Editorial for “Impact of Type 2 Diabetes Mellitus on Epicardial Adipose Tissue and Myocardial Microcirculation by Cardiovascular Magnetic Resonance in Postmenopausal Women”

Editorial for “Impact of Type 2 Diabetes Mellitus on Epicardial Adipose Tissue and Myocardial Microcirculation by Cardiovascular Magnetic Resonance in Postmenopausal Women” Epicardial adipose tissue (EAT) shares an intimate anatomical association with the myocardium and epicardial vessels. Through shared microcirculation and paracrine signaling, adipocytokines modulate the structure and function of the adjacent myocardium. Under normal physiological conditions, EAT secretes adiponectin, an adipokine that downregulates hypertrophic signals, assists in cell repair, and reduces myocardial inflammation. In disease states, such as obesity or diabetes, expansion of EAT transforms the adipose secretome into an inflammatory and atherogenic substance. Expansion and dysregulation of EAT are increasingly linked to the development of cardiovascular disease including atherosclerosis, microvascular disease, and diastolic dysfunction. In this issue of JMRI, Huang et al present “Impact of Type 2 diabetes mellitus on EAT and myocardial microcirculation by cardiovascular magnetic resonance in postmenopausal women” a retrospective study utilizing cardiac magnetic resonance imaging (MRI) to investigate association between EAT volume and derived parameters of microvascular perfusion. Patients were stratified by the presence and duration of diabetes. A total of 161 post-menopausal women were included in the analysis. There were 48 healthy controls and 113 diabetic patients (56 newly diagnosed, median duration 2 years, IQR: 0.2–4 years; 57 long-term diabetics, median duration 10 years, IQR: 8–14 years). Magnetic resonance evaluation consisted of standard volumetric assessment and EAT volume calculation indexed to body surface area (BSA). Perfusion parameters included upslope, maximum signal intensity, and time to maximal signal intensity as derived from myocardial signal time-intensity curves on first pass perfusion sequences. Demographics and clinical characteristics were well balanced between patient groups. Greater rates of left ventricular (LV) remodeling and higher LV mass indexes were seen in diabetic postmenopausal patients compared to nondiabetic controls. EAT volume was significantly higher in diabetic patients (48.4 13.4 mL/m vs. 58.4 17.3 mL/m vs. 35.8 12.3 mL/m, P <0.001). Within the two diabetic subgroups, longer duration of diabetes had higher EAT volumes than newly diagnosed patients (P = 0.024) implying a possible temporal relationship. Increased rates of microvascular dysfunction were seen within diabetic post-menopausal women with reduced upslope (2.6 1.0 vs. 2.1 0.8 vs. 3.6 1.3, P <0.001), maximal signal intensity (21.4 6.9 vs. 18.7 6.4 vs. 28.4 8.6, P <0.001) and increased time to maximal signal intensity in the longer-term diabetic group (23.6 8.7 vs. 27.1 9.4 vs. 21.4 6.0, P = 0.005). Clinical factors positively associated with increased EAT volume in diabetic patients included age, BMI, hypertension, atrial fibrillation, and LV remodeling. EAT volume (β = 0.610; P = 0.008) and menopausal age (β = 0.433; P = 0.025) were independently correlated with microvascular dysfunction in a multivariate linear regression model. Taken together, these results imply that EAT may represent a novel marker of microvascular dysfunction and therefore a potential future therapeutic target to reduce cardiovascular disease. Although a retrospective cohort study, Huang et al provide an important insight into the strong association between EAT and microvascular dysfunction for which the authors should be commended. It remains to be determined, however, if EAT is causative in the development of microvascular dysfunction or secondary to the abnormal metabolic milieu of diabetes. Future studies examining relationships between EAT and microvascular dysfunction in a younger, nondiabetic cohort may help to elucidate the role of sex hormones, EAT and microvascular dysfunction. Although enlarged and metabolically transformed EAT is described in diabetic patients, this study is the first to