lunes, 31 de marzo de 2014

Insomnio y riesgo de enfermedad cardiovascular

Durante los últimos años se han realizado un número considerable de estudios para determinar la asociación entre alteraciones del sueño y el riesgo cardiovascular. En algunos se ha encontrado una relación estadísticamente significativa. Incluso un reciente metaanálisis con estudios prospectivos de cohortes muestra una asociación significativa entre el exceso y las pocas de horas de sueño, con un aumento del riesgo de eventos cardiovasculares.
Los autores del presente estudio realizan una revisión y metaanálisis con el objetivo de aclarar la relación entre el insomnio y el riesgo de desarrollar o morir de enfermedad cardiovascular.
Tras una exhaustiva búsqueda se incluyeron los estudios prospectivos de cohortes que evaluaban el insomnio o quejas relativas al sueño en sujetos sin enfermedad cardiovascular previa y que midieran la asociación entre el insomnio y el riesgo de desarrollar o morir de enfermedad cardiovascular. Trece estudios cumplían los criterios de inclusión. De un total de 122.501 sujetos se produjeron 6.322 eventos cardiovasculares durante un seguimiento de 3 a 20 años. Se consideraban insomnes aquellos sujetos que refiriesen dificultad para conciliar o mantener el sueño o que presentasen sueño no reparador mediante cuestionarios.
El análisis acumulativo para todos los estudios mediante un modelo de efectos aleatorios arrojó un aumento del 45% del riesgo de desarrollar o morir de enfermedad cardiovascular durante el seguimiento (RR 1,45, IC 95% 1,29-1,62; p <0 a="" alteraciones="" an="" aquellos="" asocia="" aumento="" autores="" cardiovascular.="" con="" concluyen="" del="" el="" en="" estudio="" insomnio="" lo="" los="" no="" o.="" p="" por="" que="" refer="" respecto="" riesgo="" se="" sue="" sujetos="" tanto="" un="">

Comentario

El insomnio, entendido como la dificultad para conciliar o mantener el sueño o la presencia de sueños percibidos como no reparadores, puede estar presente hasta en un tercio de la población, con una prevalencia aún mayor en sujetos ancianos.
La magnitud del efecto de este trastorno en el riesgo cardiovascular es equiparable a la de otros factores de riesgo bien establecidos y recogidos en las actuales guías de prevención cardiovascular como lo son, por ejemplo, el bajo nivel socioeconómico, el estrés en el trabajo, la depresión, ansiedad, hostilidad, incluso la exposición pasiva al humo del tabaco o el efecto equivalente a un exceso de colesterol LDL de 2 mmol/l.
No se conoce con exactitud hasta qué punto la relación entre estas dos variables es una relación pura de causalidad. Esta se podría explicar por el efecto de las alteraciones del sueño en los sistemas endocrinológicos, metabólicos, inflamación… Sin embargo, no se puede descartar una cierta implicación de otros factores de confusión por la asociación del insomnio con otros condicionantes del riesgo cardiovascular (depresión, bajo nivel socioeconómico, bajo nivel de actividad física o mala salud en general).
Las recientes guías de prevención de enfermedad cardiovascular no hacen referencia a los trastornos del sueño. No obstante, y a la vista de la asociación entre el insomnio y el riesgo cardiovascular y en el intento de definir lo que se considera un estilo de vida cardiosaludable, parece razonable tener en cuenta, al menos, las medidas de higiene del sueño. Una vez más, no puede ser casualidad que estas sean algunas de las medidas habituales para controlar otros aspectos del riesgo cardiovascular.
Está aún por determinar el efecto de las alteraciones del sueño en la población de enfermos cardiovasculares y las medidas dirigidas a reducir el riesgo cardiovascular residual atribuible al mismo. Es posible que pronto se vayan aclarando algunas de estas cuestiones y tengamos noticias al respecto.

