Ji Eun Jun1, Mira Kang2, Sang-Man Jin3, Kyunga Kim4, You-Cheol Hwang1, In-Kyung Jeong1, Jae Hyeon Kim3,5. 1. Department of Endocrinology and Metabolism, Kyung Hee University Hospital at Gangdong, Kyung Hee School of Medicine, Seoul, Republic of Korea pages: 867-878. 2. Department of Health Promotion Center, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. 3. Division of Endocrinology and Metabolism, Department of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. 4. Statistics and Data Center, Research Institute for Future Medicine, Samsung Medical Center, Seoul, Republic of Korea. 5. Department of Clinical Research Design & Evaluation, SAIHST, Sungkyunkwan University, Seoul, Republic of Korea.
Abstract
OBJECTIVE: We aimed to investigate the interaction of reduced skeletal muscle mass and abdominal obesity on coronary artery calcification (CAC). DESIGN AND METHODS: A total of 19 728 adults free of cardiovascular disease (CVD) who contemporaneously underwent cardiac tomography and bioelectrical impedance analysis were enrolled in a cross-sectional and longitudinal cohort. Skeletal muscle mass index (SMI) was calculated using the following formula: SMI (%) = total appendicular muscle mass (kg)/body weight (kg) × 100 according to sex. CAC presence or incidence was defined as CAC score > 0, and CAC progression was defined as √CAC score (follow-up) - √CAC score (baseline)>2.5. Pre-sarcopenia was defined as SMI ≤ -1.0 s.d. of the sex-specific mean of a young reference group. Abdominal obesity was defined as waist circumference ≥ 90 cm for men and ≥85 cm for women. All individuals were further classified into four groups: normal, abdominal obesity alone, pre-sarcopenia alone, and pre-sarcopenic obesity. RESULTS: Individuals with pre-sarcopenic obesity showed the highest adjusted odds ratio (AOR) for CAC presence (AOR 2.16, 95% CI : 1.98-2.36, P < 0.001) as well as total CAC incidence and progression (adjusted hazard ratio: 1.54, 95% CI: 1.37-1.75, P < 0.001), compared with normal individuals. Pre-sarcopenic obesity significantly increased CAC incidence and progression compared to either pre-sarcopenia or abdominal obesity alone. CONCLUSION: Pre-sarcopenia and abdominal obesity together were significantly associated with a higher CAC presence and increased risk of CAC incidence and progression, independent of traditional CVD risk factors.
OBJECTIVE: We aimed to investigate the interaction of reduced skeletal muscle mass and abdominal obesity on coronary artery calcification (CAC). DESIGN AND METHODS: A total of 19 728 adults free of cardiovascular disease (CVD) who contemporaneously underwent cardiac tomography and bioelectrical impedance analysis were enrolled in a cross-sectional and longitudinal cohort. Skeletal muscle mass index (SMI) was calculated using the following formula: SMI (%) = total appendicular muscle mass (kg)/body weight (kg) × 100 according to sex. CAC presence or incidence was defined as CAC score > 0, and CAC progression was defined as √CAC score (follow-up) - √CAC score (baseline)>2.5. Pre-sarcopenia was defined as SMI ≤ -1.0 s.d. of the sex-specific mean of a young reference group. Abdominal obesity was defined as waist circumference ≥ 90 cm for men and ≥85 cm for women. All individuals were further classified into four groups: normal, abdominal obesity alone, pre-sarcopenia alone, and pre-sarcopenic obesity. RESULTS: Individuals with pre-sarcopenic obesity showed the highest adjusted odds ratio (AOR) for CAC presence (AOR 2.16, 95% CI : 1.98-2.36, P < 0.001) as well as total CAC incidence and progression (adjusted hazard ratio: 1.54, 95% CI: 1.37-1.75, P < 0.001), compared with normal individuals. Pre-sarcopenic obesity significantly increased CAC incidence and progression compared to either pre-sarcopenia or abdominal obesity alone. CONCLUSION: Pre-sarcopenia and abdominal obesity together were significantly associated with a higher CAC presence and increased risk of CAC incidence and progression, independent of traditional CVD risk factors.