ABSTRACT
Introduction
We aimed to investigate whether lean metabolic dysfunction‐associated steatotic liver disease (MASLD) is associated with the progression of carotid atherosclerosis in patients with type 2 diabetes mellitus.
Materials and Methods
We investigated 828 patients with type 2 diabetes mellitus who underwent baseline abdominal and carotid artery ultrasonography, followed by repeat carotid ultrasonography after 6–8 years. MASLD was confirmed by abdominal ultrasonography, and lean body mass was defined as a body mass index <23 kg/m2. Carotid atherosclerosis progression was defined as the appearance of new carotid plaque lesions on repeat ultrasonography. The association between lean MASLD, non‐lean MASLD, and the progression of carotid atherosclerosis was investigated.
Results
Among the 828 patients, 57 (6.9%), 197 (23.8%), 397 (47.9%), and 177 (21.4%) were classified as lean MASLD, lean without MASLD, non‐lean MASLD, and non‐lean without MASLD, respectively. After 6–8 years, both lean MASLD (adjusted odds ratio [aOR], 2.57; P = 0.005) and non‐lean MASLD (aOR, 1.59; P = 0.029) had a higher risk of atherosclerosis progression than controls (lean without MASLD). No significant difference was observed in the risk of atherosclerosis progression between the lean and non‐lean MASLD groups.
Discussion
In patients with type 2 diabetes mellitus, both lean and non‐lean MASLD were significantly associated with an increased risk of carotid atherosclerosis progression compared to those who were lean without MASLD. This suggests that evaluation of liver steatosis in patients with type 2 diabetes mellitus, regardless of body weight, may help identify individuals at high risk for carotid atherosclerosis progression.
Keywords: Atherosclerosis, Fatty liver, Type 2 diabetes mellitus
In patients with type 2 diabetes mellitus, both lean and non‐lean MASLD were significantly associated with an increased risk of carotid atherosclerosis progression compared to those who were lean without MASLD. This suggests that the evaluation of liver steatosis in patients with type 2 diabetes mellitus, regardless of body weight, may help identify individuals at high risk for carotid atherosclerosis progression.
INTRODUCTION
Type 2 diabetes mellitus is a heterogeneous disease with clinically diverse phenotypes 1 , arising from a complex interplay of various factors contributing to hyperglycemia 2 . Hepatic steatosis, a condition closely linked to insulin resistance, is a significant contributor to type 2 diabetes mellitus 3 . In general, hepatic steatosis is common in obese patients; however, it is also often identified in the lean population, with or without type 2 diabetes mellitus 4 . A meta‐analysis showed that lean nonalcoholic fatty liver disease 5 appears metabolically less severe than obese NAFLD 6 . However, recent studies suggest that despite having fewer metabolic comorbidities, these lean patients experience similar liver disease severity 7 and clinical outcomes 8 as their non‐lean counterparts. Patients with lean and non‐lean NAFLD also have similar risks of developing cardiovascular diseases (CVDs) and malignancies 9 .
The newly proposed criteria for metabolic dysfunction‐associated steatotic liver disease (MASLD) use five simple components of metabolic syndrome, including central or overall obesity, to encompass both lean and non‐lean patients with NAFLD. Notably, these criteria remove homeostasis model assessment‐insulin resistance (HOMA‐IR) and high sensitivity‐C‐reactive protein from the definition of the metabolic dysfunction‐associated fatty liver disease (MAFLD) criteria. This new nomenclature and criteria for MASLD were reported to be more appropriate for lean patients without type 2 diabetes mellitus compared to the previously proposed MAFLD criteria 10 .
While obesity and insulin resistance are well‐established risk factors for CVD in patients with type 2 diabetes mellitus, the association is less clear for lean individuals. Although studies have shown an increased cardiovascular risk in lean NAFLD, the evidence regarding long‐term outcomes in patients with type 2 diabetes mellitus remains inconclusive 11 , 12 . We aimed to investigate the risk of atherosclerosis progression in lean type 2 diabetes mellitus patients with MASLD.