Referencia

Insomnia and risk of cardiovascular disease: a meta-analysis
  • Francesco Sofi, Francesca Cesari, Alessandro Casini, Claudio Macchi, Rosanna Abbate, and Gian Franco Gensini.
  • European Journal of Preventive Cardiology January 2014 21: 57-64.


Fuente: http://www.secardiologia.es/practica-clinica-investigacion/blog-cardiologia-hoy/443-otras-publicaciones/5173-insomnio-riesgo-enfermedad-cardiovascular?utm_source=Sociedad+Espa%C3%B1ola+de+Cardiolog%C3%ADa&utm_campaign=13ae22386a-RSS_resumen_web+%2A%7CRSSFEED%3ADATE%7C%2A&utm_medium=email&utm_term=0_255d8eca74-13ae22386a-208961265

viernes, 28 de marzo de 2014

Diseminemos esta petición global

El Sábado 29 de Marzo de 2014 a las 20:30 horas (hora local de cada pais), WWF le pide a individuos, empresas, gobiernos y organizaciones alrededor del mundo que apaguen sus luces durante una hora, La Hora del Planeta, para demostrar globalmente su preocupación por el cambio climático y demostrar su compromiso para encontrar soluciones.
La Hora del Planeta es un llamado para que cada persona, negocio, empresa privada, gobierno o comunidad actúe. Es una alerta para asumir responsabilidades e involucrarnos en el trabajo por un futuro sustentable.


martes, 25 de marzo de 2014

CENTROAMÉRICA DESPUÉS DE LA GUERRA FRÍA

jueves, 6 de marzo de 2014
Centroamérica después de la Guerra Fría
Marcelo Colussi (especial para ARGENPRESS.info)

¿Qué es Centroamérica?

Para quienes viven fuera de Centroamérica, ésta representa una región bastante ignorada. Es, salvando las distancias, como el África negra: un área difusa, donde no se conocen con exactitud los países que la integran, y de la que existe una vaga idea del conjunto, siempre en la perspectiva de pobreza, atraso comparativo, condiciones de vida muy difíciles, impunidad y corrupción por parte de los Estados, con dinámicas sociales de alta violencia. Centroamérica, en esta lógica es, sin más, sinónimo de república bananera.


Completo aquí: http://www.argenpress.info/2014/03/centroamerica-despues-de-la-guerra-fria.html

miércoles, 19 de marzo de 2014

CV Risk and Saturated Fats: The Debate Roils On

CAMBRIDGE, UK — A meta-analysis has revived the debate over best dietary recommendations for cardiovascular health; specifically, whether there's an evidence base supporting the traditional message to consume foods rich in long-chain omega-3 and omega-6 polyunsaturated fatty acids (PUFA) and avoid those laden with saturated fats[1]. But questions about the report emerged even before its publication today. Fuente: http://www.medscape.com/viewarticle/822092?nlid=51723_2566&src=wnl_edit_medp_card&spon=2

martes, 11 de marzo de 2014

Dietary Fiber Intake Shows Inverse, Dose-Dependent Risk Ratio with CHD, CVD

Dietary fiber intake has been linked to a lower incidence of coronary heart disease (CHD) since the 1970s. Multiple mechanisms have been postulated for this relationship, including decreased absorption of low-density lipoprotein (LDL) from the intestines, increased satiety signals that result in less weight gain, and the presence of antioxidants in high fiber foods that may have a beneficial effect.
A recent meta-analysis published in the British Medical Journal combined the existing data from 22 prospective studies between 1990 and 2013 to try to characterize the association and dose-response relationship between fiber intake and CHD or cardiovascular disease (CVD). The studies were largely from the United States and Europe; there were 2 from Japan and one from Australia. A number of the studies included many different subtypes of fiber (vegetable, fruit, soluble, insoluble, cereal etc.) and all studies had a minimum follow-up of 3 years.There was an inverse dose-dependent risk ratio for CHD associated with total dietary fiber intake (RR 0.91 per 7% intake in fiber, 95% CI 0.87 to 0.94). There was some heterogeneity with respect to outcomes of interest and subtype of fiber intake as well as with the strength of risk reduction. For example, there was a lower risk of CVD and CHD associated with higher intake of insoluble, cereal, fruit, and vegetable fiber. Pooled analysis, however, showed that the association of soluble fiber with CHD or CVD and fruit fiber with CHD crossed the line of unity.Although this study, like all observational studies, is subject to confounding (ie, fiber intake is a marker of other healthy lifestyle behaviors), these findings are consistent with other studies of fiber intake and there is a plausible scientific mechanism to explain these results. It remains to be seen whether fiber intake from food sources is equivalent to synthetic fiber intake (such as Metamucil). Practically speaking, however, patients should certainly be counseled to increase their dietary fiber intake by 7 g. This can be accomplished by eating just one portion of whole grain plus beans or lentils or by consuming 2 to 4 servings of fruits and vegetables daily.

