RESUMO
RESUMEN Introducción: Estudios previos han asociado la pérdida auditiva con un acelerado deterioro cognitivo durante el envejecimiento; no obstante, esta asociación no ha sido estudiada en adultos mayores chilenos. Objetivo: Investigar la asociación entre la discapacidad auditiva y la sospecha de deterioro cognitivo a través del cuestionario Mini Mental State Examination (MMSE, versión abreviada) en esta población. Material y método: Se incluyeron 1.384 adultos mayores de 60 años de la encuesta nacional de salud 2009-2010. Un puntaje <13 puntos en el MMSE se consideró sospecha de deterioro cognitivo. La discapacidad auditiva se determinó a través de un cuestionario de tamizaje autorreportado de tres preguntas. La asociación entre estas dos variables se investigó mediante análisis de regresión logística. Resultados: Se identificó una asociación significativa entre el MMSE alterado y cada una de las discapacidades auditivas estudiadas. A su vez, existió una tendencia a aumentar en 59% la probabilidad de desarrollar deterioro cognitivo en la medida que aumentaron las discapacidades auditivas (OR: 1,59 [95% IC: 1,38 a 1,82], p <0,0001). Conclusión: La disminución de la percepción auditiva es un factor de riesgo para el desarrollo de deterioro cognitivo y posteriormente demencia. La creación de políticas públicas, orientadas al tamizaje temprano en población de riesgo, podría ser una solución efectiva para prevenir las consecuencias asociadas con esta condición.
ABSTRACT Introduction: Hearing loss has been associated with an accelerated cognitive impairment during ageing. However, this association has not been investigated in older Chilean adults. Aim: To investigate the association between hearing impairment and cognitive impairment, using the Mini-Mental State Examination (MMSE, abridged version), in the Chilean population. Material and methods: 1,384 older adults aged ≥60 years, from 2009-2010 Chilean national health survey, were included. <13 points in the MMSE were considered suspicion of cognitive impairment. Hearing impairment was determined through a questionnaire including 3 domains. The association between cognitive and hearing loss was investigated using logistic regression. Results: An association between MMSE and each hearing disabilities studied was identified. As hearing impairments increased, the odd for cognitive impairment incremented by 59% (OR: 1.59 [95% IC: 1.38 a 1.82], p <0.0001). Conclusion: Hearing loss is a risk factor to develop cognitive impairment, which could translate into a high risk of dementia. Public politics implementation, focused in an early screening, could be an effective approach to prevent the complications associated with this hearing loss in older adults.
Assuntos
Humanos , Masculino , Feminino , Demência/etiologia , Disfunção Cognitiva/etiologia , Perda Auditiva/complicações , Chile/epidemiologia , Estudos Transversais , Inquéritos e Questionários , Demência/epidemiologia , Disfunção Cognitiva/epidemiologiaRESUMO
Background: High density lipoproteins are an heterogeneous population of particles. Two main subpopulations have been identified, one contains Apo A-I and Apo A-II and is denominated LpA-I:A-II and another one contains only Apo A-I and is denominated LpA-I. Aim: To measure the concentrations of these particles in patients with stable coronary artery disease. Patients and Methods: Serum lipids, A-I and B apolipoproteins, LpA-I, LpA-I:A-II and LpB particles were measured in 73 men aged 33 to 82 years with angiographically documented coronary artery disease (CAD) and 33 control subjects aged 39 to 76 years. LpA-I, LpA-I:A-II and LpB were measured by a noncompetitive enzyme linked immunoassay using previously characterized monoclonal antibodies against ApoA-I, ApoA-II and apoB. Results: Patients with CAD had significantly higher mean levels of LDL cholesterol than the control group (p= 0.038). The mean concentration of LpA-I particles in patients with CAD was significantly lower (p= 0.031) than in control subjects, while the concentration of LpA-I:A-II particles was significantly higher (p=0.016). The percentage of coronary stenosis correlated negatively with LpA-I and positively with LpA-I:A-II. The best relative risk (RR) indicator in these patients was LDL-cholesterol. The relative risk increases 2.5 fold when LpA-I falls below the cut-off level. Likewise, the relative risk increases 3-fold when LpA-I:A-II raises over the cut-off level. Conclusions: Our findings indicate that the quantification of LpA-I and LpA-I:A-II particles might allow a more accurate evaluation of the CAD risk than HDL cholesterol. LpA-I might represent the antiatherogenic fraction of HDL