol in plasma and earlier onset of cardiovascular disease (CVD) than patients homozygous for receptor-defective, LDL receptor mutations. In contrast, it is uncertain whether the severity of atherosclerotic disease differs in heterozygous FH caused by receptor-negative and receptor-defective mutations. The present authors investigated the influence of LDL receptor mutation type on the clinical phenotype in 31 patients with heterozygous FH caused by the receptor-negative, Trp23-stop mutation and in 31 patients heterozygous for the receptor defective Trp66-Gly mutation. Untreated levels of plasma LDL-cholesterol and calculated cholesterol-years score did not differ significantly between the two groups of patients. Detection of vascular disease was based on two approaches: (1) measurement of coronary calcification by spiral computed tomography (CT) scanning; and (2) ultrasonic measurement of carotid intima-media thickness (IMT). Age was significantly correlated to the presence of coronary calcification, but controlling for relevant cofactors, there was no evidence that the receptor-negative mutation caused more calcification than the receptor-defective mutation. Furthermore, carotid IMT was significantly influenced by plasma concentrations of Lp(a) and triglycerides, as well as by age, sex and smoking status, but again, there was no statistically significant effect of LDL receptor gene mutational type. The similarity in vascular phenotypes was probably caused by a similar life-long burden of LDL-cholesterol in the two groups of patients.

The atherosclerosis epidemic: methodology, nosology, and clinical practice.

An electronic search shows that there is a small but respectable amount of research on psychiatric and neurologic nosology. There is a also a small body of literature on endocrinologic nosology, but cardiologists almost never write about the nosology of heart disease. It does not keep them awake at night. Our understanding of the 20th-century epidemic of coronary artery disease (CAD), which dominates cardiology, has nevertheless been frustrated by problems of nosology. One of the purposes of this article is to discuss how our understanding of the epidemic has depended on classification of disease events and on the methods used to detect them. The other purpose is to show how current reclassifications of CAD and the major metabolic condition conducive to CAD, type 2 diabetes, each affect the practice of cardiology and medicine.

LDL-receptor gene mutations and the hypocholesterolemic response to statin therapy.

Studies of the cholesterol lowering effect of statin therapy as a function of low-density lipoprotein (LDL)-receptor mutation type have not produced a clear picture, possibly because they included patients with several different kinds of LDL-receptor mutations. We studied the response to treatment with fluvastatin in 28 patients with heterozygous familial hypercholesterolemia as a result of a receptor-negative mutation (Trp23-stop) and in 30 patients with a receptor-binding defective mutation (Trp66-Gly) to test the hypothesis that response to treatment depends on the type of mutation. Patients were randomized to 12 weeks of treatment with fluvastatin 40 mg daily and 12 weeks of placebo treatment, preceded by a placebo run-in period of 8 weeks in a double-blind, cross-over design. Untreated plasma concentrations of lipids and lipoproteins were similar in the two groups of patients. Plasma cholesterol and LDL cholesterol response to therapy tended to be less marked in receptor-binding defective patients, but the differences were not statistically significant. A tabulation of the results of the present and earlier studies suggests that differences in treatment response as an apparent function of LDL-receptor gene mutational type occur mainly in populations with recent genetic admixture (<400 years). In such populations, persons with the same mutation in the LDL-receptor gene are more likely to share other but undetermined genetic variations affecting the pharmacology of statins.