References

Threapleton DE, Greenwood DC, Evans CEL, et al. Dietary fibre intake and risk of cardiovascular disease: systematic review and meta-analysis. BMJ. 2013;19:347:f6879. doi: 10.1136/bmj.f6879. (Full text)
- See more at: http://www.consultantlive.com/cardiovascular-diseases/dietary-fiber-intake-shows-inverse-dose-dependent-risk-ratio-chd-cvd?GUID=24510CEB-E6AD-4B62-B3CC-131041EACD56&rememberme=1&ts=30012014#sthash.dqXQn9dD.dpuf


Fuente: http://www.consultantlive.com/cardiovascular-diseases/dietary-fiber-intake-shows-inverse-dose-dependent-risk-ratio-chd-cvd?GUID=24510CEB-E6AD-4B62-B3CC-131041EACD56&rememberme=1&ts=30012014

Researchers Claim Blood Test Predicts Alzheimer's

Published: Mar 9, 2014 | Updated: Mar 9, 2014 By John Gever, Deputy Managing Editor, MedPage Today Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco save| A A For best viewing, click the bottom right corner for full screen. Action Points Blood biomarkers in cognitively normal seniors were associated with their 3-year risk of developing mild cognitive impairment or Alzheimer's disease, although the accuracy fell short of what would normally be acceptable for a screening test. Note that the researchers focused on unconventional markers considered to be components of the blood "metabolome" and "lipidome," metabolites resulting from cellular processes and lipid molecules, including 10 plasma phospholipid molecules. Blood biomarkers in cognitively normal seniors were associated with their 3-year risk of developing mild cognitive impairment or Alzheimer's disease, researchers said, although the accuracy fell short of what would normally be acceptable for a screening test. Levels of 10 plasma phospholipid molecules -- none of them conventional markers for Alzheimer's disease -- distinguished initially healthy individuals 70 and older who developed cognitive impairments during follow-up from those who remained cognitively normal in a 525-person study, according to Howard J. Federoff, MD, PhD, of Georgetown University in Washington, D.C., and colleagues. For this distinction, the 10-marker panel had an area under the receiver-operating characteristic curve (AU-ROC) of 0.92 (95% CI 0.87-0.99), with sensitivity and specificity each at 90%, they reported online in Nature Medicine. "We consider our results a major step toward the commercialization of a preclinical disease biomarker test that could be useful for large-scale screening to identify at-risk individuals," Federoff said in a Georgetown press release. But the data did not appear to fully support that optimism. If the study cohort's 5% rate of conversion from normal cognition to mild impairment or Alzheimer's disease is representative of a real-world screening population, then the test would have a positive predictive value of just 35%. That is, nearly two-thirds of positive screening results would be false. In general, a positive predictive value of 90% is considered the minimum for any kind of screening test in normal-risk individuals. On the other hand, the use of markers unrelated to the APOE gene or beta-amyloid and tau proteins may represent a welcome new direction for Alzheimer's disease risk prediction. For instance, the test could hold promise as part of clinical trials of new treatments, by enriching patient samples with those progressing quickly to clear impairment, Gisele Wolf-Klein, MD, director of geriatric education at North Shore-LIJ Health System in New Hyde Park, N.Y., told MedPage Today in an email. "[It] would be a major step in assisting the pharmaceutical industry in producing disease-modifying therapies at both early and preclinical stages of dementia," she said. Wolf-Klein added, "Further research will enable healthcare practitioners to determine the actual benefits and relevance of this test in clinical practice." For the study, Federoff and colleagues recruited 525 community-dwelling, physically healthy people who were 70 and older and followed them for up to 5 years with annual examinations. A total of 74 were determined to have either amnestic mild cognitive impairment or Alzheimer's disease