The main finding of the present study was the relationship between EAT and Strain, with significant differences between diabetic and non-diabetic patients.
This finding let us speculate that EAT may limit the deformation capacity of the cardiac myofibril. Consistently, Cho et al. found that EAT was associated with the degree of subclinical myocardial dysfunction (longitudinal strain), as well as with ventricular mass and high sensitivity C-reactive protein values . Similarly, Arnold et al. reported a significant association between EAT and longitudinal strain in subjects with metabolic syndrome, obesity and coronary artery disease .
Epicardial fat could induce dysfunction of myofibril deformity by different processes: 1) mechanical impairment: the increase in the EAT would limit the movement of the myocardium, and 2) inflammation: epicardial fat has histological characteristics of brown fat, which is in close proximity with coronary arteries and has the potential ability to secrete pro-inflammatory adipokines and free fatty acids, which can produce atherosclerosis of the coronary microvasculature and ischemia of the myofibril [13, 14]. In addition, higher free fatty acids may facilitate intramyocardial triglycerides accumulation (steatosis) and induction of cellular oxidative stress, as well as the higher activity of nitric oxide synthase and intracellular production of nitric oxide, which leads to myofibril apoptosis.
To our knowledge, the present study is the first to evaluate the role of t2DM on the relation between EAT and longitudinal strain. In this regard, higher values of EAT in subjects with t2DM had previously been reported [10, 15, 16]; while we further observed that most of the subjects with EAT > 4.2 mm and concomitant t2DM showed a limited deformation capacity of the cardiac myofibril (Table 1).
Similar observation was performed by Zhang et al. during comparison between patients with t2DM, where non-controlled t2DM preceded higher Strain values in all spatial directions and controlled t2DM affected only longitudinal Strain .
Furthermore, deformity of myofibrill may be affected by several cardiometabolic risk factors, like weight, BMI and insulin resistance. Consistent with this statement, Liu et al., observed a reduction in left ventricle tension in hypercholesterolemic rabbits, in comparison with normal controls . Likewise, Vitarelli et al., observed a higher deterioration of left ventricle’s myofibril deformation in obese/hypercholesterolemic children and adolescents .
Interestingly, multivariate analysis showed that EAT did not associate with Strain or HbA1c; but with t2DM. This is consistent with findings described by Xiaoling et al. where patients with t2DM had less myocardial deformity, being more evident in patients with HbA1c > 7% .
In the present study, the median value of the Strain was considered as the cut-off value for our analyses, which was lower than the Strain values reported in other studies: − 15.80% to − 23.40% . Such difference could be explained by characteristics of the study population and/or the equipment and software used for the measurements. In addition, EAT cut-off value obtained through ROC analysis or median value, were both useful to discriminate lower myofibril deformity. This is useful since EAT measure may be less complex to obtain than Strain determination.
Limitations of our study include the low number of patients, the lack of T2DM subgroup in male analysis and technological restrictions related with the available echocardiographic equipment, which lacks specific software for Strain determination.
In conclusion, EAT significantly related to myofibril deformation, with additional influence of t2DM.