148-OR: People with Type 2 Diabetes Are at Greater Risk for Liver Fibrosis after Recent Myocardial Infarction

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Introduction and Objective: Type 2 diabetes (T2D) is linked to increased risk of cardiovascular diseases and metabolic dysfunction-associated steatotic liver disease (MASLD, previously known as non-alcoholic fatty liver disease), both resulting in worse long-term outcomes. Non-invasive tests (e.g. non-alcoholic fatty liver disease fibrosis score (NFS), fibrosis-4 test (FIB-4)), are increasingly used for risk stratification of liver fibrosis. However, the link between myocardial infarction (MI) and risk of liver fibrosis is not yet well understood. We hypothesized that people with recent MI bear a higher risk of liver fibrosis within the first year post-MI. Methods: Participants of the DIabetes and ST-segment Elevation MI (DISTEMI) study underwent comprehensive phenotyping at 6-12 weeks after MI (0Y, n=103, age 61±9 years, 76% male, BMI 28±4 kg/m2) and were followed for one year (1Y, currently n=84). Based on a 75-g oral glucose tolerance test, participants were assigned to either normoglycemia (25%), prediabetes (46%) or T2D (29%). The ejection fraction (EF) was quantified by magnetic resonance imaging, while NFS and FIB-4 were calculated using laboratory and anthropometric parameters. Results: The EF declined by about 5% from 0Y to 1Y (53±10% vs 51±10%, p<0.01), which was mainly driven by the T2D group (52±12% vs. 48±11%, p<0.05). FIB-4 rose by about 12% (1.28±0.85 a.u. vs. 1.43±0.90 a.u., p<0.001), which was independent of age and glucose tolerance, while the NFS increased by 56% (-1.10±1.47 a.u. vs. -0.61±1.28 a.u., p<0.0001). At 1Y, EF was inversely associated with NFS (r=-0.27, p<0.05), but not with FIB-4 (r=-0.22, p=0.10). Conclusion: One year after myocardial infarction, people with type 2 diabetes show a reduction in the left ventricular ejection fraction along with a rise in indices of liver fibrosis. The intricate interaction between the liver and the heart in acute and chronic phase after recent MI deserves further studies to dissect the impact of organ specific and systemic metabolic alterations on organ function. Disclosure C. Möser: None. O.P. Zaharia: None. F.C. Michelotti: None. V. Schrauwen-Hinderling: None. S. Trenkamp: None. G. Heilmann: None. P. Bobrov: None. V. Burkart: None. R. Wagner: Speaker's Bureau; Boehringer-Ingelheim, Novo Nordisk. Advisory Panel; Sanofi. Speaker's Bureau; Sanofi. Advisory Panel; Lilly Diabetes. J. Szendroedi: Advisory Panel; Novo Nordisk, Lilly Diabetes, Novartis AG, Boehringer-Ingelheim. M. Cramer: None. C. Jung: None. M. Kelm: None. M. Roden: Research Support; Boehringer-Ingelheim. Advisory Panel; Echosens. Speaker's Bureau; Madrigal Pharmaceuticals, Inc. Advisory Panel; MSD Life Science Foundation. Board Member; Novo Nordisk. Advisory Panel; TARGET PharmaSolutions, Inc. Funding Special Research Area (Sonderforschungsbereich, SFB) 1116 B12

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