The role of inflammation in atherosclerosis has
been a topic of interest in recent years. Many studies
have shown that inflammation in plaque formation,
in addition to intimal damage and lipid accumulation,
plays a key role in the mechanism of atherosclerosis.
The accumulation of cellular and humoral structures
involving in the mechanism of inflammation has
become a guide for these studies.[
1,
2] Later studies
have attempted to identify the proinflammatory
structures having paracrine or endocrine effects on the
inflammation to discover novel treatment strategies to
overcome plaque formations in the arterial wall.[
3] In
our study, we mainly observed the numerical increase
in the inflammatory cells in EAT of the patients
having CAD.
Epicardial adipose tissue was initially thought to
be responsible for the storage of energy substrates
and behaving as a guard for myocardium; however, later studies showed several soluble products
produced by adipocytes in the EAT.[5,6] During any
inflammatory process, inflammatory cells and several
cytokines increase in the tissues nearby the culprit
lesions.[7] Mazurek et al.[8] showed in their study that
inflammatory cells and markers were significantly
higher in the EAT samples of patients with CAD. In
our study, similarly, we found a significantly higher
accumulation of inflammatory cells in the EAT tissue
samples of CAD group than the control group.
In another study of İzgi,[9] EAT was described
as a local player of atherosclerosis in the coronary
artery walls with its neighborhood. In this study, the
author emphasized by referring several studies that the
increase of the inflammatory cells and markers in the
EAT samples were not seen in the serum samples of
the same patients. Additionally, in a study of Erdogan
et al.,[10] the decrease in coronary flow was associated
with the increased epicardial adipose tissue thickness,
independent of serum CRP levels.[10] Similarly, in our
study, the measurement of inflammatory cells and
markers (CRP and ESR) in the serum samples did
not show any significant increment. Moreover, in the
study of Yeşilkaya,[11] no significant relationship was
found between systemic inflammation and mortality
after CABG. This result may suggest a consideration
about the interaction of solely local inflammatory of
EAT with coronary arterial atherosclerosis.
Beside the increase of inflammatory cells in the
EAT taken from the RAA in the CAD patients
compared to those without CAD, the increment
of inflammatory cells was also similar in the periarterial
EAT in the CAD patients. In addition to our
findings, Moos et al.[12] observed the inflammatory
cells accumulation in the adventitia rather than the
intima. Taken together, these findings indicate that
the EAT may have a proinflammatory effect on
atherosclerosis, rather than the inflammatory process
in the EAT occurred secondary to intimal injury.[13]
The main limitation of this study was its small
sample size. In addition, although sample collections
were made prospectively, preoperative data were
obtained retrospectively.
In conclusion, our study showed that both periarterial
and atrial EAT inflammation significantly
increased in patients with CAD. This result may
suggest that inflammation in EAT have a significant
relationship with the CAD’s pathogenesis. However,
further large-scale, prospective studies are needed to
confirm these findings.
Declaration of conflicting interests
The authors declared no conflicts of interest with respect
to the authorship and/or publication of this article.
Funding
The authors received no financial support for the research
and/or authorship of this article.