Lin Lin1,2,3, Jie Zhang1,2,3, Lei Jiang1,3, Rui Du1,3, Chunyan Hu1,3, Jieli Lu1,3, Tiange Wang1,3, Mian Li1,3, Zhiyun Zhao1,3, Yu Xu1,3, Min Xu1,3, Yufang Bi1,3, Guang Ning4,5, Weiqing Wang6,7, Yuhong Chen8,9,10. 1. Shanghai Institute of Endocrine and Metabolic Diseases, Department of Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Rui-Jin 2nd Road, Shanghai, 200025, China. 2. Department of Endocrine and Metabolic Diseases Rui-Jin Hospital North, Shanghai Jiao Tong University School of Medicine, Shanghai, China. 3. State Key Laboratory of Medical Genomics, Key Laboratory for Endocrine and Metabolic Diseases of Ministry of Health, National Clinical Research Center for Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. 4. Shanghai Institute of Endocrine and Metabolic Diseases, Department of Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Rui-Jin 2nd Road, Shanghai, 200025, China. gning@sibs.ac.cn. 5. State Key Laboratory of Medical Genomics, Key Laboratory for Endocrine and Metabolic Diseases of Ministry of Health, National Clinical Research Center for Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. gning@sibs.ac.cn. 6. Shanghai Institute of Endocrine and Metabolic Diseases, Department of Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Rui-Jin 2nd Road, Shanghai, 200025, China. wqingw61@163.com. 7. State Key Laboratory of Medical Genomics, Key Laboratory for Endocrine and Metabolic Diseases of Ministry of Health, National Clinical Research Center for Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. wqingw61@163.com. 8. Shanghai Institute of Endocrine and Metabolic Diseases, Department of Endocrine and Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Rui-Jin 2nd Road, Shanghai, 200025, China. chenyh70@126.com. 9. Department of Endocrine and Metabolic Diseases Rui-Jin Hospital North, Shanghai Jiao Tong University School of Medicine, Shanghai, China. chenyh70@126.com. 10. State Key Laboratory of Medical Genomics, Key Laboratory for Endocrine and Metabolic Diseases of Ministry of Health, National Clinical Research Center for Metabolic Diseases, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. chenyh70@126.com.
Abstract
AIMS/HYPOTHESIS: The cardiometabolic risk associated with metabolically healthy obesity (MHO) remains the subject of debate. It is unclear whether MHO is a transient condition that affects subclinical atherosclerosis risk. In this study, we aimed to investigate the association of MHO and its transition over time with incident subclinical atherosclerosis. METHODS: A prospective study was conducted with 6220 Chinese adults who were free of cardiovascular disease (CVD) at baseline. Obesity was defined as BMI ≥25.0 kg/m2. Metabolic health was defined as an individual having fewer than two of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (NCEP ATP III) criteria for components of the metabolic syndrome (excluding waist circumference). Subclinical atherosclerosis was measured by brachial-ankle pulse wave velocity, pulse pressure and albuminuria, separately or combined. Participants were cross-classified by BMI categories and by metabolic health status and its transition during follow-up. Inverse probability weighted logistic regression models were used to estimate ORs and 95% CIs for subclinical atherosclerosis. RESULTS: The MHO phenotype accounted for 16.3% of the total population and 32.8% of the population with obesity at baseline. Baseline MHO was not significantly associated with incident subclinical atherosclerosis. During a follow-up period of 4.4 years, 46.8% of individuals with MHO developed a metabolically unhealthy status. Those with transient MHO had an increased risk of composite subclinical atherosclerosis compared with those in the metabolically healthy non-obesity reference group (OR 2.52 [95% CI 1.89, 3.36]). A transition from metabolically unhealthy to healthy status was shown to decrease the outcome risk. The relationship between BMI and subclinical atherosclerosis was partly mediated by BP and plasma glucose. CONCLUSIONS/ INTERPRETATION: MHO is not a stable condition and transient MHO conferred an increased risk of subclinical atherosclerosis, the early stage of CVD. Hence, individuals may benefit from early behavioural or medical management in order to avoid a deterioration of metabolic status and prevent atherosclerosis and CVD.
AIMS/HYPOTHESIS: The cardiometabolic risk associated with metabolically healthy obesity (MHO) remains the subject of debate. It is unclear whether MHO is a transient condition that affects subclinical atherosclerosis risk. In this study, we aimed to investigate the association of MHO and its transition over time with incident subclinical atherosclerosis. METHODS: A prospective study was conducted with 6220 Chinese adults who were free of cardiovascular disease (CVD) at baseline. Obesity was defined as BMI ≥25.0 kg/m2. Metabolic health was defined as an individual having fewer than two of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (NCEP ATP III) criteria for components of the metabolic syndrome (excluding waist circumference). Subclinical atherosclerosis was measured by brachial-ankle pulse wave velocity, pulse pressure and albuminuria, separately or combined. Participants were cross-classified by BMI categories and by metabolic health status and its transition during follow-up. Inverse probability weighted logistic regression models were used to estimate ORs and 95% CIs for subclinical atherosclerosis. RESULTS: The MHO phenotype accounted for 16.3% of the total population and 32.8% of the population with obesity at baseline. Baseline MHO was not significantly associated with incident subclinical atherosclerosis. During a follow-up period of 4.4 years, 46.8% of individuals with MHO developed a metabolically unhealthy status. Those with transient MHO had an increased risk of composite subclinical atherosclerosis compared with those in the metabolically healthy non-obesity reference group (OR 2.52 [95% CI 1.89, 3.36]). A transition from metabolically unhealthy to healthy status was shown to decrease the outcome risk. The relationship between BMI and subclinical atherosclerosis was partly mediated by BP and plasma glucose. CONCLUSIONS/ INTERPRETATION: MHO is not a stable condition and transient MHO conferred an increased risk of subclinical atherosclerosis, the early stage of CVD. Hence, individuals may benefit from early behavioural or medical management in order to avoid a deterioration of metabolic status and prevent atherosclerosis and CVD.
Authors: Maoxiang Zhao; Wenjuan Du; Qianqian Zhao; Yating Chen; Bin Li; Zhonghui Xie; Zihao Fu; Nan Zhang; Xiaowei Cheng; Xiaoqian Li; Siyu Yao; Miao Wang; Chi Wang; Shouling Wu; Hao Xue; Yang Li Journal: Front Cardiovasc Med Date: 2022-06-28