Metabolic dysfunction-associated steatotic liver disease is associated with vascular dysfunction in type 1 diabetes

Metabolic dysfunction-associated steatotic liver disease (MASLD) is linked to atherosclerotic cardiovascular disease (ASCVD). Markers of arterial stiffness and subclinical atherosclerosis (carotid-femoral pulse wave velocity [cfPWV], and carotid-intima media thickness [CIMT]) and endothelial dysfunction (flow-mediated dilation [FMD], nitroglycerine-induced dilation [NID]) are potential ASCVD predictors. This study examined the correlation between vasculopathy and MASLD in type 1 diabetes (T1D).

We conducted cross-sectional vascular assessments in non-smoking adults with T1D without ASCVD. MASLD was determined by ultrasound and transient elastography. FIB-4 was calculated as a marker of fibrosis. ASCVD risk scores were assessed using the Steno Type 1 Risk Engine. Subjects were included in a 2:1 control-to-case ratio and matched for age and diabetes duration.

We examined 105 subjects, of whom 30 had MASLD. Mean age was 51.7 ± 15.7 years, mean diabetes duration was 29.9 ± 14.3 years. 50% were male, mean HbA1c was 55.1 ± 9.5 mmol/mol (7.2 ± 0.9%). MASLD was associated with lower NID (15.3 ± 6.3 vs. 20.1 ± 7.5%, p = 0.003). NID and cfPWV were more often impaired in people with MASLD (53.3% vs. 28.4%, p = 0.018, 56.7% vs. 35.1%, p = 0.043, respectively). In adjusted multivariable logistic regression, MASLD was associated with increased cfPWV (OR 8.30, 95% CI 1.25-55.2, p = 0.029), as was age, sex and mean arterial pressure. cfPWV and CIMT strongly correlated with 5-year ASCVD risk (cfPWV ρ = 0.76, CIMT ρ = 0.81, p < 0.001), as did FIB-4 (ρ = 0.74, p < 0.001). CIMT (0.93), cfPWV (0.88) and FIB-4 (0.88) yielded the highest AUROC to identify significant ASCVD risk.

cfPWV is the most robust vascular marker associated with MASLD in people with T1D. cfPWV, CIMT and FIB-4 correlated strongly to incident 5-year ASCVD risk. Sven Francque, Hilde Heuten and Christophe De Block have claimed equal senior authorship.