Dan Mu1, Xiuzheng Yue2, and Xiance Zhao2
1Department of Radiology, Affiliated Nanjing Drum Tower Hospital of Nanjing University Medical School, nanjing, China, 2Philips Healthcare, Shanghai, China
Synopsis
Keywords: Atherosclerosis, Cardiovascular
Epicardial
adipose tissue (EAT) is a novel factor for risk stratification of coronary
artery disease. EAT in microvascular
obstruction formation in patients with ST-segment elevation myocardial infarction
(STEMI) remain unclear. This study aimed to evaluate the correlation between
EAT and MVO volume detected by CMR on a clinical 1.5T CMR system with a
28-channel coil array in STEMI patients.
Synopsis
Epicardial
adipose tissue (EAT) is a novel factor for risk stratification of coronary
artery disease. EAT in microvascular
obstruction formation in patients with ST-segment elevation myocardial infarction
(STEMI) remain unclear. This study aimed to evaluate the correlation between
EAT and MVO volume detected by CMR on a clinical 1.5T CMR system with a
28-channel coil array in STEMI patients.Introduction
Epicardial
adipose tissue (EAT), a metabolically active fat depot between the visceral pericardium
and the outer margin of the myocardium, has gradually emerged as a novel target
for risk stratification of coronary artery disease due to its distinctive
location and multifaceted metabolic properties. Microvascular obstruction (MVO)
after primary percutaneous coronary intervention (pPCI) is identified as an
independent risk factor for poor prognosis in patients with acute myocardial
infarction (AMI). However, the clinical implications of EAT in microvascular
obstruction formation in patients with ST-segment elevation myocardial
infarction (STEMI) remain unclear. Recently, cardiac magnetic resonance (CMR)
has emerged as the gold standard technique to detect the extent of MVO and
evaluate EAT volume. This study aimed to evaluate the correlation between EAT
and MVO volume detected by CMR in STEMI patients.Methods
A
total of 129 STEMI patients who underwent pPCI successfully were enrolled
between February 1, 2022 to August1, 2022. Clinical characteristics, including
demographic characteristics, cardiovascular risk factors, laboratory data, and
angiographic parameters, were recorded from each patient by 1 trained physician.
All patients underwent CMR on a clinical 3.0T MR system (Ingenia CX, Philips Healthcare,
Best, The Netherlands) with a 28-channel body phase array coil within 1 week
following pPCI. PSIR-LGE and black-blood T2WI in three different views were
used to evaluate infarct size, MVO volume, and EAT distribution. All
CMR data were analyzed using Q-MASS MR 8.1 imaging system (Medis, Leiden, The
Netherlands) and interpreted twice by 2 expert radiologists who were blinded to
the angiographic and clinical data of patients.Results
Compared
to STEMI patients without MVO, STEMI patients with MVO presented with higher
peak troponin-T levels, an increase in neutrophil-lymphocyte ratio (NLR) and
C-reactive protein (CRP), larger infarct size, and compromised left ventricular
ejection fraction (LVEF%). Total EAT volume, EAT mass index, left atrioventricular
EAT volume, left atrioventricular EAT mass index, and thickness of EAT in the
left atrioventricular groove were unanimously associated with the occurrence of
MVO. The left atrioventricular EAT mass index in STEMI patients with MVO was
significantly larger than that in STEMI patients without MVO (24.72±5.049 g/m2 vs. 18.63±3.670 g/m2,
P<0.001). Multivariate logistic regression analysis demonstrated that NLR,
peak troponin T levels, and left atrioventricular EAT mass index were
independent predictors of MVO. Left ventricular EAT mass significantly
predicted the presence of MVO (area under the curve [AUC]: 0.83 [95% CI: 0.760
to 0.895; P<0.001). Discussion & Conclusions
The
left atrioventricular EAT mass index is an independent predictor of MVO.
Measurement of EAT using CMR could be used for risk stratification and may be a
promising target in developing new therapies to reduce myocardial reperfusion
injury in patients with STEMI. A quick identification of a high
EAT mass index could define a subset of patients in which potential therapeutic
strategies, such as GLP-1 or targeted therapy against EAT, could be developed
to alleviate myocardial damage.Acknowledgements
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