Inflammatory activity of adipose tissue.

To the Editor,

There is growing interest in inflammation, adipose tissue, and the atherosclerotic process in vessels. As a result of recent studies, it is known that obesity and increased epicardial adipose tissue are important factors affecting the pathogenesis of atherosclerosis. Adipose tissue releases inflammatory mediators like an endocrine organ. It produces cytokines, such as adiponectin, leptin, resistin, and interleukins, and these mediators cause an increase in inflammatory activation in the arterial wall. Adipose tissue acts as a source of proinflammatory activity, and it is therefore called obesity-related inflammatory activity (1).

We read the article entitled “An increase in epicardial adipose tissue is strongly associated with carotid intima-media thickness and atherosclerotic plaque, but LDL only with the plaque” published in The Anatolian Journal of Cardiology 2017; 17: 56-63 by Kocaman et al. (2) with great interest. The authors sought to investigate whether epicardial adipose tissue (EAT) has proliferative effect on carotid intima-media thickness (CIMT) and carotid plaque. They concluded that EAT had a relationship with both CIMT and the presence of carotid plaque. The authors also said that this finding suggested that EAT thickness may be a risk factor and a biomarker, playing an important role beginning in early stages of atherosclerosis. We congratulate the authors for these valuable results, which are compatible with the literature. They also drew attention to an interesting topic related to the inflammatory capacity of adipose tissue. There are hypotheses related to interactions of the heart and epicardial fat. One suggests that lack of fascia between heart and epicardial fat allows inflammatory mediators to easily diffuse to the vessels and myocardium (1). Having read the authors’ report, we want to contribute to a seemingly missing aspect. In the results of the study, it was reported that EAT correlated to BMI, waist circumference, and CRP, in addition to CIMT (p<0.001) (Table 2). CIMT, BMI, waist circumference, and presence of carotid plaque increased with increase of EAT thickness (p<0.001) (Table 3). These results show that CIMT and carotid plaque formation may also be related to obesity of the study patients, as EAP and BMI are directly proportional in the study. In the limitations section, the authors said that their study group had increased visceral adipose tissue. BMI is a widely used marker of obesity and there are many studies about obesity and inflammatory effect on progression of atherosclerosis (1). So there is a need to differentiate whether these results belong to visceral or epicardial adipose tissue. The authors were also interested in question of if CRP level increased as EAT thickness increased, and if there is a possible inflammatory link between EAT and CIMT. We think there is a need for more studies to investigate the inflammatory pathways of EAT, independent of other clinical variables like obesity, and that there is also a need for a patient group that isolates increase in EAT to obtain more significant results.