RESUMO
Abstract Introduction: Older adults may become fragile by different mechanisms that influence homeostasis, such as stroke. Objective: To investigate the relation of stroke with the frailty process in older adults, correlating body mass index, functional aspects and resulting deficits. Methods: A case-control study was performed between February and November 2015. Patients aged 60 years and older, who had suffered ischemic stroke, were evaluated using the Kihon Checklist (KCL), the modified Rankin Scale, and the National Institutes of Health Stroke Scale. Baseline data included pre-stroke information and follow-up data obtained one month after discharge. The statistical analysis was performed by paired t-test and Friedman non-parametric test. Results: The study was conducted on 16 older adults (72.19±7.20 years old), making evident the influence of stroke on the frailty process (p<0.005). After stroke, an increase was observed in the mean scores domains: total KCL score (p=0.001); instrumental activities of daily living (p=0.001); physical (p=0.002); socialization (p=0.006); mood (p=0.004). Conclusions: A significant worsening of frailty was observed after stroke. KCL was satisfactory to evaluate frailty pre and post-stroke due to its applicability and coverage of the main aspects of frailty in older adults.
Resumen Introducción. Los ancianos pueden tornarse frágiles por diferentes mecanismos que influencian la homeostasis, como por ejemplo el accidente cerebrovascular (ACV). Objetivo. Investigar la relación del ACV con el proceso de fragilización en correlación con el índice de masa corporal, la funcionalidad y los déficits resultantes. Materiales y métodos. Se realizó un estudio de caso-control. Se incluyeron pacientes con 60 años o más que sufrieron ACV isquémico y evaluados con Kihon Checklist (KCL), Escala de Rankin Modificada y Evaluación Neurológica del National Institutes of Health Stroke Scale. Se recogieron datos de baseline de información pre-ACV y de follow-up un mes después del alta hospitalaria. El análisis estadístico se realizó mediante prueba t pareada y prueba non paramétrica de Friedman. Resultados. Se incluyeran 16 ancianos (720.19±7.20 años) y se observó la influencia del ACV en la fragilización (p<0.005). Aumentaron las puntuaciones de los dominios: KCL total (p=0.001); actividades instrumentales de la vida diária (p=0.001); físico (p=0.002); socialización (p=0.006); humor (p=0.004). Conclusiones. Se observó empeoramiento de la fragilidad después del ACV. El KCL se presentó como una evaluación satisfactoria para medir la fragilidad pre y post ACV debido a su aplicabilidad y cobertura de los aspectos principales de la fragilidad en ancianos.
RESUMO
AIM: To examine whether arterial stiffness, measured by the cardio-ankle vascular index (CAVI), is associated with skeletal muscle mass index (SMI) in Japanese community-dwelling older adults. METHODS: Data were collected from 175 participants through questionnaires and specific tests; the data included demographic, lifestyle and health characteristics, body mass index (BMI), and body composition features determined by the bioelectrical impedance analysis, ankle-brachial index, the Mini-Nutritional Assessment, handgrip strength (GS), walking speed and shuttle walking tests (SW), and arterial stiffness determined by the CAVI. Absolute SMI was dichotomized according to the first quintile, which determined low (n = 35) and normal (n = 140) SMI. RESULTS: Participants with low SMI were older (P = 0.01), had more polypharmacy (P = 0.01), a lower BMI (P < 0.001), and fat mass index (P = 0.02), and had a greater risk of malnutrition (P < 0.001) than the normal group. Additionally, they showed poorer physical performance (GS and SW, P = 0.007 and 0.01, respectively) than the normal group. Furthermore, CAVI was associated with SMI even after adjustments (OR 1.82, 95% CI 1.14-2.90, P = 0.01). CONCLUSIONS: Our data showed that arterial stiffness is associated with low SMI in community-dwelling older adults, even when adjusting by multiple factors, showing a close interaction of vascular aging and muscle mass decline.