Key result
Post-acute myocardial infarction was associated with higher non-culprit perivascular adipose tissue mean attenuation compared to stable CAD (mean difference 8.01 HU; 95% CI 5.90-10.11; P<0.001).
Why the study?
To identify differences in CT-derived PVAT and EAT characteristics that may indicate inflammatory status differences between post-treatment AMI and stable CAD patients.
Does post-acute myocardial infarction status alter CT-derived perivascular and epicardial adipose tissue characteristics compared to stable coronary artery disease?
Cross-Sectional (n=410)
Does post-acute myocardial infarction status alter CT-derived perivascular and epicardial adipose tissue characteristics compared to stable coronary artery disease?
Mean Difference: 8.01 (95% CI 5.9–10.11)
p-value: p=<0.001
Post-AMI patients exhibit higher CT-derived PVAT and EAT attenuation compared to stable CAD patients, suggesting increased cardiac adipose tissue inflammation following AMI.
May reflect post-AMI adipose inflammation on CT; hypothesis-generating and should not yet change practice.
AIMS: To identify differences in CT-derived perivascular adipose tissue (PVAT) and epicardial adipose tissue (EAT) characteristics that may indicate inflammatory status differences between post-treatment acute myocardial infarction (AMI) and stable coronary artery disease (CAD) patients. METHODS AND RESULTS: A cohort of 205 post-AMI patients (age 59.8 ± 9.2, 92.2% male) was propensity-matched with 205 stable CAD patients (age 60.5 ± 10.0, 90.2% male). Coronary CT angiography and non-contrast CT scans were performed to assess PVAT mean attenuation across major coronary segments and EAT mean attenuation and volumes, respectively. For post-AMI patients, CT scans were conducted 28.6 ± 13.8 days after the AMI incidence. Post-AMI patients showed higher non-culprit PVAT and EAT mean attenuation than stable CAD patients (8.01 HU, 95% CI 5.90-10.11 HU, P < 0.001, 2.48 HU, 95% CI 0.83-4.13 HU, P = 0.003, respectively). The EAT volume percentage at higher attenuation levels was higher in post-AMI patients compared with stable CAD (33.93 cm3, 95% CI 16.86-51.00 cm3, P < 0.001), with the difference maximized at the -70 HU threshold (4.75%, 95% CI 3.64%-5.87%, P < 0.001). PVAT mean attenuation positively correlated with EAT mean attenuations and the percentage of EAT volume > -70 HU (P < 0.001 for both). CONCLUSION: Post-AMI patients showed higher PVAT and EAT attenuation than stable CAD patients, potentially indicating AMI-associated inflammatory cardiac adipose tissue changes. A total of -70 HU can act as a potential cut-off for inflamed EAT. These findings highlight the potential of using CT-derived adipose tissue characteristics to assess inflammation and guide post-AMI management strategies.
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Wang et al. (2025) conducted a cross-sectional in Acute myocardial infarction and stable coronary artery disease (n=410). Post-acute myocardial infarction vs. Stable coronary artery disease was evaluated on Non-culprit perivascular adipose tissue (PVAT) mean attenuation (MD 8.01 HU, 95% CI 5.90-10.11, p=<0.001). Post-acute myocardial infarction was associated with higher non-culprit perivascular adipose tissue mean attenuation compared to stable CAD (mean difference 8.01 HU; 95% CI 5.90-10.11; P<0.001).
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