Objective: To compare the epicardial fat volume (EFV), assessed by computed tomography angiography (CTA), in subjects with recent myocardial infarction (MI) ver-sus subjects with unstable angina. Moreover, we aimed to evaluate the relationship between increased EFV, the amount of myocardial scar tissue and left ventricular function after an acute myocardial infarction.
Methods: 18 subjects were included in the MultiPlaque trial (NCT NCT03391908) and underwent CT assess-ment for unstable angina (n=9, 50%) or for post-MI evaluation of coronary arteries, at 1 month after MI (n=9, 50%). EFV was calculated for each patient on the basis of CT scanning and left ventricular ejection frac-tion, myocardial scar was assessed on MRI evaluation, using Q-Mass software developed by Medis BV (Lei-den, The Netherlands).
Results: Mean EFV values were 158.24 +/- 55.0 mm3 (95% CI 41.3–61.2). EFV presented significantly higher values in patients with recent MI as compared to pa-tients with unstable angina (173.32 +/- 56.1, 95% CI 131.1–257.1 vs. 118.72 +/- 35.3, 95% CI 82.7-149.3, p=0.02). LVEF average values were 53.12% +/- 17.2% (95% CI 41.3–92.4%). Linear regression analysis iden-tified a good positive correlation between: (1) EFV and hs-CRP levels (r=0.62, p=0.01), indicating that increa-sed EVF is corelated with inflammatory status, and (2) between EF and EFV (r=0.46, p=0.04), showing that a larger EFV represents a marker of a decreased left ventricular performance. The amount of myocardial assessed via MRI presented a positive correlation with the amount of epicardial fat by CT (r=0.49, p=0.03), and a negative correlation with left ventricular ejection fraction (r=-0.74, p<0.0001).
Conclusions: EFV, as new imaging-derived marker of augmented inflammation, is significantly increased in patients with recent myocardial infarction and is asso-ciated with a decreased LVEF and a larger myocardial scar, indicating that: (1) the inflammatory status is more pronounced in the post-acute MI period than in unstable angina (2) the presence of a persistent increa-sed inflammatory response in the post-infarction peri-od may be responsible for the remodelling process and decreased ventricular function.