Public Health

Targeting lipid-lowering drug therapy for primary prevention of coronary disease: an updated Sheffield table

En estos últimos años diversos autores y organizaciones han desarrollado guías de práctica clínica (GPC) con recomendaciones para el manejo del paciente con riesgo vascular. El objetivo es la descripción de la variabilidad existente entre las recomendaciones de las distintas GPC.

Se comparan los autores de las distintas GPC y si están basadas en la evidencia y en el riesgo vascular (los factores de riesgo, el método de estimación y su estratificación), tanto en aquellas guías de carácter internacional, que son la referencia bibliográfica de las guías españolas, como en las GPC nacionales en Atención Primaria.

Las GPC están basadas en la evidencia o en la adaptación de otras GPC ya existentes. La importancia de las últimas versiones de las GPC radica en la llamada de atención sobre los nuevos marcadores potenciales de las enfermedades cardiovasculares (ECV): la homocisteína, los marcadores de inflamación, los factores trombogénicos, los factores genéticos, la microalbuminuria y la aterosclerosis subclínica. También prestan mayor atención al síndrome metabólico.

Existe variabilidad entre las GPC revisadas tanto en los autores como en los factores de riesgo contemplados y en el método de estimar y de estratificar el riesgo. Los nuevos marcadores de ECV todavía no se consideran aplicables en la estimación de riesgo cardiovascular rutinario de la ECV. Se espera que la combinación de los factores de riesgo tradicionales y de los factores de riesgo que emergen facilite la valoración del riesgo global de los pacientes con el fin de optimizar los esfuerzos diagnósticos y terapéuticos. Sugerimos que en la práctica clínica los médicos de Atención Primaria utilicen la GPC editada por la semFYC II.

In recent years, several authors and organizations have developed clinical practice guides (CPG) with recommendations for the management of patients with vascular risk. Description of existing variability between recommendations of the different CPG.

A comparison is made of authors of the different CPG and if they are based on evidence and vascular risk (risk factors, estimation method and its stratification) both in those international guides, that are the bibliographic reference of the Spanish guidelines, as well as in the national CPG in Primary Care.

The CPG are based on evidence or the adaptation of other already existing CPG. The importance of the last versions of the CPG is found in the call to attention on the new potential markers of cardiovascular diseases: homocysteine, inflammation markers, thrombogenic factors, genetic factors, microalbuminuria and subclinical atherosclerosis. Greater attention is also given to the metabolic syndrome.

There is variability between the CPG reviewed both in the authors and in the risk factors contemplated and in the method of estimating and stratifying risk. The new CVD markers are still not considered applicable in the estimation of routine cardiovascular risk of CVD. It is hoped that the combination of the traditional risk factors and the risk factors that emerge will facilitate the assessment of global risk of the patients in order to optimize diagnostic and therapeutic efforts. We suggest that Primary Care physicians use the CPG edited by the semFYC (Spanish Society of Family and Community Medicine) II in the clinical practice.

To determine, in asymptomatic subjects, the interstudy reproducibility of a three-dimensional (3D) volume selective fast spin echo (FSE) cardiovascular magnetic resonance sequence for the assessment of carotid artery wall volume as a measure of atheroma burden.

Interstudy reproducibility was evaluated in 16 asymptomatic volunteers (10 male, 6 female). Both carotid arteries were scanned twice with a median interscan time of 5 days. The images were acquired in cross-section, and the total carotid arterial wall volume (TWV) was calculated by subtraction of the total carotid lumen volume from the total outer carotid vessel volume.

The mean carotid T1-weighted TWV for the first and second scans was 828 and 821 mm³, respectively (mean difference 7 mm³, p = 0.45). The standard deviation (S.D.) of the differences between the measurements was 38 mm³ yielding an interstudy coefficient of variation of 4.6%. The time for each study was approximately 30 min. For the longitudinal evaluation of carotid atheroma burden with pharmacological intervention versus placebo, 32 subjects would enable a difference of 38 mm³ to be detected with a significance level of 5% with 80% power.

Volumetric analysis with carotid CMR in asymptomatic subjects using a 3D volume-selective FSE is time-efficient with good interstudy reproducibility, and is well suited for longitudinal studies of carotid atheroma with reasonable sample sizes.

Clinicians often have to make treatment decisions based on the likelihood that an individual patient will benefit. In this article we consider the relevance of relative and absolute risk reductions, and draw attention to the importance of expressing the results of trials and subgroup analyses in terms of absolute risk. We describe the limitations of univariate subgroup analysis in situations in which there are several determinants of treatment effect, and review the potential for targeting treatments with risk models, especially when benefit is probably going to be dependent on the absolute risk of adverse outcomes with or without treatment. The ability to systematically take into account the characteristics of an individual patient and their interactions, to consider the risks and benefits of interventions separately if needed, and to provide patients with personalised estimates of their likelihood of benefit is shown using the example of endarterectomy for symptomatic carotid stenosis.

The aim of this study was to determine the threshold of fracture probability at which interventions became cost-effective in women based on data from the UK. We modelled the effects of an intervention costing £350 per year given for 5 years that decreased the risk of all osteoporotic fractures by 35% followed by a waning of effect (offset time) for a further 5 years. Sensitivity analyses included a range of treatment duration (3–10 years), intervention costs (£300–400/year) and offset times (0–15 years). Data on costs and risks were from the UK. Costs included direct costs, but excluded indirect costs due to morbidity. A threshold for cost-effectiveness of £30,000/QALY gained was used.

With the base case (£350 per year; 35% efficacy) treatment in women was cost-effective with a 10-year hip fracture probability that ranged from 1.1% at the age of 50 years to 9.0% at the age of 85 years. Intervention thresholds were sensitive to the assumed costs and offset time. The exclusion of osteoporotic fractures other than hip fracture significantly increased the cost-effectiveness ratio because of the substantial morbidity from such other fractures, particularly at younger ages. Cost-effective scenarios were found for women at the threshold for osteoporosis from the age of 60 years. Treatment of established osteoporosis was cost-effective irrespective of age. We conclude that the inclusion of all osteoporotic fractures has a marked effect on intervention thresholds, that these vary with age and that available treatments can be targeted cost-effectively to individuals from the UK at moderately increased fracture risk.