Author`s Reply.

To the Editor,

We thank the authors for their interest in our study entitled “Epicardial adipose tissue thickness is associated with myocardial infarction and impaired coronary perfusion.” published in Anatolian Journal of Cardiology reporting an association between acute myocardial infarction and increased epicardial adipose tissue (EAT) (1). As mentioned, the association between coronary atherosclerosis and EAT has been demonstrated in many studies using either echocardiography or computed tomography (CT)/magnetic resonance imaging (MRI). EAT is three dimensional and its evaluation using CT or MRI would provide more accurate information about its volume. However, studies using echocardiography and CT/MRI have shown that these techniques are in good compliance (2). We think that it is important to categorize a patient as having increased EAT rather than precisely providing the exact EAT volume to classify a patient as “at high cardiovascular risk”. Echocardiography is adequate for that purpose and is advantageous because it is inexpensive, repeatedly and easily available in almost every cardiology clinic.

The authors mentioned that EAT may have cardioprotective properties because of the secretion of anti-inflammatory and anti-atherogenic adipokines such as adiponectin and adrenomedullin, and cited Iacobellis et al. (3) However, in that study, Iacobellis et al. (3) found that EAT partially contributed to the adiponectin levels in the coronary circulation. Instead, intracoronary adiponectin levels reflected the adiponectin levels in the peripheral circulation. In addition, Iacobellis et al. (4) also stated that adrenomedullin gene and protein expression in EAT were downregulated in the presence of CAD, and there was no direct evidence that EAT contributed to intracoronary adrenomedullin levels.

We agree with the authors that stable angina pectoris, unstable angina pectoris, and acute myocardial infarction (AMI) are different clinical entities with respect to pathophysiology, presentation, and clinical management; however, we think that there is some merit in showing that EAT thickness is different among different clinical entities and providing a cut-off value to predict AMI. We accept that EAT is associated with traditional risk factors such as diabetes, hypertension, age, waist circumference, and metabolic syndrome (5). However, EAT has an additional predictive value over these, as there are studies highlighting an independent association between CAD and well-known risk factors.

We provided an association between increased EAT thickness and AMI. Apparently, this was not a prospective study where patients were followed in terms of adverse cardiac events. However, there are recent follow-up studies in the literature reporting increased cardiovascular death and myocardial infarction in patients with thicker EAT, that can be considered as supportive based on our hypothesis (6).

Finally, we think that patients with increased EAT thickness should receive more aggressive risk factor modification. What we mean by saying that is to maximize proved medical therapies based on cardiovascular protection in accordance with the current relevant guidelines. Although physicians agree on the idea of prescribing mortality reducing medications in maximum applicable doses, real life experience is not so promising. These high risk patients may be followed up closer than others to check for the status of the modifiable risk factors.