Epicardial adipose tissue and nonvalvular atrial fibrillation

Abstract

\n \n \n Several studies revealed the relationship between epicardial fat tissue (EF) and development of atrial fibrillation (AF). Though pathophysiological mechanisms are not clear enough, the anatomy and location EF as a part of visceral adiposity tissue could lead to proinflammatory and fibrotic changes in atrial myocardium.\n \n \n \n To evaluate the paracrine effects of EF and detect the association of tissue Doppler imaging (TDI) parameters, EF thickness by cardiac magnetic resonance tomography (CMR) and biochemical markers of fibrosis and inflammation in patients with nonvalvular AF without concomitant coronary artery disease.\n \n \n \n Thirty-nine patients with idiopathic paroxysmal AF, normal or slightly enlarged left atria (LA) (mean LA diameter 4,5±0,6cm) were included. The mean age was 50,8±13,9 y.o., 19 (49%) were men. The absence of coronary lesions was confirmed by angiography in all cases. Besides standard ECG and ECHO, all patients underwent TDI and CMR with late gadolinium enhancement. EP thickness at anterior left ventricular (LV) wall was estimated by CMR. The myocardial fibrotic and proinflammatory biomarkers levels - matrix metalloproteinases (MMP-2, MMP-9), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) were estimated. Kendall rank correlation coefficient was used. If the |τ| >Tcr, the correlation ranked as statistically significant.\n \n \n \n The epicardial fat thickness was associated with TIMP-1 plasma level (τ=0,71; Tcr=0,18) and MMP-9 (τ=0,65; Tcr=0,16). Among clinical factors weight was slightly associated with fat thickness (τ=0,33; Tcr=0,26). Besides, we found correlation of MMP-9, TIMP-1 with E/e by TDI (τ=0,65; Tcr=0,16 and τ=0,56; Tcr=0,21, relatively); and with maximal systolic strain of lateral LV wall (τ=−0,37; Tcr=0,18 and τ=−0,44; Tcr=0,16, relatively) and interventricular septum (τ=−0,36; Tcr=0,18 and τ=−0,44; Tcr=0,16, relatively).\n \n \n \n The epicardial fat thickness by CMR is significantly associated with myocardial fibrosis markers (MMP-9, TIMP-1) in patients with AF without structural heart disease. The increasing levels of MMP-9 and TIMP-1 are associated with LV local contractility disturbances by TDI in patients with AF. This association demonstrates the paracrine effect of EF, which could lead to atrial remodeling and formation AF substrate even in patients without valvular and ischemic heart disease and with normal or slightly enlarged LA\n \n \n \n Type of funding sources: None.\n