In this study we aimed to assess the association of EAT thickness with LVDD in subjects with MetS. Using two-dimensional echocardiography we demonstrated that EAT thickness is significantly associated with LVDD in subjects with MetS, and this association remains after adjusting for age, systolic blood pressure, BMI, blood glucose level, and LDL cholesterol. Importantly, we did not observe this association in subjects without MetS.
The echocardiographic measurement of EAT was proposed and validated by Iacobellis et al. [17, 18]. Several studies have assessed epicardial fat using coronary CT or cardiac magnetic resonance imaging (MRI). However, measuring EAT by echocardiography has several advantages over CT or MRI. It is inexpensive, easier to access, and rapidly applicable especially within clinical practice, and has high reproducibility. Moreover, when compared to CT, echocardiography is radiation-free and free from contrast agent-related side effects. Considering these significant advantages and placed within the context of the current study population, which consisted of subjects without clinical signs or symptoms of heart disease who were self-referred for health exams, the data strongly suggests that the echocardiographic measurement of EAT is preferred to CT.
We found that EAT thickness was greater in subjects with MetS, consistent with previous studies [10, 11, 19]. Our data indicate that EAT thickness is associated with metabolic factors and is correlated with the main anthropometric and clinical parameters of metabolic syndrome [10, 20, 21]. This data is consistent with a previous study that reported EAT thickness increases with an increasing number of MetS components .
MetS is a cluster of several cardiometabolic risk factors and is eventually associated with cardiovascular disease. Visceral obesity and insulin resistance have been proposed as the main underlying mechanism. Both are strongly linked with hypertension, dyslipidemia and atherosclerotic coronary artery disease. In current study, we assessed functional aspect of myocardium rather than vascular disease. To avoid other possible confounding factors, we adjusted cardiometabolic risk factors using multivariate regression model. Our result still showed significant association between EAT and LV diastolic function in presence of MetS. Although the underlying mechanism is not fully understood yet, increased EAT, measured by either CT or echocardiography, has consistently shown independent correlation with impaired diastolic function. Cavalcante et al. reported that epicardial fat volume is an independent correlate of impaired diastolic function after accounting for associated comorbidities . They studied 110 apparently healthy individuals, and found that epicardial fat volume adds increment predictive value for diastolic dysfunction.
Having similar properties and origin with visceral adipose tissue, EAT has been suggested as an active organ producing several proinflammatory and proatherogenic bioactive cytokines [22–24]. Also with its anatomic proximity to the heart without fascial protection inbetween, the possible local interaction via paracrine or vasocrine effect was suggested as a mechanism that causes coronary artery disease or LVDD [1, 3, 25, 26].
As shown in our study, EAT thickness was independently associated with LVDD in subjects with MetS. LVDD is clinically significant and related to poor outcome. This was demonstrated in the longitudinal study of Olmsted County, in which increased all-cause mortality was significantly associated with presence of LVDD . The significance was still present after adjusting for age, gender and ejection fraction.
There are several limitations in our study. First, the measurement of epicardial fat tissue by echocardiography can vary depending on the experience of the cardiologist. To minimize such inter- and intra-observer variability, we repeatedly compared images and had discussions among cardiologists in our center. From these group discussions an overall consensus was drawn on the interpretation of the images. Also, our cardiologists are all well-trained individuals with much experience in echocardiography. Second, since the study is performed as a cross-sectional study, we do not have clinical outcome data. Third, assessing additional biomarkers may help strengthen our findings and aid in the interpretation of our results.