MATERIALS AND METHODS
We analyzed data from the Seoul Metabolic Syndrome Cohort, a study that included 13,296 patients with type 2 diabetes mellitus treated at the Huh Diabetes Center between November 1997 and September 2016 13 , 14 . Patients were diagnosed with type 2 diabetes mellitus according to the American Diabetes Association criteria 15 . From this cohort, we enrolled patients aged ≥19 years who had undergone abdominal ultrasonography and carotid artery ultrasonography at baseline and had repeated carotid ultrasonography after 6–8 years. Excluded criteria were as follows: patients (1) aged <19 years; (2) diagnosed with type 1 diabetes; (3) pregnant; and (4) diagnosed with liver diseases other than MASLD, such as viral hepatitis, autoimmune liver disease, or hepatocellular carcinoma 16 . "Additionally, participants with a history of heavy alcohol consumption—defined as >210 g/week for men and >140 g/week for women—were excluded to emphasize metabolic factors over alcohol‐related pathology", as it provides rationale for excluding individuals with heavy alcohol consumption in order to focus on metabolic rather than alcohol‐related causes of liver disease 17 . Patients with bilateral carotid artery plaques at baseline were excluded to ensure the detectability of new plaque development, while those with unilateral plaques were included to assess contralateral plaque progression. This selection process yielded a final cohort of 828 patients who underwent abdominal ultrasonography and repeat carotid artery ultrasonography at baseline and after 6–8 years of follow‐up. MASLD was defined as hepatic steatosis, confirmed by ultrasonography, in the presence of type 2 diabetes mellitus, a key cardiometabolic risk factor, consistent with current diagnostic criteria 18 . Patients were categorized into four groups based on MASLD status (present or absent) and BMI classification (lean or not lean). The four groups were lean without MASLD, lean with MASLD, non‐lean without MASLD, and non‐lean with MASLD. The Institutional Review Board and Ethics Committee of Inha University Hospital approved the study protocol (IRB No. 2024‐07‐006), which was conducted in accordance with the Declaration of Helsinki principles.
Measurements and definitions of clinical and laboratory parameters
Baseline information, including medical and family history, medication use, and anthropometric measurements (weight, height, and waist circumference), was collected from the participants. Venous blood samples were also drawn after an 8 h fast. Blood tests were performed to assess various parameters, including insulin resistance and β‐cell function. HOMA2‐IR and β‐cell function were estimated using the HOMA 2 calculator based on C‐peptide concentration (University of Oxford, Oxford, UK) 19 . Lean status was defined as BMI <23 kg/m2 by the guideline for Asians 20 . Individuals who consumed alcohol twice a month or more were defined as regular alcohol consumers, and those who had smoked more than five packs of cigarettes were considered ever‐smokers. Participants underwent abdominal ultrasonography after an 8 h fast to evaluate hepatic steatosis using a 3.5 MHz transducer on an iU22 ultrasound system (Philips Healthcare, Andover, MA, USA). As previously described, the degree of steatosis was assessed semi‐quantitatively (absent, mild, moderate or severe), and MASLD was diagnosed based on the criteria for patients with type 2 diabetes mellitus 18 , 21 .
Carotid atherosclerosis measurements
All participants underwent repeated carotid ultrasonography using a LOGIQ7 system (GE Healthcare, Chicago, IL, USA) by trained technicians blinded to patient information. The mid and distal common carotid artery was scanned by lateral longitudinal projection, and carotid intima‐media thickness (IMT; mm) was measured at three points: far wall of mid, distal common carotid artery, and 1 cm proximal to the carotid bulb. Mean carotid IMT was defined as the distance between the lumen‐intima interface and media‐adventitia interface, of which the mean value of three measurements on each side was used to represent carotid atherosclerosis status 22 . Carotid plaque was defined as meeting at least one of the following criteria: (1) carotid intima‐media thickness (IMT) of ≥1.5 mm, (2) atherosclerotic protrusion into the lumen exceeding 50% of the surrounding thickness, or (3) distinct areas of hyperechogenicity 23 . Progression of carotid atherosclerosis was defined as the appearance of new plaque lesions on repeat ultrasonography.
