Impact of epicardial adipose tissue accumulation on left ventricular mass and hypertrophy in non-obstructive coronary artery disease

Abstract

Introduction Increased left ventricular mass index (LVMi) and left ventricular hypertrophy (LVH) by echocardiography are common in obesity and important cardiovascular risk predictors associated with myocardial ischemia in non-obstructive coronary artery disease (CAD). Accumulation of epicardial adipose tissue (EAT) suggest a possible direct impact on LVMi and LVH. Purpose To explore the association between EAT volume, LVMi and LVH in patients with chest pain and non-obstructive CAD. Methods We included 129 patients with chest pain and non-obstructive CAD (<50% stenosis) by coronary computed tomography (CT) angiography. EAT volume was quantified using a semiautomatic analysis software on non-contrast cardiac CT images. Patients were grouped according to EAT volume, where high EAT volume was adjudicated when EAT volume was in the highest tertile (≥125 ml). Left ventricular mass was assessed by echocardiography, calculated by the Devereux formula and indexed for height in the allometric power of 2.7 (LVMi). LVH was defined as LVMi >46.7 g/m2.7 in women and >49.2 g/m2.7 in men. Coronary artery plaque burden was assessed as calcium score and segment involvement score on coronary CT angiography. Results High EAT volume was more common in men with higher BMI, waist circumference, serum triglycerides and higher prevalence of hypertension and obesity (all p<0.05). Age, coronary calcium score and coronary artery segment involvement score did not differ between groups. Patients with high EAT volume had higher LVMi compared to those with low EAT volume (42.5 g/m2.7 vs. 36.1 g/m2.7, p=0.003), while there was no difference in EAT volume among patients with or without LVH. In univariable logistic regression analysis, high EAT volume was associated with higher LVMi (OR 1.05 [95% CI 1.01–1.10] per g/m2.7, p=0.015). After adjusting for hypertension and obesity in a multivariable model, higher LVMi remained significantly associated with high EAT volume (Model 1, Table 1), but the association was attenuated after adjusting for sex (Model 2, Table 1). Conclusion High EAT volume was associated with increased LVMi in patients with non-obstructive CAD, independent of hypertension and obesity, while there was no association with LVH. This suggest that direct infiltration of adipose tissue in the myocardium may contribute to the development of increased LVMi. FUNDunding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): Western Norwegian Regional Health Authorities Table 1