Higher CMR-derived epicardial adipose tissue volume was independently associated with greater infarct size (β = 0.064, p = 0.032) and larger area at risk (β = 0.104, p = 0.018) post-AMI.
Does elevated epicardial adipose tissue volume increase acute myocardial injury in patients following acute myocardial infarction?
Increased epicardial adipose tissue volume is independently associated with greater acute myocardial injury (infarct size and area at risk) following acute myocardial infarction, suggesting a role in myocardial vulnerability.
Tasa de eventos absoluta: 0% vs 0%
Abstract Background Elevated epicardial adipose tissue volume (EATV) is increasingly recognized as a key contributor to cardiovascular disease by promoting myocardial remodeling and has been linked to adverse outcomes, including in acute myocardial infarction (AMI). However, the pathmomechanism for amplified risk after acute events like AMI remains unclear. Given that post-AMI myocardial injury drives adverse outcomes, we hypothesize that EAT-induced remodeling increases myocardial vulnerability to injury following AMI. Purpose To assess whether elevated EATV independently contribute to increased post-AMI myocardial injury, as quantified by cardiovascular magnetic resonance imaging (CMR). Methods A total of 1168 patients were prospectively enrolled in a multicentric study and underwent CMR within 10 days after percutaneous coronary intervention following AMI. After excluding cases with incomplete data or poor image quality, EATV were manually derived in 962 patients from short-axis cine images and indexed to body surface area. Left ventricular function, infarct size (IS), area at risk (AAR = myocardial edema – IS), and microvascular obstruction (MVO) were quantified (Figure 1A). IS, AAR, and MVO were indexed to myocardial mass and compared across EATV quartiles (Q1: 26.7ml/m2, n=237; Q2: 26.7-34.3ml/m2, n=241; Q3: 34.3-43.0ml/m2, n=240; Q4 43.0ml/m2, n=237). Associations between EATV and individual parameters of myocardial injury were analyzed using uni- and multivariable linear regression including patient demographics, cardiovascular risk factors, and parameters influencing severity of acute myocardial injury. Results Patients with EATV in the upper quartile were older (Q1-Q4: 63 vs. 62 vs. 62 vs. 66years; p = 0.002) and had a higher BMI (Q1-Q4: 27.4 vs. 27.8 vs. 28.0 vs. 28.9kg/m², p = 0.001) while all quartiles had a higher proportion of male patients (Q1-Q4: 76 vs. 77 vs. 70 vs. 72%; p = 0.288). As shown in Figure 1B, patients with higher EATV exhibited progressively increased IS and larger AAR. MVO demonstrated variability across EATV quartiles, while no discernible pattern emerged, and left ventricular ejection fraction and global longitudinal strain remained comparable across all quartiles (Figure 2B). In linear regression analyses, higher EATV was independently associated with greater IS (β =0.064; 95% CI: 0.005-0.122; p = 0.032), a larger AAR (β = 0.104; 95% CI: 0.017-0.190; p = 0.018), but smaller MVO (β = -0.024; 95% CI: -0.042 to -0.005; p = 0.012) (see Table 1). Conclusion Patients with increased CMR-derived EATV exhibited greater acute myocardial injury following AMI, as indicated by larger IS and AAR, whereas post-AMI left ventricular function was comparable to patients with smaller EATV. Notably, higher EATV was independently associated with the extend of myocardial injury, suggesting a role in myocardial vulnerability and underscoring the potential relevance for personalized preventive strategies.Figure 1A+B Table 1
Hagedorn et al. (Thu,) reported a other. Higher CMR-derived epicardial adipose tissue volume was independently associated with greater infarct size (β = 0.064, p = 0.032) and larger area at risk (β = 0.104, p = 0.018) post-AMI.