https://doi.org/10.1007/s00392-025-02625-4
1Universitätsmedizin Göttingen Herzzentrum, Klinik für Kardiologie und Pneumologie Göttingen, Deutschland; 2Universitätsklinikum Schleswig-Holstein Medizinische Klinik II / Kardiologie, Angiologie, Intensivmedizin Lübeck, Deutschland; 3Kerckhoff Klinik GmbH Abteilung für Kardiologie Bad Nauheim, Deutschland; 4Forum Medizin GbR Kardiologie Rosdorf, Deutschland; 5Herzzentrum Leipzig - Universität Leipzig Klinik für Innere Medizin/Kardiologie Leipzig, Deutschland
Background
Epicardial adipose tissue (EAT) is receiving increasing attention in modern day cardiology as it may represent an additional cardiovascular risk factor. While EAT is often associated with obesity and diabetes, we set out to explore implications of increased EAT volumes on the prognosis of non-obese, non-diabetic patients following acute myocardial infarction.
Methods
A total of 699 non-obese (BMI<30kg/m2), non-diabetic patients underwent cardiovascular magnetic resonance imaging (CMR) within 10 days after invasive treatment of acute myocardial infarction via percutaneous coronary intervention. Cardiac morphological and functional parameters were obtained from CMR. EAT was quantified by manual delineation in CMR-derived short-axis stacks and indexed to the body surface area. The primary clinical outcome was defined as occurrence of major adverse cardiovascular events (MACE) after 12 months.
Results
After exclusion of incomplete and non-analysable datasets, the final cohort consisted of 540 patients (61±13years, 427 (79%) male). An optimal cut-off value of 32.1ml/m2 EAT volume was found to provide most accurate risk stratification using Youden’s index. Compared to the subgroup with low EAT volumes (≤32.1ml/m2, n=256), the group with increased EAT volumes (>32.1ml/m2, n=284) was of same age (61±13years vs. 62±13years, p=0.285), had similar BMI (25.6±2.7kg/m2 vs. 25.9±2.4kg/m2, p=0.172) but a slightly lower proportion of male patients (82.8% vs. 75.7%, p=0.043). Other cardiovascular risk factors including arterial hypertension, hyperlipoproteinemia and history of smoking had a balanced distribution across both subgroups. In comprehensive CMR analyses no differences were observed regarding biventricular morphology, biventricular function including left and right ventricular strain analyses as well LA functional analysis between patients with high and low EAT volumes. Furthermore, infarct size as measured by quantitative LGE analysis was similar between both groups (low EAT: 14.9±12.4% vs. high EAT: 15.3±12.2%, p=0.720). However, patients with increased EAT had higher rates of MACE after acute myocardial infarction (8.1% vs. 3.5%, p=0.023) (see Figure 1). Increased EAT volumes above 32.1ml/m2 remained independently associated with MACE after adjusting for age, sex and left ventricular ejection fraction in a multivariable regression model (HR 2.4 (95% Confidence interval 1.1 – 5.2); p=0.025).
Conclusion
Increased EAT volumes are associated with worse prognosis of non-obese, non-diabetic patients following acute myocardial infarction. EAT may qualify as an additional, yet underrecognized cardiovascular risk factor in metabolically healthier patients.
Figure 1: Kaplan-Meier plot of the occurrence of major adverse cardiac events (MACE) after acute myocardial infarction. The red curve shows the incidence of MACE in patients with high EAT volumes (>32.1ml/m2), compared to patients with low EAT volumes (≤32.1ml/m2). AMI – acute myocardial infarction, EAT – epicardial adipose tissue