Statistical analysis
Categorical variables are presented as numbers (proportions) and compared using the chi‐squared test. Continuous variables are presented as medians with interquartile ranges (IQRs) and analyzed using the Kruskal–Wallis test for intergroup comparisons, followed by the Dunn procedure for post‐hoc analysis. Multivariate logistic regression analysis was conducted to determine the odds ratio (OR) of carotid atherosclerosis progression based on MASLD presence in lean or non‐lean BMI categories. Confounding factors were adjusted stepwise: Model 2 adjusted for age and sex; Model 3 further adjusted for the duration of type 2 diabetes mellitus, glycated hemoglobin (HbA1c) level, time of enrollment, and follow‐up duration; Model 4 additionally adjusted for low‐density lipoprotein cholesterol (LDL‐C) and high‐density lipoprotein cholesterol (HDL‐C) levels, history of hypertension, and the presence of carotid plaque at baseline. To explore the potential influence of concomitant medication use, we performed a supplementary logistic regression analysis adjusting for baseline use of diabetes medications (metformin, insulin, sodium‐glucose cotransporter 2 inhibitors, dipeptidyl peptidase‐4 inhibitors, sulfonylureas, thiazolidinediones) and antihypertensive drugs (renin‐angiotensin system inhibitors, calcium channel blockers, thiazides) in addition to the covariates in Model 4. To evaluate the robustness of our findings and address potential bias from pre‐existing plaques, we performed a sensitivity analysis restricted to participants without carotid plaques on either side at baseline. Statistical significance was set at P < 0.05. All analyses were performed using IBM SPSS Statistics (version 26.0; IBM Corp., Armonk, NY, USA).
RESULTS
Among the total 828 patients with type 2 diabetes mellitus, 197 patients (23.8%) were classified as lean without MASLD, 57 (6.9%) as lean with MASLD, 177 (21.4%) as non‐lean without MASLD, and 397 (47.9%) as non‐lean with MASLD. Table 1 summarizes the baseline characteristics of the participants. Compared to the lean without MASLD group, patients with lean MASLD had significantly higher levels of HOMA2‐IR, an indicator of insulin resistance (P < 0.05). However, no other statistically significant differences were observed between these groups. Patients with non‐lean MASLD had the highest levels of BMI, HOMA2‐IR, triglycerides, LDL cholesterol, aspartate aminotransferase, alanine aminotransferase, and waist circumference (all P < 0.05).
Table 1.
Baseline characteristics
| Study population | Lean | Lean | Non‐lean | Non‐lean | P‐value |
|---|---|---|---|---|---|
| Without MASLD | With MASLD | Without MASLD | With MASLD | ||
| N = 828 | N = 197 | N = 57 | N = 177 | N = 397 | |
| Female, n (%) | 116 (58.9) | 41 (71.9) | 113 (63.8) | 227 (57.2) | 0.117 |
| Smoking, ever, n/total (%) | 58 (33.9) | 15 (29.4) | 47 (31.8) | 126 (36.4) | 0.645 |
| Regular alcohol consumption, n/total (%) | 60 (34.39) | 11 (21.6) | 54 (34.8) | 126 (36.2) | 0.237 |
| History of hypertension, n/total (%) | 40 (20.3) | 18 (31.6) | 72 (40.7) | 152 (37.8) | <0.001 § |
| Age, years | 57.0 (11.0) | 59.0 (11.0) | 57.0 (13.0) | 56.0 (13.0) | 0.631 |
| BMI, kg/m2 | 21.5 (2.1) | 22.0 (1.0) | 25.3 (2.7)* , † | 25.8 (3.5)* , † | <0.001 |
| DM duration, years | 5.0 (8.0) | 6.0 (9.0) | 5.0 (8.0) | 5.0 (8.0) | 0.091 |
| HOMA2‐beta | 98.7 (84.1) | 107.9 (76.3) | 124.6 (79.3)* | 128.2 (85.9)* | <0.001 |
| HOMA2‐IR | 3.3 (1.7) | 4.2 (2.5)* | 4.2 (1.9)* | 5.2 (2.6)* , † , ‡ | <0.001 |
| Total cholesterol | 182.0 (51.0) | 183.0 (80.0) | 191.0 (49.0) | 200.0 (55.0)* | <0.001 |
| Triglyceride | 94.0 (71.0) | 120.0 (79.0) | 109.0 (72.0)* | 144.0 (91.0)* , † , ‡ | <0.001 |
| HDL cholesterol | 52.0 (18.0) | 49.0 (17.0) | 50.0 (16.0) | 47.0 (14.0)* , ‡ | <0.001 |
| LDL cholesterol | 106.4 (48.3) | 107.6 (48.4) | 116.0 (43.3) | 115.6 (47.4)* | 0.019 |
| AST, IU/L | 23.0 (9.0) | 22.0 (10.0) | 23.0 (9.0) | 27.0 (13.0)* , † , ‡ | <0.001 |
| ALT, IU/L | 20.0 (10.0) | 23.0 (10.0) | 21.0 (10.0) | 29.0 (20.0)* , † , ‡ | <0.001 |
| Systolic BP, mmHg | 129.0 (22.0) | 127.0 (24.0) | 134.0 (24.0)* , † | 134.0 (24.0)* , † | <0.001 |
| Diastolic BP, mmHg | 83.0 (13.0) | 81.0 (14.0) | 85.0 (15.0) | 87.0 (14.0)* , † | <0.001 |
| Waist circumference, cm | 75.0 (7.0) | 77.5 (7.0) | 84.0 (8.0)* , † | 87.0 (10.0)* , † , ‡ | <0.001 |
| HbA1c, % | 7.7 (2.9) | 8.0 (2.2) | 7.4 (2.2) | 8.1 (2.2) ‡ | 0.002 |
| Fasting blood glucose, mg/dL | 132.0 (64.0) | 136.0 (49.0) | 127.0 (50.0) | 137.0 (55.0) | 0.118 |
| Mean IMT | 0.74 (0.20) | 0.74 (0.14) | 0.76 (0.21) | 0.76 (0.21)* | 0.021 |
Variables are shown as median (IQR) or n (%).
