Author's Reply.

To the Editor,

We thank the authors for their comments and interest in our study titled “Epicardial adipose tissue thickness is associated with myocardial infarction and impaired coronary perfusion” (1) published in the Anatol J Cardiol 2015; 15: 224-31. In the last decade, many studies have highlighted an association between epicardial adipose tissue thickness (EAT) and coronary artery disease (CAD); thus, it has been proposed as a marker to detect cardiovascular risk. Of course, an ideal biomarker should reflect the degree of atherosclerosis, predict cardiovascular events, and indicate improvement after intervention. In addition, it would be further desirable if a biomarker could be easily and non-invasively measured, and if the measurement was reproducible and standardized (2).

As the authors mentioned, there has been a debate on the preferred method to measure EAT and on the range that should be considered as normal. Echocardiography is the method used to assess EAT by Iacobellis et al. (3) since 2003, and it is identified as the echo-free space between the outer wall of the myocardium and the visceral layer of the pericardium perpendicular to the free wall of the right ventricle at endsystole. Although some investigators suggested that the measurement should be made at the end-diastole to coincide with other imaging modalities such as computed tomography (CT) and magnetic resonance imaging (MRI), many authors including Iacobellis et al. (3), the investigator who first presented echocardiographic EAT thickness to the literature, prefer to measure EAT at end-systole because EAT may be compressed at end-diastole.

An important point is to set a clear and widely accepted reference range for a biomarker, as mentioned previously. Although EAT has been studied for more than a decade, there is no universally accepted cut-off point above which the EAT values can be definitely considered as abnormal. Many studies have provided cut-off values, but these studies have evaluated EAT from different points of view, such as its association with atherosclerosis, subclinical atherosclerosis, presence of CAD, extent of CAD, and plaque morphology. Thus, there are many proposed EAT cut-off values in the literature. However, in the light of the current literature, EAT thickness of >5 mm is safely considered as abnormal (4).

Another important point in the evaluation of EAT is the method of choice. Echocardiography is easily available, inexpensive, and reproducible, as mentioned previously. CT and MRI have also been increasingly used to assess the amount of EAT, and they have high spatial resolution; their most important advantage is the possibility of volumetric assessment. However, similar to echocardiography, there is no universally accepted cut-off value above which EAT is considered as abnormal (4).

The authors mentioned the study by Saura et al. (5) that reports a poor reproducibility and poor tomographic concordance for echocardiographic EAT measurement. However, it may not be appropriate to depend on a single study to conclude that echocardiography is not a reliable method. There are many other studies that report a good correlation of echocardiographic EAT determination with CT and MRI (6).

The aim of our study was to show the association between EAT thickness, myocardial infarction, and coronary perfusion. We agree that EAT still has a long way to go before universally accepted ranges are set, and other criteria that are needed to establish a marker as a routinely used one are fulfilled. Nevertheless, we think that the findings of our study add to the current literature as we provide a cut-off value to predict AMI and poor coronary perfusion among patients with a clinical diagnosis of CAD.