Sarcopenia, but not excess weight or increased caloric intake, is associated with coronary subclinical atherosclerosis in the very elderly Alessandra M. Campos a, b , Filipe A. Moura a , Simone N. Santos a , Wladimir M. Freitas a , Andrei C. Sposito a, * , on behalf of Brasilia Study on Healthy Aging and Brasilia Heart Study a Cardiology Department, State University of Campinas (Unicamp), Campinas, SP, Brazil b Pharmaceutical Sciences Department, Faculty of Health Sciences, University of Brasilia (UnB), Brasília, DF, Brazil article info Article history: Received 13 October 2016 Received in revised form 24 November 2016 Accepted 12 January 2017 Available online 18 January 2017 Keywords: Subclinical atherosclerosis Sarcopenia Excess weight Very elderly abstract Background and aims: Excess weight is a widespread condition related to increased risk of coronary heart disease (CHD). Sarcopenia is a catabolic pathway common of the aging process and also associated with CHD. In the elderly, both changes occur concurrently and it remains unclear the relative contribution on CHD risk. We aimed to investigate whether sarcopenia, excess weight, or both are associated with subclinical atherosclerosis and/or endothelial dysfunction in very elderly individuals. Methods: We performed a cross-sectional study of cohort enrolled individuals, aged 80 years or older (n ¼ 208), who had never manifested cardiovascular diseases. Blood tests, medical and nutritional evaluations, cardiac computed tomography, flow-mediated dilation (FMD) and physical performance tests were obtained at the study admission. Odds ratio (OR) was calculated by multivariate regression models using coronary calcium score (CCS) categories and FMD as dependent variables. Adjustment for potential confounders was done. Results: Muscle mass, but not fatty mass, was inversely associated with CCS categories [OR:2.54(1.06 e6.06); p ¼ 0.018]. The lowering of gait speed was negatively related to CCS>100 [OR:2.36 (1.10e5.06); p ¼ 0.028] and skeletal muscle index was directly associated with FMD [OR:5.44 (1.22e24.24); p ¼ 0.026]. Total caloric intake was positively related to fatty mass [OR:2.71 (1.09e6.72); p ¼ 0.031], but was not related to CCS. Conclusions: This study reveals that sarcopenia - comprised by reduction of muscle mass and its strength - is associated with subclinical atherosclerosis and endothelial dysfunction. Surprisingly, the excess of fatty mass seems not to be related to atherosclerotic burden in very elderly individuals. © 2017 Elsevier B.V. All rights reserved. 1. Introduction Excess weight is a worldwide risk factor for coronary heart disease (CHD) [1]. Although this condition is strongly associated with cardiovascular morbidity and mortality in middle-aged adults, the risk remains controversial in elderly individuals, given that excess weight seems to play a protective role in this age group [2]. Evidence points to a U-shaped curve where the resumption of CHD mortality risk occurs with a body mass index (BMI) 35 kg/m 2 [3]. Paradoxically, several large-scale studies have shown that overweight is related to increased mortality, including cardiovas- cular causes [4e6]. Among the elderly, the increase in fatty mass is concomitant with the decrease of lean mass, a situation in which adiposity may occur without overweight. Nutritional changes and the prevalence of redistribution of fatty mass to the abdominal region are partic- ular of this age group [7]; both factors may contribute to the development of atherosclerosis. In the same context of aging, sarcopenia has been defined as a syndrome characterized by progressive and generalized loss of skeletal muscle mass and strength, increasing the risk of adverse outcomes such as physical disability, poor quality of life, and death [8]. Sarcopenia begins at approximately 40 years of age and there is an estimated muscle mass loss of about 8% per decade, stretching until the age of 70 years; after that age, a 15% loss ensues per decade [9]. As added factor, the very process of sarcopenia has been * Corresponding author. Laboratory of Atherosclerosis and Vascular Biology (AteroLab), Cardiology Department, State University of Campinas (Unicamp), 13084-971, Campinas, SP, Brazil. E-mail address: andreisposito@gmail.com (A.C. Sposito). Contents lists available at ScienceDirect Atherosclerosis journal homepage: www.elsevier.com/locate/atherosclerosis http://dx.doi.org/10.1016/j.atherosclerosis.2017.01.005 0021-9150/© 2017 Elsevier B.V. All rights reserved. Atherosclerosis 258 (2017) 138e144