4.1 Main results
This study mainly showed an association between increasing EAT and AFACS
occurrence. To investigate the relationship between EAT volume, both
total and LA specified EAT, as well as EAT thickness and AFACS
occurrence, three different meta-analyses were conducted. The findings
were similar, which showed a positive association between increased EAT
and AFACS occurrence. Surprisingly, the similar findings in EAT
thickness and EAT volume put emphasis on the value of echocardiography
in evaluation of EAT, which is a safe and non-invasive imaging modality24.This study, the first attempt to prove the
association between EAT and AFACS occurrence, suggested a new possible
imaging marker to predict AFACS, which will require further research.
4.2 EAT and AFACS
Although the mechanism of increased EAT leading to AFACS is still
unclear, studies that demonstrated association between abundant EAT and
AF can be taken into account. EAT locates between the myocardium and
visceral pericardium, mainly on the right ventricle surface and anterior
wall of the left ventricle. It also surrounds atrioventricular grooves
and great coronary vessels, reaching the main thickness at the anterior
and lateral walls of right atrium 25. Due to the
position, It exerts local paracrine effect with findings of increased
expression of numerous inflammatory markers, and as a metabolically
active tissue modulating the adjacent myocardial tissue with abundant
ganglionated plexus of autonomic nervous system15,26,27. At the same time, abundant EAT has been
illustrated to be associated with fatty infiltration into adjacent
myocardium by histopathological evidence 28. Mahajan
and Zghaib et al 29,30 proved EAT could cause lower
bipolar voltage and electrogram fractionation as electrophysiologic
substrates for AF. Besides, there is a speculate that the imbalance
between excessive oxidative stress and the protective effect of
adiponectin ultimately leads to the occurrence of AF31.
The similarity is that AFACS associates with a combination of factors:
clinical variables, intraoperative surgical variables,
electrocardiograph markers and echocardiographic predictors. In detail,
advanced age, hypertension, male gender, right coronary artery stenosis,
depressed left ventricular function, a remote history of previous AF,
combined valve replacement/coronary artery bypass grafting procedures,
prolonged aortic cross-clamp and bypass times, PR-interval, QRS
duration, abnormal left ventricular systolic and diastolic function,
left ventricular hypertrophy and increased left atrial volume may
predispose to postoperative AF 32-36. And AFACS was
also proved to be associated with the occurrence of systemic
inflammatory response syndrome with inflammatory markers, including
IL-6, IL-8, C-reactive protein, tumor necrosis factor-α and indices of
neutrophil and platelet activation, increasing significantly in the
systemic bloodstream 37,38. Electrolyte imbalance,
especially hypokalaemia, is also considered to be a triggering factor of
AFACS 37,39.
It has been proved that obesity or a high BMI was a risk factor for AF40,41. Compared with non-obese people, obese
individuals have a higher probability (49%) of suffering with AF, which
may be related with atrial enlargement, ventricular diastolic
dysfunction and increased ectopic fat depot 41. And,
in other reports, EAT was proved to be associated with AF even after
adjustment for AF risk factors, including a high BMI13,42 . However, Echahidi et al. 37reported that metabolic syndrome and obesity were independent risk
factors for AFACS. And EAT is associated with obesity or high BMI42. So, whether EAT should be regarded as an
independent trigger or a modulator of obesity of AFACS requires further
delineation.
In this study, it is known that increased EAT is associated with AFACS,
soreducing EAT maybe potential to decrease the AFACS. Antidiabetic drugs
were used for diabetes mellitus patients, which might decrease EAT and
the accumulation of EAT, including
Thiazolidinediones43, glucagon-like peptide 1 receptor
agonists44, Dipeptidyl peptidase-4
inhibitors45 and Sodium-dependent glucose transporters
2 inhibitors46. Besides, weight loss by diet control
or exercise suggested to decrease EAT in interventricular groove, which
suggests a correlation with improved insulin resistance and insulin
sensitivity indexes47. A control study (in vivo and in
vitro) performed on aortic stenosis patients who underwent a cardiac
surgery suggested that statin therapy was related to EAT thickness
reduction, which seemed secondary to the characteristics of statins
anti-inflammatory effect48. Considering EAT containing
large amount of ganglionated plexi, an increasing number of studies
aimed at lowered AF inducibility due to injecting botulinum toxin into
canine epicardial autonomic ganglia49. Although it was
hypothetical, still promising to be a potential novel therapeutic
option. All of these therapies not only might reduce EAT, but decrease
incidence of many other diseases, especially metabolic diseases which is
closely associated with AFACS.
Ten studies fell into sub-groups as per measuring methods of EAT,
including echocardiography and CT. Comparatively, the results measured
by CT were more preferred than echocardiography, because EAT was not
uniformly distributed around the heart. Echocardiographic probe
angulation on 2-dimensional imaging could decrease reproducibility and
accuracy, as well as unable to measure periatrial fat or total EAT
volume. And echocardiographic measurement might increase the EAT
thickness, because overlapping with perivascular adipose tissue. But
when patients had coronary atherosclerosis history, which enlarged
thickness of EAT, image analysis probably provided accurate measurement.
Accordingly, Nerlekar et.al50 proved that EAT measured
by CT compared with echocardiography revealed poor correlation, and
discrepancy was particularly obvious at higher EAT thickness.