Epicardial and pericardial adiposity without myocardial steatosis in Cushing's syndrome.

CONTEXT Cardiovascular disease is the leading cause of death in patients with Cushing's syndrome. Cortisol excess and adverse metabolic profile could increase cardiac fat, which can subsequently impair cardiac structure and function. OBJECTIVE We aimed to evaluate cardiac fat mass and distribution in patients with Cushing's syndrome. DESIGN In this prospective cross-sectional study 23 patients with Cushing's syndrome and 27 control subjects of comparable age, sex and body-mass-index were investigated by cardiac magnetic resonance imaging and proton spectroscopy. Patients were explored before and after biochemical disease remission. OUTCOME MEASURES Myocardial fat measured by the Dixon method was the main outcome measure. The intramyocardial triglyceride/water ratio measured by spectroscopy and epicardial and pericardial fat volumes were secondary outcome measures. RESULTS No difference was found between patients and controls in intramyocardial lipid content. Epicardial fat mass was increased in patients compared to controls (30.8g/m 2 [20.4;34.8] vs 17.2g/m 2 [13.1;23.5], p<0.0001). Similarly, pericardial fat mass was increased in patients compared to controls (28.3g/m 2 [17.9;38.0] vs 11.4g/m 2 [7.5;19.4], p=0.0035). Sex, HbA1c and presence of hypercortisolism were independent determinants of epicardial fat. Pericardial fat was associated with sex, impaired glucose homeostasis and left ventricular wall thickness. Disease remission decreased epicardial fat mass without affecting pericardial fat. CONCLUSIONS Intramyocardial fat stores are not increased in patients with Cushing's syndrome, despite highly prevalent metabolic syndrome, suggesting increased cortisol-mediated lipid consumption. Cushing's syndrome is associated with marked accumulation of epicardial and pericardial fat. Epicardial adiposity may exert paracrine proinflammatory effects promoting cardiomyopathy. TRIAL REGISTRATION ClinicalTrials.gov, NCT02202902.