P < 0.05, vs lean without MASLD, by post‐hoc analysis.
P < 0.05, vs lean with MASLD, by post‐hoc analyses.
P < 0.05, vs non‐lean without MASLD, by post‐hoc analyses.
Significant chi‐squared test, P < 0.05.
Abbreviations: ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMI, body mass index; BP, blood pressure; DM, diabetes mellitus; HbA1c, glycated hemoglobin; HDL‐cholesterol, high‐density lipoprotein cholesterol; HOMA, homeostasis model assessment; IMT, intima‐media thickness; IR, insulin resistance; LDL‐cholesterol, low‐density lipoprotein cholesterol; MASLD, metabolically associated steatotic liver disease.
The mean carotid IMT at baseline differed among the groups (P = 0.021) and non‐lean with MASLD patients had the highest value, which is also significantly higher than the mean carotid IMT for lean without MASLD by post‐hoc analysis (P < 0.05). After an average follow‐up of 7 years, the proportion of participants who experienced carotid plaque progression differed significantly across the four subgroups (P = 0.025). Notably, the lean patients with MASLD had the highest proportion of progression among the groups (47.4%; Figure 1).
Figure 1.
Progression of carotid atherosclerosis according to body mass index and hepatic status. Proportions of carotid atherosclerosis progression in patients classified as lean without MASLD, lean with MASLD, non‐lean without MASLD, or non‐lean with MASLD. Significance level: P = 0.025 (chi‐squared test). MASLD, metabolically associated steatotic liver disease.
We compared the progression of carotid atherosclerosis among the groups using multivariate logistic regression with multistep adjustments. Compared to patients in the control group (the lean without MASLD group), those with lean MASLD had a significantly higher OR for carotid plaque progression (OR 2.16; 95% CI 1.18–3.94; P = 0.013) without adjustment. This association remained statistically significant after adjusting for other clinical variables including age, sex, duration of type 2 diabetes mellitus, HbA1c, time of enrollment, follow‐up duration, LDL‐C, HDL‐C, history of hypertension, and the presence of carotid plaque at baseline and the lean MASLD group had a significantly higher OR for carotid plaque progression compared to the control group (adjusted OR 2.57, 95% CI 1.33–4.97; P = 0.005). Similarly, the non‐lean with MASLD group also had a significantly increased OR for progression (OR 1.64; 95% CI 1.13–2.36; P = 0.008), which persisted after adjustments (adjusted OR 1.59; 95% CI 1.05–2.42; P = 0.029) as shown in Table 2. The non‐lean without MASLD group did not exhibit an increased risk of developing new plaque lesions. In a supplementary analysis adjusting for baseline diabetes and antihypertensive medication use (Table S1), the significant association between lean MASLD and carotid atherosclerosis progression persisted, consistent with the main findings, though limited to baseline medication data.
Table 2.
