Epicardial adipose tissue volume, plaque vulnerability and myocardial ischemia in non-obstructive coronary artery disease

Ingela Khan; Caroline A Berge; Ingeborg Eskerud; Terje H Larsen; Eva R Pedersen; Mai Tone Lønnebakken

doi:10.1016/j.ijcha.2023.101240

Epicardial adipose tissue volume, plaque vulnerability and myocardial ischemia in non-obstructive coronary artery disease

Int J Cardiol Heart Vasc. 2023 Jul 13:49:101240. doi: 10.1016/j.ijcha.2023.101240. eCollection 2023 Dec.

Authors

Ingela Khan¹, Caroline A Berge^{1

2}, Ingeborg Eskerud¹, Terje H Larsen^{2

3}, Eva R Pedersen^{1

2}, Mai Tone Lønnebakken^{1

2}

Affiliations

¹ Department of Clinical Science, University of Bergen, Jonas Lies veg 87, 5021 Bergen, Norway.
² Department of Heart Disease, Haukeland University Hospital, Haukelandsveien 22, 5021 Bergen, Norway.
³ Institute of Biomedicine, University of Bergen, Jonas Lies vei 91, 5009 Bergen, Norway.

Abstract

Background: Epicardial adipose tissue (EAT) accumulation has been associated with inflammation, atherosclerosis and microvascular dysfunction. Whether increased EAT volume is associated with coronary plaque vulnerability and demand myocardial ischemia in patients with non-obstructive coronary artery disease (CAD) is less explored.

Methods: In 125 patients (median age 63[58, 69] years and 58% women) with chest pain and non-obstructive CAD, EAT volume was quantified on non-contrast cardiac CT images. EAT volume in the highest tertile (>125 ml) was defined as high EAT volume. Total coronary plaque volume and plaque vulnerability were quantified by coronary CT angiography (CCTA). Demand myocardial ischemia was detected by contrast dobutamine stress echocardiography.

Results: High EAT volume was more common in men and associated with higher BMI, hypertension, increased left ventricular mass index (LVMi), C-reactive protein (CRP) and positive remodelling (all p < 0.05). There was no difference in age, coronary calcium score, total and non-calcified plaque volume or presence of demand myocardial ischemia between groups (all p ≥ 0.34). In a multivariable model, obesity (p = 0.006), hypertension (p = 0.007) and LVMi (p = 0.016) were independently associated with high EAT volume. Including plaque vulnerability in an alternative model, positive remodelling (p = 0.038) was independently associated with high EAT volume.

Conclusion: In non-obstructive CAD, high EAT volume was associated with cardiometabolic risk factors, inflammation and plaque vulnerability, while there was no association with demand myocardial ischemia or coronary plaque volume. Following our results, the role of EAT volume as a biomarker in non-obstructive CAD remains unclear.

Keywords: Cardiac CT; Coronary plaque burden; Coronary plaque vulnerability; Epicardial adipose tissue volume; Myocardial ischemia.