Author`s Reply.

To the Editor,

We would like to thank the authors for their comments on our article in their letter entitled “Epicardial adipose tissue and atrial fibrillation: the other side of the coin.” published in Anatol J Cardiol 2017; 17: 56-63. (1) epicardial adipose tissue (EAT), a special fat depot that is related to visceral fat rather than total adiposity, shares the same microcirculation with the myocardial tissue and coronary vessels. Recent studies have identified EAT as an active organ, which secretes several mediators, called adipokines, affecting the vascular system. In a prior study, we determined that EAT is associated with diastolic dysfunction and left atrial dilatation because of local or systemic effects in untreated hypertensive patients (2). We also revealed that EAT is an independent factor for adverse changes in the carotid intima-media thickness, flow-mediated dilation, and pulse wave velocity (3). Vascular structure and functions were mainly related to EAT, possibly with perivascular adiposity.

In our opinion, EAT has two main causative roles in atrial fibrillation (AF) development. The first role is the direct local interactions, which predispose the myocardial tissue to arrhythmic genesis due to abnormal atrial architecture, adipocyte infiltration, and atrial fibrosis (4). The second role is the indirect effects on left atrium reflecting from vasculature, which is mainly related to increased blood pressure because of increase in the peripheral vascular resistance after structural and functional impairment in the vascular endothelium (3). The latter mechanism is also a possible driver of the diastolic heart failure and diastolic dysfunction (2) as well as AF. Therefore, as a phrase, “peripheral resistive” may be more reason-oriented than “diastolic” in heart failure with preserved ejection fraction. These roles may be important in the prevention/management of cardiovascular diseases.