Clinically inferred MASLD was not an independent predictor of atrial fibrillation presence (OR 0.96; 95% CI 0.59-1.46), though AF subtypes exhibited a clear phenotypic gradient.
Case-Control (n=327)
No
Is clinically inferred metabolic dysfunction-associated steatotic liver disease independently associated with the presence of atrial fibrillation and its subtypes?
Clinically inferred MASLD is not independently associated with the presence of atrial fibrillation, though AF subtypes demonstrate a phenotypic gradient from metabolic to cardio-renal profiles.
Odds Ratio: 0.96 (95% CI 0.59–1.46)
Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) has been linked to atrial fibrillation (AF); however, its relationship with specific AF subtypes remains unclear. This prospective, single-center, observational case–control study investigated whether MASLD is independently associated with AF presence and its subtypes. Materials: A total of 327 participants were analyzed, including 119 controls and 208 patients with AF. Comprehensive clinical history, anthropometric measures, laboratory testing, 24 h Holter ECG, and echocardiography were performed. Clinically inferred MASLD was defined according to the current EASL–EASD–EASO guidelines using clinical and non-invasive indices (Hepatic Steatosis Index, Fatty Liver Index, Fibrosis-4 Index). No liver biopsy or imaging confirmation of steatosis or fibrosis was performed, and therefore, the diagnosis represents a clinically inferred (“probable”) MASLD. To minimize systematic bias and improve baseline comparability between groups, propensity score matching and complementary regression analyses were applied. Results: Overall probable MASLD prevalence did not differ between AF and controls (42% vs. 44%, p = 0.742). A clear phenotypic gradient emerged across subtypes: lowest in permanent AF (PermAF, 27.1%) versus paroxysmal (47.1%) and persistent AF (51.4%) (p = 0.021). PermAF exhibited the most advanced comorbidity—highest CHF (78.6%), CKD (71.4%), HFpEF (48.6%), FIB-4 (median 2.67), the lowest TG/HDL–cholesterol ratio (1.93 vs. 3.32; p < 0.001), and progressive renal impairment. Statin therapy reached 80% in clinically inferred MASLD-positive PermAF. The elevated FIB-4 observed in PermAF must be interpreted with explicit caution: this group was substantially older (median 79.5 years) and carried the highest burden of chronic heart failure and chronic kidney disease; therefore, in this subgroup, FIB-4 most plausibly reflects age and cardio-renal comorbidity rather than histologically confirmed hepatic fibrosis. After matching, MASLD was not an independent predictor of AF presence (OR = 0.96; 95% CI: 0.59–1.46) or its clinical severity. Conclusions: Probable MASLD, defined by clinical and non-invasive indices, was not independently associated with AF in this cohort, but AF subtypes exhibited a clear phenotypic gradient—from a metabolically driven profile in early AF to a cardio-renal and fibrotic pattern in advanced, elderly AF. Elevated FIB-4 values in PermAF most plausibly reflect age and cardio-renal comorbidity rather than true histologically confirmed hepatic fibrosis. These findings support a phenotype- and population-dependent MASLD–AF relationship and underscore the need for imaging- and histology-verified longitudinal studies.
Różycka-Kosmalska et al. (Tue,) conducted a case-control in Atrial Fibrillation and Metabolic dysfunction-associated steatotic liver disease (n=327). Metabolic dysfunction-associated steatotic liver disease (MASLD) vs. No MASLD was evaluated on Atrial fibrillation presence (OR 0.96, 95% CI 0.59-1.46). Clinically inferred MASLD was not an independent predictor of atrial fibrillation presence (OR 0.96; 95% CI 0.59-1.46), though AF subtypes exhibited a clear phenotypic gradient.