Risk of carotid atherosclerosis progression according to body mass index and hepatic status
| Group (Event number/Total number) | Lean without MASLD (58/197) | Lean MASLD (27/57) | Non‐lean without MASLD (68/177) | Non‐lean MASLD (161/397) | |||
|---|---|---|---|---|---|---|---|
| OR | P‐value | OR | P‐value | OR | P‐value | ||
| Model 1 | 1 (Reference) | 2.16 (1.18–3.94) | 0.013 | 1.50 (0.97–2.30) | 0.067 | 1.64 (1.13–2.36) | 0.008 |
| Model 2 | 1 (Reference) | 2.18 (1.17–4.07) | 0.015 | 1.48 (0.95–2.31) | 0.084 | 1.71 (1.17–2.49) | 0.006 |
| Model 3 | 1 (Reference) | 2.60 (1.34–5.01) | 0.004 | 1.70 (1.06–2.72) | 0.029 | 1.65 (1.10–2.47) | 0.015 |
| Model 4 | 1 (Reference) | 2.57 (1.33–4.97) | 0.005 | 1.62 (1.00–2.63) | 0.051 | 1.59 (1.05–2.42) | 0.029 |
Odds ratios with 95% CI for carotid atherosclerosis progression of each group in comparison to the control (lean without MASLD group) from multivariable logistic regression analysis are shown. Model 1 = crude model without any adjustment; Model 2 = Model 1 + age, sex; Model 3 = Model 2 + duration of diabetes, HbA1c, time of enrollment, follow‐up duration; Model 4 = Model 3 + low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, history of hypertension, and the presence of carotid plaque at baseline. HbA1c, glycated hemoglobin; MASLD, metabolically associated steatotic liver disease.
In a sensitivity analysis limited to 551 participants without carotid plaques on either side at baseline (Table S2), the association between lean MASLD and carotid atherosclerosis progression remained consistent with the main findings (adjusted OR 3.02; 95% CI 1.35–6.78; P = 0.007), indicating that pre‐existing plaques did not substantially alter the overall results.
In addition to the between‐group analysis, we attempted a within‐group statistical analysis to determine whether the presence of leanness affected plaque progression within the group of patients with MASLD. There was no significant difference in the risk of plaque progression between the lean and non‐lean patients from a crude model to a fully adjusted model in those with MASLD (all P > 0.05; Table 3).
Table 3.
Risk of carotid atherosclerosis progression according to body mass index in patients with MASLD
| Total | Non‐lean MASLD | Lean MASLD | |
|---|---|---|---|
| OR | P‐value | ||
| Model 1 | 1 (Reference) | 1.32 (0.76–2.30) | 0.330 |
| Model 2 | 1 (Reference) | 1.28 (0.72–2.28) | 0.407 |
| Model 3 | 1 (Reference) | 1.57 (0.86–2.89) | 0.144 |
| Model 4 | 1 (Reference) | 1.61 (0.88–2.98) | 0.126 |
Odds ratios for carotid atherosclerosis progression. Model 1 = crude model without any adjustment; Model 2 = Model 1 + age, sex; Model 3 = Model 2 + duration of diabetes, HbA1c, time of enrollment, follow‐up duration; Model 4 = Model 3 + low‐density lipoprotein cholesterol, high‐density lipoprotein cholesterol, history of hypertension, and the presence of carotid plaque at baseline. (Logistic regression analysis).
HbA1c, glycated hemoglobin; MASLD, metabolically associated steatotic liver disease.
DISCUSSION
This 7‐year follow‐up study of 828 patients with type 2 diabetes mellitus found that MASLD was associated with an increased risk of carotid artery plaque progression, even among lean individuals. Lean patients with MASLD exhibited a significantly higher ORs for plaque progression compared to their lean counterparts without MASLD. Within the MASLD group itself, no significant difference in plaque progression risk was observed based on lean status.
Potential mechanisms underlying lean MASLD include dietary factors (e.g., high fructose or high‐fat intake) and altered body fat distribution (e.g., visceral obesity) 24 . Recent studies have shown that while lean individuals with hepatic steatosis may have lower insulin resistance compared to overweight or obese counterparts, they still exhibit higher levels compared to healthy individuals without fatty liver disease 6 . Notably, this study also observed higher insulin resistance levels in the lean MASLD group compared to the lean without MASLD group. This association between higher insulin resistance and increased risk of atherosclerosis has been documented in previous research 25 .
Data on long‐term outcomes in lean NAFLD patients remain limited. An observational study suggested a lower incidence of cardiovascular diseases and metabolic abnormalities in lean NAFLD patients compared to non‐lean NAFLD patients 26 . However, conflicting evidence challenges this observation. For instance, an analysis of NHANES III data reported a significantly higher 15‐year cumulative mortality rate in non‐obese NAFLD patients (51.7%) compared to obese NAFLD patients (27.2%) 27 . Similarly, recent studies indicate comparable risks of cardiovascular disease (CVD) between lean and non‐lean NAFLD patients 9 . A population‐based study further revealed that lean NAFLD patients exhibited a higher atherosclerotic cardiovascular disease (ASCVD) score and prevalence of high CVD risk compared to those with obese NAFLD, with approximately 30% of lean NAFLD participants also having type 2 diabetes mellitus 12 . Moreover, prior research has established lean NAFLD as a risk factor for incident CVD 28 , 29 , 30 , and our findings align with these studies by demonstrating an increased risk of carotid atherosclerosis progression in lean MASLD patients with type 2 diabetes mellitus. Together, this evidence supports the American Gastroenterological Association's recommendation for NAFLD screening in lean individuals with type 2 diabetes mellitus 31 .
