4 Discussion
Our study mainly found that EAT thickness in front of the right
ventricular free wall measured by TEE was significantly positively
correlated with left atrial size, but significantly negatively
correlated with left atrial phasic function.
EAT is biologically active tissue that is unevenly distributed between
the myocardial and the visceral pericardium. There is no fascial barrier
between EAT and myocardial, so local EAT can slow down conduction
through fat infiltration, damage to the myocardial interstitium, and
self-tissue fibrosis, thereby affecting myocardial electrophysiology
[5]. EAT also promotes adjacent myocardial fibrosis by paracrine
release of multiple adipose cytokines [6]. Similarly, there are no
fascial boundaries between the atrium and the ventricles, thus, multiple
adipose cytokines secreted by EAT around the left ventricle can reach
the atrium and affect atrial fibrosis [7]. A variety of inflammatory
mediators secreted by EAT are also closely related to the occurrence of
AF [8]. In addition, EAT is rich in autonomic ganglion plexus, and
the excitation of sympathetic and parasympathetic nerves can increase
intracellular calcium concentration and shorten action potential
duration, thus promoting the occurrence and development of AF [9].
Left atrial remodeling is crucial in the occurrence and development of
AF, and EAT participates in this process through the above various
pathophysiological mechanisms. Moreover, left atrial remodeling is also
an important indicator of the prognosis of AF [10]. Therefore, early
identification of left atrial remodeling and timely intervention may
slow or even reverse this pathophysiological process, while improving
prognosis. Our study found that compared with control group, EAT
thickness in paroxysmal AF group and persistent AF group increased
sequentially, and the difference was statistically significant. This is
consistent with the findings of previous studies [11]. Similarly,
van Rosendael et al. [12]applied CT to quantitatively assess EAT
around the left atrium and found that it was independently associated
with AF. Through above studies, we found that EAT was closely related to
the occurrence and development of AF.
In the occurrence and development of AF, the pathological changes caused
by initial trigger factors cause atrial remodeling through the formation
of functional AF matrix [13]. The enlargement of left atrium
indicates that atrium has remodeled. Wong et al. [14] found that
pericardial fat volume by MRI was positively correlated with left atrial
volume in patients with AF. Yorgun et al. [15] used CT to measure
EAT thickness and found that it was correlated with the presence and
type of AF, and significantly related to the LAD. Our study showed that
LAD, LAImax, LAVIp and LAVImin increased sequentially in control group,
paroxysmal AF group and persistent AF group, and EAT thickness was
significantly positively correlated with left atrial size. Those results
were consistent with previous studies. According to our studies, the
increase of EAT thickness may cause structural changes in left atrium,
which can reflect the structural change trend of left atrium.
Left atrial phasic function is a sensitive parameter that reflects the
changes in left atrial structure and function, and can early detect
myocardial motion changes caused by left atrial remodeling. It mainly
includes reservoir function, booster function and conduit function.
LATEF and LASr represent reservoir function; LAAEF and LASct represent
booster function; LAPEF and LAScd represent conduit function. Our study
demonstrated that the left atrial reservoir function, booster function
and conduit function were sequentially decreased in control group,
paroxysmal AF group and persistent AF group. Hopman et al. [16]
found that compared with the control group, the left atrial reservoir
strain, conduit strain and systolic strain in AF group were
significantly reduced, and the left atrial strain in the persistent AF
group was lower than in paroxysmal AF group, but there was no
significant difference between the two groups, which is slightly
different from the results of our study, and may be affected by
different subjects. In addition, in order to further study the
relationship between EAT and left atrial, and to deeply explore the
mechanism of EAT leading to left atrial remodeling. Our study attempted
to analyze the correlation between EAT thickness and left atrial phasic
function. The results showed that EAT thickness was significantly
negatively correlated with left atrial reservoir function, booster
function and conduit function. The above studies all confirmed that with
the increase of EAT thickness, left atrial function showed a downward
trend. Compared with LAD, our study comprehensively assessed the left
atrial phasic function by RT-3DE and 2DD-STI, which more accurately
reflected the changes of left atrial structure and function. And the
results of our study showed that both LAD and more sensitive left atrial
phasic function were significantly correlated with EAT thickness.
Combined with the results of our study and previous studies, it is
further confirmed that there is a certain connection between EAT and
left atrium of patient with AF. The increased thickness of EAT may be
one of the important mechanisms of left atrial remodeling.
The result of this study showed that EAT thickness measured by TTE and
left atrial phasic function assessed by RT-3DE and 2D-STI had good
reproducibility and reliability. At present, the evaluation of left
atrial size is generally based on LAD measured by TTE, but the irregular
remodeling of left atrium makes it difficult to accurately assess left
atrial size. With the development of three-dimensional technology,
RT-3DE has achieved accurate assessment of left atrial structure and
function. MRI is the gold standard to evaluate left atrial structure and
function. Mor-Avi et al. [17] used the left atrial function
parameters measured by MRI as reference, and found that RT-3DE and MRI
had a better correlation in evaluating left atrial function, and they
were more accurate than two-dimension echocardiographic parameters. In
addition, 2D-STI is also widely used in the evaluation of early changes
in myocardial function, which can sensitively detect myocardial strain
damage in the early stage of the disease and quantitatively evaluate the
changes in left atrial function. Therefore, our study selected RT-3DE
and 2D-STI to comprehensively assess left atrial phasic function. With
the deepening of research on EAT, noninvasive examination has become the
main way to evaluate EAT, mainly including MRI, CT and TTE. Compared
with MRI and CT, TTE is more convenient, economical, and easier to
popularize in clinical practice.
Our study also has a few limitations. First, the research subjects
included in this study were relatively small. Second, EAT thickness
measured by TTE was not compared with other techniques, such as MRI and
CT. Therefore, the follow-up will continue to expand the sample size and
combine other techniques to further explore the mechanism of EAT on the
left atrial structure and function in patients with AF.