Cardiac natriuretic peptides such as brain natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP), biomarkers of left ventricular preload [1,2], are well-established biomarkers [2-8] in patients with heart failure, and are both low in obese patients [9,10]. Clearance of BNP occurs via enzymatic breakdown, receptor binding, or renal excretion, and the peripheral BNP level significantly decreases by about 20% compared with that in the left ventricle, as previously reported [11]. NT-proBNP secretion from the heart is regulated by ventricular stretching and/or ventricular preload, and our preliminary data indicated no difference between plasma NT-proBNP in the aortic root (AO) and that in the peripheral vein, suggesting that NT-proBNP is not cleared in the systemic circulation but is mainly cleared by the kidneys [12]. The reason why NT-proBNP levels are low in obese patients remains unknown. In patients with left ventricular dysfunction, both BNP and NT-proBNP correlate with left ventricular end-diastolic pressure (LVEDP) [2], and are biomarkers of left ventricular preload. In patients with constrictive pericarditis or massive pericardial effusion, low BNP and NT-proBNP secretion from the heart result from the disturbance of left ventricular dilatation [13], suggesting that the true left ventricular preload is the left ventricular end-diastolic transmural pressure (LVTMP) [14,15]. Obesity and other chronic inflammatory disorders lead to the accumulation and inflammation of epicardial adipose tissue, which may have important implications for the pathogenesis of coronary atherosclerosis and heart failure [16]. There is a highly significant correlation between the epicardial fat volume (EFV) and body mass index (BMI) [17,18]. Although obese patients exhibit an