Epicardial fat and coronary artery disease: An open debate.

To the Editor,

Epicardial adipose tissue (EAT), a source of several adipokines, is located between the outer wall of the myocardium and the visceral layer of the pericardium. The paracrine or vasocrine secretion of several bioactive molecules such as tumor necrosis factor alpha, interleukin-6, plasminogen activator inhibitor-1, and resistin from EAT may have a promoting effect on atherosclerosis (1). Indeed, several studies have reported a positive association between epicardial fat thickness (EFT) and coronary artery disease (CAD) (2, 3).

We read with great interest the article titled “Epicardial adipose tissue thickness is associated with myocardial infarction and impaired coronary perfusion” published by Tanındı et al. (4) in Anatol J Cardiol. They reported that increased EFT is associated with acute myocardial infarction (AMI), and it may prove beneficial for identifying patients who would need more aggressive approach in terms of risk reduction.

In agreement with previous studies (1-3), the present study provides further information which aims to determine the relationship between impaired coronary perfusion and EFT in a wide range of chest pain syndromes.

As mentioned by the authors, the measurement of EFT with two-dimensional echocardiography has some advantages, including easy accessibility, rapid applicability, and good reproducibility. However, EAT has a three dimensional distribution and two-dimensional echocardiography may not provide sufficient information about the total epicardial volume (1).

It has been demonstrated that EAT may display cardioprotective properties by secreting antiinflammatory and antiatherogenic adipokines such as adiponectin and adrenomedullin. It may also promote the expansion of the coronary lumen during the early phases of atheromatous plaque obstruction (5). On the other hand, stable angina pectoris, unstable angina pectoris, and AMI are different clinical entities with respect to pathophysiology, presentation, and management. It would be useful if Tanındı et al. (4) examined the association between EFT and CAD after adjusting for other cardiovascular risk factors. Therefore, the conclusion stated by Tanındı et al. (4) should be interpreted with caution because their correlations do not necessarily prove causation.

Main issues that need to be answered are as follows: Is epicardial fat a modifiable risk factor or how can we translate these encouraging results into the clinical practice? More importantly, what is the mean of more aggressive approach other than percutaneous coronary intervention, statins, anticoagulants, and other therapies in a wide range of patient population as per the present study?

In conclusion, the role of EAT in atherosclerosis is an open debate. Further clinical and experimental studies are needed to determine the function of EAT in different pathological conditions.