The mechanism underlying the increased atherosclerosis risk observed in lean MASLD patients in this study remains unclear. However, existing evidence provides some insight. Compared to obese NAFLD, lean NAFLD is associated with a more favorable liver histology, including less severe steatohepatitis and fibrosis. Nevertheless, lean NAFLD represents a distinct entity characterized by metabolic, biochemical, and inflammatory abnormalities when compared to healthy individuals without steatotic liver disease 6 . Additionally, patients with NAFLD often have abnormal body fat distribution, characterized by increased visceral adipose tissue, despite normal overall body fat mass 4 . Visceral fat tissue is linked to both NAFLD development and increased CVD risk, while subcutaneous fat can play a protective role by acting as a metabolic reservoir 32 . A recent study by Kim et al. found that lean NAFLD patients exhibit increased visceral fat despite their non‐obese status, potentially driving elevated inflammatory cytokines and insulin resistance, which could further link visceral adiposity to NAFLD progression and cardiovascular risk 33 . This mechanism may contribute to the increased carotid atherosclerosis progression observed in our lean MASLD cohort. Additionally, sarcopenia—a condition of reduced muscle mass more prevalent in lean NAFLD patients—may also heighten plaque progression risk 34 .
This study has some limitations. First, adjustments for other metabolic indicators and various event variables that changed during the study period may have been insufficient to fully account for confounding factors. Additionally, our analysis relied on baseline characteristics and did not account for changes in medication use over the 6–8‐year follow‐up period, despite their potential effects on atherosclerosis progression. A supplementary analysis adjusting for baseline medication use (Table S1) supported our main findings, but the lack of longitudinal medication data remains a limitation. Second, while ultrasonography is a valuable tool for diagnosing NAFLD in large studies, it has limitations in terms of diagnostic accuracy. Furthermore, the absence of histological information makes it challenging to determine the association of MASLD with hepatic fibrosis. In addition, this study was limited to participants who completed follow‐up carotid intima‐media thickness (IMT) assessments, potentially introducing selection bias. Individuals lost to follow‐up may have experienced cardiovascular events or mortality, which could have influenced our findings. However, our cohort was derived from a single institution with a structured longitudinal follow‐up protocol, where those completing repeat IMT assessments after 6–8 years. This systematic approach may have minimized the impact of selection bias, though it remains a limitation warranting cautious interpretation of the results.
Despite these limitations, this study found that lean MASLD was significantly associated with a higher risk of progression to carotid atherosclerosis compared to lean individuals without MASLD, similar to non‐lean MASLD in patients with type 2 diabetes mellitus. The risk of atherosclerosis progression was similar between the lean and non‐lean MASLD groups. These findings suggest that type 2 diabetes mellitus patients, regardless of weight status, should be screened for MASLD. Early identification of MASLD can inform proactive management strategies to reduce CVD risk.
DISCLOSURE
The authors declare no conflict of interest.
Approval of the research protocol: The Institutional Review Board and Ethics Committee of Inha University Hospital approved the study protocol (IRB No. 2024‐07‐006), which was conducted in accordance with the Declaration of Helsinki principles.
Informed Consent: N/A.
Approval date of Registry and the Registration No. of the study/trial: N/A.
Animal Studies: N/A.
Supporting information
Table S1. Risk of carotid atherosclerosis progression according to body mass index and hepatic status.
Table S2. Risk of carotid atherosclerosis progression according to body mass index and hepatic status in patients without baseline carotid plaque.
ACKNOWLEDGMENTS
This study was supported by the Inha University Research Grant. The funding source was not involved in conducting the research or preparing this article.
DATA AVAILABILITY STATEMENT
The datasets generated and/or analyzed in the current study are available from the corresponding author upon reasonable request.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Table S1. Risk of carotid atherosclerosis progression according to body mass index and hepatic status.
Table S2. Risk of carotid atherosclerosis progression according to body mass index and hepatic status in patients without baseline carotid plaque.
Data Availability Statement
The datasets generated and/or analyzed in the current study are available from the corresponding author upon reasonable request.