Epicardial fat thickness and serum transaminase values in myocardial infarction with concomitant metabolic-associated fatty liver disease

Aim. To assess the relationship between epicardial fat thickness (EFT) and metabolic-associated fatty liver disease (MAFLD), including hepatic steatosis (HS) and steatohepatitis, in myocardial infarction (MI), as well as to analyze the changes of transaminase levels in patients with a combination of ST-elevation MI (STEMI) and MAFLD to accurately identify liver disease.

Material and methods. A total of 163 patients with ST-elevation myocardial infarction (STEMI) (n=144) and non-ST-elevation myocardial infarction (NSTEMI) (n=19) with metabolic syndrome (MetS) were admitted for primary coronary angiography and percutaneous intervention (PCI). Eighty-two patients had concomitant MAFLD (55 with steatosis and 27 with steatosis). Liver elastometry, EFT measurement, cardiac troponin I levels, alanine and aspartate aminotransferase (ALT and AST) levels, and cytokeratin-18 fragment concentrations were measured.

Results. MAFLD in patients with MI compared to patients without liver pathology is associated with higher EFT (p<0,01). According to two-way analysis of variance, a stable increase in blood AST and ALT levels was established for the combination of MI and MAFLD (p<0,05, generalized η² effect size ≥0,11 for both aminotransferases). In STEMI combined with steatohepatitis, compared to HS and STEMI without MAFLD (control), a significantly higher EFT (p<0,01), AST (p<0,05) and ALT (p<0,001) levels were noted.

Conclusion. MAFLD in patients with MI is associated with an increase in EFT. For the combination of STEMI-steatohepatitis, compared to STEMI-HS and STEMI without MAFLD, a higher EFT was observed. This may indicate not only the role of EFT in acute coronary pathology but also the relationship of this indicator with MAFLD severity. In uncomplicated STEMI, analysis and interpretation of transaminase activity in assessing MAFLD are recommended no earlier than 10 days.

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