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.