Key result
Metabolic unhealthy status combined with hepatic steatosis significantly increased the risk of incident composite subclinical atherosclerosis compared to metabolic healthy individuals without hepatic steatosis (OR 2.57).
Why the study?
Metabolic dysfunction drives fatty liver disease progression, making it pivotal to evaluate metabolic status transitions and subsequent risk of subclinical atherosclerosis.
Does metabolic unhealthy status and fatty liver disease increase the risk of subclinical atherosclerosis in community residents?
Cohort (n=6,260)
No
Does metabolic unhealthy status and fatty liver disease increase the risk of subclinical atherosclerosis in community residents?
Metabolic unhealthy status, particularly when combined with fatty liver disease, significantly increases the risk of subclinical atherosclerosis, while regressing to a metabolic healthy status mitigates this risk.
Metabolic transitions may modify subclinical atherosclerosis risk in fatty liver; leaves open whether targeting them alters outcomes.
Background Metabolic dysfunction is a major determinant in the progression of fatty liver disease. It is pivotal to evaluate the metabolic status and subsequent transition in fatty liver population and to identify the risk of subclinical atherosclerosis. Methods The prospective cohort study included 6260 Chinese community residents during 2010–2015. Fatty liver was determined as hepatic steatosis (HS) by ultrasonography. Metabolic unhealthy (MU) status was defined as having diabetes and/or ≥ 2 metabolic risk factors. Participants were categorized into 4 groups according to the combination of metabolic healthy (MH)/MU and fatty liver status (MHNHS, MUNHS, MHHS and MUHS). Subclinical atherosclerosis was assessed by elevated brachial-ankle pulse wave velocity, pulse pressure and/or albuminuria. Results 31.3% of the participants had fatty liver disease and 76.9% were in MU status. During a 4.3-year follow-up, 24.2% of participants developed composite subclinical atherosclerosis. Multivariable adjusted odds ratios for composite subclinical atherosclerosis risk were (1.66 [1.30–2.13]) in MUNHS group and (2.57 [1.90–3.48]) in MUHS group. It seemed that participants with fatty liver disease were more prone to be remained in MU status (90.7% vs. 50.8%) and less likely to regress to MH status (4.0% vs. 8.9%). Fatty liver participants progressed to (3.11 [1.23–7.92]) or maintained MU status (4.87 [3.25–7.31]) significantly impelled the development of the composite risk, while regressing to MH status (0.15 [0.04–0.64]) were more intended to mitigate the risk. Conclusions The current study emphasized the importance of assessing metabolic status and its dynamic changes, especially in the fatty liver population. Regressing from MU to MH status not only benefited the systematic metabolic profile but also ameliorated future cardiometabolic complications.
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Xin et al. (2022) conducted a cohort in Fatty liver disease and metabolic dysfunction (n=6,260). Metabolic unhealthy status with hepatic steatosis vs. Metabolic healthy status without hepatic steatosis was evaluated on Composite subclinical atherosclerosis (OR 2.57, 95% CI 1.90-3.48, p=<0.0001). Metabolic unhealthy status combined with hepatic steatosis significantly increased the risk of incident composite subclinical atherosclerosis compared to metabolic healthy individuals without hepatic steatosis (OR 2.57).
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