at some point, including 46 at study entry and 28 who converted from normal to impaired during follow-up. These conditions were diagnosed according to standard criteria, based on a suite of 14 neurocognitive tests. To identify potentially predictive biomarkers, Federoff and colleagues analyzed baseline blood samples from 53 who showed cognitive impairments at the end of year three (including 18 who had converted from normal cognition) and 53 who remained cognitively normal. The researchers focused on unconventional markers considered to be components of the blood "metabolome" and "lipidome" -- that is, metabolites resulting from cellular processes and lipid molecules. Ten of these were ultimately found to be either significantly increased or decreased in the impaired individuals versus the normal controls. They included amino acids such as proline and lysine, the neurotransmitter serotonin, and others that Federoff and colleagues suggested were indicators of "cell membrane integrity." "We posit that this 10-phospholipid biomarker panel, consisting of phosphatidylcholine and acylcarnitine species, reveals the breakdown of neural cell membranes in those individuals destined to phenoconvert" from cognitively normal to impaired, they wrote. Statistical modeling suggested an optimal set of cutoffs for the 10 markers to distinguish impaired individuals from controls. The researchers then applied it to blood samples from a different subset of the study participants, including 10 converters, 20 normal controls, and 11 with impairments at study entry. The model actually did less well in discriminating the entire group of impaired participants from normal controls (AU-ROC 0.77) than in predicting who would convert from normal to impaired (AU-ROC 0.92). Incorporating APOE genotype into the model did not improve its performance, the researchers said. Federoff and colleagues indicated that their biomarker panel's performance in picking up incipient cognitive impairment was better than blood tests for beta-amyloid and tau proteins. Levels of these classical markers of Alzheimer's disease in cerebrospinal fluid have shown better predictive and diagnostic power, but no test requiring lumbar puncture will catch on for large-scale screening of asymptomatic people. On the other hand, at least two other blood tests for unconventional markers had shown good results for discriminating individuals with current impairment from normal controls and for predicting progression from mild impairment to overt dementia, Federoff and colleagues noted, suggesting that this is a fruitful area to explore. Keith L. Black, MD, a neurosurgeon and researcher at Cedars-Sinai Medical Center in Los Angeles, told MedPage Today that it would be important to learn more about how these markers connect with neurological dysfunction. For the biomarkers found in the study, "it's difficult to understand how they can be specifically linked to Alzheimer's disease versus some sort of diffuse neuronal abnormality or connectivity abnormality or synaptic connectivity abnormality," he said. "The question, I think, becomes for future studies how well do we understand the underlying biology of it, whether it's specific to Alzheimer's disease or whether you might see these same types of changes in these blood biomarkers with other types of diffuse neuronal loss or injury, other types of dementia, or ischemic changes, for example." In a more restrained vein than Federoff took in the press release, the Nature Medicine report concluded by saying their biomarker panel "requires external validation using similar rigorous clinical classification before further development for clinical use. Such additional validation should be considered in a more diverse demographic group than our initial cohort." The study was funded by the National Institutes of Health. Study authors declared they had no relevant financial interests. Fuente: http://www.medpagetoday.com/Neurology/Dementia/44677?isalert=1&uun=g419731d884R5519153u&utm_source=breaking-news&utm_medium=email&utm_campaign=breaking-news&xid=NL_breakingnews_2014-03-09